“Strong

Medicine by Chris Hardy, D.O. and Marty Gallagher is an exhaustively

researched, clearly written, and practically useful guide to improving your health.
Improving health is fundamentally different than treating disease. This book
represents the future of healthcare in our country. It requires the patient to assume
responsibility, learn the basics, and then enhance their health through diet, exercise,
sleep, and mindfulness.
If you are looking for a quick fix, this is not the book for you. If you understand
that there is no quick fix, then read this book and trust what you read. The
information is accurate and relevant, simple to understand, and actionable.”
—Patrick Roth, M.D., author of The End of Back Pain: Access Your Hidden
Core to Heal Your Body, Chairman of Neurosurgery at Hackensack University
Medical Center and the director of its neurosurgical residency training program.

“In the last 40-50 years we have experienced a huge rise in the chronic diseases
affecting affluent societies across the world. We are generally fatter and less healthy
than we were in the past.
In this impressive new book Chris Hardy and Marty Gallagher take the roles of
doctor and fitness coach to provide us with in-depth understanding about why this is
happening and the steps we need to take to turn this around. This includes a
comprehensive review of the latest scientific research—which is presented in an
easy to understand format. The solution is presented as an integrated ‘Battle Plan’
which includes a detailed and well-explained training regime along with excellent
nutritional advice, which will combine to provide a transformation to a fitter,
stronger, and healthier body. Most importantly they show us the best way to measure
the progress we are making towards this goal.
I would consider this as the most comprehensive and readable book I have seen
on this large topic, and it provides a thorough discussion of evidence to support the
nutritional and exercise advice. Some of the research is very new, and may be
considered controversial. However, this is all presented for the reader to evaluate.
What we have been doing as a society has not been working and this book—with its
many exciting new ideas—may provide the plan to reduce the problems created by
these chronic diseases.”
—Dr. Peter Gootjes, Public Health Medicine Specialist, New Zealand

“Strong Medicine is flat-out amazing. If you ever wanted to take your training
and your nutritional theory to an elite level—better than 99.9% of certified personal
trainers—this is the book for you. It’s all in here: genetics, gut bacteria, cutting-edge
stress biology, molecular nutrition...even better, the ‘deep science’ is all explained
so clearly (with charts, key points, photos and diagrams) that it’s almost impossible
not to understand and absorb it all fully. An automatic classic in the field, which will
surely prove impossible to surpass. I bow down to the Doc and to Marty!”
—Paul Wade, author, Convict Conditioning and Explosive Calisthenics

“Given the sad state of our society’s health and wellness literacy, Strong
Medicine is just what the doctor should order. Chris and Marty come together to
provide the reader with sound information addressing health and wellness from all
angles. Whether it’s the impact of genetics, the use of biomarkers, proper physical
training, the importance of sleep, and/or nutritional information, Strong Medicine
has it covered.
It is time that we restore and strengthen the fabric of our society by arming its
citizens with the understanding of ‘why, instead of allowing them to meander
around in ignorance from one fad to the next. Strong Medicine should be on the
bookshelf of anyone serious about their health and wellness. Gratitude, Chris and
Marty for such a fine reference.”
—Dr. Mike Davis, DPT

“Strong Medicine is a rare gem that is a must-have for anyone who wants to take
control of their health. Chris and Marty have organized an extremely thorough yet
easy to understand encyclopedia on how to maximize your health, fitness and
genetic potential.
In a day and age where we have never been more confused about how to eat, when
to eat, how to exercise and what is right vs wrong, as well as more unfit than ever
before, this is the new Bible for taking control of your life.
Why do I say controlling your life? Because this book is about your health, from
the inside out. No fads, no gimmicks, no “diets” to follow, just the truth about what
you need to do to truly be healthy and fit. Without your health, you have nothing to
enjoy in life.
This book is an essential resource for any fitness enthusiast, health practitioner or
coach.”
—Zach Even-Esh, author, The Encyclopedia of Underground Strength and
Conditioning

“Strong Medicine is one of the most informative books recently published in the
area of human health and fitness. The book not only explains bare-bone principles
of human biology and wellness, it actually translates this knowledge into a practical
strategy—hence ‘The Strong Medicine Lifestyle.’ Well written and backed by
science, Strong Medicine presents important yet controversial and perhaps arguable
concepts in the area of stress response, nutrition and mental/physical conditioning.
Highly recommended to anyone interested in ‘better survival in today’s world’.”
—Ori Hofmekler, author, The Warrior Diet

“Strong Medicine is a declaration of unconventional and asymmetrical war

against mortality. The authors’ weapon of choice is information, relayed
masterfully in the form of an easy-to-understand and richly illustrated owner ’s
manual of sorts. This is an owner ’s manual that is chock full of insights for every
level, from the seasoned physician to the absolute layman who is new to fitness.
For the grizzled coach who doesn’t have medical training, Strong Medicine lays
out crucial performance concepts like ‘hormetic dose’ in ways that are easy to
understand regardless of your background. Dr. Hardy continues with insights into
diet, nutrition myths, biochemistry demystified, intestinal fine-tuning, the chronic
stress connection with disease, and then passes the baton to Marty Gallagher, who
unleashes a plethora of exercise and training tips that are centered around five basic
exercise categories. With well-shot photographs and clear diagrams to illustrate the
important points of each posture, Gallagher lays out a beautiful plan of attack to
combat weakness and mechanical decay, including easy-to-follow training
programs.
This is a book I plan to read & re-read a number of times as both a licensed
medical professional and a strength & conditioning coach.”
—Dr. MARK CHENG, L.Ac., Ph.D, contributing editor, Black Belt Magazine

“I have had the pleasure of being with Marty Gallagher when he delivered the
‘Beta’ version of this book—and I flew home and realized that I needed to start from
zero with my coaching of the basic movements. Combine Marty’s great insights
with the clearest explanation I have ever read that ‘Food is Medicine’ and you have a
one-two punch that changes lives. An amazing book and well worth the time to read
it and digest it (pun intended).”
—Dan John, author, Never Let Go

“Strong Medicine demonstrates the paradigm shift that we currently have in the
world of physical development. We cannot put our fitness goals above our health
goals. Health provides the foundation for fitness to start the process. Fitness in turn
pays back health through maintenance and sustainability. The takeaway for this
book: learn as much about your health as you do about your fitness and you’ll do
just fine.”
—GRAY COOK, author, Movement, co-creator, FMS
 STRONG MEDICINE
How to Conquer Chronic Disease and
Achieve Your Full Genetic Potential

Chris Hardy, D.O. MPH and Marty Gallagher

© Copyright 2015, Chris Hardy and M arty Gallagher
A Dragon Door Publications, Inc. production
All rights under International and Pan-American Copyright conventions.
Published in the U nited States by: Dragon Door Publications, Inc.
5 East County Rd B, #3 • Little Canada, M N 55117
Tel: (651) 487-2180 • Fax: (651) 487-3954
Credit card orders: 1-800-899-5111 • Email: support@dragondoor.com • Website: www.dragondoor.com

ISBN 0-938045-72-5 ISBN 13: 978-0-938045-72-4

This edition first published in Fenbruary, 2015
Printed in China

No part of this book may be reproduced in any form or by any means without the prior written consent of the Publisher, excepting brief quotes used in reviews.

Book design by Derek Brigham • www.dbrigham.com • bigd@dbrigham.com

Graphics concepts by Chris Hardy and Derek Brigham
Cover illustration by Derek Rodenbeck

DISCLAIM ER: The authors and publisher of this material are not responsible in any manner whatsoever for any injury that may occur through following the instructions contained in this material. The activities, physical and
otherwise, described herein for informational purposes only, may be too strenuous or dangerous for some people and the reader(s) should consult a physician before engaging in them. The content of this book is for informational
and educational purposes only and should not be considered medical advice, diagnosis, or treatment. Readers should not disregard, or delay in obtaining, medical advice for any medical condition they may have, and should seek
the assistance of their health care professionals for any such conditions because of information contained within this publication.

Digital book (s) (epub and mobi) produced by Book nook .biz.
 — CONTENTS —
FOREWORD: Honor • Courage • Commitment
by Craig D. Thorne, M.D., MPH, MBA
PREFACE: Messages from the Authors
INTRODUCTION

Phase I: Basic Training

Basic Training I—Central Themes
• Inflammation and Oxidative Stress
• The Gene-Environment Connection
• Hormesis
• The Stress Response
• Allostasis—“The Stress Cup”
Basic Training II—Nutrition and Metabolism 101
• Introduction
• Macronutrients
• Metabolism Basics

Phase II: Knowing the Enemy

Knowing the Enemy I—The Gut: Guardian at the Gate
• Gut Health: First Principles
• Triggers of Intestinal Inflammation
• Conclusion
Knowing the Enemy II—Obesity: The Enemy Within
• Introduction: A Big Fat Problem
• The Fat Cell: Dr. Jekyll becomes Mr. Hyde
• The Plague of “Diabesity”
• How We Get Fat: the brain, hormones, and appetite
 • Intervention: The 8-step program for obesity and diabetes
Knowing the Enemy III—Chronic Stress: The Silent Killer
• Mind and Body: Descartes was wrong
• Stress and Health
• Mind Interventions: Brain Training
Knowing the Enemy IV—Circadian Disruption: Thief in the Night
• The Internal Timekeeper
• Sleep Architecture
• Edison’s Folly?
• Modern Solutions for a Modern Problem

Phase 3: BATTLE PLAN

Battle Plan I—Strong Medicine Physical Training
• Introduction
• Strong Medicine Resistance Training
• Strong Medicine Basic Cardio
• Strong Medicine Advanced Cardio
Battle Plan II—Strong Medicine Nutrition
• Food Sources and Quality
• Carbohydrate Tolerance
• Feed your activity
• A Week of Food
Battle Plan III—Putting It All Together
• Lifestyle Change: “The Neck of Roy Buchanan’s Guitar”
• Strong Medicine Lifestyle Change-Strategic Planning
Battle Plan IV—“Stuff You Can Measure”
• Introduction- biomarkers and the “Holy Grail”
• Cholesterol: What are we measuring?
• Physical Measurement
• Markers of Inflammation
 • Heart Rate Variability
Epilogue
About the Authors
Acknowledgements
Index
FOREWORD

HONOR • COURAGE • COMMITMENT

Those are the bedrock principles of the United States Navy. These values have
guided the strong men and women of the Navy to successfully meet all of their
challenges since it began during the American Revolution, even with a few small
ships, all the way to the large, powerful fleets and global reach of today.

The health and fitness communities are filled with many committed enthusiasts
who devote their time and efforts in educating and training the public towards better
habits and wellness. But few have the personal, proven experience to present fact-
based evidence that blends nutrition, exercise, and psychological truths into
strategies and techniques to truly “transform” us physically and mentally. The
authors of Strong Medicine have this rare blend of foundational scientific theory
and real-world empiricism.

Chris Hardy, the ‘doctor ’ co-author of Strong Medicine served in the Navy as a
medical officer for nearly a decade, and still holds those values very closely in his
personal daily mission to share his expertise in nutrition, strength and conditioning.
In addition to his specialty training in preventive and integrative medicine, and his
advanced public health achievements, he is also a certified strength and conditioning
specialist.

Marty Gallagher, the ‘coach’ co-author has been involved in high level sports and
athletics for over 50 years now, capturing his first national title and national records
as an Olympic weight lifter when he was only seventeen year old. In May, 2013 he
set his most recent national records as a 64 year-old power lifter. Marty is not only a
peerless athlete, coach, and writer, he is also the embodiment of “successful aging”,
achieving and maintaining physical and mental abilities superior to many who are
40 years younger.

In Strong Medicine, Chris and Marty have combined their disciplines and their
experiences and have applied a modern day military theme to provide a compelling
structure to help even those of us that lead regular lives to successfully change our
lifestyle habits for the long-term.

In our own daily lives, we experience so many threats to our physical and
psychological well-being (think of them as modern day “predators”): the pressure
to succeed in stressful work environments, commuting in traffic congestion, poor
and over nutrition with processed foods, financial pressures in a consumer-driven
environment, and even the pressure to pursue meaningful recreation and relief from
anxiety. The list goes on and on. The concomitant increasing prevalence of chronic,
deadly diseases such as obesity, diabetes, high blood pressure, heart disease, cancer
and so many more “lifestyle” conditions puts an intense spotlight on interventions
that can help turn this tide. While some of these are the result of structural and
societal changes, many are the result of individual choices and poor habits that
wreak havoc on our bodies and minds over time and rob us of our full potential for
long, healthy and productive lives.

But we have much untapped ability to change many of the antecedents and
conditions that lead to premature chronic disease and disability and help us achieve
our full genetic potential. In this information age, there are countless guides to self-
improvement, and diet fads and fitness boots camps are abounding. Chris and Marty
help us replace such “information overload” with user-friendly “know your enemy”
information and evidence-based habits and actions so that we can commit to
sustainable and manageable change.

Think about this as you read Strong Medicine:

HONOR
“I will bear true faith and allegiance…”. For the Navy, this means that officers
need to make honest recommendations and be truthful in their dealings with each
other, and with those outside the Navy. Officers should also encourage new ideas,
take responsibility for their own actions, fulfill and exceed their responsibilities, and
be mindful of their privilege to serve their fellow Americans. In Strong Medicine, the
authors provide an in-depth series of recommendations based on scientific literature
and other up-to-date information so that readers can honor themselves with the
correct information to make their own transformation.

COURAGE
“I will support and defend…” means to have the courage to meet the demands of
the mission when it is demanding or otherwise difficult. It also means ensuring that
the resources entrusted to officers are used by them in a careful and efficient way.
Lifestyle change can be daunting. This book not only provides us with the
knowledge needed to prevent disease and achieve better health but also a
transformational roadmap, both physical and psychological, that can help us find the
courage within to make the changes needed, and self-program new habits without
being overwhelmed.

COMMITMENT
“I will obey…” means to care for safety, professional, personal and spiritual well-
being of self and others, and be committed to positive change and constant
improvement. Commit to reading this book without rushing any section or trying to
take short cuts, and don’t reject out of hand any parts of the holistic expert advice
that it offers you.

Now take your time to read this book as I did, beginning with basic training, then
knowing the enemy, and continue reading and using the knowledge and practical
strategies presented all the way to the end (your new beginning) to do a crucial self-
assessment to build your own battle plan. Consider all the rock-solid scientific
principles presented as user-friendly quick medical notes, take home messages,
coach’s corner notes, and even the gourmet organic recipes …. Then use all this
latest intelligence together to honor your own life. You won’t regret it!

Craig D. Thorne, M.D., MPH, MBA, Internal Medicine/Preventive Medicine

Health Educator, Avid Runner and Lifelong Learner

Assistant Clinical Professor, Johns Hopkins Bloomberg School of Public Health

Vice President and Medical Director, Employee Health and Wellness, Erickson
Living

Washington, D.C.

November 2014
PREFACE

L et us be honest. Most of us buy diet and exercise books because we want to have a
better body. We are motivated to become involved with diet and exercise in an
attempt to change the shape and configuration of our physique. We are dissatisfied
with how we look and feel.

We are hard-wired by Nature. She has programed us to try to look and feel
attractive. We seek to attract mates and reproduce in order for our species to
survive. We need to recognize this underlying inborn need. The quest for self-
improvement is inherent and not rooted in vanity. This primal drive to attract a mate
and reproduce is the reason there is currently a multi-billion dollar industry
dedicated to dieting and “losing weight.”

Individuals spend large amounts of money every year looking for the elusive
Holy Grail of dieting and exercise plans. The truth is that all diets work and all
diets eventually fail. There is even documentation of people losing weight eating
nothing but Twinkies. If calories are restricted, body weight will be lost in the short-
term, but every “diet” invented eventually fails without exception. Dieters gain their
lost weight back—and then some. The diet industry wants the cycle of losing and
gaining to continue; it is good for business.

The exercise scene is no better. Everyone wants to follow the latest “bootcamp
style beat-down” exercise program. These programs often result in injury, burnout,
or both after a couple of months. Then, the once-enthusiastic trainee looks for the
next fitness guru to whip them into shape again to achieve the beach body of their
dreams.

The real “inconvenient truth” is that the only way for sustainable physical
transformation to occur is through lifestyle change—changing your eating and
exercise habits long-term. We will show you how to achieve your body composition
goals without starvation diets or sacrificing taste. We will show you how to build a
strong and lean body, and how to produce a physical foundation to both achieve
your fitness goals and slow the physical degeneration of aging.

The methods for achieving these physical goals are all here in Strong Medicine,
but there is a loftier purpose to this book.

Jim Morrison said, “No one here gets out alive.” Indeed the years of our lives are
a precious gift. The quality of our lives—how we live in the time we have—is
paramount. Too many of us are robbed of the irreplaceable years of our lives, by
dying prematurely from preventable chronic diseases. An equal number live their
later years in severely debilitated states of body and mind. The epidemic of chronic
disease is expanding at an alarming rate.

The military theme of this book may seem over the top to some. In our view it is
entirely appropriate given what we are facing. Make no mistake, chronic
preventable disease is killing many more people on earth every year than the total
casualties of past world wars. Diseases such as diabetes, high blood pressure, heart
disease, neurodegenerative disease (Alzheimer ’s), cancer, and obesity are the true
modern enemies. A battle plan is needed.

These diseases do not kill in the dramatic manner of bomb and bullet, but are still
just as deadly. These insidious killers wreak havoc on our bodies and minds. Many
of us have friends and family succumbing to these killers. The slow metabolic
destruction of diabetes or neurodegenerative diseases such as Alzheimer ’s dementia
rob our loved ones of the very essence of who they are (or were).

We need to pull our collective heads from the sand and look up from our
smartphones for just a minute. We need a call to action shocking us out of
complacency. Sustainable lifestyle change based on firm underlying scientific
principles is the only way to truly fight the epidemic of chronic disease while
simultaneously achieving the aesthetic physical changes we desire.
 To achieve sustainable lifestyle change you must understand the foundations on
which the recommended changes are built. We will teach you the scientific and
theoretical foundations for transformative lifestyle change. If we do not take the
time to teach you why we recommend something, we are no different from the
thousands of programs out there that just say “do this” without explanation.

If you just want to be told what to do without understanding why, you are doomed
to continue being led around by the nose by the latest fitness guru, and wandering
from diet to diet in ignorance, wondering why you continue to fail.

We will provide the tools and strategies you need to generate progress. Those
who take the plunge and institute our tactics will feel better by the end of the first
week, and will see tangible changes in body composition by the end of the second
week. Friends and family will comment on the “incredible change” at the end of the
first month. You can and will undergo an utter and complete physical and
physiological transformation in three months—90 days—without any draconian
training or concentration camp nutrition.

This book provides a framework that regular people leading regular lives can
perform at home. Strong Medicine is a roadmap that leads the serious individual
from unhealthy and uncertain into ever-improving levels of health, wellness and
fitness.

Because we are all individuals with individual needs, we have left out a certain
amount of specificity with our recommendations. This is done for a reason. You
will have to experiment and individualize our tactics to your needs; we are giving
you a foundation.

Strong Medicine offers you the opportunity to self-assess and create a

customized template that can and will enable you to transform towards the healthy
state-of-being that has eluded you for so long. You are holding the handbook of
transformation, but you have to use it. Once you understand the concepts and grasp
the consequences (of your lifestyle choices) the burden is on you. End the blame
game; let us take responsibility for our actions and choices.

We need one thing from those that seek radical transformation—a burning desire
to change. To change the body we must first change our mind. Every thwarted
physical and health goal you ever had lies within your reach.

There are no shortcuts...

DOCTOR’S RX
American society is facing a bank-busting, people-crushing crisis in which “we
the people” are uniformly unfit, unhealthy, unhappy and sickly. We continue to have
skyrocketing, out-of-control growth in preventable chronic disease. As a flat
statement of fact, this bleeding artery could bankrupt our economy. We need a
reality check:

• In 1965, the United States spent 5% of the gross domestic product on health care
expenses. For every $1 produced by the USA, only a nickel was spent on health
care during this time.
• In 2010 this grew to 17% of GDP.
• In 2030 we will spend 25% of GDP on health care expenses; for every dollar
made, a quarter will be spent on medical care.
• The United States spends more on health care per citizen than any other country
in the world, but we are ranked 37th for the effectiveness of our health care
system.

We spend more money on health care and have the most advanced diagnostic
tools and technologies found anywhere in the world. But we are still failing
miserably at treating the diseases that are costing us the most, both in human
suffering and monetary cost.

The majority of health care dollars are spent on the treatment of preventable
diseases: obesity, diabetes, and heart disease. Cancer is responsible for a
significant amount of resources and suffering, yet many cancers are preventable as
well.

Health care analysts give multiple reasons why we are spending ever more
managing these diseases and predictably point to the growing aging population,
costs of medications, costs of testing, and inefficiencies in providing medical care.
An alarming number of healthcare professionals have simply given up on the idea
of preventing these diseases.

Managing diabetes, obesity, and heart disease is incredibly expensive, but for the
most part, we should not have to manage these diseases long-term. They are
preventable and for the most part, reversible.

It has not been for lack of trying. The Public Health community is filled with
many talented and dedicated people who work daily attempting to improve public
health through prevention. Billions of dollars are spent yearly on failed (often
doomed before they start) public health campaigns. This begs the question: why do
we continue to fail? It certainly is not for a lack of funding or effort.

Why do we continue to have ever-expanding growth rates in preventable chronic

disease despite public health efforts?

Logic dictates that there are 4 possible answers to this question:

1. THE MESSAGES/RECOMMENDATIONS FOR PREVENTION

ARE WRONG
Many of the messages are sound, but there are an unacceptable number of
preventative recommendations based on outdated science that are flawed from their
foundation.

2. COMMUNICATION IS FLAWED AND INEFFECTIVE

Public health authorities seldom explain “why” people should follow the
recommendations in ways that can be easily understood, while still maintaining a
sound scientific foundation. Public health officials usually underestimate the
sophistication of the general public. The problem is not the public’s inability to
grasp physiologic concepts, it is the public health and medical community’s
inability to effectively communicate these concepts. Let us (public health) not blame
the public for our short-comings.

3. PEOPLE ARE CONFUSED BY CONFLICTING HEALTH

RECOMMENDATIONS
There is a tremendous amount of inconsistent information coming from
“authoritative” sources, which is then further jumbled by popular media (internet,
news media, etc.).

4. PEOPLE ARE UNWILLING TO CHANGE

Stopping preventable diseases usually requires lifestyle changes that many seem
unwilling to make. In an oversimplification: many people are addicted to the
substances, foods, lifestyle and habits that created their preventable disease.

The core essence of this book is the identification, and effective communication
of underlying causes of preventable health problems. We then present informed,
practical solutions that empower the reader. This empowerment and resulting self-
efficacy is essential, as many of us cannot rely on our health care providers to teach
us this type of information.

DOCERE?
The U.S. healthcare system is currently at a crossroads. A 15-minute doctor ’s
office visit is becoming the norm, driven by the economic realities of a failing
system. There is simply not enough time available for the physician to provide
detailed preventive education in an individualized manner. The word “doctor” is
from the original Latin docere, which means, “to teach.” Most of us who have
experienced a recent visit with their doctor would probably agree that there is very
little doctor-to-patient teaching happening in modern medicine. Most of the doctor ’s
time is spent managing medications to treat lab values instead of really treating the
patient—much less providing any individualized education on prevention. If given
the time, do most physicians currently have the education to impart this type of
preventive teaching?

PRIMUM NON NOCERE (FIRST DO NO

HARM)
The public trusts the opinions and recommendations given by their health care
providers. Unfortunately, most physicians simply do not have the expertise to give
science-based recommendations regarding nutrition and exercise; but do so anyway.
It is ironic that the medical education of our physicians devotes almost no time to
learning exercise science and nutrition. Instead, most of their time is spent learning
the use of pharmaceuticals. Chronic diseases are not cured by drugs, they are only
managed. Lifestyle changes such as proper nutrition and exercise can and do cure
many chronic diseases. Why are our physicians not better educated to put these
interventions into practice?

Too many doctors are put on pedestals by the public and viewed as all-knowing
oracles possessing papal-like infallibility. Obviously this is nonsense, especially
when it comes to exercise and nutrition. Many of my colleagues are just parroting
what they have heard about nutrition and exercise and pass this on to their patients.
They do not truly understand the subjects from the ground up like they do
pharmaceuticals.

Also, many doctors have long since forgotten the basics of biochemistry,
anatomy and physiology learned in medical school. If we are going to practice
prevention and health promotion, we as a profession have an obligation to really
learn our craft from the ground up, using basic science as a starting point. We need
to use a “first principles” foundational approach to critically examine current
orthodox recommendations. Physicians that use basic science as a foundation for
critical thinking about wellness practice can be invaluable in this respect.

IT’S YOUR FAULT TOO...

On the flip side, there is also a serious lack of elementary scientific literacy in
our society. I do not buy the excuse that a basic working knowledge of the human
body is beyond the grasp of most people. I know plenty of people who know
EVERY detail about baseball and football statistics—without being a pro athlete.
Countless men have an extensive knowledge of the mechanical workings of an
automobile engines—yet learning a little about how your body works is somehow
past our mental capacities? I think not.

We all NEED a basic working knowledge of the body to inform our lifestyle
choices and preventive strategies; how else can we be true partners in our own
health care?

PREAMBLE TO PREVENTION

We are all individuals with individual needs and goals, but we all belong to the
human species. So, the underlying principles of biochemistry and physiology still
apply to all of us. We will show you how to use these ‘guiding principles’ placed
within a central framework that still allows for individuality. This framework also
allows for the incorporation of exciting new scientific advances. As long as we
build on a solid foundation of underlying principles, subtle changes are easy to
make. If we need to remodel our approach as new information comes to light, no
worries—we have built our house on a strong foundation.

This is not a “lose weight quick book,” though your physical transformation will
be profound through consistent application of the principles and tactics presented
within. We are after sustainable and long-term health, not quick fixes. The goal is to
empower the reader and enable anyone to achieve their health and fitness goals
while joining the larger fight against chronic disease.

Chris Hardy — Pacific Northwest, 2014

THE COACH’S PERSPECTIVE:
IMPROVING THE FLESH MACHINE
During the Dark Ages, trade guilds emerged as craftsman bonded together to
share trade secrets. Rather than hording information, these men recognized that they
all had a common quest and by combining their collective knowledge, they could
dramatically “up” their level of collective expertise. A rising tide lifts all boats.
When a guild is formed and functioning, the tradecraft always improves.

Our guild is a group of likeminded individuals drawn together by a common

quest: how best to heal, detoxify, mold and sculpt the human body while amplifying
every athletic and health attribute. My little sliver of expertise is human performance
and how to improve it. My job entails working with the world’s best strength
athletes and finest spec ops soldiers. My role is to make the best in the world better.

The irreducible core of our guild is a doctor and a coach who are of one mind.
We want to share techniques, strategies, tactics and philosophies that actually work.
The doctor and coach have seventy years of combined experience, each operating in
distinctly different worlds—but are drawn together by the gravitational pull of
physical improvement. Not imagined or subjective improvement, but dramatic and
objective improvement.

The path of progress in each of our parallel universes (medicine and high level
athletics) eventually intersected. The doctor and the coach met, compared notes and
were struck by how the knowledge gleaned from each other ’s world upped their
own game—the coach became a better coach and the doctor became a better doctor.

This book is a transformational handbook based on proven tactics and rock-solid

science. “Strong Medicine” is the result of our alliance working in full-flight. We
have a creative synergy that allows us to describe and prescribe techniques and
tactics that are immediately useable by motivated readers.

We are big on motivation. Give me a motivated, fired-up, morbidly obese

individual over a nonchalant elite athlete any day of the week. For the truly
motivated individual lucky enough to stumble across our methodology,
transformation is not a matter of “if,” it is “when.”

Members of our guild all seek physiological improvement—across the board.

Name a physiological benchmark or category and we will start thinking about ways
to improve that capacity or benchmark. That is what we do for a living. In our world
of uber-elite military and world-class athletics, results are the only thing that matter
and the only thing that earns repeat business. We have a ton of repeat business.

We have extensive experience in engineering physical transformations; we churn

out renovated humans like Chrysler churns out Dodge Vipers. Our results are based
on the skillful blending of exercise, diet, psychology, and decades of empirical
experience. Our insider techniques and non-traditional, counterintuitive tactics are
unknown outside of a small circle of uber-elite military spec ops warriors, world-
class strength athletes, outside-the-box coaches, renegade scientists, and innovative
medical professionals.

Members of our guild-alliance all are concerned with the same eternal core
problem: how do we improve the form and function of the human body?

Any and all aspects of fitness, all of remedial medicine, every diet and exercise
tool, each and every fitness device, health profession, athletic tactic, strategy or
approach—all were created to improve the human condition in some way. The core
question is, “How exactly do we improve the human condition?” How do we
improve the form and function of—as William Burroughs labeled the human body
—“The Flesh Machine.”

Our guild is at the exact intersection of cutting-edge science and real-world

medicine melded with high-level athletics, results-producing coaching, and elite
military preparedness training.

We combine tactics from both worlds and process these volatile methods to make
them user-friendly for regular people. Our challenge was to achieve this ‘user-
friendliness’ without compromising the vital, effective essence of each protocol. We
have met this challenge by creating a multitier system that allows anyone at any
fitness level to participate.

We offer a game plan for the few with the gumption to put these ideas into
practice. It is an indisputable fact that the methods and methodologies we are
presenting work—these exact strategies are being used right now by the best in the
world.

The Tao of fitness exists and we can show you “The Way.” We can show you how
to custom design your very own transformational template—but you need to learn
some science and biology ultra-basics to be successful. We will teach you “The
Process.”
 In our world you do not get to skip ahead to the training, eating, and fun stuff
without first getting the scientific, medical, and biological facts straight. We are
teaching you how to fish—we are tired of giving you fish.

Marty Gallagher — Pennsylvania, USA, 2014

 INTRODUCTION

We are at war, and we are losing. We are losing badly. This is not a war
against countries or ideologies. This war is not fought with bullets and bombs,
but with pharmaceuticals. The frontlines of the battleground are our hospitals,
clinics, and local doctors’ offices. This is a worldwide war against chronic
disease and there are few places on Earth left untouched. The enemy is upon us
in full force and the frontlines are collapsing.

Despite being equipped with the most technologically advanced weapons, our best
soldiers—the medical professionals—seem unable to push back and destroy the
enemy. At best, they are only slowing the advance of this faceless adversary. We are
throwing more and more resources into the war effort and are still failing
miserably. The situation seems hopeless, as the war-effort is bankrupting us.

We need your help as the last and best hope for pushing back the relentless
advance of chronic disease. To become an effective fighter in this war, you will
need training. We have to teach you how the enemy works from the inside out. You
must understand the enemy before you can effectively fight and decisively win. This
war will be fought one small battle at a time, by one individual at a time. You are the
last line of defense and can become the key to ultimate victory.

You will be rewarded for your courage and effort with the optimum health of your
mind and body. You will emerge from your training with the physical appearance,
fitness, and vitality that mirrors your full genetic potential. Join us in this fight. You
are needed.
PHASE I: BASIC TRAINING
Strong Medicine Basic Training is not easy, but can be accomplished by anyone
with the requisite motivation. The foundations of your training are the central
themes that underlie health and disease, and a primer on nutritional science and
human metabolism.

It is important to have a basic understanding of this section to prepare you for the
battle ahead. You will be introduced to concepts which may not be familiar.

There is quite a bit of information in Strong Medicine Basic Training, so spend

some time here. Do not worry if you don’t get it all the first time through, because
we will reinforce this training throughout the book. We do not expect the new
Strong Medicine trainee to become a warrior overnight.

While you are learning the fundamentals in basic training, we will also give you
an early taste of the Strong Medicine Defensive Tactics. These tactics can
immediately be put into action against the enemy—even without the full knowledge
of the adversary. The Strong Medicine recruit who graduates from basic training
will be ready for advanced training to understand the enemy and advanced tactics to
stop chronic disease and optimize health.
PHASE II: KNOWING THE ENEMY
Your Strong Medicine trainers know the enemy. We have gathered the military
intelligence and analyzed their weaknesses. We know the chinks in their armor. We
will systematically impart this knowledge to you, as you are no longer a recruit, but
still have a lot to learn before you can lead your own forces into battle.

You will get in-depth defensive tactics, and will understand the reasons behind our
tactics. Our tactics are graded as gold, silver, and bronze. The gold tactics are
particularly devastating to the enemy and should be mastered early on. The silver
and bronze tactics are very effective as well, and will ensure chronic disease stays
down once it is put down.

During this phase of your training we will periodically bring out Coach
Gallagher to give you a reality check. He is a master Strong Medicine trainer and
coach. He is rough around the edges but will give you the brutal truth without
political correctness—something we need to hear from time to time.

Once you have gained the requisite knowledge about the enemy, you are ready to
put your training into practice. You will be able to turn the Strong Medicine
Defensive Tactics into a devastating offensive strategy against chronic disease.
PHASE III: BATTLE PLAN
We will formulate the Strong Medicine battle plan in Phase III. This plan will be
drawn from the knowledge and tactics you learned in Phases I and II. We will show
you how to individualize a plan that is optimum for you.

Phase III will also give you a stripped down but highly effective physical training
program using original techniques and expert tactics to transform a flaccid body
into a chiseled and powerful war machine worthy of a Strong Medicine Warrior.

You will also get a short section on measurable analytics for monitoring the
inner workings of your “flesh machine” and keeping you on the right track.

We have included the “military intelligence” we gathered on the enemy and the
foundations for our tactics in the scientific references at the end of each chapter for
your further reading and research if desired. These references are the sources and
scientific foundation on which we have built your training program.

The science is always kept as basic as possible in Strong Medicine without losing
the meaning, but trainees who want more should look for the Digging Deeper and
Technical Note boxes throughout the book.

Those of you willing to enlist and join us in the war on chronic disease, let us get
to it. Be a participant in this fight, not a casualty. Strong Medicine Basic Training
awaits...
 PART I

BASIC TRAINING
BASIC TRAINING I:
CENTRAL THEMES IN DISEASE AND
HEALTH

This section teaches the rules of war before you hit the battlefield. Some of the
concepts may be brand new to you, but it is important to spend some time here
before moving on. If you do not quite get this section the first time through, do not
worry, we will return to these five themes throughout your training. These themes
are the underlying foundations of our defensive tactics against chronic disease, and
form our template for achieving your genetic potential for health and fitness.

1. Inflammation and Oxidative Stress

2. The Gene-Environment Connection
3. Hormesis
4. The Stress Response
5. Allostasis and the “Stress Cup”

We will start with inflammation and oxidative stress. These two processes are the
underlying causes of most (if not all) preventable chronic diseases. It is crucial to
understand how they work. Get to work recruit!
CENTRAL THEMES PART I:
INFLAMMATION AND OXIDATIVE
STRESS

THE 4 CARDINAL SIGNS OF INFLAMMATION:

1. Redness (Rubor)
2. Heat (Calor)
3. Swelling (Tumor)
4. Pain (Dolor)

Two interrelated physiologic processes—inflammation and oxidative stress—

are recurrent themes in this book. These two processes are at the same time crucial
to our survival as an organism and underlying causes of disease.

INFLAMMATION
The inflammatory response is directed by cells in our immune system and is
absolutely essential to heal from injury and to combat infectious diseases.

During an acute injury or infection, redness and heat are produced from
increased blood flow to the area. Swelling is the result of fluid and protein
“leaking” from the blood vessels into the tissue. Pain results from the stimulation of
nerve endings by certain chemical “messengers” called cytokines released by
immune cells. This process can last for several days while the “battle” to clear the
invading infection takes place, or the cells damaged from an injury are cleared.
After the “battle,” things slowly return to normal. This is the basic process of acute
inflammation.

The primary generator of inflammation (and resulting oxidative stress) in our

bodies is the immune system. A basic survey of the immune system is in order. The
immune system is incredibly complex, and we will simplify immunological
concepts without drowning in the details.

IMMUNOLOGY 101

The Guardian
The cells of the Innate Immune System are like the guards at the castle gate.
They deal with anyone who “looks or acts suspicious.” In practical terms, this could
be an initial encounter with bacteria/viruses or “foreign” protein fragments. The
innate immune response is not targeted at specific antigens (targets), but is a general
protective response to anything “foreign.” Innate immune cells like dendritic cells
or macrophages can “take” foreign invaders “prisoner”, destroy them, and display
pieces of the prisoners like heads impaled on pikes mounted on the castle wall.
Some of these guardians also release inflammatory chemicals called cytokines.
 The Adaptive Assassin

Cells of the Adaptive Immune System are like assassins. They are known as T-
cells and B-cells. Once they encounter pieces of a prisoner caught by the dendritic
cells or macrophages of the innate immune system, they “adapt” themselves to
become perfect assassins for this specific type of prisoner.

The assassins target the specific patterns of proteins (antigens) unique to this
“prisoner” for destruction. Then they clone themselves to make an army of
assassins with one goal—destruction of this specific type of prisoner. These death-
dealing clones spread throughout the body and wait to encounter another invader
with a protein pattern identical to the original prisoner.

The Assassin Clone Army

These assassins are persistent, and wait in the shadows for their target to appear
again. Once they encounter their prey, they release a barrage of destructive power in
the form of antibodies and inflammatory cytokines.

 The T-regulatory cell
hippie preaching tolerance:
“Just stop the
violence man!”

It is important to note that the immune system is not completely devoted to

destruction. There is a type of T-cell in the adaptive immune system that helps
control the assassins and produces an anti-inflammatory response. This type of T-
cell is called a T-regulatory cell (Treg). Treg cells are like hippie antiwar
protesters. We need a balance between protesters and assassins to prevent the
immune system from attacking our own body tissues. Autoimmunity is the process
of the immune system attacking the body.

The immune system generates and controls the acute inflammatory response
needed for the beneficial functions of proper wound healing, fighting infection, and
recovery from exercise. Chronic inflammation is also generated by the immune
system in a process that is similar to acute inflammation, but instead of stopping
after several days, it continues for much longer.

KEY POINT:
Chronic inflammation is the result of continuous stimulation of the
immune system. The constant release of inflammatory “cytokine”
chemical messengers wreak havoc on the body and your health.
 MEDICAL TRIVIA:
It is estimated that 70-80% of our immune system lives in our intestinal
tract (our “gut”).

OXIDATIVE STRESS
Working in tandem with inflammation is oxidative stress. Most of us have seen
rust on old cars. Rust is the oxidative process at work on metal alloys containing
iron. In the presence of moisture, oxygen in the environment reacts with iron to
produce rust. Oxidation reactions also occur in our bodies. They are essential
processes in our physiology—unless they get out of control.

The oxygen free radical (also called reactive oxygen species, ROS) is a type of
molecule that causes oxidation and oxidative stress. ROS can form from various
external and internal stressors such as pollution, infection, radiation, and cigarette
smoking. ROS molecules are also products of normal metabolism in our cells.
Many processed foods contain ingredients prone to oxidation, and can increase
oxidative stress far beyond normal levels.

Chemically speaking, stable molecules have electrons that travel in pairs, but a
free radical is a molecule that has a lone unpaired electron. This unpaired electron
makes the molecule extremely unstable and chemically reactive. This type of
molecule really “wants” to pair another electron with the lone electron and will take
an electron from a nearby molecule. “Stealing” an electron from a neighboring
molecule will damage structures like cell membranes and even DNA. Long-term
DNA damage by free radicals can cause mutations leading to cancer.
The Antioxidant Defense System (ADS). This is your body’s way of dealing with
free radicals (oxidative stress). They are the “bouncers in the bar.”

The “Free Radical” drunk guy thinks he is a superhero by the end of the night,
looking for some action.

QUICK FACT:
You can think of the free radical as a drunk guy in a bar looking for a
fight. The body has mechanisms to deal with free radicals called the
 antioxidant defense systems (ADS). These systems are like bouncers in
the bar who take the drunk outside before he hurts anyone.

The balance in the body between the free radicals and the antioxidant systems
determines oxidative stress. A couple of drunk guys can make the club experience
somewhat entertaining for the other patrons, but the bouncers (ADS) will take care
of them in short order.

The ADS “bouncer” taking out the trash... a couple of free radicals are no
problem.

If the free radicals overwhelm the antioxidant defense systems (the bouncers),
there is a state of high oxidative stress. The state of high oxidative stress is the result
of free radicals starting chain reactions. The chain reactions form large amounts of
new free radicals—like a drunk who starts a bar fight that the bouncers cannot
control. A free radical chain reaction can damage the membrane of a cell and lead to
destruction of the cell. On a larger scale, it can damage your health.
 High oxidative stress overwhelms the ADS “bouncer”

THE DELICATE BALANCE OF OXIDATIVE STRESS

The antioxidant system attempts to counteract free radicals generated internally

by physiologic processes and externally from the environment (food, water, toxins,
etc.). This balance is a constant push-pull process. Tipping the balance toward free
radical generation increases oxidative stress and the antioxidant system quickly
responds. Spending too much time in either direction is not a good thing long-term.
The body actually needs some oxidative stress to maintain health, but not too
much. Too much oxidative stress creates disease.
 KEY POINT:
It is very important to understand that some inflammation and oxidative
stress is normal, necessary, and even beneficial. This beneficial “dose”
of inflammation and oxidative stress works through a process called
hormesis, part of the positive adaptation to stress known as allostasis.
Low “doses” of oxidative stress may even extend our life span.

Some beneficial effects of inflammation and oxidative stress:

1. Our immune system makes use of inflammation and oxidative stress in
a controlled manner to kill invading micro-organisms.
2. Exercise and some compounds in fruit and vegetables contribute to
beneficial inflammation and oxidative stress.

Normal physiologic processes like metabolism of glucose and fats create free
radicals (ROS). Your antioxidant systems can usually deal with these free radicals
(except in the case of diabetes). A properly working immune system generates
inflammation and oxidative stress to fight microbial invaders. Increased oxidative
stress from the outside environment can also stimulate the immune system to
produce inflammation. Inflammation and oxidative stress always travel together.

“Importing” free radicals by eating rancid fats from processed foods adds extra
oxidative stress that your system may not be able to control. Conversely, eating
organic vegetables and fruit can stimulate the body’s internal antioxidant systems
(ADS), making them stronger, more resilient, and more resistant to inflammation
and out-of-control free radicals.

KEY POINT:
Where there is oxidative stress there is inflammation. Where there is
inflammation there is oxidative stress. The two processes are inseparable.
DURATION MAKES ALL THE DIFFERENCE...
Short-term increases in inflammation and oxidative stress are necessary, normal,
and even beneficial.

Short term, low levels of oxidative stress are beneficial.

Intermittent short-term inflammation and oxidative stress are essential for proper
functioning and defense of your body. However, if these processes continue for
long periods of time, disease develops. Long-term inflammation and oxidative
stress are the underlying causes for chronic preventable diseases.

The “link” in the chain from the underlying sources (the enemy) to chronic
oxidative stress and inflammation resulting in chronic preventable disease.
 You will see the central theme of chronic inflammation and oxidative stress as
underlying causes of disease throughout the book. In later chapters, we will focus
on the sources of chronic inflammation and oxidative stress. These sources are the
underlying causes “linked” to chronic inflammation and oxidative stress and the
resulting chronic diseases. These sources are the enemy that we are fighting.

KEY POINT:
Heart disease, diabetes, cancer, high blood pressure, neurodegenerative
diseases (Alzheimer ’s), asthma, and accelerated aging all have chronic
inflammation and oxidative stress as underlying causes.

 STRONG MEDICINE
Strong Medicine is all about breaking the link between the enemy sources
of chronic inflammation and oxidative stress, thus preventing chronic
disease. We will identify the enemy in Phase II of your training.

Most chronic inflammation and oxidative stress which cause preventable diseases
are the result of our body trying to adapt to the outside “environment.” This
environment includes...

• The food we eat.

• The quality of our sleep.
• Our physical activity.
• The stress in our lives.

Our environment reacts directly with the genetic code contained in our DNA, and
affects the way our body functions in health and disease. As modern humans, we can
control many aspects of our environment, therefore we have the potential to control
how our genes are expressed in a way to optimize health and achieve our fitness
goals. The next section will describe just how this works.
CENTRAL THEMES PART II:
THE GENE-ENVIRONMENT
CONNECTION

GENETICS AND EPIGENETICS

Our genes form a foundation that determines who we are as individual humans.
The DNA contained in our genes makes each of us unique. While we have more
similarities than differences, seemingly small genetic variations make us unique
individuals. When DNA was discovered as the molecule of heredity in 1952, it was
thought that genetic preprogramming was set in stone, and we all had individual
predestined genetic fates. The idea that DNA is set-in-stone dominated the latter half
of the 20th century.

One of the central ideas in evolutionary theory is that genetic variations happen at
a relatively slow pace. The slow evolving changes in the DNA code are called
mutations. As the 21st century began, another idea took hold in genetic research—a
concept known as epigenetics, literally defined as “upon the gene.”

Our genes are collections of DNA—instruction manuals or “recipes” for making

specific proteins in our bodies. The proteins made from the DNA instructions have a
huge variety of functions.
 • Proteins make up the physical structure of our body, including organs, blood
vessels, skin, etc.

• Proteins function as the machinery that makes the necessary chemicals and
hormones our bodies need.

• Proteins make up our immune system, which defends against invaders.

The small sections of your DNA that contain specific instructions to make a
specific protein are called genes. You can think of a gene as a single recipe in a
cookbook that tells you how to make a specific meal. The human genome is the total
collection of genes in our DNA. The genome is the complete cookbook containing
over 20,000 “recipes” (genes) to make specific proteins.

KEY POINT:
The human genome is the complete DNA “cookbook” that contains over
20,000 genes. Each gene is a specific “recipe” to make a protein.

In traditional evolutionary theory, changes to genes by mutations could be

thought of as changing the recipe. This would be like taking a cake recipe that
originally called for 4 eggs, and changing the requirement to 5 eggs. Whenever you
read the cake recipe in the future you would see the instruction to use 5 eggs.
Mutations physically change the recipe. The cake produced by the new recipe
would be different than the previous cake, just as any protein produced after a
mutation would be different than the original protein.

The epigenetic system has quite a different way of acting on genes. In response to
environmental signals (signals that originate from outside the body), the epigenetic
system will “turn off” or “turn on” different genes. Epigenetics does not change
the individual recipes; the cake will continue to be made with 4 eggs. Epigenetic
signals determine how many cakes are made, or if they will be made at all.
 TURNING
“OFF”
Within the complete genome cookbook, epigenetic signals can make the
pages containing certain recipes “stick together” so that they cannot be
read. If you cannot read the recipe you cannot make the specific meal.
With DNA, if you cannot read the gene you cannot make the protein.

TURNING
“ON”
Epigenetic signals can also “bookmark” a specific recipe so it is made
more often. Genes “bookmarked” by epigenetic changes will make large
amounts of their specific proteins. Similar to a favorite recipe for pot
roast or BBQ, the bookmarked recipes in the DNA cookbook are made
often.

If you could only cook meals that were in your cookbook, you would not be able
to make meals on the recipe pages which are “stuck together.” You would make
meals with the “bookmarked” recipes more frequently.

This is a simplified explanation for how epigenetics works. Different genes

(“recipes”) will be turned off or turned on to meet the internal or external demands
placed on the body.

Some recipes will have the pages stuck together, and some will be bookmarked,
depending on your “environment.”

 YOUR “ENVIRONMENT”
The American Heritage Dictionary defines “environment” as: “all of the
biotic and abiotic factors that act on an organism, population, or
ecological community and influence its survival and development.” We
refine the definition: environment is our food and water intake, air
quality, physical surroundings, physical activity and lifestyle. Our
transformative process focuses on food selections, activity, sleep and
stress—the factors in our environment we can control.
Epigenetic changes impact how our genes interact with what we eat, our
activity level, and how we live our lives every day. Epigenetic changes can
make profound differences in our physical wellbeing. Handled
incorrectly, our bodies will fail us prematurely. Handled properly, we can
hold back the sands of time. Beneficial environmental changes in diet and
exercise will reverse preventable diseases such as type-2 diabetes.
Epigenetics suggests that modern maladies should be thought of as
mismatches between a person’s genetics and their environment. By
correcting mismatches, we can transform from affliction to health.

EPIGENETICS CASE STUDY

This hypothetical case study of identical twins illustrates how epigenetics works:
John and Steve are born identical twins. Their “cookbooks” (genomes) are exactly
the same down to every last recipe. In their late teens, John decides he wants to be a
bodybuilder and Steve wants to start training to compete in ultra-endurance running.
Before each man immerses himself in his newfound athletic passion, both stand 5’
10”, weigh 170 pounds, and have a body composition of 10% body fat.

John’s bodybuilding training consists of long hours in the gym lifting heavy
weights to self-inflict intense muscle trauma. To speed recovery, he eats large
amounts of protein. John is sending “environmental” signals to his “cookbook” for
muscle growth. The “recipes” (genes) for muscle growth are bookmarked by
epigenetic signaling.

Because of his chosen epigenetic path, John’s recipes for sustained energy output
(the kind needed for distance running) have had their pages “stuck together” and are
largely turned off. These unintended consequences happen so John can adapt to the
specific environmental stresses (lifting weights while eating large amounts of
protein) he is placing on his body. His muscles grow significantly, but he is in no
shape to run a single mile.

Steve begins his training at the same time as John. Steve stays away from the
weight room and wears out several pairs of running shoes. He is training for a 50-
mile ultra endurance race. He trains his body to maintain high energy levels for
extended periods of time. The “environmental signals” this type of endurance
training is sending his “cookbook” is for muscle endurance, not muscle growth.

Over the months, while John is packing on muscle mass, Steve is leaning out,
shedding unneeded muscle. Steve’s high volume endurance training enables his
muscles to continue to power his running for hours on end, but he is certainly not
going to win any bench press competitions.

KEY POINT
Epigenetic changes are not set in stone once they are made. As your
environment changes, your epigenetics will change.

After a year of training, the identical twins are no longer identical. John is a
muscled-up 200 pounds and gets winded running around the block. Steve is down to
a rail-thin 140 pounds and has lost a significant amount of muscle mass and
strength.

John and Steve still have identical genetics, but epigenetic changes caused by
different environmental stresses have made their bodies different—they are no
longer identical after a year of sport specific training.

Epigenetic changes are not “set” once they are made. Recipes that were once stuck
together can be bookmarked and vice-versa, depending on the signals from the
environment.

WOMB TO THE GRAVE

Your epigenetic changes started when you were developing in your mother ’s
womb. What your mother ate, drank, and the stress she experienced while pregnant
had a direct impact on your environment in utero. Epigenetic changes began in
response to this environment and persisted after your birth. There is actually good
science now which shows that some epigenetic changes can be passed from parent
to child, much like traditional genes.

A mother ’s metabolic health and stress during her pregnancy can be passed down
to the fetus in utero. The fetus’s “environment” consists solely of the mother ’s body.
If this environment is stressful, the epigenetics of the fetus will change to adapt to
the stresses. Stresses in the mother such as gestational diabetes, psychological stress,
and malnutrition WILL cause epigenetic changes in the fetus. These changes can
exist in the infant after birth.

Recent epigenetic research on mothers who have experienced extreme stress

prior to and during pregnancy has shown that their children are likely to develop
anxiety and are less able to cope with stress later in life. Epigenetic changes are
thought to be responsible for passing stress responses from mother to child.

RESEARCH UPDATE
Recent research has indeed shown that gestational diabetes in the mother
during pregnancy places the child at higher risk for developing obesity
and diabetes later in life. It is also clear that this happens through
epigenetic changes in utero.

It is important to remember that epigenetic changes take place so that we can

adapt to our current environment. This is why creating the best environment
possible (the mother ’s health) during pregnancy is crucial to the future health of the
child. This lifespan view of the impact of the environment on our genes through
epigenetic change has become a very important field of scientific study in recent
years.

In the “nature versus nurture” environment argument, genetics trumps

environment or environment trumps genetics. The balance tips in favor of “nurture”
based on the findings of cutting-edge epigenetics research. “Nurture” starts in the
womb.

Just as the genome describes your complete DNA cookbook, the epigenome
describes the current state of all of the recipes in the cookbook as “bookmarked”
or “stuck together.”

As your environment changes during your life, changes in your epigenome take
place to compensate. Mutations to DNA still happen and are important, but
epigenetics provides real-time adaptations to environmental stresses that mutation-
based DNA changes cannot match.

THE HEALTHY COOKBOOK
Your environment includes nutrition, exercise, sleep and stress. These
shifting environmental characteristics “bookmark” and “stick together”
the generecipes of your genome-cookbook—every day, month, and year.

The ability to read (or not read) the individual recipes and how much each
is made into a “meal” determines disease or health. This is highly
individual and the reason no diet or exercise plan is perfect or works for
everyone. We can optimize your epigenome by providing it with the
proper environmental signals for health.

Epigenetics has emerged as a major way that we adapt to our environmental

stressors. These stressors can change our epigenome for better or worse. Exercise
and food are beneficial in the right amounts, but unhealthy in the wrong dose.
Figuring out these beneficial doses leads us to the concept of hormesis.
CENTRAL THEMES PART III:
HORMESIS

Stress is perceived as a negative thing. Yet exercise is self-induced stress and can
be very beneficial. A central concept, common to all organisms, is a need for
environmental stresses. In order to survive, thrive, and ultimately live our lives to
their fullest potential, environmental challenges must be overcome.

Nietzsche’s axiom, “That which does not kill me makes me stronger” is

profoundly accurate in the world of DNA, genes and epigenetic science. Organisms
—human or otherwise—either adapt to challenges by becoming stronger or they
die. Challenges in the right amounts are not only beneficial, but necessary. Think of
the profound differences in overall health and appearance when comparing the
physique of an out-of-shape individual to that of a life-long athlete who exercises
regularly and eats a sound diet full of natural foods.

A life devoid of physical challenges and inactivity sets a person up for an early
death from metabolic diseases, obesity, muscle loss, fractures of weak brittle bones,
etc. Unfit people degrade rapidly as they age. In our unchallenged, unfit era, this has
unfortunately become the norm.

Physical challenges of the requisite intensity slow the aging process to a crawl.
Favorable and appropriate environmental challenges make our bodies stronger and
more resilient through a process called hormesis. The hormesis concept originated
in the study of toxicology. Although hormesis is still considered somewhat
controversial in the academic circles of toxicology, we view hormesis as a unifying
concept applicable to all environmental stressors.

“THE POISON IS IN THE DOSE”

Paracelsus: “The
dose makes the poision”.
Paracelsus, the 16th century Swiss physician and father of toxicology said,
“Poison is in everything, and no thing is without poison. The dosage makes it either
a poison or a remedy.” In other words, the amount or dose of a substance is what
makes it harmful or helpful.

Hormesis is an extension of Paracelsus’ statement. It implies that there are

necessary doses of environmental challenges. The right “doses” provide beneficial
adaption, while “overdoses” of the same challenges are harmful in the long-term.
The doses that provide beneficial adaptation are said to be “hormetic” doses.

Hormesis readily applies to nutrition, exercise, and lifestyle. While stressful

“challenges” in the right “dose” are necessary to health, overdosing will have the
opposite effect. When it comes to dosage, while “some” is good, “more” is not
necessarily better. Overdose is as negative and deadly as an under-dose.

Antioxidant supplements are heavily advertised and hyped, but research studies
have shown that when antioxidants are isolated and supplemented, beneficial effects
are not seen in humans. Some studies have shown that high-dose antioxidant
supplements (vitamin E for example) can actually make some diseases worse and
shorten life spans.

As we discussed above, we need some oxidative stress to promote an adaptive

response. This increases our internal antioxidant systems, and makes us more
resilient to future stress. High-dose antioxidant supplementation neutralizes the
small amount of reactive oxygen species (i.e. free radicals) responsible for
beneficial levels of oxidative stress. Neutralizing this beneficial oxidative stress
also neutralizes the favorable adaptive response necessary for health and
longevity.

If this seems counterintuitive, think of it this way—exercise is good for the body
in the right doses, but too much can cause you harm. Eliminating exercise
altogether, because too much can harm you, is using the same failed logic behind
the idea of trying to eliminate all oxidative stress because we know that too much
oxidative stress is harmful. Just as we need the right dose of exercise to make us
stronger and more resilient, we need some oxidative stress to thrive through the
adaptive response.

POLYPHENOLS
Polyphenols are a group of natural compounds found in fruits, vegetables,
and plant products such as olive oil. Polyphenols have been promoted for
antioxidant properties, free-radical defense, and as helping in the battle
against oxidative stress and inflammation. Recent research has shown that
their favorable action may not be directly related to polyphenols acting as
antioxidants. Instead, polyphenols stimulate our antioxidant defense and
cell protection mechanisms in an indirect way. These compounds promote
a small amount of oxidative stress and create an environmental challenge
which will stimulate a beneficial adaptive response.

EXERCISE, NUTRITION AND HORMESIS

Coaches and athletes know how to get faster and stronger by subjecting the body
to physical demands. They are unknowingly invoking hormesis. To become faster
and stronger the adaptive response must be triggered. There is a proper “dose” to
trigger the adaptive response. Too little leads to no beneficial changes, and too
much often leads to overtraining. Sickly, injured endurance exercise addicts are
examples of overtrained individuals.

Smart coaches and athletes also know the importance of recovery in making
performance gains. Adequate recovery allows for maximum adaptation to the
“exercise dose” and promotes recovery before the next training session. Consistent
exercise overdose and inadequate recovery is “poison” to the body.

The right “dose” is important for both.

High quality food and nutrition also fits into our hormesis framework.
Macronutrient ratios of protein, starch, fiber and fat can be altered on a daily basis
to fuel activity levels and serve physiologic needs. We need to account for
individual genetic differences and tailor food quality, quantity and selections based
upon different “dose” requirements, goals and preconditions such as obesity and
diabetes. Both over-nutrition and under-nutrition, outside of your individual “ideal
window” can have very real health consequences.

It will be easier to grasp the concept of hormesis visually in the diagrams that
follow...
 The above diagram illustrates the concept of hormesis. The x-axis (left to right)
measures the “dose” of environmental challenge with an increasing dose as we
move to the right. The environmental challenges can be anything previously
discussed, with food and exercise being the obvious examples. The y-axis (top to
bottom) represents the effect seen on the body that corresponds to a given “dose,”
either adverse or hormetic (beneficial).

Point A: The yellow and red sloping curve on the left could represent
inactivity (for exercise dose), or malnutrition (when looking at food
dose). The low doses of activity or food cause “adverse” effects on the
body. For food, Point A represents malnutrition. For exercise, Point A
represents sedentary/low activity.

Point B: As we move to the right with increasing doses of

environmental challenges, we see the curve turn green and rise into the
area of beneficial “hormetic” effects. This green area represents the
beneficial “doses” of environmental challenges for food and exercise in
this case.

Point C: Continuing to the right, the higher doses start making the
curve drop into the yellow and red again, the territory of adverse effects
and eventual death with high enough doses. For food, Point C represents
over-nutrition and the resulting adverse adaptation of obesity. As far as
exercise, Point C could represent overtraining.

An alternate way of visually grasping hormesis is the arrow below. It shows the
same thing as the previous graph and the descriptions of points A, B, and C still
apply.

As you go from left to right following the arrow, the “doses” of environmental
challenges (food and exercise in our example) increases.

• Point A represents malnutrition (food) or lack of activity (exercise).

• The “just right” (hormetic) doses of point B represent beneficial amounts of
nutrition and exercise. Moving out of the green zone to the right, you find point
C.
• Point C represents too much exercise (overtraining) or too much food (over
eating).

There is a proper dose for food and exercise for each individual that maximizes
favorable adaptation without taking other external sources of environmental stress—
such as sleep deprivation or psychological stress—into account. If we take into
account these other external stresses, things can change...

A bad night of sleep, a stressful day at work, or a period of financial problems,

add to “environmental stress.” This decreases the ideal “hormetic window” for
things like certain types of food and exercise because of the additional stresses on
the body. What may be a good “dose” of food and exercise while on a week long
vacation may not be right when facing a deadline at work with poor sleep.

This is your hormesis arrow after a couple of nights of bad sleep and work stress.
In this case, just a little exercise will put you in the green zone of hormetic dose. If
we did the same dose of exercise right now as we did last week (B surrounded by
the yellow box) when we were sleeping well and on vacation, we would find
ourselves in the “overdose” zone. In other words, the dose of exercise that was
beneficial for us last week will be too much this week because of the poor sleep
and job stress. A smaller “dose” of exercise this week will be the beneficial dose.

COACH’S CORNER:
We need to be aware of all the pitfalls and landmines that can drag us out
of our “hormetic dose”—sleep deprivation, intense and prolonged
psychological stress, starvation, gluttony, too much or too little exercise
to name just a few. Hormesis is a delicate gossamer strand, a fragile state.
External stresses will rip us out of the progress zone in a matter of hours
—a night of bad sleep, a super-stressful day at work, a period of financial
problems, beating yourself to a pulp in training then starving or stuffing
yourself.

It is difficult to stay in the “hormetic zone.” But if we are able to ride the
razor’s edge and stay in the zone, we are rewarded with tangible physical
gains: measurable decreases in body fat, an increase in lean muscle mass,
health, wellness, energy, improved stamina, and dramatic improvements in
every definable athletic benchmark. It all can be ours and this book shows
you precisely how to attain and maintain the hormetic zone—the requisite
precursor to all tangible physical progress.

In elite athletics, the combination of perfect training combined with

perfect eating, plentiful rest, copious amounts of organic, nutrient dense
foods, and stress-free living all combine to create a synergistic zone of
progress. The key is to balance the components. It is better to have a little
of all the interrelated elements and disciplines than a whole lot of one or
two at the expense of the others.
 TECHNICAL NOTE:
The graphics depicted on the previous pages show adverse effects at low
doses and high doses, with “beneficial” effects seen in moderate doses (the
green part of the curve or arrow).

Classically, hormesis as described in toxicology shows beneficial effects

at low doses with adverse effects at higher doses. The classical hormesis
graph differs from ours because we are extending the hormesis concept to
include lifestyle factors such as nutrition, stress, and exercise—not just
looking at chemical exposure.

With our expansion of the hormesis concept to lifestyle factors, we see

adverse effects at both very low doses (sedentary lifestyle, under-eating,
etc.) as well as high doses (overtraining, overeating, etc.), with a
beneficial moderate dose.

In an upcoming section we will discuss the concept of the “stress cup” and
allostasis. These ideas explain how something can be good for you one day when
your overall stress is low, and bad the next when your stress is high. Up to this
point, we have talked a great deal about “stress.” Let’s dig a little deeper into the
concept of stress, especially how your brain deals with stress—a.k.a. the threat
response.
CENTRAL THEMES PART IV:
STRESS AND THE RESPONSE TO
THREAT

One of the brain’s major roles is to protect us from harm. A hard-wired system
lives in the brain and expands to the body. This system responds to external and
internal threats, is crucial to our survival, and has been finetuned during the
development of the human species.

Why is this important and why is it a central theme in a health and fitness book?
Just as we must learn the science of the body we need also learn about the brain.
 COACH’S CORNER:

The brain can be an individual’s best friend or worst enemy. The goal is to
use the untapped powers-of-the-mind to amplify our training and
nutritional efforts. How do we harness the mind? How do we make it an
ally instead of a hindrance? The first step is to understand how it works—
from a scientific perspective.

Stress is a killer. Literally. Too much stress is the Black Plague of the
modern era. Everyone is mentally stressed trying to cope with life. Stress
also kills progress. No matter how intense the training, or strict and
pristine the nutrition, if you are over-stressed you will “go catabolic” and
no progress is possible.

Our distant ancestors’ brain circuitry was hardwired to instantaneously respond to

real or perceived threats from the environment. Dubbed “fight or flight,” this
instinctive reaction was critical for survival. Ingrained deeper and deeper with each
passing generation, the “fight-or-flight” response was inserted deep into our
collective psyche.

Early man had to respond to various “threats” including...

• Predators
• Unfriendly neighboring tribes
• Competition for resources
• Periods of scarce food
 • Environmental stresses such as heat and cold
• Injury and infectious disease

In modern society, humans are faced with a different set of “threats.”

• Stressful work environments

• Traffic
• Financial problems
• Disruption of circadian rhythm (artificial light at night, poor sleep, shift
work)
• Processed food supply
• Environmental toxicants (chemicals, pollution)
• Chronic disease

The differences between the threats to modern and primitive man may seem
very obvious to us, but in our brain’s hard-wired threat response system they
are treated equally, and elicit the same threat response.

Your brain treats both types of threats in a similar manner. In an escape from
immediate danger, a “bear threat” is actually preferable to the stress from a “traffic
threat.” Daily low-level chronic stresses such as traffic can add up to cause real
health problems. We are wired to deal with the bear using a short-term threat
response, but are not as suited to handle long-term stress associated with things like
daily traffic.

The big difference between primitive and modern “threats” is that primitive
threats were mostly temporary and short-lived, while modern threats are often
continuous and long-lived. The same brain-based threat response system that
allowed our distant ancestors to adapt, survive, and get stronger works overtime
every day with modern humans. Working the threat response system overtime has a
very real impact on our health.
 Chronic stress and threat response has been linked to the following diseases:

• Heart disease
• Type II diabetes
• High blood pressure
• Autoimmune disease (see the gut chapter)
• Depression
• Chronic pain
• Cancer

QUICK FACT:
Humans are not equipped to effectively deal with the chronic threats
rampant in modern society, and it is evident in the overall poor state of
public health.

YOUR BRAIN ON “THREAT”

Anything in your environment that the brain perceives as a threat will trigger a
physiologic stress response. The racing heart, jitteriness, and hyper-alert state we
have all experienced after being startled by a loud noise or narrowly avoiding a car
accident, is the stress/threat system in action. At the primal level, the system’s job is
to prepare you to fight or flee from danger.

There are two main components to this “fight or flight” system, the autonomic
nervous system (ANS) and the hypothalamic-pituitary-adrenal axis (HPA axis). Both
components work together to prepare the brain and body to deal with the threat and
to recover afterwards. Once a threat is perceived, the autonomic nervous system is
responsible for the immediate preparation to deal with the threat.

I. THE AUTONOMIC NERVOUS SYSTEM

The (ANS) operates without conscious control. The ANS operates on autopilot so
that you do not have to think about raising your heart rate or moving more blood to
muscles during a threat. It happens automatically thus the name “autonomic.” There
are three main parts of this system but only the first two are of primary importance
to our discussion of the threat response.

• The Sympathetic Nervous System (SNS) is the “flight or fight” part of the
autonomic nervous system (ANS). This is the system responsible for increasing
your heart rate when you are startled, perceive danger, or in response to exercise.
The SNS stimulates the “fast pathway” that produces chemicals to give you
energy and increase your heart rate during danger. Adrenalin (epinephrine) is
one of the chemicals produced by the adrenal gland when danger stimulates the
immediate threat response by the brain. Another chemical similar to adrenalin
called norepinephrine is also produced.

When the SNS is dominant, processes like digestion, rest and recovery are put on
hold; you do not need them or want them while fighting or running for your life.
The main job of the SNS during a threat response is to provide energy to
maintain the high states of alertness and increased muscle activity necessary to
survive “fight or flee” threats. The SNS has (primarily) inflammatory actions
and should only be periodically dominant to respond to danger.

• The Parasympathetic Nervous System (PNS) is the “rest and digest” system
that counteracts the SNS. This system brings your heart rate down after the
danger has passed, allows for movement of food through the intestines during
digestion, and is associated with a calm, relaxed state. The PNS system is critical
for the recovery process. The PNS allows your body to recuperate and prepare to
successfully face another threat in the future. The PNS has (primarily) anti-
inflammatory actions. We want the PNS to be dominant most of the time.

QUICK FACT:
Our distant ancestors lived the majority of their lives dominated by the
“rest and digest” parasympathetic system. Their sympathetic systems
sprang into action only when a threat appeared. Stressed out modern man
lives his life dominated by the SNS.
 KEY POINT:
The sympathetic and parasympathetic systems are both operating to some
degree at all times. Environmental signals determine which system is
dominant at any particular time.

• The Enteric Nervous System (ENS) is the third part of the autonomic nervous
system (ANS) that controls your gastrointestinal tract (the gut). It is sometimes
called the “second brain” due to the huge amount of nerve cells associated with
this system. We will discuss this system in depth in the gut chapter.

II. THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS

The (HPA) is the second component to the stress/threat system. It is responsible
for the slow pathway in the response to threat, and releases various hormones to
support the threat response. The first part of the HPA axis is the hypothalamus.

—HYPOTHALAMUS
Central to the brain’s threat response system is the hypothalamus—a tiny area
located at the base of the brain. If you drew a line starting at the bridge of your nose
and went straight backwards into your head, you would run into the hypothalamus.
This area of the brain is only about the size of an almond, but packed into that little
space is the central control center for how we respond to stresses perceived from
our environment. The hypothalamus regulates many processes crucial to our
survival:

• Sleep-wake cycle (circadian rhythm) in response to light

• Hunger
• Thirst
• Thermoregulation (maintaining a constant body temperature)
• Signals for reproduction (making babies!)
• Fight or flight response

You can see from the vital processes the hypothalamus controls, it is logical that
it is the part of the brain responsible coordinating the stress response. The
hypothalamus is responsible for initiating both the immediate threat response
through the autonomic nervous system and the delayed response through the HPA
axis.

—THE PITUITARY GLAND

In response to environmental stress, the hypothalamus releases hormones that
travel to another tiny structure “hanging” just below the hypothalamus in the brain
called the pituitary gland. The pituitary gland acts like a relay station, taking
signals from hormones released by the hypothalamus and making its own hormones
in response to these signals. The stress hormones produced by the pituitary gland
then travel outside of the brain down to the adrenal glands.

—THE ADRENAL GLANDS

Your adrenal glands sit on top of each of your kidneys and are about the size of
your thumb. The adrenals are the third partner in the hypothalamic-pituitary-adrenal
(HPA) axis. The adrenals secrete various hormones and chemicals in response to
both the slow and fast stress response pathways.

—HORMONES PRIMARY FOR THREAT RESPONSE:

Cortisol is released in response to stress signals from the slow pathway. Cortisol
provides the fuel to help the body recover from the threat and helps control
inflammation from the threat response.

Epinephrine (adrenalin) and norepinephrine are released in response to stress

signals from the immediate, fast pathway.

THE HPA-AXIS: HYPOTHALAMUS-PITUITARY-ADRENAL

• FAST PATHWAY:
 This pathway is triggered immediately after a threat is sensed by the brain. It
bypasses the pituitary and sends a direct signal to the adrenals to produce
epinephrine (adrenaline) and norepinephrine. This pathway immediately puts you in
an alert state, and gets you ready to “fight” or “flee” from danger.

• SLOW PATHWAY:
This pathway is also triggered by threat but responds slowly, signaling the
adrenal gland to secrete cortisol. Cortisol helps you recover from the threat after it
has passed.

MEDICAL CONNECTION:
Prednisone is the pharmaceutical equivalent of cortisol and works using
the same mechanisms in the body. Prednisone is used in modern medicine
to control inflammation in many different diseases such as severe asthma
and autoimmune diseases.

Well-known side effects of chronic prednisone (and other similar

medications) use is fat gain, muscle wasting, bone weakening, and
psychological side effects such as agitation.

High levels of cortisol from chronic stress/threat activation can result in

the same side effects as daily prednisone use.

ANCIENT PHILOSOPHY MIRRORS

MODERN SCIENCE
The Chinese philosophical concept of yin and yang mirrors the interaction
between the sympathetic (SNS) and parasympathetic (PNS) systems very well as it
relates to the stress/threat system. The yin/yang graphic has become a universal
symbol for good reason; it is an overarching concept that describes our natural
world from large-scale ecology to molecular biology. We can use the yin/yang
concept to illustrate the importance of balance in the autonomic nervous system
between the SNS and the PNS.

Prolonged activation of the stress/threat system leads to dominance by the SNS

and wear and tear on the body and brain.

ANS balance is crucial to health.

HEALTH EFFECTS OF THE

STRESS/THREAT SYSTEM

The sympathetic nervous system has the potential to produce high levels
of inflammation and oxidative stress, potentially causing significant
wear and tear on our body and brain. Optimally, the SNS should only be
dominant for short periods of time. In addition to responding to threats
and challenges, the SNS is also purposefully invoked during intense
physical training. For many of us, our sympathetic nervous system is
always on, ramped up, agitated, and frazzled from responding to chronic
stress situations. Chronic over-stimulation of the SNS results in chronic
inflammation.

The parasympathetic nervous system is associated with calm, relaxed

centeredness, and has anti-inflammatory effects. Bodily functions occur
optimally when operating in PNS. We want to cultivate the PNS and have it
maintain dominance most of the time.

Prolonged activation of the HPA axis can lead to abnormally high cortisol
levels. Cortisol is an essential part of the recovery from threat and plays
vital roles in our body. Modern stresses keep our HPA axis threat system
 on longer that it was designed, leaving us awash in cortisol. This damages
the brain, wastes muscle, weakens bones, and promotes fat accumulation
resulting in poor health.

KEY POINT:
The sympathetic “flight or fight” nervous system (SNS) generally has
inflammatory effects.

The parasympathetic “rest and digest” nervous system (PNS) generally

has anti-inflammatory effects.

Low levels of continued SNS activity can lead to chronic inflammation,

and is a key driver of chronic diseases such as heart disease, diabetes,
high blood pressure, and cancer in modern society.

Poor health and disease are the result of this imbalance—dominance of the SNS
over the PNS. Many modern humans live in a constant state of low level “flight or
fight” in response to modern “threats,” with very few of these threats being a true
immediate danger to life and limb. The following point needs repeating; the brain
will trigger the threat response to both internal threats from within the body and
external threats from the environment.

• Internal threat: swollen fat cells in an obese individual causing

inflammation.
• External threat: stressful work environment.
• Internal threat: bacterial infection or injury.
• External threat: processed food causing inflammation and oxidative stress.
• Internal threat: rumination and worry causing chronic psychological stress.
• External threat: consistent overtraining from “boot-camp beat down”
exercise programs.
• Internal threat: inadequate sleep.

This is just a handful of examples that can activate the brain’s threat response. You
will learn more about all of these threats as you continue your training. Notice that
inflammation and oxidative stress from internal and external threats such as obesity
and processed food can stimulate the threat response. In turn, the threat response of
the “flight or fight” system (SNS) can cause inflammation and oxidative stress. This
creates a vicious cycle that leads to poor health.

In the upcoming in-depth training on Chronic Stress, we will show you the
damage to your body and brain that results from the cycle of inflammation and
over-activation of the stress/threat system. You will also get defensive tactics to
break the cycle and restore balance to the system and to your health.

This very brief overview of the stress response system sets the stage for how
threats from our environment and from within impact our health. On any given day,
each of us has a specific capacity for dealing with internal and external sources of
stress. This capacity is what we call your “stress cup,” the amount of stress you can
handle on any given day. The next section expands the “stress cup” idea using the
scientific concepts of allostasis and allostatic overload, which are foundational to
the Strong Medicine view of health and disease.
CENTRAL THEMES PART V:
ALLOSTASIS: MY CUP RUNNETH
OVER…

Unlike the meaning of this phrase in the biblical context, we will use it in
reference for a way to visualize our bodies’ capacity for stress, a.k.a the “stress
cup.” You really do not want to routinely overfill this cup, as you will soon see.

The scientists who study the adaptation of the human body to stress call this
adaptation process allostasis. This word literally means achieving “stability
through change.” Put more simply, the human body always wants to achieve
balance with the environment*, and does so by changing and adapting.

If something in our environment (such as strength training) tries to disrupt this

balance, the body will adapt to meet the challenge, changing to be in a new balance
with the environment (in this example becoming physically stronger in response to
lifting weights).
 QUICK FACT:
*As a reminder, we define environment as our food and water intake, air
quality, physical activity and lifestyle.

KEY QUESTION:
How is the concept of allostasis different than hormesis?

Answer: Allostasis is the physiologic mechanism by which hormesis

operates.

What does that mean?

• Hormesis occurs when an environmental stressor produces a

“positive adaptation” or beneficial effects in the body.

• Allostasis is how the beneficial effects (adaptations) actually happen

inside the body to achieve stability with the environment.

Many of us have felt a sense of euphoria or wellbeing after intense physical

activity. Those in the endurance sport community call it the “runners high.” This
sensation is really a protective response to stress by the release of natural
morphine-like compounds called endorphins.

Endorphin release is part of allostasis—in this case, the brain is attempting to

decrease pain during intense physical stress.

Allostasis is responsible for other adaptations/responses seen in response to

various types of environmental stress:

• Release of stress hormones such as cortisol and epinephrine by the brain

and adrenal glands in response to stress in all forms.
• Increase in muscle size in response to weight training.
• Increased cardiovascular fitness in response to exercise.
• Stimulating the antioxidant protection system when exposed to free
 radicals.

QUICK FACT:
When the environmental challenges are in a high enough dose and
frequency to consistently overload the body’s ability to adapt, the body
starts to break down from “wear and tear” and disease is the result.

These adaptations through allostasis allow you to better cope with the demands of
any future environmental challenges and/or serve an immediate need for survival as
part of the “flight or fight” response.

FAILURE TO ADAPT: “THE STRESS CUP”

At any one time, your body has an upper limit to the amount of stress it can
handle and still produce a favorable adaptive response. This limit or capacity for
stress can change dramatically day to day, or slowly over months and years. A night
of poor sleep, a couple of fast food meals, traffic during your morning commute,
or a demanding boss can reduce the daily capacity for stress. It may be easier to
think of this visually using the concept of the “stress cup.”

THE “STRESS CUP”

The entire cup represents your body’s capacity to deal with stress (through
 allostasis) on a given day. In this example, the environmental stress of
work, poor sleep, and bad diet fill the cup most of the way, leaving only a
little capacity (empty space at the top) for physical stress such as strength
training.
Attempting a high intensity workout session—usually a beneficial stressor
—on a day like this could “overfill” the “stress cup” and lead to poor
adaptation and even illness or injury.

When the environmental stressors are greater than the body’s capacity to maintain
stability, scientists call this allostatic load or allostatic overload. This overload of
the system over time (the overflowing “stress cup”) produces “wear and tear” in the
body and over the long-term leads to disease.

This wear and tear can express itself as a “broken” metabolism (as in diabetes) or
physical degeneration leading to premature aging and poor health.

THE OVERFLOWING “STRESS CUP”
This is what happens when attempting a high intensity workout when your
“stress cup” is almost full from work stress, bad diet and poor sleep.

Exercise is usually a good thing, but you need to decrease “the dose” of
exercise on a day like this day to prevent your “stress cup” from
overflowing like in the picture.

The overflowing “stress cup” is called allostatic overload.

 QUICK FACT:
The end result of allostatic overload is increased chronic inflammation
and oxidative stress, which cause damage to your body and brain.

Allostatic overload represents the health consequences of more stress (of

all types) over time than your body and brain can handle—your “stress
cup” is constantly overflowing.

As you “pour” different stresses into your “stress cup”, your body and brain react
and adapt to the stress through the process of allostasis. As long as you do not
exceed the capacity of your cup, your body and brain will survive and thrive in
response to stress.

I know what you’re thinking, “I’ve got too much stress in my life. I’ll avoid
exercise so I don’t overfill my ‘stress cup’.” This is a really bad idea because the
complete lack of exercise will make your “stress cup” smaller, leaving you less
able to handle other stresses such as injury, poor diet, poor sleep, and work stress.

QUICK MEDICAL NOTE:

We can measure the results of allostatic overload with medical tests such
as:

• Blood sugar tests for diabetes

• Lipid panels for heart disease risk
• Thyroid testing
• Adrenal stress indexes for problems with cortisol
• C-reactive protein (a marker of inflammation)
• Heart Rate Variability

We will go over some of these in detail in the “Stuff You Can Measure”
chapter. Just know that conceptually, we are really measuring the markers
 of allostatic overload—or how our body is not adapting well to the
environment over time.

Lack of exercise will figuratively reduce your “stress cup” from a 24-ounce cup
to a 12-ounce cup. The smaller your cup, the more easily it will overflow, resulting
in allostatic overload and health problems.

KEY POINT:
It is very important to remember that a lack of stress—such as sedentary
behavior—can just as easily cause allostatic overload as well!

Again, these stresses are necessary for a healthy body, and it is no surprise
that arthritis and degenerated joints seen in middle age often accompany
poor muscle mass and weak bones from lack of physical training and
activity.

Regular exercise can increase the size of your “stress cup”!

SLOW THE HANDS OF TIME: “SUPER-

SIZE” YOUR “STRESS CUP”
A natural part of aging is the gradual “shrinking of our stress cup.” As we age,
we do not heal or recover from physical stresses or illness as well, and are
generally less resilient than we were as children or young adults.

The good news is that we can significantly slow the “shrinkage rate” of our
“stress cups”, and armor ourselves against stress into old age.

The “stress cup” can be “emptied” with stress reduction techniques such as the
breathing exercises, mindfulness techniques, physical exercise, and the nutritional
approaches we will cover later in the book.


Those with a history of poor nutrition, exercise, and lifestyle habits will see a
dramatic increase in the size of their “stress cup” as they adopt the comprehensive
approach to health and wellness outlined in Strong Medicine.

THE GOOD NEWS:

The size of your “stress cup” can be increased over time through smart
training, adequate sleep, good nutrition, and the use of stress reduction
techniques. We will slow the aging process by “supersizing” your “stress
cup”.

In this example, the stresses of poor sleep and bad diet have been reduced
through lifestyle change. There is still some work stress, but we now have
a large empty space that can be filled with intense training without
overfilling our “stress cup”.

THE FUTURE OF MEDICINE?

In our opinion, the concepts of allostasis and allostatic overload are the best way
to view chronic disease as a whole. High blood pressure, diabetes, high cholesterol,
obesity, and mental health problems such as anxiety and depression are all examples
of the body’s failure to adapt to environmental stresses such as chronic stress, poor
diet, and lack of physical activity. It is well known that these diseases often occur
together—which is no surprise if you view them all as results of allostatic overload,
overfilling your “stress cup.”

We need to stop treating these diseases as individual issues to be treated with

drugs. Instead, the lifestyle should be aggressively modified to reduce stress, eat
well, and exercise more. If you are unwilling to do this, you are doomed to take an
ever-increasing number of drugs in an attempt to artificially control your body’s
attempt to achieve stability in a poor environment of fast food, inactivity, and high
stress. None of the chronic diseases listed above have ever been cured by drugs,
only partially controlled at best.

Let us eliminate the causes instead of treating the symptoms. The body has an
incredible potential for self-healing. Given the right inputs of good food, exercise,
and stress reduction, it knows what to do.

USE IN DAILY LIFE

Using the visual concept of the “stress cup”, you can discover your individual
daily limits and proper “doses” of the various environmental inputs of food,
training, and lifestyle that lead to beneficial changes for you.

What works well for you may not work well for your family members,
neighbors, or co-workers, and vice-versa. You will make mistakes in the process of
experimentation with this concept, just don’t let your “stress cup” consistently run
over. The rest of this book will give you the tools to prevent allostatic overload and
the chronic diseases that go with it.

SPOTLIGHT ON A SCIENTIST:
The work of Dr. Bruce McEwen inspired this section of Strong Medicine
with his foundational work on allostasis and allostatic overload. His
contributions to this area of research have been monumental.
“MILITARY INTELLIGENCE” (REFERENCES):
Bohacek J , Gapp K, Saab BJ & M ansuy IM . Transgenerational epigenetic effects on brain functions. Biol Psychiatry 73 (2013): 313-320.

Calabrese, V. et al. Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity, Biochim Biophys Acta 1822 (2012): 753.

Calabrese, V. et al. The hormetic role of dietary antioxidants in free radical-related diseases, Curr Pharm Des 16 (2010): 877.

Cohen, S. et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk , Proc Natl Acad Sci USA 109 (2012): 5995.

Davidson RJ , M cEwen BS. Social influences on neuroplasticity: stress and interventions to promote well-being, Nat Neurosci 15 (2012): 689.

Fairfield KM . Daily multivitamin supplements did not reduce risk for major CV events over > 10 years in men, Ann Intern Med 158 (2013): J C2.

Ganzel BL, M orris PA. Wethington, E. Allostasis and the human brain: Integrating models of stress from the social and life sciences, Psychol Rev 117 (2010): 134.

Goldstein DS. Adrenal responses to stress, Cell Mol Neurobiol 30 (2010): 1433.

Gomez-Pinilla, F. The influences of diet and exercise on mental health through hormesis, Ageing Res Rev 7 (2008): 49.

Goto S, Radak Z . Hormetic effects of reactive oxygen species by exercise: a view from animal studies for successful aging in human, Dose Response 8 (2009): 68.

J oseph PG, Pare G, Anand SS. Exploring gene-environment relationships in cardiovascular disease, Can J Cardiol 29 (2013): 37.

Li G, He H. Hormesis, allostatic buffering capacity and physiological mechanism of physical activity: a new theoretic framework , Med Hypotheses 72 (2009): 527.

M aeta K, Nomura W, Tak atsume Y, Izawa S, Inoue Y. Green tea polyphenols function as prooxidants to activate oxidative-stress-responsive transcription factors in yeasts, Appl Environ Microbiol 73 (2007): 572.

M ansuy IM , & M ohanna S. Epigenetics and the Human Brain: Where Nurture M eets Nature. Cerebrum 2011(2011): 8.

M cEwen BS. Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load, Metabolism 55 (2006): S20.

M cEwen BS. Central effects of stress hormones in health and disease: U nderstanding the protective and damaging effects of stress and stress mediators, Eur J Pharmacol 583 (2008): 174.

M cEwen BS. Brain on stress: how the social environment gets under the sk in, Proc Natl Acad Sci USA 109 Suppl 2 (2012): 17180.

M cEwen BS, Getz L. Lifetime experiences, the brain and personalized medicine: an integrative perspective, Metabolism 62 Suppl 1 (2013): S20.

M cEwen BS, Wingfield J C. What is in a name? Integrating homeostasis, allostasis and stress, Horm Behav 57 (2010): 105.

M enendez J A, et al. Xenohormetic and anti-aging activity of secoiridoid polyphenols present in extra virgin olive oil: A new family of gerosuppressant agents, Cell Cycle 12 (2013): 555.

M uscatell KA, Eisenberger NI. A Social Neuroscience Perspective on Stress and Health, Soc Personal Psychol Compass 6 (2012): 890.

Novak ovic B, Saffery R. The importance of the intrauterine environment in shaping the human neonatal epigenome, Epigenomics 5 (2013): 1.

Nunn AV, Bell J D, Guy GW. Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?, Nutr Metab (Lond) 6 (2009): 16.

Ogino S. et al. M olecular pathological epidemiology of epigenetics: emerging integrative science to analyze environment, host, and disease, Mod Pathol (2013).

Pace TW, Hu F, M iller AH. Cytok ine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression, Brain Behav Immun 21 (2007): 9.

Pick ering AM , Vojtovich L, Tower J A, Davies KJ . Oxidative stress adaptation with acute, chronic, and repeated stress, Free Radic Biol Med 55 (2013): 109.

Pietsch K, et al. Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans, Biogerontology 12 (2011): 329.

Puterman E, et al. The power of exercise: buffering the effect of chronic stress on telomere length, PLoS One 5 (2010): e10837.

Radak Z , Chung HY, Koltai E, Taylor AW, Goto S. Exercise, oxidative stress and hormesis, Ageing Res Rev 7 (2008): 34.

Ristow M , Schmeisser S. Extending life span by increasing oxidative stress, Free Radic Biol Med 51 (2011): 327.

Ristow M , Z arse K. How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis), Exp Gerontol 45 (2010): 410.

Speciale A, Chirafisi J , Saija A, & Cimino F. Nutritional antioxidants and adaptive cell responses: an update. Curr Mol Med 11 (2011): 770-789.

Webster AL, Yan M S, M arsden PA. Epigenetics and cardiovascular disease, Can J Cardiol 29 (2013): 46.

Ye Y, Li J , Yuan Z . Effect of antioxidant vitamin supplementation on cardiovascular outcomes: a meta-analysis of randomized controlled trials, PLoS One 8 (2013): e56803.
BASIC TRAINING II:
NUTRITION AND METABOLISM 101:

You are now starting Part II of your Basic Training. Gaining a strong foundation
of knowledge with these concepts will protect the Strong Medicine trainee from
being led astray by the avalanche of misinformation in the popular media.

This knowledge will insulate you from fad diets and outright propaganda by
special interests trying to gain financially from your ignorance. Mastering this
section will give you the tools to analyze nutrition from its very foundations,
allowing you to pierce the fog of the “dietary war.”

Much like placing raw ore in a blast furnace to make steel, our body is made to
take pristine natural foods and use our metabolic “furnace” to produce energy and
keep us in optimal health.

Also like the steel making process, impurities in our food supply have
consequences to the quality of the end product—or in this case, our health.

Nutrition has become a controversial subject. It is ironic that what we eat as

human beings—a central element of our successful development as the dominant
species on the planet—has somehow “suddenly” become controversial in the
modern age.
 The fact that this chapter (or the entire book for that matter) has to be written puts
some perspective on how far we have fallen from the ancient synergy of food and
metabolism enjoyed by our ancestors.

We have strayed so far from eating food in its most natural form, unadulterated
by modern processing and additives, that our bodies have not had time to fully adapt
to many of the chemical concoctions sold to us as “food.” The health consequences
of this failure to adapt (allostatic overload) are readily apparent in the true modern
epidemics of diabetes, obesity, heart disease, and cancer.

This chapter will give you a basic “first principles” education in nutritional
science, and background on how human metabolism is supposed to work when in
harmony with our environment. Given that over 2/3rds of the population is obese or
overweight, and diabetes rates continue to climb to epic proportions, a “normal”
human metabolism is becoming increasing rare in modern society.

There are several fundamental flaws in the current “official” food and exercise
recommendations—lack of a scientific foundation, and poor communication. Many
of these nutrition recommendations are based on shaky science. They are built on a
“house of cards” with a poor foundation. It is also very rare to see a basic
explanation of why the nutrition recommendations are made.

Many people will actually stick to lifestyle changes if they understand what is
happening inside their bodies because of lifestyle choices such as poor nutrition.
Many public health authorities do not give people enough credit for their
intelligence and capacity for understanding. The public usually is not the problem,
the message is the problem. We need to educate the layperson on the “whys” in a
way that does the science justice, but is understandable. We need to build a scientific
foundation to evaluate any nutritional recommendations dispassionately to see if
they pass the “sniff-test.”

Following the mission of this book, this chapter will attempt to explain the
science in an understandable manner, while maintaining the careful balance between
complexity and over-simplicity.

“It can scarcely be denied that the supreme goal of all theory is to make
the irreducible basic elements as simple and few as possible without
having to surrender the adequate representation of a single datum of
experience.” (Everything should be made as simple as possible, but no
simpler.)
—Albert Einstein 1933
BASIC TRAINING II:
NUTRITION AND METABOLISM 101:
INTRODUCTION

WHAT IS “GOOD” NUTRITION?

We all have our own ideas of what we consider to be good nutrition, even if we
are not currently eating that way. But what are these ideas based on? Are they based
on what we hear and see in the popular media? Are they based on advice from health
professionals—our doctors and dietitians? Are they based on official government
recommendations? How about advice from friends and family members?

For most of us, it is usually some combination of “all of the above”. And more
often than not, the advice we hear is contradictory. What and who do we believe?
This last question is often the one people struggle with the most, and is the reason
“fad diets” are everywhere. There is always a new “lose weight quick” scheme that
people latch onto in desperation, hoping that this will finally be the miraculous
answer to their quest for a healthy body.


WHY DO ALL DIETS FAIL IN THE

LONG-TERM?
Diets fail—this has been proven time after time. They all seem to work in
the short-term, but after a while, once enthusiastic participants find
themselves back to where they were in the beginning, and sometimes even
worse!

ISSUES WITH CURRENT

NUTRITIONAL SCIENCE:
Unfortunately, when you peel back the layers to find the underlying basis for
current nutritional recommendations—the basic principles on which they are
founded—you find yourself in a sketchy place, far from solid, unbiased science.
Surely the Dietary Guidelines from our government are based on the latest and
greatest cutting-edge science, right? There are four major problems with modern
nutrition research and practice:

I. FIRST PRINCIPLES?
One major problem is that current nutritional science has no underlying guiding
principles at its foundation. Physics, chemistry, biology, and geology, all have
universal principles such as mathematics, relativity, quantum theory, and the
periodic table of the elements, as foundations. In the sciences, these foundations are
the basis for formulating and testing theories, through the design and performance
of experiments. We will refer to these universal principles as “first principles” in
this book.
 After reading through countless journal articles on nutritional research, the
underlying first principles from which to test theory and perform research seemed
to be largely absent. One would think that foundational disciplines of physiology,
biochemistry, and even anthropology would be very useful in informing nutritional
theory and clinical practice, but they are often ignored.

When we actually peeled the layers of this onion back even more, we found that
modern “official” nutrition recommendations by professional medical
organizations and government agencies sometimes contradict the basic scientific
principles on which they should be based.

Maxwell’s Equations—these equations describe how electrical and magnetic fields

interact and form the basis for all modern technology using electricity and
magnetism. I had to derive these as part of an exam in physical chemistry back in
college. Truly first principles, but a painful experience at the time!

II. STUDY DESIGN

Most nutrition research involves “observational data,” which really boils down
to study participants reporting what they eat to researchers on questionnaires. How
many of us are truly honest about what we really eat when asked, especially by a
researcher, or can even recall what we ate weeks and months ago? Do the
questionnaires allow for differences in food quality in research? For example, does
red meat from a grass-fed cow have the same biochemical composition, fat profile,
and nutritional value as a cow raised in a feedlot on pesticide-laden grains? Does
this make a difference when we claim that red meat is bad?

Nutrition research that mimics the methods used in physical sciences—tightly

controlled variables free from external influences called confounders—is nearly
impossible to perform. This is largely due to the expense and logistics associated
with a study following these standards.
 TECHNICAL NOTE:
Observational studies can be very useful to generate hypotheses that can
later be tested more rigorously, but one should be very careful when using
observational results to make nutrition recommendations. How many
contradictory studies have you seen? It seems like every year a study
comes out saying “eggs are bad,” only to have another say “eggs are
good.” These studies are based on observational data, so these
associations need to be tested. Often, good first tests for observational
study findings are:
1. What are the proposed physiological or biochemical mechanisms
behind the findings?
2. Does the finding make sense from what we know about molecular
biology or biochemistry?

Unfortunately these questions are not answered before the results are
released to the media, who once again confuse the general public about
whether or not they should eat eggs!

III. REDUCTIONISM
Another problem rampant in nutritional research and recommendations is
“reductionist nutritionism.” For example, we know that food “X” has health
benefits. We also know that compound “Y” is present in food “X”. Therefore we can
isolate “Y” and test it (and maybe even make a supplement).

The problem with this approach to food research is that other unknown factors
present in food “X” are likely working with compound “Y” to give the health
benefits. Isolating “Y” and using it as a supplement most often will not yield long-
term benefits, and may even be harmful.
 QUICK FACT:
Nutritional supplement sales are a multi-billion dollar industry in the U.S.
alone!

IV. GROUPTHINK
“If fifty million people say a foolish thing, it is still a foolish thing.” —(Anatole
France)

Groupthink is a phenomenon in which groups of people try to minimize conflict

when coming to a collective decision and course of action on a given topic.
Controversial issues are avoided, and opinions and/or thoughts outside the current
norm are not brought up or addressed.

Independent thinking is subtly discouraged in favor of group conformity. This is

very much like the peer-pressure to conform that we experienced as teenagers. This
type of peer-pressure can continue into adulthood in the form of groupthink, and
unfortunately is often rampant in the government and medical communities.

When we hear nutritional information from “fitness experts,” media, government

or physicians, we tend to blindly accept the information as true. Few among us have
the knowledge or background to critically examine “settled science” and treasured
dietary orthodoxies. It becomes nearly impossible to discover dietary information
that is sound from a scientific perspective.

Misinformation rules the day as profit becomes inexorably intertwined with

knowledge. Misinformation and sometimes outright propaganda comes in a variety
of forms and results in conflicting and confusing information:

1. Special interests push bogus dogma to sell their products for financial gain.
2. Official recommendations from government agencies are often influenced by
special interests, creating conflicts of interest.
3. Well-meaning organizations and health care providers cling to outdated
 information. They are too intimidated to take a second look at established
dogma, for fear of being ostracized or called “quacks.”
4. Groupthink is rampant and profitable.

The basic training that follows will give you the knowledge to critically examine
nutrition advice and recommendations so you will not fall prey to misinformation
from bad science and outdated paradigms.

NO DIETS HERE!
The Strong Medicine approach for healthy eating is relatively simple; eat food in
its natural form, from local sources, as unprocessed as possible, with an emphasis
on food quality. We could sum up our entire nutritional philosophy with that
sentence. We contend that the primary reason for the obesity and diabetes epidemic
in “modern” society is processed food from the industrialized food manufacturing
and distribution system. Most of us no longer get our food from the local farmer,
but from cardboard and plastic packages.

“Eat food in its natural form” is easy to say, but we will get into a more detailed
definition of that statement, and what it means for your health using the relevant
basic biochemistry and physiology.

When people know why they are doing things, behavioral changes seem to stick
longer, and we are after a long-term sustainable lifestyle change. Diets do not work
long-term; they never have, and never will.

Because of the shortcomings in most nutrition research, we will rely on the “first
principles” approach, using the foundations of biochemistry and human physiology
as a lens to view nutrition.

We combine this view with what we have observed in the eating habits of
traditional cultures not largely impacted by “Western dietary habits.” These
traditional cultures are relatively free of chronic disease. This seems to be the most
rational approach.
BASIC TRAINING II:
NUTRITION AND METABOLISM 101:
MACRONUTRIENTS

The best place to start with the science of nutrition is to understand the three
major building blocks of food, otherwise known as macronutrients:

I. Carbohydrates
II. Protein
III. Fat

It is crucial to understand macronutrients from a biochemistry perspective. These

major building blocks of food are broken down and processed through chemical
reactions in the body. Carbohydrates, protein, and fat are natural chemicals, and as
chemicals, their specific structures determine how they react in the body.

The varied chemical structures of the many different types of fat allow them to
function very differently from each other. Lumping them all together as “fat” when
we discuss nutrition and health misses the huge diversity of structure and function
found within this group.

Outdated generalizations such as “carbs are bad” or “fat is bad” are complete
nonsense when you look at macronutrients chemically. To make educated decisions,
it is imperative to understand the biochemistry involved when looking at food labels
in the supermarket.

CARBOHYDRATES
Many people think of carbohydrates as bread, pasta, bagels, and potatoes.
Carbohydrates include much more than this and are generally divided into 3 main
categories: sugar, starch, and fiber.

SIMPLE SUGARS AND STARCH:

Glucose is an example of a simple sugar. It is a single molecule called a
monosaccharide; mono = one and saccharide = sugar.

Above are the actual chemical structures for glucose, fructose, and sucrose. To
avoid seeing these chemical structures over and over, we will only show them once.
We will represent them as circles and triangles from this point forward.

Strings of glucose are connected in chains with branches to make starches.

Starches are found in bagels, bread, pasta, roots, and tubers (i.e. potatoes). Starches
are called “polysaccharides.” Poly=many, saccharide= sugar. The simple sugars are
connected by “bonds,” shown in green in the diagram below.
Glucose (circles) linked together to form starch.

These bonds link the glucose together, and the specific type of chemical bond is
one that our body has the machinery to cut. This cutting process is part of
digestion, and allows us to break starch into single glucose molecules to use as fuel.

KEY POINT:
Note that bagels, bread, pasta and other processed starchy foods are really
just fiber and large collections of glucose.

The next common simple sugar is fructose, another single molecule

monosaccharide. But, the body handles it QUITE differently than glucose. Fructose
is found in fruit in varying quantities, and large amounts are found in high fructose
corn syrup.

Fructose can only be used in the liver. The liver turns fructose into glucose or
makes it into fat. It also makes the liver a “glucose sponge” and greatly accelerates
liver absorption of glucose. Fructose consumed daily in high amounts can cause big
problems in certain situations we will discuss later. People who eat processed foods
daily are getting much more fructose (usually in the form of high-fructose corn
syrup) than their bodies can handle effectively.

DIGGING DEEPER:
How to Make a Fatty Liver
 High fructose intake is a great way to make a fat-filled liver. It is not fat
in the diet that makes the liver fatty. Foie gras is a prime example of this
fact in action. To make foie gras, ducks are consistently force fed corn so
their livers rapidly fill with fat. This happens because the large amount of
sugar (especially fructose) in corn is converted to fat in the liver.

In humans, other factors are involved with fatty liver disease, but high
fructose consumption is a major contributor. Alcoholic fatty liver disease
produced from high levels of alcohol consumption used to be the number
one cause of fatty liver disease. The new reigning champion of the fatty
liver is non-alcoholic fatty liver disease (NAFLD).

One cause of NAFLD is thought to be high fructose intake—with high

fructose corn syrup (HFCS) being a major contributor since it is an
ingredient in most processed foods. Soda and other flavored drinks with
high amounts of HFCS are thought to be a major factor in the
development of NAFLD in kids. NAFLD in children was unheard of
until the early 1980’s.

To be clear, the problem is the huge amount of fructose in the diet

from processed foods and drinks. The amounts of fructose found in
fruits and vegetables is easily handled by the liver, as long as processed
food is avoided.

 Sucrose, another simple sugar, is a double molecule (disaccharide: di=two,
saccharide=sugar) made by sticking one glucose and one fructose together (from
our previous picture, a circle and a triangle stuck together).

Sucrose is known to most of us as table sugar, the “white stuff”. When we eat
sucrose, it doesn’t stay together long. Our body rapidly breaks down the sucrose
double molecule to individual molecules of glucose and fructose.

FIBER
Strings of glucose and other monosaccharides (such as fructose) can be linked
together with specific types of bonds that we do not have the machinery to cut. These
strings are known as fiber—polysaccharides (“many sugars”) that we cannot break
down directly for energy. It is the third type of carbohydrate.

This graphic represents a small piece of fiber showing strings of glucose (circles)
connected by bonds (shown in red). Humans do not have the machinery (enzymes)
to break down fiber into glucose because the connecting bonds are chemically
different from the bonds found in starch. Note that certain types of fiber may also
be strings of fructose (triangles instead of circles).

Fiber is found in various plants and is generally favorable for your health. Here
again, the devil is in the details: all fiber is not the same. From a health and nutrition
perspective, fiber is best classified by the degree that the specific fiber can be
fermented.
 Fermentation: Over one trillion bacteria are in your colon and have the
machinery to break the bonds in fermentable fiber. They feed on the sugars that are
released, and secrete “waste” products in the form of short chain fats, butyrate and
propionate. This process is how certain types of fiber are fermented. These short
chain fats are the primary energy source for cells that line the colon (colonocytes).
Check out the gut chapter for more on fermentation.

KEY POINT:
New research has shown that colon cells begin to die without adequate
supplies of bacteria-produced fats. Butyrate and propionate also have anti-
inflammatory and anti-cancer properties. And by the way, they are
saturated fats. Here is another hole in the “saturated fat is bad for you”
argument that we will get to in the fat section. This is why fermentable
fiber is “good for you”.

HEALTHY WHOLE GRAINS?

A major problem—and point of confusion for the public—is that nutrition and
medical experts generally don’t know the difference between fermentable fiber and
non-fermentable fiber. They lump both types together as “good for you” which is
factually false—the fiber found in many grain products (especially wheat) is poorly
fermentable. Bacteria cannot break down wheat fiber very well and will not
produce significant amounts of the beneficial short chain fats as the “waste”
products responsible for the health benefits of fiber.

THE TAKE-HOME MESSAGE:

The next time you see something advertised as “high in fiber”, ask if it is
fermentable or non-fermentable. Vegetables and fruits are the best source
of fermentable fiber. Grain-based fibers are less fermentable and thus less
desirable from a health perspective. Along with being full of glucose,
 grains (for the most part) do not have the highly fermentable type of fiber
we need for health benefits. Stick with fruits and veggies for your fiber!

PROTEIN
Of all the macronutrients, patients and clients ask the most questions about
protein. How much should I eat? When should I eat it? What sources are best? This
section will help answer some of those questions. Of course, we’ll start with the
biochemistry first.

Protein is comprised of chemicals called amino acids that are linked together to
form chains. The general amino acid structure is shown in the following graphic. In
the picture, N represents nitrogen, C represents carbon, O represents oxygen, and H
represents hydrogen.

The bond shown in red in the picture below is the “link” (called a peptide bond) that
joins 2 amino acids. This “linking” process happens hundreds of times, creating
the long chains of amino acids that make up a protein.

The “R” in the squares represents chemical “side groups.” These side groups
(also called R-groups) are what make one amino acid different from another. There
are 20 standard amino acids used to build proteins, and each has a different side
group.

The side groups have different chemical properties: some are attracted to water
(called polar or hydrophilic), some are repelled by water (called non-polar or
hydrophobic). Some have positive charges and some have negative charges.

WHY DOES THIS REALLY MATTER?

These different chemical properties of the side groups determine how each amino
acid reacts to water (remember, we are mostly made of water) and how they react
to other side chains in the string. For example, two positively charged side groups
will repel each other, while a positive side chain and a negative side chain next to
each other in the string of amino acids will attract each other.

Because proteins are strings of amino acids, the specific order and type of amino
acids in the strings will cause the string to behave in different ways. Long strings of
amino acids will fold to become specific shapes of three-dimensional proteins.

For example, a group of non-polar (water repelling) amino acid side chains will
attempt to position themselves as far from water as possible. Imagine a droplet of
oil put in a glass of water. The oil will stay in drop form and “keep away” from the
water instead of dissolving in it. So a group of non-polar (water repelling) amino
acid side chains will make the string of amino acids fold in such a way that they are
kept on the inside of the 3-dimensional protein structure when it folds, and away
from water.

Conversely, a polar (water attracting) amino acid side chain will “want” to be
positioned in the three-dimensional protein structure so that it is in contact with the
surrounding water. Think of pouring alcohol (a polar substance) in a glass of water.
It readily dissolves due to the attraction of alcohol molecules to water.

WHY IS THIS RELEVANT?

The preceding, relatively long-winded discussion sets the stage for the following
point:

Because each protein has a unique order of specific amino acids linked in the
string, all with different chemical properties, all of the proteins in our body have a
unique shape once folded, and thus a unique function.

Some proteins are enzymes—biologic machinery that help vital chemical

reactions happen in the body (such as the production of energy). Some proteins are
hormones like insulin that are crucial for a properly functioning metabolism. Other
proteins are structural and form the scaffolding for our cells.

STRUCTURE = FUNCTION

Many readers will be interested in the muscle proteins actin and myosin
which allow muscle contraction to take place. Actin and myosin each have
a unique order of amino acids in their chains that make them fold a certain
way as 3-dimensional proteins. This folding gives them the unique shape
to perform their function.

ESSENTIAL?
Now that we have established the structure of proteins from amino acid building
blocks, and the importance of amino acids to body function, it is a good time to talk
about “essential” and “non-essential” amino acids.

Of the 20 standard amino acids, nine of them are essential. Essential just means
that your body must get these nine amino acids from the diet. The other 11 are of
course necessary for you to live, but they can be manufactured within the body. All
of the preceding discussion of protein biochemistry was leading up to the following
key point:

KEY POINT:
To manufacture all of the required proteins for proper functioning, your
body must get the nine essential amino acids from your diet in the
 correct amounts to support your activity level.

A deficiency in an essential amino acid will lead to sub-optimal protein

synthesis. There won’t be enough essential amino acid building blocks in
the correct order in the chains for the proper folding, formation, and
function of the crucial proteins when your body needs them—especially in
times of environmental stress.

For example, let us say you were fighting off an illness and your body needed to
generate a large immune response. The immune cells especially need certain
essential amino acids called “branched-chain” amino acids to generate the special
immune proteins they need to fight the infection.

If your diet is deficient in some of these amino acids, there will not be enough on
hand to generate the large amount of immune proteins needed, and you will not be
able to fight the infection as well as you otherwise could with adequate essential
amino acids from your diet.

THE NINE ESSENTIAL AMINO ACIDS

The nine essential amino acids are histidine, isoleucine, leucine, lysine,
methionine, phenylalanine, threonine, tryptophan, and valine.

PROTEIN QUALITY
The resistance-based exercise programs that are a central pillar of the Strong
Medicine approach require high quality protein beyond the recommended daily
allowance (we will get to this soon).

The quality of a protein food is generally graded on its ability to deliver the full
complement of the nine essential amino acids when eaten. Animal-based foods are
high quality proteins because they contain all nine essential amino acids in high
amounts. Many individual plant-based proteins are often lacking in relative
amounts of one or more of the essential amino acids to support heavy resistance
training or other high intensity exercise.

A sedentary vegetarian will motor along fine (from a protein perspective) with
plant-based protein. It is important for vegetarians engaged in resistance training to
make use of more than one source of plant protein, as one incomplete plant-based
protein will have the essential amino acid that another is lacking.

Using multiple plant-based proteins this way is called eating “complimentary

proteins” and can be a useful strategy for vegetarian lifters to get enough protein
without having to consume an inordinate amount of calories.

ONE-STOP SHOPPING FOR

ESSENTIAL AMINO ACIDS

Ounce for ounce and calorie for calorie, nothing can beat an animal
source of protein for a person engaged in regular strength training. The
nutrient density of these proteins is of course enhanced in wild game or
pastured (grass-fed) animal products.

HOW MUCH PROTEIN DO I NEED?

The current official recommendation for minimum daily protein intake for
“healthy people with moderate physical activity” is 0.8 grams per kilogram of body
weight (0.8 g/kg). This recommendation is from the Institute of Medicine, Food and
Nutrition Board and uses the concept of nitrogen balance to arrive at this number.
Remember from the previous discussion of protein biochemistry that the core
amino acid molecule contains nitrogen as part of its structure (some amino acid
side chains have additional nitrogen).

Amino acids from protein are our body’s primary source of nitrogen, and our
kidneys are in charge of getting rid of the excess nitrogen we do not use. The ratio
between intake of nitrogen (from protein) and excretion of nitrogen by the kidneys
is called the nitrogen balance.

Zero balance occurs when the intake of nitrogen is equal to excretion of nitrogen.
Positive nitrogen balance occurs when the intake of nitrogen is larger than
excretion, and is seen during anabolic states (building processes with overall body
protein gain) in the body. Negative nitrogen balance occurs when we lose more
nitrogen from excretion than we take in from diet, and is seen during catabolic
states (overall protein loss seen in muscle wasting).

QUICK FACT:
The official recommendations of 0.8g/kg/day are made to achieve zero
nitrogen balance in the average adult. The Food and Nutrition Board does
recognize that individuals have different needs and preferences with diet
and activity and set an upper limit of protein intake to 2.5g/kg/day without
any identifiable medical risk.

Going by the official recommendations, the average 70kg (155 lbs.) male would
fall into a range of protein intake from 56 grams to 175 grams per day. That is a
huge range! So how do I decide how much I need?

Many factors come in to play when deciding how much protein you really need,
including age, type and amount of physical activity, and underlying medical issues.

PROTEIN NEEDS DIFFER BY AGE AND

PHYSICAL ACTIVITY
The dietary signal for muscle building is supplied by the nine essential amino
acids.

As we age, we do not respond as well to the anabolic, muscle-building signal

provided by the essential amino acids obtained from protein in our diet. Because of
this, intake of protein higher than the 0.8g/kg body weight is recommended as we
start pushing middle age and may be especially valuable for those past retirement
age.

Regular resistance training, coupled with adequate protein intake has shown to be
incredibly effective in stimulating the muscle-building pathways in older trainees,
and preventing muscle wasting (sarcopenia) seen in old age. This age group should
shoot for 1-1.5g/kg body weight as long as they have no pre-existing kidney
disease.

TECHNICAL NOTE:
The signaling pathway for this is mTOR (mechanistic target of rapamycin
—formerly known as mammalian target of rapamycin). mTOR is the
main part of the signaling chain that drives anabolic (building processes)
and is stimulated by essential amino acids.

QUICK MEDICAL NOTE:

There is absolutely NO evidence that higher intakes of protein CAUSE
kidney dysfunction or disease. However, those that have kidneys that are
not working 100% (known as insufficiency) from other causes DO need to
monitor protein intake closely and should work with their doctor in
determining safe amounts.

No sarcopenia here—adequate protein and resistance training can stave off age
related muscle wasting

When trying to build muscle mass with resistance training, most people will need
significantly more protein than 0.8g/kg/day. This is highly individual based on your
training volume and intensity, so you will to experiment with it to see how much is
optimal for you.

OTHER REASONS FOR INCREASED

PROTEIN
Protein intake above the recommended 0.8g/kg/day has other advantages not
related to nitrogen balance. Protein has positive metabolic effects, especially if you
are overweight. Protein sends signals to the brain that you are full much more
effectively than carbohydrates (or fat).

The effect of this signaling to the brain is called satiety. Studies have shown that
eating 30 grams or greater of protein in the morning reduces total calorie intake for
the rest of the day. This effect can help you control calorie intake without being
hungry. Higher protein intake will also minimize any lean muscle loss when losing
excess body fat as calorie intake naturally decreases due to satiety. Take heed, all of
you “bagel and orange juice for breakfast” people!

You’ll be hungry by mid-morning...

FATS
Fat is a favorite subject, partly because there is so much controversy and
misinformation surrounding this macronutrient. Let us look at fat from a
biochemist’s perspective first, then deal with the controversy.

Fats—or according to chemists, “lipids”—are an incredibly versatile and

essential group of chemicals with hundreds of functions in the human body.
 TECHNICAL NOTE:
Fats are really a subgroup of a larger group of chemicals classified as
lipids. Other non-fat lipids include: waxes, sterols, phospholipids, and fat-
soluble vitamins.

Just a few functions of fats:

• Energy storage
• A major component of cell membranes
• Essential for proper brain development and nerve function
• Proper lung function and prevention of lung collapse
• Crucial for inflammatory response and immunity cell
signaling/communication

A complete chapter on fats is well beyond the scope of this book. Instead we will
concentrate on fats in the diet, beginning with classifying the three major types of
fats:

• Saturated fat
• Monounsaturated fat
• Polyunsaturated fat

I. SATURATED FAT

“THE HORROR! THE HORROR!”

Just like the plot from Joseph Conrad’s book, we will now venture into The Heart
of Darkness, the world of saturated fat. All drama aside (somewhat), it is evident in
the repeated official recommendations and relentless marketing campaigns, that the
idea of saturated fat as a villain of the nutritional world is very widely accepted.

Somehow the visual of saturated fat “clogging” arteries has taken hold in our
collective consciousness. The demonization of this type of fat has reached a quasi-
religious fervor in the dogmatic proselytizing of mainstream nutrition and medical
professionals. There has even been collateral damage caused by this message to
basic scientists (who should really know better) performing research.
 Let us take a deep breath, a step back, and look at saturated fat from a
dispassionate scientific perspective.

CAUTION, CHEMISTRY LESSON AHEAD!

So what does “saturated” mean when we talk about fat? As we will see in the
diagrams below, saturated just means that the molecule of fat has the maximum
amount of hydrogen atoms possible. Using a tree-branch analogy, everywhere
there could be a leaf, there is a leaf.

Before we go any further, let us establish a very basic chemistry rule regarding
the carbon atom. This rule guides the maximum number of hydrogens (amount of
saturation) possible for a fat.

RULE: Each carbon atom can only form 4 bonds

KEY POINT:
The single bond chain is a very important feature in the saturated fatty acid
for a couple of reasons.
1. The single bond “backbone” gives the chain flexibility.
2. There are no double bonds in the chain, making saturated fats
resistant to free radicals.

We will discuss the implications of these two facts very soon.

Single fat molecules, called fatty acids, are just long chains of carbon linked
together. The head of the fatty acid is called the alpha end. The alpha end has
oxygen molecules attached, which makes this end attract water. The tail of the fatty
acid molecule is called the omega end. The length of the tail all the way to the
omega end only has carbon and hydrogen, making this end repel water.

The long chains of carbon on a saturated fat have only one single bond
connecting each of the carbons to each other. This fact is important because of our
rule of four total bonds per carbon atom—two bonds are left open on most of the
carbons in the chain for hydrogen to bond. The omega carbon can actually bond
three hydrogens.

This is a 12-carbon saturated fat called lauric acid. Notice that every grey carbon
atom has four bonds (even the alpha carbon because the double bond counts as two
bonds).

The all-single-bond carbon backbone gives the chain flexibility. This flexibility
means that when a bunch of saturated fatty acids are together, the tails can “bend” to
form close associations with their neighbors. These close associations are why
saturated fats are solid at room temperature (but they are all liquid at body
temperature).
 TECHNICAL NOTE:
For all of the biochemists out there, I realize I have represented the carbon
chain of the fatty acid in the diagram as a straight line. In reality, the
carbon chain looks like a series of “zigzags” due to bond geometry.
Representing the bond geometry accurately in a picture complicates the
visual greatly, so it is simplified above to teach the concept.

Now that you know what a saturated fat is from a biochemistry perspective, we
will discuss the basic ways to classify the various saturated fats. You will see that
even small changes in the chain length make a huge difference in how each type
affects our body functions.

You will also see how ridiculous it is to make generalized statements about
saturated fat and health, without discussing the specific types of saturated fat
involved.

CLASSIFICATION BY CHAIN LENGTH

A general way to classify saturated fats (and other fats as well) is by chain length
of the carbon “backbone”.

1. Short-chain saturated fats have backbones two to five carbons long.

2. Medium-chain saturated fats have backbones six to 12 carbons long.

3. Long-chain saturated fats have backbones longer than 12 carbons.

We are going to profile fats from each of these three classifications, so you can
see the huge differences in function among them, while keeping in mind that they
are all saturated fats.

Profile of a
short-chain saturated fat.
BUTYRIC ACID (BUTYRATE)
From the diagram, you can see butyrate (also called butyric acid) is a four
carbon saturated fatty acid. Butyrate has some very interesting actions in
our body:
• It is the major product of fiber fermentation by the gut bacteria.
• Butyrate has very potent anti-inflammatory properties.
• Butyrate has powerful anti-cancer effects through epigenetic
mechanisms.
• Butyrate has been used in conjunction with modern cancer treatment
techniques (photodynamic therapy) on certain types of brain tumors,
killing more cancer cells.
• Butter is about 3% butyrate, and is the best direct dietary source
(fermentation of fiber is the best indirect source).

LAURIC ACID (LAURATE)

Profile of a medium-chain saturated fat.

From the diagram, you can see laurate (also called lauric acid) is a 12
carbon saturated fatty acid. Laurate has the following effects in the body:
• Comprises about 6% of the fat content in human breast milk.
• Potent antibiotic actions against bacteria and viruses.
• As a medium-chain triglyceride, laurate is used as an alternate fuel
source in the brain, showing promising results treating epilepsy and
degenerative brain disorders such as Alzheimer’s dementia.
• Increases high density lipoprotein (HDL) associated cholesterol, which
may decrease risk from developing heart disease.
• As a component of medium-chain triglycerides, lauric acid in the diet
has been shown to aid significantly in weight loss.
• Coconut oil is a great source of lauric acid, which comprises about
50% of the fat content in coconut oil.

DIGGING DEEPER:
Medium-Chain Fats and Metabolism

Coconut oil: an excellent

source of medium chain fats
Medium-chain fatty acids in the diet are metabolized much differently than
long-chain fatty acids. The medium-chain fats, in the form of medium-
chain triglycerides, are taken directly to the liver after they are absorbed
in the intestines. In the liver they are rapidly metabolized for energy use
in the body.

The long-chain fatty acids are absorbed in the intestine and travel in the
lymphatic system. They have a much higher chance of being stored in fat
cells before getting to the liver for energy use.

This may be why medium-chain triglycerides have been used successfully

as a dietary supplement for body fat loss. They are able to bypass the fat
storage sites and are used directly for energy production.

Additionally the medium-chain fats do not need the specialized fat

transporter (carnitine-acylcarnitine translocase) to get into the
mitochondria (the place in the cells where energy production takes place)
that long-chain fats need. This fact allows rapid entry of medium-chain
fats into the mitochondria for energy production.

PALMITIC ACID (PALMITATE)

Profile of a long-chain saturated fat.

From the diagram, you can see palmitate (also called palmitic acid) is a 16
carbon saturated fatty acid. Palmitate has the following characteristics and
effects:
• It is the primary fat stored by the body in fat (adipose) tissue.
• High amounts in fat cells are inflammatory.
• It is the primary saturated fat used in research studies.
• Activates an inflammatory response by immune system.
• High levels of palmitate increase insulin resistance, contributing to
diabetes.
• Palmitate levels are higher in the fat content of grain-fed animals.

WHAT IS A TRIGLYCERIDE?
 Triglycerides are simply three individual fatty acids linked together at
their “alpha” ends by another carbon backbone (made from glycerol). The
triglyceride form is the way fats are stored in fat cells. This form of fat
is also what we measure in doctor-ordered blood tests (see the Analytics
chapter).

The graphic above shows three separate lauric acid molecules (twelve
carbon saturated fatty acids) joined together by a three carbon glycerol
backbone. The area shaded in pink is where the three separate fatty acids
are joined to the glycerol to make a triglyceride.

We are going to profile another long-chain fatty acid just to show you the
difference two extra carbons in the backbone makes, concerning how the fat
“behaves” in the body. Make sure you compare the 16 carbon palmitic acid to this
next long-chain fatty acid.

STEARIC ACID (STEARATE)

Profile of a long-chain saturated fat.

From the diagram, you can see stearate (also called steric acid) is an 18
 carbon saturated fatty acid. Although differing in length by only two
carbons, stearate behaves very differently than palmitate:
• Stearic acid has been shown to beneficially reduce blood clotting and
may decrease the risk of heart disease.
• Unlike palmitic acid, stearic acid has no bad effects on insulin
resistance or development of diabetes.
• Stearic acid does not promote inflammation in fat cells.
• Stearic acid triggers the death of breast cancer cells in laboratory
testing.
• Grass-fed beef is a good source of stearic acid.

Comparing the 16-carbon saturated fat palmitic acid, with the 18-carbon saturated
fat, stearic acid, there are substantial differences in potential health effects for each.

FIRST PRINCIPLES-BASED
SPECULATION:
I think there is a reason why palmitic acid in high amounts in particular
can trigger an inflammatory response in the body. As we will discuss in
the chapter on obesity, palmitate is the specific type of fatty acid the body
makes and stores in fat cells. When fat cells become overloaded, the
immune cells are triggered as a warning response to the body that
something “bad” is happening (in this case obesity).

The immune cells trigger an inflammatory response, and an overloaded

fat cell is considered an overall “threat” to the body as a whole. Because
palmitate is generally the specific type of fat stored by the body in fat
cells, high amounts in the diet can trigger the immune system, mimicking
the threat of the palmitate-overloaded fat cell.

It is interesting that the same specific molecules (called toll-like receptors)

that palmitate triggers for the inflammatory response, are in the same
family that the immune system uses to recognize pathogenic bacteria as
“threats.”
WHY HAVE WE BEEN TOLD THAT SATURATED FAT IS BAD?
I think the reason for the “saturated fat is the devil” messaging stems from
combination of bad science, politics (big shock!), and groupthink. I encourage you
to read Gary Taubes’ outstanding book Good Calories, Bad Calories. Mr. Taubes
does a masterful job in chronicling the origins of the current campaign against
saturated fat. Just a cursory review of the differing effects of the many different
types of saturated fat on the previous pages should be enough for us to stop lumping
all saturated fats together as a harmful, homogenous, “artery-clogging” substance.
This type of fat should be regarded with a bit more nuance and thoughtfulness.

To be fair, there are many scientific studies showing that saturated fat causes
inflammation and disease in animal models. However, there is a pretty good reason
why we see so many scientists coming to this conclusion.

In 2012, a group of scientists showing a high amount of critical thinking

published an article in the American Journal of Physiology, Endocrinology, and
Metabolism, showing that a large majority of scientific studies on saturated fat used
only palmitic acid when testing the effects of saturated fats on animals and cultured
human cells. To make matters worse, it was found that many of the authors of these
studies then generalized their results to all saturated fat, even though only
palmitic acid was used.

We have shown you in previous pages that palmitic acid can indeed be
inflammatory in the right circumstances, and may be associated with health
problems. But, the effects of palmitic acid certainly cannot be generalized to all
types of saturated fat.

This type of bad science just reinforces the collective groupthink that all saturated
fat is “bad”. This information is taught to doctors and dietitians who unfortunately
do not question the science. Again, public health suffers at the hands of bad
science and groupthink.

We have spent this much time discussing saturated fat for a reason. We have to
change the public health message that all saturated fat should be avoided. Most
saturated fat is a necessary and beneficial macronutrient for optimum health, and
was an essential part of our distant ancestors’ diets.

The next time a health care provider or well-meaning acquaintance tells

you to avoid saturated fat, I encourage you to first respond, “What
specific type of saturated fat are you asking me to avoid?”
 After the likely quizzical look, hopefully a mutually-beneficial and
educational conversation can occur.

II. MONOUNSATURATED FAT (MUFA)

Now that you know what “saturated” means, discussing monounsaturated fats
should be a bit easier from a biochemistry perspective. Remember that each carbon
atom can only form four total chemical bonds. With a monounsaturated fatty acid,
two of the carbons in the “backbone” are joined by a double bond, instead of a
single bond. This double bond ties up two bonds out of the total of four that each
carbon atom can form.

You will notice that the carbons on the right have lost the bonds on top due to the
double bond. Adding the top facing bonds on the picture in the right would give five
total bonds per carbon, violating the four bond rule. This matters because when we
add a double bond to a fatty acid carbon backbone, we cannot get the maximum
amount of hydrogens on the fat. Thus it is no longer “saturated” with hydrogens, but
“unsaturated” because of one double bond. Mono=one, so we call this type of fat
a monounsaturated fatty acid (MUFA).

The “kink” in the chain from the double bond is important for the function of
monounsaturated fatty acids. When a large amount of monounsaturated fats are
lined up together, the angle of the “kink” does not allow them to get very close
together, so they are less densely packed when in a group. It would be like trying to
bundle a bunch of bent sticks.

This is why olive oil, a primarily monounsaturated oil, is liquid at room

temperature, rather than solid like the saturated fats which are able to group together
more closely.

OLEIC ACID
A monounsaturated fatty acid
CHARACTERISTICS AND HEALTH
EFFECTS OF MUFA
Oleic acid, an 18 carbon monounsaturated fat, is the primary dietary
MUFA and has generally positive health effects:
• May help reduce blood pressure and cardiovascular risk.
• It is the crucial fat for proper cell membrane function.
• It is the main fat of the Mediterranean diet, generally considered
healthful.
• High levels of MUFA are found in olive oil, avocados, macadamia nuts,
lard, and beef tallow.

THE DOUBLE BOND: UNSATURATED

FAT’S ACHILLES HEEL
Remember our discussion of free radicals and oxidative stress in the
Central Themes chapter? Free radicals are the unstable molecules with an
unpaired electron, looking to take another electron from anywhere to
complete the pair. Free radicals are attracted—like moths to a bright porch
light—to any source of electrons.


It turns out that double bonds are a particularly attractive source of

electrons, like blood in the water to a free radical shark. Free radicals will
“steal” an electron from the double bond in an unsaturated fatty acid,
turning the fat into a free radical in the process. The newly created fatty
acid free radical is a “lipid peroxide”.

Imagine a newly created lipid peroxide, formed from an unsaturated fat

previously just minding its own business as part of a cell membrane. The
free radical lipid peroxide will then find its own source of electrons to
steal, likely from a neighboring unsaturated fat in the cell membrane. This
creates a chain reaction in the cell membrane called lipid peroxidation,
and if not stopped, leads to widespread destruction of the cell membrane
and death of the cell.

Double bonds can also lose electrons when subjected to heat, light, or left
in the open air, through processes called photo-oxidation and
autoxidation. Oxidized fats are damaged fats and free radicals
themselves. You certainly don’t want to eat any of these oxidized fats, and
it is why you should not cook with unsaturated fats for health reasons.
This is the main reason fried foods are bad for you. Eating damaged
unsaturated fats from high heat cooking or processing is like importing
oxidative stress into your body.


Remember that saturated fats do not have any double bonds in their back-bone,
and are relatively resistant to oxidation at high heat. This is why saturated fats don’t
“go rancid” like other fats and why they have a long shelf life.

There are tons of health benefits to foods containing high monounsaturated fats.
Just make sure you store them away from light and heat and don’t routinely cook
with them.

STRONG MEDICINE TACTICS:

Cook mostly with saturated fats such as coconut oil to avoid fat oxidation
and importing free radicals into your body.

III. POLYUNSATURATED FAT (PUFA)

You already know what “unsaturated” means, so this will be easier. A
polyunsaturated fatty acid (PUFA) is simply a fatty acid with more than one
double bond.

The two main types of polyunsaturated fatty acids we will cover are the omega-3
and the omega-6 fatty acids. In our original diagram of a fatty acid, remember that
we called the “head” the alpha-end, and the “tail” the omega-end. When we name
polyunsaturated fats, they are named for the position of the first double bond
from the omega end.

ESSENTIAL” FATTY ACIDS:

 Only two fatty acids are known to be “essential” for humans. Essential
means that we have to get these fats from the diet, as our bodies cannot
make them from other fats. This is similar to the concept of essential
amino acids we discussed in the protein section. Both essential fatty acids
are of the polyunsaturated type. These two essential fats are:
• Alpha Linolenic Acid (ALA), an 18 carbon omega-3 polyunsaturated
fatty acid that is found in many seeds, notably flaxseed.
• Linoleic Acid (LA), an 18 carbon omega-6 polyunsaturated fatty acid
that is found in many vegetable oils such as safflower, grape seed, corn,
and soybean oils.

These two essential fatty acids are important building blocks for other
fats, but you only need a little ALA and LA in your diet to satisfy the
body’s requirement.

Following the Strong Medicine dietary prescriptions will ensure

adequate amounts of both ALA and LA.

Although we need relatively little polyunsaturated fats in our diet, they have a
profound influence on our health. We’ll start with a little background on the two
main types of PUFA, dietary sources and health effects.
OMEGA-3 FATTY ACIDS
You probably have heard a lot about the beneficial effects of the omega-3s. It
seems food manufacturers are putting them in all kinds of processed foods, even
milk and ice cream. It is important that we discuss the science behind the health
claims before you buy these products thinking that you are doing something good
for your health.

THE OMEGA-3 PUFA “BIG 3”

The following are the three most biologically important omega-3 PUFA
in the diet:
 • Alpha Linolenic Acid (ALA)— The 18 carbon omega-3 pictured on the
previous page and one of the two essential fatty acids. Flaxseed and
flaxseed oil are probably the best known food products containing high
amounts of ALA.
• Eicosapentaenoic Acid (EPA)— This omega-3 PUFA is 20 carbons
long and is one of the main fatty acids found in “oily” fish (salmon, tuna,
sardines).
• Docosahexaenoic acid (DHA)— DHA is the longest chain of the
omega-3 PUFA at 22 carbons in length. It is also found in oily fish and
fish oil. DHA has been shown to be especially important in brain health,
especially in the developing brains of children.

Research on omega-3 PUFAs have shown numerous positive health effects in

recent years against the following diseases:

• High blood pressure

• Diabetes type II
• Heart arrhythmia
• Cancer (certain types)
• High triglycerides
• Osteoporosis

They have also been found to be beneficial in the following areas:

• Reducing chronic inflammation

• Optimizing brain development in children
• Neurodegenerative disorders in the elderly

EPA and DHA seem to be the omega-3 superstars for health benefits, more so
than ALA from recent research.

WHAT IS AN “OILY FISH”?



Oily (or fatty) fish are those that carry fat in their flesh and gut, as
opposed to “white” fish that have their fat located primarily in their liver.
Oily fish usually swim in the water column away from the bottom of the
sea. White fish are usually bottom dwellers.

Oily fish include species such as salmon, tuna, sardines, and trout.

WHERE DO THE OMEGA-3 PUFAS

COME FROM?

The beneficial omega-3 PUFA found in fish and animal foods originally
come from land plants and tiny water-based plants called algae. This is
why when choosing fish and land animal flesh for food, it is extremely
important to know the diet of these animals before assuming any health
benefits.

In the wild, fish get their omega-3 from the food chain, starting with
aquatic plant-like species such as algae (a type of phytoplankton). Algae
are eaten by krill (a tiny crustacean), and krill are eaten by small fish (and
larger fish as well). The smaller fish are then eaten by the larger fish. In
 this way, the original omega-3 PUFA produced by algae are now in the
fish you eat.

It is well-established that fish traditionally high in omega-3 such as

salmon, have almost no useable omega-3 when raised in fish farms,
eating processed fish feed.

Wild game and domesticated herbivores such as cattle have significant

amounts of omega-3 from the plants they eat. Meat from grass-fed cows
has almost twice the omega-3 PUFA than cows that are grain-fed in
feedlots.

STRONG MEDICINE TACTICS:

To maximize omega-3 PUFA in your diet, eat wild-caught oily fish and
meat from grass-fed animals.

OMEGA-6 FATTY ACIDS

Chemically, the omega-6 fatty acids are simply PUFAs that have their first double
bond six carbons from the “tail,” or omega end.
 This seemingly small chemical difference from omega-3 PUFAs results in very
big differences in how omega-6s differ in function within our body.

Omega-6 PUFAs are crucial to the following processes:

• Inflammatory process of wound healing

• Regulating blood coagulation
• Stimulating growth of cells and repair processes
• Proper functioning of the immune system

WHERE DO THE OMEGA-6 PUFAS

COME FROM?

Omega-6 PUFA are found in high amounts in nuts, seeds, as well as

vegetable and seed oils. They are also present in animal-based foods, but
like omega-3 content in animal products, the amount of omega-6 PUFA is
dependent of the type of food the animal itself is eating.

Western diets high in processed food contain large amounts of omega-6

PUFA, mostly from the routine use of industrially processed seed oils
such as sunflower, safflower, soybean, and corn-derived oils. Herbal oils
such as evening primrose and borage oils are also good sources.

Grain products also contain significant amounts of omega-6 PUFA.

People in modern societies have significantly increased their omega-6

PUFA content compared to ancestral diets and the diets of traditional
cultures. As we will see, this increase is not without potential health
consequences.
 It is unfortunate that the omega-6 PUFA have recently been demonized in
nutritional circles in a similar way to saturated fat. We need to dig a little deeper and
use some critical thinking before pronouncing a sentence on omega-6.

While it is true that the large amounts of omega-6 many of us are consuming in
processed food from added industrially produced vegetable and seed oils can be
problematic from a health standpoint, balanced dietary intake of omega-6 from
natural whole food sources is an important part of our diet and necessary for
optimal health.

THE OMEGA-6 PUFA “BIG 3”

The following are the three most biologically important omega-6 PUFA
from the diet:
• Linoleic Acid (LA) is the 18 carbon omega-6 found in many vegetable
oils such as safflower, grape seed, corn, and soybean oils.
• Gamma Linolenic Acid (GLA) is another 18 carbon omega-6 with one
more double bond than LA. Unlike most omega-6, which have
inflammatory actions, GLA can have anti-inflammatory effects. Direct
dietary sources include: evening primrose oil, borage oil, and
blackcurrant seed oil.
• Arachidonic Acid (AA) is a 20 carbon omega-6 which is very important
in the inflammatory response and repair processes (such as muscle tissue
building in response to weight training). It is also very important in
growth and repair of nerve cells. Dietary sources are primarily from
animal products such as meat and eggs. It can also be synthesized from
LA, so vegetarians are usually not deficient.

We need to have a relative balance of omega-3 to omega-6 in our diets, and for
many of us currently eating processed foods, this means reducing omega-6 intake
and increasing omega-3 intake.

INVESTIGATE YOURSELF!
Read the labels on the food you buy at the grocery store. You will be
surprised how often you will see vegetable and seed oils (high in omega-
6) listed in the ingredients. They seem to be in everything, and are the
primary reason why many of us have an unbalanced dietary intake of
omega-6 fatty acids.

The balancing of omega-3 and omega-6 will happen naturally and without
supplementation if you stop eating processed foods and focus on high quality whole
food sources. The following section will discuss why balancing omega-3 and
omega-6 intake is so important.

THE OMEGA-3/OMEGA-6 BALANCE

The omega-3 and omega-6 PUFA act as building blocks for a group of
messenger molecules called eicosanoids. These messengers are central to how the
body creates and controls inflammation. The eicosanoids go by names such as
prostaglandins, prostacyclins, thromboxane, and leukotrienes.

In general (there are exceptions), the omega-3 PUFA are building blocks for
eicosanoids that have anti-inflammatory actions which control the body’s
inflammatory response.

Overall, the omega-6 PUFA are building blocks for eicosanoids with
inflammatory actions such as wound healing and the immune response.
 Having a balance of the anti-inflammatory and inflammatory eicosanoids is very
important for optimum function of our body systems.

When we are injured, or are fighting a viral or bacterial infection, we need the
inflammatory eicosanoids (derived from omega-6 PUFA) for wound healing or
mounting a strong immune response. The anti-inflammatory eicosanoids (built
from omega-3 PUFA) are there to calm down the inflammation as the injury is
healing or after the infection has been dealt with.

KEY POINT:
If we don’t have enough omega-6 PUFA to act as building blocks for
inflammatory eicosanoids, we won’t be able to recover from injury,
rebuild muscle after a workout, or fight off infection.

If we don’t have enough omega-3 PUFA to act as building blocks for anti-
inflammatory eicosanoids, acute inflammation will become chronic
inflammation. Our immune system may become overactive, and we won’t
be able to control cell growth well, which is a factor contributing to
cancer.

The high intake of omega-6 from processed food has shifted the balance in many
of us decidedly towards an excess of omega-6, promoting a general low-level
chronic inflammatory state in our body. Remember the diagram below from the
introductory section on inflammation and oxidative stress:
 It is no surprise that as processed food intake (high omega-6) increased in the
20th century (even more in the 21st), the incidence of chronic diseases such as
cancer, heart disease, diabetes and obesity have increased as well. The high intake of
omega-6 from vegetable and seed oils in processed food may be a primary
contributor.

It also makes sense that supplementation with fish oil (high omega-3) has shown
in many studies to be effective in treating some of these chronic diseases.

PUFA COMPETITION
A major way that omega-3 and omega-6 PUFA work is through their
incorporation into the cell membranes of all cells in the body. Once in the cell
membranes, they can then be the building blocks for the eicosanoids as previously
discussed.

The omega-3 and omega-6 PUFA compete for placement in the cell membranes,
so having a balance of the two in the diet is important. An unbalanced diet, heavy in
omega-6 will result in a disproportionate amount of omega-6 placed in the cell
membranes, essentially outcompeting the omega-3 by sheer numbers. This leads to
an unbalanced production of large amounts of inflammatory eicosanoids due to the
high amount of omega-6 PUFA in the cell membranes.

TECHNICAL NOTE AND RESEARCH UPDATE:

 Recent studies have shown that omega-3 PUFA also directly affects the
gene expression of inflammatory messengers by inhibiting their
formation in the cell. This effect on reducing inflammation is separate
from omega-3’s role as a building block of anti-inflammatory
eicosanoids.

You can see from the graphic that the essential fatty acids ALA and LA are converted
into their “big brother” omega-3 and omega-6 with conversion enzymes. The
omega-3 and omega-6 conversion pathways share the same conversion enzymes.
This is important because if you have an excess of dietary omega-6, the conversion
enzymes will be busy converting the LA omega-6 and won’t have room to convert
the ALA omega-3 to the highly beneficial EPA and DHA.

It is also very important to note that the conversion from ALA to EPA and DHA is
very inefficient. It is estimated that only 5% of dietary ALA is converted to EPA
and DHA. If you add in a bunch of LA omega-6, then due to competition with the
shared conversion enzymes, very little ALA is converted to EPA and DHA (now less
than 5%).

You can bypass the poor conversion by eating EPA and DHA directly from fatty
fish, but this is obviously a problem for vegetarians who try to get all of their
omega-3 in the form of ALA from sources like flaxseed.

TECHNICAL NOTE:
The preceding graphic was simplified significantly, and left out an
 important omega-6 called dihomogamma linolenic acid (DGLA). It is
synthesized from GLA and is made into AA. DGLA is interesting as an
omega-6 in that it has anti-inflammatory properties.

The conversion graphic highlights the problems encountered with shared

conversion enzymes for omega-3 and omega-6 PUFA. As noted, strict vegetarians
and vegans can have a hard time getting enough EPA and DHA—which is critical to
health—due to the poor conversion of ALA. This is especially problematic if the
same vegetarian or vegan is taking in a high amount of omega-6 PUFA at the same
time.

QUICK MEDICAL NOTE:

DHA is especially important for brain function. A full 40% of the cell
membranes of nerve cells are comprised of DHA.

DHA is especially important for children with developing brains, and

elderly with potentially degenerating brains. Women of reproductive age
show an increased efficiency over men for converting ALA to EPA and
DHA. This makes sense, as they would need to provide plenty of DHA to a
developing fetus for brain development during pregnancy.

Children do not have this conversion advantage, so it is extremely

important that kids get adequate EPA and DHA. Enforcing a strict vegan
lifestyle on a child and neglecting adequate amounts of DHA, can lead to
developmental problems if not supplemented.

SUPPLEMENTATION?
Given what we know about competition for membrane placement and competition
for conversion enzymes, the better approach to balancing omega-3 and omega-6
would be to decrease the amount of omega-6 in the diet and increase the omega-3
from whole food, high quality sources.

Supplementing omega-3 using fish oil capsules, while you continue to eat high
omega-6 processed food, has a couple of disadvantages in our opinion:
 • This approach is trying to directly outcompete the high omega-6 with high
omega-3 intake. The human body only needs small amounts of both omega-3 and
omega-6, so this has a potential to overwhelm the system.

• Omega-3s are still polyunsaturated fats, and prone to oxidation and free radical
formation because of the multiple double bonds. The process of extracting and
storing fish oil leaves these fragile double bonds exposed to heat and light,
creating omega-3 free radicals. Free radicals, omega-3 or not, are not good
things to import into your body.

Similarly, the omega-6 extracted in industrial processes to form vegetable and

seed oils, also have the potential to form significant amounts of fatty acid free
radicals!

QUICK MEDICAL NOTE AND RESEARCH UPDATE:

Recent research has starting to link an unbalanced omega-6 to omega-3
ratio (one that is high in omega-6) to an increased incidence of allergies
and asthma. This makes sense as high levels of omega-6 lead to increased
inflammatory eicosanoids and over-active immune systems. Balancing
your omega-6 and omega-3s may help decrease the severity of allergy
symptoms and asthma.

Maintain the balance for your health

 STRONG MEDICINE TACTICS:
To balance omega-3 and omega-6 PUFA, decrease high omega-6
processed vegetable and seed oils, and increase whole food sources of
omega-3 such as wild caught fish and products from pastured animals
eating their natural diet.

TRANS FATTY ACIDS (TFA)

Trans fatty acids, or “trans fats” as you may have heard them called, do exist in
small amounts in natural foods, but it is the TFA produced by man-made processes
that have negative effects on our health.

Chemically, the concept of TFA is relatively simple. As you now understand the
chemistry of the double bond, the following shouldn’t make your eyes glaze over
too much.

There are two types of double bond configurations in fatty acid carbon chains.
The most common configuration which occurs in almost all fats is called “cis.”
The configuration which is relatively rare in nature is called “trans.” Cis and trans
simply describe where the hydrogens are positioned on the double bond. This
positioning changes the structure of the fat considerably, and we have previously
discussed how important structure is to function in the body. Small changes in
structure can change function dramatically.

The cis configuration has the

The trans configuration has the hydrogens
hydrogens on the same side of the
on the opposite side of the double bond.
double bond.

This seeming small change in the double bond configuration profoundly changes
the way trans fatty acids operate in the body.

As most trans fats in our food supply are not products of nature but man-made,
our bodies treat them as foreign invaders and the result is increased inflammation
and oxidative stress. With this effect in mind, it comes as no surprise that routine
intake of trans fat has been linked to diseases associated with chronic
inflammation and oxidative stress such as heart disease, diabetes, cancer, and
neurodegenerative diseases such as Alzheimer’s dementia.

This is the 18 carbon cis monounsaturated fat, oleic acid. This is the same health-
promoting fat found in olive oil we discussed earlier. Notice that the hydrogens on
either side of the double bond are on the same side. Also notice the kinked shape this
cis double bond gives the tail.

This is the 18 carbon trans monounsaturated fat, elaidic acid. Other than the
configuration of the double bond, it is chemically identical to oleic acid. Notice
what the trans double bond does to the kink in the tail, resulting in a “straighter”
carbon backbone. This structural change makes all the difference in the world to the
body, as elaidic acid is a well-known trans fat linked to diseases such as cancer and
heart disease in humans.

INVESTIGATE YOURSELF!


Did you know that according to the Food and Drug Administration, a food
manufacturer can claim “zero trans fats” if there are less than 0.5 grams
of trans fat per serving size in the product? If something has
hydrogenated or partially hydrogenated oil of any type listed among the
ingredients, there is some amount of trans fat present, despite any
claims to the contrary.

WHERE DO TRANS FATS COME

FROM?

In the early 1900s it was discovered that you could make liquid oils solid,
by putting them through a process called hydrogenation. Hydrogenation is
a process in which hydrogen is added through a catalytic reaction to
unsaturated fatty acids. Unsaturated vegetable oils can be produced much
more cheaply than animal-based fats for use in cooking and as food
additives. As you now know, unsaturated fats have double bonds, leaving
them susceptible to oxidation when left out in the open or in storage. You
may have heard of fat going “rancid”—this is the result of oxidation of
the double bonds in unsaturated fats.
Food manufacturers had the idea of artificially adding hydrogens to the
unsaturated vegetable oils, making them saturated (or at least more
saturated) and thus resistant to “going rancid.” This extended shelf life and
created an inexpensive long lasting fat that wouldn’t go bad. Vegetable
shortenings and margarine are examples of “foods” made using this
process of turning liquid vegetable oils into products that are solid at
room temperature.

Unfortunately, the process of hydrogenation alters many of the

unsaturated fat’s double bonds, turning them from the natural cis
configuration to the rare trans configuration that our bodies are not
equipped to process.

During the 1950s and 1960s, hydrogenated vegetable fats became more
widely used than the traditional animal fats of lard and tallow for cooking
and food ingredients. It is quite interesting that heart disease, formerly a
relatively rare health problem, increased dramatically during the same
time period as the widespread use of hydrogenated and partially
hydrogenated vegetable and seed oils.

Hydrogenated and partially hydrogenated vegetable oils are industrial

concoctions not found in nature—enough said.

STRONG MEDICINE TACTICS:

Eliminate any food or food product containing hydrogenated or partially
hydrogenated vegetable or seed oils (including soybean oil) from your
diet. Read your labels!

TECHNICAL NOTE:
There are some naturally occurring trans fats in animal-based foods that
 have not shown to have bad health consequences. One of these is vaccenic
acid found in dairy products, as well as human breast milk. Vaccenic acid
is converted into a highly beneficial group of fats known as conjugated
linoleic acid (CLA). CLA has been shown to have anti-cancer properties
and has shown promise as a weight loss aid for humans. Aside from
being formed from vaccenic acid, CLA can also be found directly in milk
and meat from pastured (grass-fed) animals.

We have spent a disproportionate amount of time discussing fats, but hopefully it

was time well spent. If you are interested in further study into the world of fat, an
excellent book is “Know Your Fats,” by Mary Enig, PhD.

Now get ready to dive headfirst into the basics of human metabolism. We have to
know how the flesh machine is supposed to function to understand the consequences
and causes of a broken metabolism.
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BASIC TRAINING II:
NUTRITION AND METABOLISM 101:
METABOLISM BASICS

Any discussion about human metabolism is quickly lost in the incredible

complexity of this dynamic self-regulating system. Whole academic textbooks are
written on the subject and are still lacking in some way. We will greatly simplify the
discussion by focusing on overarching ideas and concepts. Essential details will
emerge.

ENERGY AS CURRENCY
Metabolism is the production and utilization of energy from the foods we eat.
Foods and beverages are converted into the fuel needed to run the human body. The
human body uses a specific molecule as its energy currency. Everything revolves
around making and breaking down this molecule for energy. We make money and
we spend money on essential needs. It is the same with energy—we manufacture and
distribute, or “spend,” our available energy on the body’s essential needs. This
molecule of energy currency is known as adenosine triphosphate (ATP).

Our body and brain control the metabolism. Think of metabolism as your home
thermostat: optimally, we want a fast metabolism. Through the skilled blending of
intense exercise and certain power-packed nutrients found in regular food, we can
“amp up” or accelerate the metabolism. We want to raise our metabolic thermostat.

A morbidly obese individual has a snail-paced metabolism while a super active

ten-year-old boy will have a blast-furnace metabolism. The obese person’s slow
metabolism is very efficient in its use of fuel. The burning hot metabolism of the
lean and athletic youngster is a raging bonfire; a bonfire craves big logs (lots of
food/fuel) to stay raging. We seek to build the metabolism, raise our home
thermostat, build a metabolic bonfire, and inefficiently burn a lot more fuel
(calories).

The body has an innate wisdom and preferentially sends macronutrients to where
they are most needed on an immediate basis. The metabolism regulates how much
of each nutrient needs to be present at any one body location at any one time. You
will learn how different types of food stimulate different hormones, which in turn
control what type of fuel is used to make energy—fat or carbohydrate.

METABOLISM CONCEPTS
The following are overarching ideas we will use to help you understand
metabolism:

The brain is an
energy and glucose hog.

1. The brain is an “energy hog” and requires glucose. The average human brain
weighs about three pounds. For a 170-pound person, the brain represents less
than 2% of total body weight, but uses 20% of total daily body energy.

The brain is also very particular about which type of fuel it uses. Most of the
brain requires glucose to function. In a pinch the brain can use ketones as an
alternate fuel.
 CENTRAL THEMES CONNECTION:
Because the brain requires glucose as brain fuel to make ATP, when blood
glucose starts to drop, the brain quickly notices and signals the body to
produce more glucose, or it generates a “sugar craving” so you will
consume more glucose. In the “Chronic Stress” chapter, we will further
discuss the hypothalamus and its role as the master regulator of the
stress/threat response.

The hypothalamus is also a regulator of metabolism and hunger which

ensures the brain receives a consistent supply of glucose. Low glucose in
the brain is considered a “threat.” Perceived threat in the brain (in this
case low glucose) is central to controlling our metabolism.

2. The liver is the glucose “banker” The liver receives signals from the brain to
keep blood sugar at a (relatively) constant level. The liver will store glucose
when dietary levels of carbohydrate are high. The liver releases glucose when
dietary intake is low. All the liver ’s actions are done to maintain adequate levels
of glucose and keep the brain happy.

In times of starvation (i.e. radical calorie-restricted diets) the liver will make
glucose from amino acids either from protein in the diet, or more often from
“muscle cannibalism” when the body breaks down its own muscle tissue, strip
mining it for amino acids.

Making glucose from amino acids stolen from protein is called gluconeogenesis
(gluco=glucose, neo= new, genesis= make). With prolonged starvation, the liver acts
like the Federal Reserve and will print money (make glucose from amino acids
derived from muscle) and put that energy currency into immediate circulation.
 TECHNICAL NOTE:
Gluconeogenesis actually happens all of the time, especially during the
night as we sleep. As long as you have adequate protein in your diet to
provide amino acids, the process will have minimal impact on your
skeletal muscle. Muscle wasting happens in times of starvation/calorie
restriction without adequate protein intake.

3. Skeletal muscle has a large capacity to store glucose. Muscle can store five
times more glucose (as glycogen) than the liver. The caveat with glucose stored
in muscle—when glucose goes in, it cannot come back out. The muscle holds
onto glucose in case it needs to use it for a “flight or fight” response, such as
running away from a bear at full speed.

Fat cannot fuel this type of extreme muscular effort, so the muscles store large
amounts of glucose in case it is needed as a survival mechanism. Muscle will not
and cannot share this stored glucose with the brain (even under starvation
conditions). We will use this fact to our advantage by implementing intense exercise
to create a large glucose “sink” in the muscle. Stay tuned for more on this topic.

TECHNICAL NOTE:
Red blood cells are unable to use fat for an energy source because they do
not have mitochondria. They can only use glucose for energy.

4. Our body runs more efficiently on fat but will use glucose first. Fat is the
most efficient energy source for most of the body. Even our muscles use fat as
their primary energy source while at rest. Our organs and tissues will use
 glucose before using fat for energy if we eat glucose in the diet. When glucose is
scarce, the body seeks to horde its dwindling glucose supply and shifts into a
burn-fat-for-fuel metabolic mode. Using fat when glucose is low spares glucose
for use by the brain (and red-blood cells).

5. High levels of glucose in the blood are toxic. Glucose is inherently toxic.
Excess glucose promotes inflammation and oxidative stress. The metabolism of
glucose for energy creates free radicals. Glucose “sticks” to proteins in the blood
and in the cells lining the blood vessels. This results in advanced glycation
endproducts (AGE).

AGEs promote inflammation and oxidative stress. Our bodies are always
detoxifying AGEs. The body is designed to clear low amounts of AGEs, produced
by normal blood glucose levels, but is overwhelmed if blood glucose levels stay
high. Several mechanisms keep blood glucose levels in the “goldilocks” range, not
too high, not too low, just right.

Large increases in dietary glucose will be moved out of the blood to be used for
energy (or stored in cells) by the actions of insulin. Controlling the interaction
between glucose and insulin—and its overarching relationship with inflammation—
is one key to mastering body composition.

6. Fat cells are energy storage facilities. Fat cells (adipocytes) are energy storage
facilities that dot the bodily geography. Excess energy is highly prized by the
human body and is derived from dietary fat and dietary carbohydrate. Excess
carbohydrate (glucose, fructose) intake will be stored in the liver and in the
skeletal muscles. When the liver and skeletal muscles are filled to overflowing,
the excess glucose is sent to fat cells and converted to fat for storage.

Glucose is converted to fat in fat cells for a couple of reasons:

• The glucose has to go somewhere, as it is toxic in the blood stream at high

levels. If the liver and muscles are “full” and the rest of the organs are using all
they need, fat becomes the only place left for storage.
 • Fat is over twice as energy dense as carbohydrates and protein. Fat contains 9
calories per gram while carbohydrate or protein contains 4 calories per gram. A
pound of carbohydrate contains 1800 calories while a pound of fat contains 4100
calories. You can store more energy in less space by converting glucose to fat.

Fat from the diet which is not used for energy is stored directly in fat cells. How
much dietary fat is stored depends on the current energy needs of the body and the
level of certain hormones in the blood stream.

7. The body uses both glucose and fat for energy. How much of each is used at
any one time depends on the body’s energy needs, activity levels, the relative
intensity of the activity and the brain’s requirement for glucose. The balance
between the use of glucose and fat (as fuel) is called the “Randle Cycle.” Philip
Randle first described the process in the early 1960s.

TECHNICAL NOTE:
The body is always using both glucose and fat as fuel. The hormones
insulin, glucagon, and growth hormone determine the proportions of
glucose and fat used for energy. For example, high insulin levels mean
very little fat will be burned for energy, and the body will use mostly
glucose. It is important to note that 100% fat or 100% glucose is never
burned at any one time.

Mitochondria: the
 cell’s power station.

8. Mitochondria are the “energy factories.” Mitochondria are tiny powerhouses

residing inside each cell in your body. Mitochondria break down carbohydrates,
fat and protein. Mitochondria generate energy in the form of ATP. The number of
mitochondria per cell differs depending on the type of tissue and varying needs
for energy. Cells that have a high requirement for energy, such as those found in
the liver, brain, and muscle, can have thousands of mitochondria in each cell.
Oxygen must be available for the mitochondria to make energy.

KEY POINT:
Mitochondria can only make energy (ATP) when oxygen is available.

9. Much more energy can be generated from glucose in the presence of oxygen.
A full-speed sprint can only last for a matter of seconds. During a sprint, the body
cannot provide oxygen to the muscle cells fast enough to allow glucose to be
fully oxidized. Glucose will start breaking down in the cell, outside the
mitochondria. A small amount of energy can be extracted without oxygen.
Anaerobic (literally “without oxygen”) glycolysis is the process of breaking
down glucose for energy.

• Only a very small amount of energy (ATP) can be generated with glycolysis.
The end product of glycolysis is lactate. Lactic acid ‘build-up” often occurs
during intense exercise. Lactic acid is the end product of breaking down glucose
for energy without any oxygen present.

• If you slow down the sprint, to allow oxygen to arrive in the muscle cells, some
of the breakdown products of glucose can now enter the mitochondria. With an
infusion of oxygen, the body is able to make significantly more energy.
 The above picture represents a cell in your body. The internal parts of the
cell are suspended in cytosol, the liquid inside the cell that is similar to the
water inside a water balloon.

The mitochondria (not drawn to scale) are represented in purple and

suspended in the liquid cytosol.

You do not need to know the technical names listed in the picture, just
follow the arrows from glucose in the cytosol.

When there is no oxygen present (anaerobic), the breakdown of glucose

stops at lactate, and only two ATP are produced.

When oxygen is present (aerobic), the breakdown product of glucose

can enter the mitochondria, leading to production of 38 ATP from one
glucose molecule!

10. Burning fat requires the presence of oxygen.

 From the above picture, you can see that fat (triglyceride) is broken down
into three separate 16 carbon palmitates in the cytosol, and must enter the
mitochondria to be used as energy.

Remember that since mitochondria must have oxygen to generate energy,

fat can only be burned in the presence of oxygen (called an aerobic
process).

The payoff is worth it, as one 16 carbon palmitate fatty acid can generate
104 ATP!

Because it uses both fat and glucose to generate ATP in the presence
of oxygen, you can see why aerobic exercise can be sustained for so
long (as in a marathon).

DIET, HORMONES, AND THE RANDLE

CYCLE
With the previous 10 concepts in mind, let us figure out how it all works when
applied to daily life.
 The preceding diagram simplistically summarizes the metabolic response to food
intake. We will plug in some details in different situations to help deepen your
understanding using 10 central concepts as a guide. A high carbohydrate meal
plugged into the “FOOD” box has a specific reaction.

CASE 1: HIGH STARCH/SUGAR MEAL

Foods containing processed flour are starches (example: bagels) and are
quickly broken down to large amounts of glucose by digestion.


The large amount of glucose produced by digestion (of a bagel) causes a

reaction by the pancreas. The pancreas is situated near our digestive tract
and when large amounts of glucose are present, the pancreas releases
insulin.

Insulin is a “storage and building” hormone. It has the following actions

in the body:

• Insulin allows entry of glucose into cells. The glucose is used as an

energy source or stored. Insulin can be thought of as a “gate-keeper” for
glucose. Without insulin, glucose (in most circumstances) can’t gain entry
into the cells and stays in the bloodstream. Insulin is the mechanism used
by the body to clear large amounts of glucose from the bloodstream.
• Insulin increases glycogen synthesis from glucose.
• Glycogen is the storage form of glucose and chemically looks a lot like
a starch. Glycogen synthesis is the process of taking excess glucose and
storing it as glycogen. The liver and skeletal muscle store most of the
body’s glycogen. Glycogen is stored and ready to be broken down into
glucose when needed.
• Insulin increases fatty acid synthesis and storage (making and storing
fat). When the body has had its fill of glucose, and the liver is full of
glycogen, the liver will become a fat-producing factory. This can result in
“high triglycerides” on a blood test at the doctor ’s office. Fat produced by
the liver along with dietary fat will be stored under the influence of
insulin.
• The machinery (enzymes) for fat production and storage is turned on by
insulin. Any fat eaten while insulin is high will be shuttled off to fat
storage depots instead of being used to make energy. Insulin decreases fat
breakdown and turns on the machinery for production and storage of fat.
Insulin also turns off the machinery for “burning” fat.
• Insulin increases protein synthesis and is a potent stimulator for
building protein and muscle from amino acids.
• Insulin stimulates cell growth and division, and creates an environment
favorable for new cell growth.

Large amounts of insulin prevent fat from being used as a fuel. If you
cannot effectively utilize fat for fuel it remains stored in unattractive
places. Insulin is an essential hormone, crucial for growth and building
processes while maintaining optimal blood sugar levels.

CASE #1 High insulin levels decidedly tip the balance in favor of

“burning” glucose as a fuel for energy production and stops fat from
being burned for energy.

The large insulin release from a bagel and orange juice meal will clear
glucose from the blood very rapidly (unless you have diabetes) and often
“overshoots,” resulting in a rapid drop in blood sugar that triggers
symptoms such as fatigue, difficulty concentrating and hunger. It is no
wonder that people who eat this type of meal for breakfast (or a variation
with toast, or cereal) will often be hungry by mid morning.
QUICK MEDICAL NOTE:
A condition called reactive hypoglycemia is fairly common condition in
which high carbohydrate meals produce an excessive insulin response. It
is easily treated by modifying the diet to include more protein and fat in
each meal, and significantly less starchy carbohydrates and sugars.

KEY POINT:
Any meal based on processed starchy carbohydrates (with little protein or
fat) such as pasta and bread will have the same effect on insulin and will
largely stop fat from being used for energy.

With insulin and glucose available in large amounts after a high carb
meal, other organs in the body that do not have to use glucose for energy
will use glucose, as it is available and plentiful.

Once insulin clears much of the glucose load from the bloodstream,
insulin levels will start to fall. Once insulin levels begin to fall, fat can
start to be burned as fuel. The faster insulin is able to do its job and
dispose of the glucose (shuttling it into cells for storage or using glucose
for energy) the faster insulin levels fall and normalize. Insulin sensitivity
is how well insulin is able to “trigger” entry of glucose from the
bloodstream into the cells.

INSULIN SENSITIVITY


A helpful way to think about insulin sensitivity is to visualize your house

as a cell in the body. The street and driveway outside your house is the
bloodstream. Let us say that you are hosting a party and want to impress
your friends with a new electronic front door to your house. To really
“class up” your party, you also hire a doorman to activate your front door
by pushing a button when guests arrive to let them in your house.

The doorman (playing the part of insulin) will look for your arriving
guests (guests are glucose) and meet them at the door. He will push the
button of your newly installed electronic door and the door will open to
let your guests inside your house. If the button works as it should when
pressed, the door will open and let your guests in immediately.

Let us say for some reason the button stops working well, and now takes
10 pushes before the door will open and let your guests in. As you throw
large, lavish parties with a huge guest list, the delay caused by the button
not working well causes a line to form outside of your front door and
guests waiting in the driveway (just like glucose in the bloodstream
waiting to enter the cell).

The button activating your door has lost its sensitivity to the doorman
pressing it. This is what happens in your body when sensitivity to insulin
is lost, leading to increased glucose in the bloodstream, and eventually
diabetes.

When the insulin sensitivity of a cell is low, it takes much longer for the
“triggering” process to work. When a person (who is diabetic) is not sensitive to
insulin, glucose is delayed from entering the cell and stays in the blood stream.
 As long as there are high amounts of glucose in the bloodstream, insulin levels
will not fall. The longer insulin is around, the less fat will be burned for energy. The
loss of insulin sensitivity, also called insulin resistance leads to diabetes.

CASE 2: LOW STARCH/HIGH

PROTEIN MEAL
Let’s take a look what happens when we plug this meal into our “food
box”. The lettuce wrap is carbohydrate, but has no starch to speak of. The
lettuce carbohydrate component is mostly the indigestible fiber called
cellulose. We can’t extract glucose from cellulose because we don’t have
the “machinery” to digest the chemical bonds (in red) connecting the
glucose.

Since no glucose is released from cellulose digestion, there is no insulin

response to the lettuce wrap component.

These particular tacos are made with grass-fed beef, so they have a good
amount of protein that will be broken down during digestion into amino
acids. Amino acids stimulate the pancreas to secrete a hormone called
glucagon.

Glucagon has actions opposite to those of insulin as far as glucose is

concerned:
• Glucagon breaks down glycogen stored in the liver to release
glucose. When dietary glucose is low (not eating starchy carbohydrates)
glucagon is released to break down stored glycogen. The body seeks to
release glucose into the bloodstream to prevent blood sugar from
becoming too low.
• Glucagon turns on gluconeogenesis—the liver is the glucose “banker”
and when glucose starts to run out of stored glycogen, the liver starts to
“print money” by making glucose from amino acids using the process of
gluconeogenesis. The liver uses amino acids to make more glucose—this
amino acid derived glucose can then be released into the blood stream.

The brain is an “energy hog” and has a heavy demand for glucose. When
dietary glucose sources such as starch and sugar are low, most of our
organs and tissues will burn fat as an energy source, sparing glucose
for use by the brain, glucose-dependent red blood cells and the kidneys.

The fat from the beef and avocado (used to make the guacamole) is a
good mixture of saturated, monounsaturated, and polyunsaturated (grass-
fed beef has a good omega-3/omega-6 balance) fats. Fat is “hormonally
neutral.” Dietary fat does not stimulate insulin or glucagon.

KEY POINT:
Fat alone does not stimulate insulin or glucagon release. Overall, it is
neutral for these two hormones.

Amino acids derived from a protein meal will stimulate a small release of
insulin. One of insulin’s actions is to increase protein synthesis, and to
assist in the making of protein. This is one reason why elite athletes will
consume amino acids post-workout; they want to purposefully trigger the
anabolic (growth inducing) properties associated with insulin secretion.
KEY POINT:
Amino acids from protein will stimulate a small amount of insulin release.

The carbohydrate present in the guacamole (from the avocado) is mostly

fermentable fiber, so it will not contribute to release of insulin. The
fermentable fiber will feed our gut bacteria. The resulting “waste” product
is the beneficial short chain saturated fats (i.e. butyrate).

The hormonal response is mostly glucagon with a small amount of insulin

—we tip the scales in favor of burning fat as fuel instead of carbs as fuel.
Without much glucose around, the rest of the body stops utilizing glucose
as a major fuel source and goes into fat burning mode. The body seeks to
spare the glucose given out by the liver for exclusive use by the brain.

CASE #2: Low insulin levels and high glucagon levels decidedly tip the
balance in favor of “burning” fat as a fuel for energy production, sparing
glucose for use by the brain.

DIGGING DEEPER:
Does glucagon directly stimulate fat burning?
The recent research regarding this question has shown conflicting results.
Some studies have shown that glucagon stimulates a fat releasing enzyme
called hormone sensitive lipase (HSL). But these studies were conducted
on fat cells in a test tube. The few studies conducted with humans have
shown no effect of glucagon in direct stimulation of breaking down fat
for energy. There are other hormones that definitely directly stimulate fat
burning, which we will discuss very soon.

As we have covered recently, insulin stimulates the machinery involved in

making and storing fat, AND inhibits the machinery involved with fat
burning such as HSL. Current scientific thought is that as insulin levels
drop, the “brakes are taken” off of the fat burning machinery, allowing fat
to be used as energy.

So it seems decreased insulin levels are more responsible for fat burning
than directly stimulating the effect of fat burning with glucagon.

This is still an active area of research. Soon we may know how to better
answer this question.

THE INSULIN/GLUCAGON RATIO

In CASE #2 you saw that there was some insulin released by eating our
meal, but glucagon was dominant. With any given meal, the balance
between the amount of insulin and glucagon present is known as the
insulin/glucagon ratio. High amounts of insulin will lead to using glucose
as an energy source while storing fat.

When glucagon dominates, glucose will be used by the brain, the liver
will break down glycogen to release glucose and make new glucose from
amino acids, and the rest of the body will switch to fat burning.
Insulin stops glucagon from being secreted by the pancreas. When there
are high insulin levels, glucagon levels are usually very low. The reverse
is NOT true however, as glucagon itself has NO effect on stopping insulin
secretion.

A healthy metabolism can negotiate changes in the ratio quickly and

effectively in response to food, but with a broken metabolism (diabetes),
rapid change is not possible. We’ll cover this much more in the
obesity/diabetes chapter.

CASE 3: FASTING
During sleep, insulin levels fall rapidly after the increased blood glucose
(from dinner) has been shuttled out of the blood stream. The falling
glucose levels (and insulin levels) trigger release of glucagon from the
pancreas.

We know that glucagon will release stored glucose from the liver to feed
the brain and red blood cells. We also know that glucagon will prompt the
liver to start making new glucose via gluconeogenesis.

Since we are sleeping and have not recently eaten any protein, the liver
would normally use amino acids “stolen” from the breakdown of our
muscle to make new glucose to feed the brain. But there are mechanisms
in place to prevent the loss of muscle while we are sleeping—and any
other time we are fasting.

During sleep, our muscle mass is mainly protected from amino acid
pilfering (to feed gluconeogenesis) by growth hormone (GH).
 GH is secreted by the pituitary gland in response to a signal by the
hypothalamus (technically this signal is another hormone called “growth
hormone releasing hormone”). Signals for release of GH include…
• Fasting
• Intensive exercise
• Deep sleep

SLEEP YOUR WAY THIN?

You can indeed burn your love-handles for energy while you sleep IF you
are getting good sleep. Although GH is secreted throughout the day, the
largest amount is released in the first 1-2 hours of deep sleep.

GH release is cut back significantly by poor sleep.

Bad sleep habits can stop your fat loss in its tracks!

GH is an interesting hormone because it promotes muscle building through

protein synthesis, while at the same time triggering fat breakdown for energy. These
effects make sense if you view growth hormone as a muscle mass protector during
sleep and other times of fasting.

GH is very potent in triggering the breakdown of fat cells for energy. In this way,
GH provides the majority of the body with a plentiful supply of energy from fatty
acids (fat).

The question is, “How does the brain continue getting glucose if growth hormone
shuts off the ‘theft’ of amino acids from muscle that would otherwise be used by the
liver to make glucose for the brain?”
 The liver can make a special kind of fuel called ketones. Ketones are created from
fatty acids released by GH while you are sleeping.

The brain cannot directly use most fats for energy, but two-thirds of the brain’s
energy needs can be supplied by ketones made from fat during fasting and
starvation. When the brain starts to use ketones as an energy source, the demand for
glucose plummets and muscle tissue (and the body’s reserve storage of amino
acids) is spared.

GH increases liver gluconeogenesis (making new glucose). However a different

source—lactate, lactic acid—is used.

KEY POINT:
Growth hormone spares muscle from amino acid “theft” by jump-starting
ketone production. The brain can now use ketones and doesn’t need as
much glucose.

Red blood cells and the inner parts of the kidney both produce energy from
glucose anaerobically (without oxygen). They accumulate the lactic acid waste
product and use it during fasting for making glucose in gluconeogenesis.

KEY POINT:
When growth hormone is around, lactate is the major source of new
glucose, sparing amino acids (and sparing your muscle!)

CASE #3 REVIEW:
• During an overnight fast, the insulin/glucagon ratio changes so that
glucagon is dominant.
 • Most of the body switches to fat burning in order to preserve and
reserve adequate glucose for the brain.
• Growth hormone accelerates fat burning, allowing for the liver to make
ketones from fat taken from fat cells.
• The brain can (mostly) use ketones in place of glucose during fasting;
when fasting there is also less need for glucose.
• Growth hormone spares protein, and protects muscle from being
broken down to make glucose during fasting.
• The glucose is primarily made from lactate instead of amino acids.

Glucagon and Growth Hormone work together to burn fat while

sleeping

YOUR HORMONES ON DESSERT

Looking at the effect of ice cream and cake from a hormonal perspective is
included to drive home insulin’s role as a storage hormone. Again, when large
amounts of insulin are triggered by glucose, the body will store fat and glucose. No
appreciable fat burning will take place under insulin’s umbrella.

INSULIN AND CARBOHYDRATES

ARE NOT EVIL....

All of this talk about insulin, carbohydrates, and fat storing may give you
 the (wrong) idea that insulin and carbs are bad things and need to be
avoided at all costs. This view has unfortunately become very popular of
late, and misses an important point.

Insulin and carbohydrates are crucially important to your health. It is the

chronic loss of insulin sensitivity that leads to disease. Once insulin
sensitivity is lost, the ability to handle starchy carbohydrates in the diet is
compromised as we discussed at the end of CASE #1.

An example to illustrate this point is the diet of a traditional culture such

as the Okinawans. Traditional Okinawan diets consisted of 85%
carbohydrates, mostly eaten in the form of sweet potatoes. The traditional
Okinawans were some of the longest-lived people on the planet, with
many in their population reaching over 100 years old. They were also lean
and relatively free of chronic disease. The large amount of sweet potatoes
definitely caused insulin to rise in their bodies. The key to their success is
maintaining insulin sensitivity.

Do not be in a hurry to blame insulin and carbohydrates for insulin

resistance, diabetes, and obesity. There are other important factors at play,
which we will soon explain.

Once insulin comes back down, fat burning for energy can take place again. For
someone with high insulin sensitivity, insulin will rise and fall very quickly. Once
insulin subsides, fat burning for energy purposes can take place. A metabolically
“broken” individual with poor insulin sensitivity will maintain a relatively high
insulin level long after the meal is eaten and will have a hard time burning fat for
energy.

We will show you how chronic inflammation and oxidative stress from multiple
sources can lead to insulin resistance and wreck your metabolism—slowing fat
burning to a crawl. A broken metabolism is one of the drivers of chronic diseases
such as obesity, diabetes, heart disease, neurodegenerative diseases and even cancer.
We will dive headlong into each of these underlying sources of disease now that you
have the framework and knowledge to understand what is going on “under the
hood.”
“MILITARY INTELLIGENCE” (REFERENCES):
Te xtbooks :

Frayn KN. M etabolic Regulation, A Human Perspective, 3rd Edition, J ohn Wiley & Sons Ltd, West Sussex, U nited Kingdom (2010).

Journals :

Habegger KM , et al. The metabolic actions of glucagon revisited, Nat Rev Endocrinol 6 (2010): 689.

Heppner KM , et al. Glucagon regulation of energy metabolism, Physiol Behav 100 (2010): 545.

M oller N, J orgensen J O, Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects, Endocr Rev 30 (2009): 152.

M oller N, et al. Growth hormone and protein metabolism, Clin Nutr 28 (2009): 597.

Perea A, Clemente F, M artinell J . Villanueva-Penacarrillo, M . L., Valverde, I., Physiological effect of glucagon in human isolated adipocytes, Horm Metab Res 27 (1995): 372.

Stanhope KL, Schwarz J M , Havel PJ . Adverse metabolic effects of dietary fructose: results from the recent epidemiological, clinical, and mechanistic studies, Curr Opin Lipidol (2013).

Vendelbo M H, et al. Insulin resistance after a 72-h fast is associated with impaired AS160 phosphorylation and accumulation of lipid and glycogen in human sk eletal muscle, Am J Physiol Endocrinol Metab 302 (2012):
E190.

CONGRATULATIONS ON COMPLETING STRONG

MEDICINE BASIC TRAINING.

PREPARE FOR ADVANCED TRAINING; WE ARE GOING

TO MEET THE ENEMY...
 PART II

KNOWING YOUR ENEMY

“If you know the enemy and know yourself, you need not fear the result of a
hundred battles. If you know yourself but not the enemy, for every victory
gained you will also suffer a defeat. If you know neither the enemy nor yourself,
you will succumb in every battle.”
—Sun Tzu, The Art of War
THE “PENTAVERATE” OF
PESTILENCE
These are the five enemies producing chronic inflammation and
oxidative stress. They are a cabal of health calamity. We have collected
ample intelligence on each of these nefarious characters. We will train
you to understand them from the ground up, and will give defensive
tactics to protect you from their advances. Each enemy will be briefed
in the following order:

• Gut Inflammation
• Obesity and Insulin Resistance
• Chronic Stress
• Circadian Disruption

We will discuss “Inactivity” (#5) in Part 3 in our extensive coverage of

exercise.

Notice that no matter the specific enemy, the underlying cause of most
chronic disease is long-term inflammation and oxidative stress. The
Pentaverate works together to cause the diseases listed in the black
box. Those listed are only a fraction of diseases thought to be caused
by chronic inflammation and oxidative stress.
KNOWING YOUR ENEMY I:
THE GUT: GUARDIAN AT THE GATE

Our intestinal tract will likely become a primary focus as we learn more about the
underlying causes and treatment of disease in the 21st century. Indeed the last decade
has shown tremendous progress in our understanding of just how central this organ
system is for maintaining health.

The following discussion will be fairly lengthy, but a basic understanding of how
the gut works and what happens when its function is disrupted is extremely
important to your health. If you want to attain your body composition and fitness
goals, you cannot overlook this section.

Chronic inflammation of the gut is the first member of the Pentaverate. The
intestinal tract (gut) is our first line of defense from outside “invaders” such as
pathogenic bacteria and from our modern diet.

When the gut defenses are constantly stimulated, they can transform from
protectors into agents of chronic disease. We will show you how to stop this
insidious process with Strong Medicine defensive tactics. Proceed for in-depth
training on the inner workings of the “guardian at the gate.”
GUARDIAN AT THE GATE PART I:
GUT HEALTH: FIRST PRINCIPLES

A recent case study published in the British Medical Journal described the
results of placing a 6-year old boy on a gluten free diet after he was
diagnosed with type 1 diabetes (T1D).

For those of you that do not know, T1D is an autoimmune disorder in

which the person’s own immune system destroys the insulin-producing
cells in their pancreas, typically the person will be dependent on insulin
injections for the rest of their life.

The results of the gluten free diet with this child were remarkable. Within
weeks of starting on the diet, he no longer needed insulin injections.
Twenty months after starting the diet, he still did not need daily insulin
 treatments. Essentially, the gluten free diet put his T1D into remission.

T1D is traditionally thought of as an incurable disease, so how was this

child apparently “cured” with something as simple as a gluten free diet?

A “FIRST PRINCIPLES” ARGUMENT THAT

INTESTINAL TRACT HEALTH IS
CRITICAL IN ATTAINING OVERALL
HEALTH:
• Our intestinal tract (gut) is where we absorb nutrients from the food we eat.

• The intestinal tract is the first barrier through which we “interact” with
outside environmental inputs of food and water, selectively letting in the
“good” environmental inputs and keeping out the “bad” inputs.

• This interaction is the first opportunity for the body’s defense against outside
bacterial invaders and toxins/toxicants in our food and water.

• A large proportion of our body’s immune system is located in the intestinal

tract.

• When the gut immune system is overactive, bad things can happen. Chronic
inflammation is a result of prolonged activation of our gut-associated immune
system. This creates chronic inflammation and oxidative stress in the body.

• Chronic systemic inflammation and the resulting oxidative stress are the main
contributors to chronic diseases including cancer, atherosclerosis and diabetes.

• The intestinal tract and brain are closely connected. Inflammation in the gut is
communicated to the brain, creating a body-wide stress response that can wreck
our metabolism and ruin our health if left unchecked.

THE INTESTINAL BARRIER

The intestinal tract was designed to maximize absorption within the smallest
possible space. The intestinal wall is intricately folded, creating structures called
villi. The villi themselves are comprised of individual epithelial cells with their own
folds called microvilli. The “lumen” is the space “inside the tube” of the gut
where food passes after digestion. The epithelial cells selectively absorb nutrients—
amino acids from protein, glucose and fat—from digested food. The absorbed
nutrients are sent into the blood stream, including amino acids, glucose, short and
medium-chain fats and in the lymphatic vessels, long-chain fats are absorbed.

This is a close-up view of the epithelial cells (light brown.) Each is connected by
tight junctions.(TJ). TJs keep large undigested particles of protein and harmful
bacteria from penetrating through to the blood stream. This system allows nutrients
(amino acids, sugars, fats) to travel through transporters in the microvilli. The
epithelial cell barrier is our first line of defense (The Guardian at the Gate) from
harmful things in our diet. We have a system of immune cells just below the
epithelial layer (in the lamina propria) to deal with anything trying to bypass the
tight junctions.

When the tight junctions fail, this is called intestinal permeability (IP)
or “leaky gut.” IP allows harmful bacteria and undigested protein
fragments into the lamina propria and the bloodstream. The immune
system then launches its response against the interlopers, resulting in
 inflammation.

The intestines contain most of our body’s total immune system, 70-80%
by many estimates. This is a strategic location for most of our immune
defenses, as it is one of the first places where the inside of our body
contacts things we bring in from the outside world—food and water—
which may include disease-causing bacteria and viruses.

The gut’s immune system is incredibly important for maintaining our health and
defending against invaders.

First, a brief review of the immune system, then a discussion on how the immune
system can get out of control and attack our own body in a process called
autoimmunity. Recent research has shown that the gut may be the primary place
where autoimmunity is triggered.

IMMUNE SYSTEM REVIEW

The immune system is highly complex. We have simplified the concepts
considerably. Please reacquaint yourself with the main players of the immune
system that we originally introduced in Basic Training. Because the majority of the
immune system makes its home in the gut, it is crucial that you retain a basic
understanding of how each member contributes to maintaining our first line of
defense against threats from the outside world. The members of the gut immune
system are truly the “guardians at the gate.”

INNATE IMMUNE SYSTEM:

The cells of the innate immune system are like the guards at the castle gate. They
will deal with anyone who looks or acts suspicious. This is usually the initial
encounter with bacteria/viruses and “foreign” protein fragments. Their response is
not targeted at specific individuals, but is a general protective response to anything
deemed “foreign.”

ADAPTIVE IMMUNE SYSTEM:

These assassins are called T-cells and B-cells and once they encounter pieces of a
prisoner caught by the dendritic cells or macrophages of the innate immune system,
they “adapt” themselves. They morph and become perfect assassins for this specific
type of prisoner. They form “clones” of themselves to make an army of assassins
once they have found a specific victim.

T-REGULATORY CELLS, AKA TREG CELLS:

Think of these cells as the “hippie” anti-war protestor that helps control the
assassins. Treg cells are the peace-loving part of the adaptive immune system and
produce an anti-inflammatory response. We need a balance between Treg cells and
the assassins to prevent the immune system from attacking our own body tissues in
something called autoimmunity.

AUTOIMMUNITY AND INTESTINAL

PERMEABILITY
Autoimmunity occurs when our immune system (the innate guardians and
adaptive assassins) fails to recognize tissue in our body as “self.” Instead, the
immune system gets its wires crossed and recognizes “self” tissue as foreign. As the
immune system is designed to protect us from foreign invaders, it attacks and
destroys our own tissue. This can happen in multiple tissue types.

• Celiac disease: cells lining the intestine are destroyed.

• Hashimoto’s thyroiditis: the thyroid tissue is destroyed.
• Multiple sclerosis: the “insulation” (myelin) of our nerves is destroyed.
• Rheumatoid arthritis: our joints are destroyed.

There are many theories currently being investigated why our own immune
system turns on us. Some interesting theories involve the loss of Treg cells
(hippies). We also know that individual genetics, specifically genetics of the immune
system, play a large role in autoimmunity, but there are environmental “triggers”
that jump-start the process. One leading researcher in the field has proposed that a
third factor is necessary for the development of autoimmunity, intestinal
permeability.

The theory of intestinal permeability as the third factor required for

autoimmunity came from studying people with celiac disease. Celiac disease is an
autoimmune disease triggered by intestinal permeability. People with this condition
are known to have a much higher incidence of other autoimmune diseases. It is
proposed that whatever the environmental trigger—bacteria, virus, food particle—it
must first come into contact with the immune system for a reaction. Intestinal
permeability allows the contact of the gut immune system with environmental
triggers to take place.

KEY POINT:
Intestinal permeability may be the third required factor for developing
autoimmune disease.

Review the graphic from the beginning of this section showing the intestinal
barrier. Pay close attention to the tight junctions that prevent undigested food
particles and bacterial invaders from penetrating the lining of the gut wall. When the
tight junctions fail, things that should not get past the protective gut lining take the
passage that is now open between the intestinal epithelial cells forming the barrier.
Failure of the tight junctions is the mechanism behind intestinal permeability (“leaky
gut”). When this happens, undigested food particles and bacterial invaders come in
contact with the immune system guardians that are defending the castle wall. The gut
immune system is now on alert.

DISRUPTION OF THE BARRIER:

CONSEQUENCES AND CLINICAL DISEASE
Daily exposure to things that induce intestinal permeability can lead to:

• Chronic inflammation, the precursor to developing chronic diseases—diabetes,

obesity, cancer, Alzheimer ’s dementia and heart disease.

• Autoimmune diseases, which strike those who have a genetic predisposition.

Multiple sclerosis, rheumatoid arthritis, type I diabetes, Hashimoto’s thyroiditis,
celiac disease, and Crohn’s disease are just some of the diseases influenced by
intestinal permeability.
 In this diagram, the tight junctions have been disrupted, allowing harmful
bacteria and undigested protein fragments past the epithelial barrier. The
immune system is now activated (red glow) and the inflammatory
response is initiated.

Chronic intestinal permeability can also lead to reduced numbers of the Treg
cells “hippies” and increased numbers of adaptive “assassins.” New science has
shown that Treg cells are extremely important in prevention of autoimmunity.
Having enough Treg cells is critical for preventing the adaptive assassins from
getting out of control.

Chronic intestinal permeability leads to the “assassins” outnumbering the

 “hippies.” This sets the stage for out of control inflammation and
autoimmunity because there are not enough hippies (Treg) to keep the
assassins in check.

We need to maintain the intestinal barrier and prevent chronic intestinal

permeability to maintain a proper balance between the “assassins” and the “hippies.”
Too many assassins leads to out of control inflammation and autoimmunity, while
too many hippies would leave us vulnerable to invading microorganisms such as
bacteria and viruses.

When the balance between “assassins” and “hippies” is disrupted, chronic

inflammation and autoimmunity are triggered, leading to disease.

Balance prevents autoimmunity and chronic inflammation.

We will show you strategies on how to maintain this balance in upcoming sections,
but first we will show you how chronic intestinal permeability (leaky gut) is
triggered by components of processed food, stress, and disruption of our normal
population of gut bacteria.

Recent science supports the idea that although you may have the genetics
predisposing you to getting autoimmune diseases, if your gut immune system does
not come into contact with the environmental trigger, you will remain free of
disease.

KEY POINT:
Even if you are genetically predisposed to autoimmune disease, avoiding
 the environmental triggers will prevent you from developing one of these
diseases.

In the next section, your in-depth training on the causes of gut inflammation will
continue. We will identify the environmental triggers of chronic intestinal
permeability and train you in defensive tactics to protect yourself from these
triggers. This is how we will bring down the first member of the Pentaverate and
keep the “Guardian at the Gate” intact, protecting your health from the onslaught of
chronic disease.
GUARDIAN AT THE GATE PART II:
TRIGGERS OF INTESTINAL
INFLAMMATION

TRIGGERS OF INFLAMMATION
Potential triggers for chronic inflammation in the gut leading to disease are the
following:

1. Gluten and other dietary triggers

2. Stress, the Gut-Brain Axis

3. Dysbiosis, the disruption of gut bacteria

KEY POINT:
It is very important to keep in mind that short term increases in intestinal
permeability is a normal physiologic mechanism, and is an essential part
 of our natural defenses to fight infectious bacteria and viruses in the gut,
as well as to clear them from the body (diarrhea). It is only when we have
long-term intestinal permeability and inflammation that we run into
trouble.

TRIGGER #1: GLUTEN

In Environmental Medicine, we judge the public health impact of potential
environmental toxins and toxicants on the toxicity of the compound and the potential
for exposure. With gluten, toxicity will vary depending on the person, but potential
exposure is extremely high. Gluten is always potentially problematic.

Inflammatory reactions to gluten proteins—found in wheat, barley and rye food

products—have received a lot of press over the last couple of years. The gluten
family of proteins have become whipping boys in the dietary blogosphere and
popular media. Although the demonization of gluten is somewhat justified and is
supported by recent research, we need to look at this issue dispassionately.

Gluten is an ingredient in countless processed foods (and many other products)

so our potential for exposure cannot be underestimated.

GLUTEN 101
• Gluten is the main structural protein in wheat, barley and rye. Gluten gives
bread products their soft, doughy texture. Extra gluten is often added to make
bread and bagels softer.

• The toxic components of gluten proteins are called gliadins and glutenins.
Proteins are “chains” of amino acids. Different amino acid sequences in the
chains determine the shape of the protein, the ease of digestion, and most
importantly, their biologic function.

 Amber waves
of inflammation?

• Parts of the chains in gliadins and glutenins are very resistant to our digestive
“machinery.” Small fragments of these proteins with amino acid sequences
containing high amounts of proline and glutamine, are responsible for digestive
resistance. Gluten proteins are called “prolamins” (proline + glutamine).

• Prolamin protein fragments can trigger intestinal permeability and immune

response resulting in inflammation and oxidative stress.

• Genetic differences in our immune systems result in individual differences in

the strength and type of immune response to these prolamin protein fragments.
Differing immune responses to gluten create differing classifications of gluten-
related diseases.

• Celiac disease is also called gluten-sensitive enteropathy. This condition creates

an innate and adaptive immune response.

• Gluten sensitivity is an innate, non-specific immune response.

SPECTRUM OF GLUTEN-RELATED
DISEASE

The spectrum of glutenrelated disorders: your genetics (and

epigenetics) determine the reaction of your immune system to gluten and
where you fall on the spectrum.
 Between points A and B: People are able to eat gluten without any known
adverse health effects. This group represents the majority of us.

Between points B and C: People with Gluten Sensitivity. Those in this

range have immune reactions to gluten. The range includes those with no
symptoms and a low level of inflammation to those with substantial
symptoms, including irritable bowel syndrome (IBS). About 20-30% of us
fall into this category.

Between points C and D: These people are afflicted with celiac disease.
About 1% of the population has celiac disease.

The variance among responses to gluten is largely genetic (and epigenetic). Many
of the scientists studying the effects of gluten on health have come to the conclusion
that there simply has not been enough time for humans to fully adapt to grains as a
food source. Widespread agriculture has only been in existence for 10,000 years—a
blip on the historical radar.

Another interesting hypothesis holds that the increase of gluten-related health

problems is in direct proportion to the increase in food processing. Industrial foods
are constructed using cheap, subsidized grain containing gluten. The rise in the
consumption of these artificial gluten-containing foods mirrors the increase in
gluten-related health maladies.

Traditional cultures have long used grains without nearly the degree of gluten-
related health problems Western cultures are experiencing. These cultures often
prepare their grains using sprouting and fermentation processes that decrease the
toxicity of gluten. (see Weston A. Price foundation.)

One school of thought holds that genetic modification of grains, most

particularly wheat, has changed the protein structures enough to promote an
increased immune response.

QUICK MEDICAL NOTE:

Recent research is finding links to gluten for a wide range of diseases and
metabolic disorders:


• Insulin resistance
• Leptin resistance
• Hashimoto’s thyroiditis
• Neurologic diseases
• Rheumatoid arthritis
• Irritable bowel syndrome
• Inflammatory bowel disease (Crohn’s, ulcerative colitis)
Systemic inflammation starting in the gut may be the hidden link to
these conditions.

CELIAC DISEASE (CD)

This “disease” is not really that rare, affecting as many as 1 in 100 people. It is
also under diagnosed. It is estimated that 90% of those with celiac disease are
walking around undiagnosed. Undiagnosed children with celiac are short and
scrawny for their age and are delayed developmentally.

Celiac disease is not so much a disease as it is a mismatch between a person’s

genetics and their environment. When the environmental trigger of gluten is
removed, most CD patients see complete resolution of their symptoms.

• The innate and adaptive immune systems each contribute to the problems seen
in CD.

• The undigested protein fragments of gluten proteins disrupt the tight junctions
of the epithelial barrier.

 • The “innate guardians” intercept the foreign fragments, ingest them and display
pieces on their cell surface. Individual genetics determine how these fragments
are displayed and the interaction with the T-cell “adaptive assassins”.

• The adaptive assassin T-cells recognize the displayed gluten fragments as

foreign, and form clones to specifically recognize and unleash their destructive
arsenal.

• Unfortunately, this results in the “nuclear option” as far as the intestinal barrier
is concerned. The assassins release large amounts of inflammatory cytokines in
response to gluten fragments.

• The massive cytokine release increases the intestinal permeability even further,
letting in more gluten fragments and foreign particles including bacteria. The
nuclear option physically destroys the epithelial barrier in the process—akin to
an innocent casualty of war. Destruction of the absorptive epithelial barrier
results in decreased ability to absorb nutrients in the diet. This leads to
malnutrition and “failure to thrive” in growing children.
 KEY POINT:
This process will continue as long as gluten is included in the diet for this
group of genetically susceptible people. The adaptive assassins are always
waiting to pounce on gluten fragments. This is why even a tiny bit of
gluten in people with CD results in immediate symptoms of
gastrointestinal distress and diarrhea.

The intestinal permeability and immune response in CD may contribute to the

development of a variety of autoimmune and inflammatory disorders often seen in
CD patients. These include:

• Endocrine diseases such as type I diabetes, Hashimoto’s thyroiditis (most

common form of thyroid disease), and reproductive disorders.

• Neurologic disorders such as cerebellar ataxia, peripheral neuropathy,

psychosis, epilepsy (seizures), autism and migraine headaches.

• Autoimmune liver diseases such as primary biliary sclerosis and autoimmune

hepatitis.

• Anemia, osteoporosis, rheumatoid arthritis, autoimmune heart disease

(myocarditis).

• Non-Hodgkin’s lymphoma (a type of cancer of the immune system).

Gluten activates autoimmunity (celiac disease) through intestinal permeability.
Observe the destruction of the microvilli in the epithelial cells (on the right) of the
gut lining. The damaged microvilli are now unable to absorb nutrients from food.

DIAGNOSIS OF CELIAC DISEASE

There is no clear and reliable way to definitively diagnose celiac disease.
Intestinal biopsy has been—and still is in current clinical care—the “gold standard.”
The tissue sample from the biopsy is analyzed under a microscope to look for signs
of microvilli damage in the wall of the intestine. The problem lies in the fact that not
all CD patients show microvilli damage. The most reliable way to test for a gluten
problem is by eliminating it from the diet and monitoring symptoms over a couple
of months.

RESEARCH UPDATE:
Recent research has shown that as many as 50% of patients with CD show
 no signs of microvilli destruction. This test still may be helpful as most
CD patients show infiltration of “adaptive assassin” immune cells into the
epithelial cells themselves. These are called intraepithelial lymphocytes,
or IEL.

KEY POINT:
The most reliable and practical way to determine any type of gluten-
related disorder is to completely eliminate gluten for a period of time and
monitor your symptoms.

GLUTEN SENSITIVITY
Gluten sensitivity (GS) is gaining credence as an emerging diagnosis. GS is
distinctly different from celiac disease in how the gluten proteins within the body
cause problems.

• The epithelial cells in the small intestine are usually normal, without signs of
microvilli destruction.

• The “adaptive assassins” of the immune system do not appear to be a key player
in GS; but investigations are still under way.

• The non-specific response of the innate immune system, the “guardians”

system, produces inflammation by secreting cytokines in response to gluten
protein fragments.

• Clinically, this response leads to symptoms of bloating, diarrhea, and

cramping after exposure to gluten.

• These symptoms are often classified as irritable bowel syndrome (IBS) by the
medical profession. IBS is a catch-all diagnosis for gastrointestinal symptoms
for which a specific cause cannot be found. The current research suggests that GS
may be one of the underlying causes of IBS.
 Many people have suffered with gastrointestinal symptoms all of their lives
without a clear diagnosis. This is very frustrating for most, and most learn to live
with it, although the symptoms routinely affect their quality of life. Some of these
individuals need to plan their day to ensure they have easy access to restroom
facilities wherever they go.

DOC’S RANT:
What has always been interesting to me is that many people suffering with
IBS-like symptoms will not “give up” foods like bread and pasta, even
when given the above information. As we discussed in previous chapters,
most gluten-containing grain products are not nutritionally dense, and
have anti-nutrients.

Since we are not missing anything nutritionally by eliminating these

products, why do people cling to their grain-based foods? You never hear
anyone say, “I won’t give up my broccoli!” A few scientists have looked at
this phenomenon and have shown that some pieces of the gluten protein
may mimic the effects of opiates (morphine-like compounds) in the
brain.

We have all heard of endorphins—our naturally produced feel-good

substances. Some scientists are now referring the specific pieces of gluten
proteins as “exorphins,” and think these molecules may be responsible for
the craving some people have for gluten-containing grain products.

Most of us do not have celiac disease or gluten sensitivity. However, if you have
any chronic gastrointestinal problems such as IBS, reflux disease (chronic
heartburn), gallbladder problems, or inflammatory bowel diseases such as
ulcerative colitis or Crohn’s disease, gluten may be a significant contributor to these
diseases. Gastrointestinal problems often have an inflammatory origin, so why not
eliminate a potential source of gut inflammation by eliminating gluten.

Without a clear and definitive test for determining whether you have CD or GS,
the most rational approach is to eliminate gluten from your diet. How do you feel
after a week or a month? Is your heartburn better? Are IBS symptoms decreased? If
you have an autoimmune disease, a glutenfree trial period is a must do. You have
nothing to lose (other than bread) and everything to potentially gain. There is no
nutritional benefit to eating gluten, and for as many as 30% of us, there are
significant health consequences for continuing to eat gluten-containing products.

RESEARCH UPDATE:
The focus on gluten in wheat is admittedly a bit reductionist on our part.
Gluten is certainly potentially problematic and the best studied, but it may
not represent the whole story.

New research shows that other proteins in wheat aside from gluten are
potential culprits in stimulating intestinal permeability and inflammation
and may be the underlying cause of problems previously attributed to
gluten.

STRONG MEDICINE TACTICS:

Eliminate gluten-containing grains for 1-2 months to assess their potential
effects on your individual health.

TRIGGER #2:
STRESS AND INTESTINAL PERMEABILITY
Many of us are familiar with clichéd sayings such as, “I’ve got a gut feeling about
this”, “Show some intestinal fortitude!” or “Gut it out!” Most of us have experienced
a “nervous stomach” or “butterflies in the belly” before stressful events.

There is very strong scientific and anatomical basis for a gut-brain connection.
The intestinal tract has its own nervous system that can operate independently from
the brain. This gut-based nervous system is known as the enteric nervous system
(ENS) and has been called our “second brain” by some scientists.

THE SECOND BRAIN

The ENS is extensive and contains as many nerve cells as our spinal cord. Like
the brain, the ENS has sympathetic (flight or fight) and parasympathetic (rest and
digest) systems. These systems can and do operate independently from the brain.
Also similar to the brain, the ENS has nerve cells responsible for sensation,
controlling muscle movement (peristalsis) and neurotransmitter production.
Neurotransmitters are molecules that carry messages between nerve cells. You may
be familiar with neurotransmitters such as serotonin (depression) or epinephrine
(adrenaline). The ENS alone produces over 30 different neurotransmitters!

DIGGING DEEPER:

Enteric Glial Cells

Yet another similarity between the ENS and the brain are the presence of
specialized cells that act in support of nerve cells. In the brain these cells
are known as astrocytes. These cells have a multitude of functions and act
to regulate the function of nerve cells.

Astrocytes are the primary component of the blood-brain barrier. This

barrier is crucial in preventing things from getting into the brain that are
potentially harmful. There are very specific transport systems in the
blood-brain barrier that only allow certain things (like nutrients) to pass
through.

The ENS has a cell similar in type to the astrocyte, the enteric glial cells.
These cells support the ENS nerve cells and help control gut function.
EGCs are responsible for helping maintain intestinal barrier function by
reducing intestinal permeability.
“THE GUT-BRAIN AXIS”
Even though the ENS can operate independently from the brain, there is a strong
communication link between the two, the gut-brain axis. Through this two-way
communication network, signals are passed from gut to brain, and from brain to
gut. The system of how stress is communicated between the brain and gut explains
how psychological stress can produce physical symptoms such as diarrhea.

As a system, the gut-brain axis orchestrates processes such as:

• Gastrointestinal function
• Appetite control
• Body weight control

The vagus nerve is the direct connection of the gut-brain axis. The vagus
nerve carries sensory information from the gut to the brain. The vagus
also controls motor signals for gut muscle contractions.
 KEY POINT:
Higher levels of parasympathetic activity (as in relaxed states) have been
shown to decrease inflammation, and protect the gut from intestinal
permeability. This is how stress reduction can protect your gut.

High sympathetic (fight or flight) states reduce parasympathetic signaling

leading to increased inflammation and intestinal permeability. If you are
“stressed” constantly, think how this may affect your gut!

THE BRAIN RESPONSE TO STRESS

The vagus nerve is the primary carrier of parasympathetic (rest and digest)
signals from the brain to most of our internal organs, including the gut.

During psychological stress or physiological stress (poor sleep, overtraining,

etc.) the brain releases a signaling hormone called corticotropin releasing
hormone (CRH) from the hypothalamus. This triggers the pituitary gland to release
a hormone called adrenocorticotropic hormone (ACTH). ACTH then acts on the
adrenal glands to release the stress hormone cortisol.

Cortisol is released to combat stress, and decreases inflammation. It does so by

depressing the immune system. This process is your body’s way of defending itself
after a stressful event. This works well for short-term stresses, but the system breaks
down if it is constantly stimulated from a lifestyle of daily stresses. Chronically high
cortisol levels lead to weight gain and poor blood sugar control—a risk factor for
diabetes. Stress leaves you susceptible to sickness from bacteria and viruses.
THE GUT RESPONSE TO STRESS
The “second brain,” the ENS, also releases its own CRH in response to stress
signals. The effects are different from CRH released by the brain. This CRH acts
directly on immune cells of the “innate guardian” type, the mast cells. Mast cells are
known in medical circles as cells that release histamine in allergic reactions. It is
now known that mast cells also release a full complement of inflammatory
cytokines. These cytokines increase intestinal permeability by altering the
function of the tight junctions shown in the pictures at the beginning of this
chapter.

GUT INFLAMMATION FROM STRESS

LEADS TO CHRONIC DISEASE

1. Psychological and/or physical stress leads to high sympathetic (fight
or flight) nervous system activity.
2. The brain responds by decreasing parasympathetic (rest and digest)
signaling to the gut by the vagus nerve.
3. Decreased parasympathetic signaling by the vagus nerve leads to
increased intestinal permeability.
4. Increased intestinal permeability activates the gut immune system.
“Invaders”—foreign bacteria and protein fragments—lead to
inflammation.
5. Inflammation of the gut leads to impaired function resulting in
symptoms such as diarrhea and bloating.
6. Chronic stress leads to chronic intestinal permeability, which leads to
chronic inflammation.
7. Chronic inflammation leads to diabetes, cancer, high blood pressure
and heart disease.

Locally in the Gut:

 1. Stress activates the ENS to produce CRH.
2. CRH activates mast cells that release inflammatory cytokines.
3. Inflammatory cytokines disrupt tight junctions leading to intestinal
permeability.
4. Intestinal permeability leads to inflammation.
5. Chronic stress leads to chronic inflammation.
6. Chronic inflammation leads to diabetes, cancer, high blood pressure
and heart disease.

STRONG MEDICINE TACTICS:

Stress reduction is crucial to improving your gut health and will help
prevent chronic disease. Use the stress reduction techniques in the Chronic
Stress chapter.

TRIGGER #3. DYSBIOSIS: CHAOS IN THE GUT “ZOO”

“This consortium of bacteria contains tenfold more cells than the human body,
100 times the number of genes than the human genome, and has the metabolic
capacity of the human liver.”

The quote above is from an article published in 2009 from a very prestigious
scientific journal, describing the bacteria that live in our gut. We have known for a
long time that vast amounts of bacteria call our gut home, but we are only recently
beginning to learn the profound effect they have on our health.

The gut really is a “zoo” in the truest sense of the word:

• There are approximately 100 trillion bacteria in our intestines.

• There are approximately 1,000 separate bacterial species capable of colonizing

the human intestinal tract.

• At any one time, a healthy adult has 150 to 200 of these bacterial species inside
them.
 • Which specific species are present depends on the human host’s environment. A
study has recently shown that gut bacteria species in children from rural African
communities are very different from the species found in European city dwellers.

Just as a large diversity of species is good for our planet’s ecosystem, a large
diversity of bacterial species has been shown to be an indicator of good health in
humans. In fact there has been shown to be a direct correlation with loss of gut
bacteria diversity and poor health. Sickly and obese people have fewer types of
bacteria in their guts than healthy people.

DIGGING DEEPER:
What is a Microbiome?
Many of us have heard the term, human genome. Our genome is simply
the total collection of our genes. We each have approximately 20,000
different genes. Each gene represents a message encoded in our DNA that
when activated, produces a protein of a specific structure and function.
These proteins include—among other things—hormones, enzymes,
signaling and structural proteins. The metabolic “machinery” in humans is
also made from these proteins encoded by DNA. The machinery that
creates (and breaks down) carbohydrates, protein, and fat, are all made
from specific genes.

The gut bacteria microbiome, is simply the total amount of different genes
found among the bacteria that live in our intestinal tract. There is a key
difference between the human genome and the gut bacteria microbiome:
• The human genome completely resides within a single organism—a
human.
• The gut bacteria microbiome is comprised of separate genes in each
species of bacteria. When we group the species of bacteria together (150-
200 species in our guts), we then get the total collection of genes known as
the microbiome from the populations of separate bacterial species.

You and I can have different species of bacteria present in our gut “zoo”,
but our gut microbiomes can still be similar to one another, because
 similar genes will be present in a diverse population of separate bacterial
species.

This is why high diversity (many different types) of gut bacteria is

important. Sick and obese people have less species, and this lower
diversity means that the microbiome in these people is probably lacking
some bacterial genes that are important to the person’s health. So now
when we refer to the microbiome, you know what we are talking about.

FROM CRADLE TO GRAVE

When you were still in your mother ’s womb, your insides were a sterile place,
free of any bacteria. Bacteria began to colonize your gut during and after the
birthing process. Recent science suggests that the time during and immediately after
birth is crucial for development of a diverse population of bacteria. Certain
practices in Western society affect this process with potentially profoundly negative
health consequences.

The results of a study in the Netherlands published in 2006 showed that the
specific gut bacterial species found in infants depended on a number of factors
including: gestational age (how long the fetus was carried in the mother before
delivery), type of delivery (C-section vs. vaginal), location of delivery (hospital vs.
home), type of feeding (breast milk vs. formula), and antibiotic use.

The results showed that infants born at home and breastfed exclusively, showed
the highest amount of beneficial gut bacteria and the lowest amount of potentially
pathogenic bacteria.

Hospitals are certainly appropriate places to monitor delivery of pregnancies.

Formula feeding is sometimes the only option and C-sections can be lifesaving.
That said, it seems whenever possible and safe, “natural” birth environments and
processes promote a healthy and diverse gut bacteria population for the baby.
Breastfeeding has been shown to be especially beneficial in this regard.

It is thought that the gut bacteria population has matured to mirror that of an adult
by three years of age. The first few years of life are crucial for forming a balanced
gut bacteria population.

The early development of our immune system during infancy and

 childhood is influenced by gut bacteria composition. Disruption to the
normal “balance” of gut bacteria may change the way our immune
systems develop, possibly leading to increased susceptibility to:
• Allergic disease such as asthma
• Autoimmune diseases such as type I diabetes

RESEARCH UPDATE:
Some scientists think that early in life, our gut bacteria may “program”
our metabolisms, helping determine whether we will develop metabolic
disorders such as obesity or type II diabetes. One scientist suggests that we
can help prevent obesity and diabetes in adulthood by identifying and
correcting gut bacteria imbalance in early childhood and even during
childbirth!

THE DELICATE BALANCE

It turns out that a balance exists between bacteria species beneficial to our health
and those that are potentially problematic. In medical lingo, we call the latter
“opportunistic pathogens.” They don’t cause problems if there are enough
beneficial (good guy) bacteria around, but if the population of good guys is reduced
for some reason, the opportunistic pathogen bad guys will take over with chronic
inflammation as the result.
THE HEALTH BENEFITS OF OUR
“INTESTINAL TENANTS”
The beneficial species of bacteria can do great things for us as long as we
treat them well.
• When we eat fermentable fiber—fibrous carbohydrate material mainly
from fruits and vegetables—the bacteria uses the fiber for food,
metabolizes it for us, and produces a “waste” product of anti-
inflammatory short-chain (SC) fats. Our colon uses SC fat as a primary
energy source. These SC fats are powerful and exceedingly effective at
reducing inflammation. Short-chain fat boosts the immune system and has
been shown to have anti-cancer properties.
• Our beneficial gut bacteria detoxify potentially harmful compounds in
our food and water.
• They prevent the overgrowth of infectious “pathogenic” bacteria.
• They are crucial for proper development of our immune system.
• They can help prevent insulin resistance and diabetes.
• Beneficial gut bacteria can even help protect against autoimmune
diseases.

DIGGING DEEPER:
T-Regulatory Cells and Gut Bacteria
New research has shown that beneficial gut bacteria provide the signal for
formation of new Treg cells (the “hippies”) in the gut. Remember that the
Treg cells keep the “assassin” T-cells in check, preventing them from
getting out of control and damaging our body tissues. The beneficial gut
bacteria need to be present in the proper balance to keep the “assassins”
and “hippies” in proper balance.

This signaling function to form new Treg cells by beneficial gut bacteria
may be behind the following findings in recent research:
• Beneficial gut bacteria have been shown to help prevent our immune
system from becoming overactive, thus preventing chronic inflammatory
disease.
• Specific types of beneficial gut bacteria may protect against
autoimmune disease, including inflammatory bowel diseases such as
ulcerative colitis and Crohn’s disease.
• People with inflammatory bowel diseases often show a loss of certain
types of beneficial gut bacteria.
• Beneficial strains of gut bacteria have been shown to help maintain our
intestinal barrier, protecting against chronic intestinal permeability.
• Butyrate produced from fiber (vegetables and fruit) fermentation by
beneficial gut bacteria makes more Treg cells (“hippies”) to help control
inflammation.

RESEARCH UPDATE:
Deficiencies in beneficial gut bacteria lead to deficiencies in
Treg cells
Recent research has shown that deficiencies in Treg cell populations in
humans may predispose us to asthma, inflammatory bowel disease, type I
diabetes, and multiple sclerosis.
 The importance of the balance between the “beneficial” gut bacteria
(green) and the opportunistic pathogens (red) is illustrated here. Certain
types of beneficial bacteria stimulate formation of the Treg “hippies”
while the pathogens stimulate formation of T-cell “assassins.” Imbalance
resulting in an overgrowth of pathogens is called dysbiosis. It can lead to
too many assassins around which can cause chronic inflammation. At the
same time, too many hippies and not enough assassins can lead to a poor
immune response to an infection when necessary. Just like real life, we
need both the warriors and anti-war protesters in balance so we do not go
too far in either direction.

THE BALANCE DISRUPTED: DYSBIOSIS TAKES OVER...

The term “dysbiosis” refers to any altered state of normal bacteria balance
associated with disease. A feature common to all types of dysbiosis is the loss of
bacteria species diversity. We need balance between “beneficial bacteria” and
“opportunistic pathogens.”

TECHNICAL NOTE:
The definition of dysbiosis we are using is greatly simplified. Indeed,
recent research shows that there are significant differences in the
composition and balance of gut bacterial species between obese
 individuals and non-obese and between diabetics and non-diabetics.
Classifying gut bacteria as “beneficial” or as “opportunistic pathogens” is
not as black and white in reality. We use this distinction to communicate a
concept, but it is important to note that some bacteria associated with
inflammation in the gut may not be “pathogenic” in the technical sense. We
are still classifying them under “opportunistic pathogens” because they
can promote inflammation and contribute to chronic disease when the
normal balance is disrupted, when there is a loss of bacterial diversity, and
in cases of intestinal permeability.

DYSBIOSIS HAS BEEN ASSOCIATED WITH NUMEROUS

DISEASES AND DISORDERS
• Autoimmune disorders (including inflammatory bowel disease)
• Allergic disease including asthma
• Irritable bowel syndrome
• Obesity
• Type II diabetes
• Colon cancer
• Fatty liver disease
• Atherosclerosis (heart and vascular disease)
• Acne (not surprising, acne is an inflammatory condition)

Dysbiosis—the opportunistic pathogens outnumber beneficial gut bacteria. This

leads to an imbalance between “hippie” Treg cells and “assassin” T-cells. With more
assassins around, we are more prone to out-of-control inflammation and
autoimmune disease. There are not enough hippies to balance the assassins.

WHAT CAUSES DYSBIOSIS?

 The shift to dysbiosis has been associated with multiple factors, but the primary
influence on gut bacteria populations seems to be diet, with environmental
exposures such as antibiotic use also contributing.

“Diet is the most powerful influence on gut microbial communities in healthy

human subjects” —Stig Bengmark (2012)

Evidence is mounting that processed foods containing large amounts of flour,

refined oils, and sugar may be a primary culprit in development of dysbiosis. We
are used to thinking about food in terms of carbs, fat, and protein—the
macronutrients. Diet books are best sellers and each champions a diet strategy
promoting one nutrient while damning another, i.e. “low fat/high carb” or “high
fat/low carb.”

It is interesting that many traditional cultures eat a wide range of diets, including
high fat/low carb (the Inuit tribe) and high carb/low fat (the Kitavans). These
cultures have extremely low rates of “Western” diseases such as diabetes, obesity,
and heart disease, despite the large variability in types and ratios of macronutrients.

When people from these cultures begin eating processed Western diets, high in
refined grains, sugar, and refined oils, they quickly lose their tribal health and
vitality. Obesity, formerly unheard of, becomes epidemic. The tribal members eating
“Western” succumb to “Western diseases”.

An intriguing hypothesis was put forward recently in the scientific literature by

Dr. Ian Spreadbury. He suggests that processed grain-based carbohydrate foods
affect gut bacteria very differently than natural, non-processed “whole food”
carbohydrate sources, such as root tubers (sweet potatoes,) stem tubers (potatoes)
and fruit. Dr. Spreadbury suggests that the carbohydrate density of a food is
important to how our population of gut bacteria respond.

If you are having a hard time conceptualizing density, think of how many
people are in one square mile in rural Montana versus a square mile in
New York City. As far as carbohydrate density, tubers and fruit are more
like Montana, while processed grain foods are like New York City.

Dr. Spreadbury suggests that high-density carbohydrate foods promote dysbiosis,

the overgrowth of specific inflammation-promoting gut bacteria. He further
suggests that once this type of dysbiosis has been cultivated and takes root, high
dietary fat intake (especially refined oils, corn oil, vegetable oil) promotes further
inflammation. This suggests that the fat intake in the diet may only become harmful
if processed grain foods are eaten. For promoting dysbiosis, the worst dietary sin
would be combining lots of processed grain-based foods with lots of refined dietary
fat. This combination describes the composition of most fast food.

Do not worry about eating tubers, vegetables, and fruit. These foods contain high
amounts of “fermentable fiber.” They are excellent food choices, containing the
type of fiber our beneficial gut bacteria use for fuel.

These foods will not lead to dysbiosis because the “waste” product of fiber
fermentation is short-chain fatty acids (SCFA). Butyrate, propionate, and acetate are
all SCFAs that are anti-inflammatory and have numerous health benefits, including
promoting the growth of beneficial gut bacteria.

FERMENTABLE FIBER AND GUT

HEALTH: FIRST PRINCIPLES
Current scientific thought—eating foods high in fermentable fiber
encourages the growth of beneficial bacterial species in our guts, helping
maintain the balance. “Western” processed food, largely devoid of
fermentable fiber, encourages the growth of opportunistic pathogens
leading to dysbiosis. This hypothesis of processed food leading to
dysbiosis makes sense for many reasons:

• There are several examples of traditional cultures eating no processed
food, but otherwise a relatively high fat diet without apparent health
consequences.
• Processed, grain-based high-density carbohydrates coupled with refined
oils and fats is the definition of the health-killing “Western Diet.”
• Several traditional cultures eat a diet high in unprocessed carbohydrates
from tubers such as sweet potatoes without succumbing to metabolic
diseases such as obesity or diabetes.

Here again we see the trend of “food quality,” not ratios of carbs or
fat, being crucial for health. Real food trumps processed food every
time.

STRONG MEDICINE TACTICS:

To prevent dysbiosis-related diseases such as type II diabetes, fatty liver
disease, and obesity, cut out processed, grain-based high-density
carbohydrates, and replace them with low-density carbohydrates like
vegetables, tubers and fruit.

DIGGING DEEPER:
The Link Between Obesity, Diabetes, Atherosclerosis, and
Fatty Liver Disease?
One of the ways microbiologists group some bacteria is by how well they
absorb a special type of dye—a Gram stain—in their cell walls when
viewed under a microscope. Gram-positive bacteria take up the stain well
and look purple in color under the microscope. Gram-negative bacteria
do not take up the stain, and have a light pink color. Gram-negative
bacteria have an outer membrane surrounding their cell wall, which
prevents the stain from coloring the cell wall.

Gram-negative bacteria have something called lipopolysaccharide (LPS)

in their outer membrane. LPS is also known as a bacterial “endotoxin”.
When LPS gets through our intestinal barrier and into the blood stream,
our immune system goes crazy and produces a large inflammatory
response. This is called endotoxemia. Also the epithelial cells lining our
 gut have a system to recognize LPS. When LPS is recognized either in the
blood stream by immune cells or in the gut wall, inflammation is the
result.

People with type II diabetes, fatty liver disease, and obesity have been
shown to have a greater proportion of Gram-negative bacteria in their gut
(dysbiosis), and thus more LPS than healthy individuals. It is probably no
coincidence that many type II diabetics are overweight or obese, have fatty
liver, and accelerated atherosclerosis.

In fact, there is a hypothesis that is strongly supported by recent research

that links chronic low levels of LPS in the bloodstream (chronic
endotoxemia) with Type II diabetes, obesity, atherosclerosis and fatty liver
disease. Scientists suggest that constant low levels of LPS are getting into
the bloodstream from chronic intestinal permeability.

“After millions of years of co-evolution, have societal advances paradoxically

and adversely affected human health by reducing our exposure to health-
promoting bacteria?”

The quote above is from a study published in 2009 and brings to light another
possibility for a dietary source of dysbiosis. Many people in modern society have
been “sheltered” from exposure to bacteria in our food starting early in childhood.
Our modern foods have been largely sterilized compared to traditional cultures.
There are a variety of potentially beneficial bacteria present in naturally grown
fruits and vegetables. Traditionally these vegetables are an early source of
beneficial bacteria in our diets.

We have become obsessed with food hygiene as we have modernized, and for
good reason. Our modern large-scale farming and distribution methods have led to
frequent contamination of our food supply by pathogenic bacteria. News stories
about salmonella contamination of produce or E. coli in meat are common. A recent
study showed significant differences in gut bacteria found in rural African children
versus those in a group of city-dwelling European children. The African children
had a large and diverse population of beneficial gut bacteria able to ferment fiber,
while the European kids showed decreased diversity and small amounts of
beneficial gut bacteria. A sanitized food supply in Europe was thought to be one of
factors accounting for this difference.
ANTIBIOTIC USE: A DOUBLE EDGED SWORD
Another potential contributor to dysbiosis is the use of antibiotics. The
discovery and widespread medical use of antibiotics in the 20th century has saved
countless lives. Use of these wonder drugs has become incredibly common in recent
years. Some argue that though they are clearly effective and beneficial, in many
circumstances, antibiotics may have unintended health consequences.

Antibiotic use significantly alters the balance of your gut bacteria, and in some
cases leads to dysbiosis. The main job of antibiotics is to kill bacteria that are
causing infections; unfortunately beneficial bacteria are mowed down in the process
—like innocent bystanders killed in a gang drive-by shootout. Killing beneficial
bacteria leads to imbalance and dysbiosis.

It is often the opportunistic pathogens that are resistant to antibiotics. Left to

fester, dysbiosis spins out of control, and left unchecked leads to chronic
inflammation. Pseudomembranous colitis occurs when antibiotics kill beneficial
bacteria, leading to overgrowth of an opportunistic pathogen known as Clostridium
difficile (CD). CD overgrowth leads to inflammation of the colon and diarrhea.

Pseudomembranous colitis is an extreme example of dysbiosis caused by

antibiotics. Recent science has shown that antibiotic use generally results in
significant changes in bacterial balance; the clinical significance of this change is
unclear. We know that antibiotic use changes the composition of gut bacteria, but we
have not studied it long enough to determine how or if it affects your health.
Disrupting gut bacteria equilibrium with frequent antibiotic doses is likely to have
unintended consequences.

RESEARCH UPDATE:
A new article in the journal, Pediatrics, has started to illustrate these
unintended consequences. The study found that while following a group of
464 children for 15 years, the children who received courses of antibiotics
early in childhood had a significantly higher risk for developing
inflammatory bowel disease (IBD) as they got older. The authors correctly
state that other factors are involved in developing IBD, but early antibiotic
use clearly seems to be a significant factor.
 The following is clear from current research:

• A single course of broad-spectrum antibiotics (those that kill a wide variety of

types of bacteria) causes changes in gut bacteria populations lasting from three
months to two full years.

• Combination antibiotic therapy, as used to treat Helicobacter pylori infections

(a cause of stomach ulcers), has been shown to alter gut bacteria populations for
up to four years after treatment in extreme cases.

• Widespread antibiotic use is creating strains of bacteria resistant to current

antibiotic treatment.

Antibiotic source?

Many people go to their doctor ’s office demanding antibiotics for relatively

minor maladies such as upper respiratory infections. A significant number of these
patients are successful in getting their doctor to prescribe antibiotics, even though
the majority of upper respiratory infections are due to viruses unaffected by
antibiotics.

Frequent and inappropriate use of antibiotics may end up contributing to long-

term health problems from the impact on beneficial gut bacteria. Not to mention, it
creates problems for the rest of us by developing resistant strains of bacteria.

We also unintentionally get low levels of antibiotics from environmental sources

such as meat and dairy from feedlot animals. Eighty percent of all antibiotics sold in
the U.S. are currently used for chickens, cows, and pigs to prevent infection in the
crowded environments in which they are raised. Many of these antibiotics eventually
find their way to your dinner table, and most are not destroyed in the cooking
process.

Some studies have even found antibiotics in produce such as lettuce, carrots, and
potatoes grown in fields treated with manure-fertilizer from antibiotic-treated
animals. It is currently unclear how these sources of antibiotics affect gut bacteria
and human health, but it seems logical to do your best to avoid them if possible.

Knowing where your food comes from is the best way to start. Choose locally
grown organic produce and choose meat from pastured animals, free from
antibiotics.

STRONG MEDICINE TACTICS:

To prevent dysbiosis and antibiotic resistance, avoid frequent treatment
with antibiotics for minor conditions.

Also choose meat and produce that is free from antibiotics by demanding
organic, pastured, and locally grown food.

“Let food be thy medicine and medicine be thy food”

—Hippocrates

The best way to restore bacterial balance is through diet. First and foremost—
avoid processed food. For people with dysbiosis (and gut inflammation)
consumption of probiotics in fermented foods has been found to be extremely
beneficial. The treatment of disease with probiotics is a hot topic in current medical
research and deserves further discussion.

PROBIOTICS AND FERMENTED FOODS

The World Health Organization defines probiotics as, “Live microorganisms
which, when administered in adequate amounts, confer a health benefit on the host.”
Fermented foods containing live microorganisms (such as yeast and bacteria) have
been part of traditional diets for thousands of years. It has been known for 150 years
that the bacteria and yeast in fermented foods are responsible for chemical changes
that result in health benefits.
 Fermentation is defined as a biochemical change in carbohydrates—
microorganisms such as yeast, bacteria or mold use the carbohydrate for food. The
microorganisms metabolize carbs and create “waste products.” Beneficial gut
bacteria transforms fiber into short-chain fatty acids and these short-chain fat “waste
products” (from bacterial fermentation of vegetable and fruit fiber) are crucial for
the overall health of our intestinal tract.

The product of microorganism fermentation most us are most familiar with is

alcohol. Alcohol is the waste product from yeast fermenting sugars. Alcohol is not
considered a probiotic because the yeast is filtered out of alcoholic beverages
before consuming.

For thousands of years, traditional tribal cultures have made fermented foods
from vegetables, fruit and dairy products. These primal tribesmen were not
concerned one wit about health benefits—fermentation allowed foods to be stored
for later consumption in the hard winter months. Fermented foods can be stored for
years: Korean kimchi is aged like wine. Fermented foods are always widespread
when refrigeration is not common or available. Fermented foods are still regularly
part of millions of people’s daily diets worldwide.

The medicinal and health benefits of fermented foods were recognized by ancient
cultures and used as medicine. With the advent of industrial food processing,
modern society has relegated fermented foods to the trash heap. Recently there has
been a resurgence in interest in fermented foods, driven largely by research into the
health benefits of probiotics.

The supplement industry has discovered probiotics and is attempting to

commercialize and popularize their usage. This is yet another example of
inappropriate reductionism. The supplement industry grows bacteria species
thought to be beneficial, isolates and processes them, puts the anemic concoction
into a capsule, then makes exaggerated claims for the product. Traditional cultures
obtained these beneficial bacteria in their diets—not from a pill—in the form of
fermented foods.

The most common beneficial bacteria species found in traditional fermented

foods produce lactic acid as a waste product during the fermentation process. Using
this type of bacteria for fermentation is thus called lacto-fermentation, or lactic acid
fermentation. Lacto-fermentation is used on a wide variety of fruits, vegetables, and
dairy products to produce fermented foods.
LACTO-FERMENTATION

There are vast amounts of bacteria that naturally make their homes on vegetables
and fruit. Even with a thorough washing, bacteria clings to produce in large
numbers. We all have seen fruits and vegetables “go bad” quickly or spoil if left out
in the air at room temperature for a period of time. The produce will stay fresh
longer in the refrigerator, but decomposition and rot are inevitable. Fruits and
vegetables decompose because of bacteria. Surface bacteria begin to quickly break
down the host when left exposed to oxygen at room temperature.
Lacto-Fermented Escabeche (jalapeño, sweet peppers, carrots, onions, garlic).
www.thenourishinggourmet.com

Lacto-fermentation works because the lactic-acid-producing bacteria on the fruits

and vegetables thrive in the following conditions:

• In an acidic environment

• In the presence of relatively high salt concentrations

• Without the presence of oxygen

DO IT YOURSELF!

 To start the fermentation process, vegetables and/or fruit are placed in a
container and filled with water to ensure no air is present. Salt is added
and the container is left in a dark place with the temperature between 68
and 72 degrees. This environment encourages the growth of the lactic-
acid-producing beneficial bacteria. As these bacteria multiply, they start to
use the vegetables and fruit as a fuel source and give off lactic acid as a
waste product (this is the fermentation process). The lactic acid reduces
the pH of the surrounding fluid, making it more acidic. The other bacteria
present (the ones involved in the rotting process) die because they are not
able to survive the high salt and acidic environment. This leaves the lactic-
acid-producing bacteria alone to continue the fermentation process until
the lactic acid builds up enough to slow their growth. The resulting
fermented vegetables and fruit now can be stored for long periods of time
because the high acid and salt content prevent the decomposing (rotting)
bacteria from growing.

Health benefits of lacto-fermented fruits and vegetables:

• Increased vitamin content—lacto-fermenting bacteria concentrate large

amounts of vitamins (especially B vitamins) during the fermentation process.

• Better digestibility: fermentation breaks down the indigestible parts of plants,

allowing humans to utilize them. Many traditional cultures use fermented foods
to wean young children from breast-feeding.

• Removal of natural plant toxins and anti-nutrients: many plants have their own
defense mechanisms to prevent them from being eaten. The process of
fermentation breaks down many of these defensive toxins and anti-nutrients,
leaving the plants safe to eat.

QUICK DEFINITION:
Anti-nutrients are compounds found in many plants that bind to nutrients
such as vitamins and minerals. This binding process prevents us from
absorbing these beneficial nutrients when we eat the plant. Fermentation
destroys many of these anti-nutrient compounds allowing us to better
 absorb the vitamins and minerals found in the plant.

LACTO-FERMENTING BACTERIA AND OUR HEALTH

Recent science has shown that lacto-fermenting bacteria are extremely beneficial
to our health. These bacteria shore up our immune system.

• Lactic acid fermenting bacteria (Lactobacillus) have been shown to directly

induce formation of Treg cells in the gut. Treg cells (the “hippies”) control the
“assassins” and reduce inflammation.

• Lactic acid fermenting bacteria increase tight junction formation in the

intestinal epithelial cells and reduce intestinal permeability. They also were found
to protect the tight junctions from further disruption.

It is now thought that the lactic acid fermenting bacterial species from fermented
foods do not stay in the gut as long as previously thought. We used to think that
these probiotics “repopulated” the gut bacteria directly. Current science seems to
show that most of them just “pass through” but still exert considerable beneficial
effects on our immune system and health. This is why regular consumption of
fermented foods is necessary. This may partially explain the fact that most cultures
still eating fermented foods as a regular part of their traditional diets are free from
chronic inflammatory diseases such as heart disease and diabetes.

The best way to restore the “balance” in your gut bacteria is primarily through
eating foods with plenty of fiber such as fruits and vegetables. These types of foods
provide a fuel source, and encourage the growth and reproduction of beneficial
bacteria living in your gut. Lacto-fermented fruits and vegetables not only provide
an anti-inflammatory effect from the probiotic lactic acid fermenting bacteria in the
food, but the food itself helps the beneficial bacteria that are already in your gut
multiply. Thus, taking probiotics in a pill only gives you half of the solution to
dysbiosisrelated inflammation.

 Specific preparation methods for fermented foods are beyond the scope of this
book. There are several excellent resources in books and on the internet. A
comprehensive book on the subject is The Art of Fermentation by Sandor Katz and
for beginners, Cultured: Making Health Fermented Foods at Home by Kevin Gianni.
Both are highly recommended. Go try some kimchi!

STRONG MEDICINE TACTICS:

Eat fermented food 2-3 times per week to control intestinal permeability,
inflammation of the gut, balance the immune system, and improve
digestion.

THE GUT-BRAIN-BACTERIA TRIUMVIRATE: WHO’S IN

CHARGE?
Recent research indicates that bacteria may influence our mood and behavior. The
idea that mute bacteria living within us can affect our behavior is, well, strange. In
the last several years, some intriguing research (in animals) has shown that specific
bacteria can measurably change levels of anxiety and alter responses to stress.

Scientists have shown that anxiety-related behaviors were increased in mice when
they were given small doses of “opportunistic” pathogen-type bacteria. They also
showed that when given certain probiotic strains of beneficial bacteria, the mice’s
anxiety levels plummeted. Researchers have shown that alterations in the normal gut
bacteria in young mice left them with exaggerated responses to stressful events later
in life as adults.
 Our brain and “second-brain” (enteric nervous system) communicate through the
vagus nerve—our internal communication “super highway”. We also know that our
gut bacteria can directly affect and change the function of our enteric nervous
system via intestinal permeability and dysbiosis. Our enteric nervous system
communicates these changes to our brain (primarily) through the vagus nerve.

Somehow this complex organic communication system is able to differentiate

“good” from “bad” bacteria and sends signals to decrease or increase anxiety states
in the brain.

FIRST PRINCIPLES PERSPECTIVE

An overgrowth of opportunistic pathogen-type bacteria could be
considered a “threat” to the body. No matter the source, our brain
responds to “threats” (any potentially dangerous situations) by stimulating
our “flight or fight” sympathetic nervous system. Increasing our “flight or
fight” system can certainly increase anxiety. Think about narrowly
avoiding a car accident or being confronted by a dangerous wild animal.
These two examples are external threats and produce large flight or fight
responses compared to comparatively minor “threats” such as increased
bacterial pathogens in our gut. But a minor threat to the body that happens
chronically every day can constantly keep the brain in a low state of flight
or fight. Over time, this constant low-level “threat” response can lead to
negative effects in the brain and body.

We know that chronic stress can lead to anxiety and depression, so given
our discussion above, it is not far fetched to consider that imbalances in
gut bacteria (a low level chronic stress) may contribute to mental health
problems.

Interestingly, an alternative (FDA-approved) treatment for intractable depression

is vagus nerve stimulation. As gut bacteria can stimulate the vagus nerve pathway, it
is plausible that there could be a connection between gut bacteria composition and
mood disorders like depression.
 RESEARCH UPDATE:
A recent study from 2011 provided early evidence that probiotics
improved anxiety and mood within 30 days of use. More research needs to
be performed, but these results are very interesting.

In addition to communicating with the brain through the vagus nerve, intestinal
bacteria may also affect several hormones that act directly on the brain to regulate
appetite, the sleep/wake cycle, memory retention and metabolism. These hormones
include leptin, ghrelin, gastrin, orexin, and many others.

Recent work by a French research team has shown that our immune system
produces “auto-antibodies” that actively work against some of these hormones.

QUICK DEFINITION:
Auto-antibodies are antibodies produced by our adaptive immune system
(assassins) against our own tissues. See our discussion on auto-immunity
for more on this.

The team of researchers hypothesized that these auto-antibodies are produced by

our immune system in response to “signals” sent by specific gut bacteria. The
signaling mechanism is thought to be “molecular mimicry.” Molecular mimicry is
when a certain protein sequence found in bacteria is chemically similar to a protein
sequence found in our own tissues. The immune system recognizes the bacterial
protein sequence and produces antibodies for defense against the bacteria.

The problem is that these antibodies will also bind to tissues in our body (in this
case the hormones) that have a similar protein sequence as the bacteria. By binding
to the hormones inappropriately, these antibodies (now called auto-antibodies) can
affect the way the hormones deliver their messages to the brain. Depending on the
hormone affected, signals for functions like hunger, sleep, and mood can be altered
by these auto-antibodies. The resulting hormonal chaos contributes to inappropriate
eating behavior, sleep disturbances, and depression.

The composition of gut bacteria influences what type of auto-antibodies are

produced by the immune system and what hormones are affected.

These ideas are relatively new and more investigation is needed before jumping
to any conclusions, but they were included here to illustrate another way bacteria
may profoundly influence our health and behaviors. Basic physiologic processes
like sleep, hunger and mood are regulated by chemical-signaling hormones in the
brain. Anything that can alter these processes (such as gut bacteria) will affect how
the brain functions.

Based on recent science, the idea that our gut bacteria can affect our outward
behavior may not be as far-fetched as it once seemed. One more reason to hedge
your bets and follow the Strong Medicine Defensive Tactics in this chapter to
prevent dysbiosis.
GUARDIAN AT THE GATE PART III
CONCLUSION

Chronic inflammation is a central cause of diseases such as heart disease, high

blood pressure, diabetes, and cancer. We have shown chronic intestinal permeability
and gut inflammation from a variety of sources is not only a potential source of
chronic inflammation, but perhaps a necessary component for developing and
perpetuating autoimmune diseases (such as type I diabetes).

 Using the basic dietary and lifestyle interventions given in this chapter ’s Strong
Medicine Defensive Tactics can “break the link” to chronic inflammation in the gut
and the diseases and conditions resulting from it.

TYPE I DIABETES CASE STUDY

REVISITED
Let us resume our initial case study of the 6-year-old with type I diabetes
from the beginning of this chapter. Although speculative, a rational way to
explain his fantastic results with a gluten free diet is as follows:
• Gluten was likely triggering intestinal permeability.
• Chronic intestinal permeability was setting off his adaptive immune
response by exposing the immune system to “foreign” molecules daily.
• His individual genetics left him predisposed to an “agitated” adaptive
immune system accidently targeting his own cells—in this case the insulin
producing cells in the pancreas—and started to destroy them. Again we
speculate, but it is plausible that he had dysbiosis, leaving him with fewer
Treg cell “hippies” to tame the out-of-control immune response from the
“assassins.”
• We know that proper gut bacteria balance is especially important to the
development of the immune system in infants and children.
• Removing the gluten trigger before all of his insulin-producing cells
were destroyed by the out-of-control immune attack allowed him to
recover. Without the gluten trigger, the vicious cycle of chronic intestinal
permeability and the resulting immune response stopped.
• His condition was caught and treated early enough to save sufficient
insulin-producing cells in his pancreas. He no longer needs insulin
injections.
Early intervention with a gluten free diet eliminated the problem before it
was too late. Most type I diabetics are not that lucky, and the damage is
already done by the time gluten sensitivity is caught. In my opinion, there
are no benefits in including gluten in a child’s diet—and everything to
gain by adhering to a gluten free diet at an early age. Most children are not
genetically predisposed to develop type I diabetes, but is it worth the risk
with your child?

COACH’S CORNER:
Gut Health and Body Composition
If you are focused on fat loss and muscle gain, take heed. High cortisol
levels from the HPA-axis threat response promote fat gain and muscle
loss. Inflammation and oxidative stress in the gut are interpreted as a threat
by the brain, leading to activation of the cortisol producing HPA-axis.
Stopping the threat response by controlling inflammation in your intestinal
tract will improve your health, as well as accelerate your fat loss and
muscle building efforts.
 Now that you have adequate training on the devastating health effects of chronic
gut inflammation, prepare yourself to learn about one of the most powerful
members of the “Pentaverate,” obesity.
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KNOWING YOUR ENEMY II
OBESITY: THE ENEMY WITHIN

A nuclear explosion is an uncontrolled chain reaction leading to a devastating

outcome. The obesity epidemic is an out of control chain reaction that is devastating
to both our health and healthcare system. By contributing to creating a legion of
people with chronic diseases, obesity is also killing us economically.

Obesity and its resulting health consequences, may represent the single biggest
threat to 21st century public health.

Obesity transforms our fat cells into an “enemy within.” We will show you how to
reverse this transformation and stop the metabolic corruption that ultimately results
in a devastating assault on your body and brain.

The Strong Medicine Defensive Tactics learned in this section will repel this
assault and restore the flesh machine to state of optimum function. We will
overthrow the enemy within.
KNOWING YOUR ENEMY II
INTRODUCTION: A BIG FAT
PROBLEM...

THE NEWEST MINORITY

A couple of years ago, I was preparing for job interviews after my time in the
military and needed to buy a new suit. For the previous 13 years, I wore military
uniforms for formal occasions and had not bought a business suit in years. I went to
a well-known men’s clothing store, thinking it would be relatively easy to purchase
a decent suit, without spending a fortune on custom tailoring. I was wrong.

The salesman worked with me for more than 2 hours, trying on suit after suit,
before he said with a look of dismay, “Even with extensive tailoring, I don’t have
anything here that I can make fit you. There is just too much extra material around
the waist.” I was somewhat taken aback by his statement. At the time, I had a 44-inch
chest and a 32-inch waist—hardly freakish proportions. He said there was too much
of a difference between my chest and waist size, making off-the-rack suit purchases
“impossible.”

He directed me to a competitor who carried a brand that was “athletic cut” and
which could probably be tailored to fit me. After spending an entire day looking for
a suit, I eventually found something to fit my apparently “rare” proportions. I had
no idea that my body type had become a rarity, as I had been around military men
and women—who were far fitter than the general population—for more than a
decade. I did not truly grasp the extent of the obesity problem until my sheltered
bubble was burst while shopping for a suit.

The actual statistics for the proportion of U.S. adults that are overweight or obese
—almost 3/4ths of our population—are sobering. The remaining 1/4th of us who
are not overweight or obese are the newest minority.

Data compiled by the American Heart Association, 2013.

COSTS: HEALTH AND THE ECONOMY

Excess body fat ranges from overweight to obese to morbidly obese. The health
consequences mirror the individual’s degree of obesity. These chronic diseases and
poor health outcomes are inexorably linked to obesity:

• Type II diabetes
• High blood pressure
• Heart disease
• Cancer

The current economic cost of obesity-related disease is estimated at over $250

billion each year. By 2030, it is predicted that the health care costs from obesity
could rise to over $950 billion.

Obesity and chronic disease are linked very strongly since obesity is a source of
chronic inflammation and oxidative stress. We will present what you can do to fight
your own battle with obesity—and win.

QUICK FACT:
Health care costs related to obesity could reach as high as $950 billion per
year by 2030.

TECHNICAL NOTE:
Someone is defined as overweight or obese by an indictor called the body
mass index (BMI). BMI is calculated using a person’s height and weight:

BMI = mass(kg) / height(m)) Metric version

2

BMI = mass(lbs) / height(1n)) X703 English version

2

There are several online BMI calculators on the internet, which will
automatically calculate the BMI from your height and weight
measurements.

A BMI from 25.0 to 29.9 indicates being overweight.

A BMI of 30 or over indicates obesity.

Many will correctly point out that lean, muscular people may have a BMI
in the overweight range when they are not actually overweight. For
example, I am 5’9’ tall and weigh 175 lbs. I am fairly lean—about 8-9%
body fat. My BMI is calculated as 25.8, which is considered overweight
even though I have little body fat.
Lean individuals who carry more muscle mass may find that the BMI is
not the most accurate assessment. For the general population, it is a decent
measurement for being overweight or obese. We will discuss some new
body measurements that have shown to be superior to BMI in the Analytics
Section.
OBESITY: THE ENEMY WITHIN I
THE FAT CELL: DR. JEKYLL
BECOMES MR. HYDE

The fat cells, or adipocytes are the major storage sites for fat in the body. We all
have fat in our body, and we all need fat to survive.

QUICK DEFINITION:
The word adipocyte comes from: “adipo”= fat and “cyte”= cell.
Adipocyte literally means “fat cell.”

Adipocytes do much more than just store fat. They provide crucial signals to the
brain regarding energy storage. These fat cells regulate appetite, adjust metabolism
and lower inflammation when they are functioning properly.

When fat cells are stuffed to capacity from overeating, the adipocytes undergo a
metamorphosis from being benefactors of good health into aggressive, bloated
monsters spewing inflammation and oxidative stress.

How does a fat cell transform? Why does an excessive intake of industrial,
processed food and drink transform mild-mannered Dr. Jekyll into evildoer Mr.
Hyde? The following diagram (from the Central Concepts chapter) shows chronic
inflammation and oxidative stress contributing to chronic diseases.

The over-stuffed adipocytes in an obese person are one source of chronic

inflammation and oxidative stress that “links” obesity to cancer, heart disease,
diabetes, and high blood pressure as well as accelerated aging and
neurodegeneration.
The “link” between obesity/insulin resistance and chronic disease.

THE METAMORPHOSIS OF A FAT

CELL
The normal fat cell seeks to store excess energy in the form of triglycerides—the
storage form of fat. The adipocyte, functioning correctly (as found in lean
individuals) secretes an important hormone, adiponectin. This little-known
hormone performs several health-promoting functions:

• Decreases inflammation - adiponectin controls inflammation caused by the

immune system. It decreases the number of inflammatory cytokines, the
messengers of inflammation.

• Increases insulin sensitivity - adiponectin decreases levels of inflammatory

cytokines. This allows insulin to do its intended job: pulling glucose into the cells
to prevent a toxic buildup of glucose in the blood stream.

• Increases fat burning for energy - adiponectin stimulates the machinery that
breaks down fat for energy.

The healthy adipocyte stores just the right amount of fat, and because it is not
overworked, it functions properly. When we eat food during the day, we stockpile
nutrients and have a good supply to use for energy while we sleep. The healthy
adipocyte produces high amounts of the beneficial hormone adiponectin regularly.

 When we take in more calories than we can use for energy, the adipocyte starts to
grow in size. It swells to capacity as it tries to store excess triglycerides. When
excess dietary fat and triglycerides made from extra glucose combine, they
overwhelm the storage and processing capacity of the fat cells.

Now, the bloated adipocyte starts to attract the attention of the immune system.
The immune system exists to defend us from “threats” and the bloated adipocyte has
appeared on the immune radar as a potential health threat. A very interesting process
involving an immune cell called a macrophage begins in our fat cells as they get
jam-packed with fat.

QUICK DEFINITION:
Macrophage literally means “big thing that devours”. Macro = “big”
and phage = “thing that devours” (from Greek phagos).

The macrophage is an “innate guardian” cell that “eats debris” when a cell dies.
Macrophages also fight invading bacteria and other foreign material. A type of
macrophage called an M2 macrophage “stands guard” inside an adipocyte in case
something bad happens.

When the adipocyte starts to swell with triglycerides (fat), the M2 macrophage
senses a threat and goes on “alert,” then starts to arm itself with weapons. Like
prison guards who get assault rifles and tear gas ready when they sense a riot may
start, the M2 macrophage “arms” itself by transforming into a deadly M1
macrophage. The M1 macrophage prepares for battle by secreting inflammatory
messengers called cytokines.

The swelling adipocyte, stuffed with triglycerides triggers the transformation of the
M2 macrophage to the inflammation-producing M1 version.
 The adipocyte starts secreting inflammatory cytokines as a “911 call” summoning
immune reinforcements.

If more food is eaten—despite the fact that enough fat to fuel the body for weeks
may be available for energy—the normal cellular processes break down.

Inside the swelling adipocyte fat cell, the mitochondria work overtime and
produce large amounts of oxidative stress in the form of free radicals. More of the
M2 macrophages are converted into the M1 variety, as the immune system registers
a “prison riot” in full swing inside the swollen fat cell. Higher amounts of
inflammatory cytokines are sent into the bloodstream as the fat cell tries to protect
itself from the excess energy and resulting oxidative stress.

The immune system responds by sending in more soldiers, triggering and

increasing intense, prolonged and devastating inflammation. Stressed and bloated
adipocytes create obesity-related inflammation.

Intense inflammation causes the fat cells to reduce secretion of the beneficial
hormone, adiponectin. Without the anti-inflammatory effects of adiponectin, the
inflammatory momentum picks up even more steam.

The body considers fat deposited next to vital organs—the liver, intestines, and
blood vessels—as especially threatening. This is called “visceral obesity,” as
viscera means internal organs. People with visceral obesity have the classic “apple
shape” with the majority of the fat stored in the abdominal cavity around the organs.
This type of visceral obesity is seen with the classic beer belly. People proudly
sporting a beer belly often brag that it is “hard as a rock” and not squishy like
superficial fat. This is the absolute worst type of fat and nothing to be proud of, as it
is highly inflammatory.
 QUICK MEDICAL NOTE:
Visceral obesity (also called abdominal obesity or central obesity) is
highly associated with a variety of diseases related to inflammation:
• Type II diabetes
• Heart disease
• Fatty liver disease
• Cancer
• Alzheimer ’s dementia
• Accelerated physical aging

Given what you now know about fat cell transformation and
inflammation, these associations should not be surprising.

The swollen adipocytes surrounding the vital organs in visceral obesity are no
longer recognizable as the innocent fat cells found in lean individuals. These
monsters truly have become Mr. Hyde. They spew forth massive amounts of
inflammatory cytokines into the rest of the body like an oil rig fire. These beasts
often end up dying in their attempt to protect themselves, leaving the M1
macrophages to clear their bodies away. This dying and clearing process is also
highly inflammatory.

Recent research has shown that swollen fat cells can be a substantial source of
chronic inflammation and oxidative stress. As we mentioned at the beginning of this
section, the inflammation and oxidative stress produced daily by these bloated fat
cells is likely the link between obesity and the chronic diseases of cancer, heart
disease, diabetes, and high blood pressure.
 QUICK MEDICAL NOTE:
It was once thought that by adulthood, you had all of the fat cells
(adipocytes) you would ever have, and people got fatter only by over-
stuffing their existing fat cells in a process called hypertrophy.
Hypertrophy simply means “growing bigger”.

It turns out that an overweight or obese person can actually grow new fat
cells. This process is called hyperplasia. People can increase their fat
mass by storing fat in existing fat cells (hypertrophy) AND by producing
new fat cells (hyperplasia).

Drawing on the ideas from the Central Concepts chapter, obesity can be viewed as
a process of allostasis—trying to achieve stability in a changing environment. In
this case, your body attempts to adapt to the environmental stimulus of overeating. It
increases your fat storage as a protective mechanism to keep high levels of
damaging glucose and certain fats (palmitate) out of your bloodstream. Over time,
this protective mechanism becomes problematic, causing excessive inflammation
and contributing to disease. The diseases caused by this process can be viewed as
part of allostatic overload, or the body’s failure to adapt (long-term) to an
environmental stress such as overeating.

The following sections will cover obesity’s contribution to chronic diseases,

including an appropriately detailed discussion of diabetes, given its current impact
on public health.
OBESITY: THE ENEMY WITHIN II
THE PLAGUE OF “DIABESITY”

Obesity and type 2 diabetes (T2D) have a powerfully negative relationship.

Obesity and T2D occur together so often, that amongst medical professionals the
combined affliction is often referred to as “Diabesity.” Diabetes + Obesity = Dia-
besity.

Massive public health campaigns, an increased focus on diabetes prevention, and

diabetes management in clinical settings have not been able to turn the tide. The evil
combo of diabesity is a health Armageddon—a literal tsunami leaving death and
destruction strewn in its wake. The statistics for T2D are disturbing evidence that we
are losing this fight. According to the latest update from the American Diabetes
Association (2013), 26 million people in the US have diabetes, and an additional 79
million people are pre-diabetic.

• The economic cost of diabetes has risen to $245 billion per year in the US
alone.

• If current trends continue, it is estimated that one in three adults will have
diabetes by the year 2050.

Although we know a genetic component contributes to a person’s risk for

developing diabetes, genetics do not account for the dramatic increase in diabetes
over the past half-century.
 The massive increase in T2D is parallel to a radical change in our daily
environment—degradation of food quality, lack of physical activity, increased
stress, and detrimental habits. Recent science reveals epigenetic changes—the way
environmental signals turn our genes on and off—are at the center of the T2D
epidemic. Borrowing from our earlier analogy in Basic Training (Central Themes),
we are “bookmarking” recipes that wreck our metabolism long-term.

RESEARCH UPDATE:
Recent research has shown that exposure to high amounts of glucose in
utero (in the womb)—as in gestational diabetes—will produce epigenetic
changes making the fetus much more likely to develop T2D as an adult.
Even our earliest environment (the womb) affects our epigenetics and life-
long health.

Epigenetic changes produced by the modern environment predispose us to

disaster. Left unchecked, the metabolism “breaks”—the smooth efficiency of a
normal metabolism is shattered. When a healthy adipocyte turns into a bloated
monster of a fat cell, massive amounts of inflammation and oxidative stress are
produced. These two culprits are largely responsible for the loss of insulin
sensitivity that leads to T2D over time.

Inflammation and oxidative stress cause a loss of insulin sensitivity in two main
ways:

1. Inflammatory cytokines (in this case from adipocytes) “break” the signaling
mechanism of the insulin receptor. The doorbell ringer on the “door” to the cell
is an insulin receptor, a protein on the surface of the cell to which insulin can
“dock.”

When insulin docks to the insulin receptor, it “rings a doorbell” on the cell.
Usually, a special kind of door called a glucose transporter opens and allows
glucose into the cell from the bloodstream. The inflammatory cytokines “short-
circuit” the insulin receptor. Once the insulin receptor is short-circuited, insulin can
still normally bind to the receptor, but the signal to open the glucose door does not
get through. More and more insulin is required by the malfunctioning receptor over
time. These “broken” receptors will eventually require the pancreas to produce a
tidal wave of insulin to clear glucose from the bloodstream.

KEY POINT:
Inflammatory cytokines “short-circuit” the insulin receptor. This is one of
the primary ways inflammation causes loss of insulin sensitivity and leads
to T2D.

Your body doesn’t know how to fix the receptor, it just responds to the problem
by producing more insulin to “ring the doorbell harder.” Fixing the problem
requires stopping the chronic inflammation from the bloated adipocyte-monster,
not putting more insulin into the bloodstream.

The analogy is a doorbell with a short-circuit that someone keeps hitting

harder to ring—instead of just fixing it!

Swollen adipocytes reduce beneficial secretions of adiponectin, the

inflammation-reducing hormone. Reduced adiponectin production leads to
increased numbers of inflammatory cytokines.
INSULIN SENSITIVE
The healthy adipocyte helps ensure insulin sensitivity by keeping inflammation
(inflammatory cytokines) low. The insulin receptor is sensitive to the signal
generated when insulin “docks” to the receptor.

This signal opens the “door” of the glucose transporter, allowing glucose into the
cells from the bloodstream. Glucose will not build up in the bloodstream, and
proper blood sugar levels will be maintained.

INSULIN RESISTANT
The bloated adipocyte “monster” spews forth inflammatory cytokines, which
“short-circuit” the insulin receptor. The insulin receptor is now resistant to
sending a signal to the glucose transporter when insulin docks to the receptor.

The signal does not get through and the glucose transporter “door” remains closed.
Glucose can no longer enter the cell and builds up in the bloodstream. As you
become more insulin resistant, diabetes begins to develop. Chronic inflammation
drives diabetes. In this case, the bloated adipocyte is the source of the inflammation.

2. Increased oxidative stress in the mitochondria. The second major way

obesity causes insulin resistance is through elevated stress levels in cell energy
factories. This cause of insulin resistance is similar to a smoke detector sounding an
alarm if your house catches fire. The overheated, over-stressed mitochondria are
simply overwhelmed by a flood of food/fuel.
 Mitochondrial energy factories produce ATP, the vital “energy currency”
generated from the fuel obtained from food. During normal circumstances, we eat
enough food to fuel our body’s requirements for energy—but not so much that we
overwhelm the capacity of our mitochondria energy factories. We need to eat
enough but not too much to operate within mitochondrial limits and capacities. How
do we determine such a minute and finite thing as cellular fuel capacities? Sounds
more like a biophysics equation! In more earthy terms, it is similar to running your
car ’s engine at low to moderate RPMs.

DIGGING DEEPER:
What Exactly is a Cytokine?
We have referred to cytokines extensively in this section and in
“Immunology 101.” Cytokines are signaling molecules, carrying
messages from cell to cell throughout the body. Cytokines are best known
as messengers of the immune system. A very simplified way of looking at
cytokines is to classify them by the messages they carry.

As you might have guessed, inflammatory cytokines carry the message of

inflammation. Inflammatory cytokines are generated during infections or
injury, and signal the immune system to attack an invader such as a
foreign bacteria or virus, or to start the healing process in response to an
injury. As we have just seen in chronic diseases like diabetes,
inflammatory cytokines can also disrupt normal metabolic “machinery”
such as the insulin receptor. Oxidative stress can also trigger
inflammatory cytokines.

There are also anti-inflammatory cytokines produced to keep the immune

system “in check” and to stop the inflammation response. The Treg cells
we discussed in Immunology 101 and the Gut Chapter are examples of
cells that produce anti-inflammatory cytokines. The M2 macrophage also
produces this type of cytokine.

Cytokines communicate the current “stress state” of the body between cells
and organs. In this way, the liver “knows” if there is an infection or injury
in the right leg because it is communicated by inflammatory cytokine
 messengers.
It is important for the various organs to “know” what is happening in
other parts of the body so they can respond appropriately.
Cytokines allow this to happen.

Even running at safe and moderate RPMs, the mitochondria will naturally—like a
engine’s exhaust—produce free-radicals (oxidative stress). As long as the free
radical production is relatively low, our body’s antioxidant systems can take care of
this “green level” of oxidative stress. Eating just enough food to fuel your energy
requirements will keep your “Mito-RPM” in the green.

If you consistently take in more fuel than your body needs by overeating, the
mitochondria factories go into overdrive trying to process the extra fuel. The
energy-producing machinery in the mitochondria will start to heat up and produce
high quantities of free radicals. Oxidative stress reaches “red” danger levels. The
increased oxidative stress starts to overwhelm the antioxidant systems and triggers
a stress response within the cell, similar to a 911 “call for help.”

High oxidative stress triggers alarm systems within the cell when “smoke” (free
radicals) is detected from the over-heating mitochondria. The alarm system carries
the message that something bad is happening in the mitochondria, alerting the cell to
damage from large amounts of free radicals.
 The absolute best way to stop a fire is to remove the fuel source, and that is
exactly what the cell tries to do. When we eat starches and other glucose-containing
carbohydrates, insulin is produced and docks to the insulin receptor (ringing the
doorbell). This signal would usually open the glucose transporter (door), allowing
glucose into the cell to be utilized for energy production by the mitochondria. The
cell tries to shut this door-opening signal down to protect itself.

INSULIN RESISTANCE FROM THE INSIDE

When the “Mito-RPM” is in the red from processing too much fuel, the overload
of free radicals (oxidative stress) “turns off” the insulin receptor signaling
mechanism, which stops the glucose transporter from opening. This removes the
fuel source by stopping glucose from entering the cell. The cell is trying to protect
itself from too much fuel.

TECHNICAL NOTE:
The “nuts and bolts” of how insulin resistance actually happens on the
molecular level is an active area of research. We have just presented
simplified versions of two mechanisms supported by current research.
 TAKE HOME MESSAGE:
A malfunctioning insulin receptor, broken by inflammatory cytokines or
oxidative stress in the mitochondria, is called insulin resistance (or loss of
insulin sensitivity). Insulin resistance will slow the entry of glucose into
the cells, allowing glucose to build up in the blood stream.

Any environmental stimulus that provokes long-term increases in

oxidative stress and inflammation will result in insulin resistance. This
also includes sleep deprivation and psychological stress.

As chronic inflammation and oxidative stress get worse, insulin resistance

gets worse, and blood sugar levels get higher, resulting in type 2 diabetes.

CONSEQUENCES OF OBESITY AND

CHRONIC INSULIN RESISTANCE
Insulin is a storage hormone. Insulin’s job is to store glucose and fat when food is
plentiful. When the insulin signal is not transmitted to the cell due to insulin
resistance (the doorbell is broken) several things start to happen simultaneously:

1. Stored fat in fat cells (adipocytes) starts to break down. In normal

circumstances, insulin signals the storage of excess energy as fat in the
adipocyte. Insulin usually signals the storage of fat and stops it from breaking
down. Since the insulin signal is interrupted because of chronic inflammation
and oxidative stress, the brakes are taken off. Fat is released from the adipocyte
into the bloodstream.

This release of fat is not a good thing, considering that there is no place for this
fat to go. The body already has a fuel excess at this point and there is nowhere to
“burn” the fat. The liver grabs the fat from the bloodstream and transforms it
into triglycerides before placing it on a lipoprotein carrier circulating in the
bloodstream looking for a place to drop the fat. It is like an ever-growing group
of people riding a bus with no destination and no one ever gets off the bus.

Instead of the fat getting stored in adipocytes as triglycerides, it is aimlessly

 circulated in the bloodstream on lipoproteins. This inevitably causes real
problems. The trapped, endlessly circulating triglycerides are the reason
diabetics almost always have high triglycerides when their doctor checks
their blood-work.

COMING ATTRACTIONS >>>

See the cholesterol section in the Analytics Chapter to learn how high
triglycerides in diabetes and metabolic syndrome can lead to heart and
vascular disease.

Adding fuel to the fire...

2. The liver “banker” starts making glucose. When the insulin signal is not
getting through, the liver starts to do something unthinkable—it starts making
new glucose (gluconeogenesis) and releasing it into the bloodstream. The
liver is pouring fuel on the fire by making and releasing glucose when the
bloodstream is already highly saturated with glucose.

As far as the liver is concerned, the body is in a state of stress, and the liver
needs to ensure that the brain has adequate supplies of glucose—especially when
stressed. Insulin resistance “fools” the liver into thinking that the body is starving
and needs more glucose.
 QUICK MEDICAL NOTE:
The anti-diabetic drug Metformin works by stopping gluconeogenesis in
the liver. Metformin helps stop this source of extra glucose in the blood,
and decreases blood sugar levels.

3. Insulin resistance puts the pancreas in overdrive. When the insulin

signaling system is broken and glucose builds up in the blood, the pancreas
responds to its programming by producing more insulin.

Chronic inflammation and oxidative stress short-circuit the insulin receptor

“doorbell button” mechanism. The pancreas responds by making more insulin
(more doormen to hit the button).

Because the person will not change his or her lifestyle and eating habits to
decrease inflammation and oxidative stress, the body has no choice but to
produce more insulin. Unfortunately, producing large amounts of insulin to cope
with insulin resistance burns out the pancreas over time. Eventually, the pancreas
will fail and lose the ability to produce insulin at all. A type II diabetic reaching
this stage will have major health problems. They need to take insulin at higher
and higher doses as their disease progresses.

DIGGING DEEPER:
Beta-Cell Failure in the Pancreas
The cells which produce insulin in the pancreas are called beta-cells. They
detect glucose and respond by producing insulin. As insulin resistance
develops from chronic inflammation and oxidative stress, the beta-cells
compensate by producing more insulin.

They can only compensate for so long, and the stress of constantly
producing high amounts of insulin will wear out the beta-cells. They
 eventually break down and die, leaving fewer beta-cells to carry the work-
load of insulin secretion. When many beta-cells fail, the remaining ones
can no longer effectively compensate to keep blood sugar in check. Then,
blood sugar rises into diabetic levels, and things just get worse as the
process continues.

4. Muscle wasting occurs when our lean muscle mass starts to disappear.
Insulin resistance causes muscle wasting. Recent research on muscle wasting—as
it relates to obesity and diabetes—has focused on a protein, myostatin.
Myostatin’s function is to reduce muscle mass by stopping muscle growth
(myo= muscle; statin= stop or inhibit).

Myostatin is secreted by muscle, and is thought to be the central player in muscle

loss associated with aging (sarcopenia).

A recent study has shown myostatin production is elevated in obese and insulin
resistant people. The horrific combination of chronic inflammation and insulin
resistance was found to increase myostatin production levels. The elevation of
myostatin is thought to be a major contributor to the loss of muscle mass often
seen in severe cases of obesity and diabetes.

Obesity, insulin resistance, and diabetes act as “age-accelerators” for loss of

muscle mass. All humans lose muscle mass as we age, but obese people and
diabetic people experience muscle loss at an accelerated rate. The body will
break down its own muscle tissue to strip it of amino acid content. The
cannibalized amino acids will be used to feed the now-deranged “liver-banker,”
in its mad quest to make more glucose when none is needed. In addition to
muscle-wasting myostatin secretion, the chronic inflammation associated with
obesity and diabetes directly contributes to muscle wasting. Insulin stimulates
building new protein, but the “building” signal is not getting through. As insulin
resistance increases, muscle building grinds to a halt.

KEY POINT:
Obesity, insulin resistance, and diabetes create a perfect storm for muscle
wasting.
 FIRST PRINCIPLES-BASED
SPECULATION: MYOSTATIN

It makes sense that myostatin increases in cases of insulin resistance from

chronic inflammation. The body is reacting to the “threat” of chronic
inflammation and insulin resistance much like it reacts to the threat of
starvation.

Myostatin is also elevated in times of starvation to decrease muscle mass.

From a survival perspective, maintaining muscle mass has a very
“expensive” energy cost. If the body can decrease muscle mass, it will
have more energy to keep the brain going. We can survive with reduced
muscle mass, but we don’t do well without brain function. Insulin
resistance and diabetes are interpreted by the body as a state of starvation
and/or stress—even though plenty of fuel is available—and it will
decrease muscle mass to conserve energy for the brain.

5. Fat without a home... When the adipocytes (fat cells) are too full and unable
to store excess energy as fat, the liver and muscle will start to retain some of it,
simply because it has nowhere else to go. Excess fat contributes to development
of fatty liver disease. The fat will also start to replace the muscle mass lost to
myostatin.

Large amounts of fat circulating in the bloodstream amplify the inflammatory

response and insulin resistance. Fat cells store a significant amount of fat in the
form of palmitate. In the Nutrition 101 section, we learned palmitate is a 16
carbon saturated fat that gives saturated fat a bad name.
Palmitate is the primary fat liver cells make from excess glucose. When palmitate is
released into the bloodstream by malfunctioning fat cells or when the liver produces
it from large amounts of excess glucose, it activates alarm systems normally
reserved for detecting foreign invaders such as bacteria.

The alarm system activated by palmitate ramps up the immune system promoting
increased inflammation, oxidative stress, and further increasing insulin resistance.
The fact that this specific saturated fat activates this alarm system shows that large
amounts of palmitate are a threat to the body. High amounts of palmitate occur
with obesity and insulin resistance—your body is trying to protect itself!

The middle picture is an MRI cross section of a 74 year old sedentary
man’s thigh muscle. The view in the pictures is the same as if the thigh was
cut in half, and we looked down at the stump.

You can see the fat (adipose) tissue surrounding the shrinking muscle, as
compared to the large muscle mass in both of the pictures above and
below. If you are insulin resistant or diabetic, this process is happening to
you right now. If you are not exercising, this process will happen even
faster.

Unfortunately, many young diabetics are exhibiting the dramatically

decreased muscle mass associated with much older people.
 PALMITATE—GIVING SATURATED
FAT A BAD NAME:
Without fail, almost every scientific study examining the effects of
saturated fat uses palmitate for testing—as if it were the only saturated fat
in existence. It is perplexing how very smart scientists continually
overlook this fact and in their research, generalize palmitate’s effects to
represent all saturated fat.

As previously stated, palmitate indeed has some bad effects on metabolism

and contributes to chronic disease. Of importance to this chapter, please
note that a significant amount of fat produced in the liver from excess
glucose and fructose in the obese and diabetic person is specifically
palmitate.

In high amounts, palmitate can wreak metabolic havoc:

• Palmitate causes inflammation, oxidative stress, and increases insulin
resistance.
• Palmitate decreases adiponectin secretion by fat cells, increasing insulin
resistance.
• Palmitate has been shown to increase inflammation in the hypothalamus,
which disrupts appetite regulation (causes hunger when the body already
has enough energy.)

Look back at the saturated fat section in Nutrition 101. Most saturated fats
have very beneficial effects, don’t judge them all by the actions of
palmitate.

Remember that it is normal for low levels of palmitate to be stored in

healthy fat cells, and it does not cause any of the above problems.

6. Obesity and chronic insulin resistance increase the risk of cancer. Cancer is
not a single disease, like diabetes or heart disease. Each type of cancer is very
different, depending on the original cell type. The triggers for cancer
development are just as diverse. For instance, liver cancers can be caused by
infections, exposure to chemicals, and chronic alcohol use. Since cancers come
in many different varieties, there is no one “cure for cancer.”
 However, there are several characteristics that some—and in some cases all—
cancers have in common that are important to obesity, insulin resistance, and
diabetes:

• Cancerous cells show uncontrolled, aggressive cell growth and have

transformed from previously normal cells.

• Many cancer cells become dependent on glucose as their only source of energy
(called the “Warburg Effect”).

• Some cancers such as breast and endometrial cancer are sensitive to estrogen.

• A common trigger for many cancers is chronic inflammation and oxidative

stress.

We’ll tackle these characteristics individually to show you why cancer loves
obesity, insulin resistance, and diabetes.

“Cancerous cells show uncontrolled and aggressive cell growth, and have
transformed from previously normal cells.”

Uncontrolled cell growth is the hallmark of all cancers. These cells no longer
respond to normal, healthy “check and balance” signals that control growth and
reproduction. Insulin resistance creates a “growth favorable” environment. During
insulin resistance, the pancreas responds by producing more insulin. People with
insulin resistance have relatively high insulin levels all the time. Because insulin is a
“growth, building, and storage” hormone, the presence of high insulin levels helps
cancer grow out of control.

“Many cancer cells become dependent on glucose as their only source of

energy.”

Nobel prize winner Otto Warburg first described the phenomenon of cancer cells
switching their metabolism to only use glucose without the need for energy
production from mitochondria. At first glance, this does not make sense, because
much more energy can be generated if the mitochondria finish burning glucose.
(See Metabolism Basics.)

Most cancer cells only break glucose down to lactate, generating a paltry 2
ATP, compared to the 38 ATP they could get from glucose if they used the
mitochondria.


The area shaded in pink is the energy pathway that cancer cells use, showing the
“Warburg Effect.” Only 2 ATP is generated because the mitochondria are not used.

Scientific speculation holds that because cancer cells are fast growing, they need
rapid energy production, and the mitochondria take too long. The cancer cells don’t
care if they are wasting energy, they want fuel immediately and don’t care about
sloppy inefficiencies.

Cancer cells become the ultimate glucose hogs; a raging cancer cell will burn
through glucose 200 times faster than a normal cell. They are like 500-horsepower
muscle cars that get 7 miles per gallon. They do not care about fuel efficiency, they
just go very fast. Normal cells are like Smart Cars by comparison, they use glucose
for fuel in a reasonable and highly efficient way.

The fact that cancer cells become dependent on glucose is important for those
with insulin resistance and diabetes:

• A diabetic’s high blood sugar levels give cancer cells a huge supply of glucose
to survive and thrive.

• Most cancer cells use glucose transporters (doors) that do not need to be
opened by insulin. The cells can scarf up large amounts of glucose from the
bloodstream without relying on insulin.
 QUICK MEDICAL NOTE:
If some cancer cells are dependent on glucose through the Warburg
Effect, it would make sense that a low carbohydrate diet would be a
valuable part of treatment. Most cells in the body can use fat as an energy
source, so a low carbohydrate diet could potentially “starve” and weaken
the cancer cells that need glucose to survive, allowing traditional
treatments to be more effective. This could be a “one-two punch,” weaken
the cancer cells by starvation, then kill them with the drugs.

For some reason, low carbohydrate diets have not seen widespread use in
the treatment of cancer. Recent research has shown some promise using
low carbohydrate (ketogenic) diets in conjunction with traditional cancer
treatment. Widespread use of both therapies together could potentially
help save many lives.

If the specific cancer is dependent on glucose for energy, low

carbohydrate diets really have no potential negative side effects for cancer
patients. If you are newly diagnosed with cancer, discuss starting a low
carbohydrate diet with your doctor to see if it is appropriate for your type
of cancer.

STRONG MEDICINE TACTICS:

If you have cancer, discuss the use of a low carbohydrate or ketogenic diet
with your doctor as part of your treatment plan.

“Some cancers such as breast and endometrial cancer are sensitive to estrogen.”

The point applies to obesity in general. Adipocytes (fat cells) produce an enzyme
called aromatase. Aromatase converts hormones such as testosterone into estrogen.
The more fat you have, the more aromatase present, and the more estrogen you are
producing (this also applies to men).
 Cancers such as endometrial cancer, and some breast cancers are “estrogen
sensitive.” This means estrogen can trigger them to grow. Losing fat mass will
reduce the amount of estrogen in your body, which may help reduce the growth of
breast and endometrial cancers.

If you attempt a fat-loss plan when you have one of these cancers, make sure to
discuss it with your doctor first.

STRONG MEDICINE TACTICS:

Losing fat mass through a well-constructed weight loss plan may help
reduce the trigger for breast cancer and endometrial cancer growth.
Discuss this approach with your doctor as a potential part of your
treatment plan.

“One of the triggers for many cancers is chronic inflammation and oxidative
stress.”

As we have covered extensively, obesity is a disease which produces chronic

inflammation and oxidative stress. The inflammatory cytokines produced by the
bloated “monster” adipocytes are the same ones known to trigger the development
of several types of cancer. The constant barrage of inflammatory cytokines from
deranged fat cells encourages the survival, growth, and spread of cancer cells.

The high levels of free radicals that accompany oxidative stress damage DNA in
normal cells. Under some circumstances, free radicals can transform normal cells
into cancer cells. This DNA damage caused by free radicals, will mutate the normal
cell into cancer.

Obesity, insulin resistance and diabetes are all inflammatory diseases linked to an
increased risk of cancer. Being highly inflamed is the ideal cancer hothouse.

7. Obesity and chronic insulin resistance increase the risk of heart and
vascular disease.

Obesity and diabetes greatly increase your chances of heart and vascular disease.
The statistics for this association are frightening:
 • A diabetic is twice as likely to have a heart attack or stroke than a non-diabetic.

• 66% of diabetics end up dying from a heart attack or stroke. Only 1/3 of
diabetics die from other causes.

• A recent study showed that obese men had a 60% greater chance of dying from
a heart attack than non-obese men.

• Diabetics are up to four times as likely to have vascular disease in the lower
extremities (legs, feet) than non-diabetics.

• Diabetes also causes a type of heart failure called diabetic cardiomyopathy.

• Diabetes leads to small blood vessel damage which causes nerve damage and
can lead to amputation.

These statistics are not surprising if you know that the main trigger for heart
and vascular disease is chronic inflammation and oxidative stress. Obesity and
diabetes are sources of chronic inflammation and oxidative stress.

KEY POINT:
Heart and vascular disease are triggered primarily by chronic
inflammation and oxidative stress.

COMING ATTRACTIONS >>>

The cholesterol section in the Analytics Chapter contains a thorough
discussion on why the cholesterol carriers (lipoproteins) directly cause
problems in heart and vascular disease, instead of cholesterol itself.
 8. Obesity and chronic insulin resistance can lead to accelerated aging.

Chronic oxidative stress from obesity and insulin resistance/diabetes can cause
premature aging (accelerate the rate at which you age). Dysfunctional mitochondria
in the fat cells of obese and diabetic people can produce large quantities of free
radicals. These free radicals can damage specific parts of DNA called telomeres.
Telomeres are the “caps” on the ends of chromosomes.

TECHNICAL NOTE:
We have represented the telomeres as multi-colored “caps” on the tips of
the chromosome for clarity. In reality, the telomeres look exactly like the
regular genetic DNA that contains your genes.

The telomere DNA “caps” function to protect the genetic DNA from
damage. Bad things happen when your genetic DNA is damaged, namely
cancer and accelerated aging.

Telomeres are made from DNA and protein. They function to protect DNA that
contains your genes—your genetic material.

When most cells divide to make new cells, some of the telomere structure is lost.
After a certain number of cell divisions, the telomere no longer exists. The cell is
unable to divide any further and often dies.

Most of the cells in the body do not divide often enough for this to be a problem.
The issue for people who are obese and/or diabetic is that the constant onslaught
of free radicals from chronic oxidative stress has been shown to shorten
telomeres by damaging the telomere DNA.

The telomere DNA is more susceptible to free radical damage than gene-
containing DNA. Telomeres are much like a “sacrificial lamb” when high amounts
of oxidative stress are present as in diabetes and obesity.

BIOLOGICAL VERSUS
CHRONOLOGICAL AGE:

Chronic oxidative stress and inflammation result in accelerated telomere

loss and more rapid aging. Most of us have seen obese and diabetic people
who look older than their actual age.

Biological age is how old the cells in your body are based on telomere
length, while chronological age is based on the year you were born. This
is how a 50-year-old diabetic can have the body of a 70-year-old (similar
to a rusty car) based on telomere length.
This graphic shows a single “arm” of a chromosome with the telomere cap in place.
Chronic oxidative stress from the mitochondria in diseases such as obesity and
diabetes, shorten the telomeres over time. Chromosome A shows a normal telomere
length before any damage takes place. The telomere shortening is shown in the
picture as the chromosome passes through the stages shown in B, C, D, and E.
Chromosome E is unprotected by the telomere and the DNA containing your genes
can now be damaged. (Notice the free-radical “drunk guys” wreaking havoc.)

Cells that have DNA like chromosome E can no longer divide to produce new
cells. Old worn-out cells are not replaced. This is really the definition of aging—
when your cells can no longer divide to replace the worn-out cells. Eventually the
“worn-out” cells in your organs such as the liver, pancreas, heart, kidneys, brain,
begin to die and are not replaced because they no longer have functioning
telomeres.

Shortened telomeres are seen in people with many diseases associated with
oxidative stress such as heart disease, diabetes, Alzheimer ’s dementia, and obesity,
as well as environmental exposures such as smoking, air pollution, and stress.

Researchers are now using telomere length to analyze the rate of aging and
even predict lifespans.

MITOHORMESIS: EXTENDING
LIFESPAN WITH OXIDATIVE
STRESS?


Recent research has shown that when mitochondria are not overloaded
with fuel, they increase their efficiency in producing energy. Free radials
are produced during this efficient energy production, and result in
oxidative stress.

Periodic reduction of glucose in the diet, physical exercise, and calorie

restriction all create short-term stress to the metabolism. Specifically,
these conditions increase oxidative stress in the mitochondria.

The result of these stressors and the increase in oxidative stress is an

increase in our cells’ antioxidant defense systems capacity for dealing
with free radicals. These increases can protect us from aging
—specifically they can stop telomeres from shortening from free radical
damage. Mitohormesis is the stimulation of mitochondria by oxidative
stress.

It is very important to point out that taking antioxidant supplements has not
been shown to improve health or slow aging. They may even be
detrimental because antioxidant supplements stop the beneficial dose of
oxidative stress in the mitochondria and prevent the increased capacity in
our natural free radical defense system.

In fact, most of the beneficial “antioxidants” (such as polyphenols) found

in plant products do not act directly as antioxidants. They only stimulate
our free radical defense system.

In keeping with the concept of hormesis, periodic stresses that increase

short-term oxidative stress are beneficial, while chronic increases in
 oxidative stress from obesity and diabetes overwhelm the mitochondria
and the free radical defense system. Keep your “Mito-RPM” in the green
to stimulate mitohormesis with regular exercise, and the nutritional
strategies we will cover soon. Your telomeres will thank you!

RESEARCH UPDATE: ALL IS NOT LOST

Learning how obesity and especially diabetes can accelerate aging can be
pretty discouraging. Before you update your life insurance policy, let us
discuss some findings in recent research showing that loss of telomere
length can be slowed dramatically. A study on diabetics showed that total
loss of telomere length was prevented in diabetics who maintained good
blood sugar control. In the upcoming sections, we will give you the tools
and knowledge to maintain good blood sugar control, slow down
premature aging, and perhaps even reverse the disease.

STRONG MEDICINE TACTICS:

Maintain good blood sugar control to prevent accelerated aging.

9. Obesity and chronic insulin resistance can lead to “brain wasting.”

Paralleling the increase in obesity and diabetes, neurodegenerative diseases such
as Alzheimer ’s disease (AD) are reaching epic proportions. AD is the most
common cause of dementia in our aging population.

We all have heard horror stories about friends, relatives and parents succumbing
to AD or other neurodegenerative diseases. The financial and emotional burden it
places on families is catastrophic. Family members—non-professionals—provide
80% of home care for AD patients. AD has become more and more common in
recent years and strikes people at an age when they should be enjoying life the most.
Spending the last decades of life in a tortuous existence, marked by a slow fall into
mental and physical decay is occurring with increasing regularity. Why?

“TYPE 3 DIABETES”
In 2005 a research group from Brown University Medical School described
Alzheimer ’s disease as type 3 diabetes. Their research showed AD to have
characteristics of both type 1 (decreased insulin production) and type II diabetes
(insulin resistance). Proper insulin regulation is highly important for brain cell
neurons—they die very quickly when insulin is not properly regulated.

Ketogenic diets and supplementation of ketone-producing substances (such as

medium chain triglycerides) are showing very promising results in early clinical
studies on nutritional therapies for AD. Short-term ketogenic diets and low carb
diets can also be very effective in reversing type II diabetes—a result which
supports the metabolic similarities between T2D and AD. Additionally, chronic
inflammation, oxidative stress, and formation of advanced glycation end-products
(AGE) are common to the development of both Alzheimer ’s disease and type 2
diabetes.

Obesity and the resulting insulin resistance greatly increase your chances of
succumbing to neurodegenerative diseases such as Alzheimer ’s disease.

STRONG MEDICINE TACTICS:

Prevent Alzheimer ’s disease by reversing obesity and insulin resistance
using strategies in the upcoming intervention section.

CENTRAL THEMES CONNECTION:

Most of us who have a parent or close relative with AD often wonder if we
will be likely candidates for AD and dementia.

There is no greater nightmare than for a functioning, able, independent

 and intelligent adult to—without warning—begin a slow and inexorable
descent into a state of mental infancy.

While there is a lot of talk about the “genetic risk factors” associated with
Alzheimer ’s disease, we need to look at AD and genetics through the lens
of epigenetics.

Recent research has shown a strong connection between development of

AD and diseases such as type II diabetes (T2D), cardiovascular disease and
high blood pressure. T2D was found to double the risk for dementia.
Individuals requiring insulin therapy are four times more likely to acquire
AD.

These diseases are associated with metabolic syndrome and can (often) be
prevented by altering lifestyle factors. Altering our habits and
environment can dramatically reduce the chances of acquiring brain
atrophy—no matter how strong our genetic predisposition. Alzheimer ’s
and other causes of dementia follow the same pattern: they have a strong
genetic component, but need the right environmental triggers to germinate
and take root.

STRONG MEDICINE TACTICS:

Cook with coconut oil for a “dose” of medium chain triglycerides to help
keep your brain cells healthy, especially if you have a family history or
early signs of Alzheimer ’s disease.

HOW DO I KNOW IF I HAVE DIABETES?

Do you have diabetes? Are you starting to show signs of developing diabetes or
insulin resistance? A person just does not wake up one morning with type II
diabetes. T2D and the broken metabolism that accompanies it takes years to develop.
But, there are early signals of which to be aware.

Insulin resistance and diabetes involve increases in blood sugar from

malfunctioning insulin receptors. The laboratory tests for diabetes and
“prediabetes” analyze blood sugar levels and how well you “handle” a glucose load
in the diet.

1. The first test used to diagnose diabetes (and prediabetes) is the hemoglobin
A1c (HbA1c) test. Hemoglobin is a protein inside red blood cells that carries
oxygen. Depending on how much glucose is in the blood, a certain amount of
glucose will stick to the hemoglobin. Higher concentrations of glucose in the
blood (as seen in diabetics) results in more of the hemoglobin getting glucose
“stuck” to it. The percentage of hemoglobin that has glucose stuck to it gives
the HbA1c value.

The average red blood cell has a lifespan of 120 days, so the hemoglobin in the
cell is exposed to blood glucose for the same length of time. This allows the
HbA1c measurement to give an average level of blood sugar for the past 3
months.

The percentage amounts of HbA1c is used to classify someone as normal,

prediabetic, or diabetic:

The values in this table were taken from the American Diabetes Association (ADA).
Notice that there is a “no-man’s land” for values between 5.1 and 5.6. Our personal
bias is that although this area is not officially prediabetes, the numbers in this range
may indicate a developing problem with insulin resistance. My personal bias is the
closer to 5.0 (or lower), the better.

2. The next commonly used laboratory test for prediabetes and diabetes is
fasting blood sugar. This is our least favorite test because is it only represents a
brief snapshot in time—your blood sugar at the time of the blood draw. Other
factors, such as a night of poor sleep can elevate this number even if you do not
have diabetes. Nevertheless, the official values for this laboratory test, again
taken from the ADA guidelines, are as follows:
 3. The third test is called the Oral Glucose Tolerance Test (OGTT). The OGTT
is performed by fasting for 8 hours, then drinking a glucose and water mixture
containing 75 grams of glucose. After drinking the liquid and waiting 2 hours,
your blood glucose is measured. The diagnosis is based on the ADA guidelines
below:

The idea behind the OGTT is to test your tolerance for glucose. Remember, when
people have insulin resistance (diabetes or prediabetes), the insulin signal does not
get through to allow glucose into the cells. Then the glucose builds up in the
bloodstream. Depending on how severe your insulin resistance is, and how well
your pancreas is secreting insulin, the more of the 75 gram glucose solution will
stay in your bloodstream.

As we will discuss later, when figuring out how much carbohydrate a prediabetic or
diabetic can tolerate, performing a home version of the OGTT using real food can
help you track improvement of insulin sensitivity, and figure out what kinds and
quantities of foods cause trouble for you in terms of blood sugar. We will talk much
more about this in the Intervention section.

For convenience, here is a chart compiling all three tests:

All of these charts show very definite divisions with ranges of numbers indicated
as “normal”, “prediabetic”, or “diabetic”. Insulin resistance leading to diabetes is a
long process that takes years before most people are officially classified as
diabetic by a blood test.”

A - This point represents good insulin sensitivity. Oxidative stress and

inflammation are in the green zone. But, you start to eat processed food
and stop exercising due to a hectic work schedule.
B - 2 years later your lifestyle is beginning to catch up with you. Your
blood tests are still in the “normal” range, but you are gaining weight
around your midsection. Your blood tests are normal because your
pancreas has started to go into overdrive to produce more insulin to deal
with the start of insulin resistance. Inflammation and oxidative stress are
increased and your telomeres are likely shortening. Age acceleration has
begun.
C - 3 years later you are upset after your annual checkup because your
doctor said your blood tests show you have prediabetes. The insulin
secreting cells in your pancreas are starting to fail, resulting in increased
blood sugar. You have gained 20 more pounds over the last 3 years.
Oxidative stress has further increased and your telomeres continue to
shorten, accelerating aging.
D - 2 years later you are shocked when your doctor tells you are
“borderline diabetic.” You have not gained any more weight but your
blood pressure has gotten worse, and your telomeres are quickly
shrinking.
E - Your doctor says your HbA1c is 6.8 and that you have diabetes. You
now make a resolution to change your lifestyle because you “have
diabetes”, but wonder how it happened so fast.

Do not be the person at point E, and wait too late to do something about your
disintegrating health. By the time a person has attained pre-diabetes status, a
significant amount of damage to the insulin-secreting beta-cells has likely already
occurred. This person will likely never regain full function of these cells—but they
always have the power to halt the damage.

The time for action is at point A and B, before much damage takes place. Use the
Strong Medicine prescriptions in the intervention section to prevent chronic insulin
resistance and diabetes.

If you have no symptoms and normal blood tests (points A and B) how do you
know if you are at risk? The following groups of people should be focused on
prevention, as they are at higher risk for developing diabetes:

• A family history of diabetes—your parents, brothers, or sisters have diabetes

• Recent diagnosis of high blood pressure

• High triglycerides and low HDL on blood tests
• History of polycystic ovarian syndrome (PCOS)
• History of gestational diabetes
• Sedentary lifestyle
• Ethnic groups including African Americans, Hispanics, Native Americans, or
Pacific Islanders
• Overweight or obese, especially abdominal obesity

CENTRAL THEMES CONNECTION:

Revisiting the “stress cup” from Central Themes V (Allostasis), the
graphic below is a “stress cup” overflowing from a poor diet of
processed food filled with sugar, flour, and vegetable oils. The obesity
and diabetes resulting from this type of daily diet has overfilled the
individual’s “stress cup,” and caused allostatic overload. For the obese and
diabetic, the “stress cup” does not have the capacity to handle poor sleep
and job stress. Those additional stresses will only cause more overflow.
This chronic allostatic overload—an overflowing “stress cup”—plus the
inflammation and oxidative stress that goes with it, will lead to accelerated
aging, heart disease, high blood pressure, neurodegenerative diseases
(such as Alzheimer ’s), and cancer.
 STRONG MEDICINE TACTICS:
Find out if you have risk factors for developing diabetes. If so, start a
program of early prevention.

DRIVEN TO EXCESS
We have talked extensively about the health risks of obesity, and especially
diabetes. The $64,000 question is why are so many of us getting overweight and
obese? After all, the majority of Americans are overweight or obese.

Why are we consistently eating so many of the wrong calories? Have we all
become gluttons and hedonists in the last 50 years? That is what social critics would
have us believe! Dietitians would urge us to count our calories, and limit the amount
we eat, in the attempt to gain some control of our growing waistlines. Counting
calories is not natural or sustainable, and it does not get to the root of the
underlying problem.

It turns out there are some very real problems in the modern brain—problems
that drive us to eat beyond our physiologic need for calories. Some of these
problems are coming from within our bodies and others are from our environment.
Appetite is controlled in the brain. Ergo, the brain can become our worst enemy or
best friend in our efforts to shed body fat and add lean muscle mass.

We will decrypt the hunger communication system’s “black box” and understand
how the brain controls our drive to consume food. Without understanding this system
we are doomed to fight a losing battle against hunger. Counting calories and other
neurotic practices are all destined to fail in the long term. Obesity, the “enemy
within,” will never be vanquished without an understanding of the drive to eat.
OBESITY: THE ENEMY WITHIN III:
HOW WE GET FAT: THE BRAIN,
HORMONES, AND APPETITE

THE DRIVE TO EAT

Humans are hard-wired to find high-energy foods to fuel our body. This
primordial survival mechanism is built into our brains and resides just below
conscious thought. “Hunger” is an urge created by a sophisticated communications
system in the primitive parts of our brain. Once the hunger message is received,
humans use their superior problem-solving abilities—that other animals do not
possess—to find creative ways to acquire and make decisions about food.

The hunger drive is indeed a primal one. It is based on a complex

communications system of hormones and chemical messengers within the brain—
neurotransmitters. These hormones and neurotransmitters interact with the primitive
structures in the brain responsible for the “reward system.” The reward system in
the brain produces feel-good neurotransmitters to create a pleasurable response to
eating food. This pleasure response helps us survive as a species.
 For ancient hunter-gatherers, there was a caloric cost associated with the
acquisition of food. They would expend thousands of calories bringing down and
butchering an elk—and even more calories transporting the carcass back to camp
on foot. We no longer have to expend energy to hunt, gather, or cultivate our food.
We purchase our artificial, industrial foods without burning a single additional
calorie. We need to readjust our thinking and our actions; we need reexamine our
relationship with food. Let us stop being slaves to the subconscious primordial
impulses and urges from a broken metabolism and short-circuited reward system. If
we let it, hunger can turn us into a ravenous saber-tooth tiger on the hunt. We have
to understand our drive to eat before we can exert some control.

THE HUNGER COMMUNICATION

SYSTEM
“The regulation of appetite” is exceedingly complex. To faithfully describe all the
players in the system and their interrelations would quickly lead to confusion. We
want to explain new ideas and scientific breakthroughs in a simplified way so we
can gain control of our nutritional destiny.

1. FAT IS TALKING—SO LISTEN UP!

Fat is not just a storage site for excess energy, it is an active participant in
metabolism. In the past, fat was thought to be inert material. Then scientists
discovered that normal, healthy fat cells (adipocytes) secrete a substance called
adiponectin. As discussed previously, this fat-hormone keeps inflammation down
and insulin sensitivity high throughout the body. Recent research supports that fat
tissue is highly active. Healthy fat secretes several different compounds that have
effects on the body and brain.

A major player in the hunger communication system is a hormone called leptin.

Leptin is secreted by fat cells. The more fat mass you have, the more leptin is pumped
into the bloodstream.

KEY POINT:
The more fat you have (and the larger your fat cells), the more leptin is
produced.

The more fat you have (and the larger your fat cells), the more leptin is produced.

Leptin travels from the fat cells and communicates with the brain by docking on
leptin receptors located on certain brain cells. This is similar to how insulin docks
to insulin receptors. Leptin communicates with specific cells located on the
hypothalamus (part of the Stress/Threat system we discussed earlier).

The hypothalamus is the central receiving and command center in the human
brain which responds to environmental signals. The hypothalamus is at the center
of the brain’s hunger communication system.

The brain is normally protected from the rest of the body by the “blood-brain
barrier” (BBB). Part of the hypothalamus is located at a “crack in the wall” of the
BBB and has direct access to the bloodstream. Leptin crosses into the brain through
a specialized transport system after being released by fat cells.

When leptin “docks” with the leptin receptor on the hypothalamus, the hunger
communication system generates a signal to stop eating.

The brain knows how much energy is available from fat because of the leptin
system. As fat stores decrease (from fasting or starvation), less leptin is available to
signal the hypothalamus. This results in the feeling of intense hunger. As body fat
increases, leptin increases and the signal to stop eating will be stronger.

TAKE HOME MESSAGE:

Leptin functions as a signal to keep body fat at optimum levels. When it is
working correctly, the leptin signal from fat cells to the hunger
communication system—controlled by the hypothalamus—will keep a
person’s body fat amount in an ideal range.

Low body fat = low leptin = signal to eat (hunger)

Higher body fat = high leptin = signal to stop eating (satiety)

Leptin is secreted into the bloodstream by adipocytes (fat cells). Leptin travels
through the bloodstream to the brain and docks with leptin receptors on the
hypothalamus through the break in the blood-brain barrier.

The hypothalamus receives the signal that the body has plenty of energy, and the
hunger communication system tells the body to “stop eating.”

When the leptin system is working correctly, you should be less hungry as you
collect more body fat. More body fat = more leptin. More leptin = a stronger signal
to stop hunger.

Based on what we now know about leptin and the hunger signal, how does anyone
get fat? The overweight and obese have higher leptin levels than lean people. If the
communications system was working properly, people with more fat should get a
strong signal to stop eating.

The reason overweight and obese people are still hungry even with high leptin
levels is leptin resistance. As with insulin resistance, the signal that leptin is
supposed to carry (stop eating) is not getting through to the hypothalamus.

KEY POINT:
Despite high leptin levels, the obese and overweight do not get the “stop
eating” signal because of leptin resistance.

DIGGING DEEPER:
Leptin and Having Babies...
Although we are discussing leptin’s role as a signal to stop eating when
body fat is high, this is only a piece of its greater role, that ensures
survival of not just the individual, but the human species.

One of leptin’s primary functions is to signal the brain when energy levels
are high enough to sustain a pregnancy. When there is an appropriate level
of body fat, the leptin signal from fat cells to the hypothalamus is
relatively strong. The hypothalamus “knows” body fat is adequate and
sends a signal to the pituitary gland which secretes the sex hormones
controlling ovulation, menstrual cycles, and fertility.

It is important that women have an adequate supply of energy stored as

body fat to successfully carry a fetus to term. If a woman’s body fat levels
fall, the leptin signal to the hypothalamus decreases, and fertility
hormones from the pituitary gland also decrease. This is why some young
women with very low body fat (endurance athletes, women with anorexia
nervosa) stop having their menstrual cycles and certainly have fertility
problems.

There is an ideal level of body fat for the optimum leptin levels needed to
maintain fertility. Infertility is not just a problem for women with very low
body fat. Overweight and obese women with high levels of leptin also
have fertility problems. But, should not high levels of leptin from the extra
fat mass give a strong signal for fertility based on what we just said
above? The overweight and obese develop leptin resistance, and the signal
doesn’t get through despite high levels of leptin. This concept should
sound familiar to insulin resistance in the previous section. No leptin
signal = no fertility signal.

KEY POINT:
It is important to understand that overweight and obese people (especially
diabetics) truly feel hungry most of the time, despite the large amounts of
body fat they carry.

Because leptin is not functioning correctly, their brain behaves as if they

have low body fat and sends the signal to eat. This creates a vicious cycle
of eating, more weight gain and inflammation, and more leptin resistance,
leading to more eating.

Knowing about this process can help an obese person understand why they
are always hungry, which can give them some control.

It is very helpful for friends, family members, and medical providers to

also understand this process to support the obese or diabetic person in
your life without dismissing their eating habits as gluttony or lack of will
power.


LEPTIN RESISTANCE
The bloated adipocyte “monster” is secreting high amounts of leptin and
inflammation. The inflammation breaks the transport system and short-circuits the
receptor. Now, very little leptin reaches the receptor, and the small amount that gets
through cannot transmit a signal through the broken receptor.
Without the “stop eating” signal from leptin, the hypothalamus sends the
message to eat more!

You can see from the graphic that despite high body fat and high leptin levels, the
brain “thinks” that body fat is low because the leptin signal is not received. Why?
The bloated adipocyte (fat cell) “monster” is producing large amounts of
inflammation and oxidative stress which interrupts the leptin signal.

2. THE GUT TALKS TO THE BRAIN

Having just read through the gut chapter, you know that the digestive tract
communicates to the brain through the gut-brain axis. Communication hormones
and messenger molecules are produced by our digestive system in response to the
food we eat. Trying to describe their myriad functions and how they interrelate is
beyond the scope of this book. The complexity of how the gut-brain axis works is
truly mind-blowing; even the scientists researching these amazingly complex
biological functions are mystified as they nibble around the edges of understanding.

What are the practical considerations? How does the digestive system signal the
hunger communication system? How does the brain’s response to food vary
depending on the food in question?
 Most of the digestive tract signaling messengers send a message of satiety to the
brain. Satiety is defined a feeling of fullness and satisfaction after being fed. Once
the digestive tract (stomach, intestines, gall bladder, liver, and pancreas) senses a
meal has just been eaten, it sends multiple signals—all designed to promote a
feeling of satiety—to the brain. The satiety signal stops intake of more food—the
goal is to allow time for digestion, and to prevent overeating. Most of the satiety
signaling in the digestive tract is designed to control short-term eating behavior.
This is an important distinction, leptin is not a short-term satiation solution, it is
more effective at exerting long-term control over eating behavior.

The feeling of being full after a big dinner, but still being hungry the next
morning is a short-term eating signal. Digestive tract signals are mostly
concerned with stopping continued eating in the short-term to allow for
digestion. But, the digestive tract will signal for more food when digestion
is nearing completion from the previous meal.
Long-term eating signals (leptin) control the quantity of what you eat over
multiple meals. Routinely eating large amounts of food at every meal—
greater than the fuel requirements of your body—is an example of
disrupted long-term eating signals. An example of proper long-term
eating behavior from correctly functioning long-term eating signals is
routinely eating the right amount of food to supply your body’s energy
needs without much excess.

TECHNICAL NOTE:
 There are many specific digestive tract messengers that send a “stop
eating” (satiety) signal. They include: Peptide Tyrosine (PYY), Pancreatic
Polypeptide (PP), Glucagon-Like Peptide (GLP-1), and Cholecystokinin
(CCK).

One of the only messengers from the digestive tract that triggers the
hunger response is ghrelin. Ghrelin is produced in the stomach and is
active between meals. When the stomach is empty, ghrelin is secreted to
stimulate hunger.

PROTEIN PRODUCES THE LARGEST AND LONGEST SATIETY

SIGNAL TO THE BRAIN.
Amino acids from protein digestion are sensed in the intestine. A signal is sent to
the brain through a variety of messengers, and produces a strong signal of satiety.

The satiety signal from protein is the strongest of all the food satiety signals.
Many studies have shown that high protein diets result in lower intake of total
calories throughout the day. This is because protein triggers the best short-term
signal to stop eating. People that eat a good quantity of protein with each meal are
less hungry and naturally eat less throughout the day—without discipline. Their
protein-satiated brain tells them that they do not need food.

Eating 20-30 grams of protein as part of your breakfast will keep you from being
hungry later in the morning and resorting to “snacking.” Many people succumb to
sweet, sugary snacks because they did not provide the right satiety signal to the
brain first thing in the morning with a high protein meal.

KEY POINT:
Remember this for the rest of your dietary life: protein produces satiety. It
generates the largest and longest satiety signal to the brain of any and all
nutrients. Want to kill an appetite? Eat protein!
 STRONG MEDICINE TACTICS:
Eat 20-30 grams of protein as part of breakfast to provide a strong satiety
signal to the brain first thing in the morning. This will help decrease the
calories you eat for the rest of the day without feeling hungry.

Protein is the only macronutrient that consistently produces satiety signals in the
brain. Carbohydrates and fat can produce satiety as well, but the specific types of
carbohydrates and fat are important. In some forms, carbohydrates and fat can
produce a hunger and food craving response. That leads us to our next point...

3. “PALATABLE” FOODS CAN STIMULATE

THE REWARD CENTERS OF THE BRAIN,
INCREASING APPETITE.
“Palatability” of food can be a confusing topic, and should not always be equated
with good tasting food. Palatability refers to the feeling of satisfaction or “reward”
coming from eating a particular food at a particular time. A good way to explain
this is the immediate satisfaction and “comforting” feelings you may get by eating
ice cream after a stressful day. Although ice cream generally tastes good to most
people, it may not always be satisfying to eat depending on the circumstances. For
instance, if you have not had ice cream with chocolate syrup for a month, it may be
extremely palatable because you have not had it for so long. It generates the “feel-
good” response and satisfaction. If you have ice cream nightly, it may still taste
good but you may not have the intense “feel-good” satisfaction response you
experienced after being deprived of it for a month. Having ice cream every night
has made it less palatable.

Palatability of food is very individual, but in general, calorie-dense foods that

contain sugar and fat are generally palatable to most of us. Fast-food and other
processed foods are very palatable to many people for this reason.

 Palatable foods?

Palatable foods that stimulate our reward system can override our normal “stop
eating” signals. A good way to tell if a food falls into this category (for you) is if
you feel driven to eat the food even when you are full—and will go out of your way
to acquire this specific food. The normal “stop eating” signal that emanates from the
digestive tract’s communication system will often be silenced or overruled by the
food reward system. There is a chemical reason you continue eating certain foods
even when full.

The reward system in the brain is the same area activated by drugs such as
cocaine.

When the reward system is stimulated, “feel good” chemicals like dopamine and
endorphins are produced. Stimulating the reward pathway makes us feel good and
can encourage us to stimulate it over and over.

THE REWARD SYSTEM HAS CHANGED IN OBESE PEOPLE.

Two main parts of the reward system are in the brain, and recent research has
shown that the reward system functions differently in an obese person than it does in
a lean person. The two parts of the reward system are interconnected and influence
one another.

• The first part of the reward system is controlled by the parts of the brain
involved in the actual experience of pleasure. Palatable food signals this part of
the brain to produce a chemical called dopamine. Other chemicals that increase
dopamine include opiates such as morphine, heroin, and prescription pain-
killers, as well as drugs like cocaine.

• The second main part of the reward system is the part of the brain involved in
 organizing and planning actions to obtain a reward. Once something like
palatable food stimulates dopamine release (in the first part of the reward system)
the second part of the system plans how to obtain the palatable food again. This
part of the reward system is involved when you leave your house, get in your car,
and travel to the store to pick up your favorite ice cream when a craving hits. It is
also the system that helps you imagine how good the ice cream is going to taste
before you eat it.

One current theory holds that the overeating seen in overweight and obese people
is due to the two parts of the reward system changing in a very similar way to what
is seen in drug addiction.

In an obese person, the first part of the reward system involved with experiencing
pleasure from dopamine release is suppressed. This means that just like developing
tolerance to a drug, a higher amount of the palatable food is needed to get the same
“feel-good” pleasure response.

While the “pleasure-part” of the reward system is suppressed in the obese person,
the second part of the system involved with planning to obtain palatable food, and
predicting how much pleasure will be involved with eating it, is overactive.

This broken reward system may explain why some people are compelled to seek
out palatable food more often and in larger amounts. It is a subconscious attempt to
stimulate the pleasure part of the reward system.

People will literally fantasize about how good favorite foods will taste—only to
feel unsatisfied when they actually eat the food. This creates a vicious cycle of
fantasy, fulfillment, and continuing to forage and eat because nothing satisfies.
Many people continually seek out highly palatable foods in a futile attempt to feel
pleasure and satisfaction.

FIRST PRINCIPLES PERSPECTIVE:

WHY THE REWARD SYSTEM?
The brain’s food reward system makes sense as a system to ensure
survival when food is scarce. Ancient humans did not have grocery stores
and fast food chains available when they were hungry. Access to large
quantities of caloriedense food was not a common occurrence in a hunter-
gatherer society. When these groups obtained a large source of calorie
 dense food, the ability to override the “stop eating” signal may have had
some advantages.

Periodic overeating to store excess energy as body fat would be a valuable

stored energy source to draw from when food became scarce again. In this
way, the ability to override the “stop eating” signal could be a survival
advantage.

The same food reward system that helped ensure survival of primitive
humans is ironically contributing to the poor health of modern humans.

The fat cells and the gut communicate with the brain (especially the
hypothalamus) to signal when we have eaten enough or, conversely, if we need to
eat more to derive additional energy from food. The energy system that drives us to
eat can be overridden by the reward system. An obese person may continually have
the urge to eat—even though there is no need for more energy from food—because
the reward system is in control.

TAKE HOME MESSAGE:

An obese or overweight person has two strikes against them in their
battles to control how much they eat:
1. The “energy” hunger communication system involving leptin is not
working. They are not getting the “stop eating signal” from leptin and are
hungry.
2. The “reward” hunger communication system is broken, which will
cause overeating in the attempt to feel satisfied.

If you are overweight or obese, hopefully this information can help you
realize that you are not “weak-willed,” but have a real drive to eat—even
when your body does not need the energy. This may help you gain some
control over these urges when they hit.
“...knowing is half the battle.” —G.I. Joe (1985)
KEY POINT:
The reward system can override the “energy” system for control of the
drive to eat.

DIGGING DEEPER:
Processed Food, Palatability, and Reward
Fast food and processed food tastes good to most of us. That is why multi-
billion dollar food industries are a major contributor to the obesity
epidemic. Why does this type of food maximally stimulate our food
reward centers in the brain?

Food processing removes much of the natural flavors present in whole

food ingredients. Most of the ingredients—that most of us cannot
pronounce—seen on processed food labels are preservatives to keep the
food from spoiling or flavor and color additives. Color additives make
the processed food more visually appealing, and flavor additives are
engineered to make the food palatable.

There is a whole profession of “flavorists,” chemists who specialize in

creating flavors to add to processed food, and which maximally trigger
the reward centers in the brain. Flavorists are highly trained individuals
with the primary goal of making processed food extremely palatable.
Many of us are very loyal to products like specific soft drinks (from
particular manufacturers) because of the unique and reward-stimulating
flavors created in laboratories. These flavors are manipulating your
behavior through your reward system. If they can “hook” you with a
flavor, they have a loyal customer for life. Unfortunately, the reward
system “hooked” on artificial, laboratory-concocted flavors contributes to
the rampant overeating that underlies the current obesity epidemic.

COUNTING CALORIES: ISSUES WITH

CONTROL

Daily, I overhear dieters’ conversations about the latest strategies, gadgets,

and resources for determining the calorie count of every meal. They are
counting calories in an attempt to gain some control over a broken hunger
communication system. They are not addressing the underlying problem.

The healthcare community (especially dietitians) has promoted counting

calories in a big way. This practice has done a disservice to the public and
their health. Sure, counting and restricting calories will work for short-
term weight loss, but it is not sustainable for the long-term. It is not
sustainable because we are trying to exert control over a primal hunger
system that is hardwired in our brain to ensure survival. We cannot
restrain it for prolonged periods of time.

A properly working hunger communication system will not let you

overeat. We have to restore proper operation of the hunger system with
 the right food, sleep, stress-reduction and exercise. It will take some time
to fix the hunger system but it can be done following the Strong Medicine
approach.

Restricting calories while still eating the wrong type of food (processed
foods, etc.) will not restore the hunger communication system. The brain
thinks you are starving the body and will activate the stress-threat system
producing cortisol, interrupting the actions of leptin. The result is constant
hunger and a losing battle to maintain calorie restriction. Calorie counting
often becomes a neurotic and self-defeating practice in the long term.
Have some patience when working to restore your hunger communication
system. The rest will take care of itself.

This has been a very simplified overview of what drives us to eat, and what can
go wrong when the hunger communication system breaks down with obesity and
diabetes. Now that you understand what is going on “under the hood” with obesity,
diabetes, and the drive to eat, the interventions we will discuss to fix and prevent
these problems should make a lot more sense. We are going to put obesity “on the
ropes” and prepare to deliver the knock-out punch.
OBESITY: THE ENEMY WITHIN IV:
INTERVENTION: THE 8-STEP
PROGRAM FOR OBESITY AND
DIABETES

How do we reduce the chronic inflammation and oxidative stress that promotes
obesity and diabetes? Both obesity and type II diabetes can be treated and reversed
with nutritional and lifestyle interventions. Our approach is geared towards the
systematic reduction of body fat and proven methods for controlling blood sugar.

QUICK MEDICAL NOTE:

Please work with your health care provider when implementing the
recommendations that follow in this section—especially if you are taking
medications to treat diabetes. Your medications will likely have to be
adjusted as you change your diet and lifestyle, so it is important that your
healthcare provider is in the loop. You are encouraged to take this book
 with you to your appointment to help with the conversation.

If your clinician is unwilling to support these interventions as part of your

treatment plan, consider finding another healthcare provider to work with.
There are plenty of us out there who are willing and able to help a
motivated patient.

Let’s dive right in to our stepwise approach to losing fat and controlling blood
sugar...

STEP 1
DETERMINE YOUR TOLERANCE FOR
STARCH AND SUGAR.
Reducing starch and sugar to “tolerance levels” is fundamental. If you are obese,
but without a diabetes diagnosis, it is a safe bet that you are on your way to insulin
resistance, so this step will also apply to you.

Insulin resistance—malfunctioning insulin receptors—caused by chronic

inflammation and oxidative stress leads to poor entry of glucose into muscle and fat
cells. As insulin resistance gets worse, the amount of glucose in your bloodstream
increases, damaging your blood vessels and accelerating aging. Someone with
insulin resistance cannot tolerate the same amount of glucose from starch and sugar
that a healthy person with good insulin sensitivity can tolerate.

After a meal, a healthy person with good insulin sensitivity will rarely
experience blood sugar exceeding 140 mg/dL, even directly after a starchy meal.
For the insulin resistant obese person or diabetic, small amounts of starch and sugar
may increase their blood sugar well above 140 because they cannot “dispose” of the
glucose. They cannot get it into muscle or fat cells because of malfunctioning
insulin receptors. A long-term diabetic likely has twice the problem–broken insulin
receptors and a burned out pancreas. A damaged pancreas cannot produce enough
insulin to help handle significant amounts of dietary starch or sugar.
 KEY POINT:
Someone with insulin resistance cannot tolerate the same amount of
glucose from dietary starch and sugar that a healthy person with good
insulin sensitivity can tolerate.

Depending on the severity of your insulin resistance, your tolerance for glucose
will vary. To achieve optimal results, you will have to consistently measure your
blood sugar after meals to assess your tolerance for the amounts and types of
specific foods.

Even regular people can benefit from identifying how certain foods (and amounts
of those foods) react within their bodies. I recommend purchasing a glucose meter
from your local pharmacy. Meter technology has improved considerably over the
last several years and most glucose devices are inexpensive and require very little
blood.

Remember that starches are just thousands upon thousands of glucose molecules
“linked” together. Digestion rapidly turns starch into glucose, and insulin is then
needed to clear the glucose from the bloodstream so it doesn’t stay at high levels.

Many people do not know which foods are large sources of starch and glucose.
You can favorably manipulate blood glucose and insulin by making expert use of
food. We need to understand some basic biochemistry to intelligently discern which
foods are beneficial or detrimental.
 KEY POINT:
STARCH = GLUCOSE
An important point to make is that not all of the foods listed are necessarily “bad”
for you. Tubers, root vegetables, and fruit are nutrient dense and can have high
nutritional value. The whole point of the list is to identify sources of starch and
glucose in your diet so you know what to eliminate or reduce if your blood sugar
readings are too high after a meal.

Ideally, you should eat the amount of starch/glucose that your insulin system is
able to effectively clear from the bloodstream with relative immediacy after a meal.
Using the blood sugar monitor, you can perform your own glucose tolerance test.
We will test your individual ability to clear glucose from many different types of
meals instead of just testing with a glucose solution at your doctor ’s office.

You have the power to experiment with many different food combinations to find
out what foods (and in what amounts) are beneficial or detrimental. An oral glucose
tolerance test is used to diagnose diabetes and prediabetes. You can use this as a
food tolerance test to help you plan your meals and keep blood sugar under control.

COMMON SOURCES OF STARCH

AND GLUCOSE:

• Rice is basically starch and not much else.
• Flour includes favorites such as bread, pasta, pastries, bagels, and
tortillas. ANYTHING made with flour is a large source of starch.
• Cereals are a grain-based processed breakfast food packed with starch.
• Tubers and root vegetables include potatoes and sweet potatoes, etc.
 • Soda and “fruit beverages” have high amounts of glucose and fructose
—especially in the form of high fructose corn syrup.
• Fruit juice is really the concentrated sugar from fruit and water. A glass
of orange juice contains the juice of several oranges without much of the
beneficial fiber.
• High sugar fruits include bananas, mangos, apples, pears, grapes, etc.
Dried fruit is even higher in glucose!
• Candy, sweets, pastries—enough said!

Self-testing is simple, take two readings after each meal. Use the blood glucose
meter one hour after a meal, then two hours after a meal. This will take the
guesswork out of the process—no more guessing how that lunchtime sandwich
affects your blood sugar.

A healthy person with normal insulin sensitivity will rarely have their blood
sugar elevate above 140 after a meal, so we will use 140 as a “normalcy
benchmark.” We offer these goals for appropriate (normal) amounts of
starch/glucose in the bloodstream after consuming a food or a meal or a beverage.

QUICK MEDICAL NOTE:

Why are these goals stricter than the Oral Glucose
Tolerance Test?
The first reason is that we are using real food instead of a glucose
solution. Most importantly, the “normal” ranges in the OGTT (and
diabetic testing in general) are not adequate for achieving optimal health
in my opinion. The traditional tests set the bar too low and categorize too
many people with early insulin resistance as “normal.”
 REAL LIFE EXAMPLE

“Joe” was recently diagnosed with prediabetes. He is using our self-

monitoring program and wants to find out how the baked potato he is
having for lunch today will affect his blood sugar. He eats a whole baked
potato and measures blood glucose at 180 at the first hour and 142 by the
second hour. Obviously he cannot tolerate that much starch in a meal, as
these readings are outside the goal values in the chart above.

The next day Joe has 1/3 of a baked potato for lunch. His 1-hour blood
glucose measurement is 136, and his 2-hour measurement is 118. Now he
knows that generally, he can tolerate the amount of starch in 1/3 of a baked
potato. He moves on and does the same experiment with more of his
favorite meals so he can make the necessary adjustments.

For most overweight, obese, and type II diabetics early in their disease, these
goals are achievable. You will need to reduce the amounts of starch/glucose in your
meals appropriately. How insulin sensitive (or resistant) you are will determine how
much you need to reduce the starch load in your meals. You will also notice which
foods are problematic for you.

The amount of starch you can handle will also change depending on what you
eat with the starchy food in the meal. For instance, eating fermentable fiber with
the starch will slow the release of glucose in the bloodstream allowing you to
tolerate more starch with the meal.

Measure your blood sugar this way for a while to get a sense of which specific
foods you can handle and which ones you cannot. It can also help you identify which
foods to eat with a starchy food help control blood sugar (i.e. fiber from
vegetables). There is no guesswork. Things you thought were “healthy” might shoot
your blood glucose through the roof. You will never know unless you use this
testing protocol.

Over time, you will not need to measure as much. You will have assembled
enough empirical data to intuitively know what kind of foods you should avoid. All
you need is an inexpensive glucose monitor to get started. We will now refer to what
you are measuring with this method as your individual glucose tolerance (IGT).

WHOLE GRAINS FOR DIABETICS?

SERIOUSLY?
Somewhere, somehow, someone got the bright idea that whole grains
were good for diabetics. This has never made any sense to me, and
sometimes makes me a little crazy when I hear that a well-meaning health
care provider has told a diabetic person “to eat more whole grains” as
nutrition advice to help their diabetes.

While it is true that the starch in whole grains is converted to glucose a

little slower than processed flour, eating whole grains still results in a
large glucose load the body must clear from the bloodstream. If you don’t
believe me, eat a sandwich made of “healthy whole grain” bread and check
your one and two hour blood sugars. Try a plate of “whole grain” pasta
and do the same blood testing protocol and see what it does to your blood
sugar.

Unprocessed whole grains such as oats and pseudo-grains such as quinoa

can definitely be part of a healthy diet for someone with good insulin
sensitivity, but even these foods in large amounts will often present too
much of a starch load for most diabetics and prediabetics to effectively
process.

 “Stop recommending
whole grains for
diabetics!!!!”

Diabetic educators and other well-meaning clinicians keep parroting the

whole grain mantra they learned in their training, but it is not doing their
patients any favors, believe me. It drives me a little nuts when whole
grains are recommended to diabetics, and everyone wonders why the
patient’s blood sugar is not well controlled.

Sometimes I feel like Inspector Dreyfus in the old Pink Panther movies
with the “whole grain” issue. The bumbling Inspector Clouseau’s antics
torment Dreyfus over the years, and eventually land him in an insane
asylum. I am not yet in a mental health institution, but I do get the
occasional eye twitch.

As you get leaner and healthier, you will be able to tolerate more starch. Along
the way it is your duty to experiment and verify the changes. If you have excellent
insulin sensitivity, and can tolerate high starch levels, eat it, enjoy it, and clear it
with no worries. Do not lie to yourself about having high insulin sensitivity if you
do not. The IGT will not lie to you.

QUICK MEDICAL NOTE:

Type II diabetics (especially those who have had the disease for a while)
may need additional help from pharmaceuticals to control their blood
sugar. Drugs like Metformin control the release of glucose the “liver
banker” produces from gluconeogenesis (see item #2 in the Consequences
of Obesity and Insulin Resistance from the previous section) and can
definitely help some achieve their blood sugar goals.
Again, if you are currently on diabetes medication, please work with your
doctor while implementing the starchy carbohydrate reduction as
described in step one. Your medication may need adjustment to keep your
blood sugar from falling too low.

Type I diabetes can be more complicated to manage. Type I diabetics

definitely need medical supervision if they try dietary changes.

COACH’S CORNER:
Recent research strongly supports the contention that restricting starchy
carbohydrates and sugars is of substantial benefit for the type II diabetic
and the insulin-resistant obese.

Welcome to the orthodox elite who showed up to the party 30 years late to
proclaim that starchy carbs, grains, liquor, man-made industrial food and
artificial chemically poisoned proteins are BAD for us and contribute to
obesity and type II diabetes. Thank you for confirming what the athletic
elite already knew in 1983!

Individuals with a broken insulin system should reduce stress on the

system by decreasing dietary glucose (created from starch and sugar) to
an amount that their system can effectively process. It is so simple! Again,
the amount each person can tolerate will differ between individuals.

The more insulin resistant you are, the less starch and sugar you will be
able to tolerate. Get serious about regaining your health and use the
science and technology available for identifying your individual glucose
tolerance.

REAL LIFE EXAMPLE

 Lettuce wraps are a
great alternative to
reduce the amount of
starch in your favorite
wrap recipe.
Maintaining healthy
blood sugar levels
can still be tasty.

“Sally” has had the diagnosis of type II diabetes for 4 years, and probably
had insulin resistance developing for more than a decade. She could not
figure out why her blood glucose kept reading high after her lunch. She
had switched from making her sandwiches with bread to making wraps
with corn tortillas. Her glucose readings improved but were still
considerably high after lunch.

During a clinic visit, Sally was reminded that corn tortillas are made with
corn flour and are mostly starch. Since Sally has had her condition for a
while, she cannot tolerate much starch with her meals while keeping her
after-meal glucose within the goal range. Switching from corn tortilla
wraps to lettuce wraps did the trick and now her after-lunch blood glucose
readings are well within the goal range.

STEP 2
STOP EATING FOODS THAT CONTAIN
GLUTEN!
Obesity and diabetes are inflammatory disorders. For many individuals, gluten
adds fuel to the inflammation fire by causing gut irritation, intestinal permeability,
and inflammation. Gluten-containing products provide no nutritional advantages.
There is no downside to eliminating gluten from your diet.

“GLUTEN-FREE” DOES NOT

NECESSARILY EQUAL HEALTHY!

I have seen plenty of people cut out gluten from their diets only to run to
the gluten-free section of their grocery store to buy a bunch of processed
glutenfree replacement products.

Many of these processed products are far from healthy. Most are just
highly dense sources of starch with very little nutritional value. A gluten-
free cake is still a cake, and a gluten-free cookie is still a cookie—the only
difference is they do not contain a potentially gut-irritating protein
(gluten).

These gluten-free processed products will wreak havoc on your blood

sugar and waistline. Do not fool yourself into thinking that these are health
foods!

Do gluten-free the right way and stay away from these processed products.

STEP 3
ELIMINATE PROCESSED SEED OILS
FROM YOUR DIET
Processed seed and vegetable oils are some of the largest contributors to
inflammation and oxidative stress in modern society. These rancid concoctions are
in 99% of all processed (man-made) foods. Fast food manufacturers find ways to
include seed and vegetable oils in nearly every food product they make—from milk
shakes to burger “meat,” from the hot apple pie crust, to the bacon bits sprinkled
over your salad, these bad fats are everywhere.

Processed seed and vegetable oils are high in omega-6 PUFA and contribute to
chronic inflammation and oxidative stress.

• High dietary intake of omega-6 PUFA can disrupt the omega-3/omega-6

balance leading to a chronic inflammatory state.

• Omega-6 PUFA, like all polyunsaturated fats are prone to free radical damage
because of their multiple double bonds. This leads to free-radical chain reactions
in the body, which quickly produce large amounts of oxidative stress.

This is linoleic acid (LA) an omega-6 PUFA. High amounts of LA are

found in many processed foods and in the vegetable/seed oils used to cook
fast food.

Free radicals are attracted to double bonds!

The last thing you need if you are obese or diabetic is to “import” more oxidative
stress and inflammation from vegetable and seed oils found in processed food and
fast food.

KEY POINT:
Insulin resistance is triggered by chronic inflammation and oxidative
stress. Do not make it worse by “importing” more inflammation and
oxidative stress by eating high amounts of omega-6 PUFA from fast food
and processed foods. Read your labels!!

OMEGA-6 CONTENT OF VEGETABLE

AND SEED OILS

Corn Oil
• 24% MUFA
• 60% Omega-6 PUFA
• 12% SFA

Sunflower Seed Oil

• 19% MUFA
• 65% Omega-6 PUFA
• 10% SFA

Safflower Oil
• 14% MUFA
 • 75% Omega-6 PUFA
• 6% SFA

Soybean Oil
• 23% MUFA
• 51% Omega-6 PUFA
• 6% Omega-3 PUFA
• 14% SFA

You can see the high percentage of omega-6 PUFA in each of these oils.
Check processed food packages and salad dressings for these oils. Many
of them are even advertised as being healthy for you!
• MUFA = monounsaturated fatty acid
• PUFA = polyunsaturated fatty acid
• SFA = saturated fatty acid

WHAT SHOULD I USE FOR SAUTÉING FOOD OR FOR SALAD

DRESSING?
Why not use the choice of the world’s elite chefs, olive oil or coconut oil? Do
you really think the world’s best chefs use trashy, highly processed vegetable oil for
sautéing top quality ingredients? Of course not! They use the finest extra virgin
olive oil, or the purest of high MCT coconut oil—these magnificent fats are highly
beneficial and introduce great flavors into your foods.

If we are going to ask you to stop using something, we will give you substitutes:

Use extra virgin olive oil to make your own homemade salad dressing instead of
using store-bought dressings. I challenge you to find a store-bought salad dressing
low in omega-6 PUFA.

For cooking, coconut oil is superb. It is high in medium-chain triglyceride

saturated fats (including lauric acid) that have amazing health benefits. Because it
contains saturated fat, coconut oil will not oxidize and produce free radicals when
you cook with it. Medium-chain saturated fats aid in weight loss and provide some
benefit to people with Alzheimer ’s disease. They are “heart safe” and do not
aggravate risk factors for heart and vascular disease.

Medium-chain triglycerides go to the head of the fuel-burning line as soon as

they are consumed; MCTs are used directly for energy instead of being stored as
excess body fat. MCT consumption is especially helpful for insulin resistant
individuals cutting back on starchy carbohydrates. The medium chain-fats can
provide “replacement energy” for the “lost” starchy carbs. Ironically, this is the
identical strategy (replace starch calories with MCT calories) used by competitive
bodybuilders leading up to competitions where 5% body fat percentages are
common.

Overall, the high content of medium chain saturated fats makes coconut oil an
excellent alternative to vegetable oil for most cooking needs.

Also, coconut oil does not impart a strong coconut flavor to food as you might
imagine. Try it when making a vegetable stir-fry and see for yourself.

STRONG MEDICINE TACTICS:

As alternatives to processed seed and vegetable oils, use olive oil for
homemade salad dressings and coconut oil for cooking.

STEP 4
EAT AT LEAST 20-30 GRAMS OF PROTEIN
WITH EVERY MEAL
Every time you eat, consume some protein: at least 20 grams if you are smaller
and 30 grams if you are a larger person. Protein provides the amino acids critical
for maintaining (or increasing) lean muscle mass, and protein is also an appetite
suppressor. Protein satiates, nourishes, and quells hunger. Quality protein triggers
the brain’s satiety (the “fullness”) centers, and eating protein throughout the day will
quench hunger.

Determining how much protein you are eating with a meal is relatively easy using
the following “rule of thumb” estimates for protein. All you need is a kitchen scale
that measures cooked protein sources in ounces.
 PROTEIN ESTIMATOR: THE EASY
WAY
The following are good “rules of thumb” for figuring out protein
amounts from animal sources. For plant sources, we recommend using the
National Nutrient Database (http://ndb.nal.usda.gov/ndb/search/list) since
plant sources are highly variable in protein amounts.
• Cooked chicken, turkey, beef, or pork have about 7 grams of protein
for every 1 ounce of meat. Four ounces of any of these cooked meats
provide approximately 28 grams of protein, and are well within the 20-30
gram goal.

• Ground meats such as hamburger are less dense, and have about 7
grams of protein for every 1.5 ounces of cooked meat. You will need 6
ounces of cooked ground meat for the same 28 grams of protein.
• 1 egg has about 7 grams of protein. So, 4 scrambled eggs provide 28
grams of protein.
• Fish and fatty poultry (duck) have about 7 grams of protein for every
1.5 ounces. Six ounces of fish or duck contain 28 grams of protein.
Over time you should be able to literally “eye-ball” the amount
of food you need to get within the 20-30 gram protein goal for
each meal.

STEP 5
INCREASE PLANT-BASED FOODS FOR
FERMENTABLE FIBER AND
ANTIOXIDANT DEFENSE.
Fruit and vegetable fiber is fermented (broken down) by our gut bacteria. This
process produces beneficial “waste” products including short chain saturated fats
like butyrate.

Unlike our digestive machinery, the beneficial bacteria that live in our gut can
break the connecting bonds in fiber and they can feed on the released glucose. These
bacteria secrete the short chain fats (butyrate) as “waste” products, but these waste
products have amazing anti-inflammatory properties.

Here is a quick review on the benefits of butyrate:

• Butyrate has potent anti-inflammatory properties. Obesity and diabetes are

inflammatory conditions, therefore substances like butyrate and other short chain
fatty acids produced from the fermentation of fiber help counteract the chronic
inflammation produced from bloated fat cells.

• Butyrate has been shown to have anti-cancer properties, and potential anti-
cancer action—especially with colon cancer.

KEY POINT:
The main health benefits from fiber result from the short chain fat
(butyrate) production from fermentation of fiber by the gut bacteria. Fiber
from many types of grains (especially wheat) is not as fermentable.

WHAT ABOUT THE FIBER IN WHOLE

WHEAT?

The fiber found in whole wheat is not nearly as fermentable as the fiber in
most fruits and vegetables. The beneficial gut bacteria cannot break down
the whole wheat fiber as well, so very little butyrate is produced.

The main health benefits from fiber result from the short chain fat
(butyrate) production, so fiber that is not as fermentable (like whole
wheat) is not the best choice.

Whole wheat is also very dense with starchy carbohydrates, making it a

poor choice (like many of the whole grains) for people with obesity and
diabetes.

STRONG MEDICINE TACTICS:

To help stop chronic inflammation, choose vegetables and fruit over
grains as your sources of fermentable fiber.
 Eating fermentable fiber from a wide variety of fruits and vegetables can help
decrease the level of glucose in your bloodstream after meals. This will help you
meet the one-hour and two-hours after-meal glucose goals discussed in step one.
Make fibrous vegetables and fruits a cornerstone of your nutrition.

Fermentable fibers can slow the rate in which food is moved from the stomach
during digestion. This can help create a feeling of satiety (fullness).

The following list is some of the best sources of fiber from fruits and vegetables,
but it is not nearly a complete list.

GOOD SOURCES OF FERMENTABLE

FIBER

The Vegetables:
• Leafy green vegetables such as kale, spinach, and chard
• Stem tubers such as potatoes
• Root tubers such as sweet potatoes
• Root vegetables such as carrots, turnips, rutabaga, daikon, radish,
parsnips, jicama

Fruit:
• Berries such as strawberries, blueberries, blackberries, raspberries
• Avocados
• Pears, apples, oranges, bananas (be aware of the sugar content)

INCREASING ANTIOXIDANT
 DEFENSE WITH PLANT-BASED FOOD

There are certain health-promoting compounds found only in plant foods.

Many of these compounds stimulate our body’s antioxidant defense
systems and counteract the chronic oxidative stress linked to obesity and
diabetes.

Many fruits and vegetables are “edible pharmacies” containing hundreds

of different compounds to combat inflammation and oxidative stress—
especially important for diabetics and the obese.

For a long time it was thought that these plant compounds acted as
antioxidants, scooping up free radicals and preventing them from
damaging the body. Some of these compounds may work in this fashion to
a limited extent, but current research shows that many of these chemicals
work primarily by stimulating our natural antioxidant defense and
detoxification systems. Some of these plant-chemicals also work by
stopping inflammation.

Some grains such as oatmeal do contain a relatively high amount of fermentable

fiber, but also have a pretty high starch load, so use with caution if you are diabetic.

Legumes such as beans, peas, and lentils have high amounts of fiber, but can
cause gut inflammation in some people. If you are going to use legumes as a fiber
source, make sure you soak them for 24 hours then cook them thoroughly to reduce
some of the toxic compounds found in dried legumes. If you tolerate legumes, they
can be an excellent source of fiber if prepared correctly. Vegetable and fruit-based
fiber generally causes less irritation than legumes and is generally preferable from
a gut health perspective.

There are thousands of plant-derived chemicals, and many have positive health
benefits. Some are outstanding and deserve to be singled out because they are
especially beneficial to the insulin resistant obese or diabetic person.

SULFORAPHANE: BROCCOLI’S
BOUNTY

Sulforaphane is a chemical found in all cruciferous vegetables (broccoli,

cauliflower, cabbage, bok choy, horseradish, mustard seed, wasabi,
rutabagas, radishes, turnips and others).

Sulforaphane stimulates the central controller of the antioxidant response

system, which fights oxidative stress from the free radicals inside your
cells. It also directly helps to stop the inflammatory response.

Since obesity and diabetes are diseases of chronic inflammation and

oxidative stress, sulforaphane can be especially helpful for diabetes in
particular.

Sulforaphane has also shown potent anti-cancer activity in some types of

cancer, and may inhibit the growth of the ulcer-causing bacteria,
Helicobacter pylori.

Additionally, sulforaphane can stimulate the body’s natural detoxification

system, helping to detoxify certain types of toxins and toxicants from the
air, water, and food.

The best dietary source of sulforaphane is from broccoli sprouts (3-5 day
old broccoli plants). Broccoli sprouts have 20 times the sulforaphane
content as full-grown broccoli plants.

TECHNICAL NOTE:
Sulforaphane is produced from a chemical building block in broccoli
called glucoraphanin. A special enzyme in the plant is needed to convert
glucoraphanin to sulforaphane. You must damage the plant through
chopping or chewing for the conversion to sulforaphane to take place
directly from the plant. Glucoraphanin can also be converted to
sulforaphane by the gut bacteria.

KEY POINT:
Broccoli sprouts must be damaged by chewing or cutting to get
sulforaphane directly from the plant.

RESEARCH UPDATE:
A recent study has shown that sulforaphane can alter the epigenetic
programming of certain cancer cells. Researchers found that sulforaphane
“turns off” a gene responsible for growth in these cancer cells. This is
important, since cancer is uncontrolled cell growth.

This research suggests that sulforaphane can stop uncontrolled growth in

some cancer cells by “switching off” growth genes, through an epigenetic
process.

If you need a review on the epigenetic process, go back to the Central

Concepts section on Gene-Environment Interaction.

RESEARCH UPDATE:
Of special interest for diabetics—new research has shown that adding
foods with high sulforaphane content such as broccoli sprouts to the diets
showed substantial benefit for diabetics.

All of the diabetic patients in the study showed improvements in insulin

resistance, and overall decreased oxidative stress and inflammation after
adding broccoli sprouts to the diet.

DO IT YOURSELF!
Broccoli sprouts are easy to grow at home. An internet search will yield
several sites with instructions on how to grow your own sprouts. Given
the benefits of sulforaphane, having your own indoor broccoli sprout
garden is well worth the effort, and they will be fresher and more effective
than sprouts from the grocery store.
STRONG MEDICINE TACTICS:
Eat cruciferous vegetables such as broccoli, cauliflower, cabbage, bok
choy, horseradish, mustard seed, wasabi, rutabagas, radishes, and turnips
to get the benefits of sulforaphane. Broccoli sprouts are the best source.

POLYPHENOLS: DARK CHOCOLATE

ANYONE?
Polyphenols are a large group of plant-chemicals found in most plant
species. Laboratory studies have shown they have strong anti-oxidant
effects and inhibit inflammation.

Studies in a test tube (called in vitro) show that polyphenols act as

antioxidants, scavenging free radicals. However, recent research has
shown that in the body, polyphenols do not have as much direct
antioxidant effect themselves, but activate the antioxidant defense
system (see the “bouncers in the bar” from the Central Concepts chapter).

Polyphenols are found in many plant-based foods, but the highest

concentrations are found in cocoa beans, coffee, red wine, green tea, black
tea, and olive oil. The bitter taste in many of these foods comes from the
polyphenol content. The higher the polyphenol content, the more bitter the
flavor.

Pure cocoa has one of the highest polyphenol contents of any food, but is
inedible because of the bitter taste. 85% dark chocolate is an excellent
source of polyphenols and tastes pretty good once you are accustomed to
the flavor (and lack of sugar).

Research on polyphenols is still ongoing, but recent studies have shown

that polyphenols may be of some benefit for diseases of inflammation and
oxidative stress such as diabetes, heart disease, cancer, and Alzheimer ’s
dementia.

Incorporate a variety of polyphenols in your diet—there are plenty of

sources to choose from.

STRONG MEDICINE TACTICS:

Incorporate polyphenol-rich foods like dark chocolate (80-85% cacao),
coffee, red wine, green tea, black tea, and olive oil into your diet.

FIRST PRINCIPLES PERSPECTIVE:

PLANT CHEMICALS AND HEALTH
There are multiple theories as to why so many plant-based chemicals
show health benefits. But, the theory that these chemicals act as direct
antioxidants is slowly losing favor.

Plant-based chemicals such as polyphenols are produced inside the plant

in response to environmental stresses on the individual plant. Poor soil
nutrients, insect predators, and lack of water can all produce a stress
response in plants, increasing polyphenols.

Recently an intriguing hypothesis was put forward—chemicals such as

polyphenols, produced in plants during stressful conditions, are known to
activate stress defense mechanisms (antioxidant defense) in our bodies
when eaten, and they act as an environmental stress sensor. The authors
of this hypothesis think that these plant-chemicals (when eaten) allow us to
sense stress in the food supply (stress to the plants) and prepare our bodies
for an upcoming threat to the food supply such as a drought or insect
 infestation.

In the hunter-gather societies of our distant ancestors, the ability for our
body to prepare for a food shortage by “sensing” stress in the food supply
would be a survival advantage. It may be one reason why so many
chemicals in plants have health benefits for humans.

This is still just a hypothesis, but it makes sense through the first-
principles lens.

STEP 6
CUT OUT HIGH FRUCTOSE CORN SYRUP
AND SUGAR.
Like alcohol, fructose can only be metabolized in the liver. The liver does two
things with fructose—converts it to glucose or body fat for storage at one of the
many fat-storage depots dotting the bodily landscape.

The amount of fructose in the fruit we eat is relatively small and can be easily
processed by the liver without causing problems. It is the added sugar and high
fructose corn syrup in processed foods causing the health problems in many
modern societies.


When the liver has stored as much glucose as possible in the form of glycogen, it
will convert the extra glucose into fat, specifically triglycerides. Usually these
triglycerides are transported to fat cells for storage, but if you are somewhat insulin
resistant, the fat cells are not storing triglycerides well. The liver and muscles
become the new “storage sites” for fat. This process damages the liver leading to
“fatty liver disease”, also known as Non-Alcoholic Fatty Liver Disease (NAFLD).
Overloading the liver with glucose and fructose leads to NAFLD.

KEY POINT:
The primary causes of NAFLD are:
• Insulin resistance
• Intestinal permeability (see Gut chapter)
• Excess sugar in the diet

Recent research has shown that a combination of insulin resistance, intestinal

permeability, and excess dietary sugar (especially fructose) causes NAFLD.

High-fructose corn syrup continues to get bad press as a “dietary devil.” Some of
this portrayal as a nefarious character is deserved, but further discussion in the
following “Digging Deeper” section is warranted to establish its role in health
problems in a scientific context.
DIGGING DEEPER:
Why the fuss over high-fructose corn syrup?
High-fructose corn syrup (HFCS) is almost identical to table sugar
(sucrose) when you compare them as chemicals. Most HFCS is 55%
fructose and 45% glucose, while sucrose is 50% fructose and 50%
glucose. Eating either in large quantities can cause health problems,
especially if you have insulin resistance or outright diabetes.

The reason behind the bad press on HFCS is because food manufacturers
add it to most processed foods and fast food to improve taste and
palatability. The primary reason they can do this is because the
government subsidizes farmers growing corn, which makes HFCS very
cheap. Processed food manufacturers can use large amounts of HFCS in
their products more cheaply than sucrose harvested from sugar cane or
sugar beets.

The body can handle small amounts of HFCS or sucrose, but the amount
consumed by the average American is causing health problems.

The average American eats an estimated 80 to 100 pounds of added sugar

in the forms of sucrose and HFCS annually. “Added sugar” simply means
sugar not naturally present in real foods. It is a large part of processed and
fast food.
 This staggering amount of added sugar in our diet is certainly
contributing to NAFLD, obesity, and diabetes. HFCS is not chemically
different from sucrose, but the large amount we are exposed to in
processed food is the real issue.

SUGAR AND “AGE”

Sugar, consumed in large amounts over a protracted period of time, inevitably
creates serious health problems, especially for diabetics. Table sugar and HFCS are
large concentrations of glucose and fructose. Large amounts of these simple sugars
leads to increased formation of Advanced Glycation End-products (AGE). AGEs
are formed when glucose and fructose undergo chemical reactions that allow them
to “stick” to proteins inside and outside cells.

Low amounts of AGEs are normal. They are naturally produced on a constant and
ongoing basis as part of a healthy metabolism. Health problems occur when large
amounts of AGEs form in part from high amounts of sugar and HFCS in the diet,
then trigger inflammation. If the cause is dietary, then we can control it.

Just as there is a receptor, or “dock”, for insulin, leptin, and countless other
molecules in the body, there is a receptor for AGEs as well. This receptor is the
Receptor for Advanced Glycation End-products (RAGE).

When AGEs “dock” with RAGE, an inflammatory response is generated. The

more AGEs present in the body, the more inflammation is produced when they dock
with RAGE. The chronic inflammation from high levels of AGEs, contributes to
accelerated aging of the body. AGE makes you age faster, but we can control this
with diet.

KEY POINT:
As the amount of AGEs increase in the body, so does the level of
inflammation. This worsens chronic diseases and contributes to
accelerated aging.

Fructose forms AGEs eight times faster than glucose. Some organs in your
body—kidneys, brain and blood vessels—will produce AGEs rapidly when
subjected to high levels of glucose and especially fructose. High amounts of
glucose and fructose (as found in high fructose corn syrup) damage these organs
and turn them into AGE-producing machines.

The kidneys and blood vessels prone to AGE-caused inflammation are damaged
in diabetes. Kidney failure, vascular, and heart disease are often seen in long-term
diabetes.

KEY POINT:
When overall sugar is high, the blood vessels and kidneys are especially
prone to forming AGEs. Chronic inflammation from AGEs in these
organs contributes to the high incidence of heart disease and kidney
disease seen with diabetes.

ADVANCED GLYCATION END

PRODUCTS IN FOOD

We have just discussed how levels of sugar can lead to AGE formation
inside your body, but AGEs can also be preformed in the food you eat,
even before it gets into your body.

The type of food and cooking process greatly affects how much AGE is
present. High temperature cooking, such as deep frying, can elevate AGE
formation by up to 100 times.
Animal-based foods are protein-rich and are especially vulnerable to AGE
formation with cooking methods such as frying. Processed foods often
contain sugar and proteins subjected to high temperatures during the
manufacturing process. They are often loaded with AGEs.

Alternate cooking methods can greatly reduce the amount of AGEs in

your food. So-called “moist” cooking methods using water and lower
temperatures (slow cookers/crock pots) are excellent for reducing AGE
formation. Also, adding acidic liquids such as lemon juice and vinegar
will also reduce AGEs formed from cooking.

Making stews, soups, and slow cooker meals are all great ways to prepare
your food to avoid high levels of AGEs, especially if you are diabetic.

STRONG MEDICINE TACTICS:

Reduce AGEs by decreasing sugar and HFCS in your diet and follow low-
AGE cooking methods.

HOW TO ACCELERATE DISEASE

AND AGING: THE NUCLEAR OPTION

If you are diabetic or overweight/obese, the best way to accelerate disease

and aging is to continue to eat fried fast food and processed food. There is
no doubt that fried chicken and French fries from your favorite fast food
restaurant taste amazing. It is why the fast food industry makes billions of
dollars per year from consumers. But, these foods are
inflammation/oxidative stress nuclear weapons in your body:
• The processed vegetable oils (PUFA) used to fry the food create huge
 amounts of free radicals.
• The breading (starch) and protein cooked at high temperatures creates
AGEs by the bucket-load.
• Most of these foods have added sugar and HFCS to make them more
palatable, which potentially increase the AGEs produced in your body.
• Most of these foods have large amounts of gluten that can contribute to
inflammation in the gut if you are sensitive.

These foods taste great and generate strong reward signals in your brain,
but are deadly to your health. If you are obese or diabetic and continue to
eat these foods regularly, you are simply not serious about getting healthy.

The following graphic summarizes how preformed AGEs in processed and fried
food, as well as AGEs generated in the body from high glucose levels—seen with
diabetes and insulin resistance—lead to chronic inflammation and oxidative stress.

SOFT-DRINKS, ENERGY DRINKS,

FRUIT DRINKS: HEALTH-KILLING
SMART BOMBS
Soft drinks, energy drinks, and “fruit-flavored” drinks are devoid of any
nutrition and will slowly wreck your metabolism. If you already have pre-
diabetes, diabetes, or obesity, you need to steer clear of these beverages.

They are all filled with sugar and HFCS. They are taste-engineered to
stimulate your food reward system. Many of us have “soda addictions”
which are hard to kick. Clever marketing is also involved in fruit-drink
labeling such as “made with real fruit”, yet they are all loaded with sugar!
Some children are even showing signs of fatty liver disease in their early
teenage years largely due to soft-drinks, fruit beverages, and energy
drinks.

Energy drinks are hugely popular with teenagers and young adults. Not
only are they loaded with caffeine, but some have almost 3 times the sugar
as a soft drink! Here are some numbers:
• One 12-ounce can of soda can have between 10-15 teaspoons of sugar. A
20-ounce bottle has 16-25 teaspoons of sugar depending of the brand.
• Energy drinks can have as much as 40 teaspoons of sugar in one can!
Most brands have 25 to 30 teaspoons of sugar per can.

Fruit drinks marketed to children can have just as much, if not more sugar
than soft drinks.

WHAT ABOUT FRUIT JUICE?



It is a big shocker for most people, but fruit juices can have just as much
sugar (glucose and fructose) as soft drinks. While juice has some
nutritional value in the form of vitamins and minerals, they also have huge
sugar loads for the body:
• One glass of orange juice is equivalent to 10 teaspoons of sugar.
• One glass of apple juice has 10-12 teaspoons of sugar.
• One glass of grape juice can have up to 15 teaspoons of sugar.

Fruit can be a part of a healthy diet and is a good source of fermentable

fiber, vitamins, and minerals. Remember that it takes 4-6 good-sized
whole oranges to make one 8-ounce glass of orange juice.

Eat the whole fruit rather than the juice to get the nutrition without the
huge sugar load.

HOW DO I KNOW HOW MUCH

SUGAR IS IN A FOOD OR DRINK?
1. Read the label to find the amount of sugar in grams.
2. Divide the number in grams by 4 (there are about 4 grams in 1
teaspoon of sugar). For example, 40 grams of sugar, divided by 4, equals
10 teaspoons of sugar.
3. Watch “serving size.” This is a small deception often used by food and
beverage marketers. The amount of sugar is labeled by serving size. If a
beverage is labeled as having 40 grams of sugar in a 16 oz. bottle, but with
a serving size of 2, you are really consuming 80 grams of sugar if you
drink the whole bottle.
 STRONG MEDICINE TACTICS:
Limit the amount of soft drinks, energy drinks, and fruit juice in your diet.
If you are obese and/or diabetic, cut them out completely.

STRONG MEDICINE TACTICS:

Read food labels to determine how much sugar is in the processed foods
you are eating (If you are eating unprocessed food without a label, you
generally do not have to worry).

STEP 7
INCREASE INSULIN SENSITIVITY WITH
EXERCISE.
Step 7 is probably one of the most powerful ways to increase insulin sensitivity
and help normalize blood sugar for a type II diabetic or insulin resistant obese
person.

Even the conservative Centers for Disease Control (CDC) recommends at least
2.5 hours per week of “moderate intensity” aerobic exercise or 75 minutes per week
of “vigorous intensity” aerobic exercise. They also recommend 2 or more days of
resistance training in addition to aerobic exercise. These recommendations are
often lacking when it comes to exercise specifics—but we have them for you. We
can show you how to get fit with maximal time efficiency.

Out-of-shape people avoid fitness and exercise for a variety of reasons. Some of
their reasons are legitimate—mistreatment by fitness professionals and personal
trainers, incompetent exercise instruction, or from using exercise modes incapable
of producing results. We will guide you through setting up a proven exercise
template used to this day by elite athletes. Every intelligent exercise program needs
a cardiovascular training regimen (builds and strengthens heart and lungs, flushes
arterial highways), and a resistance training regimen (builds and strengthens the 600
+ muscles on the human body.) We will successfully blend these two exercise
modes.

Exercise is one of the best ways to restore insulin sensitivity.

You do not have to spend hours in the gym to obtain the insulin-sensitizing
benefits of exercise. Recent research shows the possibility of getting these benefits
using short exercise protocols—if the protocols are sufficiently intense. Exercise
intensity is measured by the percentage of maximal heart rate achieved during the
exercise.

As a preview to our exercise approach, we will present an abbreviated exercise

protocol that has been tested in a lab with actual diabetic patients, and which showed
excellent results. The key to the success of this protocol is the intensity of the
exercise.

In this case, we are measuring exercise intensity of exercise by the percentage of

maximal heart rate achieved during exercise.

Let’s back up a bit to explain more about exercise intensity before we dive into
the protocol. The CDC defines “moderate intensity” exercise as anything that gets
your heart rate between 50% and 70% of your maximum. “Vigorous intensity” is
defined as exercise that causes heart rates between 70% and 85% of maximum.

WHAT IS MAXIMUM HEART RATE?

The maximum heart rate (HRmax) is the highest heart rate you can expect
to achieve during exercise. HRmax is mostly affected by a person’s age—
the older you get, the lower your maximal heart rate. In other words, a
younger person can generally achieve a higher heart rate during exercise
than an older person.

HRmax varies considerably among individuals, but some general

formulas have been developed to provide reasonably good estimates of
your personal maximum heart rate. We used to rely on the simple “220
minus age” formula to calculate HRmax, but that was found to be
 relatively inaccurate.

Some of the more recently developed formulas will better suit our
purposes for determining your HRmax:

For men: 208 - (0.7 X Age) = HRmax

For women: 206 - (0.88 X Age) = HRmax

Example 1: Chris is 43 and wants to calculate his maximum heart rate. He
will multiply his age (43) by 0.7, which equals 30.1. He will then subtract
30.1 from 208 to get 177.9 (we will round to 178). So Chris’s HRmax is
about 178 beats per minute.

Example 2: Carrie is 46 years old. To calculate her HRmax, she would

multiply her age (46) by 0.88 to get 40.5. She would then subtract 40.5
from 206 to get 165.5 (we will round up to 166). Carrie’s HRmax is 166
beats per minute.

Following the CDC’s recommendations for “moderate” intensity exercise, Chris

needs to keep his heart rate between 50% and 70% of his maximum heart rate during
exercise. He will take the HRmax of 178 that he just calculated and multiply that
number by 0.5 (50%) and 0.7 (70%):

• 178 X 0.5 = 89 beats per minute

• 178 X 0.7 = 125 beats per minute

When Chris is exercising at “moderate” intensity for 2 1/2 hours per week
as recommended by the CDC, he will keep his heart rate between 89 and
125 beats per minute.

Carrie decides she doesn’t have 2 1/2 hours per week to devote to exercise, so she
is going to exercise with a little more intensity. She wants to go into the heart rate
zone the CDC classifies as “vigorous.” With this intensity she only needs to exercise
for 75 minutes (half the time of the moderate exercise goal) per week.

Carrie uses the HRmax she just calculated and figures out her “vigorous” target
zone of 70% to 85% of her HRmax. She takes her HRmax of 166 beats per minute
and multiplies this number by 0.7 (70%) and 0.85 (85%):

• 166 X 0.7 = 116 beats per minute

• 166 X 0.85 = 141 beats per minute

When Carrie is exercising at a “vigorous” intensity for 75 minutes per

week as recommended by the CDC, she will keep her heart rate between
116 and 141 beats per minute.

Exercising 3 times per week, Chris will need to work for 50 minutes per session
to get his 2 1/2 hour total at moderate intensity.

Carrie will schedule 25 minutes per exercise session, 3 times per week for her 75
minute weekly total at a vigorous intensity.

EXERCISE TIP:
Do not rely on the heart rate monitors built into the handles of exercise
machines. They are notoriously inaccurate. Invest in a personal heart rate
monitor with a chest strap and watch receiver. This is a worthwhile
investment if you are serious about your fitness.

HIGH INTENSITY BEATS MODERATE OR VIGOROUS

INTENSITY
High intensity, short duration exercise protocols have more physiological
benefits than the “steady-state” exercise recommended by the CDC. One of these
protocols, High Intensity Interval Training (HIIT), is especially beneficial to people
who are insulin resistant. As the name implies, HIIT is exercise ramped up to a high
intensity for short bursts. For example, a burst or sprint, stop and recover, burst or
sprint again, over and over until the session is complete. This method has been
shown to reduce high blood sugar as seen in type II diabetes and prediabetes.
 HIGH INTENSITY INTERVAL
TRAINING PROTOCOL
The HIIT protocol involves pushing your heart rate to approximately 90%
of your maximum heart rate for short periods of time with rest breaks in
between. Let us use Carrie as an example:

Carrie has already calculated her HRmax at 166 beats per minute, then she
multiplied her HRmax by 0.9 (90%) to get approximately 149 beats per
minute.

• 166 X 0.9 = 149 beats per minute (her target heart rate).
• While wearing her heart rate monitor, Carrie will choose a piece of
cardio equipment such as a bike, elliptical, treadmill, stair climber, etc.
• She will start at a slow pace for 2-3 minutes to get her muscles warmed
up.
• She starts exercising as hard as possible to get her heart rate up to her
target of 149 beats per minute, and continues until the 60 second interval is
complete.
• After the 60-second exercise interval, she will rest for 60 seconds (or
pedal/walk very slowly).
• After resting for 60 seconds, she will start another 60-second exercise
interval to achieve her target heart rate of 149 beats per minute.

Carrie will repeat this pattern for a total of 10 60-second exercise intervals
before cooling down for 2-3 minutes.

The HIIT protocol is only 10 total minutes of exercise (10 60-second intervals),
and 10 total minutes of rest (10 60-second rest periods). These intervals combine to
only 20 minutes in total—and you are done. “I don’t have time for exercise” is no
longer a valid excuse.

KEY POINT:
The most common excuse for not exercising is “I don’t have enough
time...” If that is the case, then use the HIIT protocol.

Short bursts of activity at a high intensity, followed by rest periods has been
shown to be just as—and in many cases more—effective as traditional sustained
lower intensity exercise. While Chris is plugging away for 50 minutes of
“moderate” intensity exercise, Carrie has finished her workout, showered, and is
back to the day’s business. Despite the short duration of her workout, she has also
gained some advantages that Chris won’t get from “moderate” intensity workout.

The benefits of short duration high intensity training come from the effect it has
on glucose storage in muscles.

FLASHBACK
Quickly review concept #3 and #10 in the Metabolism Basics section,
before reading onward.

As intensity is increased from “moderate”, “vigorous”, and finally to the 90%

HRmax seen in our HIIT protocol, more glucose is used by the muscle for energy.
This is because the body cannot supply oxygen to the muscle fast enough to keep up
with the demands of high intensity exercise. As a result, the muscle is forced to use
glucose without oxygen for energy. This produces lactic acid buildup as a waste
product, and starts to empty the muscles of their stored supply of glucose. Fat needs
oxygen to be used as fuel, so the low oxygen in the muscles during intense exercise
shifts the primary fuel source to glucose.
 Wait a minute! I want to burn fat with exercise. You are saying that I
will mostly be burning glucose with the HIIT protocol, and I want to get
rid of fat!

You will burn plenty of fat during the rest periods and after this workout,
especially. This type of high intensity workout will keep your metabolism
working at a higher rate for the next 24 to 36 hours, and will primarily burn fat
as fuel. The point of burning up all of this glucose will become evident in the
following discussion.

The reason we want to use high intensity interval exercise to empty the muscles’
storage supply of glucose is because of what happens after the exercise. As far as
your body and brain are concerned, the high intensity exercise may have happened
because you ran from a wild animal to escape getting killed. Your body wants to
replenish the supply of glucose in case you need to escape from an animal again in
the near future. You know that you are riding a bicycle, and not running from a
predator, but your body responds to the high intensity stimulus as a threat and wants
to make sure you are prepared to survive for another day.

In response to the high intensity exercise “threat,” the muscle does a neat trick and
bypasses the insulin signaling mechanism we saw in the “Diabesity” section. After
intense exercise, muscle cells do not need an insulin signal to open the glucose
transporters to let glucose in from the bloodstream. Even if you have substantial
insulin resistance, after intense exercise the glucose transporters are “unhooked”
from the insulin signal. Going back to our “electronic door” analogy, high intensity
exercise is like installing a manual door-opening mechanism which bypasses the
insulin receptor ’s electronic door system.

High intensity interval exercise not only opens the glucose transporters, but it
also signals the muscle to make more glucose transporters. This allows the glucose
that has been accumulating in a diabetic’s bloodstream to push its way into the
muscle cells, thus lowering blood sugar.

KEY POINT:
After intense exercise, muscle cells do not need a signal from insulin to
 open the glucose transporters to let glucose in from the bloodstream.

The great thing about high intensity exercise is that the benefits continue for the
next 1-2 days after a single 20-minute session. Glucose transporters stay active well
into the next day. When this protocol was tested on diabetics, not only was their
fasting blood sugar lower the following day, but their blood sugar levels after
meals were also lower for 24-36 hours after the workout.

This is the normal state of a type II diabetic (let’s call him Jim) with bloated fat cells
spewing out inflammation which blocks the insulin signal from opening the glucose
transporter. Glucose is left in the bloodstream and builds up to toxic levels.

Jim is not engaging in any exercise at this point because he thinks that he doesn’t
have time to spend hours in the gym.
Jim has now started a high intensity exercise protocol. He likes the fact that he only
has to spend 20 total minutes a day, with only 10 minutes of actual exercise. Jim has
calculated his HRmax and is using the HIIT protocol with a target heart rate of 90%
of his HRmax.

The high intensity intervals are decreasing his muscle glucose storage, and the
muscle responds by “unhooking” the glucose transporters from the insulin signal,
and by making more transporters.

The fat cells are still shooting out inflammation which block the insulin signal, but
it does not matter since the transporters have “bypassed” the insulin signal. Glucose
from his bloodstream is now pouring into his muscles and is decreasing his blood
glucose levels.

To grasp the concept, it may be easier to think of your muscles as “containers” that
store glucose (as glycogen) for emergencies like running from a bear. HIIT
depletes muscle glucose and creates an open storage area for the glucose from the
bloodstream. If you did not deplete the muscle glucose with HIIT, the extra glucose
would build up in the bloodstream causing high blood sugar, or it would be
converted and stored in the fat cells as fat.

For these reasons, HIIT is a very powerful protocol for diabetes and pre-diabetes.
It can substantially help keep your after-meal blood glucose levels within the target
ranges discussed in earlier sections.

If you consistently apply this protocol with a proper diet, over time the better
blood sugar control will result in increased insulin sensitivity. The pancreas will
now secrete less insulin because there is less glucose in the bloodstream for it to
process.

Also, now that the extra glucose will be stored in the muscles, the fat cells will
not need to process the excess glucose and turn it into fat for storage. The fat
cells will start shrinking, and return to their “happy state” with decreased
inflammation.
This is how you lose fat with HIIT

As fat cells return to their normal size over time, the decrease in inflammatory
cytokines will also increase insulin sensitivity. Chronic inflammation is a major
cause of “broken” insulin signaling. You can modify the HIIT protocol to fit any
type of exercise. You just need to ensure your heart rate is sustained at 90% of your
HRmax for 60 seconds. Find the exercise or equipment that works for you.

In the exercise chapter we will discuss other high intensity exercise strategies and
resistance training extensively. Resistance training coupled with HIIT will give
diabetes and prediabetes a knockout punch!

IMPORTANT MEDICAL NOTE:

 As beneficial as high intensity exercise is for diabetes, it is extremely
important that you first discuss it with your doctor before starting a
protocol like HIIT. This is especially true if you have had prior heart
attacks or chest pain with physical exertion. If you fall into these
categories, you MUST get approval from your physician first for safety
reasons. There are plenty of other exercise routines that you can safely do
and that will still be beneficial. We will cover some of these in the exercise
chapter.

HIIT is highly beneficial, but make sure your heart can tolerate high
intensity exercise before you dive in.

STRONG MEDICINE TACTICS:

Once cleared by your doctor, high intensity interval training is a great
method if you are short on time. Incorporate three sessions a week of HIIT
in your exercise program.

STEP 8
FIX YOUR SLEEP AND USE STRESS
REDUCTION TECHNIQUES.
If you are not getting at least 7-9 hours of restful sleep per night, your fat loss and
blood sugar control goals will come to a screeching halt.

We are going to extensively discuss sleep and stress reduction in following

chapters, but will get started with the main points.

Studies have shown that more than a third of adults in the U.S. are getting
inadequate sleep—and the health consequences are more than just being tired the
next day.

Sleep deprivation is a large stressor and turns on the body’s “threat response.”
Part of the threat response due to poor sleep is increased oxidative stress and
inflammation.

KEY POINT:
Poor sleep triggers your body’s threat response.

Just 1-2 nights of poor sleep have been shown to put healthy people into a nearly
diabetic state of insulin resistance! Imagine what this would do to someone who is
already obese or has prediabetes or diabetes. Poor sleep also promotes weight gain
as a likely effect of chronic insulin resistance.

Although the amount of sleep one needs can be substantially different among
individuals, The National Sleep Foundation recommends between 7-9 hours of sleep
per night for adults.

KEY POINT:
Inadequate sleep leads to inflammation and oxidative stress, making
insulin resistance and other chronic diseases worse.

STRONG MEDICINE TACTICS:

To stop making insulin resistance and weight gain worse, ensure you are
getting between 7-9 hours of sleep per night.

We are not going to delve any deeper into sleep here, since there is a whole
chapter devoted to it later in this book. Just be sure to make sleep a priority; you
will not achieve your weight loss goals or healthy blood sugar levels without
consistent, adequate sleep.

Chronic psychological or “life stresses” also activate the threat response in the
brain, leading to chronic inflammation and oxidative stress. Stress reduction
techniques are crucial for the chronically stressed and will be covered in detail in a
forthcoming chapter devoted to chronic stress.

COMING ATTRACTIONS >>>

Make sure you read the Chronic Stress and Sleep chapters to fully
understand the concepts, then incorporate the recommendations from
those chapters into your 8-step plan.

PARTING THOUGHTS ON THE 8-STEP

PLAN:
In closing, make sure you pay close attention and adhere to as many of the 8 steps
as possible. In doing so, you will achieve better and faster results. It is important to
note that use of Step 1 will vary depending on your situation. If you are not diabetic,
testing your blood sugar after meals a couple of times can still give you valuable
information. If you have prediabetes or diabetes, Step 1 is extremely important to
follow until you figure out what foods consistently put you out of the target ranges
for blood sugar.

The key to this 8-step program is consistency, and the enemy of the program is
convenience. Preparing good food is time consuming, and getting fast food is
convenient.
 KEY POINT:
Consistency is your friend with the 8-step plan.
Convenience is the enemy.

Spend a couple of hours on a weekend to prepare a large quantity of food for

your lunches the following week. Soups and stews work well because they are
relatively easy to make in large quantities. We will cover more of these ideas in the
Strong Medicine Nutrition: Individualized Strategies chapter near the end of the
book.

Over time, consistency with the 8-step plan will lower chronic inflammation and
oxidative stress, fix your leptin signaling, restore insulin sensitivity, and help you
achieve your weight loss and blood sugar goals without counting calories and being
constantly hungry.

“BREAKING THE LINK”

The Strong Medicine 8-Step Program for Obesity and Insulin Resistance will “break
the link” in the chain between obesity/insulin resistance and chronic disease, thus
defeating the “enemy within.”
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KNOWING YOUR ENEMY III:
CHRONIC STRESS: THE SILENT
KILLER

Chronic psychological stress affects us all to varying degrees. Psychological

stress is a serious problem that can lead to physical maladies.

Sustained stress in particular causes tangible, medically definable harm to the

body and brain. Chronic stress causes premature ageing while those who have
conquered stress look years younger than their chronological age.

Very real physical changes occur to those who have continual chronic stress.
Chronic stress can be overcome by using proven stress-relieving strategies and
methods. Stress has been called the silent killer, but can be overcome with
knowledge and a game plan.

Chronic stress is a master assassin that kills with a thousand small cuts over time.
He will worm his way inside your brain and wreak havoc. As you will see, this
silent member of the Pentaverate will actually change your brain and affect your
body from the inside.

The Strong Medicine training team has studied the ways of this killer and devised
effective defenses against him.
CHRONIC STRESS AND DISEASE
Recent research has linked chronic stress to a multitude of diseases. For many of
these diseases, stress is either thought to be the actual cause of the disease, or at the
very least, stress makes any disease worse.

DISEASES ASSOCIATED WITH

CHRONIC STRESS

• Obesity
• Diabetes
• Alzheimer’s dementia and other neurodegenerative diseases
• High blood pressure
• Heart disease
• Depression and anxiety
• Chronic pain
• Cancer

Even with the association of chronic stress to the above diseases, most patients do
not bring up their chronic stress when discussing their health concerns with their
doctor, and most doctors don’t ask their patients about stress levels. There are
roadblocks for having this crucial discussion...

• Many physicians feel they are physical custodians, not mental custodians, and
refuse to offer advice or recommendations regarding stress reduction.

• Most physicians don’t have specific advice or recommendations to give their

patients to effectively reduce stress.

• Chronic stress is still not recognized as a serious risk factor leading to disease.

• Historically there have been no good medical tests to evaluate chronic stress.
 This is starting to change.

• Mental health and physical health are still viewed as separate and distinct and
obviously that is flawed thinking.

Your mental health is really an extension of your physical state. Mind and body
need be addressed as an organic whole. Chronic stress will prevent us from
attaining any and all body-composition and fitness goals.
CHRONIC STRESS I
MIND AND BODY: WAS DESCARTES
WRONG?

Rene Descartes
(1596- 1650) French
mathematician and
philosopher

Rene Descartes (1596 - 1650) was a brilliant 17th century mathematician and
philosopher widely considered the father of modern philosophy. One of his central
philosophical tenets is the idea of dual nature—we have a mind and we have a body.
Descartes proposed the theory of mind-body dualism—the body and the thinking,
conscious mind exist in separate parallel universes. For Descartes, the body was a
material object following the laws of nature, while the thinking conscious mind was
“nonmaterial,” and not subject to these laws. He contended that the body and mind
can influence each other, but ultimately remain separate and distinct.

Descartes’s philosophy founded the idea that psychology and neuroscience are
separate and distinct disciplines—and should remain that way. Psychology deals
with the “non-material” thinking mind while neuroscience explores the actual
mechanical workings of the physical brain. Increasingly, modern science is
discovering that this is not how the mind and body function. Both form an
intertwined, indivisible whole. New fields of study such as neuropsychology and
psychoneuroendoncrinology explore this mind/body connection.

UNION OF MIND AND BODY

Our conscious and subconscious mind is responsible for so many things on many
levels. The brain is Command Central, Headquarters, the place where projection and
reflection reside. It is able to switch tasks, compute, calculate, interface ongoing
changes in our environment, then determine our next actions and reactions.
Consciousness always occurs in the exact present time.

The brain monitors critical operations of the body, such as the second to second
function of the heart and lungs for example. Though the brain itself is a physical
organ, it has produced the non-physical consciousness of our mind and is able to
manifest our intellect, personality and behavior. The actual physical brain is
constantly shaped, changed, and literally reconfigured, based on our
experiences, thoughts and perceptions.

THE CHANGING BRAIN

Ideas, thoughts, attitudes and perceptions can literally change the brain’s
“hardwiring.” New technology now allows us to track these brain circuitry changes.
Brain plasticity is not new age nonsense designed to fleece hippies—technical
advances are allowing us to actually see how the human brain can rewire itself. If
the rewiring is in response to repeated, ongoing physical and psychological stress,
then it is a bad thing—but, if the rewiring is in response to activating new and
exciting areas of the untapped brain, then it is a fabulous thing.

Change to the physical structure and function of the brain in response to internal
and external stimuli is known as neuroplasticity. The original definition of the
word plastic is, “Easily modeled or molded, capable of adapting to various
conditions.” The human brain is “plastic” as well, and can mold or adapt itself to
various conditions throughout a lifetime.

KEY POINT:
Neuroplasticity refers to the brain’s ability to physically change its
structure and function to adapt to changing environmental conditions.

The most current research shows that the human brain contains approximately 86
billion nerve cells (neurons) and almost an equal amount of “support cells” (glial
cells). There are about 25 times more cells in a single human brain than there are
people on the planet. Even more mind-blowing is the fact that each of the 86 billion
nerve cells can form up to 1000 connections with other cells in the brain. The total
number of potential connections formed between nerve cells has been estimated at
several hundred trillion. The possibilities are literally endless.

Let us take a look at the nerve cells and how they make these trillions of
connections.

The synapses, or “connections” between axons and dendrites of neighboring

nerve cells are “made” and “unmade” constantly, depending on environmental
circumstances. The making and unmaking of these connections is the definition of
neuroplasticity.

The picture above is a drawing of a nerve cell (neuron):

• The cell body of the neuron is the cell’s “control center” and the
location of the energy-producing machinery keeping the neuron alive.
• The dendrites receive signals from the other nerve cells. You can think
of them as satellite dishes receiving incoming transmissions to the neuron
cell body.
• The axons transmit signals from the nerve cell to other nerve cells in
the brain, and also to other cells (like muscle cells) in the body.

The light blue “blocks” covering the axon in the picture above act as
insulation allowing the signals transmitted by nerve cells to travel farther.
This insulation is called myelin, and acts just like the insulative coating
around electrical wires, which allows electricity to flow without “short
circuits.”

THE ULTIMATE WIRING DIAGRAM

Billions of nerve cells communicate with each other via the dendrite
“receivers” and the axon “transmitters.” This graphic only shows 6 nerve
cells (neurons) connecting and communicating. Imagine the complexity
of billions of nerve cells each forming up to 1000 connections!

The yellow glow at the connection (synapse) of an axon “transmitter”

between one neuron to the dendrite “receiver” of another neuron
illustrates the communication signal passed along the chain of neurons.

This is how your brain communicates within itself and the rest of the body.
When you want to move your leg, this is how the signals pass from the
 brain all the way to your muscles to tell them to move. This system is also
how the body communicates changes in your outside environment to the
brain. This is how signals about touch, taste, smell, sight, hearing, heat,
cold, and danger are communicated from body to brain.

KEY POINT:
Neuroplasticity occurs because of nerve cells making and unmaking
connections. This process can start just minutes after a new stimulus to the
brain.

Like a muscle, the human brain has a “use it or lose it” quality. When we stop
performing regular physical activity, our muscles shrink, and bones become brittle.
Stressing our body purposefully and intelligently with exercise halts these negative
physical processes. The brain is no different.

Your brain will adapt to the challenges you give it by forming new connections.
Without challenges, the circuit connections wither away. We challenge the brain by
taking on new and mentally complex tasks outside our normal scope of activities.
This includes difficult tasks like learning a foreign language, taking up a musical
instrument, reading classical literature, composing poetry, sculpting, painting, or
mastering another new and different skill. There are two elements critical to
invoking positive brain plasticity. First, the new skill needs to be different from the
skills you already possess—new skills activate new regions of the brain. Second, the
skill needs to be sufficiently complex—we need intellectual stimulation, not
moronic “stupefaction.”

Mental challenges cause an “adaptive response” to take place in the brain, just like
a muscle. Challenges build axon-dendrite “transmitter-receiver” connections.
Passive activities such as watching “reality” television do not stimulate or build
these connections. We need to be actively involved with our activities, instead of
being passive observers. Making and unmaking nerve cell connections
(neuroplasticity) dictates how well the brain can handle stress.

THIS IS YOUR BRAIN ON STRESS

 Stress actually changes the brain’s structure and function through neuroplasticity.
Brain cell changes and alterations will affect how you think, act and behave. The
duration and intensity of psychological stress makes a huge difference in how the
brain responds to stress.

• Isolated, short-term stresses such as an argument with your friend or spouse,

final exam week at college, or an unexpected expense temporarily causing
financial stress, can all actually lead to resiliency. Resiliency means that after the
short-term stresses, you rebound and are able to deal with future stresses that
come along much better. Think of the difference between a college freshman
going through her first exams, versus a graduate student who has spent the last 4-
5 years dealing with exams. The graduate student is much less stressed about
exams than the freshman. The grad student has survived the short-term final exam
stress many times before and is now more resilient. Her brain has made axon-
dendrite “transmitter-receiver” connections that allow her to deal with the stress
of final exams better. The freshman is just starting the process of building the
brain connections that enhance exam resiliency.

FLASHBACK
Do a quick review of Central Themes IV, “Stress and the Response to
Threat,” before you read on.

The freshman has never encountered this level of exam stress before and
her brain registers the exams as a significant threat. This produces the
threat response. The graduate student’s brain, fortified against the stress of
final exams from years of experience, perceives the exams as far less of a
threat. Short-term, intermittent stressors of relatively low intensity will
build resiliency to future stress and decrease the threat response.

KEY POINT:
 Occasional, relatively low intensity stressors will build resiliency and
protect you from future stress through “re-wiring” the brain
(neuroplasticity).

• Chronic stress, or high intensity stress alters the brain much differently, and
much more radically—in a negative, detrimental way—than short term, low
intensity stress. Chronic stress and high intensity stress (such as combat stress,
auto accidents, or other traumatic events) alter brain “transmitter-receiver”
connections that strengthen the stress response over time to threats. The
connections that strengthen the stress response do not make you more resilient to
future stress; instead you become more vulnerable to the effects of psychological
stress. Intense trauma makes you more sensitive to threats in your daily life.

Many of us under chronic stress can relate to having “little things” set us
off, and not being able to handle minor stresses that we used to take in
stride. This feeling of being always “stressed out” is because our brain’s
threat system has been rewired in response to chronic stress. From a
strictly survival standpoint, your brain is trying to protect you from a
persistent threat. Remember from Central Themes IV that the brain’s threat
response doesn’t know if your “threats” are a nasty boss at work, financial
worries, or dealing with a troubled teenager. All it knows is that you are
under a daily “threat” and it responds by strengthening your threat
response. The problem is, the strengthened long-term threat response
is not good for your health.

KEY POINT:
Chronic stress “re-wires” the brain to strengthen the stress response to
threat. This physical change in the brain will make you more sensitive to
 future stress with poor long-term health effects.

We will diagram the “re-wiring” of the brain to help you visualize what happens
to certain regions of the brain during chronic stress. The Hypothalamic-Pituitary-
Adrenal axis (HPA axis) is a “hard-wired” stress response system. The HPA axis and
the Sympathetic Nervous System produce stress hormones such as cortisol,
epinephrine, and norepinephrine. These hormones are released when preparing for
a “fight or flight” situation.

THE HPA-AXIS: HYPOTHALAMUS-

PITUITARY-ADRENAL
• The fast pathway is triggered immediately after the brain senses a
threat. It bypasses the pituitary and sends a direct signal to the adrenals to
produce epinephrine (adrenaline) and norepinephrine. This pathway
immediately puts you in an alert state, and prepares you to “fight” or
“flee” from danger.
• The slow pathway is also triggered by threats, but responds slowly,
signaling the adrenal gland to secrete cortisol. Cortisol helps you recover
from the threat after it has passed.

The HPA axis induced hormones—cortisol, epinephrine, and norepinephrine

have the following actions on the body and brain:

• They increase the energy available to the body by increasing blood sugar.
 • They increase heart rate and blood pressure.
• They increase blood flow to muscles
• They produce hyper vigilant behavior (watchfulness, anxiousness, alertness)

The HPA axis—both slow and fast pathways—is triggered in response to any
stress perceived as a threat by the brain. It is a well-designed system, but is only
meant to operate in response to “threats” in our environment.

The fast pathway triggers the sympathetic nervous system (flight or fight). The
result is the release of epinephrine (adrenaline), and a hormone that closely
resembles epinephrine called norepinephrine. Both of these hormonal messengers
increase alertness, release stored glucose from the liver into the bloodstream,
increase heart rate, stop digestion, and increase blood supply to the muscles—all in
anticipation of either fighting hard or running away fast. This particular pathway
will make you jittery after a heated confrontation or disoriented after a car accident.

The slow pathway goes through the pituitary gland on the way to the adrenal
glands. This pathway is the most active about 30 minutes after the threat has passed.
Cortisol is the primary hormone that helps you recover from the threat, and it
prepares the body and brain for any future threats. Cortisol releases glucose from
the liver to ensure the brain has enough fuel to deal with the threat. Cortisol will
also “assist” in breaking muscles down (muscle cannibalism) so the amino acids in
the muscle protein can be used to make more glucose for the brain. In certain
circumstances, cortisol helps the body eat itself. One reason many marathon and
ultra-marathon runners look emaciated is they are awash in cortisol to the point that
caloric shortfalls are fed with the runners’ own muscles.

As far as our
brain is concerned,
many of us are
 “chased by bears”
daily.

This system was never meant to be used daily. A majority of the population
overuses and over-works this system in response to modern threats such as abusive
bosses, snarled traffic, domestic relationship and financial problems or poor sleep.

As far as our brain is concerned, many of us are “chased by bears” daily. While
the degree to which the system is activated will not register as high as actually being
chased by a bear or an assailant, we still activate it in lesser degrees when
responding to the constant daily stresses of modern life. Our stresses add up to the
proverbial “death of a thousand cuts.”

THREAT AND THE STRESS RESPONSE

What determines if the HPA axis is activated to produce the stress response?
Anything the brain perceives as threatening from within the body or from our
external environment will activate the HPA and produce a stress response.

• Potential threats arising within the body include infection, injury, toxins or
sickness. Internal threats do not have to be processed by higher levels of the
brain. The subconscious perceives the internal threat and triggers the HPA axis to
greater and lesser degrees.

• Higher levels of the brain process external threats that arise in our environment
and enter into our consciousness. External threats require a series of “decisions”
which need be made—the seriousness of the threat is assessed, and a course of
action is devised.

KEY POINT:
Potential threats from our external environment are first processed by
higher levels of the brain before they are determined to be threatening or
non-threatening.

Degree of threat and threat response will vary radically from individual to
individual. What is perceived as threatening to one person is considered no threat
whatsoever to a harder type. The difference between individuals in the perception of
threat is experiential: a Navy SEAL under fire during combat will show a lower
threat response and less agitation than a distraught teenager dumped by a boyfriend
or girlfriend.

For simplicity’s sake, our discussion will be limited to the three parts of the
higher brain instrumental in perceiving threats and initiating the stress response.
The workings of the brain are staggeringly complex, and the following is
substantially simplified from the current science of the brain and threat response.
Let’s meet the main players in this game:

• The Prefrontal Cortex (PFC)

• The Hippocampus
• The Amygdala

THE PREFRONTAL CORTEX (PFC)

The PFC is the area in the front of your brain (behind your forehead)
responsible for what brain scientists call “executive function.” Executive
function is the description given for tasks such as:
• Assigning “value” to something (“good” versus “bad”).
• Paying attention to something.
• Controlling your behavior (you lose this when you are drunk).
• Solving complex problems, and task switching (commonly called multi-
tasking).
• Distinguishing “same” versus “different” when viewing two objects.
The PFC can help stop a stress response by the HPA if executive
function is intact. The PFC is one of the brain structures that separates us
from animals. It helps us evaluate a potential environmental threat by
“thinking” about it before deciding if it is threatening or not. Animals
don’t have the executive function, and react to potential threats
instinctively without “thinking” about it.

THE HIPPOCAMPUS

This part of the brain is thought to be responsible for functions such as:
• Putting short-term memory into long-term memory (learning).
• Forming memories of “new” situations or environments.

The hippocampus is one of the only areas in an adult brain that

regularly grows new nerve cells. The hippocampus also helps stop stress
responses from the HPA axis by recalling memories about your
environment when you come across a potential threat you have seen
before.

THE AMYGDALA
The amygdala is an area of the brain in charge of:
• Forming memories associated with strong emotions.
• Controlling aggressive behavior.
 • Controlling emotional reactions.

The amygdala can activate the stress response by the HPA axis. It is
also the structure of the brain responsible for “learned fear.” For example,
hearing a bell does not provoke fear for most people. However, if every
time you heard a bell ring you received a painful electric shock soon after,
you would quickly learn to “fear” the sound of a bell. This is an example
of a learned fear produced by the amygdala.

When working properly, the PFC hippocampus and amygdala act together to
produce stress responses appropriate to the threat. The three will also halt the stress
response when the danger has passed—an overactive stress-response system is
counterproductive and detrimental.

The PFC and hippocampus can stop the stress response by using executive
function and memory to determine that something is not really a “threat.”

The amygdala triggers the stress response to external stimuli in the environment
that are perceived to be “threats.”
 This is the normal “threat-stress circuitry” in the brain of a healthy person.

The PFC and hippocampus can stop the stress response by using executive
function and memory to determine that something is not really a “threat.”

The amygdala triggers the stress response to external stimuli in the environment
that are perceived to be “threats.”
CHRONIC STRESS REWIRES “THREAT-
STRESS” CIRCUITRY
The hippocampus is especially sensitive to over-activation of the HPA-axis. Over
time, the high levels of cortisol from chronic stress will actually shrink the
hippocampus, reducing its function. Studies using special types of MRI have shown
that people under chronic stress (and people with depression) have smaller,
shrunken hippocampi, which are decidedly smaller than those in healthy people. The
mechanisms and rationale for how and why stress shrinks the hippocampus include:

• Decreased dendrite “receiver” and axon “transmitter” connections between

bundles of nerve cells.

• Decreased formation of new neurons in the hippocampus. The hippocampus is

one of the few regions in the adult brain that regularly produces new nerve cells
(neurons). The hippocampus relies on the formation of new nerve cells to
maintain its numbers. When fewer new nerve cells are formed, the overall
population decreases, shrinking the entire hippocampus.

The shrinking hippocampus results in poor short-term memory and problems

when coping with new situations and environments. A shrunken hippocampus is
woefully ill prepared to deal with stress, and does a poor job of controlling the
activation of the HPA axis.

The nerve cells in the prefrontal cortex (PFC) also shrink. The dendrite
“receivers” shrink, due to high cortisol levels released by chronic stress. When the
dendrite “receivers” shrink, they cannot form as many connections with other nerve
cells. These connections are critical for cell communication. The “executive
function” of the PFC is also diminished. Without good executive function, we have
trouble paying attention, controlling our behavior, solving complex problems,
organizing thoughts and distinguishing “good” from “evil.”

Chronic stress changes the amygdala in a opposite way as compared to the PFC
and the hippocampus. “Receiver-transmitter” connections between nerve cells in the
amygdala will grow stronger and more numerous in response to continual chronic
stress. High fear and anxiety levels increase the activation of the HPA-axis. The
strengthened amygdala can result in increased aggressive behavior.

Physical changes due to chronic brain stress include:

 • Non-threatening stimuli are perceived as “threatening” to the stressed-out brain.
Tension and stress provoke the HPA-axis stress response causing a decrease in
function of the PFC and the hippocampus. Stress strengthens the amygdala and
these effects combine to create stress responses to events that were previously
non-threatening. Many of us in modern society are “set off” over trivialities,
which causes us to engage in aggressive behavior like “road rage”, overreacting,
or snapping at friends and family over minor issues.

• The poorly functioning PFC and hippocampus do not allow us to evaluate

situations well using our higher brain functions. We start reacting to things much
like animals do. One way to view the physical changes of chronic stress is that
our brains will function in a more “animal-like” way.

• More stress leads to higher threat perceptions, which leads to more activation
of the HPA-threat system. More HPA-axis activity leads to higher cortisol and
adrenaline, which leads to poorer function of the PFC and hippocampus. This is a
vicious cycle of chronic stress and has real health consequences.

THE “STRESSED-OUT BRAIN”

Notice the shrinking of the PFC and the hippocampus along with the strengthened
amygdala. These changes will result in an overactive threat response and HPA-axis
 activation.

The environment can physically alter our brain. It not only affects our physical
health, but can alter our behavior and even our personality. If Descartes were living
in our modern age, would he change his assessment based on what modern science
has discovered in respect to the mind/body?

FIRST PRINCIPLES PERSPECTIVE:

STRESS AND BRAIN CHANGES

What advantage would physical changes in the brain in response to

chronic stress give us? If you take us out of modern society for a minute
and think about what chronic stress might mean in a different
environment, these brain changes may make more sense.

If an individual from a primitive society was under a constant threat from

his or her environment—predators, aggressive neighboring tribes—it
would make sense for the brain to change to help this person survive. If
the brain changes to interpret most things in the environment as a potential
threat (whether they are or not), the person will never be caught off guard.

They will always be alert and anxious about every noise in the woods at
night, and it would be unlikely that a predator or human enemy could
sneak up and kill them. They are always ready for “fight or flight.”

In this primitive, survival situation, it seems better for them to react to the
unknown like an animal, instead of using any higher brain functions (PFC
and hippocampus) to further evaluate the “threat.” In the long-term, this is
bad for their overall health, but it could certainly help them live another
day in a dangerous environment.
CHRONIC STRESS II
STRESS AND HEALTH

THE “NEGATIVITY BIAS”

Human beings are hard-wired to react more strongly to negative things in our
environment than positive things. Due to our higher brain function, we are generally
much more capable at evaluating potential threats than an animal, but we still carry a
“negativity bias.”

In psychology, a negativity bias means that a negative stimulus (pain, conflict,

criticism) will elicit a much stronger reaction and memory formation than a
positive stimulus (comfort, reassurance, compliment) of equal intensity. Many of us
intuitively know this is true from our own personal experiences.

• One critical comment from a supervisor can erase ten previous compliments
from your mind.
• One argument or fight with a friend can end a friendship that has existed for
years.
• We learn more from making mistakes than we do by “getting things right.”

The negativity bias exists, and our brain reacts this way for a reason.
 FIRST PRINCIPLES PERSPECTIVE:
NEGATIVITY BIAS
We already discussed the survival advantage for the brain changes from
chronic stress. These changes can be thought of as an extension of the
negativity bias. The negativity bias helps us survive when exploring a new
environment or situation.

If a situation is perceived by the brain to have an equal amount of negative

and positive characteristics—such as a potential source of food located
close to an aggressive bear ’s home—the potential danger from the bear
gets a stronger response from the brain than the potential benefit of
getting the food. Even though food is necessary for survival, the potential
danger from the bear may stop you from pursuing this food source.
Starvation is surely a threat, and acquiring the food is a powerful positive
reward, but the bear is potentially an immediate danger to life and limb.
The negativity bias wins the day for immediate survival.

Knowing about the negativity bias may help you moderate your reactions to
negative events and stimuli. Our higher brain functions allow us to override systems
like the negativity bias, once we understand them.

Many of us know people whom seem unfazed by genuinely stressful situations.

“Nerves of steel,” “courageous” and “crazy” are how others view the rare few who
have learned how to put non-life threatening and life-threatening stresses into the
proper context. Let’s not have a total freak-out over a traffic jam; or grossly
overreact when confronted by everyday modern stressors.
 KEY POINT:
Understanding the negativity bias can help you react less negatively to
things that are not life or limb dangers.

EARLY LIFE EXPERIENCES SHAPE THE

STRESS RESPONSE
Traumatic events experienced in childhood (abuse, loss of a parent, hunger,
neglect) have a profound impact on a child’s developing brain—especially the
developing stress-threat system. As these children enter adulthood, they are
disproportionally afflicted with depression and anxiety. Their brains are physically
and functionally different than a normal adult who did not have traumatic childhood
experiences. The developing brain of a child is much more susceptible to stress—
from childhood into adulthood.

FLASHBACK
Do a quick review of Central Themes II, “The Gene-Environment
Connection,” before continuing further.

CENTRAL THEMES CONNECTION:

Early life Stress and Epigenetics
In Central Themes II “The Gene-Environment Connection,” we discussed
 how epigenetic changes alter how a gene is expressed. Some changes
“bookmark” the gene, causing it to be turned on all of the time, and other
changes “stick the pages of the recipe together,” in effect turning the gene
off.
Early life stress causes these types of epigenetic changes in the areas of
the brain involved in the stress-threat system.

Specifically, early life stress “turns on” many of the genes involved with
making the HPA-axis function more often. This leads the HPA-axis to be
very sensitive to any “threats” in the environment, and will turn on very
easily. Adults with a history of significant early life stress can have their
stress systems turned on most of the time, even in response to minor
stresses.

Remember from the previous section that the prefrontal cortex (PFC) and
the hippocampus normally function to help stop the stress response of
the HPA-axis. Adults with a history of early life stress have epigenetic
changes that interfere with normal PFC and hippocampus function. For
these people, the PFC and the hippocampus don’t stop the stress response
well, and it can get out of control.

Research has also shown that children raised with abuse or other
significant stresses have epigenetic changes affecting the function of the
amygdala, making it strongly trigger the stress response of the HPA-axis.

Recent research shows how continual and repeated stress rewires the brain to
make it even more susceptible and inclined to trigger stress. There are epigenetic
mechanisms responsible for these changes. Epigenetic changes can be reversed over
time. If you are an adult with a history of childhood stress, seek to normalize the
stress-threat system. This is accomplished with consistent and dedicated brain
plasticity training. The adult brain is still very “plastic” or changeable, if you give it
the right inputs.

BRAIN CHANGES AND “MENTAL

HEALTH”
Epigenetic changes to the brain of those afflicted with chronic stress (particularly
childhood stress) have been shown to increase depression, anxiety and other mental
health conditions. The brain is a physical organ that is adversely affected, literally
changed by chronic stress. This leads to mood and behavior changes. Thus, “mental
health” is just another aspect of your physical health and should be treated as
such.

Supporting this notion, people with major depression have been shown to have
smaller hippocampi than non-depressed individuals. These are physical brain
changes associated with depression and other mental health disorders, not just a
“mental” defect.

It should be no surprise that many of the self-treatment approaches covered in

following sections for chronic stress, have also been shown to be effective in
treating disorders traditionally thought of as mental health problems.

STRESS AND CHRONIC DISEASE

The long-term health consequences of chronic stress are primarily related to
chronic inflammation and oxidative stress. It is therefore no surprise that chronic
stress has been linked to...

• Heart disease
• Diabetes
• Accelerated aging
• Autoimmune disease
• Cancer
• Obesity
• Depression- new research is showing that depression is an inflammatory
disease!
CENTRAL THEMES CONNECTION:
A primary mechanism behind how long-term stress leads to chronic
inflammation and oxidative stress is over-activity of the sympathetic
(“flight or fight”) nervous system. We covered this at the beginning of the
book in Central Themes IV, but it bears repeating. Activation of the
“flight or fight” (sympathetic) part of the nervous system can lead to
an increase in inflammation and oxidative stress.

Short-term activation of the sympathetic nervous system from stimuli such

as exercise produces short-term inflammation and oxidative stress, which
is beneficial for health through hormesis, as we have discussed
extensively.

Long-term, low level activation of the sympathetic (flight or fight)

nervous system from chronic stress leads to the chronic inflammation and
oxidative stress that is the underlying cause of many diseases.

Cortisol produced as part of the stress response is supposed to help with

recovery by decreasing inflammation and oxidative stress, after a short-
term stress such as exercise, injury, or escaping a predator. In short,
cortisol “puts the brakes on” inflammation and oxidative stress produced
by the “flight or fight” system after the “danger” has passed.

This system of checks and balances between the sympathetic nervous

system (inflammation) and cortisol (anti-inflammation) works extremely
well with short-term stressors. The problem lies when cortisol (HPA-axis)
is activated constantly. New research proposes that the body develops
“cortisol resistance” similar to insulin resistance and leptin resistance.
Similarly, it also leads to uncontrolled inflammation.
TECHNICAL NOTE:
Cortisol receptor resistance is a relatively new area of research, but the
idea seems conceptually sound. Receptor resistance—as found with insulin
receptors in diabetes, and leptin receptors in obesity—is commonly found
in bodies with disease. It is not surprising that another hormone, like
cortisol, could follow this same theme.

DIGGING DEEPER:
Cortisol Receptor Resistance
Chronic stress and resistance to the effects of cortisol is a new area of
research. As discussed before, cortisol usually has anti-inflammatory
effects on inflammation produced by cells of the immune system (both the
“innate guardian” and “adaptive assassin” types). To make this anti-
inflammatory effect happen, cortisol binds to receptors on the immune
cells to signal for them to stop producing inflammatory messengers
(cytokines).

Remember from the Obesity chapter, we discussed how in insulin

resistance, the insulin receptor stops working and the normal signal from
insulin does not get through to the cell. Cortisol resistance is similar to
insulin resistance in this manner. With chronic stress, the receptors for
cortisol on the immune cells start functioning insufficiently over time.
When this happens, the immune cells no longer get the signal to “turn off”
inflammation after a threat has passed. This results in long-term
uncontrolled inflammation and oxidative stress leading to chronic
diseases such as heart disease, diabetes, obesity, autoimmune disease and
cancer.

In summary, chronic stress causes the “flight or fight” sympathetic

nervous system to trigger chronic inflammation from our immune cells.
The normal anti-inflammatory “checks and balances” produced by
cortisol are working insufficiently due to cortisol resistance.
 FLASHBACK
Remember the hunger communication system with its food reward in the
obesity chapter? High levels of cortisol produced by chronic stress also
trigger the food reward pathway. This causes hunger and cravings for
high-calorie, palatable foods. This makes since from a survival
perspective.

As far as your brain is concerned, cortisol means that you just survived a
significant stress and need to refuel. High calorie sources of fuel would be
desirable to prepare you for the next “fight or flight.”

Unfortunately in modern society, most of our “threats” don’t require re-

feeding for recovery. The stressed out brain is more “animal-like” and
gets the signal to refeed anyway. When you are stressed, recognize what is
happening and don’t “feed the beast.”

BODY AFFECTS BRAIN; BRAIN AFFECTS

BODY
From the Gut Chapter, we saw that problems with our body can affect the function
of our brain. Recent research shows that metabolic diseases such as diabetes can
affect both the structure and function of the brain over time. Studies have shown that
diabetes can have the same “shrinking” effects on the hippocampus as chronic
psychological stress.

This should not be too surprising as diabetes is an “internal” physical stress

recognized as a threat by the brain, in the same way as a chronic “external”
environmental stress is seen as threatening. Diabetics experience chronic activation
of the HPA-axis because the brain thinks the body is starving since the leptin and
insulin signals not getting through to the brain. The inflammatory “threat” of
diabetes perceived by the brain creates a vicious cycle…

• The internal threat of inflammation triggers the HPA-axis, producing cortisol.

This process shrinks the hippocampus.

• High cortisol triggers the hunger communication system, signaling you to eat
 more.

• Eating more makes the diabetes condition worse.

• As the diabetes gets worse, it produces more inflammation, which triggers the
HPA-axis, ad infinitum...

Diabetes makes people more susceptible to depression since a shrunken

hippocampus and inflammation are indeed contributors to depression. The physical
brain changes generated by continual chronic external stress are made worse with
the addition of chronic internal stress from diabetes.

KEY POINT:
No matter the source (external or internal), chronic stress makes the brain
change in ways that activates the threat-stress system (HPA- axis) more
often. This leads to chronic diseases and increased susceptibility to future
stress—a vicious cycle.

CHRONIC STRESS AND PREMATURE

AGING
Chronic stress has been associated with accelerated aging in humans. Chronic
stress activates the HPA-axis/sympathetic nervous system’s threat-stress response
system. Long-term and continual activation of the threat-stress response system
leads to chronic inflammation and oxidative stress. One of the consequences of
chronic inflammation and oxidative stress is damage to the protective “caps”
(telomeres) on your chromosomes (DNA). Losing telomeres leads to DNA damage.
Damaged DNA eventually stops your cells from dividing to regenerate the tissues
and organs in your body. When your tissues and organs can no longer regenerate,
they start to fail—leading to death. Chronic stress accelerates this process.

Many of us know people who’ve seemed to age before our eyes during a period
of intense stress. The perfect example of this is how a U.S. President will appear to
rapidly age during their term in office.
 The most health-damaging and age-accelerating aspects of chronic stress are two
stress behaviors—rumination and worry.

STRESS FROM “NOTHING”—

RUMINATION AND WORRY
Rumination and worry are stress-related behaviors that amplify the negativity
bias. The stress-threat system perceives rumination and worry as two sides of the
same coin. These behaviors are the largest contributors to chronic stress.

Rumination is defined as having persistent negative thoughts about past

experiences. Rumination is a negative process that adversely impacts self-image and
self-worth. Rumination can be caused by critical comments or embarrassing
situations. Insecurity triggers rumination.

If you find yourself mired in continual and ongoing rumination, be aware that
this will have a devastating impact on your mental and physical health over time.
Rumination is in some ways “stress over nothing.” Rumination is created in the
mind, and in the same way, the mind can kill rumination by not engaging in it, or
silencing rumination before it has an opportunity to fester and grow. We want to
avoid reliving stressful situations over and over in the mind, since this prolongs
activation of the HPA-axis. The ruminator is creating “stress from within” when
there is no real stress currently present in the environment.

Worry is the opposite side of the same stress coin. Worry is the anticipation of a
future stressful or threatening event. With worry, the stressful event has not actually
happened yet, but you are activating the stress-threat response system when the brain
“worries” about the future event.

CENTRAL THEMES CONNECTION:

Hormesis and Chronic Stress
The arrow below should look familiar. It was taken from Central Themes
III, Hormesis. The stress of rumination and worry follows a hormesis-like
response:

Point A represents an individual with no worry or rumination. Finding a

human without any worry or rumination would be extremely difficult.
Many animals fall into this category. As previously discussed, having no
worry or rumination would not be a survival advantage.

Point B represents an individual with occasional, short-term worry and

rumination. This “hormetic dose” of worry and rumination provides a
survival advantage by making this individual more resilient against future
stress.

Point C represents an individual with chronic daily worry or rumination.

The stress-threat system (HPA-axis) is constantly activated by “stress from
nothing”, leading to chronic diseases such as heart disease, diabetes,
obesity, depression and anxiety.

Scientists call this the anticipatory threat response. In effect, we are anticipating a
future stressful event, but causing a stress response in the present moment—without
an actual environmental stressor. This is why we also classify worry as “stress from
nothing.”

A certain amount of short-term periodic rumination or worry can make us

resilient to future stresses. Rumination and worry provide humans a survival
advantage over animals. With reasonable and appropriate worry, we anticipate and
prepare for future stresses.

RESEARCH UPDATE:
Recent research has shown that anticipatory stress (worry) activates the
stress-threat system more than experiencing the actual future stressful
situation you are worrying about! Rumination and worry are very hard to
control with the environmental stresses of modern society.

THE 24-HOUR NEWS MEDIA,

CHRONIC STRESS, AND THE
NEGATIVITY BIAS
The modern news media is now operating 24/7, constantly reporting on
war, murders, plane crashes, abductions, economic forecasts, and other
negative events and subjects to anyone tuned in. Negativity brings good
ratings and feeds our negativity bias. Over time, habitual watchers of the
modern news media have increased chronic stress that keeps their “flight
or fight” system constantly in low-level activity. Worriers seem to be the
most affected.

Most people don’t even know what has happened to them until they
“unplug” for a period of time. Many people who voluntarily restrict their
viewing of the 24-hour news cycle for a week or so report lower levels of
anxiety and depressive thoughts. Taking a “news holiday” is always a
good idea.
 Rumination allows us to learn from past threats—specifically, how to adapt and
better deal with similar threats in the future. But, long-term, chronic rumination and
worry over-activate your stress-threat system (HPA-axis), fill your stress cup and
eventually lead to chronic disease.

Modern stresses amplify our inborn, human negativity bias to such a degree that
our health is negatively impacted by the thoughts, ideas, projections, and reflections
which occur in our consciousness. Understanding this mental stress is the first step.
The second step is developing “mental antidotes”. Awareness of potential triggers
or mental land mines, that over-activate the stress-threat system empower you to
avoid, temper, or alleviate stress when it first appears.
CHRONIC STRESS III
MIND INTERVENTIONS

BRAIN-TRAIN:
WHERE EASTERN MEDITATION TACTICS
MEET WESTERN HIGH TECHNOLOGY
The previous chapters showed that chronic stress physically changes the structure
and function of the human brain by over-activating the stress response, filling the
stress cup to overflowing, contributing to age acceleration, and developing chronic
disease.

What if there was a mental approach or strategy that you could consistently use to
relieve stress, and minimize projection, reflection, rumination and worry?
Additionally, this same brain-train mind method can be used to improve discipline,
adherence, steadfastness and human performance.

 Training the brain will have a beneficial carry-over to physical effects
with the body. Training the body will beneficially affect the structure and
function of the brain.

We live in the information age where there are no more secrets. If you want to
learn details about anything under the sun, just Google it. Mental training techniques
used by Eastern mystics and shrouded in mystery for centuries are now available to
anyone. Want to learn Dogen Zenji’s tactical approach to meditation? No problem!
Want to learn about the breakthrough mental preparation of elite athletes in the old
Soviet Union? Google Dr. Aladar Kogler and read about his pioneering work with
autogenic and auto-suggestive practices.

Experts in the East and West have offered up complex and effective systems for
transforming the human mind from an individual’s worst enemy into their best
friend. Our user-friendly mind methodology is a blend of Eastern contemplative
techniques and Western athletic and technological techniques and tools. All the
religiousness and supernatural aspects of Eastern meditational techniques, and
overly mechanistic shortcomings of the uber-rational Western approach have been
stripped away. Our synthesis of East and West—with understanding and practice—
will be immediately applicable for you in your current life situation.

View the interventions in this chapter as mental exercise—we are literally training
the brain in the same way we train to make our bodies stronger and more resilient
with physical exercise. Just as we need consistency in our physical exercise, we need
consistency in our brain-train protocols.

The three main interventions are:

1. Mindfulness practice
2. Biofeedback
3. Physical exercise

I. MINDFULNESS PRACTICE
Mindfulness training originated in traditional Buddhist meditation practices, but
has been used extensively in modern medicine for well over 20 years.
 WHAT IS MINDFULNESS?
In its simplest definition, mindfulness means focusing your attention and
awareness on the present moment. With mindfulness, you are aware of
internal processes like breathing, and external stimulus from the
environment—while not “holding on to” any thoughts or experiences after
they pass from the present moment.

Seamus the
“mindful cat”

Focusing your attention and awareness to the present moment sounds easy until
you try it for a couple of minutes. At first, it is common for beginners in
mindfulness training to have intrusive or distracting thoughts—that have nothing to
do with the present moment—pop into their heads.

Thinking about what you need to get at the store for tonight’s meal, or the jerk
that cut you off on the way home from work, will take you away from your focused
attention on the present moment. You can be aware of what goes on in your
environment moment to moment, but don’t hold on to or make judgments on these
stimuli, just label them as what they are and let them pass. For instance, during
mindfulness practice you can be aware of the sound of a jet passing overhead, but
don’t think about how annoying the sound is, or how you wish you hadn’t bought a
home so close to the airport.

Being consistently mindful for even a couple of minutes can be challenging at

first. Try this simple breathing exercise to get you started.
MINDFUL BREATHING
Many mindfulness meditation techniques involve focusing on your inhalation and
exhalation during slow breathing. The way you breathe in these exercises is critical
to the desired effect on your nervous system. It is important that you primarily
breathe “into your belly” instead of your chest. In other words, we are trying to
almost exclusively use our diaphragm for breathing instead of the chest and neck
muscles.

There are scientific reasons for breathing in this specific way:

• Inhalation (breathing in) activates the sympathetic nervous system.

Breathing in using your chest and neck muscles strongly activates the flight or
fight sympathetic system. This makes sense when you are running away from
danger or fighting—you will take in huge gulps of air by using your chest and
neck muscles to assist your diaphragm. This helps your muscles get the
maximum amount of oxygen during the physical stress of a flight or fight
situation. The brain associates “chest and neck breathing” with the flight or
fight response and increases sympathetic nervous system activation. Many
people under chronic stress habitually breathe this way without the presence of
immediate danger to life and limb. Breathing this way causes chronic low-level
sympathetic nervous system activation. We have previously mentioned that
constant high levels of sympathetic flight or flight activation result in high alert
levels, increased inflammation, and oxidative stress that can lead to chronic
disease. For this reason, don’t use your chest and neck muscles for breathing.

• Exhalation (breathing out) activates the parasympathetic nervous system.

We want you to breathe with slow exhalations that are longer than inhalation so
we can tip the balance of your autonomic nervous system in favor of the
parasympathetic system, which has anti-inflammatory and calming effects on
your body. By breathing out for a longer time than breathing in, we are
spending a longer time activating the parasympathetic system and a shorter
time activating the sympathetic system. The effect over time is less activation
of the stress-threat system that we discussed in the previous section. Try to
practice breathing like this throughout the day so it becomes a natural way to
breathe. Many of us with chronic stress have fallen into the “chest and neck”
breathing pattern without even realizing it.

• Find a comfortable position, either seated or somewhat reclined.
• While you are first learning to breathe correctly, place one hand on
your belly and the other on your chest.
• Breathe in slowly through your nose, and make sure that you mostly
feel the hand on your belly move during inhalations, and only minimal
movement in the chest area.
• Exhale slowly. The time spent breathing out (exhalation) should be
longer than the time spent breathing in (inhalation). If you are having
problems exhaling slowly, purse your lips at the beginning of the
exhalation. This makes your mouth smaller and it will be easier to control
the air passing out of your mouth.
• Focus on the sensation of the air passing in through your nostrils,
filling your belly, and then passing out of your mouth.

Mentally count each cycle of inhalation and exhalation, attempting to

reach 10 without any “intruding” thoughts other than the sensation of
breathing. If you find your mind has wandered before you get to 10
breaths, start over.

• Focusing on the sensation of breathing without letting your mind wander with
distracting thoughts has the benefit of directly attacking rumination and worry.
Remember that your prefrontal cortex is involved with maintaining attention. By
focusing attention on breathing, you are strengthening the connections in this
area of the brain. By not allowing rumination, worry, and negative thoughts
—“stress from nothing”—we decrease activation of the stress response.
Decreasing chronic activation of the threat-stress system over time with this type
of mindful attention to the present moment and breathing will strengthen the
prefrontal cortex and hippocampus while weakening the amygdala. The
downstream effects of this seemingly small breathing exercise performed
 routinely over time can slowly physically rebuild the stressed brain so it
functions normally again.

With proper breathing, we can maximize our time with high
parasympathetic activation, and only using the high level activation of the
sympathetic “flight or fight” system sparingly when necessary.

Review Central Themes IV for more on the balance of the autonomic

nervous system.

The following graphic shows the “rebuilding” process of the brain through daily
mindful breathing exercises:

• Decreased rumination and worry, which decreases the activation of the threat-
stress system.

• Decreased activation of the sympathetic system with increased activation of the

parasympathetic system caused by slow “belly breathing” with long exhalations,
reduces overall activation of the threat-stress system.

• Prolonged reduction of the stress-threat system activation allows the prefrontal

cortex and hippocampus to strengthen their connections.


The bottom picture illustrates how regular mindfulness breathing restores the
healthy brain over time. The previously overactive amygdala from the top image of
the “stressed out brain” is now “shrinking” and has a smaller activation signal to the
stress-threat system. Now that the prefrontal cortex and hippocampus are
strengthened, they can stop the stress response better with stronger inhibition
signals. This will give you more resilience against future stress. Mindfulness not
only helps with present time stress reduction, it prepares you to cope with future
stress by physically rebuilding and restoring the stress-threat system to a healthy
state.

This is how brain training with mindfulness practice is similar to strength

training for your muscles. In both cases, regular training causes beneficial physical
changes.

KEY POINT:
Regular mindfulness practice can physically rebuild your brain in the
same way that regular strength training can build your body.

Start out by trying to spend at least 10 minutes each day with mindfulness
breathing, working up to 30 minutes a day over time. You may begin to sleep better,
have less depression and anxiety, and cope with daily stresses more easily. Make
time for mindfulness breathing whenever you can. The benefits are too great to be
ignored. Make the time to practice.

STRONG MEDICINE TACTICS:

Start with 10 minutes a day of mindfulness breathing practice and work
your way up to 30 minutes a day over time.

THE BODY-SCAN
This is not a high-tech device at airport security checkpoints! Body scanning
refers to systematically visualizing and “paying attention” to each part of your body.
Like mindful breathing, you can perform this exercise in a relaxed seated or
reclining position.

Start by focusing your attention on one of your big toes for 20-30 seconds and
register all of the sensations coming from this toe. Don’t let any “intrusive
thoughts” take hold and cause your mind to wander. Move on from your big toe to
the rest of your foot and proceed slowly up your ankle, leg, knee, and thigh. At all
times, focus on the sensations coming from those specific areas. Then start at the
big toe on the other foot and do the same thing until you get to the waist area. Next,
move up your torso with the same focus on your abdomen, rib cage, and chest.
When you get to your neck, start with individual fingers on one hand and move up
the arm to the shoulder. Then begin with the other hand, moving up to the shoulder
on that side. Lastly, move up the neck into your head until you reach the top of your
scalp.

STRONG MEDICINE TACTICS:

Add the body-scan technique as part of your mindfulness training after
you have worked up to 20-30 minutes of mindful breathing practice.

The body scan may seem strange, but it is similar to the mindful breathing
exercise. Both exercises involve being in the moment while focusing on the
immediate sensations coming from your body. While doing the body scan, if your
mind wanders—especially with negative thoughts of rumination and worry—stop,
then start again at the big toe.

Focusing on the three dimensional space in and around your body during the
body scan is an additional strategy recommended by Dr. Les Fehmi in his book, The
Open-Focus Brain. In this approach, with your eyes closed, imagine the three
dimensional space occupied by each body part as well as the distance between them.
Dr. Fehmi asserts that focusing on 3-D space further assists the mindful-state and
enhances the body scan.

The body-scan technique is a somewhat advanced mindfulness technique, and

should be added after you have trained with the mindfulness breathing technique for
several weeks or months. Once your breathing technique has become automatic, you
can continue breathing properly while performing the body scan.

With either the mindfulness breathing or the body-scan, you should attempt a total
20-30 minutes of mindfulness training daily.

This is just the very tip of the iceberg with mindfulness training. You may find
many other techniques that work better for you. There are some fantastic
mindfulness systems and books to explore if you like the results you get from the
basics:

• Jon Kabat-Zinn, PhD, brought mindfulness practice into mainstream

medicine. He founded the Mindfulness-Based Stress Reduction (MBSR) course
currently taught around the world. His books and programs are excellent
resources.

• Rick Hanson, PhD, is a neuropsychologist and author of Buddha’s Brain. He

has some excellent audio-based mindfulness programs that are definitely worth
looking into. He also discusses the science behind mindfulness in a very clear
and easy to understand way.

• Les Fehmi, PhD, is a pioneering scientist in the field of neurofeedback

(biofeedback for the brain) and the author of The Open-Focus Brain. His
scientific perspective on mindfulness is a great place for a beginner to start.

Mindfulness “brain training” is no longer just for Buddhist monks or Zen

masters. It has become mainstream in a big way over the past 10-15 years along with
very strong scientific evidence for health benefits. This type of training interrupts
the vicious negative mental thought cycles of chronic rumination and worry. As
rumination and worry are large contributors to chronic stress, it’s no surprise that
recent research shows very promising results with mindfulness training for chronic
“body” diseases such as diabetes, heart disease, high blood pressure, and
autoimmune disease.

You can’t try mindfulness exercises once and decide “they don’t work for you.”
That would be like going to the gym once and saying “exercise doesn’t work for
me.” This is brain training, and daily mindfulness practice is key if you want to
rebuild a stressed brain.

II. BIOFEEDBACK
Biofeedback is a technique for stress reduction in which you use devices to
monitor your body’s heart rate, muscle tension, or skin conductance in the attempt
to exert some type of control over these processes. A biofeedback device will give
you instant “feedback” so you can be aware of your body’s state in real time. For
instance, a device monitoring your muscle tension can give you instant feedback to
your stress state, since increased muscle tension equals increased stress. You can
also monitor the sweat response in your skin with skin conductance biofeedback.
Increased stress leads to increased sweating, causing increased electrical
conductance measurable by the device. Monitoring muscle tension and skin
conductance provides a real-time window to your current state of stress—second by
second.

The idea of biofeedback is to use real-time information in an attempt to change

your stress level. If the device shows increased muscle tension—that you might not
be aware of—then you can actively try to relax your muscles to change the muscle
tension readings. You will be able to change your behavior based on the feedback.

KEY POINT:
Biofeedback uses monitoring devices to train you to reduce stress-related
body responses.

Many of us walk around during the day with high amounts of muscle tension
from underlying stress. We may “carry” the stress in our neck or chest muscles.
Biofeedback brings this muscle tension to your awareness so you can change it by
relaxing. Once we are aware of the behavior, we can eventually “catch” ourselves
and stop the tensing behavior without using the biofeedback device.

Monitoring muscle tension and skin conductance can require expensive

equipment and technical expertise. These types of biofeedback sessions are best
done in a clinic with a biofeedback professional.

A type of biofeedback many of us can perform at home with relatively

inexpensive equipment monitors something called heart rate variability.

Heart rate variability (HRV) does not measure the slowing down and speeding up
of the heart rate as the name might imply. HRV measures the variation in the time
between each heartbeat.
 The best way to illustrate this concept is to show how the heart behaves in a
person with a resting heart rate of 60 beats per minute (one beat every second).

Low Variability: the heart beating exactly once every second. The time between
each beat is exactly the same (in this case 1 second). This machine-like precision is
not how a healthy person’s heart beats. Low variability is a marker of poor health.

High Variability: the heartbeats do not happen on exactly every second. Sometimes
the time between heartbeats is less than a second, or more than a second. This
person would still have 60 heartbeats in a minute on average, but would not have a
heart beat exactly every second. High variability is a marker of good health.

LOW HRV = BAD

Low HRV, the machine-like heart, has been linked to a high amount of
sympathetic nervous system (“fight or flight”) activity. Low HRV is seen
in people with chronic diseases and indicates poor health overall. Chronic
stress and activation of the stress/threat system causes the heart to beat in a
more “machine-like” way, causing low HRV.

HIGH HRV = GOOD

High HRV corresponds to higher activation of the “rest and digest”
parasympathetic nervous system. High HRV is associated with good
physical health and low stress states.

New technology has allowed for portable HRV biofeedback devices that you can
use at home. These devices monitor your HRV moment to moment by tracking your
pulse with different types of sensors.

Using the mindful breathing techniques covered earlier in this section,

biofeedback can track how proper breathing reduces “flight or fight” system
activation and raises your HRV. The device will also alert you if your attention
drifts into worry or rumination which both raise your anxiety levels and lowering
your HRV.

Biofeedback devices that use HRV are useful for daily practice at home to reduce
your stress levels. There are plenty of portable systems on the market, but our
current favorite personal HRV biofeedback system is Inner Balance made by
HeartMath. It is an application and ear sensor that works with the iPhone.

With biofeedback, you can train your brain to maintain low stress states with real
effects on your body. Give it a try...

STRONG MEDICINE TACTICS:

Try a personal HRV biofeedback device to reduce chronic stress and raise
your heart rate variability. Use it daily for maximal health benefits.

III. EXERCISE
Similar to mindfulness practice, exercise decreases activation of the stress-
threat system (HPA-axis). But, it also helps to regrow stress-shrunken brain
structures such as the hippocampus by stimulating the release of Brain Derived
Neurotrophic Factor (BDNF).

DIGGING DEEPER:
Exercise, BDNF, and the Hippocampus
Exercise stops the shrinking hippocampus by not just decreasing the
 excess cortisol from stress activation of the HPA-axis, but by stimulating
the growth of the hippocampus by an additional mechanism.

Exercise is a potent stimulator of Brain Derived Neurotrophic Factor

(BDNF). BDNF is a protein that stimulates nerve cell growth and is a
central player in neuroplasticity (adaptive brain changes to environmental
stimuli). Exercise stimulates BDNF, which stimulates the growth of nerve
cells in the hippocampus, rebuilding this part of the brain that was
“shrunken” by stress. Recall that the hippocampus is a key player in
preventing the stress-threat system from getting out of control. Regrowth
is good for controlling stress.

Exercise has proven to be beneficial for stress relief. Recent research shows that
exercise specifically decreases rumination and worry—both major contributors to
chronic stress. Exercise has been shown to be extremely effective for reshaping the
stressed brain through neuroplasticity. Reshaping the brain connections with
exercise is thought to be responsible for helping the anxiety and depression-related
symptoms that often accompany chronic stress.

Exercise is a true mind-body intervention. While you can train both the body and
the brain directly, not all exercise is optimal for targeting brain training.

COACH’S CORNER:
We love outdoor exercise such as chopping wood, running or biking steep
mountain trails, running along the seashore, swimming, intense games
and sports. Think big athletic cardio—not being stuck indoors like a
gerbil riding or operating an aerobic stationary bike or machine while
 watching the built-in TV to distract you from the horror of the mindless
activity you are doing.

Meanwhile the mountain biker or runner—tearing along wooded trails of

serene natural beauty—is having a transcendental, altered-state experience
while working his lungs until they sear and generating innumerable
rivulets of sweat.

Outdoor exercise gives maximum stimulus from the environment. It is superior

for keeping you in the moment, mindful of what you are doing. It is easy to fall back
into worry or rumination when you are plodding away on a treadmill or elliptical
machine.

The authors engaged

in “physical
mindfulness”

Chris has always been drawn to sports such as mountain biking, rock climbing,
trail running, and surfing. There is no room for rumination or worry while flying
downhill on a narrow mountain bike trail, or when dropping in on a big wave.
Marty is a life-long powerlifter. He is not thinking about anything but the present
moment while pulling a 500lb deadlift. Both of us have been drawn to sports such as
these because of the mindful aspects built in to the performance of these activities.

You certainly do not have to engage in powerlifting or rock climbing to tap into
physical mindfulness activities. A short hike in the woods can quickly reset your
stress-threat system. Also, yoga and the ancient Chinese internal martial art of T’ai
chi ch’uan (known as tai chi in the West) are embodiments of physical mindfulness
and can be practiced by anyone regardless of fitness level or athletic experience.
STRONG MEDICINE TACTICS:
Get regular exercise for stress relief. Outdoor exercise and “physical
mindfulness” activities are especially beneficial to reverse stress-related
brain changes. Let Nature be your trainer, get outdoors!

COMING ATTRACTIONS >>>

There will be extensive coverage on the Strong Medicine exercise
approach in Part 3, Battle Plan.
KNOWING YOUR ENEMY IV:
CONCLUSION

Chronic stress causes structural and functional changes in the brain that “link”
to significant health consequences and leads to premature aging. The human mind
and body are not separate entities, but tied together inextricably.
 Chronic stress can also affect other organs such as the gut, multiplying chronic
inflammation and oxidative stress. Remember the Gut-Brain Axis?

The triumvirate of brain training—mindfulness, biofeedback, and exercise—will

repair the damage of the stressed brain and combat chronic disease by reducing
inflammation and oxidative stress.

If you still think this is all new-age nonsense, be aware that recent research using
sophisticated brain imaging techniques has shown that brain training does indeed
physically reshape the brain. Several studies show that people who exercise and
practice mindfulness regularly have structurally and functionally different brains
than those who do not. People who exercise and practice mindfulness also have
much lower rates of stress-induced chronic disease and mental health disorders. Just
as weightlifters grow their muscles, and runners improve their cardiovascular
fitness through training, brain training does the same for the brain.

In our stressed-out modern world, brain training can help prevent chronic disease
and is truly part of the fountain of youth for your mind and body.
BREAKING THE LINK
The Brain Training Triumvirate (mindfulness, biofeedback, and exercise) can stop
chronic stress in its tracks, “breaking the link” between chronic stress and chronic
disease. The Strong Medicine Defensive Tactics in this section will expose the
lurking “Silent Killer” and stop his subversive plan to destroy your health.
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KNOWING YOUR ENEMY IV
CIRCADIAN DISRUPTION: THIEF IN
THE NIGHT

Our body and mind follow a natural rhythm of activity and rest that few of us
appreciate or follow. The modern environment is at odds with this ancient internal
rhythm that developed at the origin of our species.

Failure to follow this circadian rhythm creates dissonance and disruption in the
internal workings of our body—with profound consequences to our health that
modern science is just now beginning to appreciate.

Circadian Disruption is one of the more slippery members of the Pentaverate. He

operates in ghostly silence and attacks relentlessly. You cannot touch, taste, smell, or
hear him. The only evidence of his attack is constant fatigue and the slow
destruction of your health.

We will show you how to spot him and stop him in his tracks. We have his
number.
CIRCADIAN DISRUPTION I
THE INTERNAL TIMEKEEPER

A master clock resides deep inside the brain. It governs cycles of sleeping,
waking, eating, fasting, body temperature, and controls the ebb and flow of the
various hormones that control our metabolism.

This clock is not constructed of metallic gears, it is a molecular clock made of

genes and protein located within specific nerve cells of the hypothalamus. Recall
that the hypothalamus is the control center of the brain that responds to signals from
the environment. It controls many of the body’s processes, so it makes sense that the
hypothalamus houses the master clock.

QUICK DEFINITION:
Circadian is from the Latin circa = “about” dies = “day”. Processes that
follow circadian rhythm fluctuate over a time period of approximately 24
hours or “about a day.”

The inner workings of our master molecular clock are just now being understood
by very sophisticated cutting edge science and will not be covered in Strong
Medicine due to the extreme complexity.

Science has recently shown that most cells in the body contain their own circadian
clocks, but only the master clock in the hypothalamus can maintain a circadian
rhythm without external influences from the environment. Scientists have
removed master clock cells and locked them away from environmental influences
like light and dark, fueling and fasting, and yet they maintain their rhythm of
slightly more than a 24-hour cycle (between 24.2 and 24.5 hours).

The master clock in the hypothalamus regulates all of our major organs
including the liver, lungs, heart, kidneys, gastrointestinal tract, and our muscles.
Each organ has its own internal clock that is influenced by the master clock.
This ensures that each organ system is adjusted to meet the metabolic and functional
demands of activity during waking hours, and allows for “sleep mode” regeneration
during rest and sleep. This rhythm of the metabolic and physiologic ebb and flow
allows for maximal efficiency in operation and repair of the “flesh machine.”
THE CONDUCTOR OF THE ORCHESTRA
The master clock in the hypothalamus coordinates the activity and regeneration
rhythms of the organs in the body. The individual organs’ clocks also communicate
with each other through hormonal signals to coordinate optimum functionality for
activity during the day, and repair and regeneration at night.

This timing system and the organs’ coordinated rhythms are crucial for ensuring
precious energy is not wasted and each organ system is prepared to function
individually and in harmony with the other organs.

The whole system must be coordinated to deal with the extremes of the circadian
cycle: full throttle physical activity during the day, and deep sleep during night time
hours.

The master clock is the conductor of this symphony orchestra. The various organ
clocks are the musicians who must listen to each other while following the
conductor. One organ clock out of sync with the system is like a violist playing a
different tune than the rest of the orchestra—disastrous to the overall performance,
and in the body, this is disastrous to long-term health.

Peripheral body “organ clocks” are set by the “master clock” in the
hypothalamus. Each organ clock controls organ functions during activity and
regeneration modes. They are crucial in ensuring the organ systems work together
in a synchronized manner. As we will see, desynchronized (broken) clocks lead to
chronic disease.

The adrenal gland’s clock helps maintain the timed secretion of cortisol
in the early morning to prepare for activity by increasing glucose release
from the liver. It reduces cortisol levels in the evening and through the
night to promote rest and regeneration.

The heart clock helps prepare the heart for daytime by making it more
responsive to the demands of physical activity with heart rate and strength
of contraction. At night, the clock allows the heart to be less responsive
during sleep.

The liver clock helps control the “glucose banker” so that the liver can
store glucose during daytime activity and meals, then release and make
glucose at night during fasting to supply the brain.

The pancreas clock sets insulin secretion at the highest during daytime
activity to allow for energy storage. At night, insulin secretion is set low
to ensure the brain receives a steady supply of glucose for regeneration.

The fat clock controls the release of the hormones adiponectin and leptin.
Adiponectin is higher during daytime activity to increase insulin
sensitivity, allowing the storage of nutrients. Leptin is higher at night,
delivering the “stop eating” signal necessary for fasting during
regeneration.

The muscle clock helps prepare our muscles for optimum performance
during the day. The clock sets a metabolic rhythm, making it easier for
muscle to burn glucose during the day, then using fat for energy at night.

The immune clock has the immune system on alert for threats such as
bacteria and viruses in the daytime, then at night the adaptive assassins
create “immune memories” for the threats encountered during the day.

The kidney clock helps control fluid and electrolyte balance in the body.
To support daytime activity, blood pressure is increased, then at night
there’s a 10-20% drop in blood pressure during regeneration.

The gut clock regulates gastrointestinal function to increase digestion,
absorption of food, and motility (movement of digested food) during the
day. It signals for repair of the gut lining at night when digestive processes
are minimized.

During daylight hours, hormone levels are controlled by the master

clock in the hypothalamus to support increased physical activity.
• Cortisol levels are highest in the morning. This increases glucose after
night-time fasting, making energy available for the brain and body. It also
helps “wake you up”.
• Leptin levels are low in the morning and during daylight hours, this
gives the brain the “GO” signal to eat. Hunger is high with low leptin
levels, this promotes eating to satisfy the energy requirement for physical
activity during the day.
• Melatonin levels are suppressed by light, which brings the brain and
body out of resting/sleep mode to prepare the mind and body for activity.
• Growth hormone is low, suppressed by increased cortisol in the
morning as the body comes out of the regeneration/repair mode of sleep.

During the onset of night, hormone levels are controlled by the master
clock in the hypothalamus to support repair and regeneration.
 • Cortisol levels are lowest at this time to prepare the body and brain for
sleep. Low cortisol allows for growth hormone secretion during sleep.
• Leptin levels are high at night, giving the brain the signal to “stop
eating”. Hunger is low with high leptin levels, which promote fasting
during the repair/regeneration phase and allow for uninterrupted sleep (no
need for midnight snacks).
• Melatonin levels start to rise as the sun sets, giving the brain and body
the signal to slow down in preparation for sleep and the repair and
regeneration that happens during this time.
• Growth hormone is high especially during deep sleep in the first part
of the night. Growth hormone increases the burning of body fat for
energy during fasting, and increases muscle repair and regeneration.

Because the organs in the body function differently if we are in the activity or
regeneration phases of the circadian rhythm, are there optimal times to perform
activities such as exercise and eating so these activities match up with the rhythm of
organ function?

• Is it better to exercise in the morning or evening?

• Is a late night snack a good idea?

• Are there any health consequences to shift work?

We’ll answer these questions in upcoming sections, but they are important to
consider now.

LIGHT RESETS THE MASTER CLOCK

While the master clock in the hypothalamus can keep running without any
external influence, the clock can be reset to match the external environment through
outside influences such as light. It is important to reset the clock daily as most
people’s internal master clock runs in a cycles a bit longer than 24 hours. The
majority of the general public has an internal timekeeper genetically set to about
24.5 hours. Some people may have longer cycles up to 26 hours.

Without external cues from the environment (such as light), the internal
timekeeper would slowly advance out of sync with the environmental 24 hour cycle
ruled by the rising and setting of the sun. Most people’s internal time would end up
being about 30 minutes off “environmental time” each day, adding up to over 3
hours out of sync in a week.

KEY POINT:
Most people’s master clock is genetically set for a cycle of about 24.5
hours. We need external “cues” from the environment to “reset” our clock
each day.

The external environmental clock setters are called “zietgebers,” which is

German for “time givers.” Light is the most powerful zeitgeber that resets our
master clocks on a daily basis.

KEY POINT:
Light is the most powerful environmental cue to reset the master clock.

The circadian master clock regulates our daily rhythm of activity and
regeneration through key hormones as shown in the previous diagram. Of these
hormones, melatonin is of particular importance to how we enter and exit the
body’s regeneration mode.

When light—especially short-wave length blue light—hits our eyes in the

morning, specialized cells in the back of our eyes transmit this signal to the
hypothalamus (master controller). The hypothalamus transmits the “light signal” to
a tiny structure in the brain called the pineal gland, which is responsible for
producing melatonin. The “light signal” tells the pineal gland to stop producing
melatonin so we can enter the activity phase of the circadian cycle.
 KEY POINT:
Light signals the pineal gland to stop producing melatonin. Decreased
melatonin levels send a message to the master clock and the organ clocks
to prepare for the activity phase.

After the physical and mental stress of our daily activities, the body and brain
desperately need time to regenerate and repair. Our flesh machine enters
regeneration mode primarily through the actions of the hormone melatonin. The
dimming light—with longer wavelengths of red and orange—in the evening signals
the hypothalamus to tell the pineal gland to start making melatonin. Melatonin
production starting at twilight is the gateway into regeneration mode.

KEY POINT:
The dimming light of the evening sky signals the pineal gland to start
producing melatonin. Melatonin is the gateway into the regeneration
phase.

MELATONIN: THE GATEWAY TO

REGENERATION MODE
Melatonin is indeed the “gateway” hormone for entering the regeneration mode,
and it is essential for overall health with multiple actions in the body:

• Melatonin prepares the brain and body for sleep, allowing a smooth transition
between waking and sleeping.

• Melatonin signals the organ clocks to start shifting from activity mode into
regeneration mode.

• Melatonin is a potent antioxidant and greatly increases the body’s internal

antioxidant defense system to decrease oxidative stress.

• Melatonin has anti-inflammatory properties that can counteract chronic

inflammation.

• Melatonin is a crucial signal for cellular and DNA repair. This is important
because damaged cells and DNA contribute to accelerated aging and cancer.

Given the many actions of melatonin which enhance regeneration of the flesh
machine, and protect against chronic disease, anything that decreases melatonin
during the evening and night has the potential to cause health problems. Melatonin
interacts with the master clocks as well as the organ clocks to help keep the flesh
machine “orchestra” perfectly synchronized as the brain and body weave in and out
of the activity and regeneration modes in the 24 hour circadian rhythm.

KEY POINT:
Interrupting the natural cycle of melatonin secretion at night has far-
reaching health consequences and contributes to many chronic diseases.

One of the gravest consequences of low melatonin at night is sleep disturbance.

Poor sleep has emerged as one of the most important public health issues of the
modern age. Chronic poor sleep doesn’t just result in fatigue during the day, it plays
havoc on the regeneration mode at night. Recent research shows that poor sleep is a
major contributor to chronic disease. Building a perfect night’s sleep is a challenge
in a modern world polluted by artificial light. Read on for a description of sleep in
its optimum form.
CIRCADIAN DISRUPTION II
SLEEP ARCHITECTURE: BUILDING A
GOOD NIGHT’S SLEEP

There is a lot happening in the body and brain from the time you lay your head
down at night until you wake in the morning. Sleep is much more than escaping the
conscious world when the lights go out. The health benefits of the regeneration
mode happen during high quality sleep.

An episode of sleep is actually a very structured process built on a cycle of

sequential stages that repeat approximately every 90-120 minutes, with four to five
total cycles during a night of sleep. The structured cycle of sleep is called sleep
architecture.

BUILDING BLOCKS
There are two distinct types of sleep that occur during the night—non-rapid eye
movement sleep (NREM) and rapid eye-movement sleep (REM):

• NREM sleep makes up about 75% of total sleep time during the night. It is
divided into 3 distinct stages: NREM-1, NREM-2, and NREM-3. As you fall
 asleep you descend down through the stages: awake NREM-1 NREM-2
NREM-3. The electrical activity of your brain slows as you descend through the
stages to NREM-3. Brain electrical activity is very slow at NREM-3, also named
slow wave sleep (SWS). Slow wave sleep happens mostly in the first part of the
night.

TECHNICAL NOTE:
Non-rapid eye movement sleep (NREM) was traditionally broken up into
four separate stages. In 2008, the American Academy of Sleep Medicine
merged stages three and four—both characterized by slow wave sleep
(SWS)—into one phase. The NREM-3 we refer to in this book is the
combination of stages three and four, to be consistent with the new
classification system.

• REM sleep makes up about 25% of total sleep time. In this type of sleep, the
brain shows electrical activity similar to waking states. REM sleep is also known
as “active sleep.” REM sleep is when most dreaming takes place, The length of
time spent in REM sleep increases at the end of the night.

IMPORTANCE OF SLOW WAVE SLEEP

(NREM-3)
Slow wave sleep (SWS) during the first part of the night has some very
important functions in the regeneration mode of circadian rhythm:

• Most of the daily supply of growth hormone is released during slow

wave sleep. Recall that growth hormone is essential for sparing muscle
mass while burning fat for energy during the fasting period at night.
Reduced slow wave sleep leads to reduced growth hormone. Reduced
growth hormone leads to muscle wasting, and slows fat loss to a crawl.

• Events from the previous day are stored in long-term memory during
slow wave sleep. This is especially true for storing new information
learned during the day into long-term memory for later recall.

• Much of the cellular and DNA repair in the body and brain is performed
during slow wave sleep.

COACH’S CORNER:
You will not achieve your body fat reduction or muscle gain goals if you
are not getting enough sleep—no matter how dialed-in your nutrition and
exercise plans. Inadequate sleep = reduced slow wave sleep = reduced
growth hormone= poor body fat loss and increased muscle wasting.

THE FIRST HALF OF THE NIGHT—(NREM-3)

The first half of the night is dominated by slow wave sleep (NREM-3).
Notice that as you descend into sleep, you spend a relatively brief time in
NREM-1 and NREM-2 before spending the majority of time in the deep
SWS of NREM-3. The mind is quiet with slow electrical activity.

Much of the restorative and healing processes of the regeneration

mode happen during NREM-3 in the first part of the night. Disrupting
NREM-3 has significant health consequences of which few are aware.

THE SECOND HALF OF THE NIGHT—(REM)

 The second half of the night is dominated by REM sleep, when dreaming
takes place. During this time, the mind is very active with electrical
activity similar to waking states. During REM sleep, although the mind is
active, the muscles of the body are paralyzed.

REM sleep is extremely important for health, but for different reasons
than SWS as we will discuss shortly. Most people don’t appreciate the
potential health consequences of reduced dreaming.

IMPORTANCE OF REM SLEEP

The importance of rapid eye movement (REM) sleep to human health and
function is less clear than that of slow wave sleep, but some theories are
emerging from recent research...
• In REM sleep, we can play out stressful situations in the safe
environment of dreaming. This process is thought to give us resiliency,
leaving us less vulnerable to the effects of actual stresses encountered
during waking hours. Recall from the Stress Chapter how stress can cause
significant health problems. REM sleep may help shield us from actual
stressful events by “rehearsing” stressful situations in our dreams.
• REM sleep is thought to significantly enhance creativity and problem
solving. Historically, great works of art and scientific breakthroughs have
been reported as happening after dreaming. Recent science has shown us
that REM sleep activates areas of the brain thought to be responsible for
problem solving and creativity.

Sleep research is still in its infancy and we are only beginning to crack the
surface of what happens at night in the mind and body when we leave the conscious
world. But, the nasty health effects of sleep deprivation are already well defined.
Before we launch into the health problems caused by poor sleep, it is crucial to
understand what causes us to fall asleep, and the transition from activity mode to
regeneration mode. We cannot fix sleep problems such as insomnia if we do not
understand the internal processes that allow us to fall asleep under ideal
circumstances.
THE DRIVE TO SLEEP
There are two primary processes that work together to promote falling asleep
and staying asleep. If these two systems are synchronized, we will enjoy a smooth
plunge into a restful and regenerative sleep period. If these systems are uncoupled,
insomnia and restless, fragmented sleep may occur.

SLEEP DRIVE #1: THE CHEMICAL

SYSTEM
The first sleep system is the “chemical system” because it is primarily driven by
the build up of a certain chemical—adenosine—in the brain. The name of this
chemical may seem familiar; it is part of the “energy currency” molecule adenosine
triphosphate (ATP) introduced in the Metabolism 101 section.

Recall that the brain is an “energy hog” and uses 20% of the body’s supply of
ATP even though it is only 2% of the body’s weight. When adenosine triphosphate
(ATP) is used for energy it loses its phosphates and becomes adenosine. Adenosine
could be understood as an energy waste-product. The brain goes through a
mountain of ATP during the high activity of waking hours. Adenosine, the energy
use “waste-product,” begins to build up in certain parts of the brain. This build up of
adenosine is the chemical signal that produces fatigue and drives sleep as night
approaches.

KEY POINT:
 The “energy waste product,” adenosine, accumulates in the brain during
the day. Once adenosine builds up to a certain level in the brain, it triggers
the drive to sleep.

Adenosine building up during the day is analogous to adding debt on an “awake-

time credit card.” Once this credit card reaches its awake-time spending limit for
adenosine, it must be paid off. The only way to pay off this credit card is by
sleeping. After several hours of sleep, a large amount of the adenosine will have
cleared out—the “credit card” will be close to paid off, and waking is triggered.

SLEEP DRIVE #2: THE CIRCADIAN

SYSTEM
The second sleep system is the one driven by the circadian rhythm. The circadian
sleep system follows the light-dark cycles of your environment and works side by
side with the chemical (adenosine) system. The circadian system sets the threshold of
how much adenosine can be accumulated on the chemical system’s “awake-time
credit card” before triggering sleep.

The circadian sleep system sets the adenosine threshold (“credit-limit”) primarily
through the actions of melatonin. During darkness, the circadian system secretes
melatonin and sets the adenosine “credit limit” low. Lower amounts of adenosine
will easily trigger sleep with the lower “credit limit”. When daylight hits the eyes,
the circadian system stops secreting melatonin and the adenosine credit limit is set
higher. Now it will take higher amounts of built up adenosine to trigger sleep.

KEY POINT:
 The adenosine “credit limit” is the amount of adenosine build-up
necessary to trigger sleep. This “credit limit” is set by the circadian
sleep system.
• A high “credit limit” requires a large amount of adenosine to trigger
sleep.
• A low “credit limit” only needs a small amount of adenosine to trigger
sleep.

The morning sunlight triggers the circadian system to stop secreting melatonin.
The circadian sleep system issues a high credit limit “gold card” for adenosine for
use during the day.

The adenosine gold card issued by the circadian system allows the brain to
accumulate relatively high amounts of adenosine during the day without triggering
sleep.

As the sun sets, low light levels trigger melatonin. At this time, the circadian sleep
system issues a low credit limit “gray card” for use at night.

The low credit limit gray card issued by the circadian sleep system lowers the
amount of adenosine necessary to trigger sleep.

The card switch from gold to gray as the sun sets allows the amount of adenosine
that accumulated during the daylight waking hours to trigger sleep under the low
adenosine credit limit of the gray card. The gray card’s lower credit limit requires
that the adenosine “debt” be paid immediately by sleeping.
 The card switch from gray to gold as the sun rises allows the brain to accumulate
adenosine during waking hours without reaching the high credit limit. The gold
card’s high credit limit prevents the accumulating adenosine from triggering sleep
during the day, so we can wait to pay the sleep debt.

SLEEP SYSTEM SYNERGY

The chemical and circadian systems are synergistic for a reason. It makes sense
to sleep when the master clock and organ clocks of the circadian system are primed
for the regeneration mode. Using the circadian sleep system, the brain will allow
sleep to be triggered more easily by the chemical sleep system if the master clock
and organ clocks are prepared to enter regeneration mode.

It also makes sense to wake up when the master clock and organ clocks are
primed for activity mode. The brain will resist the chemical signal (adenosine) to
sleep if the circadian master clock and organ clocks are primed for activity mode.

When working properly, the circadian system will keep you asleep under the
effects of melatonin even though your levels of adenosine are decreasing during
sleep. The regeneration mode of the circadian system will set the low gray card
“credit limit” for adenosine. This means you can clear out adenosine to relatively
low levels by sleeping and remain asleep because the low adenosine levels are still
triggering sleep because of the “low credit limit.”

During waking hours the circadian system in activity mode counteracts the rising
levels of adenosine as the day progresses, allowing you to stay awake. The
circadian system in activity mode sets the adenosine “credit limit” high with the
gold card so you can accumulate adenosine without falling asleep during the
daytime.

The two sleep systems ensure that our circadian clocks and organ clocks are
optimized to our activity levels. We should be awake during the circadian activity
mode and asleep during circadian regeneration mode. To do otherwise will cause
significant stress on our mind and body. Out of phase sleep systems result in using a
gold card at night and a gray card during daytime. This is called circadian
disruption and leads to poor sleep and eventually chronic disease.

We are going to cover the health consequences of inadequate sleep in the next
section, but first we will describe how the circadian system gets out of sync with the
chemical-adenosine sleep system. Before we can fix something, we have to know
the cause of the problem. The alternative is to try treating sleep symptoms with
medications without addressing the underlying causes.
CIRCADIAN DISRUPTION III
EDISON’S FOLLY? THE
CONSEQUENCES OF A BROKEN
CLOCK

Thomas Edison,
American inventor
 Thomas Edison, the prolific American inventor of the late 19th century, brought
us the first electric light bulb suitable for widespread consumer use. Edison also
patented an early electrical distribution system, paving the way for the accessible
electrical power we enjoy in our homes and businesses today.

There is no doubt that Edison’s contributions to the Industrial Age have allowed
the transition to the modern Information Age, supported by trillions of kilowatt-
hours of electrical power annually. Businesses can now operate around the clock,
and we can engage in late night recreation because of the ubiquitous bright
electrical lighting in our world.

Prior to electric light, the world primarily woke and went to sleep with the light
and dark cycles from the rising and setting of the sun. Prior to 130 years ago, our
circadian rhythms were entrained with the sun since the origin of our species.
Electric light has enabled us to live out of sync with our natural circadian rhythm by
extending waking activity well into the night. It has also enabled us to start working
well before the sun comes up in the morning.

From a circadian perspective, the regeneration mode has been significantly

shortened in exchange for extended activity time. Science is now starting to
understand that the artificial disruption of the circadian system may not be so good
for our health.

Light is the most powerful stimulator of the circadian system. Natural light is
broken up into a spectrum of different colors, each corresponding to different
wavelengths. You can see the light spectrum when it is refracted by water droplets in
a rainbow or when viewed through a crystal prism. Otherwise, you cannot
distinguish the full spectrum of colors hiding within daylight.

The short wavelength—primarily blue light—portion of natural light stimulates

our circadian system. Blue light signals the brain to stop melatonin production and
prepare us to enter the activity mode of the circadian cycle.
 The blue light from the sun rising in the morning signals the master clock and the
organ clocks to prepare the mind and body for the increased energy demands of
activity. Natural light’s effects on melatonin keep us in activity mode during the day.
The circadian system issues us a high credit limit “gold card” to prevent the build
up of adenosine from triggering sleep.

KEY POINT:
Blue light, the short wavelength part of natural light, is the primary
stimulator of the circadian cycle. Blue light turns off melatonin
production and signals the activity mode to start.

Before incandescent light bulbs were widespread, the setting sun reduced the blue
light signal that triggered melatonin production. The circadian system issued the
“gray card” with the low credit limit as melatonin increased and the adenosine
build-up triggered sleep. Light from candle flames and fire have less blue light in
their spectrums and did not significantly affect the circadian systems of preindustrial
citizens.

In modern times, widespread use of indoor electric light at night has effectively
extended the daylight. Although indoor electric light is lower in intensity than
sunlight, it still has a significant amount of blue in its spectrum. It does not take
much blue light to stop melatonin production, and recent science has shown that
most nighttime indoor light significantly reduces melatonin production. This light
at night (LAN) extends the activity mode of the circadian cycle at the expense of the
regeneration mode. Computer screens and television sets also give off significant
amounts of blue light.

Light at night (LAN) is not just from indoors. If you live in or around a
metropolitan area, it will be difficult to see the starts at night. Many places in our
country simply no longer have true darkness at night. Street lamps and illuminated
signs shine through bedroom windows, potentially disrupting melatonin production
and sleep. This constant outdoor electric light at night is known as light pollution.

FALLING ASLEEP WITH LAN

The light at night (LAN) exposure many of us have produces an abnormally long
activity mode with no gradual transition from wake to sleep. Without exposure to
LAN, melatonin production starts approximately 2-4 hours after natural light starts
to dim at sunset. This delay in melatonin production 2-4 hours after sunset
corresponds well to bedtime for many people who do not have the influence of
artificial light at night.

Recent research has shown that exposure to artificial light at night not only delays
the onset of melatonin production, but also reduces the total amount of melatonin
produced overnight. Many of us try to go to sleep right after exposure to artificial
light for most of the evening hours. Even though we have turned off the lights, we
will have to wait an additional 2-4 hours for melatonin production to start in full
swing. Since melatonin is the gateway to the regeneration mode for the mind and
body, we have delayed and shortened the time for recovery and repair.

Light at night (LAN) also makes it difficult to fall asleep. Recall that melatonin
generated by the circadian sleep system issues the low-credit limit “gray card” for
the adenosine sleep system. In this way, melatonin allows the built-up adenosine to
trigger sleep. If we have delayed melatonin production with LAN, we are still in the
activity mode of the circadian sleep system. We are still carrying the high credit
limit “gold card” for the adenosine sleep system while trying to fall asleep. The
gold card credit limit will not allow the adenosine built up during the waking hours
to trigger sleep. Insomnia is the result.

Using the adenosine

“gold card”
at night = insomnia

Compounding the problem, light at night decreases the melatonin produced when
we finally enter the regeneration phase. The low levels of melatonin do not produce
a strong “keep sleeping” signal as adenosine levels of the chemical sleep system
drop during sleep. The result is frequent waking during the night, especially
towards the early morning. Valuable sleep is lost.

Many people in modern society wake before dawn to a home illuminated by low
intensity artificial light. Then they go to offices with only low intensity artificial
light which does not completely shut off melatonin production. To truly reset the
circadian system in the morning and strongly enter the circadian activity mode, we
need the high intensity natural light from outdoors. Outdoor natural light has a high
enough intensity and a significant amount of blue light in its spectrum to absolutely
turn off melatonin.
 KEY POINT:
High intensity natural outdoor light is the best way to reset the circadian
system and enter into activity mode.

While anemic indoor light is enough to stall the start of melatonin production at
night, it does not sufficiently shut off melatonin production in the morning once the
regeneration mode has picked up steam during the night. The low intensity indoor
lighting sends mixed signals to the master clock and organ clocks. The internal
clocks do not fully initiate the activity mode, and your brain and body are not
optimized to meet the challenges of the day.

Many people who suffer from disrupted circadian systems and the resulting poor
sleep at night turn to stimulants like caffeine to keep them going during the day. The
out-of-sync circadian sleep system lets relatively small amounts of adenosine build
up and trigger an intense feeling of fatigue and need to sleep. It is no surprise that
caffeine works by interfering with adenosine signaling.

A significant number of us carry around enough chronic adenosine sleep debt that
we need caffeine and other stimulants on a daily basis to keep functioning.

QUICK MEDICAL NOTE:

Caffeine keeps you alert for activities such as all night study sessions, late
night parties, or to help you get through your day after poor sleep. It
stimulates us and delays sleep by stopping the actions of adenosine in the
brain.

In effect, caffeine—and the theophylline in tea—slows down the chemical

sleep drive system, keeping you awake. Unfortunately you will have to pay
your sleep debt at some point after the effects of the caffeine wear off.
LAN AND CIRCADIAN DISRUPTION
The end result of high amounts of indoor light at night and the lack of outdoor
natural light in the daytime is a broken circadian system. This shortens the duration
of restorative sleep at night and leaves us struggling to survive the day without
falling asleep. Over time, this pattern leads to chronic disease through allostatic
overload.

Noted scientists and chronobiologists Michael Terman, PhD, and Ian McMahan,
PhD, state in their groundbreaking book Chronotherapy, “Most of us live a twilight
existence.” They are describing modern life with no true daylight in indoor offices
during the day, and light pollution obscuring true darkness at night creating
perpetual twilight.

Circadian disruption
and poor sleep
significantly fills
your stress cup

Circadian disruption and the accompanying lack of restorative sleep are major
contributors to filling your daily stress cup. Light at night (LAN) allows us to
uncouple the synergy between the circadian cycles of activity and regeneration
modes, and our actual patterns of waking and sleeping. The long-term health effects
of this circadian disruption cannot be underestimated—the clocks are broken.

CONSEQUENCES OF A BROKEN CLOCK

Long-term circadian disruption often leads to chronic poor sleep with significant
health consequences. It is hard to separate the adverse health effects of circadian
disruption from those of inadequate sleep as they so often occur together.

Circadian disruption leads to sleep problems, and poor sleep can negatively effect
the circadian system. Not all sleep disorders are caused by circadian disruption but
these sleep problems do impact the circadian system. Trying to tease out the cause
of these long-term health effects is like the “chicken or the egg” argument. We do
know that long-term inadequate sleep is strongly associated with the following
conditions:

• Obesity
• Insulin resistance and diabetes
• Cancer
• High blood pressure
• Increased susceptibility to infectious disease
• Heart and vascular disease
• Depression
• Aggravated symptoms of autoimmune disease
• Accelerated aging

The chronic disruption of the circadian system seen in long-term night shift
workers has also been associated with all of the conditions listed above. This
supports the strong reciprocal link between sleep disruption and circadian
disruption regarding health consequences.

THE MALFUNCTIONING MASTER CLOCK

When the master circadian clock in the hypothalamus is “broken”, it has far
reaching effects on the mind and body. Recall that the hypothalamus is the master
controller for many functions of the flesh machine including: metabolism,
reproduction, stress-threat response, hunger, thirst, and body temperature. The
master circadian clock orchestrates the timing of all of these crucial processes in
the hypothalamus based on anticipated activity and regeneration cycles.

When the master clock is out of phase it affects the body’s organ clocks as well.
With overall direction by the hypothalamus, the organ clocks are finely tuned with
functions optimized to activity or regeneration, depending on their place in the
circadian cycle. Exercising when the organs clocks are in regeneration mode, or
sleeping during activity mode places stress on the body.
 When the organ clocks are out of sync with your waking and sleeping activity,
they are not prepared to function optimally to support your activity. Waking activity
during circadian regeneration mode leads to poor physical and mental performance
as well as wear and tear on the body. Attempting to sleep in circadian activity mode
promotes poor mind and body repair and regeneration. Some possible scenarios are
outlined below.

Cortisol timing is off and may peak when you are trying to go to bed at
night instead of the normal time—just before waking. Cortisol at night is
stimulating to the mind and body and will disrupt sleep.

A heart clock still in regeneration mode while you begin the increased
activity of the day is not prepared to respond to the increased demands of
physical activity. Wear and tear on the heart is the result.

A liver clock still in regeneration mode while you are having a meal in the
morning will cause the liver to mishandle glucose or fat. Insulin
resistance, diabetes and fatty liver disease are possible long-term
consequences.

A pancreas clock still in regeneration mode during the day may not
produce adequate insulin to handle food intake, contributing to diabetes. If
the clock is in activity mode while you are sleeping, the inappropriate
insulin release may make your blood sugar too low at night.

A disrupted fat clock will cause adiponectin and leptin to be released at the
wrong times. The result will be hunger at night, disrupting sleep and loss
of insulin sensitivity leading to diabetes.

A muscle clock still in regeneration mode during physical activity will
lead to poor athletic performance. Muscle clock dysfunction can also
cause improper glucose handling leading to insulin resistance and
diabetes.

A broken immune clock can lead to a poor defense against “invaders”
during the day and poor formation of long-term immunity. It may also
lead to out of control inflammation which contributes to heart disease,
diabetes, cancer, and autoimmunity.

A broken kidney clock can cause poor regulation of fluid and electrolyte
balance contributing to high blood pressure, a risk factor for heart
disease and stroke.

A gut clock still in regeneration mode during a meal can lead to poor
digestion and poor movement of food through the GI tract. A gut clock in
activity mode during sleep leads to poor intestinal barrier regeneration
contributing to chronic inflammation.

TECHNICAL NOTE:
The organ clocks can adopt circadian rhythms independent of the master
clock with signals such as food intake and exercise. This can cause
problems with various organ clocks being on their “own schedule,” and
out of sync with each another. That is why the orchestrating function of the
master clock is so important, it ensures that the organ clocks work
together optimally.
THE MELATONIN CONNECTION?
One of the primary ways exposure to artificial light at night may slowly destroy
your health and vitality is through diminishing the amount of the hormone
melatonin. We previously described the potent effects melatonin has during the
regeneration mode as a powerful antioxidant and antiinflammatory agent. In
addition to acting as a direct antioxidant to scarf up free-radicals, it also strongly
stimulates the body’s own antioxidant defense system, protecting against oxidative
stress. Melatonin has been shown to protect against cancer and accelerated aging.
There are melatonin receptors (“docks”) in almost every type of cell in the body.
Melatonin truly has a long reach, potentially affecting every part of the mind and
body during its activity after dark as the gateway hormone to regeneration.

The benefits of melatonin are not a surprise given its protective effects against
oxidative stress and inflammation. Diminished melatonin at night due to circadian
disruption and reduced sleep is likely a primary mechanism through which sleep
and circadian disruption contribute to chronic inflammation and chronic oxidative
stress. These two processes are the well-known deadly duo leading to chronic
disease.

This is not to say that melatonin deficiency is the sole cause of all chronic
diseases arising from circadian disruption and poor sleep. It is a likely major
contributor, but circadian disruption and poor sleep activate the brain’s stress-threat
system on their own. The stress-threat system greatly increases the flight or fight
sympathetic nervous system activity level, resulting in inflammation and oxidative
stress.

KEY POINT:
Circadian disruption and poor sleep result in decreased melatonin
production, chronic activation of the stress-threat system, and physiologic
“wear and tear” on the internal organs.

This all adds to the growing pool of chronic inflammation and oxidative
stress which lead to chronic disease.
CIRCADIAN DISRUPTION, SLEEP, AND
DIABETES
When the body’s organs are forced to operate out of phase with their own
individual circadian clocks, the resulting metabolic derangement and physiologic
stress causes additional inflammatory responses and oxidative stress. This is
especially true of the liver, muscles, and the pancreas. Disruption of the natural daily
rhythm of these three organs is thought to contribute significantly to the
development of insulin resistance leading to diabetes.

The effects of circadian disruption and poor sleep on the development of insulin
resistance and diabetes can be profound. Several recent scientific studies have
shown that even a couple nights of poor sleep can increase insulin resistance to
prediabetic levels in healthy young people.

It was found that the loss of slow wave sleep (NREM-3) is the biggest contributor
to insulin resistance.
 KEY POINT:
A couple nights of poor sleep have been shown to increase insulin
resistance in healthy young people to prediabetic ranges.

Loss of slow wave sleep seems to be the most damaging.

If circadian disruption and reduced slow wave sleep can give a healthy young
person insulin resistance to prediabetic levels, imagine what metabolic havoc poor
sleep can have on an obese or diabetic person. For diabetes, we often focus on
nutrition and exercise to help control blood sugar levels. This is hugely important,
but a diabetic with disrupted sleep will have great difficulty meeting blood sugar
goals no matter how good they are doing with their nutrition and exercise.

QUICK MEDICAL NOTE:

If you are obese and/or diabetic, fixing your sleep must be a top priority.
Good nutrition and exercise are a great start, but you most likely be
unable to reverse type II diabetes without mastering your circadian rhythm
and getting recuperative sleep.

The next section will give the Strong Medicine Tactics to fix your sleep.

OTHER EFFECTS ON THE BRAIN AND

BODY

 Circadian disruption and sleep loss result in poor long-term memory formation
and difficulties with concentration. Both can also lead to anxiety and depression due
to their effects on the brain. Slow wave sleep (NREM-3) and REM sleep are crucial
for the brain’s recovery after a day of activity. During sleep, memories and
information are stored, emotional events are processed to promote resiliency, and
irrelevant “mental debris” from the previous day is cleared away.

Circadian disruption tears away the carefully structured sleep architecture, often
reducing slow wave sleep and REM time in favor of lighter sleep stages such as
NREM-1 and NREM-2. This results in light, non-regenerative, restless sleep. You
can get a full eight hours of this non-recuperative sleep and still feel like a truck hit
you in the morning.

BODY FAT, MUSCLE, AND SLOW

WAVE SLEEP
Remember that slow wave sleep is the primary time for growth hormone
release. Growth hormone is a major player in fat burning, muscle growth,
and muscle repair during the regeneration mode. Circadian disruption
leads to reduced slow wave sleep, a one-way ticket to body fat gain and
muscle wasting.

You will not reach your body composition goals unless you fix your
sleep.

A night of poor sleep will limit your productivity the next day, make it difficult to
concentrate or make decisions, and will decrease your ability to handle stress. Your
reaction time will slow to the equivalent of having a blood alcohol level above the
legal limit. A sleep-deprived driver can be just as dangerous as a drunk driver with
impaired ability to react in traffic. Make sure you get your slow wave sleep before
you drive.

QUICK FACT:
A sleep-deprived driver can be just as dangerous as a drunk driver. Studies
have shown that sleep deprivation results in reaction times as slow or
slower than a person with a blood alcohol level above the legal limit of
0.08 g/dL.

It’s likely that there are many more sleep-deprived drivers than drunk
drivers on the road. Driving while sleep-deprived is a real safety concern
and public health issue.

Spending time to fix circadian disruption can be especially important for people
suffering with depression. One of the interventions shown to be effective for
improving depressive symptoms is bright light therapy (BLT). We will discuss BLT
in the next section as a method to reset the circadian rhythm. The anti-depressive
effect of BLT in the morning supports the theory that a significant contributor to
depression may in fact be circadian disruption.

A final note to dieters struggling to control cravings and food intake.—circadian

disruption and sleep loss stimulate the drive to eat. The threat/stress response that
results from poor sleep puts the food reward system into overdrive. Poor sleep
results in a strong drive for palatable and rewarding foods that are often the same
foods a dieter is trying to avoid. Fixing your sleep and circadian system will put the
reigns on food cravings.

KEY POINT:
Circadian disruption and poor sleep put the food reward system into
 overdrive. Your goals of sustained lifestyle change will be sabotaged by
cravings if you do not address circadian and sleep issues.

SHIFT WORK: A CIRCADIAN NIGHTMARE

Part of the formal training in Occupational and Environmental Medicine (OEM)
includes chronobiology. Chronobiology is simply the study of natural biological
rhythms such as the circadian system. OEM physicians apply the knowledge of
chronobiology to shift workers. As much as 20% of the U.S. workforce participates
in some type of shift work.

Night time shift work is the ultimate circadian nightmare. It puts the worker at
complete odds with the natural cycle of the sun’s rising and setting for activity and
sleep.

• The night-shift worker starts his or her day during the darkness of night. They
are gearing up for physical and mental activity when the mind and body should
be entering regeneration mode.

• They are exposed to relatively low-intensity indoor light during their work
shift. This somewhat suppresses melatonin but does not give the strong circadian
signal for activity mode that high-intensity natural light provides. They often rely
on caffeine to block the sleep promoting effects of the adenosine which
accumulates while they are working.

• The night-shift worker often finishes their work shift as the sun rises in the
morning. During their drive home, the high intensity outdoor light is stops
melatonin production and places them in the circadian activity mode. The
circadian system issues them a “gold card” for adenosine with a high credit limit,
and prevents the accumulated adenosine in the brain from their time at work from
triggering sleep.

• The worker will go home and attempt to sleep while their circadian system is in
activity mode. The outside daylight seeps into their home during sleep and
decreases melatonin. The adenosine build up becomes so high that it is able to
override the circadian system to fall asleep but only for a short while. Most night
shift workers report only getting 5-6 hours of sleep at best in the daytime. The
sleep they do get has a significantly disrupted sleep architecture with shortened
slow wave recuperative sleep.

• The night-shift worker wakes in the afternoon and prepares for the physical and
 mental activity of their upcoming “day”. The sun sets during the hours when they
are preparing for work.

• These workers often eat their meals during the regeneration mode of the
circadian system, a time that the organs are not prepared to process and store
nutrients from food. This leads to metabolic derangement such as insulin
resistance.

The extreme circadian disruption and poor sleep of the shift worker results in
significant health consequences. Night-shift workers are at greater risk for
developing chronic diseases such as diabetes, obesity, high blood pressure, heart
disease, depression, accelerated aging, and cancer. In fact, the World Health
Organization has classified shift work as a carcinogen (cancer-promoting).

Many people have no choice but to perform shift-work to make a living and
provide for their families. In the next section, we will show some easy strategies
shift workers can implement to minimize the circadian disruption of and improve
their health.

EDISON’S FOLLY?
The point of this section was not to blame circadian disruption in modern society
on Thomas Edison’s amazing invention. There is no doubt that artificial light in the
modern world has dramatically altered how we live our lives and has allowed
increased productivity and an exponential rate of technological advancement over
the past century. Unfortunately, substantial negative impacts to our individual and
public health have resulted from this advancement as a tradeoff.

Modern problems require modern solutions. We will now provide some very
simple and science-based interventions that can go a long way in fixing your broken
clocks and restore the healing power of circadian regeneration mode.
CIRCADIAN DISRUPTION IV
MODERN SOLUTIONS TO A MODERN
PROBLEM

U.S. citizens are working longer hours than the citizens of any other
industrialized nation in the world. We are taking full advantage of artificial light at
night to work longer hours, making us especially vulnerable to circadian disruption.
Many other countries are not far behind us, with sleep disorders and circadian
disruption emerging as a worldwide public health problem—if not an epidemic.
Fueled by artificial light, our recreational activities are extending further into the
evening hours as well, with time spent in front of computer and television screens
constantly increasing.

Statistics from the National Sleep Foundation support the notion of inadequate
sleep as a public health epidemic.

• Over 60% of American adults experience sleep disruption on two or more

nights per week.

• Approximately 40 million Americans report chronic sleep problems.

 • Approximately 30% of Americans report routinely getting only 6 hours or less
sleep per night.

Additionally, the increased hours Americans are working do not translate into
increased productivity on the job. Sleep deprived workers are not efficient or
productive. An estimated $18 billion is lost every year in decreased productivity
from sleep loss in the U.S. alone.

We rely on stimulants such as caffeine during the day to keep us going while
adenosine levels keep piling up in the brain. Caffeine does not solve the problem
and we carry the accumulated adenosine as sleep debt, since we’ve artificially
stopping the sleep trigger. Most of us put off this sleep debt all week with stimulants
and try to repay it on the weekends by “sleeping in.” This pattern is hard on the body
and brain, and overfills our stress cup (allostatic overload).

We switch off the bright lights as we hit the bed, already well into the night. Then
we are frustrated that we can’t fall asleep immediately, as we struggle against a
circadian system disrupted by light at night. We resort to alcohol or prescription
drugs as sleep aids instead of fixing the underlying problem, a disrupted circadian
rhythm.

Alcohol and many of the drugs used to help people fall asleep dramatically alter
sleep architecture. Slow wave restorative sleep time (NREM-3) is reduced and
replaced by an increased time in the “light sleep” stage of NREM-2. You may fall
asleep faster, but you are missing the period of slow wave sleep crucial for your
health.

KEY POINT:
Alcohol and many of the sedative prescription medications alter sleep
architecture, reducing time spent in slow wave sleep.

Sending your circadian system the right signals at the right times can reset your
clock and will help break the cycle of using stimulants to keep you going and
sedatives to make you sleep. Stop fighting your broken internal clock. There are
some simple ways to realign your internal clock with your personal wake-sleep
needs, even if you are a shift-worker.

FIXING YOUR CLOCK

We can use light (even artificial light) to “train” your circadian system to match
up with your waking and sleeping schedule. Training the circadian system with light
exposure is what chronobiologists call entrainment. The timing of meals, body
temperature, and exercise can also be used to entrain the circadian rhythm, but light
remains the most powerful “trainer”.

The goal of training your circadian system is having your activity mode fall inline
with your time awake, and the regeneration mode synchronized with your sleep. This
is more difficult with extreme situations such as night-shift work, but still doable to
some extent. We will begin by showing you how to use light as a “circadian trainer.”

KEY POINT:
Fixing your clock involves getting the activity mode of the circadian cycle
to fall inline with your time awake, and the regeneration mode
synchronized with your sleep.

LIGHT AS THE MASTER-TRAINER

Recall that short-wavelength light in the “blue range” is a potent signal to turn off
melatonin and start the activity mode of the circadian system, while the dimming
light at the end of the day will trigger melatonin release in preparation for
regeneration. The following interventions will get you started in becoming a master
of your circadian rhythm...

 Dawn simulator

• Use a dawn simulator to make the transition from sleeping to waking gentle
and natural. Most people experience a startling transition from sleeping to
waking with the piercing sound of an alarm clock. Often they are in the middle of
REM sleep and the sudden loud noise rips them out of their dream state, leaving
them disoriented and with an elevated stress/threat system response. This is not an
ideal way to start your day. A relatively new technology allows a light to
gradually increase in intensity starting about 20-30 minutes before you plan to
wake. This technology is called a dawn simulator and is very valuable for those
who have to rise before the sun comes up.

The idea behind using a dawn simulator is to provide a very gradual transition
from darkness to light, mimicking the sun rising at your planned time to wake. The
gradual increase in light (even through closed eyes) signals the circadian system to
start shutting down melatonin production and prepare for activity mode. The
decreasing melatonin from the slowly increasing light will naturally and gradually
pull you out of sleep without the violent stimulus of an alarm clock. You can always
set the alarm as a backup, but you will only rarely need it when using the dawn
simulator. Philips makes a great dawn simulator.

• Get as much bright natural light as possible in the first hours after waking
up. After gently transitioning to the waking state with the dawn simulator,
continue to get exposure to bright natural spectrum light. Ideally this “natural”
light would be the sun, but realistically many of us will need to resort to artificial
sources of light that mimic the broad spectrum light of the sun. The most
practical way to do this in the morning is to buy light bulbs that emit a substantial
amount of “blue spectrum” light.

Many of these light bulbs are advertised as “natural” light on the package and are
rated with a scale called Correlated Color Temperature (CCT). The CCT scale relates
to the color of light produced and is measured in units of Kelvin (K). Low CCT
lights emit more yellow and orange light (longer wavelengths) and high CCT bulbs
emit more blue light (shorter wavelengths). Look for light bulbs that are rated in
the high CCT range, between 5000K and 6500K on the CCT scale for use in the
morning. CCT in these ranges has a substantial amount of blue light in the spectrum
and is the most similar to natural sunlight.
The left picture shows a low CCT and high CCT bulb next to each other. You can’t
tell which is which just by looking at them. The picture on the right shows the bulbs
in identical fixtures. You can tell the difference when the lights are on in the picture
on the right. The high CCT bulb is on the far right and the light emitted is “whiter”
(representing more blue light in the spectrum) compared to the light on the left that
looks yellow in comparison.

Install 5000-6500K CCT bulbs in areas of your home where you spend the most
time in the morning getting ready for work—the bathroom, bedroom, and kitchen.

You can find these compact fluorescent light bulbs at most large home
improvement stores and online as well. The blue light emitted from these bulbs is
enough to provide a strong signal to the circadian system to start activity mode.

STRONG MEDICINE TACTICS:

Install light bulbs with a CCT between 5000-6500K in areas of your home
where you spend the most time getting ready for work in the morning to
maximize your blue light exposure after waking.

RESEARCH UPDATE:
Recent research has shown that exposure to light with high blue spectrum
content in the first few hours after waking increases alertness, decreases
 feelings of fatigue, increases brain function for problem solving, and
enhances productivity at work.

This will help synchronize your initial waking time with the start of the circadian
activity mode.

Using high-range CCT artificial light just after waking is especially important if...

• You do not have time to spend outdoors in the morning sunlight.

• You need to wake up before the sun rises.
• You live in a region predominated by gray skies and rain with little sunshine.
• You work indoors.

Giving a strong signal to start the circadian activity mode with blue spectrum
light will ensure that your waking time is supported by the master clock and organ
clocks, optimizing mind and body functions for the demands of the day. This simple
intervention will ensure your circadian system issues you an adenosine “gold card”
to prevent fatigue during your waking hours.

As your waking time draws to an end, we have to give an equally strong signal to
start the circadian regeneration mode and prepare for sleep. The strategies to
synchronize entering regeneration mode with your planned bedtime are the opposite
from the morning strategy. We need to eliminate blue spectrum light exposure.

• Eliminate exposure to blue spectrum light 2-3 hours prior to your planned
bedtime. You can still use artificial light after the sun goes down, but the type of
light used is crucial to prevent circadian disruption. Recall that it will take about
2-3 hours after the last blue spectrum light exposure for melatonin levels to start
to rise, signaling the start of regeneration mode. If you can synchronize the start
of melatonin production with your planned sleep time, your transition into a deep
recuperative sleep will be effortless.

The easiest way to avoid blue spectrum light but still have artificial light for
evening activities is to use compact fluorescent light bulbs that are yellow/orange
in color. These bulbs are traditionally sold as “bug lights” in home improvement
stores. The yellow/orange bulbs should be installed in the areas of your home
where you spend most of your late evening hours.

Approximately 2-3 hours before you plan to sleep, turn off all the light sources
except for the yellow/orange “bug lights.” This will allow you to continue
evening activity without disrupting melatonin production. By the time you get
ready to sleep, melatonin production and the beginning of regeneration mode
will have started. Sleep should come much easier.

SCIENCE TRIVIA
Yellow “bug lights” block most of the blue spectrum in visible light. Bug
lights do not repel insects as many people believe, they just do not attract
bugs. Many insects are very receptive to short wavelength light (blue
spectrum) and use it as a navigational aid. If they detect blue spectrum
artificial light at night they are drawn to it. They will not detect the light
from the yellow bulbs because most of the blue spectrum has been
blocked.

STRONG MEDICINE TACTICS:

Install yellow/orange light bulbs (“bug lights”) in areas of your home
where you spend the most time in the late evening to eliminate blue light
spectrum exposure 2-3 hours before planned sleep time.

QUICK TIP:
 Many people spend a significant amount of time in some areas of the
house in both the morning and the evening (kitchen, bathroom, etc.). Many
of these “dual use” areas have more than one light source. Take advantage
of this and install the high CCT natural light in one source for morning
use, and the “bug lights” in another source. This way you can use certain
light switches for the morning to get blue light exposure and the other
switches for turning on the “bug lights” in the evening to avoid blue light
exposure before bedtime.

• Use amber-tinted glasses to eliminate blue light exposure from computer

monitors or TV screens. Modern computer and television screens emit LED-
generated light with a substantial amount of blue light in the spectrum. Staring at
these screens until bedtime will ensure that your circadian rhythm is disrupted by
delaying melatonin production and regeneration mode. There are blue light
filters you can purchase for television and computer screens but a simpler option
is just to wear amber-tinted glasses to block the blue spectrum light.

The glasses are a great option for people with family members or roommates
that will not support the use of the “bug lights” at night. Just put the glasses on 2-3
hours before your planned bedtime to ensure melatonin production happens on
schedule.

Amber-tinted glasses- an inexpensive circadian solution

The amber-tinted glasses are also very valuable for night-time shift workers who
have to drive home as the sun is coming up. The glasses will block the blue
spectrum part of the morning sunlight and prepare you for sleep when you arrive
home. More on this use to come...
 STRONG MEDICINE TACTICS:
Wear glasses with amber-tinted lenses to block blue spectrum light from
televisions and computer screens at night. The glasses are also valuable to
shift-workers.

• Ensure your bedroom environment is optimum for sleep. These interventions

are crucial for ensuring a night of regenerative sleep. Your sleep environment
should be similar to a cave.
— Keep the bedroom cool (usually between 65-72 degrees depending on
individual preference). Part of the regeneration mode is a slow fall in body
temperature as the night progresses. A cool room encourages this natural fall in
body temperature.
— Keep the bedroom dark. Use “black-out” curtains to block outside light
from neighbors’ porch lights and streetlights. You can buy black-out curtains at
most major retailers. Cover any light-emitting electronic devices as well.
— Move televisions out of the bedroom. Bedrooms should be dedicated to
sleeping. If this is not an option, make sure you wear the amber glasses while
watching TV before bed.

STRONG MEDICINE TACTICS:

Make your nighttime sleep environment “cave-like” to ensure
uninterrupted regenerative sleep.

These relatively simple interventions strategically using light to train your

circadian system are extremely effective. They all have been tested in research
settings with positive results. Although light is the most powerful “trainer” of your
circadian system, exercise can have dramatic effects as well as long as it is properly
timed.

EXERCISE AND THE CIRCADIAN SYSTEM

 Your muscles, heart, liver, and adipose tissue are all directly involved in
supporting exercise. Each has its own organ clock governing function during
activity and regeneration modes. Obviously, exercise should take place in the
activity mode of the circadian cycle, since the body is not optimally primed for
exercise during regeneration mode. Most people do not wake up in the middle of
their sleep to exercise, but many do perform exercise near the transition zones
between activity mode and regeneration mode which can be problematic.

The benefits of regular exercise can be obtained anytime during the activity mode
of the circadian system. Exercise timing falls more to individual preference and
schedule requirements. There are two general guidelines to follow:

• Ensure that your body and brain have received a strong signal to enter activity
mode before exercising first thing in the morning. Use the early morning light
exposure strategies discussed previously to ensure your circadian clocks are set
to activity mode before starting exercise.

• Avoid exercise 2-3 hours before planned bedtime. Exercise during this time
acts much like blue light and can delay the onset of melatonin production and
delaying entry into regeneration mode.

STRONG MEDICINE TACTICS:

Perform exercise consistently at the same time of the day. This will train
your clocks to anticipate physical activity, and prepare your body to
optimally support exercise.

RESEARCH UPDATE:
Recent research has shown that muscle is able to generate the most force
near the end of activity mode. Late afternoon or early evening exercise
may be the natural time in the circadian cycle for peak performance.
 This does not mean that exercise at different times of the day is less
effective in promoting favorable adaptive gains in strength and fitness.
The muscle clock can be “entrained” to anticipate exercise at different
times during the activity mode if you consistently train at the same time of
day.

Consistency in training time seems to be the best way to ensure that your
system is prepared for exercise, whether your training sessions are in the
morning, lunchtime, afternoon, or evening.

COACH’S CORNER:
If you are a competitive athlete and have an upcoming event, adjust your
daily training time to the event’s time. If your competitive event is at 4PM,
you should adjust your daily training time to as close to 4PM as possible,
allowing your body clocks to support maximal performance at that time.

While exercising within 2-3 hours of planned sleep will delay entry into
regeneration mode, an exercise session 4-6 hours before sleep (late afternoon/early
evening) will have the opposite effect on the circadian system. Research has shown
that late afternoon/early evening exercise can actually help stimulate melatonin
production and the beginning of regeneration mode.

Scheduling exercise 4-6 hours before planned sleep and avoiding blue light
exposure will send a strong signal to enter regeneration mode, greatly aiding your
transition to recuperative sleep.

STRONG MEDICINE TACTICS:

Exercise 4-6 hours before planned sleep time to aid in priming melatonin
production and the onset of regeneration mode.
 The sleep enhancing effects of exercising 4-6 hours before planned bedtime is the
only reason to advocate a specific time for exercise. If your schedule will allow for
it, this is a pretty good reason to switch over to late afternoon or early evening
exercise.

MELATONIN SUPPLEMENTATION?
Recently there has been a substantial amount of research on melatonin
supplementation and chronic disease. In some scenarios, supplementing melatonin
may show some benefit, but the Strong Medicine approach is to support the body’s
own production of melatonin with the proper environmental cues—light, exercise,
etc.

Most melatonin supplement dosage is well beyond what the body will produce
naturally and may cause problems by inhibiting the body’s natural production of
melatonin with long-term use. The other problem with melatonin supplementation is
that it has a very short half-life in the body. The melatonin only lasts for about 20-40
minutes in the bloodstream before it is metabolized and eliminated.

The pineal gland in the brain constantly produces new melatonin during the night
so this is not an issue the during regeneration phase. However, a single supplement
will only last for 20-40 minutes. You would have to take melatonin approximately
every 30 minutes to mimic the pineal gland’s natural production during sleep.
Supporting the natural cycle of melatonin production through the right
environmental signals such as light and exercise is a much better solution to
circadian problems.

MELATONIN SUPPLEMENTS AND

JET LAG
Temporary use of melatonin can be useful for adjusting to rapid time
changes from jet travel. Taking a low dose (usually 0.3 mg) of melatonin
before bedtime after arriving in a new time zone may help you fall asleep
for the first couple of nights as your circadian system adjusts.
 RESEARCH UPDATE:
A longer acting melatonin supplement is currently being researched for
use with the elderly and those with Alzheimer ’s. As we age, melatonin
production declines. There may be some benefit to using a long-acting
melatonin formulation to counteract the declining melatonin production to
help restore normal sleep for the elderly. Use of melatonin for
Alzheimer ’s (AD) patients is also an active area of research as AD also
decreases melatonin production.

SHIFT WORKER CASE STUDY

The circadian disruption from nightshift work is very difficult to correct since
the schedule is completely at odds with the natural cycle of light and dark that
entrains the human circadian rhythm. With careful planning and smart use of light
exposure strategies it is possible to improve the quality of life—and likely the long-
term health—of the nightshift worker. One possible strategy:

• Get blue spectrum light exposure upon waking and if possible, during the first
couple hours of work. Some corporations have installed high CCT (more blue
spectrum) lighting during night shifts to increase alertness and enhance
productivity. If you are able to change the lighting in your work area yourself to
this type of light, do it. There portable blue light emitters are available that can be
powered by a USB port on your computer and can be mounted on your monitor
or laptop.

• Make sure your eating cycles correspond to your waking time. Eat when you
get up for work, eat “lunch” mid-shift at work, and eat a meal when you get home
in the morning. This will help keep your organ clocks working with your master
clock.

• When driving home after the end of your shift, wear amber-tinted glasses to
block the blue spectrum light from the rising sun. Keep the glasses on after work
to block the blue spectrum light from outside and from lighting inside the home.
A nightshift worker has to be a little more aggressive with their time spent
wearing amber glasses because they are working against daylight permeating
everything.

• Ensure that no sunlight intrudes into your bedroom from outside. You will have
to be extremely diligent about blocking the sun from your room which may
require covering your windows with opaque material in addition to using
 blackout curtains. This is where shift workers often fall short in their attempts to
sleep—even a little outside sunlight in the bedroom will stop melatonin
production and bring them out of sleep.

A similar strategy to the one outlined above was recently used in a research study
with small groups of shift workers such as nurses and police officers. The results
showed improved quality and duration of sleep time, and improved alertness and
productivity. Much more research needs to be done in this area but the initial results
are promising. These strategies are worth trying if you are a nightshift worker
struggling with sleep.

CONCLUSION
Circadian disruption is widespread in modern society. Artificial light pollutes the
total darkness that once existed during the night. Not all sleep disorders are
primarily circadian problems, obstructive sleep apnea and anxiety are conditions
that result in fragmented sleep without circadian disruption. However, it is very
likely that optimizing your circadian rhythm will make treating these sleep
problems easier.

Losing weight using the Strong Medicine Tactics in the obesity chapter will
certainly help obstructive sleep apnea, and interventions from the chronic stress
chapter will go a long way towards squashing anxiety. The integrative approach to
chronic disease in this book will have crossover effects, often improving seemingly
unrelated conditions. The mind and body are not a collection of separate organ
systems; everything works together in harmony when everything is functioning
correctly. This chapter hopefully illustrated the importance of the circadian system
as a master conductor which ensures the synergy of the entire flesh machine.
Incorporating the strategies in this section will go a long way towards helping you
improve your overall health and prevent chronic disease.

By using the Strong Medicine Defensive Tactics in this section, you can
reestablish the synchrony of your internal clocks with your waking and sleeping
times—and master your circadian system. The “Thief in the Night” will no longer
steal the restorative sleep so crucial for your health.
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 PART III

BATTLE PLAN
“The best defense is a good offense.”
—Jack Dempsey


You now have the latest intelligence on the on the inner workings of the enemy
—and defensive tactics at your disposal to repel the advances of the
Pentaverate. It is time to put your training into action by formulating your
individual battle plan. Before you move your troops to the front line, we will
give you some training in battle strategy.

In Part III you will develop a foundation in Strong Medicine physical training,
learn the importance of food quality, and strategies for the optimum feeding of
the flesh machine. You will put together an individualized plan for lifestyle
change using your previous training and defensive tactics, and finally track
your progress with analytics (“stuff you can measure”). Put your pieces on the
board and we will show you how to place the Pentaverate in checkmate with a
devastating offensive strategy.

I. Strong Medicine Physical Training

II. Strong Medicine Nutrition: Individualized Strategies
III. Putting It All Together
IV. Analytics: “Stuff You Can Measure”
BATTLE PLAN I
PHYSICAL TRAINING: UNLOCKING
YOUR BODY’S POTENTIAL

STRONG MEDICINE PHYSICAL

TRAINING
Regular, mindful, intense physical training is central to the Strong Medicine
transformational plan. The body and mind need physical stress to thrive, and the
absence of regular exercise results in physical and mental deterioration over time.
The necessity of physical stress through exercise is supported by the health benefits
shown by scientific research.

• Exercise slows the aging process.

• Exercise protects us from bone and muscle wasting (osteoporosis and
sarcopenia).
• Exercise dramatically increases insulin sensitivity, protecting us from diabetes
and obesity.
• Exercise strengthens the heart and prevents heart attacks and stroke.
• Exercise rebuilds the stressed brain, making us resilient against chronic stress.
• Exercise protects us from neurodegenerative diseases such as Alzheimer ’s
Dementia.
 • Exercise helps us build a strong immune system and recover from illness
faster.
• Exercise makes us more physically resilient, preventing injury and allowing
for faster recovery after injury.
• Exercise helps reset a broken circadian rhythm.

Without exercise and its protective benefits in your daily life, the aging process is
accelerated and you are vulnerable to disease and injury.

In the terms of hormesis, inactivity represents an inadequate “dose” of exercise

and physical stress. We are going to show you how to train smartly and effectively
to maximize your health benefits by staying in the “green zone” of the proper dose
of exercise. We will also keep you out of the “overdose” zone that so many people
fall victim to if they’re following a regular high volume “boot camp beat down”
program.

The Strong Medicine physical training program does not require gym
memberships, huge time investments, or fancy equipment. We are going to strip
things down to the basics and give you a foundation for a lifetime of health and
fitness.

Inactivity is the fifth member of the “Pentaverate,” the cabal of chronic preventable
disease. Like the other four members, inactivity results in chronic inflammation and
oxidative stress.

We can break this link to chronic disease with a scientifically-based training

program, informed by an elite-level coach’s years of experience.

We will start with a primer on progressive resistance training—a true fountain of

youth—then present a scientific approach to cardiovascular training. These exercise
defensive tactics are the equivalent of a tactical nuclear weapon against the
Pentaverate. This is high-yield training for your war against chronic disease and a
keystone for achieving your genetic potential.

We are only going to cover a few critical exercises to build a progressive

resistance training foundation. You may add other exercises to create your own
individualized program, but these core movements should be the pillars of your
program:

• The Squat
• The Deadlift
• The Bench Press and Military Press
• The Row
• Abdominal Training
PHYSICAL TRAINING I
STRONG MEDICINE RESISTANCE
TRAINING: INTRODUCTION

USE IT OR LOSE IT
In a fundamental sense, muscle and strength follow a “use it or lose it” scenario—
but that would imply that the aging population (over 60) “had it” to begin with—yet
flaccidity is epidemic in most of the Western population long before the sixth
decade is reached.

A cursory glance at traditional hunter-gatherer cultures (the few still in existence)

reveals that their senior citizens are muscular, ripped and functional. They always
had “it” and never lost “it.” They were lean with functional muscularity in their
youth, maintained their physique through mid-life and retained it in late life. The
elders in tribal cultures are active, fit, disease-free and exhibit the lean muscle mass
that twenty-year-olds of modern society would envy.

Their secret is simple; they maintained their primitive diets, eating the food-fuels
they were designed to use. They inherited excellent genetics and attained a
miraculous degree of functional fitness in their youth. They never stopped using
their bodies in intense and prolonged ways, and as a result their flesh-and-blood
machinery retained a magnificent readiness. Instead of driving carts around a golf
course, these senior citizens lift, carry, run, jump, and hunt.
 Compare this to the classical ‘civilized man’ born in a controlled environment,
and who has never attained fitness. Fueled by artificial ‘foods’—just like running a
race car on cheap kerosene instead of nitro-methane—this ‘civilized man’ has never
exerted himself in the slightest. With no muscle tone or strength gained earlier in
life, physical functionality continues to diminish from an ever-increasing lack of
late life activity. The end result is a pathetic, weakened creature unwilling, unable
and incapable of being functionally mobile. Weak flaccid muscles grow weaker,
bones which have never been stressed become lighter than air. Further immobility is
compounded with fragility. Next they might fall down—if they are lucky, they’ll
avoid shattering a hip as fragile as a glass figurine on concrete—at best they will
have fallen and are incapable of standing back up.

We have all seen the commercial with the pathetic plaintive cries of the elderly
person helpless on the floor after a fall. The advertisers are saying, if you are old
you need their “alert system” so you can be safe and secure in your own home. The
not-so-subtle underlying message is that this situation is inevitable for everyone in
the last decades of life. But, this could be your fate if you succumb to sarcopenia and
osteoporosis in your “experienced” years.

We are seeing sarcopenia at younger and younger ages in modern society. It’s
caused by a lack of resistance-based activity in an increasingly sedentary population.

SARCOPENIA
Sarcopenia literally means “loss of skeletal muscle mass”—and the resulting loss
of strength—as we age. You may think it is natural and expected for everyone to
lose muscle as we age. Yet, we can do plenty to slow the decline of muscle-mass
through the expert use of resistance training. Sadly, the majority of us are needlessly
sarcopenic.

• The rate of muscle loss in adults is 1-2% every year after age 50.
• Strength loss after age 60 is 3% every year.
• The healthcare cost of sarcopenia is 18 billion dollars every year.
• Sarcopenia has been associated with increased risk of death.

MUSCLE MASS MAINTENANCE IS CRUCIAL FOR HEALTH.

• Retaining muscle mass and strength keeps a person biologically young,
regardless of their chronological age. Many adherents to resistance training are
able to retain lean muscle mass and tremendous strength late into their 70s and
80s. Many 50 year olds have a body significantly more capable and functional
than sedentary 25 year old men and women.
 • Maintaining muscle mass is the best defense against insulin resistance and
diabetes. Muscle is the largest insulin sensitive organ in the body. The loss of
muscle mass (sarcopenia) disrupts the body’s ability to handle glucose
effectively. Loss of muscle mass has been shown to be an extremely strong
predictor of the development of insulin resistance and diabetes.

• Progressive resistance training is hugely beneficial in treatment and

prevention of sarcopenia. Clinical studies repeatedly show the benefit of
progressive resistance training in treatment and prevention of sarcopenia.
Impressive improvements in strength are routine; power is gained from specific
workout protocols. Strong Medicine protocols can increase power, strength, and
can stop sarcopenia in its tracks.

OSTEOPOROSIS
Our bones are the body’s central support structures which allow us to function
upright against gravity. Our muscles can only exert force when they are attached to
our bones, so maintaining a robust skeletal system is of upmost importance—
particularly as we age. Osteoporosis is the thinning of bone tissue as mineral
content decreases. The body constantly builds new bone while reabsorbing old bone.
Osteoporosis and osteopenia (the early stages of osteoporosis), occur when bone
break-down exceeds bone construction.

Osteoporosis is rampant in women after menopause. One out of five women over
50 have some degree of osteoporosis. Half of women over the age of 50 will suffer
a hip, wrist, or spine fracture in their lifetime. Men get osteoporosis later in life than
women, but are still at risk. There are many contributors to the development of
osteoporosis, but inactivity—specifically lack of resistance training—is the
primary factor that enables osteoporosis to take root.

If we view osteoporosis through our “first principles” lens, bone physiology is

simple—bones respond favorably to systemic, prolonged and consistent resistance
training by becoming thicker, denser, and more resistant to breaking, chipping or
cracking. Bone subjected to weight training grows dense and strong.

The age-defying benefits of resistance training do not require a complicated

approach. The Strong Medicine approach uses simple stripped-down strength
training protocols accessible to everyone.

KEY POINT:
If you want to age successfully, prevent life altering fractures, and stave
off insulin resistance and diabetes, then resistance training is not optional.

DOING FEWER THINGS BETTER

Long before the current economic crisis forced fitness-minded individuals to
reexamine and reduce their fitness spending, barebones approaches were
prophetically championed by retro experts. These men insisted that modern fitness
—fancy health clubs, ineffectual personal trainers, expensive exercise machines,
elaborate supplements and miracle fat burners—was bogus, false and not nearly as
productive as the old-school methods first used in the 1950s.

This back to basics approach is always a tough sell, especially during good
economic times. But now, people are taking a second look at minimalistic training
methods.

• The most result-producing methods of progressive resistance training use free-

weights—barbells, dumbbells, and kettlebells. The goal of resistance training is
to build and strengthen the 600-plus muscles in the human body. Compound
multi-joint exercises using barbells and dumbbells cause groups of muscles to
work together in synchrony to stimulate muscle fibers in a way unobtainable
using resistance machines.

• Exercise machines that mimic free-weight movements are demonstrably

inferior since they eliminate the “third dimension of tension.” Free-weight
exercises require activation of the muscle stabilizers to control side-to-side
movement. Free-weight exercises always result in more muscle fiber stimulation
 (the goal of resistance training) than resistance machines mimicking free-weight
exercises. Free-weight exercises also translate better to real-life movements such
as lifting, carrying, pushing and pulling.

MAKING LIGHT WEIGHTS HEAVY

Although one of us is a top powerlifting coach, we are not here to make you a
powerlifter. You do not need to fear getting crushed under a heavy barbell or
otherwise injuring yourself with heavy weights with the Strong Medicine approach.
Our techniques use relatively light weights to maximum benefit by “making light
weights heavy.” This will protect you from injury while you make transformative
gains in strength and function. There is no need to fear free-weights.

The Strong Medicine program is truly strength training for anyone. It doesn’t
matter if you are very experienced or have never performed a squat in your life. We
will build you from the ground up with technique, strength, and confidence.

You will learn free-weight lifting techniques step-by-step from a master coach
with 50 years of experience. The squat, deadlift, bench press, overhead press, and
the “statue row” will be the pillars of the program. Even if you are experienced with
the lifts, you will improve your technique and maximize your strength gains. We
will also show you how to maximally train the abdominal muscles without ever
doing a sit-up or crunch.
PHYSICAL TRAINING II
KING SQUAT

“KING SQUAT”

Friends don’t
let friends squat high.
Why is the squat the king of all progressive resistance exercises? When it comes
to building leg power, proper upright squats performed with a perpendicular torso
and significant weight is unsurpassable. Properly performed, full, deep squats
stimulate more muscles than any other single progressive resistance exercise.

No one does proper full squats anymore for numerous reasons. “Experts’’ of
every kind have either condemned full squats as dangerous—or worse, they teach
some perverse technical abomination instead of the productive classic deep squat.
Our core technique for all squat variations—front squats, back squats, kettlebell
squats, or squats with no weight—is identical. The hardcore squatter ’s motto is,
“Shallow squats are worthless squats. Friends don’t let friends squat high.”

SOME TRAINERS AND MEDICAL

PROFESSIONALS WILL SAY, “DEEP
SQUATS ARE BAD FOR THE KNEES.”

My response—after watching them demonstrate a squat—is, “The way

YOU squat is bad for the knees.”

A deep squat with the correct biomechanics (body positioning) is far from
“bad for the knees.” The forces on the knee joint in a proper deep squat
are significantly less than in partial or parallel squats.

The damaging forces in question are joint shear and compression stress.
Compression stress is the stress on the knee from force pushing the knee
cap backwards onto the knee joint. Joint shear is a force attempting to
move the upper leg bone (femur) either backwards or forwards over the
tibia (a lower leg bone).

Many trainers will tell you not to squat below parallel. This is bad advice
since the greatest compression stress on the knee occurs at parallel (90
degrees). These trainers want you to stop your squat then exert more force
to stand up from the point of maximum compressive force on the knee
joint. This makes NO sense.
 Also, most people squat by initiating the movement from the knees first,
shooting the shins way out in front of the feet. This knee poison puts huge
joint shearing forces on the knees.

Force measurements of the deep squat with vertical shin position show
less compression stress and less joint shear than the “safe” parallel or
partial squat.

The deep squat is not only safe for knees, but may actually help strengthen the
knee joint and make it more resilient in daily physical activities and sports. Olympic
weightlifters routinely go into ultra-deep squat positions with heavy loads and have
one of the lowest rates of knee injuries in any sport. This is a proven fact.

We have taken countless clients who previously avoided squats because they “hurt
their knees” and have helped them perform full depth, pain-free squats in a matter of
minutes.

MAKING LIGHT SQUATS HEAVY

No other progressive resistance exercise triggers the primal “fight or flight”
psychological response to the same degree as limit squats. Limit squatting unleashes
tremendous hormonal benefits. We seek ways in which to increase squatting’s
degree of difficulty. Why would we want to exponentially increase the difficulty of
the world’s most excruciating exercise? Why are we requiring butt-to-heels depth
on every rep of every set—with a purposeful pause at the bottom of each super-deep
rep? Because this will strengthen the squatter over the entire range of motion
(ROM). This will simultaneously maximize muscle growth and exponentially
increase our brute power. Strict attention to technique will limit the amount of
weight we’re able to handle—we will reap maximum physiological results by
lifting a minimum amount of weight.

The Strong Medicine squat technique makes light weights heavy by achieving an
ultra-deep squat depth and pausing at the bottom of the rep before ascending.

• The ultra-deep squat involves starting the upward movement from a

compromised position—as far as leverage allows and the optimum length the
muscle will stretch. There is no need to load up on the weight. The ability to get a
potent neurological stimulus (our goal with strength training) from relatively
light weight, has many advantages. You can generate much more strength
(technically, torque) in a curl when your elbow is flexed to 90 degrees than when
it is fully extended. The ultra-deep squat puts you at a leverage and muscle length
 disadvantage, requiring much more effort from the nervous system to drive you
out of the bottom. This allows us to use light weights and still trigger the adaptive
response. Light weight also decreases load on the spine, making our squat safer
for those with a history of back injuries.

• The pause at the bottom of the squat makes light weights heavy by taking away
an important advantage—the stretch shortening cycle (SSC). This a reflex
similar to the one produced when a doctor hits your patellar tendon with a reflex
hammer. The SSC is most active in plyometric exercises, but research has shown
that it is also significant in normal-speed squats. The lowering portion of a
normal speed squat increasingly stretches the leg muscles. This stretch primes
them for greater activation, and adds to the force used when ascending from the
squat. Think of it as a “turbo boost” from the bottom of the squat. But, there is
only a very short window for taking advantage of this SSC reflex. Our insistence
on a one second pause at the bottom of the squat takes away this “turbo boost”
reflex.

COACH’S CORNER:
When we champion maximum range-of-motion squats, we are accused of
resistance training malpractice. Delicate people claim squatting that deep
will blow out knees and cause the deep squatter to become permanently
confined to a wheelchair. Despite being called out on it, and despite the
lack of deep-squat cripples or blown knee victims, the seriousness of the
accusation has gained traction in the wider athletic training community
who largely believe super deep squats are dangerous.

Meanwhile, trainees who squat super deep using precise techniques

develop injury-proof knees and astounding muscle and strength results.

BASIC SQUAT MECHANICS DESCENT

 BASIC SQUAT MECHANICS ASCENT

SQUAT PROGRESSION 1: THE

BODYWEIGHT SQUAT
1. The bodyweight squat is the key squat progression, the foundation on
which all subsequent squat variations are built. Learn it, master it.
2. Start with a shoulder-width stance, and toes slightly turned outwards.
3. Sit back and down while keeping your shins vertical. Do not let the
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Imagine a stake driven through the mid-foot to keep you rooted into
the floor.
6. On ALL squat variations, the knees are FORCED out to the sides
(laterally) during descent and ascent.
7. Inhale into the lower belly as you descend.
8. Knees should stay over the ankles as much as possible, and not shoot
out in front of the toes.
9. Sink all the way to the bottom, going as far as you can while
maintaining correct form.
10. In the bottom position, exhale; relax and sink further, losing all
tension. (Only do this with bodyweight or light loads).
11. After a one second pause, using diaphragm breathing, inhale to
ascend while pushing your gut out against your thighs.
12. For heavier loads, use this alternate technique: inhale, sink to the
bottom, maintain tension and pause for one second. Exhale at the top of the
ascent.
13. When ascending DO NOT let the tailbone shoot up first! The tailbone
and upper body should move as one unit during ascent. “Grind” out of the
bottom position.
14. Perform three sets of 10 reps before moving up to loaded squat
variations. Stop immediately if your technique breaks down.

“GRIND” THE SQUAT

After sinking as low as possible while maintaining a bolt-upright torso,
the squatter pauses a beat before ascending. How someone rises from a
paused, upright, ultra-deep squat determines the amount of benefit he or
she will derive.

Never let the tailbone “shoot upward” when the ascent begins from the
bottom of the squat. Fight this natural inclination to “make the move
easier” on the legs. When the tailbone shoots upward, allowing the legs to
extend, they’re put in a much more favorable position to push. But, it’s a
devil’s bargain—allowing the tailbone to shoot up causes your weight (or
bodyweight) to shift forward, in front of the feet. Now the spinal column
must be hoisted erect, using the hip-hinge and a few tortured vertebra on
the verge of ruptuing.

Instead, we should “grind” out of the bottom, embracing the sticking point
and slowly pushing through it with perfect technique, the tailbone and
upper body rising as one unit.

A purposefully slowed “grind” speed is an expression of low-end torque.

The actual speed of the grind rep is not—and should never be—radically
slowed down. Slow rep proponents continually make this fatal mistake.
Grind speed is purposely slow, just barely slow enough.

We “make light weights heavy” by adding “intensity boosters” to full

range-of-motion squats. We add pauses at grind rep speed to create the
ultimate excruciating exercise. Repeatedly grinding full ROM paused
squats optimally trains proper technique.

THE BODYWEIGHT SQUAT

Side view of squat descending sequence

 Front view of squat ascending sequence

SQUAT PROGRESSION 2: THE

GOBLET SQUAT
The second squat progression, uses added weight held with both hands out
front like a goblet. Otherwise, it is performed exactly like the bodyweight
squat.

The added weight in front acts as a counterbalance to make sitting

backward in the squat feel more stable.
1. Hold a single appropriately-sized kettlebell or dumbbell at chest height
with both hands.
2. Start with a shoulder width stance, toes slightly turned outwards.
3. Sit back and down while keeping your shins vertical. Do not let the
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Inhale into your lower belly as you descend.
6. Force your knees out to the sides (laterally) during descent and ascent.
7. Knees should stay over ankles as much as possible, they should not
shoot out in front of the toes.
8. Sink all the way to the bottom, or as far as you can descend while
maintaining correct form.
9. In the bottom position, exhale then relax and sink further, losing all
tension. Only perform this step with bodyweight or light loads.
10. After a one second pause, using diaphragm breathing inhale to
 ascend while pushing your gut out against your thighs.
11. For heavier loads, use this alternate technique: inhale then sink to
bottom while maintaining tension. Pause for one second. Exhale at the top
of the ascent.
12. When ascending, DO NOT let the tailbone shoot up first! The
tailbone and upper body should move as one unit during ascent. “Grind”
out of the bottom position.
13. Follow the sets and reps of your current program. Stop immediately
if your technique breaks down.

THE GOBLET SQUAT

Goblet squat descending sequence: note that the knees are forced out to the sides as
he initiates the movement from the hips, sinking back and down. The spine stays
straight into the bottom position. He will pause for one second at the bottom
position and then ascend with his tailbone and upper body moving together.

SQUAT PROGRESSION 3: THE FRONT

SQUAT
The third squat progression, uses added weight in each hand, held at
shoulder level. Otherwise, it is performed exactly like the bodyweight
squat.

The added weight held at shoulder level makes the abdominal muscles
work hard to maintain a stable upright posture.
1. Hold a single appropriately-sized kettlebell or dumbbell in each hand
at shoulder level. Arms are kept tight against your ribs.
2. Start with a shoulder width stance, and your toes slightly turned
outwards.
3. Sit back and down while keeping your shins vertical. Do not let your
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Inhale into your lower belly as you descend.
6. FORCE your knees out to the sides (laterally) during descent and
ascent.
7. Your knees should stay over your ankles as much as possible, they
should not shoot out in front of your toes.
8. Sink all the way to the bottom, or as far as you can descend while
maintaining correct form.
9. In the bottom position, exhale then relax and sink further, losing all
tension. Only perform this step with bodyweight or light loads.
10. After a one second pause, using diaphragm breathing inhale to
ascend, pushing your gut out against your thighs.
11. For heavier loads use this alternate technique: inhale then sink to the
bottom while maintaining tension. Pause for one second. Exhale at the top
of the ascent.
12. When ascending, DO NOT let the tailbone shoot up first! The
 tailbone and upper body should move as one unit during the ascent.
“Grind” out of the bottom position while keeping an upright posture.
13. Follow the sets and reps of your current program. Stop immediately
if your technique breaks down.

THE FRONT SQUAT

Front squat: the higher center of gravity of the weight makes for a increased
challenge for the core to maintain a straight spine during the movement.

HELP FOR BEGINNERS WITH KNEES

THAT SHOOT FORWARD
Newcomers to the squat often struggle to start their descent with a hip hinge.
Instead, they will immediately shoot their knees forward to squat, putting significant
shearing forces on the knees. People with this motor pattern avoid squatting because
it hurts their knees—and no doubt it does!

The most direct way to stop the “shooting knee” pattern is to position the lower
body so that shooting the knees forward is almost impossible. This will force the
correct pattern of beginning a squat with a hip hinge. Simply place the forefoot on a
1-2 inch board as shown below.
 Practice with the board until the hip hinge feels natural, then remove the board
and start training.

Knees shooting forward is poor squat form and bad for the knees.

Placing the board under the feet does not allow for the knees to come forward, and
helps train starting the squat movement from the hips.

KNEE COLLAPSE?
 Knees collapsing inward (called “valgus collapse” in medical terminology)
during the squat is the most common fault seen in those who include the squat in
their training. It is an easy trap to fall into, especially as loads increase, but it is
relatively easy to fix. We will provide a minimal force to push the knees inward,
using physiotherapist Gray Cook’s idea of “feeding the mistake.” We can use a
simple Theraband to provide the force. The nervous system will respond to the
inward force by reacting against it with the natural reflexive response of forcing the
knees outward—which is what we want. This technique is good for correcting
beginners, and also useful for priming the nervous system of experienced trainees
for correct movement before a squat workout.

The arrows show the valgus (inward) collapse of the knees.

Adding the band cues the nervous system to resist the inward collapse, correcting
the knee position.

THE ASSISTED SQUAT

If you have not squatted deeply since childhood, and are having difficulty getting
started with the bodyweight squat, begin with our multi-phase assisted squat
progression.

PHASE I: THE SHORTENED REP-STROKE SQUAT

We will use proper technique for partial squats. Establish an initial rep stroke
depth that is comfortable, and adjust a seat to this level. Work up to one set of 10
perfect reps, lightly touching the seat, not bouncing, and standing back up. Sit back
and down, inhaling on the descent, exhaling on the ascent. When you can perform a
perfect set of 10 reps, add a second set. Finally, in a few sessions or few weeks, add
a third set. When you are capable of three sets of ten reps, lower the seat FOUR
inches. Start from the beginning with one set of 10 reps and repeat the process
above until you can perform 3x10 at this height.

After you have lowered the seat height over time and are now capable of
squatting 3x10 to parallel, we will begin squat school, phase II.

PHASE II: THE DOORWAY/POLE SQUAT

Stand facing a doorjamb or pole and grab the support at waist height. Now squat
down and back, allowing your arms to pull on the doorway/pole as you descend.
Inhale until you reach parallel. Now exhale, relax any leg tension, and allow the
weight of your torso to push your hips to the lowest possible position. Use your
arms to offset your bodyweight and to keep your torso upright (critically
important). Inhale and stand up, using only your legs to lift your torso. Pull upward
with your arms as necessary to stand up while maintaining perfect technique. Pulling
with your arms will take weight off of the torso as needed, helping you to push
though the squat sticking point. You are self-assisting a forced rep.

Using a pole for assisted squatting instead of a door jam (phase II). Anything stable
you can grab with your hands will do. The phase III assisted squat will use a towel
or rope to increase instability and thus difficulty.

PHASE III: TOWEL OR ROPE SQUAT

Loop a rope or towel over the top of a chin-up bar or other sturdy overhead
anchor-point. Grab one end of the rope or towel in each hand, then lower yourself
down into a perfectly ultra-deep full squat. Pull on the rope or towel to lighten the
load as you descend, then pull on the rope or towel as much as needed when
standing back up.

We can learn perfect squatting by self-assisting—reducing the amount of weight

lifted—with the rope or towel. When we learn squatting from absolute weakness, we
will develop a series of bad habits when “sneaking” through sticking points. Gains
in strength and hypertrophy lie in battling through sticking points—not developing
questionable techniques that allow us to avoid them.

GRADUATION
Once you have increased your basic leg strength and are able to perform three
sets of ten reps of ultra-deep bodyweight squats with correct technique, you are
ready to work with dumbbells or kettlebells for the weighted squat.

STRONG MEDICINE TACTICS:

Use the squat as one of the foundations of your resistance training
program.
PHYSICAL TRAINING III
THE DEADLIFT = THE HEALTHLIFT

THE CROWN PRINCE OF THE

POSTERIOR
The squat is the undisputed king of resistance exercises, but the deadlift certainly
has a place in the royal family. Many would argue that the deadlift is a stiff
competitor with the squat for the overall title of the “king of exercises.” That is
debatable, but the “Crown Prince” is surely eyeing Dad’s throne.

The proper deadlift is the undisputed prince of the posterior chain—the back and
gluteal muscles.

No other progressive resistance exercise adds strength and muscle to the back
(traps, upper lats, lower lats, erectors, rhomboids, teres, and rear deltoids) and your
gluteal muscles than a perfectly executed deadlift.

Like Bubba Gump’s endless shrimp possibilities, there are a seemingly infinite
number of deadlift variations. Deadlifts can be performed while standing on a plate
or box of varying heights for different results. Box deadlifts are also much more
difficult at the start. Stiff-leg deadlifts can be done “Chaillet Style”, the lifter drags a
super heavy barbell up the thighs. A lighter and more precise “bodybuilder stiff-
leg” deadlift requires that the lifter purposefully allows the barbell to swing away
from their body, this subtly shifts the muscular stress from the erectors to the
hamstrings. You can do speed deadlifts or halting deadlifts. You can even
incorporate partial rep deadlifts using a power rack.

Other options include ultra-wide-stance sumo deadlifts, and various “double

overhand” deadlifts to build an eagle talon grip. You can also use straps to allow for
overloading the back muscles. There are enough legitimate deadlift variations to
keep a serious trainee very occupied for the rest of his natural life.

THE HEALTH LIFT

From a medical perspective, no other exercise translates better to
protecting the back and preventing injuries during daily activities than the
deadlift. Regular deadlifters are never in the doctor ’s office with back pain
complaints; the deadlift has made their backs virtually indestructible when
faced with the physical trials of work and home. This may sound contrary
to the idea many people have of the deadlift being “bad for the back.” With
a properly executed deadlift, nothing could be further from the truth. The
deadlift can even be restorative for a previously injured back.

WHY THE SUMO DEADLIFT IS ALL WE

NEED
For our purposes, the only deadlift variation we need is the “sumo-style” deadlift.
It is the easiest to teach, to perform, best translates to daily activities. It is also safer
for the beginner while still providing plenty of challenge for the experienced lifter.

“One technique, deeply ingrained, is ten times better than

ten superficial techniques.”
—Bruce Lee

In a perfect world, we could effortlessly teach athletes the sumo and

conventional-style deadlift with equal ease and effect. 50 years of experimentation
tells us something quite different. If an individual takes the time and effort to learn
our particular upright posture squat technique, learning the sumo deadlift will be as
easy and natural as taking a walk.

The conventional deadlift is a sophisticated exercise that requires accurate

positioning and the discipline to maintain the strict, straight, upward pull. The
conventional deadlift has many more opportunities for breaking form. Repeatedly
breaking technique to skirt a sticking point is shortsighted—both immediately and
ultimately detrimental. Over time, bad habits become ingrained and almost
impossible to break or correct.

The conventional deadlifter can find a lot of ways to work around or completely
avoid sticking points. Resorting to these shortcuts is not clever or advisable. Elite
trainers and master deadlifters understand that the essence of deadlifting (and of
resistance training) is to find and embrace the resistance. These elite purposefully
power through the sticking point, pushing or pulling with all their might straight
ahead with no variation—and fail wherever they may fail.

The maximum muscle and strength gains are born from the struggle of these
barely completed reps. We should live to struggle through the sticking point instead
of trying to find clever—and ultimately shortsighted—ways to slip by the resistance.
Those who truly understand seek muscular conflict will regularly and routinely
push up to (and past) momentary capacity.

How a trainee deals with the sticking points and the struggle associated with
effective resistance training will ultimately determine the degree of his success. We
define successful progressive resistance training in two ways—a radical increase in
raw strength with a radical increase in lean muscle mass. Nothing more, nothing
less. Acquiring these two attributes is profound.

WHY THE SUMO DEADLIFT?

Experience has repeatedly shown that teaching proper sumo deadlift is far
easier than teaching the conventional deadlift. First, there is a lot of
technical similarity between a correct squat and a proper sumo deadlift.
Think of the sumo deadlift as a “reverse squat” as there are far more
similarities than differences.

The perfect sumo deadlift is similar to a partial rep squat—only instead of

the weight being on your clavicles (as in a front squat) or on your back
(back squat) the weight is in front, hanging down from your hands.
Using an upright torso style for a sumo deadlift puts the emphasis on leg
power. Those with weak legs will try to neutralize their relative lack of leg
strength by compensating with high hips to start the lift. The lifter will
invariably end up struggling to force their out-of-position torso into the
final lockout.

THE SUMO DEADLIFT

1. Grip a barbell, kettlebell(s), or dumbbell (around one end) and assume
the start position.
2. Feet should be wider than shoulder width, with the torso as vertical as
possible.
3. Tense the upper back, attempting to pull the shoulder blades together.
Tense the gluteal muscles, lower back, and thighs, then take a big breath
into the bottom of the belly.
4. Smoothly bring the weight off the floor with your legs. Do not jerk the
weight.
5. The tailbone and upper body rise together, initially maintaining an
upright torso. Do not let the tailbone shoot up first!
6. The reverse hip hinge powered by the gluteal muscles finishes the lift.
The lower back and torso must be locked into one unit.
7. Maintain muscle tension at the top (the standing portion of the lift)
during exhalation.
8. Inhale into the belly and start to lower the weight using the reverse squat
technique—squatting down and back while maintaining an upright torso.
9. Lower the weight in a controlled grind speed and gently place it on the
ground with minimal noise. This controlled lowering technique is an
exercise unto itself with profound benefits.
10. If you are performing multiple reps, do not lose tension as the weight
touches the floor. Break the weight off the floor (#4) and start another rep.

The Strong Medicine Robots demonstrate optimal sumo start position.
Now, simply push your thighs downward. Your leg and torso length will
determine how vertical your torso will be at the start. The robots have
long legs which necessitate a more inclined torso. Try to achieve a spine
position as vertical as your anatomy will allow. A wider stance will enable
a more vertical torso.

Sumo Deadlift starting position.

DEADLIFT TACTICS
EMBRACE THE HARD START.
Our deadlifts have a signature technique rooted in structural architecture,
physics and safety. The idea is to never lose tension once the deadlift set
starts. Do not let the weight “settle” on the floor between reps, this
prevents a loss of body tension. We want to create maximum body tension
at the start of the first rep of the first deadlift set, and never lose that
tension for an instant. Optimally, the weight will lightly touch the floor
between reps.

BRAKING THE “NEGATIVE”.

As the barbell approaches the floor between reps, the muscular brakes are
applied with increasing tension, like a car approaching a brick wall.
Slowing the weight down causes a new level of muscle fiber stimulation,
maximally stimulating the back, glutes, upper thighs, and hamstrings. The
braking effect enables the lifter to exert maximum control at the “turn-
around” where descent becomes ascent. Slow, slower, slowest—lightly
touch the weight to the platform and begin the next rep.

NO SHORTCUTS.
If the legs are not strong enough to break the weight from the floor while
maintaining the proper start position, then go back and work on squats
until your legs are strong enough to deadlift. Stop playing to your biases
and strengths—correct your weaknesses. Those who think the hip-hinge
trumps the legs are missing the point. The question is not whether the hip-
hinge trumps leg power or if the legs are better than strength from the hip-
hinge. The Taoist answer is, ‘Not one, not the other, both!’ The optimal
deadlift technique uses both the legs and hip-hinge.

EMBRACE THE STICKING POINT...

In the sumo deadlift, as long as the torso is held erect and only leg power
is used to break the bar from the floor, there is no opportunity to avoid a
sumo sticking point. Bouncing reps are not allowed. To reduce
momentum, we use heavy breaking on the eccentric movement and
accelerate during the concentric pull.

In the sumo, the sticking point occurs when breaking the barbell from the
floor. The first six inches of a sumo pull is 100% leg power. To keep the
sumo deadlift simple, and to increase the amount of weight you’re able to
lift, increase your squat and leg power.

Once the bar approaches the knees, the lift is as good as done. The upright
torso allows for a perfect, straight-line pull. The pull becomes easier the
closer you are to the lockout. A limit set of deadlifts activates every
muscle on the human body to some degree.

EDDIE PENGELLY: SUBLIME SUMO

 Note the wide stance allowing a near vertical torso. The vertical torso
requires almost 100% leg power to break the weight from the floor. Once
off the floor, the hips and back can finish the lift.

SINGLE DUMBELL/KETTLEBELL SUMO

DEADLIFT

Sumo Deadlift side view with single kettlebell: from the starting position, the
tailbone and upper body ascend together (arrows) as the legs break the weight from
the floor at grind speed. As the weight passes the knees the hips extend to an upright
position to finish the lift. Reverse the sequence to bring the weight down slowly
enough so there is minimal sound when the weight touches the floor.

DOUBLE KETTLEBELL SUMO DEADLIFT

Sumo Deadlift front view with double kettlebells: The technique is identical to the
single kettlebell lift except for a wider stance. Double kettlebells allows for heavier
loads as you get stronger.

Start position for the Sumo Deadlift with a barbell: the stance width is wide enough
so that your arms can be positioned inside of you knees. You can alternate grip
position with your hands (shown here) or put both hands in a pronated (palm down
grip).
Sumo Deadlift with a barbell: the technique remains the same with the tailbone and
upper body ascending together as the legs break the weight from the floor at grind
speed. As the weight passes the knees the hips extend in a reverse hip hinge to an
upright position to finish the lift. Reverse the sequence to bring the weight down
slowly enough so there is minimal sound when the weight touches the floor.

To the trained eye, a perfect deadlift—sumo or conventional—is every bit as

beautiful and technically intricate as a golf swing, a tennis serve, or a baseball
pitcher ’s windup. Careers are built on coaching the raw mechanics of athletic
swings and throws. Every pro baseball team has a batting coach; every NFL team
has a quarterback coach who drills quarterbacks on an ideal technical template for
throwing and releasing a football. Definable coaching specialists and technical
experts exist for improving raw athletic mechanics in every sport—a quicker
release for a young NFL quarterback, a faster bat speed for a pro baseball power
hitter, a more refined power serve for a grand prix tennis player, or a better golf
swing for a PGA circuit pro.

Sadly, in the deadlift, there’s no equivalent—anybody can claim to be a deadlift

expert and “teach” deadlift technique. It seems every self-proclaimed deadlift expert
is blissfully ignorant of deadlift technique, and prefers to lecture about sets, reps
and frequency. Or, worse yet, they will teach some sort of “spinal cracker” deadlift
technique that works well initially, quickly plateaus, and ultimately runs a high risk
of spinal column injury. Bad deadlift technique forces a poorly positioned spinal
column to straighten for the lock out on a limit deadlift rep. Proper deadlift
technique keeps the spinal discs stacked as the lifter pulls the bar straight up.

BUILT-IN SUMO SAFETY”

We insist on breaking the weight from the floor with leg power first then
 finishing with the hip hinge not just for strength, but for safety.

Breaking the weight from the floor with the hip hinge with high hips and
an inclined torso at the starting position, puts significant shearing stresses
on the lower back. The upright, more vertical torso position we require
stacks the vertebrae of the back, and minimizes stress on your spine.

It’s less likely with our more vertical torso position for the lower back to
“round” (a common cause of back injury) when fatigued under load.

COMMON FLAWS IN FORM

1. THE HYPEREXTENDED SPINE

This back position is called “hyper-lordosis” in medical terminology. It happens
when the upper torso becomes unlocked from the lower body during the initial part
of the lift. This occurs when the legs are not strong enough to break the weigh from
the floor. The upper part of the torso will change position to become more upright
without the legs moving. This puts the entire initial load on the back, and places the
spine in a bad position.

Reduce the amount of weight and concentrate on keeping the lower back and
upper torso locked together. The rule—if the legs do not move, the upper body does
not move. Use a weight that will allow you to break the weight off the floor using
only your legs.
Here the trainee’s upper body rises before her tailbone at the start of the lift causing
hyperextension (backward bend) of the spine. This form error usually means the
weight is too heavy and the legs are not strong enough to break the weight from the
floor. Lighten the load in this case so that the tailbone and upper body can rise in
unison, maintaining a straight spine during the lift.

2. ROUNDING THE BACK DURING DESCENT

Avoid the temptation to bend forward while descending with the barbell. Using a
precise and slow lowering technique will maximize the strength and muscle
building attributes associated with the heavy eccentric/negative phase of the deadlift
rep.

Maintain an upright posture during descent, similar to a reverse squat. Rounding

the back during the descent of a deadlift is asking for a ruptured disc. The deadlift
should look exactly the same during the ascent and descent. If we took pictures of a
lifter during the upwards and downwards parts of the lift, they should be identical.

Poor descending technique with the Sumo Deadlift: the trainee lets her back bend
forward (flexion) instead of maintaining the neutral spine position as she lowers the
weight. This is usually a sign of fatigue and is a sure way to injure your back.

The sumo deadlift is a required part of your resistance training program. It will
protect your back from injury and forestall the hands of time by potently preventing
sarcopenia and osteoporosis.
STRONG MEDICINE TACTICS:
Implement the Sumo Deadlift as part of the foundation of your resistance
training program.
PHYSICAL TRAINING IV
BENCH PRESS AND OVERHEAD
PRESS

When it comes to building front torso muscles, no other progressive resistance

exercise comes close to duplicating the results from proper, repeated and intense
flat bench pressing. You might think lying flat on a bench and pressing a barbell or
pair of dumbbells to arms’ length would be the simplest task imaginable. But, we are
confronted by a myriad of choices...

What technical pathway will we use for the lowering phase? Where will we touch
on the chest? Will we pause the rep, or touch-and-go? If we pause, for how long?

Will we push on a straight or curved arc path?

The trajectory and speed of the bar ’s path during the lowering and raising phases
dramatically affects muscular targeting, and overall effectiveness of the exercise.
We need to consider these things before every set. Become conscious and attuned to
what you are doing during every rep of every set.

BENCH PRESS TECHNIQUES,

TACTICS AND TOOLS
 We want to make the bench press maximally difficult, while the rest of the fitness
world wants to make their bench presses easier with half-reps, machine pressing,
reps bounced off the chest, or raising the butt off the bench at the sticking point.
These are ego-inflating techniques that degrade strength and hinder results.

Anyone who consciously or unconsciously makes their bench presses easier is

defeating the purpose of resistance training. They don’t understand why they are
lifting weights! Our mission is to resurrect the ancient tactics used by champion
bench pressers, men who sought ways to increase the difficulty when they benched.
Difficultly in resistance training is the pathway of progress. Making resistance
training easier makes resistance training less effective.

Our goal is not to present a comprehensive set of bench press techniques

and variations. We will provide our strategy on sets, reps, frequency and
workout duration. The goal is to produce dramatic increases in lean
muscle mass and equally dramatic increases in pure pushing power. A
universe of pushing possibilities exist within the tight confines of flat
benching. But, we will focus on a single variation, and hone the dumbbell
bench press to perfection.

LEARN TO LOVE DUMBBELLS

Elite trainers love the cumbersome and awkward nature of the unwieldy
dumbbell. In the right hands and used the right way, dumbbells are unrivaled for
stimulating the pecs, shoulders and triceps. Dumbbells cause muscle stabilizers to
fire to a higher degree than two-handed barbell work, or any of the resistance
machines that mimic the bench press.

We will pair the dumbbell’s inherent instability (an advantage) with our intensity-
enhancing techniques. In our first dumbbell variation, pause with the dumbbells at
the bottom of the rep, then actually release the tension in the chest and arm muscles
with an exhalation. This relaxation tactic is considered heretical by the resistance-
training mainstream. After the pause, re-engage the stretched, relaxed pecs, inhale
and use a purposefully slow speed on the concentric (push) phase to increase the
difficulty of the rep. All of our subsequent bench press variations are constructed
based on our ultra-basic dumbbell techniques.

DUMBBELL BENCH PRESS TECHNIQUE:

RELAX, PAUSE, GRIND
The most difficult bench press technique you will probably encounter is a limit
set of ultra-deep, relaxed, paused, dumbbell bench presses performed with a
purposeful “grind” (slightly slowed) rep speed. Mastery of the paused dumbbell
bench using grind speed is our very own version of bench press boot camp—a
bench press version of SEAL BUDs Hell Week. Once you have paid your dues with
long and prolonged bouts of paused dumbbell bench presses, everything else seems
like a walk in the park.

DUMBBELL BENCH PRESS

TECHNIQUE
1. Select two dumbbells and sit on the end of the exercise bench with both
dumbbells. The handles should be vertical with the plates in your lap.
2. Lie back and simultaneously turn the handles outward. You are now
lying on the bench with the dumbbells in the bench press start position.
3. Exhale and allow the dumbbells to sink. Maintain control, even though
the pecs and shoulders are relaxed, the grip stays tight. The dumbbells are
now in push position.
4. Relax, feel the dumbbells stretch the pecs and shoulders downward.
Perform this “pre-stretch” at the start of every single rep.
5. We have maximally inhaled and are full of air at the same instant the
dumbbells touch the chest at the bottom of the descent. Then, we exhale,
relax, and stretch.
6. After allowing the bells to stretch downward, consciously re-engage
the pecs, delts, and triceps. Shift from stretching and relaxation into
pushing and contracting.
7. When it is time to push, inhale mightily and push upward. The rep
speed is not fast or super slow—but it is consciously slowed.
8. This consciously-slowed rep speed is called “grind.” We grind the
dumbbells to a “hard” (full-and-complete) lockout. We synchronize our
exhalation to end at lockout.
9. This unorthodox strategy accomplishes two monumental tasks: it
ingrains perfect technique and isolates/stimulates the maximum number of
muscle fibers.
10. This fundamental bench press technique succeeds in making light
weights heavy, and stays true to our overall philosophy.
11. All subsequent bench press variations spring from this pause-relax-
and-grind technique. After practicing this technique, all other forms of
benching are easy.

Dumbbell Bench Press set up position.

Dumbbell Bench Press start position (top view and floor level).
Dumbbell Bench Press: start from relaxed bottom position, produce tension, press at
grind speed to top lockout, descend slowly, pause at the bottom, repeat…

DUMBBELL BENCH PHASE II: BEYOND

PAUSE, RELAX, GRIND
Our bench press theme is the pause-relax-and-grind dumbbell technique. As we
introduce each subsequent new bench press variation, it will be easier than its
predecessor. This the natural order of proper progressive resistance training.
Human nature is to jump ahead to the sexier bench press variations without
mastering the basic theme.

This is a big mistake. How can we develop a deep understanding of any variations
without first mastering the theme?

The first step—which includes all the physiological benefits of bench press
expertise—is to master the dumbbell bench press with the pause-stretch-relax-in-the-
bottom-position technique, then using the grind speed to push the dumbbells to
lockout.

All subsequent bench press and barbell variations are built on this core technique.
Do not skip ahead before mastering the “pause-relax-and-grind” style. Without
mastering this technique, the trainee cannot appreciate the “easing effect” as they
master each subsequent bench press variation.

We adhere to an overarching philosophy of using ultra-strict, ultra-simplistic, but

sophisticated techniques to make light weights heavy. By design, any bench press
techniques after the pause-relax-and-grind approach with dumbbells will seem light
and easy by comparison.

ADVANCING THE DUMBBELL

BENCH PRESS
After mastering the core technique, we can proceed with the next two
dumbbell variations:
1. Pause at the bottom like before, but instead of pushing with a slow
“grind” speed, push the dumbbells up explosively.

Compared to the excruciatingly slow pause-relax-and-grind technique,

dumbbell bench presses with an explosive push seem easy by comparison.
2. The second variation eliminates the pause. Lower the dumbbells to the
bottom position, then immediately push them up explosively. This is the
“touch and go” variation.

The second variation (touch-and-go) allows for maximal loads. Strong

Medicine trainees coming from the hell of pause-and-relax grind
benching to touch-and-go explosive dumbbell bench press technique will
feel as though they are cheating. Now we can choose to use a barbell—or
not.

THE OVERHEAD DUMBBELL PRESS

The ability to push in the vertical plane is important in daily life. The overhead
dumbbell press will train this ability, giving you specific strength that not many
people possess. While big bench press numbers are impressive, overhead pressing
arguably translates better to real-life applied strength. In our opinion, “How much
can you press?” should be the benchmark question for upper body strength, not,
“How much can you bench?”.

COILED ENERGY: FROM BOTTOM TO

TOP
The perfect press starts with the lower body, not the upper body. You must have a
strong, steady foundation. A flaccid lower body during the press is a very serious
“energy leak”. Energy which could help push the weight overhead is lost to an
unstable lower body if improper technique is used. Your press should start by
tensing the entire lower body, as if you are compressing a coiled spring.

COACH’S CORNER:
A successful standing overhead dumbbell press depends on a super stable
push platform. The thighs and legs are maximally contracted, glutes are
clenched, and there is tremendous tension in the mid and upper back.

THE OVERHEAD PRESS

Dumbbells and kettlebells are the ultimate tools for overhead pressing.
You can press one are at a time, or both at once. We will be using two
dumbbells or kettlebells for the double arm press.
1. Grab a set of appropriately sized dumbbells or kettlebells. Be
conservative and err on side of “too light” if you are in doubt.
2. Position the bells in the clean position at shoulder height.
3. Clench your calves, thighs, glutes, and abdominal muscles maximally
before pressing. This is the start position.
4. Press the bells explosively overhead to full elbow lockout.
5. Pause with the bells overhead while maintaining maximal tension
throughout your body.
 6. As you lower the bells slowly, build even more tension in your body.
You are compressing the coiled spring. Do not let gravity take control of
the bells in an uncontrolled drop. The negative (lowering) part of this
exercise is just as important as the push upwards.
7. The coiled spring tension generated will prepare you for the next rep.
Pause briefly at the bottom then explosively push the bells upward again to
lockout.
8. Repeat until the desired number of repetitions are completed.

Dumbbell Overhead Press: start the press from a strong base with legs and glutes
contracted. Build tension (coiled spring) during the descent to power the explosive
push on the next repetition.

The dumbbell bench press and overhead press are the pinnacle of upper body
pushing movements. After you have developed good technique in both, you can
move forward in your training. With every push, we need a pull to maintain balance.
For our purposes, the row is the best option for an upper body pulling exercise.
STRONG MEDICINE TACTICS:
Use the dumbbell bench press as one of the foundations of your resistance
training program.

STRONG MEDICINE TACTICS:

Implement the overhead press as one of the foundations of your resistance
training program.
PHYSICAL TRAINING V
THE ROW

When selecting an appropriate pulling exercise, the choices are extremely

limited. The elite choose from chin-ups and pull-ups done with various set and rep
combinations. For those able to perform them, proper chin-ups or pull-ups from a
dead-hang stretch to chin-over-bar is unparalleled for activating, building, and
strengthening every muscle of the back. But, few have the requisite strength-to-
bodyweight ratio needed to perform this difficult exercise.

Chin-ups and pull-ups are difficult because we are forced to handle 100% of our
bodyweight—and most people are not that strong. There are clever gym machines
for assisted chin-ups and pull-ups with counterweighted knee platforms that push
upwards—but how many of us have access to such a marvelous device? We are
forced to look around for exercise alternatives.

After experimenting with different back exercises, one that seems to fit all the
criteria as a successful chin-up/pull-up replacement is the “frozen statue row.” But,
before we can do the “frozen statue row” (FSR), we will start with the single arm
row to build a foundation of perfect technique before advancing.
The Chin-up: works the back like nothing else.

COACH’S CORNER:
We realize that a row pulls in the horizontal plane while a chin-up pulls in
a vertical plane. While the row is not a true substitute, it works for us
because it is the direct opposite of a dumbbell bench press. The row will
help us build symmetry by offsetting the horizontal push of the bench
press with a horizontal pull.

PHASE I: THE SINGLE ARM

SUPPORTED ROW
1. Use a dumbbell that is lighter than you think you need, and put it next
to the bench.
2. Grab one end of the bench with your left hand and place your left knee
and shin on the bench. The left side of your body is now supported on the
bench.
 3. Bring your right leg directly out from the bench and plant your right
foot with a stance wider than shoulder width. You now have 3 points of
support—your left hand, left knee/shin, and your right foot.
4. Keep this position. Reach down and grab the dumbbell with your right
hand. Now raise your right shoulder (keeping your arm hanging straight
down) until it is level with your left shoulder. Let the weight of the
dumbbell stretch your back muscles but do not let your shoulder drop.
Your spine should be straight (do not “hunch” your back). This is the
starting position.
5. First, retracting shoulder blade (scapula) towards your spine. Your
elbow should not bend at this point. The dumbbell will start to rise as you
move your shoulder blade towards the spine (imagine trying to pinch
something between your shoulder blade and your spine). Do not jerk the
weight up from the starting position, move at a slow “grind” speed.
6. Direct your elbow up towards the ceiling. It will naturally bend when
you do this, but we are not curling the dumbbell. Bring the elbow up as
high as possible but do not let the front of your right shoulder rise much
above the level of your left shoulder. This mistake results in twisting the
spine and poor technique.
7. Briefly pause at the top position and lower the dumbbell with a slow
“grind” speed back to the start position.
8. After completing your reps, switch to the other side and repeat the
above steps.

Single Arm Supported Row: the shoulders stay level and the forearm pulling the
weight stays vertical. The elbow is directed toward the ceiling in a vertical line.

THE “FROZEN STATUE” ROW

 The single arm dumbbell row performed at grind speed with a pause truly makes
light weights heavy. You can build incredibly strong and dense lats, rhomboids,
lower trapezius, and posterior deltoids with this technique while using minimal
weight.

After several months of training, you can progress to the double dumbbell row,
the “frozen statue” row (FSR).

EXERCISE SAFETY
Do not attempt the “frozen statue” row until you have developed the
requisite posterior chain (back, glutes, hamstring) strength and postural
stability from training the sumo deadlift and squat with perfect technique
for several months. The postural demands from this exercise could result
in back injury if you are insufficiently prepared.

The FSR involves holding your body in a static position “like a statue.” Instead of
using a bench for support as in the single arm row, the “frozen” position is the base
of support for the double dumbbell row. Holding this base of support adds a
significant level of difficulty and a much higher stimulation of the central nervous
system. Stabilizing this position while just holding dumbbells is a workout in itself.
Rowing the dumbbells from this position is maximally stimulating for the adaptive
response we want from our resistance training.

WHY MOST FREE-WEIGHT ROWS

ARE WORTHLESS
The classical barbell row and all its variations are often fundamentally
flawed in their execution.

The problems are numerous:

• Stances tend to be too narrow—widen your stance to at least shoulder
width.
• The spine is often bent, make sure to maintain a neutral spine position
without bending the back.
• Most rowers jolt the weight upward to start the movement. The
latissimus (lats) muscles are not engaged (and not exercised) by jerking
the weight at the start. This is also very bad for the spine, and places
significant, abrupt shearing forces on your vertebrae.
• Lifters make most of these “mistakes” on purpose and are driven by
ego. These technical errors allow for heavier weights to be “rowed.”
Moving the weight in this manner is not a row and misses the muscles we
want to exercise. These attempts to impress others are just a setup for
injury.

Heavy weight is not needed for maximum benefits from a correctly

performed row.

PHASE II: THE “FROZEN STATUE”

ROW
1. Grab a pair of dumbbells that are lighter than you think you need and
hold them at your sides while standing erect.

 2. Move your feet at least shoulder width apart.
3. While maintaining a flat, neutral spine, hinge at the hips and lower the
angle of your torso until it is almost parallel to the floor. We avoided this
high hip position with the deadlift, but the lighter weights used for the
FSR, ensures that the stress on the spine is safe and manageable as long as
the spine remains locked in to a neutral position. The dumbbells will hang
relatively close to the floor at this point. This is the starting “frozen
statue” position.
4. Hold this position as you begin the row. If initiating the row causes you
to break the “frozen statue” position, the weight is too heavy.
5. The first movement is retracting your shoulder blades (scapula)
towards your spine. Your elbows should not bend at this point. The
dumbbells will start to rise just from moving your shoulder blades
towards the spine (imagine trying to pinch something between your
shoulder blades and your spine). Do not jerk the weights up from the
starting position, move at a slow “grind” speed.
6. Point your elbows up towards the ceiling. They will naturally bend
when you do this, but do not curl the dumbbell. Bring the elbows up as
high as possible while keeping yourself locked in the “frozen statue”
position with a flat, neutral spine. Keep squeezing your shoulder blades
together.
7. Pause at the top position briefly and lower the dumbbells with a slow
“grind” speed back to the start position.
8. Start another repetition and repeat until your set is complete.

Frozen Statue Row: the spine remains flat (almost parallel to the floor) during the
lift. The elbows are directed in a vertical line toward the ceiling with the forearms
remaining perpendicular to the floor. (Note that the trainee has a hyperextended
(bent back) neck in the start position but fixes it during the lift itself).
 SIMPLE IS AS SIMPLE DOES
Many people have a hard time making the mind/muscle connection with
the main muscles we’re trying to target—the lats. Here is a bit of muscle
trivia I heard eons ago: the lats are the least used muscles on the human
body. Because of this, they are the easiest muscles to strengthen and grow
—assuming the smart trainee uses techniques that actually stimulate the
lats to a significant degree.

The muscle elite had a saying, “Show me a man with great lats, and I’ll
show you a man with sub-par biceps; show me a man with outstanding
biceps and I’ll show you a man with terrible lats.” In other words, if you
can “arm pull” your rows by activating the biceps, you are not using your
lats. We must concentrate on pulling our rows with the muscles of the
back. Become a dumbbell row technician and really learn, hone and
develop your technique over time.

You have now learned the five core exercises which form the Strong Medicine
resistance training foundation. But no resistance training program is complete
without mentioning abdominal training.

We will show you how to develop rock hard abdominal muscles without ever
doing a sit-up or crunches. Before you think this sounds like a television
infomercial, read on.

STRONG MEDICINE TACTICS:

Incorporate the row as one of the foundations of your resistance training
program.
PHYSICAL TRAINING VI
STRONG MEDICINE ABS

We all want a hard, chiseled abdominal region—a “six-pack” to show off. There
are literally hundreds of abdominal training videos that promise to give you the
coveted six-pack. The truth is, only proper nutrition and lifestyle management (good
sleep, stress control) will give you six-pack abs, not endless crunches and sit-up
variations.

SIT-UPS ARE A BAD IDEA...

Not only will you fail to achieve the “six-pack” look from sit-ups, they may lead
to injury. Most sit-up variations involve anchoring the feet and significantly
engaging your hip flexors (psoas) to achieve the sit-up movement. This is a
problem for a couple of reasons...

• The abdominal muscles are not optimally activated or strengthened since the
hip flexors are doing most of the work.

• High activation of the psoas (a major hip flexor) puts major compressive
forces on the spine. A look at the psoas anatomy explains why. According to Dr.
Stuart McGill, a leading spine biomechanics expert, the average sit-up generates
about 730 lbs. of compression on the spine with every repetition. This amount of
compression is known to lead to disc injuries over time. Doing hundreds of sit-
 ups will not do your back any favors.

SIT-UPS ARE LOW BACK “POISON”

As Dr. McGill has studied in his spine biomechanics laboratory, sit-ups put
a huge compressive load on the spine. To make matters worse, this large
compressive force is applied when the lower back is in a flexed position.

According to Dr. McGill’s research, the best way to herniate a disc is with
high compressive forces and repeated flexion, which exactly describes a
sit-up!

Many clinicians are still telling their back pain patients to do sit-ups to
strengthen their abdominals. But, situps are the exact opposite of what
you should do for a healthy back.

The abdominal muscles’ function is to stabilize the spine during activities such as
lifting, carrying, pushing, and pulling. We need to train them as they were meant to
function, instead of isolating them with exercises such as sit-ups and crunches.

If you have progressed to the dumbbell front squat, you will recognize the
inherent difficulty in maintaining a neutral spine position while holding
the weights at shoulder level during the squat. You should feel your
abdominal muscles struggling to maintain an upright spine position while
you are squatting.

The abdominal muscles are meant to stabilize the spine during activity. So,
this is how we will train the abdominals.

ABDOMINAL TRAINING PHASE I:

THE BASIC PLANK
A properly performed plank fits the bill for a great abdominal exercise
that works the abs with the rest of the body and strengthens their function
as a spine stabilizer. The Strong Medicine plank can seriously test your
resolve. There will be no doubt that your abdominal muscles are working.
1. Find a relatively level space on the ground; use a mat if needed. Put
your forearms on the ground with your elbows directly underneath your
shoulders. Your forearms should be shoulder width apart on the ground.
You are in a kneeling position at this point.
2. Keeping your forearms in place, come off of your knees and
straighten your legs. Now, only your forearms and the balls of your feet
are touching the ground. Your feet are positioned next to each other.
3. Flatten your back (no sag in the middle), then tighten your glutes and
your thigh muscles. Do not look up; keep your eyes and head downward.
4. Push your heels away from you while keeping the balls of your feet
 planted (you will feel a stretch in your calf muscles). This is the starting
position.
5. To begin your repetition, push your forearms and elbows down into
the ground while simultaneously “pulling” them toward your feet. Your
forearms and elbows will not move from their position. This “down and
backwards” force is isometric, like pushing against a wall.
6. At first, try to hold this position with the “down and back force” on the
forearms and elbows for 10 seconds per repetition. Work your way up to
sustained 30-second holds.

The Plank (phase 1): the spine remains neutral and the entire body is under tension.
Push the heels backwards while you press your forearms down and back.

ABDOMINAL TRAINING PHASE II:

THE HIGH PLANK
Once you can hold the basic plank for several sets of 30-second holds,
move up to the high plank. This variation is exactly like the basic plank
except that you are on your hands instead of your forearms.
1. Find a relatively level space on the ground; use a mat if needed. Put
your hands on the ground directly underneath your shoulders with your
fingers facing foreword. Your hands should be shoulder width apart on
the ground. You are in a kneeling position at this point.
2. Keeping your hands in place, come off of your knees and straighten
your legs. Now, only your hands and the balls of your feet are touching
the ground. Your feet are positioned next to each other.
3. Flatten your back (no sag in the middle), then tighten your glutes and
your thigh muscles. Do not look up; keep your eyes and head downward.
4. Push your heels away from you while keeping the balls of your feet
 planted (you will feel a stretch in your calf muscles). This is the starting
position.
5. To begin your repetition, push your hands down into the ground while
simultaneously “pulling” your hands toward your feet. Your hands will
not move from their position. The “down and backwards” force you are
using is isometric, like pushing against a wall.
6. At first, try to hold this position with the “down and back force” on the
hands for 10 seconds per repetition. Work your way up to sustained 30-
second holds.

The High Plank (phase II): this variation uses the same technique as the plank but
from the hands instead of the forearms. Push the heels backwards while you press
your hands down and back. The One-hand Plank (phase III) will use the same
technique but holding one hand out in front of your body reaching toward the wall
in front of you.

ABDOMINAL TRAINING PHASE III:

THE ONE HAND PLANK
Once you can hold the high plank for several sets of 30-second holds,
move up to the one hand plank. This variation is exactly like the high
plank except you use only one hand for support. This adds an extra layer
of challenging instability.
1. Find a relatively level space on the ground; use a mat if needed. Put
your hands on the ground directly underneath your shoulders with your
fingers facing foreword. Your hands should be shoulder width apart on
the ground. You are in a kneeling position at this point.
2. Keeping your hands in place, come off of your knees and straighten
your legs. Now, only your hands and the balls of your feet are touching
the ground. Your feet are positioned about shoulder width apart. You
will need a wider base of support from your feet at first.
3. Flatten your back (no sag in the middle), then tighten your glutes and
your thigh muscles. Do not look up; keep your eyes and head downward.
4. Push your heels away from you while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). This is the starting
position.
5. To begin your repetition, lift one hand off of the ground and hold it
out in front of you. Generate the same isometric “down and back” force
with the hand on the ground. Try to hold this position for 5 seconds. Keep
your shoulders level with each other with no twisting of the spine.
6. After holding the one hand position for 5 seconds, switch hands and
lift the opposite hand up in front of you. Continue to switch hands every 5
seconds for the duration of the repetition (10-30 seconds).

“ANTI-ROTATION”
The one hand plank is more difficult since the abdominals not only
stabilize the spine from flexing or extending (in the sagittal plane), but
also must stabilize the spine against rotation (in the transverse plane).

This stabilization against rotation (Dr. McGill calls it “anti-rotation”) is an

extremely important function of our abdominal muscles. Anti-rotation is
trained with the one hand plank by keeping the shoulders level during the
hand switch.

ABDOMINAL TRAINING PHASE IV:

THE PLANK ROW
Once you have worked up to several sets of 30-second sustained one hand
planks, you are ready for the plank row. This exercise is a huge challenge
to the stabilizing function of the abdominal muscles. You will definitely
feel it.
1. Find a relatively level space on the ground; use a mat if needed. Grab
two light dumbbells and place them in front of you, parallel to the long
 axis of your body (see photo). Instead of placing your hands on the
ground, you will grab the dumbbells firmly and use them as your front
base of support. Be sure that the dumbbells are directly below your
shoulders.
2. Keeping your hands in place on the dumbbells, come off of your knees
and straighten your legs. At this point only the dumbbells and the balls of
your feet are touching the ground. Your feet are positioned about
shoulder width apart (or greater if needed).
3. Flatten your back (no sag in the middle), then tighten your glutes and
your thigh muscles. Do not look up; keep your eyes and head downward.
4. Push your heels away from you while keeping the balls of your feet
planted. This is the starting position.
5. To begin your repetition, lift one dumbbell off of the ground with the
identical technique used in the previous section for the single arm row.
Lift the dumbbell at grind speed and pause at the top. While one arm is
rowing, generate the isometric “down and back” force with the hand
grasping the dumbbell on the ground. Keep your shoulders level with each
other and do not twist your spine during the row. Do not allow your back
to bow or sag.
6. Row on alternate sides for up 2-10 repetitions per side.

The Plank Row (phase IV): the starting position (not shown) is a plank position on
top of dumbbells or kettlebells. Shoulders remain level and the supporting hand
pushes the dumbbell or kettlebell into the floor keeping the wrist straight. Use the
same rowing technique you learned previously leading with the elbow directed
toward the ceiling. Notice that he has a wider foot position for stability.
SAFETY TIP:
Make sure you use hexagonal style dumbbells or kettlebells with a large
flat bottom for this exercise. A rounded bottom surface on dumbbells or
kettlebells will not work, and will put you at risk for injury.

Phases I-IV of Strong Medicine abdominal training will progressively

work the abdominals as they are meant to work in daily life. This
progression will also help your deadlift and squat since both lifts require
significant stabilization of the spine.

The deadlift and squat by themselves are already training the stabilizing
function of the abdominal muscles.

There are many excellent ways to train the abdominals as stabilizers

(including the “anti-rotation” function). The progression covered here
only scratches the surface.

Stop training the abdominals in isolation with back-busting sit-ups and

crunches. The Strong Medicine abdominal training program will give you
a six-pack (if your nutrition and lifestyle are locked on) and a bullet-proof
back.

STRONG MEDICINE TACTICS:

Use Strong Medicine abdominal training to build an iron core and prevent
back injuries.
 The last six sections have been a primer on Strong Medicine resistance training.
These exercises should form the foundation of your weight training. Feel free to
add exercises to this foundation to suit your individual needs and goals. We will
now transition to cardiovascular training for both the beginner and the experienced
trainee.
PHYSICAL TRAINING VII
STRONG MEDICINE BASIC CARDIO

High Intensity Interval Training (HIIT) is the preferred way to maximize the
adaptive response of the body and lose fat in the shortest amount of time exercising.

But, not everyone is ready for HIIT from both a fitness and psychological
perspective. The effort and high target heart rates of HIIT can be overwhelming and
intimidating to the new trainee. For an obese or diabetic trainee, making
monumental changes in nutrition while starting an intensive exercise program at the
same time is often too much to handle at once.

We have created a Basic Cardio “ramp-up” for those in the above categories, or
who are new to training and are substantially deconditioned. The Basic Cardio
program can be progressed to subsequent advanced training using Strong Medicine
tactics.

PREPARATION
All you need to start is a basic heart rate monitor and your calculated theoretical
maximum heart rate (HRmax). You will use your HRmax to plan your basic cardio
training “ramp-up.”
 MAXIMUM HEART RATE CALCULATION REVIEW
For men: 208 - (0.7 X Age) = HRmax
For women: 206 - (0.88 X Age) = HR max
Example 1: Chris is 43 and wants to calculate his maximum heart rate. He
will multiply his age (43) by 0.7, which equals 30.1. He will then subtract
30.1 from 208 to get 177.9 (we’ll round to 178). Chris’s HRmax is about
178 beats per minute.

Example 2: Carrie is 46 years old. To calculate her HRmax, we would

multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from 206
to get 165.5 (we’ll round up to 166). Carrie’s HRmax is 166 beats per
minute.

At this stage, our preferred cardio method is outdoor “power walking.” This is
purposeful walking at a pace that will bring your heart rate up to a predetermined
level. It is not a leisurely stroll chatting with friends. Train outdoors exclusively as
long as your environment is safe. Outdoor training has added benefits (stress relief,
etc.) that slogging away on a treadmill will not provide.

The following is a sample 10-week basic cardio “ramp-up” using the heart rate
monitor and a waist to height ratio to track your progress. (Find directions for
calculating your waist-height ratio in the “Stuff You Can Measure” section at the end
of the book.) Carrie, a 46 year old female, is our example. Her HRmax was
previously calculated to be 166 beats per minute (bpm). We will calculate her
weekly target heart rate as a percentage of her HRmax of 166 (bpm).

The goal of Strong Medicine Basic Cardio training is to help someone start an
exercise program from the beginning very slowly at a low intensity and volume.

They will steadily increase both volume and intensity over 10 weeks and will be
well prepared for the full Strong Medicine physical training program.

Carrie calculated
her week 1 target
By week 5, Carrie is
heart rate of 91
power walking 5 times a
bpm by taking
week for 20 minutes per
her HRmax of
session. She is keeping
166 and By the tenth week, Carrie’s waist
her target heart rate as
multiplying it by size has decreased significantly. She
close to 112 bpm as
0.55 (55%). is wearing clothes 2 sizes smaller
possible during the entire
than when she started. She is
session.
166 X 0.55 = 91 exercising at a relative high
bpm. She will We have steadily intensity (80% of HRmax) every
keep her heart day of the week for 35 minutes per
increased both the
rate at this level volume and intensity of session.
for the duration of
her workouts over the
her session. She is ready to move on to Strong
She will do 3 past 5 weeks. She has Medicine High Intensity Cardio.
sessions during already seen the benefits
week 1 for 8 with a decreasing waist-
minutes per height ratio.
session.

Use Strong Medicine Basic Cardio as an “on-ramp” to your fitness

program. You can also use power-walking as an active recovery exercise
instead of a complete rest day. Basic cardio can also be used any time you
feel your stress cup is near overflowing and high intensity exercise may
be too much that day.

STRONG MEDICINE TACTICS:

Build your cardiovascular training foundation with Strong Medicine
Basic Cardio.

Now that you have a cardio training foundation, we will progress to the more
advanced high intensity interval training to work the cardiovascular system to its
fullest capacity. This will provide increased health benefits and accelerated fat
burning.
PHYSICAL TRAINING VIII
STRONG MEDICINE HIGH INTENSITY
CARDIO

Most official physical activity guidelines from exercise and public health
authorities recommend “at least 150 minutes per week of moderate to vigorous
aerobic exercise.” For many people, fitting this much exercise into their hectic
schedules means at least 30 minutes of mind-numbing monotony on a treadmill,
bike, or elliptical machine 5 days each week.

It is no wonder that over 50% of those who start a new exercise program will not
continue with it for even 6 months. The most common excuse for not exercising is a
lack of time. Also, a half hour of moderate-intensity exercise on a machine is just
plain boring. The boredom factor is a big part of exercise non-adherence.

Strong Medicine addresses the time and boredom problems with our advanced
cardio program centered on High Intensity Interval Training (HIIT). This type of
exercise uses very brief periods of very high effort/intensity separated by periods
of rest/recovery. HIIT protocols allow you to get all of health and fitness benefits of
sustained moderate exercise (though HIIT is superior is some aspects) in a short
amount of time. HIIT not only cuts down on the time needed for an effective
exercise session, but it also only requires you to do cardio 3 days per week, instead
of 5 days or more with traditional moderate intensity cardio.

Recent medical research supports the use of HIIT as a superior form of

exercise for people with heart disease, diabetes, high blood pressure, and
obesity.
• A single session of HIIT improves blood glucose control in diabetics
and non-diabetics for 1-3 days after the exercise session.
• For people with heart disease, HIIT results in better heart health
improvements as compared to moderate intensity exercise, even when the
amount of calories burned are the same.
• HIIT was superior to moderate intensity exercise for improving heart
and blood vessel function in heart failure patients.
• HIIT is more effective than moderate intensity exercise for controlling
and preventing high blood pressure.
• HIIT is far superior to moderate intensity exercise for reducing body
fat, especially around the belly.

The secret to the effectiveness of HIIT is the high intensity. HIIT protocols
require you to push your heart rate up to 90% (or more) of your maximum heart
rate for brief periods of time. The small amount of time spent at these high heart
rates produces incredible beneficial adaptations in the body that moderate intensity
exercise cannot touch.

MAXIMUM HEART RATE

CALCULATION REVIEW
For men: 208 - (0.7 X Age) = HRmax
For women: 206 - (0.88 X Age) = HR max
Example 1: Chris is 43 and wants to calculate his maximum heart rate. He
will multiply his age (43) by 0.7, which equals 30.1. He will then subtract
30.1 from 208 to get 177.9 (we’ll round to 178). Chris’s HRmax is about
178 beats per minute.

Example 2: Carrie is 46 years old. To calculate her HRmax, we would

multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from 206
to get 165.5 (we’ll round up to 166). Carrie’s HRmax is 166 beats per
minute.

KEY POINT:
High Intensity Interval Training (HIIT) involves periods of high intensity
exercise separated by rest and recovery periods.

HIGH INTENSITY INTERVAL

TRAINING PROTOCOL
The HIIT protocol involves pushing your heart rate to approximately
90% of your maximum heart rate for short periods of time with rest
breaks in between. Let’s use Carrie as an example:

Carrie has already calculated her HRmax at 166 beats per minute. She will
multiply her HRmax by 0.9 (90%) to get about 149 beats per minute.
166 X 0.9 = 149 beats per minute. This is her target heart
rate.
1. She will put on her heart rate monitor and choose a cardio machine (a
bike, elliptical, treadmill, stair climber, etc.).
2. She will warm up her muscles at a slow pace for 2-3 minutes.
3. She will then exercise hard enough to get her heart rate up to her
149bpm target, for a total exercise time of 60 seconds.
4. After the 60-second exercise interval, she will rest for 60 seconds (or
pedal/walk very slowly).
5. After the 60-second rest period, she will start another 60-second
exercise interval at the target heart rate of 149 beats per minute.
6. Carrie will repeat this for a total of 10 60-second exercise intervals,
then cool down for 2-3 minutes after finishing.
 7. The basic HIIT protocol has been used in many research studies and
works great for weight loss and reversing diabetes.

IMPORTANT MEDICAL REMINDER:

As we discussed in the obesity chapter, it is extremely important that you
speak with your doctor first before starting a protocol like HIIT. This is
especially true if you have previously had a heart attack or chest pain with
physical exertion. If you fall into these categories, you MUST get
approval from your physician first for safety reasons. There are plenty of
other exercise routines that you can do safely and will still be beneficial.

HIIT is highly beneficial, but make sure your heart can tolerate high
intensity exercise before you begin.

You can use the HIIT protocol with a variety of different exercises. You can even
set up your HIIT session with alternating exercise types after every 60-second
interval. For example, rowing for the first interval, cycling on the second interval,
elliptical on the third.

There is something very primal about pushing your cardiovascular system to

90% (or higher) of your maximum heart rate. It is hard to get bored or preoccupied
with worry or rumination when you are exercising at this level. The stress relieving
effects and endorphin (feel-good brain chemicals) rush are second to none with
these protocols.

HOW MUCH IS TOO MUCH?

There are circumstances when the basic HIIT protocol is too much of a good
thing. A night of bad sleep or an exceedingly stressful day at work may not leave
room in your stress cup for the demands of the basic HIIT protocol. How can we
make sure to get the optimum (hormetic) dose of exercise on any given day?
We want to be in the “green zone” with exercise intensity, the “hormetic dose.”

We do not want to under-train and miss the benefits of the adaptive response to
exercise, and we certainly do not want to overtrain and overfill the stress cup.

To address this problem we have devised an alternate HIIT protocol that

automatically takes into account the “fullness” of your stress cup on any given day,
and ensures that you get the right “dose” of exercise. It also automatically adjusts
for fitness levels, and will not overtrain the novice while still giving the veteran
trainee all that he or she can handle. We call it the “Burst Cardio” protocol.

BURST CARDIO—INDIVIDUALIZED
HIIT
“Burst Cardio” is a 20 minute protocol for getting the most out of your
workout without overfilling your stress cup.

A 20 minute Burst Cardio session:

• Burst up to 90-95% of your predicted max heart rate (HRmax), then stop
 as soon as you reach it.
• 90% HRmax is the requirement, 95% is the goal.
• Recover until your heart rate slows to 70% of HRmax.
• Burst again up to 90-95% of your HRmax.
• Repeat the burst cycle until 20 minutes have elapsed.

Using a heart rate monitor with Strong Medicine “Burst Cardio” will ensure you
don’t overfill your stress cup.

On a day when stress is low and you feel rested, you will have a relatively low
sympathetic (flight or fight) nervous system drive. Once you “burst” up to 90-95%
of HRmax you will recover to 70% of HRmax relatively quickly. This quick
recovery will allow you to do more cycles up to your 90-95% HRmax in the 20
minute time period.

There is plenty of room in the stress cup for high intensity exercise when
overall stress is low. The sympathetic (flight or fight) nervous system will
have relatively low overall sensitivity, allowing for quick heart rate
recovery. More “burst cycles” can be completed in that 20 minute session.
You will be able to do more work in the session without overflowing
 the stress cup.

On a day when your overall stress is high, your sympathetic nervous system will
be sensitive to further “threats,” including exercise. Once you burst up to 90-95% of
heart rate max, it will take longer for you to recover to 70% HRmax because the
nervous system is overactive from work stress, poor sleep, etc. Longer recovery
times mean you will not be able to do as many cycles of the burst protocol in the
20 minute workout. More time will be spent in the recovery period.

High stress at work, a bad diet, and poor sleep have filled most of your
stress cup today. Using the Burst Protocol with a heart rate monitor will
protect you from overfilling the cup. You will need longer recovery times
for your heart rate to drop back down to 70% HRmax, which will ensure
that your body is gets the rest it needs between “bursts” on a stressful day.

THE BUILT-IN SAFETY SYSTEM

Using the heart rate monitor allows you to plug into the state of your nervous
system, and ensure you get adequate rest between bursts. On low stress days, your
fast heart rate recovery may allow you to get 10 burst cycles in 20 minutes. On high
stress days, your slower heart rate recovery may only allow for 4-5 burst cycles.
 Getting only 4-5 burst cycles on a high stress day is a good thing. You are
listening to your nervous system by monitoring recovery and not overtraining
(overfilling the stress cup). Remember that consistently overfilling the stress cup
leads to chronic inflammation, oxidative stress, and chronic disease.

KEY POINT:
Using the heart rate monitor with the burst protocol is a built in safety
system that allows you to get the most out of your workout on any given
day. It automatically adjusts the protocol to the other stresses in your life
and your fitness level.

Individual heart rate recovery also allows a very fit person to train with a
beginner. The person with a high fitness level will be able to do more intervals
because their recovery time will be much shorter than the beginner ’s. Their well-
conditioned heart and nervous system will require a higher relative intensity to
reach their target heart rate. The beginner will shoot up to their target heart rate
relatively quickly, but will take considerably more time to recover than the fit
person. The beginner will do fewer total intervals in during the 20 minute session
by design. Monitoring heart rate will ensure both get exactly the right amount of
exercise to trigger beneficial adaptations without overtraining. As the beginner
becomes more fit, they will recover faster and be able to increase their number of
intervals in 20 minutes.

You can use any modality or tool for your burst cardio protocol:

• Running

• Elliptical or stair stepper

• Biking

• Cross country skiing (or simulation)

• Burpees, medicine ball slams, kettlebell swings, or any other bodyweight

circuit training exercise.
 We prefer “4-limb” cardio that activates arms and legs at the same time. Cross
country skiing, rowing, and many bodyweight circuits work well. Be creative with
your choice of exercises for your intervals and mix it up.

We will look a little deeper into the Burst Cardio protocol, and see it in action. We
will also show you how use it to fine-tune your nervous system, and as a potent tool
for stress relief.

Take a look at the graphic on the next page. There are some important things to
note on the two profiled workouts.

• The recovery periods get longer as the workout progresses. The recovery
interval needed between exercise periods automatically adjusts itself as you
become more fatigued during the workout. Your nervous system is dictating how
much recovery time you need, instead of using a set interval as in the basic HIIT
protocol.

• When your “stress cup level” is low (as in workout #1), you can spend more
time in the higher intensity heart rate zones because you can perform more
exercise intervals in the 20 minutes. Although workout #1 and #2 were
performed by the same person in the same week, you could easily imagine the
data from workout #2 being generated from a beginner or deconditioned trainee.

• It is easy to see how much a night of bad sleep—or anything else that fills the
stress cup—has an impact on your nervous system. You would never know this
unless you were monitoring your heart rate. This is the built in safety system that
prevents overtraining and allostatic overload (an overflowing stress cup).

• During the recovery periods, you never drop below the 70% moderate
intensity level. You are still burning significant calories during the recovery
 intervals.

BURST CARDIO: FURTHER ANALYSIS

Chris uses the Polar® Beat application for iPhone or Android, and the Polar®
Flow website to track workout data. Both are free and highly recommended. All you
need is a Bluetooth heart rate monitor. The following graphics have been taken
from actual workout data from his Polar® Flow account.

The following are examples of the Burst Cardio protocol in action with data from
Chris’s actual workouts. At the time, Chris was 43 years old. His HRmax was
calculated at 178 bpm, putting his 90-95% target heart rate range between
approximately 160 and 169 bpm (0.95 X 178 = 169 and 0.90 X 178 = 160). His 70%
HRmax is about 125 bpm (0.70 X 178 = 124.6).

WORKOUT #1:
Chris was able to do 6 total intervals in 20 minutes, with relatively quick recovery
times between intervals. Notice the proportion of time spent in the higher intensity
“zones” (zones 4 and 5) is relatively high in this workout.
WORKOUT #2:
This workout was 5 days after the first workout above and took place after a night
of bad sleep. Notice that Chris was only able to do 4 intervals in the 20 minute
workout with long recovery periods needed to get back down to 70%. Also notice
the time spent in zones 4 and 5 is relatively low compared to workout #1.

TRAINING THE RECOVERY, BALANCING

YOUR FITNESS
The Burst Cardio protocol also allows us to do something almost never discussed
in modern fitness—using the recovery period as a trainable event. Modern society is
hyper-competitive, always looking to achieve higher levels of performance in the
speed of our cars, our computers, and certainly our workouts. This is why “boot
camp beat-down” fitness programs are really popular. In Chinese philosophy, we
are too much in the “yang” direction without the balance of “yin.”

The time it takes to recover from the “burst” up to 90-95% of max heart rate
down to the 70% level will vary depending on your fitness and stress levels. We can
actively train during the recovery time with the mindfulness breathing techniques
and biofeedback we learned in the chronic stress chapter.

• Once you have hit 90-95% of your maximum heart rate with the first interval,
stand in a relaxed posture and start the breathing exercises. We are calming the
sympathetic (flight or fight) nervous system in a mindful manner to reduce our
heart rate.

• Watch your heart rate monitor display as you breathe, using it as a biofeedback
device. Follow your heart rate as it slows, slowing your breathing and releasing
muscle tension. Follow your heart rate down to 70% then start your next interval.

Using this technique for training your recovery, you will be able to bring your
heart rate down faster between intervals and ultimately complete more total intervals
in your 20-minute burst protocol. Referring again to Chinese philosophy, we are
balancing the interval training (yang) by actively enhancing the recovery (yin). In
Western scientific terms, we are balancing the sympathetic nervous system stimulus
of the exercise interval by training the parasympathetic nervous system during the
recovery period.

Training the recovery has carryover effects into our daily life. Being able to quiet
your mind and focus your breathing during recovery from a high intensity exercise
interval (often in the midst of the noise and distraction of a busy gym) is a very
valuable health-enhancing skill.

Imagine the benefits of training to be calm in the middle of the “storms” of your
daily life. This is another approach—built in to your workout—to help master your
stress/threat system and reduce the effects of chronic stress.

AN ADAPTABLE SYSTEM
The burst cardio system also takes into account the type of exercise you are
performing in your interval. Heavy kettlebell swings will take more of a toll on
your nervous system than the elliptical machine. It will take longer to recover from
the kettlebell swing interval than the elliptical machine interval. It is no problem to
mix different exercises as your nervous system will adjust automatically for the
proper recovery time between exercises. This is important since most injuries
happen when the nervous system is fatigued and exercise form breaks down. The
protocol will help prevent injury from poor form due to nervous system fatigue.

KEY POINT:
Most injuries happen in a state of nervous system fatigue. The Burst
Cardio protocol will help prevent injury by monitoring the state of the
nervous system with the heart rate.

The total time of the burst cardio protocol can be adjusted if you are really
feeling run down, have limited time, or have performed intense strength training
directly before your cardio session. Burst cardio sessions of 10 minutes are still
highly effective in the right circumstances. You can use this protocol in your home,
the gym, or ideally immersed in a natural setting.
 TRAINING TIP:
If you are having difficulty achieving at least 90% HRmax during your
intervals, find another exercise. You may have become too efficient at a
single exercise (i.e. elliptical) and your nervous system has adapted. Mix
up your exercises!

TRAINING TIP:
HIIT has been shown to significantly improve performance capacity in
endurance athletes like marathon runners, cyclists, and triathletes.
Research has shown that endurance athletes were able to cut as much as
25% of their regular training and replace it with HIIT protocols without
losing any performance capability during competition. This is a great way
to cut down on training volume and potentially prevent overuse injuries
for competitors in endurance-based sports.

A trail run in the woods is an ideal way to do the Strong Medicine burst cardio
protocol.
 Burst interval: pushing up to 90-95% of HRmax.

Burst recovery: mindful breathing and biofeedback down to 70% of HRmax.

The Strong Medicine burst cardio protocol will give you the health benefits of
HIIT with an extra built in safety system to prevent overtraining and injury. We are
now going to show you how to program your exercise sessions weekly, combining
strength training and cardio for an individualized template of physical
transformation.

STRONG MEDICINE TACTICS:

Implement Strong Medicine “Burst Cardio” to supercharge your
metabolism, enhance fat burning, sensitize insulin, and train your
recovery without overfilling your stress cup.
PHYSICAL TRAINING IX
EXERCISE PROGRAMMING

TRANSFORMATIONAL FITNESS
“Eventually, after all the books are read and all the
thoughts are thought, it becomes time to actually train—
what to do: how to do it.”
—Marty Gallagher

We need a transformational template and we need to structure our lives to “make

room” for fitness. Once we have the game plan and have set aside training time, it is
time for the rubber to meet the road for some actual training. Training is split into
two generalized disciplines: resistance training and cardiovascular training. The
idea is to mix and meld these two training disciplines to elicit specific physiological
effects. There are enumerable variations within each discipline.

We won’t throw you into the deep end of the pool—most professional fitness
trainers require new trainees to engage in drills past the limits of their capacity. It is
cruel and counterproductive to make an untrained person—who has done nothing
more strenuous than walk to the refrigerator for decades—suddenly and
immediately begin high-impact jogging at a pace past their capacity on day one.

Our approach eases the trainee into our methodology: we establish initial
performance benchmarks and improve upon the previous week’s performance, in
some way each week. By asking slightly more of ourselves each week we
continually trigger the adaptive response and the extremely beneficial hormonal
tsunami that accompanies it. We want to safely and consistently exceed our best
efforts—that is where the progress lies.

DAY ONE, WEEK ONE, SESSION ONE

We will assume you have spent the time to develop your technique for the five
core exercises—the squat, deadlift, bench press, overhead press, and the row—
before launching into a formal program. Once you have done your homework with
the lifts, you can start training.

TACTICAL TEMPLATE: WEEKLY TRAINING REGIMEN

DAY RESISTANCE TRAINING CARDIO
Superset of Squat with overhead
Monday Power-walk or Rest
press
Burst Cardio session 10-20
Tuesday None
minutes
Superset of Dumbbell Bench Press
Wednesday Power-walk or Rest
with Row
Thursday None Power-walk or Burst Cardio
Friday None None
Saturday Sumo Deadlift Power-walk or Rest
Burst Cardio session 10-20
Sunday none
minutes

Using the Tactical Template as a guide, the following is a six-week plan for
progressing the exercises from week to week.

Use the Tactical Template to determine what exercises you will do on specific
days of the week, and use the weekly progression charts to determine how you are
doing the specific exercise as it relates to sets, reps, time, and intensity.
 WHAT IS A SUPERSET?
A superset consists of two exercises performed one after another without
pause. For example, on Monday we will alternate or ‘superset’ ultra-deep
squats with overhead dumbbell presses. First perform a technically perfect
set of ultra-deep paused squats. Upon completion of the squats, walk to the
dumbbell station, pull the dumbbells to your shoulders and complete the
press reps, then rest.

The athlete will perform the pattern three times in succession—squat,

press, rest, squat, press, rest, squat, rest, press. This strategy is used again
on Wednesday alternating the dumbbell flat bench press with the statue
row—bench, row, rest, bench, row, rest, bench, row, rest.

The superset alternating exercise strategy is a major time saver. The trick
is to pair up “non-conflicting” exercises. For example, you would never
pair up, or superset overhead presses with bench presses because these
two exercises use many of the same muscles. We would never superset or
alternate deadlifts and squats as they also use many of the same muscles.

How long should you rest between supersets? Wait until your breathing
normalizes then hit it again.

WEEK 1
Exercise Sets/Reps/time/intensity
Squat Bodyweight, 3 sets, 8 reps
Overhead Press 3 sets, 8 reps (enough weight so 8 reps is hard)
Dumbbell Bench Press 3 sets, 8 reps (enough weight so 8 reps is hard)
Row 3 sets, 8 reps (enough weight so 8 reps is hard)
Sumo Deadlift 3 sets, 6 reps (enough weight so 6 reps is hard)
Power Walk 15 minutes at 60% HRmax
Burst Cardio 10 minutes with exercise(s) of choice
Example: Using the Tactical Template, our workout on Monday of Week 1 would
be: supersets of bodyweight squat and overhead presses, for 3 supersets of 8 reps
per exercise. You could power walk for 15 minutes (60% HRmax) after lifting or
skip the power walk and rest.after lifting or skip the power walk and rest.

WEEK 2
Exercise Sets/Reps/time/intensity
Squat Bodyweight, 3 sets, 10 reps
Overhead Press 3 sets, 10 reps (maintain poundage from last week)
Dumbbell Bench Press 3 sets, 10 reps (maintain poundage from las week)
Row 3 sets, 10 reps (maintain poundage from last week)
Sumo Deadlift 3 sets, 10 reps (maintain poundage from last week)
Power Walk 25 minutes at 65% HRmax
Burst Cardio 11 minutes with exercise(s) of choice
Example: Using the Tactical Template, our workout on Tuesday of Week 2 would
be: no resistance training today, perform an 11 minute Burst Cardio session.

WEEK 3
Exercise Sets/Reps/time/intensity
Goblet Squat, 3 sets, 6 reps (enough weight that 6 reps is
Squat
hard)
Overhead Press 3 sets, 6 reps (use 5 lbs heavier dumbbells than last week)
Dumbbell
3 sets, 6 reps (use 5 lbs heavier dumbbells than last week)
BenchPress
Row 3 sets, 6 reps (use 5 lbs heavier dumbbells than last week)
Sumo Deadlift 3 sets, 6 reps (use 10 lbs heavier than last week)
Power Walk 30 minutes at 68% HRmax
Burst Cardio 12 minutes with exercise(s) of choice
Example: Using the Tactical Template, our exercise on Wednesday of Week 3
would be: supersets of dumbbell bench presses and rows for 3 supersets of 6 reps
per exercise, using dumbbells 5 lbs. heavier than last week. After lifting, you could
power walk for 30 minutes (at 68% HRmax) or rest.

WEEK 4
Exercise Sets/Reps/time/intensity
Front Squat, 3 sets, 10 reps (enough weight that 10 reps is
Squat
hard)
Overhead Press 3 sets, 8 reps (maintain poundage from last week)
Dumbbell Bench
3 sets, 8 reps (maintain poundage from last week)
Press
Row 3 sets, 8 reps (maintain poundage from last week)
Sumo Deadlift 3 sets, 8 reps (maintain poundage from last week)
Power Walk 30 minutes at 70% HRmax
Burst Cardio 13 minutes with exercise(s) of choice
Example: Using the Tactical Template, our workout on Thursday of Week 4 would
be: no resistance training today, power walk for 30 minutes (at 70% HRmax) or
choose a 13 minute Burst Cardio session.

WEEK 5
Exercise Sets/Reps/time/intensity
Squat Front Squat, 3 sets, 6 reps (use dumbbells 5lbs heavier)
Overhead Press 3 sets, 10 reps (maintain poundage from last week)
Dumbbell Bench Press 3 sets, 10 reps (maintain poundage from last week)
Row 3 sets, 10 reps (maintain poundage from last week)
Sumo Deadlift 3 sets, 10 reps (maintain poundage from last week)
Power Walk 30 minutes at 73% HRmax
Burst Cardio 14 minutes with exercise(s) of choice
Example: Using the Tactical Template, our workout on Friday of Week 5 would be:
No training. A complete rest day.
 WEEK 6
Exercise Sets/Reps/time/intensity
Front Squat, 3 sets, 8 reps (maintain poundage from last
Squat
week)
Overhead Press 3 sets, 6 reps (use dumbbells 5 lbs heavier than last week)
Dumbbell Bench
3 sets, 6 reps (use dumbbells 5 lbs heavier than last week)
Press
Row 3 sets, 6 reps (use dumbbells 5 lbs heavier than last week)
Sumo Deadlift 3 sets, 6 reps (use 10 lbs heavier than last week)
Power Walk 30 minutes at 73% HRmax
Burst Cardio 14 minutes with exercise(s) of choice
Example: Using the Tactical Template, our workout on Saturday of Week 6 would
be: sumo deadlift, 3 sets of 6 reps using weights 10 lbs. heavier than in week 5.
After the weight training, power walk for 30 minutes (at 73% HRmax) or rest.

ADVANCED PROGRAMMING: SEASONAL

“PRIMORDIAL CYCLING”
Elite athletes know that the optimal length of time to peak the human body for
athletic competition is twelve weeks. This is empirically-based experiential
knowledge based on 70 years of observation and preparation. Elite athletes and
coaches at the highest levels try to avoid preconceptions. Preconceptions interfere
with the perception of reality.

• The fundamentalist has a set of frozen, fossilized beliefs and will reverse
engineer an elaborate rationale to justify their belief system. The fundamentalist
rejects new input and knowledge as it could potentially threaten or undermine
their beliefs.

• The scientist continually expands his knowledge, and seeks new data. Without
clinging to beliefs, the human performance scientist has loyalty to one master—
tangible, measurable, physiological results.

Empirical science has formulated a loose consensus for the optimal time period
of a serious fitness effort. All this assumes the athlete has a goal—by definition, all
athletes have a goal—to improve performance within their sport. We have learned
through hard-earned gym wisdom that twelve weeks (84 days, three months) is an
optimal length of time for building muscle mass, power, strength, conditioning,
leanness, stamina and endurance.

PRIMAL CORRELATIONS
We think it is no accident that the optimal length of time to peaking human
performance is three months is one season. Summer, winter, spring and fall are
three month chunks. Primal hunter-gatherers migrated with animal herds for
hundreds of thousands of years. Widespread agriculture was only implemented
about 10,000 years ago, a mere blip compared to the total time we have been on this
planet.

Prior to agriculture, we spent our time foraging and following migrating herds
of animals for protein sources. Walking, moving, running, chasing, being chased,
living on pristine animals, supplemented with whatever wild fruits, roots, and
vegetables could be found. Humans were parasites living off of massive migrating
herds of animals.

In temperate regions to a great degree, and all geographic regions to a lesser

degree, each passing season caused humans to adjust to nature’s whims. Even in a
desert, a summer drought can wreak havoc on all living things. By all accounts,
these primal hunter-gatherers, would physically wipe the floor with modern man.
The primal ancients were far leaner, more muscular, had greater endurance, no
cardiovascular or insulin-related maladies, and no cancer or obesity. These people
continually adjusted their lives, based on nature, the seasons, and their impact on the
herd.

The animal herd sustained them. In a time of drought, if the herd suffered, then
humans suffered. Optimally, the herd moved south as cold weather set in. The
migration reached the southernmost point as spring gave way to summer. With the
onset of the warm months, the herd moved north until fall gave way to winter and
the cycle repeated. Indigenous tribes worldwide were synced up to the weather-
induced migratory habits of animals.

Flashing forward to the present day, is it any surprise that modern elite strength
athletes have discovered that a three-month training cycle is optimal? Once we
understand and embrace this idea, the next logical step is to sync a transformational
goal with the seasonal cycle of 12 weeks. It would make sense to meld seasonally
appropriate training and eating in an attempt to reconnect with our primal encoding.

Winter: the best time for goals of gaining muscle mass and strength. What better
time than the dead of winter for hardcore, barebones, ultra-heavy strength training
when the thick soups, root vegetables, and heavy rich foods taste better. Add some
muscle mass and add 20% to your strength during winter ’s 12-weeks.

Spring: when the magnificence of the true spring arrives, shift physiological
gears. After a winter strength training cycle, shift to more volume, more sessions,
less weight, and more cardio. Shift to seasonally appropriate lighter meals with
more carbohydrates.

Summer: as the deep summer takes root, we want to become maximally lean.
During the summer heat, our activities peak, our appetite is low and we want the
lightest proteins, more salads, fruits, vegetables and less food volume. Weight
training becomes high-rep, high-volume, and high-frequency. We will do a lot of
cardio with plenty of moving and sweating.

Fall: with the onset of true fall, we will add more substance to our weight
training. Richer, more savory foods suddenly taste delicious as the weather becomes
colder. The fall phase peaks over the holidays—we want to be maximally large and
lean heading into the almost hibernation-like strength-training winter phase.

Give seasonal training a try to see how it works for you. It makes sense from a
“first principles” perspective and also aligns with our “feed your activity” concept.
CONCLUSION

We have presented a template for training that incorporates foundational

resistance training with proper doses of cardiovascular training. This is a template
that may be especially useful to the beginner but it remains only a template. Use it as
a starting point. Entire books have been written on exercise modes and periodized
training, and deeper coverage of these topics is well beyond the scope of Strong
Medicine.

We have given you a foundation of ideal techniques and tactics for resistance
training that can be progressed as you advance. This is a rock solid program to
begin your fight against inactivity, the fifth member of the Pentaverate.

Inactivity is no match for Strong Medicine physical training.

“MILITARY INTELLIGENCE” (REFERENCES):
Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab Syndr Obes 6 (2013): 113-122.

Bird SR, & Hawley J A. Exercise and type 2 diabetes: new prescription for an old problem. Maturitas 72 (2012): 311-316.

Burd NA, et al. M uscle time under tension during resistance exercise stimulates differential muscle protein sub-fractional synthetic responses in men. J Physiol 590 (2012): 351-362.

Ciolac EG. High-intensity interval training and hypertension: maximizing the benefits of exercise? Am J Cardiovasc Dis 2 (2012): 102-110.

Gibala M J , et al. Physiological adaptations to low-volume, high-intensity interval training in health and disease. J Physiol 590 (2012): 1077-1084.

Gillen J B, et al. Acute high-intensity interval exercise reduces the postprandial glucose response and prevalence of hypergly-caemia in patients with type 2 diabetes. Diabetes Obes Metab 14 (2012): 575-577.

Hartmann H, et al. Analysis of the load on the k nee joint and vertebral column with changes in squatting depth and weight load. Sports Med 43 (2013): 993-1008.

Hawley J A, & Gibala M J . What’s new since Hippocrates? Preventing type 2 diabetes by physical exercise and diet. Diabetologia 55 (2012): 535-539.

Larsen I, et al. High- and moderate-intensity aerobic exercise and excess post-exercise oxygen consumption in men with metabolic syndrome. Scand J Med Sci Sports (2013).

Li G, & He H. Hormesis, allostatic buffering capacity and physiological mechanism of physical activity: a new theoretic framework . Med Hypotheses 72 (2009): 527-532.

Little J P, et al. Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. J Appl Physiol (1985) 111 (2011): 1554-1560.

M cGill S. U ltimate Back Fitness and Performance. Stuart M cGill, PhD (2007).

M cGill S. Low Back Disorders, Second Edition. Human Kinetics (2004).

M eyer P, et al. High-intensity aerobic interval exercise in chronic heart failure. Curr Heart Fail Rep 10 (2013): 130-138.

M olmen-Hansen HE, et al. Aerobic interval training reduces blood pressure and improves myocardial function in hypertensive patients. Eur J Prev Cardiol 19 (2012): 151-160.

O’Donovan, G, et al. Changes in cardiorespiratory fitness and coronary heart disease risk factors following 24 wk of moderate- or high-intensity exercise of equal energy cost. J Appl Physiol (1985) 98 (2005): 1619-1625.

Rehn TA, et al. Increasing physical activity of high intensity to reduce the prevalence of chronic diseases and improve public health. Open Cardiovasc Med J 7 (2013): 1-8.

Rognmo O, et al. High intensity aerobic interval exercise is superior to moderate intensity exercise for increasing aerobic capacity in patients with coronary artery disease. Eur J Cardiovasc Prev Rehabil 11 (2004): 216-
222.

Shaw K, et al. Exercise for overweight or obesity. Cochrane Database Syst Rev CD003817 (2006).

Tjonna AE, et al. Aerobic interval training versus continuous moderate exercise as a treatment for the metabolic syndrome: a pilot study. Circulation 118 (2008): 346-354.

Tjonna AE, et al. Aerobic interval training reduces cardiovascular risk factors more than a multitreatment approach in overweight adolescents. Clin Sci (Lond) 116 (2009): 317-326.

Trapp EG, et al. The effects of high-intensity intermittent exercise training on fat loss and fasting insulin levels of young women. Int J Obes (Lond) 32 (2008): 684-691.

Whyte LJ , et al. Effects of single bout of very high-intensity exercise on metabolic health biomark ers in overweight/obese sedentary men. Metabolism 62 (2013): 212-219.

Wisloff U , et al. Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation 115 (2007): 3086-3094.
BATTLE PLAN II
STRONG MEDICINE NUTRITION:
INDIVIDUALIZED STRATEGIES

I. FOOD: SOURCES AND QUALITY

II. CARBOHYDRATE TOLERANCE

III. FEED YOUR ACTIVITY

IV. ONE WEEK OF FOOD

INDIVIDUALIZED STRATEGIES I
FOOD: SOURCES AND QUALITY

CULINARY CONSENSUS
The world’s best chefs insist on seasonally appropriate, locally grown, natural,
fresh, organic fruits, vegetables and proteins. They want the freshest local
ingredients, and the less time between harvest and consumption the better. Flavor
intensity (for any fruit, vegetable or protein) is at its peak the instant it is picked or
caught. Every minute after the food was gathered adds another degree of flavor-
degradation.

But, flavor is not the only thing that degrades as the time from harvest passes. The
nutrient density of produce significantly and rapidly degrades in fruits and
vegetables soon after picking. It is convenient to get out of season fruit from New
Zealand, but it has a long journey from the grove to your home, and will sacrifice
nutritional potency along the way.

The world class chef and the Strong Medicine trainee want the same foods for
entirely different reasons. Above all else, the chef wants potent flavor and vibrancy.
Trainees intent on triggering transformation understand that nutrition can be an art
and a science—optimally fueling the body to provide exactly what it needs at exactly
the right time, in direct proportion to the duration and intensity of the exercise
session and the severity of the training protocols.
 To grow muscle mass requires that we stress the body—then feed it what it wants
in the proper amounts; then we rest the body and muscle grows. We can also set up
physiological situations which cause the body to use its stored body fat to power
activity.

Taste goes hand in hand with potency. With nutritional potency, you also find the
most intense taste and flavor. This is a divine coincidence—the smartest “dieter”
eats potent gourmet meals made from the finest, freshest, most flavorful seasonally
appropriate local ingredients. Organic, locally-produced food is suited for both the
flavor-crazed chef and the athlete seeking nutrientdense food/fuel.

Amongst the world’s finest chefs there is surprising unanimity regarding the best
way to prepare fresh food—make the ingredients the star of the dish, not the chef.
We should learn how to amplify, not smother or overwhelm the perfection of
nature’s bounty, eaten at its finest, freshest and most potent state.

“ORGANIC”
To earn the US Department of Agriculture “organic” label, fruits and
vegetables must be grown and processed within strict guidelines.
• Most synthetic pesticide chemicals are not allowed.
• Synthetic fertilizers or sewage sludge cannot be used.
• No genetically modified organisms (GMOs).

Livestock must meet the following guidelines to be USDA certified

“organic”.
• No antibiotics or growth hormones used with the animals.
• Livestock must be fed 100% organic feed containing no animal
byproducts.
• Animals must have access to the outdoors.
 30% of the animals’ food must come from grazing. 70% may come from
organically produced dry feed.

The Strong Medicine trainee needs potency. Most of the foods purchased at the
local chain grocery store are nutritionally impotent compared to locally grown
foods from the farmer ’s market. One trip to the Farmer ’s Market dispels the
misconception that quality food is expensive. At the Farmer ’s Market the prices are
equal or better to the mega-chain grocery store and significantly cheaper than most
upscale organic food markets. Plus, you are supporting your local farmers.

DON’T BE FOOLED BY APPEARANCES...

LOCAL IS BEST
Local food is simply more nutrient dense. It may not look as pretty as the waxed
and polished fruit and vegetables in most supermarkets trucked in from thousands
of miles away (or from across the globe). But local food makes up good looks with
more health benefits.

The longer fruit and vegetables have been stored after harvesting, the more
nutrients they lose. The buffed and shined supermarket food has often lost over half
of its beneficial natural minerals, vitamins, and cancer fighting chemicals by the
time they reach the dinner table. Most supermarket produce is all show and no go.

We want nutrient-dense fruits and vegetables harvested by your local farmer,

eaten only days after harvesting. This local produce may not look as polished, but it
retains most of its health-promoting vitamins and minerals beneath a humble
outward appearance.

FOOD QUALITY FOR THE OMNIVORE

Homo sapiens developed as omnivores. Good foundational science shows that the
introduction of nutrient dense animal-based food—especially marine animals—into
our diet allowed for both the expansion of our relatively large brains, and the
shrinking of our digestive tract as compared to our nearest hominid relatives.

Humans especially need the polyunsaturated omega-3 fat DHA (see Nutrition
101) for proper brain function. Provocative new research theorizes that we were
able to develop our large brains by obtaining DHA from marine animal food
sources (fish and other seafood). Recall that we can convert very little alpha linoleic
acid (18 carbon omega-3) to the “big brother” omega-3, EPA and DHA. This is why
it is important to get some pre-formed EPA and DHA from our diets. Fortunately
large amounts are naturally found in animal-based foods.

As discussed previously, adequate DHA is critical for the early brain development
period from infancy through adolescence. Plant-based omega-3 (such as ALA in
flax seed) is not converted to DHA in high enough quantities to support healthy
brain development. For this reason, incorporating high quality animal-based foods
in the diet is important from a health perspective, especially for children. Animal-
based foods are also—calorie for calorie—the best sources of protein to support the
flesh machine’s need for essential amino acids.

The conversion from ALA to EPA and DHA is very inefficient

It is estimated that only 5% of dietary ALA is converted to EPA and DHA. High ALA
foods like flax seed are a poor way to get EPA and DHA. You can bypass the poor
conversion by eating EPA and DHA directly from fatty fish and grass fed
animals.

For animal food sources, quality is paramount. Unhealthy animals raised in

confinement, pumped full of antibiotics and growth hormones, then fed processed
pesticide-laden feed are poor nutrient sources for omnivores. There are significant
ethical and humane issues with animals raised in confinement as well. A template for
an optimum high-quality omnivorous diet:

• Locally produced fruits, vegetables, and tubers grown with organic

farming principles. (Some small farms are not large enough to pay for official
“organic” certification.) This category should comprise the largest proportion of
your meals by weight. The fermentable fiber, minerals, and disease-fighting
phytonutrients in these foods should form the foundation of your nutrition plan.

• 25-30 grams of protein per meal from a high quality source:

— Beef from 100% grass-fed cows or bison.
 — Wild game (deer, elk, boar, turkey, etc.).
— Poultry (chicken/turkey) should be “pasture-raised” with organic feed.
— Wild-caught oily fish such as salmon, tuna, sardines, mackerel, and trout.
— Crab, oysters, lobster, mussels.
— Eggs from pasture-raised chickens.
— Pork from pastured pigs.

PRISTINE PROTEIN

The quality of animal foods is directly related to the environment where

they are raised. Animals free to roam and eat natural foods are the most
nutritious for the omnivore.
• Cows eat grass; it is their natural food! Grass-fed beef is leaner overall
and has significantly more long chain omega-3 (EPA and DHA)fats, B-
vitamins, Vitamin E, Vitamin K, and the anti-inflammatory fat conjugated
linoleic acid (CLA), than beef from cows eating grain in the feedlot.
Grain-fed cows confined to feedlots are awash in antibiotics and growth
hormones. Beef from grain-fed cattle has almost no beneficial long chain
omega-3 fats.
• Chickens and turkeys are omnivores, eating insects as well as grain.
Poultry meat from pasture-raised organic chickens and turkeys is higher
in EPA and DHA (omega-3) and lower in omega-6 fats. Commercially
produced poultry are confined to cages and crowded indoor poultry
houses. These birds are sickly, require antibiotics, and have almost no
omega-3 fats in their meat. Avoid this type of poultry.
• Wild-caught oily fish such as tuna, salmon, sardines, mackerel, and trout
are DHA superstars. Farmed fish fed a diet of fishmeal (often containing
pesticide residues and antibiotics) have only trace amounts of the
beneficial long chain omega-3 fats. Stick with wild-caught fish and avoid
farmed fish.
• Pigs are omnivores, and pork from pasture-raised pigs (allowed to
graze and forage) is leaner and has more beneficial omega-3.
Conventionally raised pigs eat grain-based pig feed and live in horrific
crowded conditions requiring antibiotic use.

Healthy animals which have eaten their natural foods, and are pasture-
raised or wild caught, are the healthiest for us to eat.

GRASS-FED = EXPENSIVE?

Grass-fed beef and wild game meat purchased from retail stores can be
very pricy. But, you can find local sources of grass-fed beef, pasture-
raised poultry, eggs, and pork, and buy large quantities relatively cheaply.
Many local farmers will sell grassfed beef in bulk in quantities such as a
whole, half, or quarter cow. Even after processing and packaging fees, the
price per pound is often comparable to conventional feed-lot beef sold in
stores. Buy in bulk and store in your freezer.

The best resource for finding a local farmer selling pastured animal
products in your area is www.eatwild.com. Go check it out! You will get a
great deal on a healthy protein source and support your local farmer at the
same time.

If you do not hunt wild game, talk to any hunters you know. You can
probably work out a good deal on a portion of the wild game they kill
during hunting season. Elk, deer, and boar are fantastic protein sources.
DOC’S RANT:
Many people who complain about the cost of food are the same ones who
spare no expense on the latest big screen televisions, buy daily $5 coffees,
and have the most up to date smart phones.

Food quality is simply not a priority for most of us. People in this country
are used to buying low cost processed food and scoff at the idea of having
to spend more of our income on what we eat. Americans spend on average
less than 7% of their income on food, the lowest proportion in the world.

The U.S. is one of the most prosperous and productive nations on Earth
but with one of the worst rates of chronic preventable diseases. There
seems to be a connection between our poor health and the unwillingness to
demand high quality food and spend a higher proportion of our income to
purchase good food.

Perhaps we need to rethink our priorities…

ANIMAL WELFARE
The Strong Medicine omnivore should insist on pasture-raised animals as
protein sources for more than health reasons. Conventional feed-lot
operations are equivalent to concentration camps for animals and deprive
them of their health with crowded disease-promoting conditions. We
understand these animals are raised as food sources, but we have an
ethical obligation to ensure they are treated humanely.

Find a local source for your protein and visit the farm yourself to observe
the treatment of the animals you are eating. Reconnect with your food
source.

WHAT ABOUT MERCURY IN FISH?



Elemental mercury from the environment is converted to “organic

mercury” (methylmercury) in fish. Methylmercury (MeHg) is extremely
damaging to nerve cells in the brain.

Small fish contaminated with mercury are eaten by large predatory fish—
tuna, king mackerel, tilefish, sharks—and marine mammals such as
whales. Methylmercury (MeHg) is concentrated or bioaccumulated in the
larger predatory fish.

Methylmercury is especially damaging to the developing brains of fetuses,

infants, and young children, prompting warnings to avoid the above fish
as sources of protein and omega-3, especially for pregnant or nursing
mothers and young children.

The advice to avoid these specific fish for this group of people is still
prudent, but there is a little more to the story.

Methylmercury (MeHg) produces its toxic effects by directly stopping the

action of many antioxidant defense enzymes, which are crucial for
protecting us from damaging free radicals. Many of these enzymes are
dependent on the nutrient selenium for proper function. MeHg can directly
inhibit the enzymes AND bind to selenium. The binding of MeHg to
selenium effectively removes selenium, and stops the antioxidant defense
system enzymes which are dependent on it. Without the protection of the
antioxidant defense enzymes, the nerve cells are damaged by free radicals.

A key point is that an increase in dietary selenium can counteract the

damaging effects of methylmercury from these fish.

As long as the fish have higher selenium levels than MeHg levels, the
antioxidant defense enzymes are still able to function because they have
adequate selenium. The damaging effects of MeHg are greatly diminished
in this case.

Recent research was conducted on the Canadian Inuit population, a group

whose diet consists largely of seafood with a relatively high MeHg
content. It was found that the high selenium levels in the fish appeared to
protect the Inuit from neurological oxidative damage from HeMg. This
research implies that as long as selenium content in the fish is adequate,
the effects of MeHg may be minimal.

Most ocean fish have more selenium than mercury, making them
theoretically safe to eat despite their mercury levels. Exceptions are sharks
and pilot whales. Meat from these two species has more MeHg than
selenium, making them potentially toxic for your brain.

QUICK MEDICAL NOTE:

This research is still preliminary, so it is still wise to be cautious by
minimizing predatory fish consumption (tuna, swordfish, tilefish, king
mackerel) for pregnant and nursing mothers, as well as infants and
children until more studies are performed.

KEY POINT:
Most ocean fish have higher selenium content than methylmercury,
making them theoretically safe to eat for most adults. The high selenium
content protects the brain from the effects of methylmercury.
QUICK MEDICAL NOTE:
This research is still preliminary, so it is still wise to be cautious by
minimizing predatory fish consumption (tuna, swordfish, tilefish, king
mackerel) for pregnant and nursing mothers, as well as infants and
children until more studies are performed.

KEY POINT:
Most ocean fish have higher selenium content than methylmercury,
making them theoretically safe to eat for most adults. The high selenium
content protects the brain from the effects of methylmercury

IS THE CHOLESTEROL AND FAT IN

ANIMAL-BASED FOODS CAUSE FOR
CONCERN?

We have all been warned about eating too much saturated fat and
cholesterol from animal food as it will surely lead to “clogged arteries
and heart disease”. Let us tackle the issues one at a time.
• Dietary cholesterol: eating cholesterol from natural food sources such
 as eggs and animal meat has no impact on the health of your arteries. For
most people, cholesterol from the diet has a minute effect on their blood
cholesterol levels. Please see our extensive discussion of cholesterol in
the Analytics section of this book. That section should ease your fears
about the “dangers” of eating cholesterol-containing foods.
• Fat in animal foods: after reading the Nutrition and Metabolism 101
section in the beginning of the book, we are now much more
knowledgeable about fat, especially saturated fat.
i) Remember that most types of saturated fats are beneficial the body.
Pastured animals have higher amounts of beneficial saturated fats (such as
stearic acid) and lower amounts of the potentially inflammatory palmitic
acid.
ii) Almost half of the fat in animal-based foods is monounsaturated fat.
This is the same health-promoting fat in olive oil (oleic acid).

The idea that high quality animal-based foods from pastured sources
contribute to heart disease has no scientific foundation and is a very
outdated way of thinking. This erroneous message really needs to be
stopped once and for all.

“DEADLY MEAT”
There are countless news stories about recalls of meat contaminated with
bacterial pathogens such as E. coli O157:H7, a potentially deadly strain of bacteria
responsible for several deaths. Almost without fail, the contaminated ground beef
and pork on the news is from “factory-farming” operations. The crowded
conditions and improper feeding practices (using processed animal feed instead of
the animal’s natural food) lead to overgrowth of deadly pathogens such as E. coli
O157:H7.

In the attempt to stop this type of contamination, factory-farms give the animals
high doses of antibiotics which are still present in the meat when you bring it home
from the grocery store. High levels of antibiotic use in factory-farms is also
thought to greatly contribute to the development of antibiotic-resistant “super bugs.”
These are additional reasons to obtain your protein from pastured animals, living in
un-crowded conditions, eating their natural foods.

The massive amounts of animal waste (manure, etc.) from these operations have
huge potential effects on our environment as well. Some factory-farms are
ecological disasters waiting to happen.
 Investigative journalist David Kirby has brilliantly illustrated the potential
impacts to human health and the environment posed by factory farming in his recent
book Animal Factory—highly recommended reading.

INSIST ON FOOD QUALITY

We are making a big case for pastured animals and wild-caught fish as omnivore
protein sources. As more people demand high quality, humanely raised pastured
animals, more local farms will appear and increase the supply. As supply and
competition increase for this type of food, prices will go down. This change must
be driven from the ground up by the consumer, otherwise the food industry will
continue to push factory-farmed animal products because of their high profitability.
Even though factory-farms are profitable, it is at the expense of animal health,
animal welfare, the environment, and your long-term health. The Strong Medicine
omnivore should demand high quality protein from pastured animals or wild game.

FOOD QUALITY FOR THE VEGETARIAN

Given the current state of the animal-based food supply from factory farming, it
is no wonder that an increasing number of people are becoming vegetarian.
Vegetarianism can be a healthy way to eat if done correctly, but can be disastrous if
done improperly.

Strong Medicine completely respects those who turn to vegetarianism for strong
moral and ethical reasons. However, it is a fallacy to state that a vegetarian diet is
healthier than an omnivorous diet based on wild/pastured animal protein and
organically grown fruit, vegetables, and tubers. There are some potential issues
with the vegetarian (and especially vegan) dietary practices that need to be
optimized.

• Deficiency in essential amino acids- vegetarian and vegan diets can be

relatively deficient in certain essential amino acids. Recall from Nutrition 101
that essential amino acids cannot be made by the body and must be obtained from
food.

Most animal proteins have large amounts of essential amino acids, but
vegetarians will need to make a little more effort to get adequate amounts during the
day. The essential amino acid lysine is often deficient in vegetarians who base their
diets on grains. Legumes such as lentils, black beans, garbanzo beans (chick peas),
and pseudo-grains such as quinoa are relatively good sources of lysine and should
be eaten daily to ensure an adequate supply of essential amino acids. Obtaining
plant-based protein from a combination of sources is called eating complimentary
proteins.

Please note that plant-based protein is not as easily digested or utilized as well as
animal protein. This means that a vegetarian will need to eat a larger amount of
plant-based protein to get the same amount of useable (bioavailable) protein as an
omnivore.

• Inadequate Vitamin B-12. Vitamin B-12 is a crucial B-vitamin. Deficiency in

this vitamin can lead to neurological problems, anemia (low blood cell count),
and may increase the risk for heart disease from inflammation. Vitamin B-12 is
produced by bacteria in the soil and is concentrated in animal-based foods.

It has often been erroneously thought that vegetarians can obtain B12 from plant-
based sources such as mushrooms and nutritional yeast. Unfortunately the laws of
biochemistry and several scientific studies refute these claims. Plant-based “vitamin
B-12” analogs are not true vitamin B-12. They are also not biologically active in
humans. In other words the analog B-12 found in some plants does not work for
humans. Nutritional yeast does not naturally contain vitamin B-12 since yeast
cannot make it. Nutritional yeast with vitamin B-12 has been fortified or
supplemented from other sources of vitamin B-12.

Without a regular supply of vitamin B-12, vegetarians (and especially vegans)

will become deficient. It is easy to correct this deficiency by using a vitamin B-12
supplement and working with your doctor to monitor the effects of supplementation.
Vitamin B-12 supplements are made from bacteria sources, so vegans and
vegetarians can supplement without worry.
LEGUME PREPARATION IS KEY TO
PREVENT TOXICITY

Legumes (beans) contain natural chemicals called lectins that can be toxic
to humans and other animals. It is thought that plants have them in their
seeds (legumes) to protect against predators. Legumes in particular can
have a high amounts of a compound called phytohemagglutinin (PHA).
PHA can cause several toxic effects and can even be fatal in high enough
doses.

Proper preparation of legumes is important to reduce levels of lectins and

prevent toxicity. Soak raw legumes for 24 hours before cooking. Rinse the
legumes after soaking. Then boil the legumes for at least 30 minutes.
These steps will reduce lectin levels to a safe range.

Never slow cook beans. Cooking them at temperatures below boiling

can actual concentrate lectin levels and lead to toxicity.

QUICK MEDICAL NOTE:

Vitamin B-12 deficiency can lead to neurological problems, anemia, and
an increased risk for heart disease. Low vitamin B-12 leads to increases in
an inflammatory marker called homocysteine. High homocysteine levels
are a strong predictor for developing heart disease.
 The best way for a vegetarian to detect a vitamin B-12 deficiency is to
have their doctor test their blood and measure levels of methylmalonic
acid (MMA). High MMA levels indicate a possible vitamin B12
deficiency. Supplement with B-12 and monitor MMA levels with your
doctor.

• Inadequate long chain omega-3 fats. Animals concentrate long chain omega-3
(EPA and DHA) from the food they eat (grasses, algae, etc.). This makes animal
sources (especially cold water fish) optimal for getting adequate EPA and DHA.
Vegetarians and vegans often think they are getting adequate omega-3 in their
diets by eating short chain omega-3s such as alpha linolenic acid (ALA) from
plant sources. As we have discussed extensively, ALA is very poorly converted to
the longer chain EPA and DHA in the human body. Also recall from Nutrition 101
that omega-6 and omega-3 compete for the same conversion enzymes to turn
them from short chain to long chain. This means that if a vegetarian or vegan has
a relatively large amount of omega-6 in their diet from grains or vegetable oils,
the already poor conversion of ALA to EPA and DHA will be even worse!

Vegetarians and vegans can ensure they get adequate long chain omega-3 (EPA
and DHA) by supplementing with preparations of EPA and DHA from algae sources.
These algae-based products and supplements are available at health food stores or
online. It is also helpful to reduce the amount of omega-6 in the diet (from grains
and vegetable oils) so that as much of the short chain omega-3 from plant-based
sources like flax seed as possible is converted to the long chain forms of DHA and
EPA in the body (this is not much, but every little bit helps).

Maintaining a balance of long chain omega-3 with omega-6 is crucial to avoiding

chronic inflammation (and the chronic diseases that go with it) from high levels of
omega-6. Getting adequate long chain omega-3 is especially important for the
developing brains of children.

• Inadequate iron and zinc. Vegetarians and vegans are also at risk for
 developing iron and zinc deficiencies, especially if they are consuming large
amounts of grain-based foods or raw vegetables. Iron from animal foods is
predominantly in the form of heme iron which is more easily absorbed in the
body than the non-heme iron found in plant-based foods. But, vegetarians and
vegans generally have diets high in vitamin C which helps absorption of non-
heme iron. The real problem with vegetarian diets based on grains, nuts and
legumes (soy is a good example) is a molecule called phytate. Phytate is present
in the germinating portion of plants (seeds, legumes, etc.) and binds minerals
such as calcium, magnesium, iron, and zinc.

The plants use phytate to ensure the developing “baby plant” growing from the
seed has enough minerals to support its growth. Plants are able to release the
minerals bound by phytate using an enzyme called phytase which dismantles the
phytate molecule, releasing the minerals to the developing plant. Humans do not
have the phytase enzyme and are unable to absorb many plant-based sources of
minerals (iron and zinc especially) because they are still bound to phytate.

The best way to lower phytate in grains, nuts, and legumes is through proper
preparation. Soaking nuts for 24 hours before eating them will reduce phytate
considerably. Soaking legumes and then boiling them will also decrease phytate
content, allowing the absorption of iron and zinc.

SPROUTING IS THE WAY TO GO...

Sprouting (germinating) seeds, legumes, nuts, or grains not only reduces
phyate levels making iron and zinc more absorbable, but also greatly
increases the vitamin content of these foods. Sprouting makes use of the
biochemical changes that take place when the plant begins to grow. It takes
a couple days to sprout grains, legumes, nuts, or seeds, but it is well worth
it from a nutritional perspective.

There are plenty of guides to sprouting on the internet, but you can also
find a good overview in Sally Fallon’s excellent cookbook, Nourishing
 Traditions.

Using the simple recommendations above, a vegetarian or vegan diet can be well-
balanced and healthy. The Strong Medicine vegetarian should stay away from
processed grains and use properly prepared plant-based powerhouse foods such as
legumes, tubers and pseudograins such as quinoa for protein. They should also take
full advantage of the incredible health promoting “natural pharmacies” in
organically grown fruits and vegetables.

The Strong Medicine omnivore and vegetarian should maximize their intake of
locally-grown organic produce, and make them the cornerstone of a nutrition battle
plan against chronic disease.

ORGANIC VERSUS CONVENTIONAL

PRODUCE

There has been significant hand-wringing in the public health and

scientific research communities on whether conventionally grown or
organic produce is the most nutritious. They are missing the bigger
picture.
• The amount of time from picking to eating is the most important
variable for nutritional value. Produce (conventional or organic)
imported from across the globe, which spends several weeks in transport
and storage will lose its nutritional value in the from of vitamins, minerals
and other health promoting plant chemicals.
• We insist upon organic produce not as much for nutritional value but to
avoid the pesticides and antibiotic contamination often found in
conventionally grown produce.
 • Locally-grown organic produce has the highest nutritional value
because it has been recently harvested and has not been transported and
stored for weeks. Organic farming practices ensure that we are not
subjected to toxic contaminants such as pesticides.

Insist upon local and organic produce. Your local farmer’s market is
your best source.

SPICE UP YOUR HEALTH

Food tastes best when we add in herbs and spices. Variations in herbs and spices
create a flavor profile for our meals. Most of the herbs and spices that we casually
place in our food has a long history of medicinal uses. Research is beginning to
catch up with what traditional healers have known for centuries—that these
seemingly simple and tasty additions to our food are actually beneficial to our
health.

Let’s add another word of caution here. Science is an amazing tool and this book
is based on the most current research and foundational science. Scientific research,
especially as it pertains to food, can also be reductionist and lose sight of the big
picture.

Many of the “active constituents” found in modern spices and herbs are extracted
from the whole portion of the plant (which would traditionally have been used).
These medically active chemicals are studied in isolation by modern science. We
must keep an open mind to the potential of these substances. But, before you run to
the supplement store or dump an entire bottle of turmeric on your food, we need a
little more understanding of herbs as medicine. Herbal medicine is an entire aspect
of medicine that requires a thorough understanding of when to use each herb, the
right time to harvest, the correct part of the herb to use, the proper method for
obtaining the benefits, and correct dosing.

QUICK MEDICAL NOTE:

Before you run to the supplement store and stock up on herb extracts and
pills, keep in mind that some herbs can have unwanted side effects. If taken
in large enough quantities they can interfere with other pharmaceuticals.
 Make sure that you consult your physician if you intend to use any product
for medicinal purposes. This section is intended as information about
some of the potential health benefits of using spices in your cooking, not
as a cure for diseases.

Below is a brief overview of some of our favorite herbs and spices along with
their potential supportive role in your health.

GARLIC (ALLIUM SATIVUM)

Garlic doesn’t just keep vampires away, it is used both as a seasoning as well as
in medicine. Recent research has revealed potential health benefits from this pungent
beauty.

• Aged garlic may help prevent development of Alzheimer ’s disease.

• Garlic stimulates the antioxidant defense system (ADS “bouncers”) to a high
degree. Sprouted garlic seems to maximize this stimulation.
• Garlic can help keep you insulin sensitive and also may help increase heart rate
variability and improve heart function.

GINGER (ZINGIBER OFFICINALE)

Ginger is widely used in Asian cuisine. The ginger root has taste enhancing and
health promoting characteristics. Traditional medical uses for ginger have included
relief for maladies such as diarrhea and nausea.

Modern science is showing that ginger can help reduce inflammation. As chronic
inflammation drives most of the diseases we have discussed in this book, adding
ginger to the diet may benefit those with diabetes, high blood pressure, and heart
disease.

CINNAMON (CINNAMOMUM SPP)

Cinnamon comes from the bark of several species of the cinnamon tree and can
be used in both sweet and savory dishes. Recent research has shown that this tasty
spice also can be good for us.

• Cinnamon has been shown to have significant benefit for diabetics, sensitizing
insulin function and decreasing blood glucose levels.
• Cinnamon may also help control high blood pressure and improve insulin
 function in the brain (remember that Alzheimer ’s disease shows impaired insulin
function in the nerve cells).

TURMERIC (CURCUMA LONGA)

Turmeric is widely used in Indian cuisine and has been prized as a medicinal
compound in traditional cultures. The active ingredient in turmeric is curcumin.

Curcumin from turmeric has been the focus of substantial research over the last
few years. Curcumin has significant anti-inflammatory actions.

• Curcumin was found to be as effective as ibuprofen for symptoms in a study of

people with osteoarthritis.
• Curcumin was found to be beneficial for the symptoms of inflammatory bowel
diseases such as ulcerative colitis.
• Curcumin has been shown to help prevent prediabetics from progressing to
diabetes.
• Turmeric extracts are actively being studied as cancer therapy adjuncts.

CAYENNE (CAPSICUM ANNUM)

Cayenne is a popular ingredient for those who like their meals on the “spicy”
side. Capsaicinoids are a group of natural chemicals derived from cayenne (and
other hot peppers) that has been used as a pain reliever when applied externally.
Research has recently shown other beneficial effects of using capsaicin-containing
cayenne.

• Capsaicinoids may help decrease food intake by suppressing the drive to eat.
• These compounds may also help increase fat burning activity in fat cells and the
liver.
• Capsaicinoids increase adiponectin, the anti-inflammatory hormone produced
by fat cells.

The five spices profiled in this section are only a small handful of the natural
compounds available which will not only make your food taste better, but can
support your healthy lifestyle change as part of the Strong Medicine program. A
helpful link for exploring more natural herbs and spices is the excellent website
built by the University of Maryland: https://umm.edu/health/medical/altmed/herb/

You should now understand the importance of food quality as the foundation of
your nutrition. We will now show you how to individualize your plan with training
on carbohydrate tolerance and nutrient timing strategies to “feed your activity.”

Five health-promoting spices

INDIVIDUALIZED STRATEGIES II
“CARBOHYDRATE TOLERANCE”

You now have an understanding of the importance of the quality of your food,
whether you follow an omnivorous or vegetarian eating pattern. Although food
quality is the rule, some trainees will need to adjust the amount of starch/sugar in
their eating pattern depending on their current metabolic health.

During Basic Training we showed you how glucose (one of the simplest
carbohydrates and a primary fuel for the brain) can become toxic at high levels in
the bloodstream. Many of the nasty effects from diabetes come from high blood
glucose levels leading to chronic inflammation and oxidative stress. We showed you
how to assess your Individual Glucose Tolerance (IGT) in the Obesity section. The
IGT is crucial for ensuring that you do not eat more glucose—a product of starch
and sugar digestion—than your body can tolerate at any given time.

Organic oatmeal and sweet potatoes are examples of fantastic high quality foods
that can become problematic for people with a poor capacity to tolerate high starch
loads (i.e. trainees with insulin resistance and outright diabetes).

THE CASE FOR “LOW CARB” EATING

The Strong Medicine trainee now understands there is more to carbohydrates
than starch and sugar. Fiber is the forgotten carbohydrate. Most people associate a
“low carb diet” with an eating pattern containing very little starchy carbohydrates
and sugar. These diets are often high in fiber so they are not technically “low carb.”
In Strong Medicine, we will refer to this type of eating as a “low starch/sugar”
(LSS) eating pattern.

An LSS eating pattern can be an extremely powerful approach for repairing a

diabetic’s broken metabolism. LSS diets can be very nutrient dense and healthful if
done correctly for defined periods of time. In extreme cases—such as advanced
diabetes with compromised pancreas function—LSS may be appropriate for the
long-term.

LSS works amazingly well (this is supported by an ever-expanding body of

research) in the obese/diabetic/insulin resistant population to restore metabolic
health, increase fat loss, and in some cases put type 2 diabetes into remission. LSS
works because the low dietary glucose intake allows the body to sensitize itself to
the effects of insulin.

FLASHBACK
Go back to the “Diabesity” section in Part II “Knowing the Enemy” and
Metabolism Basics in Part I “Basic Training” for a review of insulin,
glucose toxicity, and insulin resistance.

The trainee with insulin resistance (especially diabetes) simply cannot tolerate the
same amount of starch with their meals as the trainee with good insulin sensitivity.
This is true no matter how “good for you” the starch-laden food is thought to be.
We went on a bit of a rant about whole grains and diabetes in the Obesity chapter,
and with good reason. Oatmeal, quinoa, fruit, and tubers (potatoes, etc.) can be
highly nutritious but may not be tolerated well by the trainee with insulin resistance
or diabetes. Dealing with the glucose load from digesting these foods may be too
much for those trainees.

In our opinion, the toxic effects of high blood glucose insulin resistant trainees
may experience from eating these foods certainly outweighs the potential benefits. If
you are obese/insulin resistant/diabetic you would certainly benefit from an LSS
approach to eating until your metabolism heals and you become insulin sensitive
again. We do not need to overcomplicate LSS. Some principles of LSS follow.

LOW STARCH/SUGAR (LSS) EATING

PATTERN
• Make fibrous vegetables such as leafy greens, cucumbers, peppers,
broccoli, cauliflower, jicama, radishes, carrots, parsnips, onions, etc. the
foundation of your meals. Mushrooms (obviously not a vegetable) are
also good choices.

• Limit tubers such as potatoes and sweet potatoes and starches such as
rice.

• Limit fruit to lower sugar varieties such as blueberries, raspberries,

blackberries, and avocados (yes they are fruit).

• Cut out all processed foods made from grain-based flours (bread, pasta,
etc.).

• Eat 25-30 grams of high quality protein with every meal. Vegetarian
diabetics should use properly prepared legumes.

• Most fat should come naturally from high quality protein sources
(pastured animals and wild-caught fish). You could consider
supplementing fat from high medium chain triglyceride (MCT) sources
such as coconut oil (cooking vegetables with it). MCTs can supply a quick
source of energy while you are reducing starch/sugar. Adding olive oil on
your salad is also a good way to supplement beneficial fats.

• Use the Individual Glucose Tolerance (IGT) from the Obesity chapter to
 periodically assess your tolerance for starch. After several months of LSS
eating, you will likely be able to add nutrient dense starchy/sugary foods
such as sweet potatoes, apples, pears, and oranges.

While LSS has been shown to be highly effective in improving metabolic health
in obese, insulin resistant, and diabetic trainees, long-term use can cause problems
for some people. LSS is not needed in trainees with good insulin sensitivity and can
slow their metabolism over time. Conversely, trainees who have sustained damage
to the pancreas from long-term diabetes may never again have normal tolerance to
starch and sugar. They may need to stay on a relatively low starch/sugar eating
pattern for life, and can use the IGT to determine their individual tolerances.

Optimizing blood sugar levels to within a safe range is crucial for preventing the
ravages of a broken metabolism such as heart disease, accelerated aging, cancer,
high blood pressure, Alzheimer ’s dementia, kidney failure, and stroke. Controlling
blood sugar levels with the sophisticated but simple approach of adjusting eating
patterns to carbohydrate tolerance is the key restoring your metabolism.

We will move on to an individualized dietary pattern using nutrient timing

around exercise that will keep your body fat low, performance levels high, and
stoke your metabolic furnace to white-hot levels. This approach will greatly benefit
the obese and diabetic trainee as well. You will master the concept of feeding your
activity.
INDIVIDUALIZED STRATEGIES III
FEED YOUR ACTIVITY

We have given you a food quality template to follow whether you are an
omnivore or vegetarian. We have also discussed the concept of carbohydrate
tolerance for those with diabetes and insulin resistance. Now we will show you how
to optimize your metabolic “blast furnace”, improve physical performance, keep
body fat low, and prevent muscle wasting through strategies using nutrient timing to
support your activity levels.

During your Strong Medicine Basic Training, you learned some of the inner
workings of the flesh machine:

• The brain is an energy hog and requires glucose. It is true that much of the
brain can use ketones (the breakdown products of fats) for energy, but there is
still a requirement for glucose. Without adequate glucose, the stress response
(HPA axis) will be triggered to produce cortisol. If there are inadequate stores of
glucose (from glycogen in the liver) cortisol will ensure that adequate glucose is
available by making it from amino acids “stolen” from the protein in your
muscles. Thus, depending on your activity, eating too little glucose (starch) can
 result in muscle wasting, and shrinking of your hard-earned muscle mass.

• Conversely, eating too much starch (chains of glucose) will result in excess
glucose converted into triglycerides (fat) by the liver and adipose cells which
will be stored as fat. Too much starch over the long term can make you fat. The
excess glucose is also toxic to the body, forming high levels of advanced
glycation endproducts (AGE) which we discussed in the obesity chapter.

How does a Strong Medicine trainee, eating high quality foods and following a
high intensity exercise program, ensure that they get enough glucose to the brain to
avoid a stress response (and the high cortisol that goes with it) without consistently
eating too much glucose (starch) and increasing their body fat?

The answer to this is a relatively simple strategy and eating pattern summed
up by the phrase “feed your activity.”

FEEDING YOUR ACTIVITY

The high intensity resistance and cardiovascular training we prescribe needs
proper post-exercise nutrition for optimal recovery of the body. This type of
exercise is stressful to the flesh machine but will produce a beneficial adaptive
response (through allostasis) if we give it the building blocks to recover
successfully.

It stands to reason that what and when you eat on your training days should be
different than what you eat on your off days. Feeding the body for recovery when
there is nothing to recover from makes no sense. You would not fill your car up
with fuel if it already has a full gas tank, so do not do the same to your body. The
following is a template for planning food (fuel) intake around your exercise
program.

I. NON-TRAINING DAYS
There is not a big need for glucose on low activity days. Your body needs protein
for muscle growth during recovery and the majority of the body can run very
efficiently on fat from the diet and stored body fat. Muscle is running on mostly fat
during this time so the available glucose can be sent to the brain for use. The
breakdown products of fat burning (ketones) can also be used by the brain to run
efficiently. The muscles’ glucose storage (glycogen) is high so a relatively low
intake of dietary glucose during this time will ensure that excess glucose will not be
turned into fat and stored. Some general rules on for non-training days to ensure the
system works optimally during this time:

• Eat the majority of your carbohydrates as fermentable fiber from

vegetables. Fermentable fiber will be converted by gut bacteria into anti-
inflammatory short chain fats such as butyrate which will help recovery.
Vegetables also contain the “edible pharmacies” of phytonutrients, vitamins, and
minerals to replenish the body’s machinery on recovery days.

• Reduce the amount of sugary fruit intake and starchy foods such as tubers
(potatoes, sweet potatoes). Eat low sugar fruits like berries on these days.
Berries have compounds that will stimulate the antioxidant defense system (ADS)
to control the free radicals that were generated during the adaptive response to
exercise. We need some exercise induced oxidative stress for adaptation but do
not want it to get out of control. The ADS “bouncers” ensure things go smoothly.

• Eat 25-30 grams of high quality protein with every meal. We want to ensure
that the muscle has both the stimulus and the building blocks to recover after
exercise. The essential amino acids in high quality protein will meet these
requirements for muscle rebuilding.

• Ensure adequate fat intake primarily from your protein sources if you are
an omnivore. Also consider cooking your food in medium chain saturated fats
such as coconut oil. These medium chain saturated fats (also known as medium
chain triglycerides or MCTs) will provide an instantly available energy source to
use while starch (glucose) from the diet is low. MCTs are also anti-inflammatory
and provide the brain with extra ketones to use for energy in place of glucose.
Metabolically, this will spare muscle mass by preventing high levels of cortisol
from the stress response. MCTs are also much less likely to be stored as fat in
adipose tissue.

II. TRAINING DAYS

Directly after high intensity resistance and cardio training there is an increased
need for starch (glucose) in the diet to refill the glucose stored in muscle tissue, the
“glycogen tanks”. It is important to remember that the brain considers intense
exercise to be a potential “threat” and will activate the stress-threat system to ensure
that the brain has adequate glucose, and that muscle glucose storage tanks are
refilled. As far as your brain is concerned, your intense exercise could have been
running away from a bear or other predator.

The stress-threat system responds to ensure that you are prepared to flee a
predator in the near future and will jumpstart the physiological processes to make
these preparations. The primal parts of the brain do not know that your exertion was
a grueling set of squats and a burst cardio protocol of kettlebell swings. The brain
will default to the predator scenario to ensure survival. Without adequate nutrition
(especially glucose) after an intense workout, the brain will go into alert mode and
start breaking down the body for energy while slowing the metabolism (and fat
loss) to a crawl. After all, why would the brain speed up metabolism during an
energy conservation mode induced by stress. You would not race around in your
car, flooring the gas pedal if you were low on fuel. The brain acts the same way and
will slow metabolism down.

To prevent the stress-threat system from inducing a catabolic (breaking down the
body) state, we need to feed the flesh machine post workout. This ensures the brain
is happy and the adaptive recovery process will make us stronger instead of
breaking us down to protect the brain. It will also prevent the slower metabolism
that accompanies a low fuel state. The strategy for doing this is very simple and will
vary subtly depending on the intensity of the exercise.

We need to refill the container after high intensity exercise to prevent a catabolic
state.

The higher the intensity of the exercise, the more glucose from muscle storage
will be used. Review your Basic Training (Metabolism Basics, concepts #3 and #9)
to recall that exercise of a high enough intensity that adequate oxygen cannot be
supplied for the metabolic demand is called “anaerobic” exercise.

Exercise such as high intensity interval training (HIIT) is highly anaerobic and
must use glucose as primary energy source. Anaerobic training burns through
muscle glucose in very little time creating a large empty “storage tank” in the
muscle to be filled with glucose from the diet post-workout.
 Metabolically, after a high intensity workout you can (and should) replace the lost
glucose with a relatively large amount of starch from your post-workout meal. This
will ensure that the muscles’ “glucose tanks” are topped off and the brain has
enough glucose to avoid a catabolic stress response. We also do not have to worry
about a huge long-lasting insulin spike from the post-workout starch meal because
high intensity exercise turns muscles into a “glucose sponges” which do not require
insulin to transfer glucose from the bloodstream to the muscles.

This relatively high intake of starch does not result in high amounts of glucose in
the bloodstream (it is absorbed quickly by the depleted muscle glucose “tanks”) and
does not result in fat production from excess glucose. This strategy also ensures that
the brain does not trigger a catabolic state from the stress response, the metabolism
stays high and results in fat burning for days after the workout during the non-
training days.

Summarizing the training day strategy for eating...

 • Your post-workout meal should consist of 25-30 grams of high quality
protein. This will ensure enough essential amino acids are present to stimulate
and build new muscle through the adaptive process (allostasis) after being torn
down by exercise.

• Eat starch from nutrient dense foods such as sweet potatoes, potatoes, and
sugary fruits. Grains and pseudograins such as rice, gluten free oatmeal and
quinoa will do the trick as well. The glucose from the starch will rapidly refill
the muscles’ glucose “storage tanks” and keep the metabolism revved up.

• Limit extra sources of fat during this refueling time. We are stimulating a
building process, and extra fat in the diet will likely be stored as fat during this
time. Fat naturally present in high quality protein sources is fine.

• Ideally, training would be performed in the late afternoon with a protein/starch

meal post workout at dinner time. This strategy will help you sleep better
preventing high cortisol spikes at night. If you train in the morning, fill your
muscles’ glucose storage tanks slowly throughout the day with smaller starch
loads with each meal as you may have daytime activity to feed during your post-
workout recovery.

Plan your meals around your training schedule. If the planned training falls
through, adjust your meals accordingly by lowering the starch and increasing the
fat. It is really that simple. Just make sure your food quality stays high.

You will need to experiment with different amounts of starch with your post-
workout meal, your needs will vary depending on workout intensity and your
individual metabolism. If you are starting to gain fat around the midsection, cut back
a little of the starch amount. If you are losing muscle mass, add some back in. Do
not fool yourself into thinking that a couple sets of barbell curls are going to
significantly deplete muscle glucose and require a large glucose replacement with
starchy food. Activities like HIIT, mixed martial arts, mountain biking, sprinting,
and intense ‘superset” resistance training will deplete your glucose stores. You will
have to play with this for a while to dial in your own “sweet spot” for post workout
meals. This is just a template.

CALORIC RESTRICTION AND “LOW

CARB” DIETS
Diets that prescribe periods of caloric restriction such as intermittent fasting can
be useful in some situations but have no place in a wellness plan that involves
regular intense exercise. Caloric restriction in general will generate a stress
response and is hard on the flesh machine, significantly filling the daily “stress
cup.” Getting any long-term benefit from diet strategies that involve significant
calorie restriction require that you have everything else in your life optimized to
reduce overall stress (minimal social/psychological stress, restful sleep, and low
intensity exercise). For most of us, this is not reality.

THE “CALORIE RESTRICTION CUP”

Extreme calorie-restricted diets cause high stress on the body, filling your
stress cup significantly. Calorie restriction with the other stresses of daily
life leave little room in the stress cup and can quickly lead to allostatic
overload and activation of the stress response. High levels of cortisol
from the stress response associated with extreme calorie restriction can
lead to muscle wasting. There are better ways to improve body
composition.

Long-term diets that are very low in starchy carbohydrate (LSS) do not mix well
with high intensity exercise programs. The mixture of the two creates stress in the
body due to inadequate amounts of glucose in the diet to support anaerobic exercise.
It is a set up for failure, and will consistently overflow the stress cup. If you are
temporarily on a LSS diet to reverse a broken metabolism (diabetes) you have to be
careful with high intensity exercise. Our recommendations are to still include some
starch post-workout and monitor your response with the Individual Glucose
Tolerance (IGT) test discussed in the obesity section.

If you want to stay on an LSS eating pattern and it is working well for you, we
advise that you limit your exercise to lower intensity protocols such as light
resistance training and low intensity cardiovascular training to prevent your “stress
cup” from overflowing and reversing the progress you have made.
 QUICK MEDICAL NOTE:
Extreme caloric restriction diets (we’ve seen some limiting calories to
500 kcal per day!) are never a good idea. Yes, you will lose weight for
sure, but a significant amount of it will be lost as muscle mass. This is
terrible for your health.

Diets like this also put the brain in starvation mode, slowing the
metabolism and priming the body for fat storage the next chance it gets.
This is why so many people who lose weight with extreme caloric
restriction gain it all back (and often more) when they stop the restrictive
diet. The brain remembers!

The loss of muscle mass has consequences as well. Muscle is a metabolic

engine and a big fat burner. Lost muscle mass can slow your metabolism
to a snail’s crawl. Remember that adequate muscle mass can protect
against insulin resistance and diabetes.

STRONG MEDICINE TACTICS:

Feed your activity to keep your metabolism high and minimize storage of
excess body fat.

Now that you know the strategies for feeding your activity, we will give you
several example recipes for simple and great tasting meals made with high quality
ingredients you can use to fuel your flesh machine.
INDIVIDUALIZED STRATEGIES IV
ONE WEEK OF FOOD

There are countless recipes available on the internet and in cookbooks. The
purpose of this section is not to tell you what to eat, but to give examples of easy to
prepare meals which emphasize food quality. As long as you have quality
ingredients and stay away from processed foods you really cannot go wrong.

Continue to use the principles covered in “Feed Your Activity” when planning
meals that are optimum for training and non-training days. Examples of this will be
given. The following is a sample five day menu with recipes to follow.

EGG SCRAMBLE
Ingredients:
The vegetables listed will change based on seasonal availability.
Vegetables should be organic if possible.
• 6 eggs from pasture-raised chickens
• 3-4 tbs coconut milk
• 3 oz organic frozen spinach
• 6-8 slices bacon from pastured pigs
• ¼ of small onion, chopped
• 1-2 cloves garlic, chopped
• 1 small rutabagas/potatoes/parsnips, etc. (thinly sliced or grated)
• salt and pepper to taste

Directions:
In a glass bowl, beat the eggs with coconut milk. Add salt and pepper to
taste and set aside. In a sauté pan, cook onions and garlic. Add potatoes
and cook for 5 min. Add in the bacon. Once the bacon is mostly cooked,
add in the beaten egg mixture and cook until the eggs are set to your
desired texture.

This recipe is designed for 2 servings. Refrigerate the leftovers for

tomorrow’s reheated breakfast.

Comments:
This recipe will given you plenty of protein to start your day and a good
balance of omega-3 and omega-6 polyunsaturated fats (make sure the
eggs are from pasture raised chickens). The coconut milk will also
provide medium chain fats that can be immediately used for energy.

SPICY BURGER WITH JICAMA CHIPS

Ingredients:
Spicy Burger

• 2lb ground beef (from pastured cows, bison, etc.)

• 1 tbsp. cumin
• 1 tbsp. smoked paprika
• 1 tbsp. powdered garlic
• 1 tbsp. powdered onion
• 1 tbsp. dried oregano
• salt to taste
• pepper to taste
• 1 tsp. coriander
• ½ tsp. cayenne (less if you like it less spicy)
• ¼ tsp. cinnamon
• zest of 1 lime

Jicama Chips
• jicama
• juice of 1 lime
• ancho chili powder

Directions:
Combine all ingredients in a bowl and mix thoroughly. If you are using
lean ground beef you may want to consider adding an egg to the mixture
to help keep your burgers moist. Divide the ground beef into 4 burgers
and cook to your desired temperature.

Jicama Chips:
Peel and slice the fresh jicama. Squeeze the fresh lime (which you used for
the zest) over the jicama and sprinkle with ancho chili powder.

Comments:
This is a good recovery day meal with plenty of protein and fermentable
fiber from the jicama. Add an avocado for more fiber and a good dose of
healthy monounsaturated fat.

CHIPOTLE BUTTERNUT SQUASH

SOUP
Ingredients:
• 2-3 lbs chicken thighs; boneless and skinless
• 1 butternut squash
• 2 medium apples
• 1 can chipotle peppers in adobo sauce
• 2 small onions
• 10 cloves of garlic
• 2 tsp salt
• 2 tsp coriander powder
• 2 tbs dried oregano
• 2 tbs dried thyme
• 1 can coconut milk
• 2 cups of chicken broth
• juice of 2 limes

Directions:
1. Preheat the oven to 375
2. Roast apples, butternut squash, 1 onion and 5 cloves of garlic
• Peel and cube the butternut squash (don’t forget to remove the seeds)
• Peel, core and chunk the apples
• Peel and chunk onion
• Remove the skin of the garlic
• Place all vegetables listed immediately above + the apples on a baking
sheet lined with parchment paper and roast for about 30-45 minutes until
the vegetable poke tender
• While this is roasting start on remainder of the soupl
3. Prepare remainder of soup
• Cut the chicken into bit size chunks
• Mince 6-8 chipotle peppers
 • Mince 1 onion, 5 gloves of garlic
• Place chicken, onion and garlic in a stock pot and and remainder of
ingredients listed above. Cook for about 30 minutes over medium heat
4. Puree roasted vegetable.
• Once vegetables are cooked, remove from oven and puree in blender
with a small quantity of liquid from soup.
• BE CAREFUL…Hot liquids in a blender increase the pressure inside
and can cause harm.
• Add pureed vegetables and apples back to soup
5. Heat for about 5 minutes and serve

This meal is excellent post-workout with a good amount of starch to refill

muscle glycogen tanks.

MEXICAN CHICKEN WITH SAUTÉED

KALE
Ingredients:

• 2lbs of pastured chicken thighs cut into bite sized pieces

• 1 small onion, chopped
• 1 jalapeno, chopped
• 3 cloves of garlic, chopped
• 2 tbsp. Mexican oregano
• 2 tsp. cumin
• 1 tsp. ground coriander
• 1 tbsp. red pepper flakes
• 1 tbsp. ancho chili powder
• 2 tsp. smoked paprika
• zest of 2 limes
• juice of 2 limes
• salt and pepper to taste
• raw milk cheese (Monterey jack), grated
• 2 bunches of kale cleaned and torn

Directions:
Sauté garlic, onion, jalapenos, and lime zest with salt and pepper in
coconut oil until softened and slightly browned. Add in the remaining
seasonings and cook for another 2 minutes. Add in the chicken and juice
of 2 limes. Cook until the meat is done. During the last 10 minutes of the
chicken cooking, in a separate pan, sauté the torn kale in coconut oil, salt,
pepper and garlic powder until it is lightly wilted. Place the kale in the
bottom of each serving bowl, top with chicken and cheese.

Comments:
This dish is high in protein with a super dose of fiber and antioxidant
defense stimulation from kale.

SPICY CHICKEN SOUP

Ingredients:
• 2-3lbs of boneless, skinless chicken thighs, cut into bite sized pieces
• 1 bag of frozen sweet corn
• 2-3 jalapenos, chopped
• 2-3 medium sized sweet potatoes, cubed
• 1 sweet onion, chopped
• 3-4 cloves of garlic, chopped
• 2 tbsp. oregano
• 1 tbsp. cumin
• 1 tsp. cayenne
• 1 tsp. Ancho chili powder
• 2-3 cups of chicken stock
• zest of 1 lime
• fresh cilantro (optional)
• salt and pepper to taste
• 1 tsp. coconut oil for sauté


Directions:
Sauté the onion, garlic, and jalapeno in a small amount of coconut oil (or
rendered duck fat) until softened. Add in chicken, seasoning, and chicken
stock. Cook on medium to low heat covered for 20 minutes. After chicken
has cooked, add in sweet potatoes, lime zest, and corn and cook for an
additional 20 minutes (or until the potatoes are easily penetrated with a
fork). Garnish with fresh cilantro and serve.

Comments:
This is a great post workout meal with a good dose of a nutrient dense
starch from the sweet potatoes. This dish will refill lost muscle glycogen
and stimulate muscle growth after a tough exercise session.

PASTURED PORK CHILI

Ingredients:
• 3-4 lb. boneless pork shoulder roast from a pastured pig
• 2-3 jalapenos, seeded and diced
• 4-6 garlic cloves, minced
• 1 large onion, minced
• 1 large can of diced tomatoes
• ¼ cup apple cider vinegar
• 1 cup vegetable broth
• 1-2 tbsp. chili powder
• 1 tsp. cayenne
• 1 tbsp. cumin
• 2 tsp. coriander
• 2 tbsp. oregano
• salt
• pepper

Directions:
Cut boneless pork shoulder roast into bite size chunks. Combine all
ingredients into a slow cooker and cook on low for 8 hours or high for 4
hours.

Comments:
This is another great lunch meal that you can prepare ahead in a large
quantity and have several portions ready for reheating for a couple of
days.

SALMON WITH CARROT NOODLES

Ingredients:
• 1lb wild caught salmon (cut into 2 pieces)
• 1 tsp. coconut oil
• ½ tsp. salt
• ½ tsp. pepper
• ½ tsp. dried dill

Season the salmon on both sides with salt, pepper and dill. In a sauté pan,
melt coconut oil. Once the oil is warmed, add in the seasoned salmon.
Sauté on both sides for approximately 4 minutes over medium to high
heat. If salmon has skin on it, cook skin side down first. If the oil begins to
smoke, turn down the heat.

Carrot Noodle Ingredients and Directions:

• 8 medium to large carrots cut into carrot noodles
• 1 tsp. coconut oil
• 3 cloves garlic, minced
• ½ ciopollini onion, minced
• salt and pepper to taste

Once the carrots are cut into noodles, set them aside. Melt coconut oil in
sauté pan and add onion and garlic. Season with salt and pepper and sauté
until onions and garlic are translucent. Add in carrot noodles and cook to
desired tenderness.

Comments:
This meal is a delicious way to get plenty of long chain omega 3 fatty
acids (DHA and EPA). The carrot “noodles” are a great way to enjoy
nutrient dense noodles and avoid the processed high-density
carbohydrates found in traditional pasta.

MAKING “NOODLES”
Making carrot noodles is simple. Use a peeler and strip the carrot until
you hit the core. Turn the carrot over to the other side and continue the
process. You can peel the carrot on four sides to make excellent tasting
realistic noodles.
ROASTED CHICKEN WITH ROASTED
CELERY ROOT

Ingredients Roasted Chicken:

• 3-4lb whole chicken
• 5-6 sun-dried tomatoes in olive oil
• 3 cloves garlic
• 1 bunch fresh thyme (leaves only)
• 1-2 tbsp. coconut oil, melted
• 1 small onion, peeled and cut in quarters
• Salt and pepper
Directions:
Preheat oven to 450 degrees.
In a food processor, combine garlic, sundried tomatoes with their oil,
thyme, salt and pepper. Pulse until well combined. Add in 1-2 tbsp. of
melted coconut oil until the mixture’s consistency is paste-like. Using your
finger, gently lift the skin from breast meat on each side of the breast
bone. Place 1 tbsp. of the mixture over each breast. Place 1 tbsp. into the
chest cavity and rub remaining over the outer surface of the chicken.
Generously salt and pepper the inside of the chicken cavity. Add in the
quartered onion.

Bake at 450 degrees for 1 hour. Allow the chicken to rest for 15 minutes
prior to carving.

Ingredients and Directions Roasted Celery Root:

• 2 whole celery roots, peeled and diced
• 2 tbsp. coconut oil, melted
• 2 tbsp. garlic granules
• salt and pepper

Preheat oven to 450 degrees (you can use the same oven as the chicken).
Peel and dice celery root, place it in a Ziploc bag and coat the diced root
with melted coconut oil. Spread coated root on a cookie sheet lined with
parchment paper. Dust the coated root with garlic, salt and pepper. Roast
celery root until done, approximately 45-60 minutes so it can be cooked in
the same oven with the chicken.

Comments: Celery root is low in starch and is a great substitute for

potatoes for those with diabetes/insulin resistance. You can roast them as
above or make celery root mash (like mashed potatoes).

BEEF POT ROAST

Ingredients:
• 3lb beef chuck roast (grass-fed of course)
• 1 medium onion, peeled and cut in to quarters
• 6 cloves of garlic, peeled and crushed
• ¼ cup raw apple cider vinegar
• ¼ cup tamari sauce (gluten free soy sauce)
• 2 cups vegetable broth
• 3 tbsp. Italian seasoning
• Generously season roast with salt and pepper

Directions:
Place all ingredients in the slow cooker and cook on low for 8 hours or
on high for 4 hours. *Purists will want to brown the meat before placing it
in the slow cooker. If you are one of these, coat the chuck roast in oat
flour with salt and pepper. Brown it in coconut oil for approximately 5
minutes per side.

Serve with a large salad for a great tasting and simple to prepare meal.

Comments:
This is an excellent choice if you know you will be having a busy evening.
You can start the slow cooker in the morning, and dinner will be ready
when you get home from work.

PULLED PORK WRAPS WITH

MANGO JALAPEÑO RELISH
Pulled Pork Ingredients and Directions:
• Pork shoulder roast (boneless from a pastured pig)
• 1 can of diced pineapple and the juice
• 2 tbsp. garlic powder
• 2 tbsp. ginger powder
• 2 tsp. cumin
• 2 tsp. cinnamon
• 2 tsp. coriander
• salt and pepper to taste

Season your pork roast and place it in slow cooker. Add in pineapple and
juice. Cook on low for 7 hours. Shred the pork with forks and cook for an
additional hour on low. Serve with a simple mango and jalapeno relish.

Mango Relish Ingredients and Directions:

• 1 ripe mango diced
• 2 cloves garlic minced
• ½ red onion minced
• 1 jalapeno seeded and minced
• 1 lime, juiced
• Salt and pepper to taste

Combine all ingredients and allow to sit at room temperature for 1 hour
before serving.

Place pulled pork into a lettuce or cabbage wrap. Savoy cabbage leaves
make an excellent wrap. Add the mango relish and enjoy.

Comments:

This is a great tasting recipe with a healthy cabbage wrap substituted for a
traditional flour tortilla.

STEAK AND POTATOES (OR KALE)

Steak Ingredients and Directions:
• 2 boneless ribeye steaks
• salt
• pepper
• smoked paprika
• garlic
• 1 tsp. coconut oil, divided in half

Allow the steaks to come to room temperature for 1 hour prior to

cooking. Dust steaks with salt, pepper, garlic, smoked paprika. We use a
cast iron skillet to cook our steaks, but you can also grill them. If using the
oven for the steaks, preheat the broiler to 500 degrees and move the rack
to the top position in the oven. Once the oven has come to temperature,
place the seasoned steaks into the skillet and add ½ tsp. of coconut on top
of the steaks. Cook for 5-6 minutes and flip. Cook an additional 4-5
minutes. Allow steak to rest on the cutting board for 5 minutes prior to
serving.

Potato Ingredients and Directions:

• 2 medium sweet potatoes
• 2 tbsp. melted coconut oil
• salt
• pepper
• garlic
• cayenne

Preheat oven to 375 degrees. Peel and dice the sweet potatoes and place in
a Ziploc bag. Coat the potatoes with melted coconut oil. Place the coated
sweet potatoes on a cookie sheet lined with parchment paper. Dust potatoes
with salt, pepper, garlic and cayenne. Cook in the oven for 45 minutes
(until potatoes are “fork tender”). Serve.

Comments:
This is another great post-workout meal high in protein and starch. If you
 miss the workout, just replace potatoes with a less starchy choice such as
kale (pictured).

PROTEIN BERRY BREAKFAST

SHAKE
Ingredients and Directions:

• ½ can full fat coconut milk (6-7 ounces)

• 6-8 ounces of water
• 25-30 grams whey protein
• ½ - 1 cup organic berries (blueberries, raspberries, blackberries,
strawberries, etc.)
• 1 tsp. of local honey (optional)

Place all ingredients in a blender and blend to a smooth consistency.

Comments:
This is a quick meal replacement shake to ensure you get adequate protein
first thing in the morning. The medium chain fats in the coconut milk will
provide a great source of immediate energy and the berries are one of the
top foods for stimulating the antioxidant defense systems in your body.

COOKING STRATEGY
The “week of food” example was just to illustrate several possible meals. The
preparation time necessary to stick to a schedule as outlined in the 5-day plan is not
doable for most people with busy lives. Our suggestion is to take one day (usually
on a weekend) and prepare lunches for the week.

For us, this involves making a big batch of one of the meals in a slow cooker and
portioning it out for lunches for the week. The drawback is that you will be eating
the same thing for lunch every day, but it is much healthier than eating out for lunch.
It is also very convenient to grab a pre-made lunch in the morning and heat it up at
work.

Try to also loosely plan your meals around your workouts. On days when you
have an intensive exercise session planned, make sure you have enough starch in
your post-workout meal to replenish your muscles’ glycogen. If life gets in the way
and you miss your workout, you can make minor changes on the fly; instead of
having steak and potatoes, make steak and kale.

The recipes here are only given as examples. Be creative and experiment with
your own recipes, use the highest quality ingredients, and feed your activity. It really
is as simple as that.

CONCLUSION
You now have the knowledge and the tools to implement defensive tactics and
individualize them to your needs. It is time to put everything you have learned
together into a cohesive strategy to start launching assaults in your war against the
“Pentaverate.”
STRONG MEDICINE NUTRITION “MILITARY
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Chuengsamarn S. Curcumin extract for prevention of type 2 diabetes. Diabetes Care 35 (2012): 2121-2127.

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Craig WJ . Health effects of vegan diets. Am J Clin Nutr 89 (2009): 1627S-1633S.

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Fernandez M L, & Calle M , Revisiting dietary cholesterol recommendations: does the evidence support a limit of 300 mg/d? Curr Atheroscler Rep 12 (2010): 377-383.

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Gupta SC, Patchva S, & Aggarwal BB. Therapeutic roles of curcumin: lessons learned from clinical trials. AAPS J 15 (2013): 195-218.

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Z evallos VF, et al. Gastrointestinal Effects of Eating Quinoa (Chenopodium quinoa Willd.) in Celiac Patients. Am J Gastroenterol 109 (2014): 270-278.
BATTLE PLAN III
PUTTING IT ALL TOGETHER

“Though no one can go back and make a brand new start, anyone can
start from now and make a brand new ending.”
—Carl Bard

“If you always put limits on everything you do, physical or anything
else, it will spread into your work and into your life. There are no
limits. There are only plateaus, and you must not stay there, you must
go beyond them.”
—Bruce Lee
PUTTING IT ALL TOGETHER I
LIFESTYLE CHANGE: “THE NECK OF
ROY BUCHANAN’S GUITAR”

Underground guitar
legend- Roy Buchanan

The authors are both musicians; Chris is a guitarist and Marty a jazz pianist.
Many of our conversations together center on our mutual love for music and
musicians. Sometimes there are some universal truths that can be applied to health
and fitness lurking beneath our shared anecdotes. Marty’s tale of the guitar neck of
Roy Buchanan is one of these...

I was always struck by the modesty of Roy Buchanan’s guitar gear. His beat-to-
hell scarred-wood Telecaster was as plain as an Amish farmer. When he had a few
beers and was feeling good and relaxed, he was incredible. His playing was
extremely subtle with lots of soaring, sustained anthem-like riffs. Roy was majestic,
elegant, loud, and crystal clear. His patented “ghost tones” and effortless three-
octave speed runs were all done with the greatest of ease, as he exhibited ho-hum
nonchalance that added to the effect. He was a relaxed, laid back, rural dude creating
amazing music with effortless pyrotechnics.

I once watched Roy from a front table, stage left, from a distance of perhaps 15
feet. He rolled into an extended arpeggio with his pick-holding right hand tracing a
perfect oval on the six strings; touching each string at precisely the right instant in
time over and over, creating a cascade of crystalline glass notes, all perfectly timed.
I imagined if he had a piece of chalk in his hand instead of a guitar pick, and a
blackboard instead of a guitar, the result would be a series of perfectly drawn ovals.

Often, Roy would turn his back to the crowd as he played. Early on I noticed the
back of the neck of his Telecaster was rubbed raw in a one-inch wide pathway up the
exact center. Over the years, this path had been worn away as a direct result of
nothing more than Roy’s palm repeatedly passing lightly up and down the neck. He
would move his hand with great smoothness, gentleness, and dexterity—he used the
lightest of touches. I wondered how many passes up and down the neck of Roy
Buchanan’s guitar it took to wear off that varnished finish?

Undoubtedly, hundreds of thousands of ever-so-light palm passes were needed to

wear off the factory varnish—perhaps a million hand passes were needed. There is
a great lesson to be learned: virtuosity comes with a price, and lifestyle change
doesn’t happen overnight. While Buchanan was certainly gifted, the more he
practiced, the more gifted he became. When talent collides with a serious time
investment, and you add in patience and a single-minded dedication to a craft, the
results are astounding.

Physiological quantum leaps happen in direct proportion to the amount of quality

time invested in lifestyle change. Roy didn’t baby himself; he immersed himself. In
your own more limited and modest way, you too should seek to emulate Roy’s
dedication to his art. Train smart, train intense, eat right, and rest big. Do copious
amounts of healthy outdoor cardio training to keep the internal plumbing working
at peak efficiency. Let’s follow Roy’s example and put in the work.

When all the elements are in place and executed in that consistent, balanced
fashion for weeks on end, synergy occurs and results accelerate. Our system relies
on the expert use of basic tools with simplistic and effective methods—with periods
of enforced rest and the support of nutrient-dense and seasonally appropriate food.
 Transformation is achieved by implementing a bare bones basic strategy in a
systematic fashion. We need to understand the simple core themes, plan how to
weave minimalistic new activities into our lifestyle and reality. You must
incorporate “the process” within the time constraints of your life. This takes
planning, patience, and persistence, but is achievable for all.

We are not here to be your personal cheerleaders; you only need to supply
the motivation and we’ll take you the rest of the way.
PUTTING IT ALL TOGETHER II
STRONG MEDICINE LIFESTYLE
CHANGE—STRATEGIC PLANNING

PUMMEL THE “PENTAVERATE”

Circadian disruption, chronic stress, obesity, gut inflammation and inactivity are
the enemy. They are the prime sources of chronic oxidative stress and inflammation
—the real underlying causes of chronic disease.

The effects of each of these sources add up to cause the preventable diseases
listed in the black box. To achieve optimal health of your mind and body, you will
have to implement the Strong Medicine tactics from each chapter to attack each
enemy.

Any of the 5 sources left unchecked will overflow your stress cup (allostatic
overload), and over time result in destruction of your health.

Keep reading and we will show you how to strategically plan your own assault on
chronic disease, achieving victory with optimal health.

The Strong Medicine Defensive Tactics will break the links of the Pentaverate, and
prevent the chronic inflammation and oxidative stress that lead to disease. Start by
assessing which member(s) of the Pentaverate is(are) most problematic for you.

STEP 1: SELF ASSESSMENT

As Sun Tzu said in the Art of War, “If you know the enemy and know
yourself, you need not fear the result of a hundred battles.” As a result of
your hard training, you now know the enemy. It is time to take a look at
the current state of your mind-body and your environment.

Decide which members of the “Pentaverate of Pestilence” are your biggest

enemies in your own private war against poor health. For some, circadian
disruption and the poor sleep that accompanies it is the biggest obstacle.
Chronic stress affects most of us and most likely is a problem for you as
well. Do you have recurrent digestive problems or gastrointestinal issues?
Are you overweight, diabetic, or have the activity level of a three-toed
sloth? You get the idea.

It is crucial that you do this self-assessment and be honest with yourself.

Once you have identified which members of the “Pentaverate” are most
problematic, you can formulate an initial assault plan.

STEP 2: TARGETED ASSAULT

Once you have identified which enemy is your biggest obstacle to health,
pick a few Strong Medicine Defensive Tactics from that section. If you are
overweight or diabetic, pick a couple of tactics in the Obesity section. If
poor sleep is your biggest issue, start with tactics from the Circadian
Disruption Section.

Implement these tactics in your daily life to start your targeted assault on
your selected “enemy.” Only implement the amount of defensive tactics
that you can handle at once. Change itself (even positive change) is
inherently stressful. Many new trainees are super-motivated at first and
charge the enemy lines with all of their guns blazing, trying to change too
much too soon. These trainees inevitably fail to truly incorporate the
defensive tactics into their lifestyle change.

Stick with a few of the defensive tactics and incorporate them consistently
until they no longer feel like stressful changes, but become part of your
normal routine.

STEP 3: REASSESS THE
BATTLEFIELD
Once you have had an initial successful assault on your enemy, go back to
STEP 1 and reassess the battlefield. Try to identify the next enemy that
represents the biggest obstacle to achieving your health and fitness goals.

Do not hurry and try to conquer the enemy in one massive assault by
attacking all of your obstacles at once. This is what happens to millions of
people every year around January when they try to “fix” themselves as
part of a New Year ’s resolution. By mid-February they realize they have
tried to make too many changes at once. Their battle plan collapses and
they lose the ground they have gained, allowing the enemy to advance
again—lost weight is gained back, and their gym memberships go unused.
This pattern repeats itself the following January. No true progress is ever
made.

Our slow and methodical approach will ensure that you truly make lasting
lifestyle changes which can be built upon. By the time next year rolls
around, you will be leaner, healthier, and more fit, instead of starting from
square one. If it takes you several years to achieve complete victory over
your enemy, so be it. This is how wars are won, battle by battle. Instant
gratification with quick weight loss plans and “Hollywood” exercise
programs will fail and have no place in true lifestyle change.
 IT’S ALL CONNECTED...
Using the Strong Medicine battle plan, assaulting one member of the
“Pentaverate” often causes collateral damage to the others.
 Over time you will assimilate the Strong Medicine Defensive Tactics into your
lifestyle. You will truly be on your way to becoming a Strong Medicine Warrior
ready to recruit new trainees for the war against chronic disease.

For those of you who like to track your accomplishments and enjoy goal setting
we have created a Strong Medicine “rank structure.” The rank structure makes use
of a point system; you will progress to a higher “rank” as you accumulate a defined
number of points.

STRONG MEDICINE TACTICS: “GOLD” = 15 POINTS

 STRONG MEDICINE TACTICS: “SILVER” = 10 POINTS

STRONG MEDICINE TACTICS: “BRONZE” = 5 POINTS

Points will be awarded for every Strong Medicine Defensive Tactic you
incorporate successfully into your lifestyle. If you have used a defensive tactic
consistently for 90 days, it is safe to say it is part of your lifestyle and you may
claim the points.

Some of the tactics will not apply to your situation (i.e. tactics for trainees with
cancer). Do not concern yourself with missing possible points from these tactics as
the rank progression in the Strong Medicine will account for the “special
population” tactics (such as cancer) in the point ranges.

You can promote yourself to the next rank once you have achieved the requisite
points for each (note that you can also be “demoted” to a lesser rank if you lose
enough points by “falling off the wagon” if you stop consistently using a previously
incorporated defensive tactic).
 Use of the rank structure is not required, but can be motivating for many trainees.
It will keep you honest by forcing you to periodically assess your progress.

As we move up the ranks, it will be beneficial to have other measures of our

progress besides points. We want to see the beneficial changes that accompany
promotions in the Strong Medicine rank structure. The following section on
Analytics will cover “stuff you can measure” for tracking the physical, physiologic,
and metabolic changes in your flesh machine as you progress through your battle
plan.

There are countless metrics we can measure as potential markers of health

(biomarkers). We have picked the four biomarkers we find to be the most useful
and meaningful for tracking physical improvement during lifestyle change.
BATTLE PLAN IV
ANALYTICS: “STUFF YOU CAN
MEASURE”

“Not everything that can be counted counts, and not everything that
counts can be counted.”
—Albert Einstein
STUFF YOU CAN MEASURE:
INTRODUCTION
BIOMARKERS AND THE “HOLY
GRAIL” OF CORRELATION AND
CAUSATION

The conceptual framework of the “stress cup”—using the concepts of hormesis

and allostatic load to inform your daily health and wellness decision making—
makes sense on an intellectual level. But, many of us would like some way to
measure our self-experiments in lifestyle management as we wage our war against
chronic disease.

In this section, we will cover some of these measurements, known as

“biomarkers.” They can be measured with procedures like blood work and heart
monitoring.

CORRELATION ≠ CAUSATION
Keep in mind that many of these biomarkers only correlate with health and
disease. This means that they do not necessarily cause health or disease, but are
associated with it.

In the first section discussing cholesterol and lipoproteins, we’ll see that small-
dense LDL and oxidized LDL measured from our blood in a laboratory test are
associated with an increased risk of heart disease—but higher LDL hasn’t been
proven to cause heart disease. In other words, when heart disease is present, this type
of LDL seems to be around more, but we haven’t fully determined exactly how it
causes heart disease (although there are some strong theories).

Correlations from things we can measure to disease can lead us astray if we are
not very careful. This is especially true with observational studies as we discussed in
the nutrition section very early in the book.

Here is an example of jumping to the wrong conclusion based on correlations

found in observational studies:

100,000 people filled out questionnaires regarding their lifestyle (food and
activity) and any diseases that they may have. We analyze the questionnaires and find
that the people who drank the most coffee had the highest rate of lung cancer. From
the data we see that coffee drinking is correlated with having lung cancer. The
media gets wind of our early study results and releases a story saying that drinking
coffee will give you lung cancer. This scenario isn’t that far-fetched as we see
stories every day in the news media about red meat, eggs, and saturated fat all
stemming from observational studies.

After coffee sales start drop as a result of the news media releasing their
“coffee=lung cancer” story, we realize that we forgot to ask about smoking in our
questionnaire. When we re-analyze the data, we find a very strong correlation with
cigarette smoking and lung cancer. It also turned out that the coffee drinkers in
our study were also more likely to smoke.

Coffee drinking was correlated with lung cancer, but was not the cause of
lung cancer seen in our observational study. Smoking, a known cause of lung
cancer (proven with actual laboratory studies), was not accounted for in our
original study. In the study results, smoking is a confounder.
 Coffee drinkers were more likely to smoke, and smokers are more likely to get
lung cancer. Coffee was correlated with lung cancer because of the relation of
coffee drinking to smoking in our study, not because coffee causes lung cancer.

The hard part with any observational study is controlling confounders.

Researchers try to think of all the other possible things in the environment that
could have an effect on a correlation with an exposure (coffee) and the disease (lung
cancer). It is impossible to control for all confounders—which is why observational
studies should primarily be used to form hypotheses for future studies when a
correlation is found.

Finding a correlation with coffee drinking and lung cancer doesn’t make much
sense from what we know about the mechanism of lung cancer. There isn’t a
plausible mechanism for coffee to cause lung cancer. The researchers could have
used the correlation of coffee and lung cancer to generate a hypothesis that they
could test further, but certainly should never draw any conclusions that coffee
causes lung cancer. Unfortunately, this happens very often, and the news media does
all of us a real disservice by generating sensational headlines. This leads to further
confusion among the general public. Invariably, another observational study will
come out the following month showing an opposite correlation.

We are spending time talking about this because many of the biomarkers we will
discuss have correlations with disease. Some have stronger correlations than
others, and some have been studied enough to approach showing that they contribute
to a cause for the disease.

We have to use biomarkers as “engine warning lights” (a car analogy) that we

may be going the wrong direction with our lifestyle choices, but the biomarkers
themselves may not be a cause of disease.

The “witch scene” from the classic movie, Monty Python and the Holy Grail is a
great example of how correlation can go wrong with disastrous consequences.

The scene starts with the villagers trying to decide if a woman is a witch, and Sir
Bedevere and King Arthur come in to “school” them on correlation and causation...

BEDEVERE: Quiet, quiet. Quiet! There are ways of telling whether she is a witch.
CROWD: Are there? What are they?
BEDEVERE: Tell me, what do you do with witches?
VILLAGER #2: Burn!
CROWD: Burn, burn them up!
BEDEVERE: And what do you burn apart from witches?
VILLAGER #1: More witches!
VILLAGER #2: Wood!
BEDEVERE: So, why do witches burn? [pause]
VILLAGER #3: B--... ‘cause they’re made of wood...?
BEDEVERE: Good!
CROWD: Oh yeah, yeah...
BEDEVERE: So, how do we tell whether she is made of wood?
VILLAGER #1: Build a bridge out of her.
BEDEVERE: Ah, but can you not also build bridges out of stone?
VILLAGER #2: Oh, yeah.
BEDEVERE: Does wood sink in water?
VILLAGER #1: No, no.
VILLAGER #2: It floats! It floats!
VILLAGER #1: Throw her into the pond!
CROWD: The pond!
BEDEVERE: What also floats in water?
VILLAGER #1: Bread!
VILLAGER #2: Apples!
VILLAGER #3: Very small rocks!
VILLAGER #1: Cider!
VILLAGER #2: Great gravy!
VILLAGER #1: Cherries!
VILLAGER #2: Mud!
VILLAGER #3: Churches—churches!
VILLAGER #2: Lead—lead!
ARTHUR: A duck.
CROWD: Oooh.
BEDEVERE: Exactly! So, logically...,
VILLAGER #1: If... she.. weighs the same as a duck, she’s made of wood.
BEDEVERE: And therefore—?
VILLAGER #1: A witch!
CROWD: A witch!
BEDEVERE: We shall use my larger scales!

DON’T GET NEUROTIC

The best way to use the biomarkers covered below is to periodically monitor
them so you can correlate the results with “how you are feeling”. If your periodic
testing shows “bad” results, and you have gained fat mass and generally feel lousy,
it stands to reason in this case the tests are reinforcing the conclusion that you are
on the road to poor health. Those of you who have type-A personalities and/or
obsessive “tendencies” could easily fall into the trap of stressing over this testing,
or testing too frequently. The idea behind using these biomarkers is to hone your
intuitive sense of your body’s state, day-to-day. Ideally, as you dial-in the ability to
“listen” to your body, you will need to use the biomarker testing less and less.

We’ll discuss in detail the background and rationale for measuring the following
biomarkers. These sections are very technical, but are necessarily so for
understanding what you are measuring and its significance—along with each
biomarker ’s limitations. Here’s what will be covered:

I. Lipid Panel (AKA Cholesterol)

II. Physical Measurements

III. Markers of Inflammation

IV. Heart Rate Variability

 We’ll start by measuring cholesterol, which shouldn’t be controversial if you
understand the science. Unfortunately, a great deal of misunderstanding and outright
misinformation surrounds cholesterol in general, not to mention the blood testing
of “cholesterol.” Hopefully we can clear things up a bit before we come to the
conclusion that cholesterol is “a witch.”
STUFF YOU CAN MEASURE I
CHOLESTEROL: WHAT ARE WE
MEASURING?

“Saturated fat and cholesterol in the diet are not the cause of
coronary heart disease. That myth is the greatest ‘scientific’ deception
of the century, and perhaps any century.”
—George V. Mann, M.D.

SCIENTISTS AS HERETICS
Dr. Mann was one of the co-directors of the Framingham Heart Study, and spent
his career attempting to determine risk factors for heart disease. His contention that
cholesterol (and saturated fat) from the diet was not a contributor to heart disease
was very controversial to say the least. As a society, we have been completely
“brainwashed” by constant messages about the evils of cholesterol, that statements
such as Dr. Mann’s are like going against gospel.

Cholesterol has been demonized more even than saturated fat in the past 50 years.
The marketing of “low cholesterol” foods and anti-cholesterol public health
messaging has been so effective that to even suggest taking a second critical look at
the basis for these recommendations puts us at risk of being labeled “medical
heretics”. The anti-cholesterol movement has approached a level of religious
fervor. As with saturated fat in the nutrition section, let’s take a step back, look at the
science, and make informed opinions regarding cholesterol.

WHAT IS CHOLESTEROL?
Before we discuss measuring cholesterol as a biomarker, it is crucial to
understand the biochemistry and physiology of cholesterol and lipoproteins (more
on this in a bit). Only with this foundation will you be able to make sense of the
laboratory testing and make informed decisions about your health.

CHOLESTEROL
This is what the fuss is all about......

Cholesterol is an absolutely ESSENTIAL compound for normal brain and body

function. Here are a few of its uses:

• Proper cell membrane function. Cholesterol is a stabilizing structure and an

antioxidant in the cell membranes (remember our lipid peroxidation discussion)
that can stop membrane-damaging free radical chain reactions.

A piece of cell membrane in cross-section, showing the double layer of fats called
phospholipids, and cholesterol in the roles of membrane stabilizers and
antioxidants. Without cholesterol to stabilize the membrane surrounding the cell,
our cells would need a cell wall like plants have, and would be susceptible to
damage by oxidation.

• Cholesterol is necessary for effective nerve cell communication—it is an

integral part of the nerve “insulation” called myelin. Myelin is wrapped around
the axon “transmitters” on nerve cells, similar to the insulation/coating on
 electrical wiring. It ensures that nerve signals can be carried quickly and
efficiently from one nerve cell to another.
In fact, cholesterol has been found to be the “rate-limiting step” in the formation of
myelin in the brain and nerves outside the brain. In other words, the speed of myelin
production depends on a steady supply of cholesterol. It is therefore no surprise that
cholesterol is crucial for the developing brain during childhood, and for slowing
the rate of the degeneration of brain connections in old age. Recent studies have
shown that as people approach old age, those with the highest cholesterol have
been shown to live the longest.

• Cholesterol is the molecular building block for the making many important
hormones, including cortisol, aldosterone, progesterone, testosterone, estrogens,
and vitamin D.

• Cholesterol is the molecular building block for making many important

hormones, including cortisol, aldosterone, progesterone, testosterone, estrogens,
and vitamin D.
A simplified pathway showing some of the important hormones made from
cholesterol. The hormones testosterone and estrogen have obvious importance to
us. Aldosterone is involved in maintaining electrolyte balance in the kidneys and
cortisol is a critical hormone involved in the stress response.

• Cholesterol is also the building block for bile salts, crucial for digestion and
absorption of dietary fats (and fat soluble vitamins, A, D, E, and K).

• Cholesterol is present in significant amounts in human breast milk—a vital

component for infant brain development.

Because of cholesterol’s very important functions, your body has a system to

keep levels adequate for these vital functions. Because of this system, you can’t
significantly alter cholesterol levels by changing dietary intake.

CAN YOU CHANGE CHOLESTEROL

LEVELS IN YOUR BLOOD BY
CHANGING HOW MUCH
CHOLESTEROL YOU EAT?
Research has shown that most people can only change their blood levels
of cholesterol about 5% in either direction by changing how much
cholesterol they eat in their diets. When you do get a small increase in
cholesterol in your blood from increased dietary cholesterol, there also is
an increase in HDL associated cholesterol, and more of the large buoyant-
type of LDL cholesterol carriers. (More about this later, but both are good
things!)

Changing how much cholesterol you eat (despite what you may have
heard) does not alter blood levels of cholesterol much for most people.
The small change that may happen doesn’t affect your risk for heart
disease, according to recent scientific studies.

If you take in less cholesterol than your body needs in the diet, the body will
produce more. If you take in more cholesterol in the diet, the body will produce
less. The bottom line is that your body knows what it is doing with cholesterol
(even if you or your doctors don’t).
 Based on the above information, it would follow from a “first principles”
perspective that artificially lowering cholesterol levels with pharmacology may
have unintended consequences.

We are seeing more of these unintended consequences in some of the side effects
recently observed by artificially lowering cholesterol levels using drugs.

• Memory loss (cholesterol is needed for proper nerve functioning in the brain)

• Muscle damage (thought to be due to depletion of CoQ10, a crucial antioxidant

which shares part of the same pathway as cholesterol for its synthesis)

• Erectile dysfunction (possibly due to low testosterone from depleted

cholesterol, testosterone’s building block)

QUICK MEDICAL NOTE:

There are certainly some individuals who can benefit from cholesterol
lowering medication, such as males who have already had a heart attack.
Most of us can change our “lipid profiles” in the right direction with
proper nutrition, lifestyle, and exercise—without any of the side effects
listed above.

Current science is starting to catch up with the “first principles,” even though
many in the scientific and medical community can’t seem to let go of the idea that
cholesterol itself is the problem. The current science points to problems arising
from lipoproteins, the carriers of fat and cholesterol.

KEY POINT:
As we will soon show you, cholesterol itself does not lead to heart
disease, but certain types of cholesterol carriers that are thought to be
problematic.
LIPOPROTEINS 101
Fat and cholesterol transport (carrier) molecules—lipoproteins—come in a
variety of “flavors” and have very different functions. An important idea to keep in
mind is that recent research has shown that it is the amount and type of dietary
carbohydrate which is one of the biggest factors in how lipoproteins can “go
bad”—not dietary cholesterol or saturated fat. This overview is very simplified, but
hopefully the message is clear.

The major classes of lipoproteins are: chylomicrons, VLDL, LDL, and HDL.
You may have heard about a couple of these lipoprotein “carriers” of fat and
cholesterol while talking with your doctor. The message we will keep repeating is
that none of these are cholesterol, they are carriers of cholesterol!

TYPES OF LIPOPROTEINS (CARRIERS)

CHYLOMICRONS
Chylomicrons are the primary form of lipoprotein that transport dietary lipids
(i.e. the fat that you eat).

• Triglycerides (fat) from the diet associated with chylomicrons are transported
through the lymph system first before they enter the bloodstream (except for
short chain and medium chain fats). This prevents a large amount of lipids from
rapidly entering the bloodstream.

• Tissues with a high need for triglycerides (skeletal and cardiac muscle for
energy, adipose tissue for storage) have an enzyme called lipoprotein lipase in
nearby blood vessels. This enzyme separates the dietary triglycerides from the
chylomicrons to allow the cell to use the fat (for energy or structural
requirements).
 The picture above depicts the basic structure of a lipoprotein particle in
cross-section. The actual particle is a 3 dimensional sphere. The
phospholipids lining the outside have 2 tails (in black) each composed of
an unsaturated fatty acid. These unsaturated fats with double bonds are
susceptible to oxidation (from our discussion of fats in Nutrition 101).
The apolipoprotein part of the particle (in red) is the protein responsible
for recognition by various receptors. The type of apolipoprotein present
on the particle is the “calling card” that distinguishes LDL, HDL, and
chylomicrons. Free cholesterol (yellow) is present in the phospholipid
membrane, helping to give it structural support and to act as an
antioxidant. The inner core consists of the fats called triglycerides (in
green) and cholesterol esters (yellow outlined in orange).
The core contains the “cargo” of cholesterol and triglycerides, which is
delivered to the various cells of the body for use. Cholesterol esters are
made of cholesterol with a “tail” consisting of various types of fatty acids.

VERY LOW DENSITY LIPOPROTEIN (VLDL)

• VLDLs are produced and released by the liver.

• VLDLs carry internally produced fat and cholesterol. Very low density
lipoproteins carry the triglycerides produced from excess glucose when the liver
“glycogen tank” is full. They are also the initial carrier for cholesterol produced
in the liver that is needed by tissues for the crucial functions cholesterol provides
(mentioned above).

• VLDLs also interact with lipoprotein lipase, an enzyme that releases fat from
 the VLDL carrier for storage in fat cells or utilization by other tissues for
energy or structural uses.

• After much of the triglyceride has been removed, the VLDL is transformed
into a relatively cholesterol-rich LDL.

LOW DENSITY LIPOPROTEIN (LDL)

LDL is the carrier unfortunately known as “bad cholesterol”. It is neither
cholesterol nor always bad. Its function is to carry cholesterol from the liver to
supply the body’s various cells with needed cholesterol. This cholesterol is then
used by the cells to perform the essential functions listed above. Under normal
circumstances, the LDL travels through the blood vessels and “docks” with an LDL
receptor at its delivery site. You can think of LDL as a commuter bus that arrives at a
station (the LDL receptor) and drops off its cargo of cholesterol.

KEY POINT:
LDL is not cholesterol, despite being called “bad cholesterol.” Cholesterol
is cholesterol regardless of what carries it. LDL is a cholesterol carrier.

As always, the “devil is in the details”. It turns out that the LDL carrier exists in
subclasses according to size: small-dense LDL (sdLDL), and large-buoyant LDL
(lbLDL). The latest science shows that these subclasses may act VERY differently in
contributing to heart and vascular disease, and the amounts of each can be largely
influenced by diet. Much more on this soon.

HIGH DENSITY LIPOPROTEIN (HDL)

Known as “good cholesterol”, even though it also is NOT cholesterol, but
another cholesterol carrier. In basic terms, this carrier takes the excess cholesterol
not used by tissues, and carries it back to the liver.
 KEY POINT:
HDL is not cholesterol despite being called “good cholesterol.”
Cholesterol is cholesterol regardless of what carries it. HDL is another
cholesterol carrier.

SMALL-DENSE LDL AND LARGE-BUOYANT LDL

We just introduced the idea that the LDL carrier has size “sub-classes”. The
differences between the two main subclasses of large buoyant LDL and small dense
LDL are much more than just size—they act very differently in the body for the
development of heart disease.

Both types of LDL carry cholesterol. The cholesterol they carry is identical,
but the carriers themselves are different. Just as you are the same person
whether you travel by bus or by taxi.

The different types of LDL, small-dense and large-buoyant are formed from
VLDL. Genetic factors determine the ratio of lbLDL to sdLDL someone has, but
what we eat is a huge player in how much of each will be formed.

The key point to understand is that the cells in your body need cholesterol and
the liver makes the lipoprotein carriers which deliver the amount of cholesterol the
body needs at any one time. Large-buoyant LDL carries more cholesterol than a
small-dense LDL carrier, so it takes fewer large-buoyant LDL particles to carry
the same amount of cholesterol. If you are making small-dense LDL particles, you
need more of them to carry enough cholesterol to meet the body’s demands. This
has extremely important health consequences as we will see shortly.

Put simply, think of large buoyant LDL as a commuter bus that can carry many
“passengers” (cholesterol) and small dense LDL as a taxi that can carry far fewer
“passengers” (cholesterol).

The following section will use the “commuter bus” and “taxi” analogy to show
you how the different types of lipoproteins are formed. Once you understand this,
you will better understand the lab tests your doctor draws to look at your
cholesterol levels.
CHOLESTEROL “TRANSPORTATION”
To briefly review, lipoproteins are the carriers of fat (triglycerides) and
cholesterol:

• Chylomicrons are the carriers that transport the fat and cholesterol that you get
directly from food when you eat.

• VLDL and LDL are the carriers that transport the fat (triglycerides) and
cholesterol made or processed in the liver.

• LDL is the primary transporter of cholesterol from the liver to the rest of the
body.

• HDL is the carrier that takes any excess cholesterol from the body and
transports it back to the liver for “recycling.”

The process starts when VLDLs are made in the liver and “packed” with
triglycerides (fats) and cholesterol. The amount of triglycerides in each VLDL
depends on your diet and your “metabolic health.”

A quick review of STEP 6 in the Diabesity Intervention section will remind you
that excess glucose and fructose in the diet will be made into triglycerides (fat) by
the liver. Also remember from the Diabesity section that if you have insulin
resistance or diabetes, the fat cells are not doing their storage job well and are
releasing triglycerides to be processed back in the liver. Both excess sugar in the
diet and insulin resistance will cause more triglycerides to be either created or
processed by the liver (usually both are happening). These triglycerides are
packaged into the VLDL carriers by the liver, in the hope that they can be delivered
to muscle or fat cells for use or storage. The liver is trying to get the triglycerides
out of the liver so they don’t build up and become toxic (as in forming a “fatty
liver”).
VLDL packed with triglycerides with a small amount of cholesterol.
If there are high amounts of triglycerides from excess dietary sugar and/or insulin
resistance, the “packaging” process will load the VLDL with triglycerides, without
much room left for shipping out the cholesterol to the body.
VLDL with more cholesterol as “cargo” and fewer triglycerides.

A healthy person who doesn’t eat excess sugar or have insulin resistance will not
have an excess of triglycerides created in the liver. When the VLDL is made to
transport triglycerides and cholesterol out to the body, there is more room to
“package” cholesterol in the VLDL because there are not as many triglycerides
around.

The VLDL will leave the liver and travel to deliver the triglyceride cargo first to
muscle or fat cells for energy use or storage. Once the triglyceride cargo is
offloaded, the VLDL undergoes processing and is transformed into a LDL. The
LDL is left with a cargo of cholesterol to deliver to the body.
 The type of LDL formed depends on how much triglyceride content was present
in the original VLDL.

• A VLDL that was “stuffed” with triglycerides will be transformed into a small
dense LDL after the triglyceride cargo is dropped off. The resulting small dense
LDL has relatively little cholesterol cargo, because there wasn’t much room for
cholesterol in the original triglyceride-packed VLDL.

• A VLDL with a “normal” amount of triglycerides and more cholesterol, will be

transformed into a large-buoyant LDL once the triglyceride cargo is dropped off.
The large-buoyant LDL has more cholesterol cargo because there was more
room for cholesterol in the original VLDL.

LARGE-BUOYANT LDL (LBLDL)

Large-buoyant LDL formed from normal VLDL carry a relatively large
amount of cholesterol cargo on each “particle” of lbLDL. These particles
travel to the cells in your body that need cholesterol and drop off their
“cargo”.
 When the lbLDL arrives at a cell to drop off cholesterol, it pulls up to a
designated “station” (like a bus pulling up to a bus station). The “station”
is an LDL receptor. The lbLDL particle “docks” with the LDL receptor to
drop off the cargo of cholesterol. This is what LDL particles are supposed
to do as a transporter of cholesterol.

The larger lbLDL particles are also less prone to damage from free
radicals and can stay in the bloodstream longer without becoming
oxidized.

The lbLDL is like a commuter bus with cholesterol as passengers. A bus is

large, sturdy, less prone to damage, and also less likely to be in an
accident while traveling—much like an lbLDL particle.

The large-buoyant LDL “Commuter Bus” packed with cholesterol.

INNOCENT BYSTANDER?
The cholesterol theory of heart disease started early in the 20th century after
cholesterol was found in the walls of the arteries from people who had recently died
from heart attacks. This finding started the demonization of cholesterol as a cause
of heart disease, especially in the last 50 years.

Recent science has shown that cholesterol itself that is not leading to the buildup
of plaques and narrowing of the arteries, but the lipoprotein carriers, especially the
small-dense LDL we just described.

SMALL-DENSE LDL (SDLDL)

The small-dense LDL particles formed from triglyceride-packed VLDL
don’t act like the large-buoyant LDL. First, they are only transporting a
small amount of cholesterol, so it takes more of them to carry the same
amount of cholesterol “passengers” than the large-buoyant LDL.
 Small-dense LDL particles (sdLDL) are also more susceptible to damage
by free radicals, which turns them into a highly reactive and dangerous
particle called “oxidized LDL” (oxLDL).

Small-dense LDL particles are also more likely not to arrive at the
designated “stations” (LDL receptors) to deliver their cholesterol cargo.
They are more likely to get in “accidents”—stuck in the walls of your
arteries.

To summarize, the sdLDL is a particle that can’t carry much cholesterol, is

susceptible to damage by free radicals, and gets into “accidents” by
crashing into the walls of your arteries. They are also not reliable for
arriving at the designated drop-off stations for cholesterol.

The small-dense LDL “taxi” with little cholesterol.

Early studies showed that cholesterol is present in “artery clogging” plaques, and
that continues to be true. We now know that cholesterol was more of an innocent
bystander, carried into the walls of the arteries by the lipoprotein carriers,
especially small dense LDL.

Blaming cholesterol for causing artery plaques is like blaming the fare-paying
taxi passenger for an accident on the interstate. The passenger (cholesterol) was just
riding in the taxi, and had nothing to do with the accident. The faulty logic would be:
we found the passenger at the scene of the accident, so they must be responsible for
the damage.

It obviously makes no sense to leap to the conclusion of blaming the passenger,

so why are we doing it with cholesterol?
The large-buoyant LDL (lbLDL) are operating as they should, transporting large
amounts of cholesterol from the liver, through the bloodstream to their designated
“stations” (LDL receptors) on the various cells in the body that need cholesterol for
the vital functions we discussed at the beginning of this section.

Large-buoyant LDL—for the most part—don’t cause problems by crashing and

lodging themselves into the sides of the artery walls. Many medical providers and
public health entities continue to refer to the cholesterol carried by LDL particles in
general as “bad cholesterol.” The lbLDL is unfortunately lumped in as “bad
cholesterol,” even though your doctor does not measure what types of LDL particles
you have; they only measure the cholesterol passengers. We will discuss this much
more very soon.

This is a “cross-section” of an artery. Imagine looking at your artery as you would

the end of a garden hose. You can see the lumen where the blood travels has no
narrowing or “blockages”. The healthy cholesterol transport system of mostly
lbLDL is operating correctly and not causing problems.
The small-dense LDL particles (sdLDL) are very prone to cause serious problems
in the walls of your arteries while carrying their “cargo” of cholesterol along with
them. The sdLDL can bind with the artery walls in places that they are not supposed
to bind. These are unap-proved stops in their journey to deliver cholesterol. Instead
of stopping at designated dropoff stations (LDL receptors) for their cholesterol
passengers, sdLDL particles are prone to “crash” into the walls of the arteries,
damaging the cells lining the arteries (endothelial cells).

Once the sdLDL particle penetrates the endothelial cells lining the artery wall, and
move into the muscular layer of the artery, they are readily oxidized by free
radicals. Now the sdLDL is a highly reactive oxidized LDL (much like a car on fire
after crashing into the guard rail). The immune system goes on high alert. Cells of
the “innate guardian” immune system, known as macrophages, respond to the scene
of the accident, much like police do in an automobile accident on the interstate.
These macrophages “know” that the sdLDL particle (with cholesterol passengers) is
not supposed to be inside the artery wall. To protect the body from this reactive
oxidized sdLDL, the macrophages engulf the sdLDL particle. The macrophages that
engulf the sdLDL particles turn into foam cells.
The body recruits more of the immune system to wall the area off, turning the area
into an atheroma. This atheroma bulges up through the artery wall from the inside
and leads to the narrowing of the arteries in heart disease.

Looking at the cross-section of the artery again, the atheroma described below has
narrowed the area in the artery where blood flows (lumen). Also note that the area
of the atheroma is highly inflamed. This is how sdLDL in particular, contributes to
heart disease. Imagine this process in the very small blood vessels supplying your
heart. Over time the narrowing will become worse, leading to a heart attack.

TESTING CHOLESTEROL
When my doctor tests my cholesterol, what are we testing?

The typical lipid panel (cholesterol test) reports HDL cholesterol, VLDL,
triglycerides (TG), total cholesterol, and LDL cholesterol. The VLDL, LDL, and
HDL numbers represent the amount of cholesterol associated with these
lipoproteins.

In other words, we are measuring the amount of cholesterol “passengers” that are
riding on each of the different carrier lipoproteins.
 KEY POINT:
Conventional cholesterol laboratory tests only measure the amount of
cholesterol (passengers) associated with each type of lipoprotein carrier.

These values tell us very little about the number and size of the lipoproteins
themselves. Additionally, the value measured for LDL-associated cholesterol is not
even a direct measurement, it is calculated by a mathematical formula known as the
Friedewald equation.

The Friedewald equation gives us only an estimate of the passengers

(cholesterol) being carried by LDL particles.

THE FRIEDEWALD EQUATION

To estimate the amount of cholesterol associated with your LDL particles,
the following equation is used:
LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Again, the LDL cholesterol tests are measuring cholesterol “riding” on LDL
carriers, and do not tell us how many LDL carriers are present or what type of LDL
is present. Both of these missing pieces of information are extremely important
to predict your risk of developing heart and vascular disease.

Conventional cholesterol testing is measuring…

cholesterol passengers…

and is not measuring lipoprotein carriers.

 Knowing your particle number and particle size is important because recent
research shows that both are more predictive of developing heart disease than just
measuring the amount of cholesterol passengers associated with the LDL particles.
To illustrate why this makes sense, let’s create a scenario.

“PATIENT A”
Patient A goes to his doctor and has a cholesterol test. His results show a
(calculated) LDL cholesterol of 150 mg/dl. His doctor is concerned and says it is
too high. He is told to reduce the amount of cholesterol he is eating in his diet—this
advice continues to be given despite the science! After arguing with his doctor, he is
given a second test that evaluates his LDL particle size and number. The results show
a relatively low actual LDL particle (carrier) number, and mostly large-buoyant
LDL particles (mostly “buses”).

Patient A has mostly “commuter buses” carrying his cargo of 150 mg/dl of
cholesterol, and the actual number of the buses was normal when checked, but he
was given advice to lower his cholesterol based only on the initial blood test
showing 150 mg/dl of cholesterol “passengers.” Patient A has a relatively low heart
attack risk with our information on particle number and size, despite his “high”
initial cholesterol test.

“PATIENT B”
Patient B comes in the following day for his annual check up. He gets his
cholesterol test and it shows an LDL (calculated) cholesterol level of 125 mg/dl. His
doctor tells him his “bad cholesterol” level is pretty good, but a little on the high
side, and tells him he should watch how much cholesterol he eats. One month later,
Patient B has a minor heart attack and was found to have blockages in the small
arteries of his heart. He gets a stent placed and the cardiologist caring for him in the
hospital also orders an LDL particle size and particle number test.
 The test results show a higher than normal particle number and mostly small-
dense LDL particles (mostly “taxis”). Patient B is mystified and tells the cardiologist
that his “bad cholesterol” was normal on a check-up 1 month ago. The cardiologist
explains that although the amount of cholesterol “passengers” counted was normal,
they are being carried on a high number of small-dense particles, known to
correlate strongly with heart disease.

You can see how Patient A could have a larger amount of cholesterol
“passengers” carried in his large-buoyant LDL commuter buses, than Patient B. but
have a fewer number of particles (he has a fewer number of “buses” than Patient B
has “taxis”). Unfortunately, Patient B had a larger number of LDL particles overall,
and most were of the small-dense type associated with heart and vascular disease.
Because the small-dense particles carry less cholesterol per particle, the standard
cholesterol test came back as normal because it was just counting the passengers.

Patient A had more passengers overall, but less LDL particles, because his large-
buoyant LDL particles can carry more passengers. The large-buoyant LDL particles
are also less likely to cause problems in the walls of his arteries. His “high bad
cholesterol” in this case was not a risk to his heart health.

The different scenarios of Patient A and Patient B show some of the problems
with relying solely on conventional cholesterol testing when figuring your risk for
heart disease. However, the conventional lipid panel is far from useless. We will
show you how to gather some very valuable information from this test outside of
the LDL cholesterol amount. First, let’s discuss particle size in a bit more depth.

WHAT AFFECTS MY LDL PARTICLE SIZE?

While genetic factors certainly predispose some people to have more small-dense
LDL, nutrition plays a larger role for most people in determining how much
large-buoyant vs. small-dense LDL they have.
 KEY POINT:
Genetics contribute, but nutrition plays the largest role in determining
LDL particle size.

We already discussed the role of nutrition in particle size previously, but it bears
repeating:

Forming small-dense LDL particles happens from the following diet and lifestyle
factors:

• Consistently eating more sugar and starch than your body can handle leads to
more triglycerides made from the excess sugar.

• Insulin resistance from inflammation and oxidative stress (diabetes, obesity,

poor sleep, gut inflammation, chronic stress) can lead to decreased fat storage
in fat cells (they are already stuffed full with fat). The excess comes to the liver
for processing.

• The liver deals with the triglycerides (fat) from both of these sources and
packages the triglycerides into VLDL. These VLDL are stuffed with triglycerides,
and have little room for cholesterol.

• A small-dense LDL is formed after the triglyceride-stuffed VLDL drops off the
triglycerides.

You can see that excess starch and sugar coupled with insulin resistance is
primarily responsible for formation of small-dense LDL.

If you are already insulin resistant, and eat a diet heavy in starch and sugar, the fat
in the diet will contribute to formation of small-dense LDL by increasing
triglycerides further. However, fat in the diet is not the specific underlying problem
as many would have you think. The problem is fat eaten with sugar and starch in an
insulin resistant state.
 TECHNICAL NOTE:
The type of fat that you eat is also very important. High amounts of
omega-6 PUFA in vegetable oils from fast food and processed food will
increase inflammation, oxidative stress, and worsen insulin resistance.

As insulin resistance becomes worse, it will decrease carbohydrate

tolerance, resulting in more triglycerides produced and processed by the
liver—leading to more sdLDL.

The sdLDL that is formed is more prone to oxidation as some of the

omega-6 PUFA will be incorporated into the sdLDL particle.

Notice that cholesterol in the diet does not lead to small-dense LDL.
Reducing cholesterol in the diet only causes the body to produce more
cholesterol “from scratch” as needed.
Forming large-buoyant LDL particles happens when you are insulin sensitive
and don’t eat more starchy carbohydrate and sugar than your body can handle. The
liver does not have to produce triglycerides from excess sugar and starch, and the
fat cells are able to store triglycerides so the liver does not have to process them.

• With fewer triglycerides for the liver to package in VLDL, a “normal” VLDL is
formed with more room for cholesterol “passengers.”

• After the small amount of triglycerides is dropped off, the VLDL is

transformed into a large-buoyant LDL.

• Not eating high amounts of pro-inflammatory omega 6 PUFA will also help
reduce inflammation, reduce oxidative stress, and help maintain insulin
sensitivity leading to fewer triglycerides and more lbLDL.
 TECHNICAL NOTE:
Eating more dietary cholesterol causes your body to produce less
cholesterol. Any short-term small increase in cholesterol in the body from
eating more cholesterol will cause a small short-term increase in large-
buoyant LDL, not small-dense LDL.

Most dietary saturated fat has the same effect of a short-term small
increase in large-buoyant LDL. Saturated fat and cholesterol in the diet
also increase the amount of HDL, the cholesterol scavenger (known as
“good cholesterol”). The only saturated fat to avoid is the pro-
inflammatory palmitic acid that we have discussed extensively in previous
sections.

IS STANDARD CHOLESTEROL TESTING

USELESS?
There is some very useful information in a standard cholesterol test (commonly
called a lipid panel), without resorting to testing for particle size and particle
number.
I. It is generally accepted that higher HDL-associated cholesterol levels are
correlated (remember correlation vs. causation) with a lower risk of heart
disease. A high HDL-associated cholesterol value says that HDL is doing a good
job of carrying excess cholesterol back to the liver. As cholesterol itself is not
causing vascular disease, it is unclear what the actual mechanism resulting in
decreased risk may be, but it is an active area of research. There is not much
more we can say about HDL, except that higher levels generally show lower
risk of heart disease.

KEY POINT:
High HDL-associated cholesterol is well correlated with a lower risk of
heart and vascular disease.

II. High triglycerides are well correlated with a higher risk of heart disease. The
medical community generally used to ignore the triglyceride level on laboratory
 tests unless it was very high. We have established a pretty strong mechanism
showing how high triglycerides lead to the formation of small-dense LDL—a
strong risk factor for heart disease. As we have repeatedly discussed, high
triglycerides are associated with obesity, diabetes, and fatty liver disease, which
are all inflammatory diseases. We also know that heart disease is primarily an
inflammatory disease and is accelerated by obesity and diabetes. More medical
providers are paying closer attention to triglyceride levels for this reason.
III. A pattern usually seen on standard lipid panels is high triglycerides with low
HDL. It is also common to have low triglycerides associated with high HDL
levels. Recent science has shown that the HDL/triglyceride ratio is a better
predictor of risk of heart disease and diabetes than standard LDL cholesterol
levels:

• High HDL and low triglycerides = LOW RISK

• Low HDL and high triglycerides = HIGH RISK

IV. There is also a pattern seen with the HDL/triglyceride ratio and LDL particle
size:

WHAT NUMBERS ARE “GOOD” ON THE

STANDARD LIPID PANEL?
First remember that any lab values on cholesterol testing are only correlated with
health and disease. Remember to use them as “engine warning lights” and make sure
they are viewed in the context of any other risk factors for heart disease you may
have. Family history of heart disease, high blood pressure, obesity, diabetes, and
smoking all are well-known risk factors for heart and vascular disease. The lipid
panel (cholesterol and triglycerides) is just another piece of the puzzle.

We have just spent a great deal of time showing the differences between large-
buoyant and small-dense LDL, especially sdLDL’s proposed contribution to heart
and vascular disease. Keep in mind that all the risk factors listed above contribute to
the development and progression of heart and vascular disease, and the underlying
main mechanisms of disease are chronic inflammation and oxidative stress.
 “Bad” lipid profiles such as the pattern of low HDL, high triglycerides, and
small-dense LDL are usually seen in the setting of inflammatory conditions such as
diabetes, obesity, and high blood pressure. Most people with heart disease have most
of the risk factors present at the same time, not just unfavorable lipid panel values in
isolation. “Fixing” obesity and diabetes lowers inflammation and oxidative stress,
and often “fixes” high blood pressure and abnormal lipid panels, changing small-
dense LDL to large-buoyant LDL without directly “treating” cholesterol.

The purpose of this long-winded discussion is to emphasize that we shouldn’t be

looking at any of these laboratory tests in isolation, without taking other factors into
account. We should also avoid the habit of “treating” laboratory values, instead we
need to treat the person, and often the lab values “fix” themselves. Use the lipid
panel as one of the measures to gauge your progress in your pursuit of health. All
this being said, below are some suggested targets for the traditional lipid panel:

PATTERN A (FAVORABLE)

• Triglycerides 100 mg/dl or less

• HDL 60 mg/dl or greater
• LDL-associated cholesterol may vary, but this pattern is generally
associated with large-buoyant LDL particles

Note that the triglyceride target is set at 100 mg/dl or less. Most tests set
“normal” at less than 150 mg/dl. My bias is to set the target a bit lower for
triglycerides. I don’t consider 150 mg/dl to be “metabolically healthy.”

 PATTERN B (UNFAVORABLE)
• Triglycerides 150 mg/dl or greater
• HDL 40 mg/dl or less
• LDL-associated cholesterol may vary (can be “normal”), but this pattern
is generally associated with small-dense LDL particles

TECHNICAL NOTE & RESEARCH UPDATE :

Tests to measure LDL particle size are currently available but sometimes
don’t give consistent results. The tests will likely become more reliable as
technology improves, so ask your doctor which test is currently the most
reliable if you want to test particle size directly (especially if you are
considering starting medication).

The NMR test for particle number is currently the most reliable and can be
very useful if you are trying to sort out a confusing lipid panel, and are
trying to make a decision about starting medication.

Current science shows that the total LDL particle number (not LDL
cholesterol number) has the best correlation with heart disease. A high
LDL particle number is often associated with small-dense particle size
(but not always).

IT GETS MORE COMPLICATED .......

Believe it or not, the topic of cholesterol and lipoproteins is even more
complicated. No wonder people are confused! Here are some highlights for those
who want to dig deeper:

• Lipoproteins such as LDL are involved in the immune response to bacterial

invasion, and are elevated when we have to fight off an infection. If your blood
work is done during this time, your numbers may be abnormal.
 • The amount of LDL receptors (“stations”) can change in response to various
situations. For instance, thyroid hormone controls how much LDL receptor is
made. If you have low thyroid function (hypothyroidism), you will have low LDL
receptors. Low LDL receptors can cause some major problems:
— The lipoproteins need to “dock” with the LDL receptors (“stations”) to
offload their cholesterol cargo for the cells to use.
— If there are not enough LDL receptors (“stations” to drop off passengers),
the normal sized large-buoyant LDLs stay in the bloodstream longer.
— The longer the LDLs stay in the bloodstream, the more susceptible they are
to oxidation (even large-buoyant LDL). You can think of this as a ship in the
water too long. Even the hulls of the best-made ships will rust if they are in the
water for long enough.
— “Fixing” a poorly functioning thyroid can “fix” your cholesterol and
lipoprotein problem by making more “stations”(LDL receptors) for LDL
particle “docking.”

• Statin-type cholesterol drugs don’t change the proportion of small-dense LDL;

they theoretically may even make the proportion worse. This may be because one
effect of statins is to cause cells to make more LDL receptor. This is good for the
large-buoyant LDL, but remember that small-dense LDLs don’t bind well to
normal LDL receptor “stations.” This will preferentially leave more small-dense
LDL in circulation—and small-dense particles are more easily oxidized! There
are plenty of people having heart attacks with “normal” cholesterol while taking
statins. This may be why.*

*A recent article by a group of researchers addressed the observations that

statin-type drugs make the proportion of small-dense LDL greater during
cholesterol lowering therapy. While it is true that the clinical significance
of the higher small-dense LDL proportion with statin therapy is somewhat
uncertain, there is strong biological plausibility to support the altered
proportion of small-dense LDL may indeed be problematic.

The point of this technical note is that the researchers authoring the article
in question dismissed the increase in proportion of small-dense LDL with
statin therapy as a potentially problematic finding. Of particular interest
is that ALL of the authors of this paper had strong ties to the
pharmaceutical companies that make statin drugs. Several of the
authors are even employees of the pharmaceutical companies, making
their opinions/findings subject to massive potential conflict of interest.
This type of conflict of interest in cholesterol research is unfortunately far
 from rare.

• The amount of oxidative stress and inflammation produced from processed

food, environmental pollution, and metabolic derangement (diabetes) contributes
to how fast LDL is oxidized in the bloodstream.

• Small-dense LDLs carry a relatively low amount of cholesterol with each

sdLDL particle. Remember that cholesterol itself is an antioxidant, and the low
amount of cholesterol may be a reason for the increased oxidation rate of sdLDL.

The subject of lipoprotein and cholesterol is complex enough even at this level to
make your head swim when wondering how to really interpret your lab values. The
bottom line is that laboratory values for cholesterol and lipoproteins only correlate
with health and disease. Although we are getting a pretty good idea that oxidized
lipoprotein particles and their interaction with our immune system play a MAJOR
role is the development of heart disease, they still just represent a strong correlation
with the disease process. We still can’t definitively call what we measure in blood
work causative. There are so many other factors in play and context is extremely
important.

SUMMARY, TAKE HOME MESSAGES,

CONSIDERATIONS
1. High triglycerides and low HDL usually indicate an unfavorable metabolic
state and can be greatly modified by diet.

2. High triglycerides and low HDL are often associated with small-dense LDL,
which is more susceptible to oxidation and formation of atherosclerotic plaques.
High triglycerides and low HDL are strong predictors of insulin resistance and
diabetes.

3. Very high overall cholesterol numbers on a lipid profile (high total

cholesterol and high LDL—even high HDL) can be due to several underlying
issues which need to be addressed:

• Poor thyroid function: treat the thyroid and cholesterol numbers will likely
improve.

• Recent infection: lipoproteins are involved in the immune response to invading

bacteria.
 • An underlying genetic abnormality resulting in poor LDL receptor function.
This is called familial hypercholesterolemia. Be sure to discuss this possibility
with your doctor, especially if there is a family history of the condition.

• Very high cholesterol levels are often associated with an LDL receptor
dysfunction and should be approached cautiously. Remember that even large-
buoyant LDLs left in circulation too long are susceptible to oxidation.

4. Look for number patterns moving in the right direction, and don’t get too
hung up on the specific numbers themselves. For instance, triglycerides
decreasing below 100 with increasing HDL is generally a good sign. Don’t
wring your hands over whether a triglyceride value of 70 is better than 80.

5. Current science shows that total LDL particle number (not LDL cholesterol
number) has the best correlation with heart disease. High LDL particle number is
usually associated with small-dense particle size (but not always). High total LDL
particle numbers may require statin use while the underlying cause (genetic,
thyroid, etc.) is being determined.

6. Dietary cholesterol (and most saturated fat) has very little to do with heart
disease risk. Altering how much you eat either way does little to change blood
cholesterol levels. Maybe Dr. Mann isn’t such a heretic after all.

7. Laboratory values of lipoproteins and cholesterol are correlates of disease

or health. Remember to use them as “engine warning lights”. The body is
INCREDIBLY complex and we haven’t completely figured out all of the moving
parts.

Hopefully this section at least gives you the knowledge to clear up

misconceptions and misinformation, and can help you make a more informed
decision regarding your health. If you are still somewhat confused, you are not
alone. As science advances, we will get a clearer picture of the role lipoproteins and
cholesterol play in our health. If all we have done is to stop you from saying “good
cholesterol” and “bad cholesterol,” then it has all been worth it!
STUFF YOU CAN MEASURE II
PHYSICAL MEASUREMENTS

AN UNHEALTHY OBSESSION WITH

WEIGHT
In popular culture, measuring lifestyle change success has focused on “weight
loss” as measured on the scale. People often brag about how much weight they have
lost in short amounts of time on the latest fad diets. Rapid weight loss often comes
with radical caloric restriction, and as discussed previously, a significant amount of
the weight is lost from valuable muscle mass.

But, it is not just popular culture that is centered on weight as a measurement of

health. The scientific and medical communities have long used the Body Mass Index
(BMI) as a health marker. The BMI formula incorporates height along with weight
and is the method currently used to determine if someone is “normal,”
“overweight,” or “obese.” Recent science has shown that BMI may not be the best
marker to gauge body fat and health.

The problem with using BMI is that it does not adequately account for muscle
mass.
 • People with large amounts of muscle mass can be classified as “overweight”
even though their body fat percentage is low. Many athletes’ BMIs categorize
them as “overweight” when it is obvious by looking at their lean bodies that they
are far from overweight or unhealthy.

• People with very low muscle mass (not a good thing) are categorized by BMI
as “normal” even though they have a significant amount of body fat and may
even have a metabolic disease such as insulin resistance or diabetes.

“NORMAL WEIGHT OBESITY”

Using the weight-focused BMI has given us a new classification of unhealthy
people—normal weight obese. These people have a “normal” BMI, but also have a
high amount of body fat as compared to their muscle mass. They often carry this
excess body fat around their midsection (central obesity). Recall from the Obesity
chapter that this type of body fat is highly inflammatory and certainly far from
healthy even though their weight is considered “normal.”

GET RID OF YOUR SCALE

Weighing yourself to gauge progress with lifestyle changes is not a scientific way
to measure health benefits. It also creates a source of stress and can become
neurotic. Body weight can fluctuate on a day to day basis, primarily due to shifts in
fluid gain and loss, not body fat loss. We have seen many frustrated and stressed
dieters weighing themselves daily and not understanding how they gained two
pounds overnight. They respond by restricting calories further or crushing
themselves in the gym based solely on what they saw on the scale that morning.

This practice is not good for mental health and contributes to creating an
unhealthy relationship with food and exercise. This is a huge factor in the long-term
failure of dieting and can create the vicious cycle of weight gain, weight loss,
rebound weight gain, and the demoralization that goes with it. The diet industry is
invested in continuing this futile cycle and reinforces the message of “weight loss”
in their advertising. Stop falling victim to obsessive weighing and put your scale out
with the other garbage.

We need another simple but scientifically sound measurement to monitor our

progress that does not focus on the unreliable measurement of body weight. We
want a measurement that correlates well with health. The waist to height ratio is such
a measurement.

THE WAIST TO HEIGHT RATIO (WHR)

The waist to height ratio (WHR) is a simple formula that is easily calculated.

1) Measure the circumference of your waist at the level of the umbilicus (belly
button). You can use inches or centimeters as long as you are consistent when
you measure your height.

2) Measure your height (most of us know this already).

3) Divide your waist measurement by your height measurement. The result is

your waist to height ratio (WHR).

WAIST TO HEIGHT RATIO (WHR)

EXAMPLE CALCULATION
RecUsing one of the author ’s (Chris) measurements, the WHR is
calculated as follows:
• Chris’s waist measurement (circumference) at the level of the umbilicus
(belly button) is 32 inches.
• Chris’s height is 69 inches (5 feet 9 inches).
• To find the WHR, we divide 32 by 69.
• 32/69= 0.46
 Chris’s waist to height ratio (WHR) is 0.46

We want to keep our WHR below 0.5 for optimum health and to avoid
chronic diseases.
WHRs above 0.5 have been correlated with the following diseases:

• Diabetes
• High blood pressure
• Heart disease
• High triglycerides from metabolic syndrome

These are the same diseases associated with the chronic inflammation and
oxidative stress from obesity.

KEY POINT:
Keep your waist to height ratio (WHR) below 0.5 to prevent development
of chronic diseases such as diabetes, heart disease, and high blood
pressure.

It is important to note that many people at risk for these diseases may be
classified as healthy if we used the weight-based BMI for screening. The
“normal weight obese” person would be classified as healthy by the BMI,
but would be correctly identified as unhealthy by the WHR. Using only the
BMI would miss people at risk for the above diseases.

Most of us strive for a healthy, lean physical appearance—even if we are not

particularly concerned about our health. Most people would not approach a
prospective mate and say, “Sure you look really fit, but I will have to pick you up to
make sure you don’t weigh too much.” This scenario sounds ridiculous but isn’t that
the message we are sending by being preoccupied by weight? A lean, well-muscled
person is healthy and attractive regardless of what the scale shows.

The WHR is the best measure of how healthy you are and how your clothes will
fit. Developing lean muscle mass is also the best prevention from chronic disease
and accelerating aging. Lean mass will increase body weight. Here are a couple of
scenarios to illustrate the advantages of using WHR over scale weight:

SCENARIO 1: JILL
Jill started at 5’6 inches tall, 180 lbs., and had a 38” waist. Jill went on a
calorie restricted crash diet and monitored her weight loss with a scale. At
the end of 4 months her results were:
• Weight dropped from 180 lbs. to 150 lbs. (30 lbs. lost)
• Waist circumference dropped from 38” to 34”.
• BMI dropped from 29 (overweight) to 24.2 (normal).
• WHR dropped from 0.58 to 0.52.

SCENARIO 2: KATHERINE
Katherine started with identical proportions to Jill at 5’6 inches tall, 180
lbs., and a 38” waist. Katherine started lifestyle change using Strong
Medicine tactics. At the end of 4 months her results were:
• Weight dropped from 180 lbs. to 155 lbs. (25 lbs. lost)
• Waist circumference dropped from 38” to 31”
• BMI dropped from 29 (overweight) to 25.0 (overweight).
• WHR dropped from 0.58 to 0.47.

SCENARIO ANALYSIS
If you look just at weight loss, it would seem that Jill’s crash diet was more
effective that Katherine’s Strong Medicine approach. After all, Jill lost 5 more
pounds than Katherine, right? If we followed BMI as a measure of progress, Jill
went from overweight to normal while Katherine was still technically classified as
overweight at the end of 4 months.

If we look beyond weight loss, we see that Jill only lost 4 inches off of her waist
circumference while Katherine dropped 7 inches. Jill finished her 4 months of
dieting with a WHR still above 0.5 and still at risk for chronic disease. Katherine’s
WHR dropped into the healthy range at 0.47. Katherine is also leaner and able to
wear smaller sized clothes than Jill despite less total weight loss. What gives here?
Jill lost more weight so why isn’t she leaner than Katherine?
 Jill went on a calorie restricted crash diet with inadequate food to fuel her activity.
As far as her brain was concerned, her reduced food intake was a threat and the
threat response system was initiated to prevent starvation. High levels of cortisol
from the stress-threat system cannibalized muscle mass to produce glucose to feed
the brain during starvation mode. The high cortisol levels made body fat loss
around her belly very slow. Upon further investigation, it was found that of the 30
pound weight loss, 10 pounds were lost from muscle and only 20 pounds were lost
as fat.

Katherine followed Strong Medicine tactics and fed her activity levels. The
emphasis on food quality helped restore her hunger communication system in her
brain. She spontaneously ate enough calories to fuel her activity without sending a
threat message to the brain, preventing high cortisol levels. She also followed the
Strong Medicine exercise plan and added 5 pounds of muscle in 4 months (while
Jill lost 10 lbs. of muscle starving herself). Further investigation showed that
Katherine lost 30 pounds of fat. Despite losing less overall weight than Jill,
Katherine lost 10 pounds more fat and added muscle mass. Katherine also looks
leaner and more physically fit even though she weighs 5 pounds more than Jill.
She also now wears clothes 2 sizes smaller than Jill.

From these scenarios you can see how following weight (and BMI) can be a poor
measure of progress with lifestyle change and can even lead you astray. The WHR
is a much better measure of improvement both inside your body from a health
perspective, and outside from an aesthetic sense. As you make your journey through
lifestyle change using Strong Medicine tactics, heed the two take-home messages
from this section.
TAKE HOME MESSAGE:
1) Keep your waist circumference less than half of your height.
2) Throw your scale away and replace it with a tape measure!
STUFF YOU CAN MEASURE III
MARKERS OF INFLAMMATION

Long-term low level inflammation and oxidative stress are the underlying causes
of preventable chronic diseases as we have discussed throughout this book.

C-REACTIVE PROTEIN (CRP)

Laboratory tests to reliably measure chronic oxidative stress are not readily
available in the clinic setting at this time, but there is a good marker for chronic
inflammation. This “marker of inflammation” is called C-reactive Protein (CRP).

CRP is a protein produced by the liver in response to inflammation. Doctors

classify CRP within a group of proteins called acute phase reactants. The acute
phase reactant proteins are produced during periods of high levels of inflammation
as part of a defense response to stresses such as injury—especially invading
bacteria.
 Recall from Basic Training that immune cells produce chemicals called cytokines
to carry the inflammatory message throughout the body to stimulate wound healing
after an injury, or to repel the attack of foreign bacteria. When the liver detects
cytokines produced by immune cells, it starts making acute phase reactants such as
C-reactive protein to aid in defense of the body.

TECHNICAL NOTE:
There are many potential markers of inflammation that are currently
being studied for use as predictors of risk of chronic inflammatory
diseases such as heart disease and diabetes. CRP has been shown to be the
most predictive and the only one we recommend following to track your
progress if you are engaged in lifestyle change to treat or prevent
diabetes, obesity, or heart disease.

Modern medicine has used the fact that CRP levels are elevated during
inflammation, and physicians can routinely measure it with blood tests. In the clinic,
CRP can be used to help differentiate bacterial and viral infections. We will use CRP
to help identify the low level chronic inflammation that is a risk factor for
numerous preventable diseases. Indeed, CRP has been shown to be highly predictive
as a marker for the development of diabetes and heart disease, and CRP is
consistently elevated in obesity.

KEY POINT:
Elevated CRP is highly predictive for developing type II diabetes and heart
disease. CRP is also elevated in obesity.

CRP AND RISK OF HEART DISEASE

 Elevated C-reactive protein has been found to be a better predictor of
developing heart disease in the future than LDL cholesterol levels or high
blood pressure.

The National Academy of Clinical Biochemistry Laboratory Medicine

recently found that CRP was the only biomarker that met criteria for use in
the prevention of heart disease.

HIGH SENSITIVITY C-REACTIVE

PROTEIN (HSCRP)
When CRP was first used as a laboratory test for inflammation, the technology to
measure low levels of CRP was not available. Since chronic inflammation is usually
present at very low levels, we needed to develop testing that could accurately
measure low levels of CRP. This was accomplished with the development of the
high sensitivity C-reactive protein (hsCRP) test. Now we are able to measure the
very low levels of CRP that accompany chronic inflammation.

Each member of the Pentaverate produces low level chronic inflammation, so it is

no surprise that elevated levels of hsCRP have been found with each one.
CRP IS NON-SPECIFIC
The often cited “drawback” of using hsCRP is that it is a nonspecific marker for
inflammation. That means that it can be elevated by anything that increases the
inflammatory response by the immune system. The test may not be useful for
doctors trying to diagnose a specific disease. For the Strong Medicine trainee using
hsCRP to monitor progress in reducing the sources of chronic inflammation
leading to preventable disease, the non-specificity of hsCRP is a strength.

Circadian disruption, chronic stress, obesity, gut inflammation, and inactivity all
produce low levels of inflammation and will elevate hsCRP.

The nonspecific nature of hsCRP elevation from any source of low level
inflammation means we can follow hsCRP levels as a marker of progress as we
attack each member of the Pentaverate.

KEY POINT:
The nonspecific nature of hsCRP elevation with any source of low level
inflammation means we can follow hsCRP levels as a marker of progress
as we attack each member of the Pentaverate.

WHAT IS A GOOD LEVEL OF HSCRP?

Most of the research with hsCRP has studied the correlation of hsCRP levels with
the risk of heart disease. These levels are shown in the table below:

hsCRP level Risk for Heart Disease

Less than 1.0 mg/L LOW
1.0 to 3.0 mg/L INTERMEDIATE
Greater than 3.0 mg/L HIGH
The Strong Medicine trainee’s goal is to keep hsCRP below 1.0 mg/L.
 KEY POINT:
The goal is to keep hsCRP levels below 1.0 mg/L as you are tracking your
progress in the battle against the Pentaverate.

TECHNICAL NOTE:
Increased hsCRP above 1.0 mg/L will also increase risk for developing
other preventable chronic diseases such as diabetes, high blood pressure,
and cancer but the actual correlated levels of hsCRP and risk for these
diseases are not as well characterized as it is for heart disease.

QUICK MEDICAL NOTE:

Since CRP is a non-specific marker for inflammation, people with
inflammatory diseases such as rheumatoid arthritis or active cancer will
have elevated CRP far above the normal levels.

Active infections or injury will also cause very high levels of CRP. If any
of these situations applies to you, measurement of hsCRP to monitor risk
for chronic diseases will not be useful.

High sensitivity C-reactive protein can be a useful part of the “Stuff You Can
Measure” to monitor your progress in your personal battle to prevent chronic
disease.

• Correcting circadian disruption and getting regenerative sleep will lower

 hsCRP levels.

• Controlling chronic stress with brain training will diminish your hsCRP.

• Reducing body fat and insulin resistance through the 8-step program will
minimize hsCRP levels.

• Stopping gut inflammation will bring down high hsCRP.

• Exercise crushes inactivity-induced inflammation and brings down hsCRP

levels as well.

As part of your Strong Medicine battle plan, work with your doctor to get a
hsCRP blood test (along with a lipid panel) at your regular preventive checkup.
STUFF YOU CAN MEASURE IV
HEART RATE VARIABILITY

If you had to pick just one single biomarker of health to measure, heart rate
variability (HRV) would be the one. HRV is your “desert island” biomarker.

In our opinion, HRV deserves this exalted status because it is the best window to
view the day to day status of your stress cup.

REVIEW OF HEART RATE VARIABILITY

(HRV)
 We discussed HRV briefly in the Chronic Stress chapter along with the subject of
biofeedback. HRV in simplistic terms is the natural variation of the length of time
between each heartbeat. Heart rate is controlled by the two branches of the
autonomic nervous system (ANS), specifically the sympathetic “flight or fight”
nervous system (SNS), and the parasympathetic “rest and digest” nervous system
(PNS). Go back and review your Basic Training on the Stress-Threat system if you
need a refresher on this topic.

The “flight or fight” sympathetic nervous system (SNS) causes the heart rate to
speed up in response to any threat. It also causes the heart to beat with a machine-like
regularity, with minimal variation of the time between each heartbeat.

The SNS (flight or fight) causes heart rate to increase, and for the heart to beat with
precise regularity—very little variation in time between each heartbeat. This
regularity is shown by the nearly identical lengths of the red arrows above. These
arrows show that the time between each heartbeat is the same. This is called LOW
heart rate variability (Low HRV).

When the “flight or fight” SNS is dominant, heart rate variability (HRV) is LOW.
There are no health consequences to having periodic SNS dominance, such as while
actively exercising or responding to an emergency. The health consequences show
themselves when the SNS remains dominant most of the time due to chronic stress
and diseases.

The “rest and digest” parasympathetic nervous system (PNS) slows down the
heart after a threat has passed. For most of the time, the PNS should be the active
system controlling how the heart beats. A healthy heart controlled by a relaxed (PNS
dominant) nervous system shows differing times between each heartbeat.

The PNS (rest and digest) causes the heart rate to decrease after the threat has passed
(or exercise is completed) and for the heart to beat with a variation of time between
each heartbeat. This variation is shown by the different lengths of the green arrows
above. These arrows show the time between each heart beat is different, with arrows
having darker shades of green correlating with increased time between heart beats
and lighter green arrows for shorter times between beats. This variation in time
between beats is called HIGH heart rate variability (High HRV).

HRV AS A WINDOW INTO YOUR “STRESS

CUP”
Chronic stress, poor fitness, poor sleep, and a broken metabolism are all sensed
as “threats” by the brain. In response to these daily threats, the “flight or fight”
sympathetic nervous system is always on. The low level of “flight or flight” in
which many of us live our daily lives causes chronic inflammation and oxidative
stress. The always-on “flight or fight” system overfills our stress cup on a daily
basis leaving the brain and body fighting a losing battle to adapt.

Measuring heart rate variability (HRV) lets us see the current state of our
autonomic nervous system—is it dominated by the “flight or fight” SNS, or by the
“rest and digest” PNS? For optimum health, we want PNS dominance most of the
time.

Most of the Strong Medicine defensive tactics in this book have the
ultimate effect of maximizing PNS dominance, and turning down the
level of the “flight or fight” SNS.
We can track our autonomic nervous system status over time as we incorporate
Strong Medicine defensive tactics to measure our progress.

• Low HRV corresponds to dominance of our nervous system by the “flight or

fight” SNS. This is not a good sign. We are moving in the wrong direction for
our health, and low HRV indicates that our “stress cup” has been overflowing.

• High HRV corresponds to dominance by the “rest and digest” PNS. This is the
natural state of the flesh machine and leads to optimum health. High HRV is a
good sign that we are currently within the limits of our “stress cup”.

We used a variation of this idea in the high intensity “burst cardio” protocol when
we measured heart rate recovery after exercise, even though we were not measuring
HRV.

HRV AND HEALTH

Our view that HRV is a window into the “stress cup” is supported by recent
scientific research. Recall from Basic Training that we presented allostasis and
allostatic overload (the state of your “stress cup”) as a way of looking at chronic
disease as a whole. Current research shows that allostatic overload (overflowing the
“stress cup”) has been associated with obesity, diabetes, heart disease, high blood
pressure, anxiety, and depression. The same diseases are also associated with low
HRV.

HRV is emerging as a predictive marker for the development of chronic disease

(and of health).

• Low HRV has been shown to predict the development of high blood pressure.

• Low HRV predicts poor glucose tolerance and insulin resistance seen in
diabetes.

• Low HRV predicts development of heart disease better than most other risk
factors such as high blood pressure and lipid testing.

• High HRV predicts longevity. The longest lived people have the highest HRV
into old age.

• Exercise is the most powerful stimulus to raise HRV (as long as you do not
overfill your “stress cup” by overtraining).

The overarching concept that links low HRV to poor health is chronic activation
of the stress-threat system.
 The stressed-out brain constantly activates the threat system which keeps the
“flight or fight” sympathetic nervous system (SNS) turned on. This creates
dominance of the SNS and reduces HRV. This is why low HRV is associated with so
many diseases, and is present even before the diseases become clinically apparent
(before they can be detected by your doctor). In this way, HRV is the “canary in the
coal mine” for heading down the road to poor health. As you learned in Basic
Training, both external and internal “threats” activate the stress-threat system.

• An internal threat of swollen fat cells in obesity causes inflammation.

Inflammation activates the stress-threat system and lowers HRV.

• An external threat—a stressful work environment—will activate the stress-

threat system, decreasing HRV.

• An internal threat of bacterial infection or injury will lower HRV in the short-
term for these types of threats.

• An external threat of processed food will cause inflammation and oxidative

 stress. The stress-threat system is activated as the free radicals from processed
food overwhelm the ADS “bouncers.” This causes low HRV and predicts the
development of a broken metabolism.

• An internal threat of rumination and worry causing chronic psychological

stress will lower HRV because of the “ramped-up” flight or fight system.

• An external threat of consistent overtraining from “boot camp beat down”

exercise programs is a threat to the body causing reduced HRV.

• Chronic stress is a threat that leads to anxiety and depression. People with
anxiety and depression have low HRV.

• An internal threat of inadequate sleep and disruption of the circadian rhythm is

a huge threat to the brain. It also results in low HRV.

HRV AND CIRCADIAN RHYTHM

HRV follows a natural circadian rhythm with increased HRV during
regeneration mode. This makes sense, as increased HRV is associated with
the dominance of the “rest and digest” parasympathetic system.

An overflowing “stress cup” results in loss of the high HRV during the
night and leads to poor recovery and regeneration. Loss of high HRV at
night also predicts development of diabetes.

You can see why HRV is potentially a very good measurement for assessing the
state of your “stress cup” and overall health. There are some scientists who even
think that measuring HRV should be done in the clinic as part of a preventive
checkup to help predict development of disease. You doctor could potentially use
HRV to measure both physical and psychological wellness, something that blood
tests cannot capture. As a Strong Medicine trainee, you know that the physical and
psychological are one, linked by the mind-body.

MEASURING HEART RATE VARIABILITY

Not so long ago, measuring HRV required specialized equipment costing tens of
thousands of dollars and was beyond the reach of the average person. Now we can
get fairly accurate measurements of HRV with a smart phone and a chest strap heart
rate monitor.
 Calculation of HRV is fairly complex and requires some relatively sophisticated
mathematics. Modern smart phone applications read the heart beat input from the
chest strap and do the calculations for us. The result is a HRV score that is scaled
from 0-100. Higher scores correlate with high HRV.

High HRV scores usually correlate with a healthy state of the nervous system and
low levels indicate activation of the stress-threat system. The higher your HRV
score, the more you are in a parasympathetic nervous system (PNS) dominant state
—a good thing. The lower your HRV score, the more you are dominated by the
“flight or fight” sympathetic nervous system (SNS) which indicates an overflowing
“stress cup”.

FOLLOWING YOUR HRV SCORE

The HRV score is a very individual measure and should not be compared with
scores from other people. But, higher HRV scores are often found in physically fit,
healthy people. The idea is to get a baseline score to evaluate the current state of
your health and fitness, then follow it as you incorporate defensive tactics from the
Strong Medicine program. Your overall HRV scores will slowly improve as you
reduce your stress, get better sleep, clean up your nutrition, lose body fat, and get
regular exercise.

It is important to note that your HRV will fluctuate day to day depending on your
current situation. A night of bad sleep, increased stress, overdoing your exercise, or
a particularly bad couple of days of “dietary indiscretion” will cause your scores to
drop temporarily.

WHEN AND HOW TO MEASURE?

Ideally, HRV measurement should be done at the same time every day and while
attempting to reproduce the same method of measurement as closely as possible. We
prefer to measure HRV immediately after waking in the morning while still in bed.
This way the time of day is the same (and accounts for circadian changes in HRV)
and the body position during measurement is the same. HRV is very sensitive to
changes in your environment. We also like waking measurements because the
various stresses of the upcoming day have not yet affected your body and brain,
giving a measurement that has fewer variables to affect it.

You can use these measurements to make lifestyle decisions—especially

regarding exercise—and avoid overfilling your “stress cup”.

USING HRV TO PLAN ACTIVITY

 To illustrate the use of a daily HRV score, let us construct a hypothetical case.

HRV CASE REVIEW:

Chris is a 44 year old male with no chronic diseases and a relatively high
level of fitness. His HRV scores usually fall in the range of 80 to 85.

He normally exercises three to four times per week and generally gets
good sleep. Chris wakes up after a restless night of sleep due to an upper
respiratory infection. His HRV score (usually in the 80s) is 68 that
morning. His exercise schedule had a planned squat workout that evening.
Chris comes home after work (an unusually stressful work day) and
performs his squat workout with a 10 minute burst cardio protocol
afterwards.

The next morning his HRV is down to 58. He feels exhausted and the upper
respiratory infection is worse.

Chris had a drop in his usual HRV score of at least 12 points after a night of bad
sleep due to an illness. Instead of modifying his workout plan, he continued with his
planned workout of squats and a burst protocol that put a high amount of stress on
his body. This caused an already mostly full “stress cup” (from poor sleep and
illness) to overflow. We saw the results of Chris not heeding his falling HRV score
the next day with a further 10 point drop in HRV. He should have altered his workout
plan that day to be either a rest day, or at most a short walk instead of the taxing
squat workout. He is now at risk for the relatively minor upper respiratory infection
to become much worse due to his immune system becoming suppressed from an
overfilled “stress cup”.

If he would have taken a rest day on the morning of the HRV score of 68, he
would have recovered. Most likely, he would have had a higher score the next day
and been able to do his squat workout without overfilling his “stress cup”.

 GUIDELINES
There are no hard and fast rules for responding to a falling HRV score,
but we do have some suggestions.
• If your score drops 10 points or more, consider taking a rest day from
exercise and add a brain training session.
• If you score drops for two consecutive days, you really need to pay
attention to what could be causing the drop. Sleep is the usual culprit for
this so prioritize getting regenerative sleep that night (using tactics from
the Circadian Disruption chapter) and certainly forget about any heavy
physical training.

Following your HRV can be very powerful for making sure you do not overtrain.
You can also use it to see the impact of various Strong Medicine defensive tactics. If
Chris would have replaced the planned squat workout that day with a 30 minute
session of mindfulness breathing practice, his HRV score the next day would likely
have been back up in the 80-85 range instead of 58 and feeling sick and exhausted.

You can use a falling score as motivation to incorporate an appropriate defensive

tactic that day to bring you back from an overflowing “stress cup”. A dropping HRV
score might motivate you to pay more attention to your sleep that night, clean up
your diet, or engage in some brain training.

HRV EQUIPMENT
As technology advances, there will be more options available to perform daily
HRV monitoring at home. There are currently some good products available. To get
you started, here are two systems we have personally used (we have no financial or
personal relationships with either developer):

• SweetBeat™ by SweetWater Health. This is a smartphone application that is

low priced and is reliable for measuring HRV. It requires a Bluetooth heart rate
 monitor strap such as the Polar® H7. It has other features related to food
sensitivity and weight loss that we have not used or evaluated, so we cannot
comment on these features.

• BioForce HRV. This is a HRV measurement package developed by top MMA

(mixed martial arts) trainer Joel Jamieson. This product is a bit more pricey but
comes with an excellent guide on using HRV with physical training. The
BioForce HRV uses a smartphone application and a Bluetooth heart rate monitor
chest strap. It also has a good website to track your measurements. Chris used this
product for 3 months and found it reliable for tracking HRV and to plan his
training. Special Note: The accompanying manual has extensive technical
information on HRV and allostasis (much to our surprise and pleasure). From
reading the manual, it is obvious that Mr. Jamieson is extremely well versed on
allostasis, allostatic load, and has applied the concepts very well to training
high-end athletes. Highly recommended.

CONCLUSION
HRV measurement truly is a window to the state of your nervous system and your
“stress cup”. This is one of the most powerful and relevant biomarkers in this
Analytics section. We strongly suggest you consider routinely checking your HRV
to keep your “stress cup” from overflowing. Managing your “stress cup” effectively
will have downstream benefits and HRV is currently the best way to keep an eye on
it.

By successfully managing your “stress cup” with HRV, you will likely see the
other three biomarkers in this section improve as well. This is truly your “desert
island” biomarker.

This also marks the end of the Stuff You Can Measure (Analytics) section. Use
these biomarkers appropriately, remembering the difference between correlation
and causation. Also, do not get neurotic when measuring these biomarkers and turn
them into sources of stress.
ANALYTICS “MILITARY INTELLIGENCE”
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DOC’S REFLECTION
Strong Medicine is a reflection of everything I wanted to say when my patients
asked me “What can I do to get healthier?” There were only so many preventative
recommendations I could impart to them in a 30 minute appointment.

The idea for this book started as a series of in-depth informational handouts that I
could give my patients for “homework” reading between office visits on topics such
as nutrition, stress relief, exercise, sleep habits, etc.

I researched the handouts by combing the scientific literature for the latest up-to-
date information that would support my recommendations. After compiling dozens
of handouts, I realized that I had the skeletal framework for a book. The project
took on a life of its own, growing far beyond the original scope.

Originally projected to take a month or so, this small project became a two year
obsession that eventually became Strong Medicine. It spanned life events such as
leaving the military, finding a new job, and relocating to a new state.

This book was truly a labor of love fueled by a passion for science, medicine,
and the need to contribute something meaningful to public health. I have always
been frustrated when hearing flawed recommendations for health promotion and
prevention that lacked any scientific foundation. I found myself ranting about this
fact with increasing frequency.

Strong Medicine was cathartic for me. I finally put my own cards on the table and
did something instead of continuing to complain about the inadequacies of
conventional recommendations for disease prevention. Through Strong Medicine, I
offer solutions instead of complaints and criticisms.

So many of our friends and family members are afflicted by chronic preventable
disease and desperately want effective solutions that they can implement. We live in
the information age, and in the face of so much conflicting information it is difficult
to find the needle in the proverbial haystack. My hope is for this book to give people
the foundational knowledge to sift through the haystack of misinformation and find
their “needle.”

After reading countless scientific research articles on seemingly disparate

subjects, I felt the best course of action was to start with the basic processes that are
the sources of chronic disease and build a prescriptive framework around them.
 Looking at the proposed mechanisms, it became obvious that sleep, nutrition,
physical activity (or a lack thereof), stress, and obesity all contributed to a variety of
chronic diseases. There was an underreported, underlying commonality that linked
these maladies.

Chronic inflammation and oxidative stress were the underlying mechanisms that
tied together the many causes of chronic disease. Allostatic overload, the “Stress
Cup,” was the overarching concept that showed how chronic stress, gut
inflammation, circadian disruption, obesity, and inactivity all join hands to promote
long-term inflammation and oxidative stress, the precursors to chronic disease.

The irony of writing a book on wellness, while working at a full time medical
practice, was that I consistently overflowed my own stress cup. I was more stressed
and sick than I had ever been in my life! I certainly was a case study and proof of
concept of allostatic overload! Hypocrisy abounded for two years while writing this
book as I gave advice to my patients on stress relief while being the perfect
illustration of the overflowing stress cup. I am sure I lost several layers off my
telomeres. After the book was complete, my road back to health put into play the
concepts outlined in this book: “Physician Heal Thyself!”

The goal of Strong Medicine was to explain difficult concepts of human

biochemistry, physiology, and pathology in a way the lay-person could
comprehend. These interlinking, interrelated concepts would create a foundation of
knowledge that could empower normal people to make beneficial lifestyle
decisions.

I wanted to demystify chronic disease by opening the “black box” of the flesh
machine for all to see. One goal was to help people understand the effects of their
lifestyle choices and the scientific foundations for our prevention recommendations.
 I continue to hold strongly to the notion that when people understand and can
visualize what is going on inside the body and brain as a result their lifestyle
decisions, it becomes easier to become motivated and implement sustainable
change. Ignorance is truly bliss, and once the veil of the unknown and unseeable is
lifted by knowledge, your bad habits become harder to ignore. When bad habits are
transformed into good habits, the resulting positive impact on the body creates
enthusiastic momentum.

The military theme of this book was comfortable to me since I spent thirteen
years of my life serving our country in the military—in both the Army and Navy.
More importantly, I used the military theme to portray the true peril of our current
public health crises. If you do not believe we are in a war against preventable
disease, you are choosing to live with your head in the sand.

Is it not shocking that reliable prognosticators indicate that the current generation
will be the first in modern history projected to live shorter lives than their parents
or grandparents?

Why is this? What has bought about this horrific situation and is it preventable?
Optimum health is difficult and near impossible to attain while existing in our
modern environment. To acquire optimal health requires knowledge, diligence,
planning and methodical application.

We no longer live in the pristine environments of our distant ancestors, but can
certainly learn a lot from them. They “exercised” intensely, got lots of cardio and
ate pure, natural food. That template works in our present time quite nicely.
However modern problems require modern solutions.

We need to jettison dogmatic and unyielding paradigms—is it impolite to note

that they don’t work? Strong Medicine seeks to approach the battle against chronic
disease and the search for optimal health with a combination of the wisdom and
practices of our ancestors and advances of modern science.

Strong Medicine will empower those that truly are motivated. If you have the
motivation, we have shown you the game plan. If you have had enough and are “sick
and tired of being sick and tired” then put into play the very real and very concrete
steps we outlined. We told you why something is the way it is, then related how to
improve it. Every one of us can achieve our health goals, but there are no shortcuts.

COACH’S CONCLUSIONS
 What is the “take away” message of this book? Self-empowerment.

There is really should be no more confusion on your part regarding what you
need to do to renovate your body and your life. You have a transformational
roadmap. You supply the requisite mental motivation and disciplined application of
our battle-tested methodology. It works every single time it is enacted fully and
completely.

Our systematic and appropriate strategies for exercise and nutrition are not the
ever popular, one-size-fits-all mainstream health and fitness strategies. Our
strategies are elite athlete practices, diluted and made user-friendly, pared down
without losing the core essence that makes them effective.

You can now create customized training templates that fit your lifestyle and time
constraints. We have made provisions for the out-of-shape to gradually adapt to our
fitness practices and procedures. Unlike the Sergeant Fury boot camp types, we
don’t throw you into the proverbial deep end of the fitness pool in the first minute
of your first session. We teach you how to swim first.

We have established parallel strategies in related disciplines. By enacting these

strategies simultaneously, we have engineered a physical transformation and
psychological recalibration. Someone undergoing a profound physical
transformation also undergoes a profound psychological transformation.

Oscar Wilde once noted, “Perception is everything.” He was right about

everything and this observation about how we see ourselves and our surroundings
is no exception. While a negative self-perception is a psychic boat anchor hung
around one’s neck, convert that negative perception into a positive perception—
complete with some very real detoxification and high intensity, endorphin-releasing
exercise—and a man or woman is reborn physically and psychologically.

I have facilitated hundreds of dramatic physical transformations, and one of the

defining characteristics of true transformation is self redefinition. We enable people
to reinvent themselves. Camille Paglia once described bodybuilding (the
combination of nutrition and exercise to reengineer and reconfigure the human
body) as “a struggle against nature.” Indeed, rather than be swept away by life and
force of habit, the individual can seize control of their life. They can fight against
“inevitability” and the idea of settling for whatever life hands them. We are either
compliant with our seemingly preordained fate or we fight.

We who choose to embrace the fight understand that life itself is a struggle and
embrace it. Compliant living is mere existing. We want more—we want to improve
our quality of life by methodically engaging in our parallel disciplines. Over time
our practices will transform us, and we will attain and maintain vibrant muscular
health and virility.

We subscribe to old school methods, rooted in intensity, sweat, and common

sense. We believe in the idea of doing fewer things better; we will detoxify
ourselves by practicing power nutrition and gourmet organic eating. Using
powerhouse nutrients, we can expertly prepare meals we look forward to eating. We
combine power nutrition with power training.

Everything you need to engineer your very own radical physical transformation
is contained within the two covers of this transformation manual. This book is
meant to be a workbook—so put our ideas into play and breathe life into the
strategies we have shared with you. Try to avoid the cafeteria syndrome of cherry-
picking our methodology. Avoid the temptation to only embrace the aspects of our
system that appeal to your preconceptions and prejudices. Don’t reject parts of this
holistic system that you deem unpleasant, stupid or ill-informed.

Our strategies are purposefully interrelated. Break them apart and the results will
be substandard. There is a tangible physical synergy when all the aspects are
practiced systematically and simultaneously. If you come to love this vibrant way of
living, then transformation is no longer a question of “if” but “when.”
ABOUT THE AUTHORS

CHRISTOPHER G. HARDY, D.O., MPH, CSCS

Dr. Chris Hardy is emerging as a leader in public health, merging his expertise in
nutrition, strength and conditioning, and in clinical and preventive medicine into a
comprehensive approach to treat chronic disease.

Dr. Hardy has a diverse background, including 13 years active military service in
both the U.S. Army and U.S. Navy. He is a previous graduate of the Naval Diving
and Salvage Training Center and Underwater Construction Basic Course, going on
to serve as a military deep sea diver. He left the military the first time after four
years of service to start his higher education.

Dr. Hardy is a graduate of Old Dominion University, earning a bachelor of

science in biochemistry. He went on to medical school at WVSOM in Lewisburg
WV, graduating as a Doctor of Osteopathic Medicine.

After medical school and internship, Dr. Hardy reentered the military as a Navy
physician, serving aboard the USS WASP (LHD-1) as medical officer and joining
the ship on deployment in support of Operation Enduring Freedom. He then served
another operational tour as a medical officer before attending Johns Hopkins
University for medical specialty training.

Dr. Hardy completed his specialty training in Occupational and Environmental

Medicine at the Johns Hopkins School of Public Health where he served as Chief
Resident, also earning a Master of Public Health degree with a concentration in
toxicology.
 Dr. Hardy is Board Certified in Occupational and Environmental Medicine under
the American College of Preventive Medicine. He has also completed formal
training in medical acupuncture and is a Certified Strength and Conditioning
Specialist by the NSCA. He is currently enrolled in the Fellowship in Integrative
Medicine at the University of Arizona.

Chris lives in Everett Washington and is passionate about guitars, mountain

biking, and health and wellness. He is still active as a trainer and gives nutrition
lectures around the local community. He is married to his talented wife Carrie, a
former biochemist and current student in Naturopathic Medicine at Bastyr
University. His daughter Anna is a graduate student in Geophysics at Virginia Tech
University.
ABOUT THE AUTHORS
MARTY GALLAGHER
Marty Gallagher has been involved in high-level athletics for over 50 years. He
captured his first national title and set his first national records as a 17-year old
teenage Olympic weightlifter in 1967. In May of 2013 he set his most recent national
records as a 64-year old powerlifter. He won the 1992 IPF world masters
powerlifting title and has taken silver and bronze medals in world championships.
He is a six-time national champion masters powerlifter.

As a coach he guided Team USA to the IPF world team title in 1991 and coached
Black’s gym to five national powerlifting team titles. He was mentored by the 1st
world powerlifting champion Hugh “Huge” Cassidy and Gallagher in turn
mentored hall-of-fame powerlifting world dominator “Captain” Kirk Karwoski.
Gallagher competition coached Ed “King” Coan, the world’s greatest powerlifter,
along with iron immortals Doug Furnas, Lamar Gant and Mark Chaillet. Marty
works with the military elite spec ops fighters (in this country and abroad) along
with governmental special units within various agencies.

As a writer Gallagher is widely read and considered one of the finest writers
operating within the health, nutrition, bodybuilding, strength and athletic training
genre. He has had over 1,000 articles published since 1978, including 232 weekly
‘ask the expert’ fitness columns for the Washington Post.com and 89 articles
published during a ten year relationship with Muscle & Fitness and Flex magazine.
Gallagher ’s biographic on Ed Coan was called, “the greatest powerlifting book ever
written,” by the late Joe Weider. Rock star Henry Rollins called the Coan book,
“Awesome!” Dr. Jeff Everson described Gallagher ’s Magnus opus, The Purposeful
Primitive “A literary masterpiece.” Gallagher lives in rural Pennsylvania.
ACKNOWLEDGEMENTS
FROM CHRIS HARDY

Attempting to give the appropriate appreciation to those who directly and

indirectly supported this project is daunting. I have been fortunate to have incredible
family members, friends, colleagues, and teachers over the years and will certainly
have missed some who deserved to be mentioned.

Thanks to John Du Cane, Derek Brigham and the Dragon Door team for making
this book a reality.

From the strength and conditioning world, my thanks go to: Dan Cenidoza, Chuck
Miller, Mike Krivka, Lauren Bunney, Donna Pierce, Susan Simpson, Sandor
Sommer, and Rob Miller.

Thanks to my colleagues: Steve English, M.D., Don Berry, D.C., Maegan Knutson,
N.D., Kim Broom, M.D., Dianna Chamblin, M.D., Gail English, M.D., Fran Read,
M.D., Jiho Bryson, M.D. MPH, Bob Handel, M.D., Marti Bradley, R.N., Kathy
Schram, R.N., Gavin Gordon, M.D., Joe Divita, M.D., Brad Olson, M.D., Chris
Hoernig, R.N., Jenny Tinch, M.D. MPH, Erin Duffy, M.D. MPH, Bob Klem, M.D.,
Colleen Clark, John Trueblood, PA-C, Mike Puckett, CIH, Carolyn Ramos, R.N.,
Osama Boulos, Phd., Carole Stonnell, and Stephanie Cramer.

Thanks to my teachers over the years whom provided friendship, mentorship and
an excellent education. The three that deserve special mention are Mark Elliott, Phd.,
Craig Thorne, M.D. MPH, and Virginia Weaver, M.D. MPH.

Thanks to my military ship-mates: Rory Miller, Sean Pearson, Ken Richards, Walt
East, John Broom, Rob White, and Ryan De La Cruz.

A very special thanks to my family and surrogate family: Marty and Stacy
Gallagher, Brian and Gina Knoll and the rest of the Knoll family, the entire Randall
and Thomas clan, Dennis and Karen Polli, Joe and Charlotte Coddington, Riddhi
and Eric Blow, and especially to Cathy Hardy (greatest Mom on Earth), Jason and
Reagan Hardy for all the love and support.

Finally, there is not enough gratitude that can be expressed to Anna Hardy for
being a constant inspiration and a wonderful daughter. To my best friend, colleague,
and incredibly talented wife Carrie, you were with me every step of the way. Strong
Medicine would not exist without your love and support.
ACKNOWLEDGEMENTS
FROM MARTY GALLAGHER

I wish to acknowledge two people: Chris Hardy and my wife Stacy.

When Chris first proposed that we do a “public health” book, I was dubious – but
curious. I was a huge fan of Chris and his amazing life story; I knew of him and
about him before I met him and came to consider him a friend and confidant long
before our book collaboration began. We had so many mutual interests past the
strength, power, physical transformation-genre that initially drew us together. He
was the Navy’s top medical man at Johns Hopkins and our Baltimore friend Sandy
Sommer introduced us.

Our mutual interests were many; Chris was a musician working in the jazz/fusion
realm and a scientist and a medical doctor. In his short life had been in both the
army and the navy and recently completed a thirteen-year military career. He had
life experience galore and was drawn to hardcore resistance training. We both had a
fondness for Weston A. Price, Krishnamurti, the Mahavishnu Orchestra and Trailer
Park Boys. So you can see why he and I hit it off immediately. He loved gourmet
organic food and we consumed much together while continuing our ongoing
conversation about bringing elite training and nutrition methods to the general
public.

I work with the elite and he works with the afflicted. I shared my idea that
“detuned” and “diluted” elite methods are what is needed by the general public.
Obviously, the methods of the elite work. The misconception has been that these
elite methods are too harsh, too demanding and beyond the reach of ‘regular folk.’
Instead, the fitness mainstream teaches John Q. and Mary J. all about “moderate” and
“sensible” fitness strategies. These mild methods don’t do a damned thing. They
ever have and they never will; softball methods never work on account of
insufficient intensity. Without herculean effort, there is no compelling reason for the
body to favorably reconfigure itself.

True, the elite methods need be defanged and declawed before being handed over
to innocent civilians. Chris understood this. We had initial talks on how to construct
user-friendly (for normal people) yet effective transformative training and
nutritional protocols. This book is an outgrowth of our weird synergy. We had both
arrived at the same eventual and identical conclusion to two entirely different
questions: he sought to rehab the damaged, I sought ways to make the best better.

This book reveals the totality and breadth of Chris’ cinematic vision. While I
might claim to be an inch wide and a mile deep, Chris is truly a mile wide and a
mile deep. I am proud to be associated with bringing his Chekov-like vision of a
better healthier world to fruition.

I also want to acknowledge the herculean contribution of my wife, Mrs. Stacy

O’Neal Gallagher, my Amazon, Spartan, tomboy, farm girl, horse whisperer, man
whisperer, girlfriend. Stacy put up with my ever-increasing hermetic eccentricities
and mood swings. By the end of the book writing process, I was, according to her,
“One bus stop away from morphing into the Unibomber, living alone in the woods,
mailings bombs to enemies.” Thank you Stacy Girl for your humor, patience and
wild exuberance….

Gallop your horse

Down the edge of the sword,
Hide in the middle of the flame.
17th century Zen poem obviously written for Stacy
 INDEX

Note: Entries in this index, carried over verbatim from the print edition of this title,
are unlikely to correspond to the pagination of any given e-book reader. However,
entries in this index, and other terms, are easily located by using the search feature
of your e-book reader.

A
AA. See Arachidonic acid
Abdominal muscles, 413
Abdominal obesity. See Visceral obesity
Abdominal training, 419
and anti-rotation, 416
basic plank , 414
high plank , 415
one hand plank , 416
plank row, 417–418
sit-ups
as low back “poison,” 413
problems caused by, 412–413
variations, 412
Accelerated aging. See also Premature aging and chronic stress
and AGEs, 244
chronic stress, 285
and exercise, 362
obesity and chronic insulin
resistance, 197–198
and processed food, 246
sleep problems, 334
ACTH. See Adrenocorticotropic hormone
Actin and myosin, 62
AD. See Alzheimer’s disease
Adaptive immune system, 8–9, 128
Adaptive response
and oxidative stress, 23–24
triggering, 24
Adenosine, in brain, 325
Adenosine triphosphate, 325, 326
as energy currency, 98
production of, 104
Adipocytes. See Fat cells Adiponectin
functions of, 176
production and inflammatory
cytok ines, 182
release, 209
Adrenal glands, 35
Adrenalin, 33
Adrenocorticotropic hormone, 143
ADS. See Antioxidant defense system
Advanced glycation end-products, 201
“dock ” with RAGE, 244
and elevated sugar levels, 244
in food, 245
formation of, 244
inflammation and oxidative
stress by, 101, 244, 246–247
Aerobic exercise recommendation, 249–250
AGE. See Advanced glycation end-products
Age and protein intak e, link between, 65–66
ALA. See Alpha linolenic acid
Alcohol consumption and fatty liver disease, 58
Algae, 83–84
Allergies, 91
Allium sativum, 462
Allostasis, 12, 206
definition of, 39
endorphin release, 40
 vs. hormesis, 40
responses in environmental stress, 40
Allostatic load, 206
harmful effects of, 41–42, 45
measuring mark ers of, 43
and obesity, 179
Allostatic overload. See Allostatic load
Alpha linolenic acid, 80, 89–90, 459
Alzheimer’s disease, 202, 353
Amber-tinted glasses, 350
Amino acids
essential, 63
side groups of
chemical properties of, 61
non-polar, 61
polar, 62
structure of, 60
Amygdala, 275, 277, 278
Anaerobic glycolysis, 103–104
Animal-based foods, 63
and AGE formation, 245
nutrient density of, 64
Animal Factory, 456
Animal foods, fat in, 455
ANS. See Autonomic nervous system
Antibiotics
and dysbiosis, 155–157
from environmental sources, 157
IBD risk with, 156
Antibodies, 9
Antigens, adaptive immune response to, 8–9
Anti-inflammatory response, 9
Anti-nutrients, 160
Antioxidant defense system, 338
and free radicals, balance
between, 11–13
functions of, 10
plant-based foods, 236
Antioxidant supplements, 23
Anti-rotation and abdominal training, 416
Apolipoprotein, 515
Arachidonic acid, 86
Aromatase, 195
Assisted squat
doorway/pole squat, 381
shortened rep-strok e squat, 380
towel or rope squat, 381–382
Asthma, 91
Astrocytes, 141
Atheroma, 523, 524
ATP. See Adenosine triphosphate Auto-antibodies, 163
Autoimmune disease, 129
chronic stress, 285
genetically predisposed to, 132
sleep problems, 334
Autoimmunity
definition of, 9, 128
factor required for, 129
in tissue types, 128
Autonomic nervous system
functions of, 33
parts of
enteric nervous system, 34
parasympathetic nervous system, 33
sympathetic nervous system, 33
Autoxidation, 79
Axons, neighboring nerve cells, 269
Axon transmitter, synapse of, 270

B
Bagels, metabolic response to
glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
Basic cardio “ramp-up,” 420–422
Basic plank abdominal training, 414
Basic training, foundations of, 2
B-cells, 8, 128
BDNF. See Brain derived neurotrophic factor
Bedroom environment, 350
Beef pot roast, 487
Belly breathing, 297
Bench press technique, 396
dumbbell, 397
advancing, 401
overhead, 402–404
“pause-relax-and-grind”
style, 398–400
physiological benefits of, 401
Beta-cell failure, 189
Biofeedback technique, for stress
reduction, 301–303
HeartM ath, 303
heart rate variability, 302
monitoring muscle tension and sk in conductance, 302
muscle tension, 302
real-time information, 302
BioForce HRV, 554
Biological vs. chronological age, 198
Biomark ers
cholesterol, 509–534
correlations with health and disease, 504–508
as engine warning lights, 506
heart rate variability and, 546–553
of inflammation, 541–545
physical measurements of, 535–545
Blood sugar control, stepwise approach to, 260–261
adequate sleep, 258–259
avoiding HFCS, 242–247
gluten-containing products, avoiding, 229
insulin sensitivity with exercise, 249–258
plant-based foods, 234–241
antioxidant defense with, 236
fermentable fiber content, 235–236
fermentation by gut bacteria, 234
legumes, 237
polyphenol content, 239–240
sulforaphane content, 237–239
and whole wheat, 235
processed seed oils, avoiding, 229–232
omega-6 PU FA, 230
for salad dressing, 231–232
protein consumption, 232–233
starch/glucose tolerance determination, 222–227
stress reduction techniques, 259
Blood sugar level. See also Blood sugar control, stepwise approach to person with normal insulin sensitivity, 224, 225
pharmaceuticals to control, 227
unprocessed whole grains and, 226–227
BLT. See Bright light therapy Blue light signals, brain, 330
BM I. See Body mass index
Body
affects brain, 288
anti-inflammatory/calming effects, 296
composition and gut health, 166
union of mind, 268
Body mass index, 173, 535–536
problem with, 536
weight-focused, 536
Body-scan technique, 299
Bodyweight squat, 372–373
Box deadlift, 384
Brain, 288
axon-dendrite, transmitter-receiver, 271
changing, 268
first principles perspective, 281
survival advantage, 283
chased by bears, 274
as energy and glucose hog, 99–100
epigenetic changes, 285
“fight-or-flight” response, 31
functions of, 30
and gut, 125
hypothalamus, 313, 314
k etones as energy source, 116
and mental health, 285
negativity bias, 282
response to stress, 143
threats, 275
Brain-based threat response system
“fight or flight” system. See “Fight or flight” system primitive and modern threats, 32
Brain derived neurotrophic factor, 303, 304
Brain training, 307
Brain Training Triumvirate, 308
Brain-train mind method, 293
“Brain wasting,” 201
“Branched-chain” amino acids, 62
Breast cancers, 195
Breastfeeding, 147
Breathing belly, 297
exhalation time, 296
 inhalation time, 296
sympathetic nervous system, 295
Bright light therapy, 341
Broccoli sprouts, 237–239
Buddha’s Brain, 300
Buddhist meditation practices, 294
Bug lights, 350
“Burst Cardio” protocol, 428– 429, 432–435
Butyric acid (butyrate), 70, 234

C
Caffeine, 334, 345
Caloric restriction diet, 474–476
Calories calculation, 207
and hunger communication system, 220
Cancer cells, phenomenon of, 193
Cancers
characteristics of, 192–193
chronic stress, 285
dependent on glucose, 193–195
link with obesity and chronic insulin resistance, 192–196
sensitive to estrogen, 195
sleep problems, 334
trigger for, 193, 196
uncontrolled cell growth, 193
Capsaicinoids, 463
Capsicum annum, 463–464
Carbohydrates, 55
fiber, 59
health effects of, 119
misconception about, 119
starches, 57
sugar, 56–57
fructose, 57
glucose, 56–57
sucrose, 58
Carbohydrate tolerance, 465–468
low carb eating, 466–468
LSS eating pattern, 466–468
overview, 465
Cardio training foundation, 420–422
Cardiovascular training, 250, 363, 436, 444
Carrot noodles, 485
Cayenne, 463–464
CCT. See Correlated color temperature
CD. See Clostridium difficile
CDC. See Centers for Disease Control
Celiac disease, 129
Centers for Disease Control
exercise recommendation
“moderate intensity” aerobic, 249–251
“steady-state” exercise, 252
“vigorous intensity,” 251–252
Chain reactions of free radicals, 11
Chin-ups, 405–406
Chipotle butternut squash soup, 480
Cholesterol, 509–534
in artery clogging plaques, 521
building block for bile salts, 512
for cell communication, 511
cell membrane function of, 510
chemical structure of, 510
for developing brain during childhood, 511
dietary, 455
in human breast milk , 512
lipoproteins, 514–517
as molecular building block for hormones, 511–512
standard lipid panel, 529–531
testing of, 524–527
transportation, 517–524
Cholesterol esters, 515
Cholesterol levels, in blood, 513
Chronic disease, 45
Chronic inflammation, 129, 164, 221
causes of, 125
and chronic preventable disease, 14–15
definition of, 9
of gut, 123
sources of, 14
outside “environment,” 15
Chronic intestinal permeability, 130–131, 164
Chronic preventable diseases, 14
Chronic stress and threat response, 32
Chronobiology, 342
Chronological vs. biological age, 198
Chylomicrons, 514
transport of fat and cholesterol, 516
Cinnamomum spp, 463
Cinnamon, 463
Circadian disruption. See Sleep problems, circadian disruption
Circadian rhythm, 312, 500
CLA. See Conjugated linoleic acid Clostridium difficile, 155
Coconut oil, 71, 72, 232
Coffee drink ing
correlation with lung cancer, 505–506
relation to smok ing, 506
Colonocytes, 59
Color additives, 219
Combination antibiotic therapy, 156
Complimentary proteins, 64
Compound multi-joint exercises, 367
Confounders, 51
Conjugated linoleic acid, 95
Conventional vs. organic produce, 461
Cook ing
methods and AGEs, 245
strategy, 49–491, 490–491
Correlated color temperature, 347, 348
Corticotropin releasing hormone, 143
Cortisol, 274
Cortisol receptor resistance, 286, 287
C-reactive protein, 541–542
high sensitivity, 544–545
nonspecific, 544
and risk of heart disease, 542
CRH. See Corticotropin releasing hormone
CRP. See C-reactive protein Culinary consensus, 447–464
deadly meat, 455–456
food quality
demand for, 456
for omnivore, 449–455
for vegetarian, 457–460
herbs and spices, 461–464
cayenne, 463–464
cinnamon, 463
five health-promoting, 464
garlic, 462
ginger, 462
turmeric, 463
local food and, 449
Curcuma longa, 463
Curcumin, 463
Cytok ines, 8, 9, 177–178, 182, 184

D
Dawn simulator, 346
Deadlift, 383
“bodybuilder stiff-leg,” 384
box. See Box deadlift
common flaws in, 393–394
conventional, 384
stiff-leg. See Stiff-leg deadlift
sumo. See Sumo deadlift
tactics, 388
variations, 384
Deep squat, 369, 371
Defensive tactics, 2–3
Dementia, 202
Dendrites, neighboring nerve cells, 269
Depression
and chronic stress, 285
and sleep problems, 334
Descartes, Rene, 267
DGLA. See Dihomogamma linolenic acid
DHA. See Docosahexaenoic acid Diabesity, 180
Diabetes. See also Blood sugar control, stepwise approach to; Type 1 diabetes; Type 2 diabetes
causes of, 53
and chronic stress, 285
and depression, 288
muscle mass maintenance as
defense against, 365
nutrition and exercise, 340
and “prediabetes,” laboratory
tests for
charts, 205
 fasting blood sugar, 203–204
HbA1c test, 203
OGTT, 204
risk for developing, 206
and sleep problems, 334
Diabetics, whole grains for, 226–227
Dietary cholesterol, 455
Dietary sources
arachidonic acid, 86
gamma linolenic acid, 86
linoleic acid, 86
Diets, 21
and epigenetic changes, 18
failure in long-term, 50, 54
Digestion, 222
Digestive tract messengers, 215
and satiety, 214–215
Dihomogamma linolenic acid, 90
DNA
damage by free radicals, 10
discovery of, 16
mutation, 20
Docosahexaenoic acid, 82, 89–90
Dopamine release, 217
Double bonds, 79
Dumbbell bench press technique, 397
advancing, 401
overhead, 402–404
“pause-relax-and-grind” style, 398–400
Dysbiosis causes of antibiotic use, 155–156
LPS levels, 154
processed foods, 152–153
sanitized food supply, 155
definition of, 149–150
dietary source of, 155
diseases and disorders associated with, 151

E
Eastern meditation tactics, 293
E. coli O157:H7, 455
Edison, Thomas, 329
EGCs. See Enteric glial cells Egg scramble, 478
Eicosanoids, 87
Eicosapentaenoic acid, 82, 89–90
Elaidic acid, 93
Elite athletes, 442
Endometrial cancer, 195
Endorphin release and allostasis, 40
Endorphins, 140
Endotoxemia, 154
Endotoxin, 154
Energy drink s, 247–248
Energy generation
from fat catabolism, 105
from glucose catabolism, 103–104
ENS. See Enteric nervous system Enteric glial cells, 141
Enteric nervous system, 34
and brain, similarity between, 141
components of, 141
enteric glial cells, 141
gut-brain axis
stress reduction, 143
two-way communication network , 142
vagus nerve, 142
neurotransmitters, 141
response to stress, 143
as “second brain,” 34
Environment, 18
Environmental challenge. See
Environmental stresses
Environmental signals
changes in epigenome, 20
epigenetic system response to, 17–18
for health, 21
Environmental stresses
adaptations/responses in, 40
adaptations through allostasis in, 40
dosage of, 23
dose of food and exercise, 26–27
and hormetic window, 27
importance of, 22–23
Environmental stressors, 21
Environmental stress sensor, 241
EPA. See Eicosapentaenoic acid Epigenetics, 21, 202, 284
case study, 19
definition of, 16
of fetus, 20
response to environmental signals, 17–18
Epigenome, 20
and environmental stressors, 21
Epinephrine. See Adrenalin
Epithelial cell barrier, 126
Essential amino acids, 63
Essential amino acids deficiency, 457
Essential fatty acids, 80–81
Excess fat, 190–191
Exercise, 21, 24, 351–352. See
also Progressive resistance training
benefits of regular, 351
CDC recommendation for, 249–250
defensive tactics, 363
and epigenetic changes, 18
health benefits of, 361–362
and hormesis, 26–27
and insulin sensitivity, 249–258
HIIT. See High intensity interval training
“moderate intensity” aerobic, 249–251
“steady-state,” 252
“vigorous intensity,” 251–252
reasons for avoiding, 250
recommendations, fundamental flaws in, 48
for reducing obesity and chronic stress, 500
scheduling, 352
sleep enhancing, 352
and “stress cup,” 42–43
timing, 351
Exercise intensity
definition of, 250
and HRmax, 250–252
Exhalation time, 296
Exorphins, 140

F
“Fad diets,” 49
“Fast pathway,” 33
Fast pathway and HPA axis, 35
Fat cells
adiponectin release, 209
definition of, 174
as energy storage facilities, 102, 177
functions of, 174
metamorphosis of, 175, 177–179
bloated adipocyte, 177
cytok ine release, 177–178
obesity-related inflammation, 178–179
Fat loss, stepwise approach to, 260–261
adequate sleep, 258–259
avoiding HFCS, 242–247
gluten-containing products, avoiding, 229
insulin sensitivity with exercise, 249–258
plant-based foods, 234–241
antioxidant defense with, 236
fermentable fiber content, 235–236
fermentation by gut bacteria, 234
legumes, 237
polyphenol content, 239–240
sulforaphane content, 237–239
and whole wheat, 235
processed seed oils, avoiding, 229–232
omega-6 PU FA, 230
for salad dressing, 231–232
protein consumption, 232–233
starch/glucose tolerance determination, 222–227
stress reduction techniques, 259
Fats, 55
in animal foods, 455
break down, 187
burning for energy, 119
functions of, 67
glucagon stimulating burning of, 113
and glucose, balance between use of, 102–103
glucose conversion into, 102
metabolism, 102
as primary energy source, 101
saturated. See Saturated fat (triglyceride) catabolism, 105
Fatty acids
carbon chain double bond
configurations, 92–93
carbon chain of, 69
Fatty liver, 58
Fatty liver disease, 58
Feeding, for training and activity, 470–476
 caloric restriction diet, 474–476
in high intensity interval training, 472–473
low carb diet, 474–476
LSS eating pattern, 475
in non-training days, 470–471
carbohydrates as fermentable fiber, 470
fat intak e from protein sources, 471
25-30 grams of high quality protein, 471
sugary fruit and starchy food intak e, 471
in training days, 471–474
“Feel-good” satisfaction response, 216–217
Fermentable fiber
and gut health, 153
health benefits of, 235
and non-fermentable fiber, 60
in plant-based foods, 235–236
sources of, 235–236
Fermentation, 59
definition of, 157
product of, 158
Fermented foods and probiotics, 157–158
Fetus, epigenetics of, 20
Fiber, 59
health benefits of, 60
in whole wheat, 235
“Fight-or-flight” response, 31, 40
“Fight or flight” system, 297, 338
components of autonomic nervous system. See Autonomic nervous system hypothalamic-pituitary-adrenal axis. See Hypothalamic-pituitary-adrenal axis conditions triggering, 38
decreases activation of, 303
health effects of, 37
sympathetic nervous, 162
yin/yang concept, 36
Fish oil capsules, 90
Flavor additives, 219
Flaxseed, 80
Flesh machine, 314
Foam cells, 523
Foie gras, 58
Food, 53. See also Diets
and exercise, 26–27
and nutrition, 25
Food and Drug Administration, 93
Food label, 86
trans fats, 93
Food processing and gluten-related diseases, 135–136
Food quality
demand for, 456
for omnivore, 449–455
for vegetarian, 457–460
Formula feeding, 147
Free radicals
and ADS, balance between, 11
chain reactions, 11
DNA damage by, 10
“importing,” 13
and premature aging, 197–198
unpaired electron of, 10
and unsaturated fatty acid, 79
Free-weight exercises, 367
Free-weight lifting techniques, 367
“Frozen statue” row, 408–411
Fructose, 57
and AGE, 244
chemical structure of, 56
in energy drink s, 248
in fruit drink s, 248
in fruit juices, 248
in fruits, 242
intak e and fatty liver disease, 58
in soft drink s, 247
“Fruit-flavored” drink s, 247–248
Fruit juices, 248
FSR. See “Frozen statue” row

G
Gamma linolenic acid, 86
Garlic, 462
Gastrointestinal problems, 140
Genes
collections of DNA, 16
definition of, 17
expression and environment, 15
functions of, 16
mutations, 17
“turning off,” 17–18
 “turning on,” 17–18
Genetic variations, 16
Genome, 146
definition of, 17
GH. See Growth hormone Ginger, 462
GLA. See Gamma linolenic acid Gliadins and glutenins, 134
Glucagon
functions of, 111–112
release, 111
stimulating fat burning, 112–113
Gluconeogenesis, 100, 188
Glucoraphanin, 238
Glucose
as brain fuel, 99–100
chemical structure of, 56
connected in chains, 57
conversion into fat, 102
in energy drink s, 248
and fat, balance between use
of, 102–103
in fruit drink s, 248
in fruit juices, 248
and insulin, controlling interaction between, 101
metabolism, 101
anaerobic glycolysis, 103
production of, 188
in soft drink s, 247
tolerance, 222
Glucose meter, 222
Gluten-containing products
health consequences for, 140
Gluten free diet, 124
for type 1 diabetes, 165–166
Gluten-free processed products, 229
Gluten-related diseases
celiac disease, 135
autoimmune and inflammatory disorders IN, 137–138
causes of, 136–137
diagnosis of, 138
microvilli destruction, 139
prevalence of, 136
food processing impact on, 135
gluten sensitivity, 135
and celiac disease, difference between, 139
symptoms of, 139
and metabolic disorders, 136
spectrum of, 135
Good nutrition, 49
Google, 294
Grain-based fibers, 60
Grains
genetic modification of, 136
Gram-negative bacteria, 154
Groupthink , 52–53
Growth hormone
functions of, 116
release during sleep, 116
signals for release of, 115
Gut
bacteria species, 145
and brain, 125
chronic inflammation of, 123, 125
as first barrier, 125
intestinal lumen, 125
nutrient absorption, 125
response to stress, 143
villi, 125
Gut bacteria
and auto-antibodies, 163
beneficial
African children, 155
European children, 155
fiber transformation by, 157
health benefits of, 148
opportunistic pathogens and,
balance between, 148, 150
signaling Treg cells formation, 149
in traditional fermented foods, 157–158
diversity of, 145
and enteric nervous system, 162
imbalance, correcting, 147
in infants, factors influencing, 146–147
influence on hormones, 163
influence on mood and behavior, 161–163
microbiome, 146
restoring “balance” in, 161
and Treg cells, 149
Gut-Brain axis, 307
Gut health
and body composition, 166
and fermentable fiber, 153
Gut immune system, 125
adaptive immune system. See
 Adaptive immune system
as first line of defense, 126–127
innate immune system. See
Innate immune system
members of, 127
stimulation of, 123
T-regulatory cells. See Treg cells
Gut inflammation, 164
and chronic disease, 144
Gut inflammation, triggers for, 133
dysbiosis, 145
gluten
and gluten-related diseases. See Gluten-related diseases prolamin protein, 134
toxic components of, 134
variance among responses to, 135
stress and intestinal permeability, 141–144

H
HDL. See High density lipoprotein HDL/triglyceride ratio, 101
Health
and lacto-fermenting bacteria, 160–161
and muscle mass maintenance, 365–366
Heart and vascular disease risk , 196
Heart disease, chronic stress, 285
HeartM ath, 303
Heart rate variability, 302, 546–554
and circadian rhythm, 550
equipment, 553–554
exercise and, 549
and health, 548–551
high, 547, 548
high/low, 302
low, 547, 548
measurement of, 551–553
for plan activity, 552–553
review of, 546–547
scores, 551–553
stress-threat system and, 550
Heart/vascular disease, sleep problems, 334
Heat (Calor), 7
Heme iron, 459
Herbs and spices, 461–464
cayenne, 463–464
cinnamon, 463
five health-promoting, 464
garlic, 462
ginger, 462
turmeric, 463
High blood pressure, sleep problems, 334
High carbohydrate meals (bagels), metabolic response to
glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
High-density carbohydrate foods and dysbiosis, 152
High density lipoprotein, 516
High-fructose corn syrup, 242 and AGEs, 244
bad press on, 242–243
comparison with table sugar, 243
consumption by average
American, 243
and NAFLD, 58
High intensity interval training, 252–258, 420
benefits of, 253, 425
glucose transporters, 255–256
increased insulin sensitivity, 257–258
muscle glucose storage, 254–255
built-in safety system, 430–431
“Burst Cardio,” 428–429, 432–435
for diabetes and pre-diabetes, 257–258
effectiveness of, 425
effort and high target heart
rates of, 420
example of, 426
with exercise types, 427
feeding for training and activity in, 472–473
and glucose levels, 472–473
and hormetic dose, 427–428
HRmax calculation, 425, 428–429
preparation, 420–421
for short periods of time, 252–253, 424
and stress cup, 427–429
High plank abdominal training, 415
High sensitivity C-reactive protein, 543, 544–545
in chronic disease, 545
level of, 544–545
nonspecific CRP, 544
High temperature cook ing and AGE, 245
HIIT. See High intensity interval training
Hippocampus, 276, 278
 stress, 275
Hormesis, 12, 21, 362
adverse and beneficial effects, 28–29
vs. allostasis, 40
concept of, 25–27
definition of, 23
food and nutrition, 25
graph of, 26, 27
Hormetic zone, 26–28
Hormones
cortisol, 35
epinephrine and norepinephrine, 35
Hormone sensitive lipase, 113
HPA axis. See Hypothalamic-Pituitary-Adrenal axis;
Hypothalamic-pituitary-adrenal axis
HRmax. SeeM aximum heart rate
HRV. See Heart rate variability
HRV score, 552–553
hsCRP. See High sensitivity C-reactive protein
HSL. See Hormone sensitive lipase Human genome, 17
Hunger, 208
Hunger communication system, 209
gut-brain axis and satiety signal
digestive tract signaling messengers, 214–215
protein, 215–216
leptin, 209
communicating with brain, 210
functions of, 210–212
and hypothalamus, 210
in obese people, 211–212
resistance, 211, 213
palatable foods and reward
center, 216–217
and restricting calories, 220
signal to stop eating, 210–213
Hunger drive, 208–209
Hunter-gatherer cultures, 364
Hydrogenation, 94
Hyperextended spine, 393–394
Hyper-lordosis, 393
Hyperplasia, 179
Hypertrophy, 179
Hypothalamic-pituitary-adrenal axis
adrenal glands, 35
diabetics experience chronic
activation, 288
fast pathway, 274
fast pathway and, 35
health effects of, 37
hormones
cortisol, 35, 37
epinephrine and norepinephrine, 35
hypothalamus, 34
pituitary gland, 34
slow pathway, 274
slow pathway and, 35
stop, stress response, 284
stressed-out brain, 280
stress response, 273, 275, 276, 278
sympathetic nervous system’s threat-stress response system, 288
Hypothalamus, 34, 100

I
IBS. See Irritable bowel syndrome Ice cream and cak e, metabolic response to
fat storage, 118–119
insulin release, 118
IEL. See Intraepithelial lymphocytes
IGT test. See Individual glucose tolerance test
Immune system, 8, 13
adaptive. See Adaptive immune system
early development of, 147
inflammatory response, 9
innate. See Innate immune system
Individual glucose tolerance test, 226–227, 465
Inflammation, 6, 285
acute and chronic, 9, 87
acute, basic process of, 8
beneficial effects of, 12–13
benefits of, 12
cardinal signs of, 7–8
insulin sensitivity loss by, 181–183
long-term, 14
and omega-3 PU FA, 87–88
and oxidative stress
by AGE, 101
allostatic overload by, 42
 stimulating threat response, 38
trans fatty acids link ed with, 92–93
primary generator of, 8
short-term increases in, 13–14
Inflammation mark ers, 541–545
C-reactive protein, 541–542
high sensitivity C-reactive protein, 543, 544–545
Inflammatory cytok ines
and insulin receptor, 181–182
oxidative stress triggering, 184
Inflammatory response
by cells, 8
palmitic acid triggering, 76
Inhalation, sympathetic nervous system, 295
Inhalation time, 296
Innate immune system, 8, 127
Insulin
functions of, 107–108
glucose and fat for energy, 103
health effects of, 119
misconception about, 119
Insulin/glucagon ratio, 114
Insulin receptor
resistant, 183
sensitive, 182
short-circuited, 181–182
Insulin resistance, 110, 188
causes of, 187, 222
chronic, consequences of
accelerated aging, 197–198
“brain wasting,” 201
cancer risk , 192–196
excess fat, 190–191
fat break down, 187
gluconeogenesis, 188
heart and vascular disease risk , 196
high insulin levels, 188
high palmitate levels, 190–191
muscle wasting, 189
definition of, 187
inflammation reduction and, 500
from inside, 186
muscle mass maintenance as defense against, 365
Insulin-resistant obese
restricting starchy carbohydrates and sugars in, 228
Insulin sensitivity
and blood sugar levels, 222
of cell, 110
definition of, 109–110
and exercise, 249–258
HIIT. See High intensity interval training “moderate intensity” aerobic, 249–251
“steady-state,” 252
“vigorous intensity,” 251–252
loss by inflammation and oxidative stress, 181–183
Internal timek eeper, 313–319
adrenal gland’s clock , 316
fat clock , 317
gut clock , 317
heart clock , 316
immune clock , 317
k idney clock , 317
liver clock , 316
muscle clock , 317
pancreas clock , 316
Intestinal barrier
as first line of defense, 125–127
Intestinal permeability, 127
and autoimmunity, 129
consequences of, 129–131
short term increases in, 133
Intestinal tract. See Gut Intraepithelial lymphocytes, 139
IP. See Intestinal permeability Iron deficiency, 459–460
Irritable bowel syndrome, 139

K
Ketogenic diets, 201
Ketones, 116
Kidney dysfunction and protein
intak e, 66
Knees
collapsing inward, 379–380
shooting forward, 378–379
Krebs cycle, 104
L
LA, 89–90
Lactic acid, 103
Lacto-fermentation, 158–159
Lacto-fermented fruits and vegetables
anti-inflammatory effects of, 161
health benefits of, 160
Lacto-fermenting bacteria and health, 160–161
LAN. See Light at night Large-buoyant LDL, 517, 519, 520, 522
particles, formation of, 529
Lauric acid (laurate), 71
LBLDL. See Large-buoyant LDL
LDL. See Low density lipoprotein
LDL particle number, 534
LDL receptors, 532–533
LED-generated light, 349
Legume preparation, for toxicity, 458
Legumes, 237
Lifestyle change, 54, 494–502
defensive tactics in, 497–502
neck of Roy Buchanan’s guitar, case study, 494–495
strategic planning, 496–502
Light at night, 331
asleep, 332–333
chronotherapy, 333
circadian disruption, 333–334
exposure, 332
poor sleep, 333
caffeine, 334
space at night, 331
Light pollution, 331
Light squat, 370–371
Linoleic acid, 80, 86, 230
Lipid peroxidation, 79
Lipid peroxide, 79
Lipopolysaccharide, 154
Lipoproteins, 514
chylomicrons, 514
high density, 516
low density, 516
structure of, 515
types of, 514–517
very low density, 516
Liver cancers, 192
Liver metabolism, 100
Local food, 449
Long-chain fatty acids
long chain omega-3 fats, 459
and metabolism, 72
Long-chain saturated fat
palmitic acid, 73
stearic acid, 75
Long-term eating signal, 214
Low carb diet, 466–468, 474–476
Low density lipoprotein, 516
Friedewald equation for, 525
in immune response, 532
large-bouyant, 519
oxidized, 523
particle number, 534
particle size, 527–529
small-dense, 519
transport of fat and cholesterol, 517–519
Low starch/high protein meal, metabolic response to
carbohydrate component, 111
fat burning, 112–113
glucagon release, 111–112
insulin release, 112
Low starch/sugar (LSS) eating pattern, 466–468, 475
LPS. See Lipopolysaccharide

M
M acronutrient ratio, 25
M acronutrients
biochemistry perspective, 55
carbohydrates. See Carbohydrates
fat. See Fat
protein. See Protein
M acrophages, 177, 523
M alnutrition and hormesis, 26–27
M argarine, 94
M ast cells, 143
M aster clock
cortisol levels, 318
hormone levels, 318
in hypothalamus, 319–320
leptin levels, 318
malfunctioning, 335–337
blood sugar, 336
diabetes, 336, 339–340
diabetes, loss of insulin, 337
disrupt sleep, 336
fatty liver disease, 336
heart, 336
heart disease, 337
inflammation, chronic, 337
insulin resistance, 336
poor athletic performance, 337
sleep, 339–340
strok e, 337
melatonin levels, 318
M aximum heart rate, 250–251
definition of, 250
determination of, 250–251, 420–421
M axwell’s Equations, 51
M BSR. See M indfulness-based stress reduction
M CTs. See M edium-chain triglycerides
M edicine, future of, 45
M editation tactics
biofeedback technique, for stress reduction, 301–303
HeartM ath, 303
heart rate variability, 302
monitoring muscle tension and sk in conductance, 302
real-time information, 302
eastern/western high technology, 293–294
exercise, 303–305
interventions, 294
mindfulness practice, 294
body-scan, 299–301
mindful breathing, 295–298
M edium-chain fatty acids lauric acid, 71
and metabolism, 72
M edium-chain triglycerides, 232, 471
M elatonin
benefits, 338
connection, 338–339
gateway hormone for regeneration mode, 321
natural light’s effects, 330
supplementation, 353
temporary use of, 353
M ental challenges, 271
M ental defect, physical brain changes, 285
M ental health and brain changes, 285
M etabolic response to food intak e, 106
high carbohydrate meals (bagels)
glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
ice cream and cak e
fat storage, 118–119
insulin release, 118
low starch/high protein meal
carbohydrate component, 111
fat burning, 112–113
glucagon release, 111–112
insulin release, 112
during sleep
GH release, 115–116
k etone production, 116
liver gluconeogenesis, 116–117
M etabolism, 95
fat, 101–103
gluconeogenesis, 100
glucose, 99–101
lean and athletic youngster, 99
liver, 100
mitochondria, 103
muscle, 101
obese person, 99
M etformin, 188, 227
M ethylmercury (M eHg) in fish, 453–454
M exican chick en with sautéed k ale, 481
M ind, 31
M indfulness-based stress reduction, 300
M indfulness training, 294–301
M ind, union of body, 268
M isinformation, 53
M itochondria
as energy factories, 103
fat catabolism, 105
glucose catabolism, 104
 oxidative stress in, 183, 185–186
M itohormesis, 200
“M oderate intensity” exercise
definition of, 250
HRmax of, 251
M odern and primitive threats, 31–32
“M oist” cook ing methods, 245
M olecular mimicry, 163
M onosaccharide, 56
M onounsaturated fatty acid
characteristics of, 78
chemical bonds, 77
health effects of, 78, 80
liquid at room temperature, 78
oleic acid, 78
Monty Python and the Holy Grail, 506
M other’s womb and epigenetic changes, 20
M U FA. See M onounsaturated fatty acid
M uscle building, dietary signal for, 65
M uscle cannibalism, 100
M uscle mass and strength
retaining, 365–366
“use it or lose it” scenario, 364
M uscle mass maintenance and health, 365–366
M uscles
glucose storage by, 101
primary energy source of, 101
M uscle tension, 301, 302
M uscle wasting, 189
M utations
definition of, 16
of genes, 17
M yelin, 269
M yostatin, 189–190

N
NAFLD. See Non-alcoholic fatty liver disease
National Sleep Foundation, 259, 344
“Nature vs. nurture” environment argument, 20
Negativity bias
brain reacts, 282
first principles perspective, 283
Nerve cells
connections, 271
dendrite receivers, 279
drawing of, 269
glial cells, 268
prefrontal cortex, 279
signal direction, 270
Nervous system and long-term
stress, 286
Neuroplasticity
brain’s ability to physically
change, 268
definition of, 269
Nightshift work , 354
Night-shift work er, 342, 343
Nitrogen balance
concept, 64
positive/negative, 65
Non-alcoholic fatty liver disease, 58, 242
Non-rapid eye movement sleep, 322, 324
light sleep stage, 345
slow wave sleep, 340
Non-training days, feeding in, 470–471
carbohydrates as fermentable fiber, 470
fat intak e from protein sources, 471
25-30 grams of high quality protein, 471
sugary fruit and starchy food intak e, 471
Norepinephrine, 33
Nourishing Traditions, 460
NREM . See Non-rapid eye movement sleep
Nutrient timing around exercise, 468
Nutrition, 48
and food, 25
recommendations
fundamental flaws in, 48, 50
observational results to mak e, 52
Nutrition research and practice, problems with
first principles, 50
groupthink , 52–53
reductionism, 52
 study design, 51

O
Obesity, 170. See also Fat loss, stepwise approach to
causes of, 53
chronic diseases link ed to, 172
and chronic stress, 285
consequences of
accelerated aging, 197–198
“brain wasting,” 201
cancer risk , 192–196
excess fat, 190–191
fat break down, 187
gluconeogenesis, 188
heart and vascular disease risk , 196
high insulin levels, 188
high palmitate levels, 190–191
muscle wasting, 189
definition of, 179
insulin resistance caused by, 181–183
elevated stress levels, 183
short-circuited insulin receptor, 181
prevalence of, 172
reward system of brain in, 217–218
and sleep problems, 334
and stop eating signal, 218
and type 2 diabetes, 180
Obesity-related disease, cost of, 172
Observational data, 51–52
Observational studies, 52
Occupational and Environmental M edicine, 342
OEM . See Occupational and Environmental M edicine Official recommendations, 53
OGTT. See Oral glucose tolerance test
Oily (or fatty) fish, 83
Ok inawan diets, 119
Oleic acid, 93
Omega-3 fatty acids
alpha linolenic acid, 82
docosahexaenoic acid, 82
eicosapentaenoic acid, 82
food sources of, 83–84
health effects of, 82–83
omega-3 and omega-6 conversion pathways, 89–90
and omega-6 fatty acids, balancing, 87–88, 91
structure of, 81
supplementation, 90–91
Omega-6 fatty acids balanced dietary intak e of, 85–86
dihomogamma linolenic acid, 90
food sources of, 85
harmful effects of, 88
health effects of, 85
and omega-3 fatty acids, balancing, 87–88, 91
vs. omega-3 PU FAs, 85
structure of, 84
supplementation, 90–91
Omega-6 PU FA
biologically important, 86
inflammation and oxidative stress by, 230
in vegetable and seed oils, 231
Omega-6 to omega-3 ratio, unbalanced, 91
One hand plank abdominal training, 416
Open-Focus Brain, 299
Opportunistic pathogen, 148
CD overgrowth, 155
overgrowth as threat to body, 162
Oral glucose tolerance test, 223, 225
Organic vs. conventional produce, 461
Osteoporosis, 366
Outdoor “power walk ing,” 421
Overhead dumbbell bench press technique, 402–404
Over-nutrition, 25, 26–27
Overtraining, 26–27
Oxidation reactions, 10
Oxidative stress, 6, 221, 285
and adaptive response, 23–24
and ADS, 10–12
balance between free radicals and ADS, 11
beneficial effects of, 12–13
and chronic preventable disease, 14–15
definition of, 10
delicate balance of, 12–13
importance of, 12
insulin sensitivity loss by, 181–183
long-term, 14
in mitochondria, 183, 185–186
primary generator of, 8
short-term increases in, 13–14
sources of, 14
 outside “environment,” 15
unsaturated fats and, 79
Oxygen free radical. See Reactive oxygen species

P
Pain (Dolor), 7, 8
Palatable foods and reward system, 216–217
Palmitic acid (palmitate), 73, 190
alarm system activated by, 191
obesity and chronic insulin resistance, 190–191
scientific studies on, 76–77
triggering inflammatory response, 76
Pancreas, 188
beta-cell failure in, 189
Paracelsus, 23
Parasympathetic activity, 143 Parasympathetic nervous system, 33, 296
and SNS, interaction between, 35
parasympathetic nervous system
anti-inflammatory actions, 33, 37
“rest and digest” system, 33
Pastured pork chili, 483
Pentaverate, 362, 496–502
PFC. See Prefrontal cortex
PHA. See Phytohemagglutinin
Phospholipids, 515
Photo-oxidation, 79
Physical functionality
of ‘civilized man,’ 365
of tribal, 364
Physically rebuilding, 298
Physical mindfulness, 305
Physical stress and exercise, 361–362
Phytate, 459–460
Phytohemagglutinin, 458
Pituitary gland, 34
Plank row, 417–418
Plant-based chemicals and health
polyphenols, 239–240
sulforaphane, 237–239
Plant-based proteins, 63–64
PNS. See Parasympathetic nervous system
Poison, 23
Polyphenols, 24, 239–240
Polysaccharides, 57
Polyunsaturated fatty acid, 80–81
Preconceptions, 442
Prediabetes
laboratory tests for
charts, 205
fasting blood sugar, 203–204
hemoglobin A1c (HbA1c) test, 203
Oral Glucose Tolerance Test (OGTT), 204
self-monitoring program, 225
Prednisone, 36
Prefrontal cortex, 276, 278
stress, 275
Pregnancy, epigenetic changes during, 20
Premature aging and chronic stress, 197–198, 288–289
Primal correlations, 442–444
Primitive and modern threats, 31–32
Probiotics
definition of, 157
effect on anxiety and mood, 162
and fermented foods, 157–158
Processed foods, 53
and accelerated aging, 246
and AGEs, 245
and dysbiosis, link between, 152–153
omega-6 fatty acids in, 85–86, 88, 90
palatability and reward, 219
processed grain-based carbohydrate foods and dysbiosis, 152–153
Processed seed and vegetable oils, 229
inflammation and oxidative stress with, 229
omega-6 PU FA, 230
omega-6 PU FA content, 230
omega-6 PU FA content of, 231
Progressive resistance training, 366. See also Exercise
for building front torso muscles
bench press. See Bench press
deadlift. See Deadlift
 primer on, 363
result-producing methods of, 367
row. See Row
squat. See Squat
Prolamins, 134
Protein berry break fast shak e, 490
Protein food, quality of, 63–64
Protein intak e
dependence on age and physical activity, 65–66
and k idney dysfunction, 66
reasons for increased, 66
recommendation for minimum daily, 64–65
Proteins, 55
chemical properties, 61
composition of, 60
consumption, “rule of thumb” estimates for, 232–233
formation of, 16
functions of, 17, 62, 232
metabolic effects, 66
and satiety, 215–216
structure of, 61
Pseudomembranous colitis, 155
Psychological stress, chronic, 265
Psychological stress duration and intensity, 271
PU FA. See Polyunsaturated fatty acid
Pulled pork wraps with mango
J alapeño relish, 488
Pulling exercises, 405
Pull-ups, 405

R
RAGE. See Receptor for advanced glycation end-products
Randle Cycle, 102
Rapid eye-movement sleep, 323, 324, 325
Reactive hypoglycemia, 109
Reactive oxygen species
definition of, 10
formation of, 10
Receptor for advanced glycation end-products, 244
Recipes, 477
beef pot roast, 487
carrot noodles, 485
chipotle butternut squash
soup, 480
cook ing strategy, 49–491
egg scramble, 478
M exican chick en with sautéed k ale, 481
pastured pork chili, 483
protein berry break fast shak e, 490
pulled pork wraps with mango J alapeño relish, 488
roasted chick en with roasted celery root, 486
salmon with carrot noodles, 484
spicy burger with jicama chips, 479
spicy chick en soup, 482
steak and potatoes, 489
Red blood cells, 101
Redness (Rubor), 7, 8
Reductionist nutritionism, 52
REM . See Rapid eye-movement sleep
Resistance training, 63, 250, 436, 444
benefits of, 366
goal of, 367
and protein intak e, 65–66
Reward system of brain
in obese individuals, 217–218
palatable foods stimulating, 216–217
processed food and palatability, 219
“stop eating” signal, 218
sugar and HFCS stimulating, 247
Roasted chick en with roasted celery root, 486
ROS. See Reactive oxygen species
Row, 405
“frozen statue,” 408–411
single arm supported, 407–408
“Runners high” sensation, 40

S
Salad dressing, olive/coconut oil for, 231–232
Salmon with carrot noodles, 484
Sanitized food supply and dysbiosis, 155
Sarcopenia, 65–66
causes of, 365
definition of, 365
Satiety, 66
definition of, 214
and digestive tract messengers, 214–215
and proteins, 215–216
Saturated fat
butyric acid (butyrate), 70
carbon chain of, 68–69
classification of
by chain length, 70
definition of, 68
lauric acid, 69
lauric acid (laurate), 71
misconception about, 67–68, 76–77
palmitic acid (palmitate), 73
resistant to free radicals, 68
structure of, 68
SCFA. See Short-chain fatty acids
SDLDL. See Small-dense LDL
Seasonal “primordial cycling,” 442
Sedentary/low activity and hormesis, 26–27
Sedentary vegetarian, 64
Selenium, 453–454
Short-chain (SC) fats, 148
Short-chain fatty acids, 153
Short-term eating signal, 214
Sit-ups
as low back “poison,” 413
problems caused by, 412–413
variations, 412
Sk eletal muscle, glucose storage by, 101
Sk in conductance biofeedback , 301
Sleep deprivation, 27
health consequences of, 258–259
Sleep problems, circadian disruption, 312
amber-tinted glasses, 349–350
bedroom environment, 350
brain/body, effects, 340–341
caffeine, 345
chronic disruption, 334
correlated color temperature, 347, 348
credit-limit, 326, 327
dawn simulator, 346
eliminate exposure to blue spectrum light, 348
exercise, 351–352
internal timek eeper, 313–319
adrenal gland’s clock , 316
fat clock , 317
gut clock , 317
heart clock , 316
immune clock , 317
k idney clock , 317
liver clock , 316
muscle clock , 317
pancreas clock , 316
light at night, 331, 333–334
asleep, 332–333
exposure, 332
light pollution, 331
malfunctioning master clock , 335–337
blood sugar, 336
diabetes, 336, 339–340
diabetes, loss of insulin, 337
disrupt sleep, 336
fatty liver disease, 336
heart, 336
heart disease, 337
inflammation, chronic, 337
insulin resistance, 336
poor athletic performance, 337
sleep, 339–340
strok e, 337
master clock
cortisol levels, 318
hormone levels, 318
in hypothalamus, 319–320
leptin levels, 318
melatonin levels, 318
melatonin
connection, 338–339
gateway hormone for regeneration mode, 321
natural light’s effects, 330
supplementation, 353
National Sleep Foundation, 344
natural light, 346
in night, 312
non-rapid eye movement sleep, 322
rapid eye-movement sleep, 323, 325
shift work , 342–343, 354
sleep drive
adenosine gold card, 327
chemical system, 325–326
circadian systems, 328
gray card, 327
 slow wave sleep, 323
wak ing and sleeping schedule, 345
Slow pathway and HPA axis, 35
Slow wave sleep, 323
Small-dense LDL, 517, 521, 522, 533
Small-dense LDL particles, 521
SNS. See Sympathetic nervous system
“Soda addictions,” 247
Soft drink s, 247
Spices. See Herbs and spices Spicy burger with jicama chips, 479
Spicy chick en soup, 482
Sprouting, 460
Squat
assisted. See Assisted squat bodyweight, 372–373
deep, 369, 371
grind, 373–374
health benefits of, 368
k nees collapsing inward during, 379–3, 379–380
k nees shooting forward, 378–379
light, 370–371
limit, 370
mechanics descent, basic, 371–372
pause at bottom of, 370
progression, 372–373
bodyweight squat, 372–374
front squat, 377–378
goblet squat, 375–376
ultra-deep, 370, 373
variations, 368
SSC. See Stretch shortening cycle Starch, 57, 222–224
Steak and potatoes, 489
Stearic acid (stearate), 75
Stiff-leg deadlift, 384
“Stop eating” signal, 218
Stress, 22, 31
brain response to, 143
gut inflammation from, 144
gut response to, 143
Stress, chronic, 265, 266, 271
brain
re-wiring of, 273
transmitter-receiver connections, 272, 279
and brain training, 307
health-damaging and age-accelerating aspects, 289
physical changes, 279–281
higher threat perceptions, 279
non-threatening stimuli, 279
PFC and hippocampus functioning, 279
and premature aging, 288–289
and resistance, 287
rewires threat-stress circuitry, 278–280
self-treatment approaches, 285
structural and functional changes in the brain, 306
“Stress cup,” 206
concept of, 41
definition of, 38
lack of exercise and, 42–43
overflowing, 42
super-sizing, 44
use in daily life, 45
Stressed-out brain, 280
Stress reduction techniques, 44, 259–260
biofeedback , 301–303
HeartM ath, 303
heart rate variability, 302
monitoring muscle tension and sk in conductance, 302
muscle tension, 302
real-time information, 302
Stress-related behaviors, 289
Stress response
amygdala, 275
changing, 281
early life experiences, 284–285
high intensity. See Stress, chronic
hippocampus, 275
HPA axis, 275
isolated, short-term, 271
nerves of steel/courageous/crazy, 283
prefrontal cortex (PFC), 275
rumination, 289
stop, 284
turned on, 284
Stress/threat system. See “Fight or flight” system
Stretch shortening cycle, 370
Strong M edicine Defensive Tactics, 355
Sucrose, 56, 58
Sugar. See also Specific types
cravings, 100
in energy drink s, 248
in fruit drink s, 248
 in fruit juices, 248
in soft drink s, 247
Sulforaphane, 237–239
Sumo deadlift, 384–387
with barbell, 392
built-in sumo safety, 393
double k ettlebell, 391
health benefits of, 384–385
hyperextended spine with, 393–394
poor descending technique with, 394
procedure, 386
single k ettlebell, 390
starting position, 387
and stick ing point, 389
sublime, 389
tactics, 388
Superset, 438
Supplement industry, 158
SweetBeat™, 553
Swelling (Tumor), 7, 8
SWS. See Slow wave sleep Sympathetic nervous system, 273, 295
functions of, 33
inflammation and oxidative stress by, 37
and PNS, interaction between, 35
short-term activation of, 286
Systemic inflammation, 136

T
Table sugar. See Sucrose
Tai chi, 305
T-cells, 128
functions of, 8, 9
T1D. See Type 1 diabetes
T2D. See Type 2 diabetes
Telomeres, 197–199
TFA. See Trans fatty acids
The Open-Focus Brain, 300
Threats, 38
to modern man, 31
to primitive man, 31
Three-dimensional proteins, 61–62
Tight junctions, 126
failure of, 129–130
TJ . See Tight junctions
Training days, feeding in, 471–474
Trans fatty acids
double bond configuration, 92
as foreign invaders, 92
Transformational fitness template
importance of, 436
seasonal “primordial cycling,” 442and superset, 438
week ly training regimen, 437, 439–441
Treg cells, 9, 128, 130–131
and gut bacteria, 149
T-regulatory cells. See Treg cells
Triglycerides, 74, 242, 514–515, 531
medium-chain, 72
“Turbo boost” reflex, 370
Turmeric, 463
Type 1 diabetes
definition of, 124
and gluten free diet, 165–166
treatment of, 227
Type 2 diabetes
economic cost of, 180
fatty liver disease, obesity and LPS, link between, 154
medication for, 227
prevalence of, 180–181
and resistant insulin receptor, 182
restricting starchy carbohydrates and sugars in, 228
risk factor for, 181
Type 3 diabetes, 201
U
U ltra-deep squat, 370, 373
U nder-nutrition, 25
U nhealthy obsession with weight, 535–540
U nsaturated fatty acid
double bonds, 79
and free radicals, 79
oxidation of double bonds in, 94
U nsaturated vegetable oils, hydrogenation of, 94
U S Department of Agriculture organics, 448
V
Vaccenic acid, 95
Vagus nerve stimulation, 162
Vegetable shortenings, 94
Vegetarians, EPA and DHA needs of, 90
Very low density lipoprotein, 516
with more cholesterol as “cargo,” 518
normal, 519
pack ed with triglycerides, 518
transport of fat and cholesterol, 517–519
triglyceride-pack ed, 519
“Vigorous intensity,” 250
Visceral obesity, 178
Vitamin B-12 deficiency, 457
VLDL. See Very low density lipoprotein

W
Waist to height ratio, 535–540
“Warburg Effect,” 193
Weight, unhealthy obsession with
Body M ass Index, 535–536
normal weight obesity, 536
scenario analysis for, 539–540
waist to height ratio, 535–540
Western diets
and dysbiosis, link between, 152–153
habits, 54
Western high technology, 293
Whole grains for diabetics, 226–227
Whole wheat, fiber in, 235

Y
Yin/yang concept, 36

Z
Z ietgebers, 319
Z inc deficiency, 459–460
Zingiber officinale, 462
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 Table of Contents
FOREWORD: Honor • Courage • Commitment
PREFACE: Messages from the Authors
INTRODUCTION
Phase I: Basic Training
Basic Training I—Central Themes
• Inflammation and Oxidative Stress
• The Gene-Environment Connection
• Hormesis
• The Stress Response
• Allostasis—“The Stress Cup”
Basic Training II—Nutrition and Metabolism 101
• Introduction
• Macronutrients
• Metabolism Basics
Phase II: Knowing the Enemy
Knowing the Enemy I—The Gut: Guardian at the Gate
• Gut Health: First Principles
• Triggers of Intestinal Inflammation
• Conclusion
Knowing the Enemy II—Obesity: The Enemy Within
• Introduction: A Big Fat Problem
• The Fat Cell: Dr. Jekyll becomes Mr. Hyde
• The Plague of “Diabesity”
• How We Get Fat: the brain, hormones, and appetite
• Intervention: The 8-step program for obesity and diabetes
Knowing the Enemy III—Chronic Stress: The Silent Killer
• Mind and Body: Descartes was wrong
• Stress and Health
• Mind Interventions: Brain Training
Knowing the Enemy IV—Circadian Disruption: Thief in the Night
• The Internal Timekeeper
• Sleep Architecture
• Edison’s Folly?
• Modern Solutions for a Modern Problem
Phase 3: BATTLE PLAN
Battle Plan I—Strong Medicine Physical Training
• Introduction
• Strong Medicine Resistance Training
• Strong Medicine Basic Cardio
• Strong Medicine Advanced Cardio
Battle Plan II—Strong Medicine Nutrition
• Food Sources and Quality
• Carbohydrate Tolerance
• Feed your activity
• A Week of Food
Battle Plan III—Putting It All Together
• Lifestyle Change: “The Neck of Roy Buchanan’s Guitar”
• Strong Medicine Lifestyle Change-Strategic Planning
Battle Plan IV—“Stuff You Can Measure”
• Introduction- biomarkers and the “Holy Grail”
• Cholesterol: What are we measuring?
• Physical Measurement
• Markers of Inflammation
• Heart Rate Variability
Epilogue
About the Authors
Acknowledgements
Index
 Table of Contents
FOREWORD: Honor • Courage • Commitment
PREFACE: Messages from the Authors
INTRODUCTION
Phase I: Basic Training
Basic Training I—Central Themes
• Inflammation and Oxidative Stress
• The Gene-Environment Connection
• Hormesis
• The Stress Response
• Allostasis—“The Stress Cup”
Basic Training II—Nutrition and Metabolism 101
• Introduction
• Macronutrients
• Metabolism Basics
Phase II: Knowing the Enemy
Knowing the Enemy I—The Gut: Guardian at the Gate
• Gut Health: First Principles
• Triggers of Intestinal Inflammation
• Conclusion
Knowing the Enemy II—Obesity: The Enemy Within
• Introduction: A Big Fat Problem
• The Fat Cell: Dr. Jekyll becomes Mr. Hyde
• The Plague of “Diabesity”
• How We Get Fat: the brain, hormones, and appetite
• Intervention: The 8-step program for obesity and diabetes
Knowing the Enemy III—Chronic Stress: The Silent Killer
• Mind and Body: Descartes was wrong
• Stress and Health
• Mind Interventions: Brain Training
Knowing the Enemy IV—Circadian Disruption: Thief in the Night
• The Internal Timekeeper
• Sleep Architecture
• Edison’s Folly?
• Modern Solutions for a Modern Problem
Phase 3: BATTLE PLAN
Battle Plan I—Strong Medicine Physical Training
• Introduction
• Strong Medicine Resistance Training
• Strong Medicine Basic Cardio
• Strong Medicine Advanced Cardio
Battle Plan II—Strong Medicine Nutrition
• Food Sources and Quality
• Carbohydrate Tolerance
• Feed your activity
• A Week of Food
Battle Plan III—Putting It All Together
• Lifestyle Change: “The Neck of Roy Buchanan’s Guitar”
• Strong Medicine Lifestyle Change-Strategic Planning
Battle Plan IV—“Stuff You Can Measure”
• Introduction- biomarkers and the “Holy Grail”
• Cholesterol: What are we measuring?
• Physical Measurement
• Markers of Inflammation
• Heart Rate Variability
Epilogue
About the Authors
Acknowledgements
Index