Vous êtes sur la page 1sur 28

20 In defense of the bros.

By Bryan Krahn, CSCS

22 Should you stop counting calories and macros?
By Armi Legge

24 Does reverse dieting build metabolic capacity?

By Alan Aragon
Copyright February 1st, 2014 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

26 Interview with Tom Venuto.

By Alan Aragon

Hormones and addiction.

By David A. Wiss, MS, RDN, CPT

11 Structural balance theory: does your butt care

about your biceps?
By Menno Henselmans

15 Overfeeding polyunsaturated and saturated fat

causes distinct effects on liver and visceral fat
accumulation in humans.
Rosqvist F, Iggman D, Kullberg J, Jonathan Cedernaes J,
Johansson HE, Larsson A, Johansson L, Ahlstrm H, Arner
P, Dahlman I, Risrus U. Diabetes. 2014 Feb 18. [Epub
ahead of print] [PubMed]
16 Can we say what diet is best for health?
Katz DL, Meller S. Annu Rev Public Health. 2014 Mar
18;35:83-103. [PubMed]

17 Effects of supplementing n-3 fatty acid enriched

eggs and walnuts on cardiovascular disease risk
lacto-ovovegetarians: a randomized, crossover, free-living
intervention study.
Burns-Whitmore B, Haddad E, Sabat J, Rajaram S. Nutr J
2014, 13:29 [Epub ahead of print] [PubMed]

18 Resistance training in overweight women on a

ketogenic diet conserved lean body mass while
reducing body fat.
Jabekk PT, Moe IA, Meen HD, Tomten SE, Hstmark AT.
Nutr Metab (Lond). 2010 Mar 2;7:17. [PubMed]
Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 1

Hormones and Addiction.

David A. Wiss, MS, RDN, CPT
It has been known for some time that individuals with substance
use disorders (SUDs) have significant vitamin and mineral
deficiencies.1-6 In the past decade, investigators have begun to
explore alterations in both neuro-circuitry and nutrition-related
hormones (i.e. leptin, ghrelin, insulin) in the SUD population to
better understand eating behavior during drug use, recovery, and
long-term abstinence. The connection between nutrition
behavior and addiction recovery have important implications
that are not frequently addressed in clinical practice. According
to Virmani et al,7 drug abuse appears to be a risk factor for
metabolic syndrome, which is a cluster of risk factors for
cardiovascular disease. Given that weight gain following
abstinence from drugs is a source of major personal suffering,
there is a pressing need for a more detailed understanding of the
effects of drug addiction on dietary intake.8
It is well known that drug addicts share many of the same brain
imaging9 and behavioral10 characteristics as compulsive
overeaters. However, since the "reward" or hedonic value
associated with food in humans is tied to memory, emotions, and
individual characteristics, food perception is difficult to assess at
a group level.11 Meanwhile, evidence supporting the concept of
food addiction is becoming widely accepted. The purpose of this
review is to examine both drugs of abuse and contemporary
palatable food to determine if there is a link addiction between
hormones acting on reward-related dopamine pathways that
stimulate or inhibit feeding. The majority of neuro-hormonal
research is conducted in animal models, so unless specified as
human research, it can be assumed that physiological
observations of the brain are extrapolated from rodents.
The mesolimbic dopamine system is considered a primitive part
of the brain that consists of the ventral tegmental area (VTA)
which contains dopamine neurons that project to cortico-limbic
structures such as the nucleus accumbens (pleasure center),
medial prefrontal cortex (cognition), hippocampus (memory),
and amygdala (emotional reactivity). The VTA receives direct
and indirect input from the hypothalamus, which governs several
endocrine processes through communication with various
glands. The VTA is involved in somatic processes including
body temperature, sleep, and appetite, and influences
neurological mechanisms that underlie mood and motivational
states. Direct evidence that leptin and ghrelin modulates the
hypothalamic pathway has begun to emerge, implying rewardrelated information that drives feeding behavior at the level of
the VTA.

initiation and termination. Adam and Epel13 have highlighted the

role of chronic stress and elevated cortisol (a glucocorticoid
controlled by the hypothalamus) in the dysregulation of this
finely balanced system. This may cause impaired sensitization
of satiety signals leading to increased food intake and
subsequent visceral fat accumulation. Corticotrophin-releasing
factor is released during stress, which stimulates the reward
system.14 Stress has been linked to drug relapse and is a
significant cause of failure in dieters, and can actually become a
conditioned incentive for food, possibly explaining the
phenomenon of "comfort food." 15 Wiss found that individuals
with a history of substance abuse reported more difficulty
controlling overeating when depressed.16
Food addiction
Highly palatable food can stimulate endogenous opioid release 17
and trigger dopamine activity in the brain. 18 Palatable food is
processed food that typically contains added sugars, salt, and fat.
Recent evidence depicts dopamine circuits as a major site of
convergence where metabolic/hormonal and visceral sensory
cues interact to regulate eating behavior by way of a "gut-brain
dopamine axis."19 Food addiction has been associated with binge
eating disorder as well as obesity.20 According to Heber and
Carpenter,21 obesity-associated inflammation modulated by
leptin in the brain may promote addictive behaviors leading to a
self-perpetuating cycle of addiction to food, as well as
drugs/alcohol and process addictions such as gambling.
Other researchers have challenged the notion that drug addiction
and food addiction are near-identical processes, since there are
unique evolutionary contexts across species with different
environmental pressures, resulting in significant differences
between rodents and humans.22 Such differences can include
food availability, visual appeal, economics and incentives, social
routines for eating, alternative reinforcement, and the impact of
advertising.23 Other differences in the prefrontal cortex (which
weighs pros and cons) are not sufficiently integrated into the
current animal models of food intake. The full behavioral
consequences of metabolic hormones acting on dopamine
neurons will require further investigation. Meanwhile, several
authors have identified leptin as the indirect link between
overeating and addiction, suggesting that many leptin-deficient
individuals meet criteria for food addiction.14

Coll et al12 have suggested the presence of an integrated system

in which adipocyte-derived signals (i.e. leptin) provide longterm information to the brain about the state of nutrient stores,
whereas a variety of signals (many not addressed in this article)
triggered by eating have important roles in influencing meal

Leptin is produced and secreted by adipose tissue to increase

metabolic rate. In human populations plasma leptin is positively
associated with fat mass.24 Leptin is described as anorexigenic
because it is responsible for initiating the starvation response
(decreases food intake). Evidence suggests that leptin-mediated
modulation of central dopamine circuits provides a neural
pathway by which changes in leptin levels lead to adaptive
behavioral responses in feeding.25 De Araujo et al showed that
the reward value of sucrose was increased by fasting, yet
decreased by leptin via a reduction in dopamine signaling.26 In
other words, a hungry individual with lower leptin levels will
assign a higher reward value of food compared to an individual
who is satiated (dopamine release and firing is inhibited in the
nucleus accumbens when satiated). Interestingly, high

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 2

circulating levels of leptin have no pronounced effect on

metabolism and feeding, whereas low levels may trigger a
physiological condition where the body perceives a hungry state
and simultaneously enhances motivation for obtaining food. 27
The failure of elevated leptin levels to control or reverse obesity
suggests the possibility of a leptin-resistant state. High-fat diets
can induce leptin resistance and is emerging as a cause and
consequence of weight gain.28 Leptin resistance is considered
analogous to the concept of insulin resistance, both of which can
correlate to obesity. According to Coll et al,12 leptin resistance
occurs when circulating leptin fails to reach its target receptors
in the brain, when leptin receptors have decreased expression,
when there is attenuation of the intracellular leptin signaling
cascade, or when enzymatic dysfunction exists. Additionally,
altered leptin signaling due to genetic mutations have been
implicated in obesity.29 Meanwhile, the concept of leptin
resistance remains controversial.
As evidence that leptin regulates the activity of the mesolimbic
dopamine system by its actions on VTA dopamine neurons
continues to grow, recent data indicates that leptin not only
regulates the homeostatic center of the hypothalamus but also
the hedonic system by affecting subjective desires for food. 30
Food deprivation decreases circulating leptin levels, which has
been used to study the impact of leptin on brain reward centers.
While still not fully understood, it is known that leptin has action
extending to the brain reward circuits thereby contributing to
preference for highly palatable foods. Recent research suggests
that the leptin-dopamine interaction appears to be bi-directional,
as dopamine has been shown to negatively influence leptin
action in the lateral hypothalamus.31 Data collected by Davis et
al indicate that leptin signaling within the lateral hypothalamus
regulates energy homeostasis and metabolism, whereas midbrain
leptin modulates effort-based responding for food via
mesolimbic dopamine.32 Hormone-influenced neuroplasticity
infers behavioral changes that include an elevated preference for
high-fat and high-sugar diets commonly associated with the
phenomenon of food addiction.33
Human research using functional magnetic resonance imaging
(fMRI) measured responses to visual food stimuli in obese
subjects compared to controls.34 As expected, obese participants
had significantly higher plasma leptin concentrations, possibly
experiencing a state of leptin resistance. Meanwhile, Kalra states
that hypothalamic leptin insufficiency rather than "leptin
resistance" leads to decreased energy expenditure, increased
energy intake, and consequential obesity.35 Grosshans et al found
a significant positive correlation between plasma leptin
concentration and brain activation in the ventral striatum (area
which includes the nucleus accumbens) during the presentation
of visual food cues,34 strongly suggesting that the homeostatic
feedback mechanism between leptin and mesolimbic reward
function is impaired in obese subjects.

hippocampus, and amygdala.36 Both ghrelin and leptin play a

central role in the neuroendocrine regulation of food intake and
energy homeostasis.30 Ghrelin is stomach-derived and will
decrease after eating thus contributing to satiety. Leptin counters
the effects of ghrelin thereby decreasing relentless hyperphagia.
The sight of food significantly elevates ghrelin levels in nonobese healthy volunteers.37 In obese human subjects, ghrelin
levels are lowered, whereas post-meal ghrelin levels remain
higher than in lean individuals.38 Direct injection of ghrelin in
the VTA and nucleus accumbens increases feeding behavior.39
Recent findings suggest that the VTA but not the nucleus
accumbens is the direct target site for ghrelin's action on sweet
food motivation.40 Ghrelin also enhances intake of artificially
sweetened food (saccharin), implying a role in feeding behavior
regardless of caloric content.41
Dickson et al suggest that the ghrelin system alters the set point
of the dopaminergic neurons in the VTA, thereby enhancing the
ability of rewarding substances to activate the midbrain
dopamine system.42 Anticipatory physiological responses to
scheduled meals can be learned through ghrelin's interaction
with central nervous system (CNS) reward pathways that
stimulate motivation to eat28 via increased release and activity of
VTA dopamine.23 While regular or palatable food by itself
activates the mu opioid receptor pathway in the VTA, systemic
ghrelin switches the dominant opioid receptor pathway from mu
to kappa only for highly rewarding food.43 These findings
suggest a pivotal role of ghrelin in regulation of food incentives
and hedonics. Meanwhile, other investigators have concluded
that ghrelin primarily exerts motivational effects on feeding,
rather than hedonic or opioid-related effects.44
The central ghrelin signaling system interfaces neurobiological
circuits involved in reward from both food and chemical drugs
including alcohol. Increased ghrelin signaling could contribute
to the overconsumption and preference for high-calorie food45
and alcohol, a high-calorie beverage.46 Whether or not ghrelin
plays a significant role in losing control over drug-taking
behavior is yet to be determined. Humans subjected acutely to
psychosocial stress displayed increased plasma ghrelin,
particularly "emotional eaters" where ghrelin did not decline
acutely following food consumption.47 Since stress has been
linked to drug relapse and is a significant cause of failure in
dieters, it is possible that stress-related increases in ghrelin are a
risk factor for substance-seeking behavior. Some authors have
suggested that ghrelin antagonists have therapeutic potential for
the treatment of obesity by suppressing overconsumption of
sweet food.48 Similarly, ghrelin agonists might increase the
motivation to eat, which could be helpful in cases where the
drive to eat is insufficient.44 Kawahara et al recommends further
study on the role of ghrelin in regulating the mesolimbic
dopamine system in response to drugs of abuse and alcohol. 43

Ghrelin has opposing effects with leptin, stimulating appetite by

activating orexigenic neurons in the hypothalamus. Additionally,
ghrelin receptors have also been identified in the VTA,

While widely studied in connection with the regulation of blood

glucose, the CNS effects of insulin remain to be elucidated.
Much like leptin, insulin is an adiposity signal, is anorexigenic,
and attenuates food reward. Leptin gene therapy represses
insulin secretion and can potentially ameliorate diabetes.35 In

Alan Aragons Research Review February/March 2014

[Back to Contents]


Page 3

metabolic circumstances in which plasma insulin or leptin levels

are low (starvation and reduced adiposity), signaling would be
decreased and drive for food intake increased. Insulin and
dopamine work together to orchestrate both the motivation to
engage in consumptive behavior and to calibrate the associated
reward, particularly related to hedonic feeding. 49 More
specifically, insulin depresses dopamine concentration in the
VTA, which may suppress salience of food once satiety is
Similar to ghrelin, there are insulin receptors in the
hypothalamus, VTA, hippocampus, and amygdala. 36 In humans,
insulin secretion is decreased by ghrelin, and vice versa. 50,51
There is also evidence that the insulin receptor signaling
pathway interferes with leptin signaling, indicating that
hyperinsulinemia contributes to the pathogenesis of leptin
resistance.52 Chronic hyperinsulinemia promotes obesity by
interfering with leptin extinguishing of dopamine clearance in
the nucleus accumbens, which is a hallmark of addiction. 53
Insulin resistance may directly or indirectly impact neural
pathways driving desires to consume highly caloric foods and
ultimately influence further adiposity.54 These authors also
reported that during exposure to stress, desire to eat is
exacerbated in obese humans but not lean individuals. In obese
individuals, evidence of insulin resistance can lead to alterations
in food craving even in a relaxed state.
Daws et al reviewed the potential impact of impaired insulin
signaling in obesity and stimulant abuse suggesting that insulininfluenced dopamine transmission can affect the ability of drugs
to exert their neurochemical and behavioral effects.55 According
to these authors, insulin receptors are present in brain and are
found on midbrain dopamine neurons, and the interplay between
insulin signaling and drug-induced increases in extracellular
dopamine may contribute to the high comorbidity of eating
disorders and drug abuse. Improvements in brain dopamine
function by normalizing or bypassing disruptions in insulin
signaling might be effective in treating addictions.
The course of alcoholism is associated with suppressed secretion
of ghrelin and leptin, both of which influence the hypothalamicpituitary-adrenal system.56 Increasing leptin concentrations have
been correlated with the course of alcohol withdrawal in human
females.57 While alcohol attenuates the secretion of leptin in the
short run (6-8 hours) in non-alcoholic, non-obese human
subjects,58 chronic alcoholism has been linked to elevated
leptin.24 This may indicate that fat tissue of alcoholic patients is
sensitized to release more leptin than controls, however levels do
normalize after six months of abstinence.24 Lenz et al reported
that lower levels of leptin were correlated with lower levels of
alcohol craving in males,59 while the opposite is true for
women.57 There is epidemiological support for a link between
familial alcoholism and risk for obesity in women, and possibly
for men.60 Some authors have suggested that alcoholic men
outnumber women four to one, highlighting neurological and
hormonal differences that may account for these observed
Alan Aragons Research Review February/March 2014

difference.61 Further investigations into the relationship between

leptin and alcohol craving accounting for differences in gender
as well as the nutritional status of subjects are clearly warranted.
The rewarding properties of alcohol require ghrelin. 62 Alcoholdependent patients have increased ghrelin levels when
intoxicated and during early abstinence, increasing during the
first week of alcohol withdrawal.57 It is likely that elevated
ghrelin can account for measurable changes in hunger and
appetite during alcohol withdrawal. The common practice of
healthy individuals drinking an alcoholic beverage before a meal
suggests that alcohol stimulates appetite. Jerlhag et al suggest
that by increasing the incentive value of rewards such as alcohol,
hyperghrelinemia may play a pathophysiological role in the
disease process that leads to addiction.62 The authors conclude
that modulation of ghrelin signaling constitutes a potential target
for treatment of alcohol-related disorders. Other human research
led by Leggio and colleagues have confirmed the findings that
ghrelin plays a key role in alcohol-seeking behavior,46
highlighting the key role of dopamine in the neurobiology of
alcohol craving. The authors conclude that antagonizing ghrelin
via homeostatic stabilization might lead to new and innovative
ways to provide effective treatment for alcohol use disorders.
Abstinent alcoholic human subjects have exhibited significantly
blunted responses in blood glucose when exposed to intravenous
2-Deoxy-D-glucose.63 Subjects exhibited trends towards both
blunted responses in glucagon and insulin. Authors speculate
that that nervous system damage attributable to the effects of
alcohol exposure is responsible for the insufficient hormonal
response, particularly neurons in the hypothalamus, as well as
the adrenal medulla. It has been established that alcoholdependent subjects during the first month of abstinence report
maximal pleasure response to the sweetness significantly more
frequently than control subjects,64 consistent with the concept of
"reward deficiency syndrome.65 The percentage of alcoholdependent subjects preferring the maximum concentration of
sucrose decreased over time. Those alcohol-dependent subjects
who reported abstinence at six months were significantly less
likely to prefer the maximum sweetness than were the subjects
who did not maintain abstinence. Krahn et al propose that sweet
preferences should be tested as a predictor of future abstinence. 64
Positive associations between the consumption of any type of
alcoholic beverage and anthropometric markers of adiposity
have been reported.66
Taken together, the apparent link between alcohol abuse and
sugar abuse and the subsequent blunted hormonal responses
highlight the negative impact of substance use on the endocrine
system, providing support for the need for dietary intervention in
supporting long-term abstinence and recovery. Manipulation of
the insulin signaling system should not rely solely on
pharmacological intervention but rather should focus on
normalizing the altered dopamine-glucose link via interventions
in nutrition behavior, which has proven to be challenging in the
light of the science on food addiction.

[Back to Contents]

Page 4

Crystal methamphetamine (meth) use may be associated with the
onset of disordered eating or used as an efficient weight loss
mechanism for those with established eating disorders.67 Food
restriction has been shown to enhance the central rewarding
effect of amphetamine.68 Research by Jerlhag et al demonstrates
that the ghrelin signaling system is required for indirect
measures of the rewarding properties of amphetamine, as well as
cocaine.69 The authors highlight the fact that food restriction
leading to elevated ghrelin facilitates the acquisition of drugseeking behavior in rats, attributable to the dopaminergic regions
of the nucleus accumbens and VTA. Hyperghrelinemia
observable in SUD patients raises important questions regarding
the physiological role of ghrelin influencing not only food intake
and appetite, but also a broader role in reward induced by
addictive drugs such as alcohol, amphetamine, and cocaine.69
The potential for a gradual normalization of ghrelin levels
through medical nutrition therapy appears indicated for patients
with methamphetamine use disorders.
Research using positron emission tomography (PET) brain
imaging has suggested that deficits in dopamine signaling are
similar for cocaine-addicted and obese rats.11 The authors
suggest that dopamine binding ability in the D2R/D3R sites can
be used to predict future body weight and cocaine preference. A
small sample of human cocaine addicts in an inpatient setting
reported preference for the highest concentration of sweet
solutions, which is in agreement with sweet-preference
expressed by alcoholics.64,72 Clearly sugar reinforces depleted
reward pathways in the brain resulting from cocaine abuse.
Meanwhile, research conducted on rats has shown that
antagonism of ghrelin receptor function has reduced the
development of cocaine sensitization, strongly supporting the
view that ghrelin receptors are partially responsible for
modulating reinforcement/reward function.70
A sample of female crack cocaine users presented with lower
levels of plasma leptin during early abstinence in comparison
with healthy controls, consistently increasing during
detoxification.71 The authors speculate that leptin levels may
increase in abstinence only as a consequence of improved diet or
weight gain. Consistent with the link between leptin and
inflammation reported by Heber and Carpenter 21 and
Levandowski et al71 highlights the fact that disruption of energy
homeostasis could interfere with clinical responses to cocaine
treatment, since cocaine addicts demonstrate increased immune
response inflammation both at the baseline and in response to
stress and cue imagery conditions.73

inhibition of leptin production that facilitates overeating. The

overeating in cocaine-dependent individuals often pre-dates
recovery, with the effect masked by lack of weight gain. Taken
together, investigators found that cocaine abuse results in an
imbalance between fat intake and storage, leading to excessive
weight gain during recovery.8 For many individuals, it is likely
that dysfunctional eating pre-dates the initiation of drug use as
well. According to Wiss and Waterhous,74 patients with SUDs
often develop disordered and dysfunctional eating patterns
during abstinence, and eating disorder patients can similarly
progress into substance abuse. Traditionally addiction has been
addressed first, however delaying eating disorder treatment can
hinder recovery, therefore it is important to alert treatment
providers who treat patients with dual diagnoses how to assess
and address both disorders simultaneously.
Ecstasy is a popular club drug classified as an empathogen or
entactogen often mixed with stimulants. In humans, abuse of this
drug reduces eating, although there is research to suggest that
women who use ecstasy are not necessarily taking it as
deliberate means of weight control.75 In rats, ecstasy was shown
to cause significant decreases in serum leptin and increases in
serum ghrelin, both of which recovered to baseline after 24
hours.76 Long-term effects of altered hormonal levels related to
ecstasy and stimulant abuse require further evaluation, with
more emphasis on behavioral parameters such as food intake.
Acute food deprivation (24 hours) reinstated heroin-seeking in
rats, and this effect was attenuated by leptin infusions. 77 Similar
to other substances of abuse, decreased activity in the
mesolimbic dopaminergic reward system (VTA and nucleus
accumbens) following leptin administration is likely to account
for this effect. Not surprisingly, Nolan and Scagnelli found that
methadone-treated human patients had a higher consumption of
sweets, a higher eagerness to consume sweet foods, and a
willingness to consume larger quantities desired by controls.78 In
another sample of human patients on methadone maintenance,
basal serum leptin concentrations were significantly decreased
compared to controls.79 These findings were independent of
BMI, body fat, and insulin sensitivity.

According to recent research conducted by Ersche et al, 8

cocaine-dependent men (not abstinent) reported increased food
intake, specifically foods high in fat and carbohydrate. There
was an expected trend towards lower levels of circulating leptin
in the cocaine group, directly interfering with metabolic
processes (impaired energy balance). In other words, the higher
fat intake was associated with less fat storage, suggesting an

Recent research has also shown that chronic food restriction (14
days of mild restriction) led to robust heroin-seeking behavior in
rats.80 The authors acknowledge the "stress aspect" of food
restriction on reward-seeking behavior, meanwhile recognizing
that the state of hunger by itself was not sufficient to induce
augmentation of heroin-seeking. D'Cunha et al concluded that
ghrelin is likely more responsible than leptin for mediating the
effect of food restriction on heroin-seeking following prolonged
abstinence.80 These findings are in agreement with Maric et al
who provided evidence that activation of ghrelin receptors is
sufficient to induce increases in drug-taking and drug-seeking
behaviors.81 Meanwhile, these authors point out that ghrelin is
not required for this mechanism since treatment with a ghrelin
receptor antagonist had no effect on drug-taking or food
deprivation-induced reinstatement of extinguished heroinseeking.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 5

Nutrition and addiction treatment


Disordered Eating

The most substantial health burden arising from addiction lies

not in the direct effects of intoxication but in the secondary
effects on physical health.8 There is strong evidence to support
that food and drugs are competing for overlapping reward
mechanisms. When the immediate crisis of substance abuse has
been resolved, there is a likely compensatory increase drive for
food intake to achieve weight recovery and a likely overshoot,
leading to increased adiposity.13 Ravenous food consumption
may be due to "rebound appetite" in the wake of the
hypothalamic suppression from drug use. Making healthful food
choices after abstinence has been achieved may be very
challenging. Sobriety is associated with new emotions, anxiety,
and uncertainty. It is easy to seek a predictable and comforting
response from food. This may lead to overeating, relapse,
compromised quality of life, and the development of chronic
disease. Caffeine and nicotine abuse should also be addressed
since they are highly addictive substances that can perpetuate
substance-seeking behavior. Additionally, the impact of stress
and adequate sleep should not be ignored, as they too can have
profound effects on the endocrine and reward systems.

Drug abuse is a risk factor for eating disorders82 and has been
shown to have both genetic and environmental influences.83
Even a remote history of SUD can negatively impact weight loss
in adults84 and adolescents.85 Sobriety time has been positively
associated with increased sugar use.86 Substance abuse linked to
low distress tolerance can lead to excessive consumption of
food.87 Fischer et al found that problems of alcohol use were
associated with binge eating and purging, and that a tendency to
act rashly when distressed was associated with both behaviors.88
In one study, nearly 40% of women in SUD treatment met
criteria for an eating disorder most commonly binge eating
disorder followed by bulimia nervosa.89 Men in SUD treatment
reported bingeing and the use of food to satisfy drug cravings
during the first six months, with weight concerns and distress
about efforts to lose weight during months 7-36.90
Interventions and Outcomes
Positive associations between nutrition interventions and
substance abuse outcomes have been reported, where nutrition
education was the differentiating factor.91 An educational
intervention on the nutrition behavior of alcohol-dependent
patients led to 80% of participants reporting continual abstinence
after six months.92 A six-week environmental/educational
intervention to improve dietary intake and reduce excessive
weight gain among men in residential treatment reported greater
reductions in total energy, percentage of energy from sweets,
daily servings of fats, oils, and sweets, and BMI over the
intervention period.90 The findings provide evidence that such
interventions can be successful despite challenges met in
residential substance abuse facilities. A series of nutrition
workshops in a substance abuse program (SAP) in the US prison
system led to significant improvements in nutrition and general
health, with a trend towards improvements in social ties. 93 A
review article on the drug-addicted prison population in the UK
builds a convincing argument for the inclusion of more
nutritious options in prisons, concluding that such changes are
overall likely to make sound economic sense in terms of prisoner
health, mood, behavior, and recidivism rates.94

The modern epidemic of obesity may be in part related to reward

and hedonic mechanisms, and that failure of regulatory systems
might be related to dysregulation of reward systems.
Normalizing the disrupted leptin signaling cascade in the obese
brain may be sufficient to decrease motivation for food reward,
and interventions targeting the central leptin system and/or other
hypothalamic hormones regulated by leptin should be considered
for the treatment of drug addicts with comorbid eating disorders.
Kalra has proposed trials involving gene therapy aimed at
reinstating leptin circuitry in drug addicts.35 More realistically,
weight gain during substance abuse recovery should be
monitored and controlled (gradual rather than drastic) in order to
counter the associated adaptations in nutrition-related hormones.
In order to accomplish this, exposure to highly palatable foods
with addictive potential should be minimized.

Betty Ford is a world-renowned treatment center in California

that has recently merged with Hazelden in Minnesota. Betty
Ford utilizes a treatment model that includes measures to prevent
post-detoxification overeating. Patients are provided with access
to dietitians and exercise is emphasized, helping patients to plan
for expected changes in eating and the reinforcing effects of
food. At Breathe Life Healing Center in Los Angeles, a
registered dietitian nutritionist is an integrated member of the
treatment team, approving all food and beverages that enter the
campus, planning nutritionally balanced meals and snacks,
teaching educational courses, and working with patients
individually to mediate dysfunctional eating behavior and
disrupt addictive tendencies. Exercise is also a mandatory
component of treatment. It is possible that data supporting the
effectiveness of improved nutrition and exercise behavior during
the course of treatment will eventually be reported.

Educational efforts alone have not reduced use of drugs of

dependence. Successful efforts have required both individuals
and societal intervention including taxation, regulation, and/or
interdiction. Similar efforts targeting the food industry may be
required to combat the rising epidemics of food addiction,
obesity, and binge eating disorder. Given that individuals with a
history of SUD are at higher risk for developing food-intakerelated dysfunction, there is a substantial need for nutrition
interventions in addiction recovery, and registered dietitian
nutritionists should become vital members of the treatment team.
Currently, there is no requirement for nutrition education and
counseling in substance abuse treatment. Anecdotal reports
suggest that most treatment centers allow unlimited or excessive
amounts of highly palatable foods to patients. While food
restriction can lead to relapse, over-indulgence can perpetuate
the cycle of addictive behavior and contribute significantly to
healthcare burden. The best intervention appears to lie
somewhere in between these extremes, which will require
additional clinical expertise in treatment settings. The need for
firm commitment to intervention protocols as well as ongoing
supervision and consultation is warranted for successful program
implementation in residential drug-treatment facilities.90

Alan Aragons Research Review February/March 2014

[Back to Contents]

Upcoming Trends

Page 6

It is important to acknowledge other relevant hormones,

cytokines, and neuropeptides not mentioned in this article, which
can include but are not limited to: neuropeptide Y, peptide YY,
agouti-related peptide, cholecystokinin, galanin, melanocortin,
adiponectin, thyroid hormones (i.e. thyroxine), reproductive
hormones (i.e. prolactin), posterior pituitary hormones (i.e.
Conclusions and Further Implications for Nutritionists
Restoration of nutritional status in SUD recovery should look
beyond correction of vitamin/mineral status and body weight,
but should also account for recovery of dysfunctional neural
circuitry and altered hormones. Before a successful nutrition
intervention can occur, it is of paramount importance to heal gut
function to promote optimal nutrient absorption throughout the
gastrointestinal tract. Next, preventing over-exposure to highly
palatable foods is critical in repairing addictive processes in the
brain. Finally, restoration of hormone levels should occur
through gradual yet progressive changes in eating behavior,
although there is limited data to support this approach given the
presence of confounding variables over extended periods of
time. From my own experience in clinical practice, utilizing
several small feedings throughout the day is an effective
approach towards preventing spikes and subsequent drops in
insulin. Given that insulin can block leptin, this technique may
be effective in gradually normalizing leptin levels, although to
my knowledge there is no data in the SUD population to support
this claim. Similarly, stable insulin levels achieved through
regular and consistent feeding patterns may prevent ghrelin from
increasing to abnormal levels. The mantra I encourage with my
SUD patients is "never hungry, never full" and the evidence
reviewed herein provides strong support for this approach.
Gradual increases in fiber intake throughout the recovery
process can improve gut function, minimize undesirable insulin
spikes, and promote satiety. For detailed recommendations
regarding nutrition therapy during SUD recovery for specific
substances of abuse, refer to Wiss and Waterhous.74
The current trend towards over-medicating SUD patients while
failing to address and improve nutrition behavior should be
aggressively challenged. Consider this is a call to order for data
collection linking drug addiction to reward-related hormones,
specifically demonstrating the importance of medical nutrition
therapy in SUD recovery over short periods (1-6 months) and
longer periods (6-36 months). Without this data, it will be
difficult to substantiate the need for nutrition interventions in
addiction recovery at the policy level. Nutrition interventions
during recovery may prevent or minimize the onset of chronic
illness, improving resource allocation. Public health measures
should be considered critical.
David A. Wiss, MS, RDN, CPT, is the founder of
Nutrition In Recovery, which specializes in the
nutritional management of: Food Addiction,
Substance Abuse, Eating Disorders, Weight
Management, Sports Nutrition, and General
Wellness. Mr. Wiss has shared his expertise with
a myriad of eating disorder and addiction
facilities throughout the greater Los Angeles
area. He is on the executive committee of the
Alan Aragons Research Review February/March 2014

Behavioral Health Nutrition Dietetic Practice Group, and is the Research

and Grants Committee Chair for the Los Angeles District of the
California Dietetic Association. David is a co-founder of Dietitians for
Professional Integrity (www.integritydietitians.org). Learn more about
his private practice at:
Twitter: @DavidAWiss
Email: DavidAWiss@NutritionInRecovery.com


Estevez, J. F. D., Estevez, F. D., Calzadilla, C. H., Rodriquez,

E. M. R., Romero, C. D., & Serra-Majem, L. (2004).
Application of linear discriminant analysis to the biochemical
and haematological differentiation of opiate addicts from
healthy subjects: A case-control study. European Journal of
Clinical Nutrition, 58, 449-455. doi:10.1038/sj.ejcn.1601827
2. Heathcote, J., & Taylor, K. B. (1981). Immunity and nutrition
in heroin addicts. Drug and alcohol dependence, 8, 245-255.
3. Hossain, K. J., Kamal, M. M., Ahsan, M, & Islam, S. N.
(2007). Serum antioxidant micromineral (Cu, Zn, Fe) status of
drug dependent subjects: Influence of illicit drugs and lifestyle.
Substance Abuse Treatment, Prevention, and Policy, 2(12).
4. Islam, S. K. N., Hoassain, K. J., & Ahsan, M. (2001). Serum
vitamin E, C, and A status of the drug addicts undergoing
detoxification: influence of drug habit, sexual practice and
lifestyle factors. European Journal of Clinical Nutrition, 55,
1022-1027. [PubMed]
5. Ross, L. J., Wilson, M., Banks, M., Rezannah, F., & Daglish,
M. (2012). Prevalence of malnutrition and nutritional risk
factors in patients undergoing alcohol and drug treatment.
6. Saeland, M., Haugen, M., Eriksen, F. L., Wandel, M.,
Smehaugen, A., Bohmer, T., & Oshaug, A. (2011). High sugar
consumption and poor nutrient intake among drug addicts in
Oslo, Norway. British Journal of Nutrition, 105, 618-624.
doi:10.1017/S0007114510003971 [PubMed]
7. Virmani, A., Binienda, Z. W., Ali, S. F., & Gaetani, F. (2007).
Metabolic syndrome in drug abuse. Annals of the New York
Academy of Science, 1122, 50-68. doi:10.1196/annals.1403.004
8. Ersche, K. D., Stochl J., Woodward, J. M., & Fletcher, P. C.
(2013). The skinny on cocaine. Insights into eating behavior
and body weight in cocaine-dependent men. Appetite. Advance
http://dx.doi.org/10.1016/j.appet.2013.07.011 [Elsevier]
9. Volkow, N. D., & Wise, R. A. (2005). How can drug addiction
help us to understand obesity? Nature Neuroscience, 8(5), 555560. [PubMed]
10. Davis, C., Curtis, C., Levitan, R. D., Carter, J. C., Kaplan, A.
S., & Kennedy, J. L. (2011). Evidence that 'food addiction' is a
valid phenotype of obesity. Appetite, 57, 711-717.
doi:10.1016/j.appet.2011.08.017 [PubMed]
11. Michaelides, M., Thanos, P. K., Kim, R., Cho, J., Ananth, M.,
Wang, G., & Volkow, N. D. (2012). PET imaging predicts

[Back to Contents]

Page 7
















future body weight and cocaine preference. Neuroimage, 59,

1508-1513. doi:10.1016/j.neuroimage.2011.08.028 [PubMed]
Coll, A. P., Farooqi, S., & O'Rahilly, S. (2007, April 20). The
hormonal control of food intake. Cell, 129, 251-262.
doi:10.1016/j.cell.2007.04.001 [PubMed]
Adam, T. C., & Epel, E. S. (2007). Stress, eating and the
reward system. Physiology and Behavior, 91, 449-458.
Albayrak, O., Wolfle, S. M., & Hebebrand, J. (2012). Does
food addiction exist? A phenomological discussion based on
the psychiatric classification of substance-related disorders and
addiction. Obesity Facts, 5, 165-179. doi:10.1159/000338310
Dagher, A. (2009). The neurobiology of appetite: Hunger as
addiction. International Journal of Obesity, 33, S30-S33.
Wiss, D. A. (2013). Nutrition and substance abuse (Master's
thesis). Retrieved from http://hdl.handle.net/10211.2/3444
Yeomans, M. R., & Gray, R. W. (2002). Opioid peptides and
the control of human ingestive behaviour. Neuroscience and
Biobehavioral Reviews, 26, 713-728. [PubMed]
Stice, E., Spoor, S., Bohon, C., & Small, D. M. (2008,
October). Relation between obesity and blunted striatal
response to food is moderated by TaqIA A1 allele. Science,
332, 449-452. doi:10.1126/science.1161550 [PubMed]
De Araujo, I. E., Ferreira, J. G., Tellez, L. A., Ren, X., &
Yeckel, C. W. (2012). The gut-brain dopamine axis: A
regulatory system for caloric intake. Physiology and Behavior,
106(3), 394-399. doi:10.1016/j.physbeh.2012.02.026 [PubMed]
Gearhardt, A. N., White, M. A., Masheb, R. M., Morgan, P. T.,
Crosby, P. T., Crosby, R. D., & Grilo, C. M. (2012). An
examination of the food addiction construct in obese patients
with binge eating disorder. International Journal of Eating
Disorders, 45, 657-663. doi:10.1002/eat.20957 [PubMed]
Heber, D., & Carpenter, C. L. (2011). Addictive genes and the
relationship to obesity and inflammation. Molecular
Neurobiology, 44, 160-165. doi:10.1007/s12035-011-8180-6
DiLeone, R. J., Taylor, J. R., Picciotto, M. R. (2012). The drive
to eat: Comparisons and distinctions between mechanisms of
food reward and drug addiction. Nature Neuroscience, 15(10),
1330-1335. doi:10.1038/nn.3202 [PubMed]
Volkow, N. D., Wang, N. J., Tomasi, D., & Baler, R. D.
(2013). Obesity and addiction: Neurobiological overlaps.
doi:10.1111/j.1467789X.2012.01031.x [PubMed]
Nicolas, J. M., Fernandez-Sola, J., Fatjo, R., Casamitjana, R.,
Bataller, E., Sacanella, E, ... Estruch, R. (2001). Increased
circulating leptin levels in chronic alcoholism. Alcoholism:
Clinical and Experimental Research, 25(1), 83-88. [PubMed]
Hommel, J. D., Trinko, R., Sears, R. M., Georgescu, D., Liu,
Z., Gao, X., Thurmon, J. J., Marinelli, M., & DiLeone, R. J.
(2006). Leptin receptor signaling in midbrain dopamine
neurons regulates feeding.
Neuron, 51,
doi:10.1016/j.neuron.2006.08.023 [PubMed]
De Araujo, I. E., Deisseroth, K., Domingos, A. I., Friedman, J.,
Gradinaru, V., & Ren, X. (2011). Leptin regulates the reward
value of nutrient. Nature Neuroscience, 14, 1562-1568.
doi:10.1038/nn.2977 [Nature]
Pandit, R., de Jong, J. W., Vanderschuren, L. J. M. J., & Adan,
R. A. H (2011). Neurobiology of overeating and obesity: The
role of melanocortins and beyond. European Journal of

Alan Aragons Research Review February/March 2014















Pharmacology, 660, 28-42. doi:10.1016/j.ejphar.2011.01.034

Pandit, R., Mercer, J. G., Overduin, J., la Fleur, S. E., & Adan,
R. A. H. (2012). Dietary factors affect food reward and
doi:10.1159/000338073 [PubMed]
Zessen, R. V., van der Plasse, G., & Adan, R. A. H. (2012).
Contribution of the mesolimbic dopamine system in mediating
the effects of leptin and ghrelin on feeding. Proceedings of the
doi:10.1017/S0029665112000614 [PubMed]
Schloegl, H., Percik, R., Hortsmann, A., Villringer, A., &
Stumvoll, M. (2011). Peptide hormones regulating appetite focus
Diabetes/Metabolism Research and Reviews, 27, 104-112.
doi:10.1002/dmrr.1154 [PubMed]
Leinninger, G. M. (2011). Lateral thinking about leptin: A
review of leptin action via the lateral hypothalamus. Physiology
doi:10.1016/j.physbeh.2011.04.060 [PubMed]
Davis, J. F., Choi, D. L., Schurdak, J. D., Fitzgerald, M. F.,
Clegg, D. J., ...Benoit, S. C. (2011). Leptin regulates energy
balance and motivation through action at distinct neural
doi:10.1016.j.biopsych.2010.08.028 [PubMed]
Alsio, J., Olszewski, P. K., Levine, A. S., & Schioth, H. B.
(2012). Feed-forward mechanisms: Addiction-like behavioral
and molecular adaptations in overeating. Frontiers in
doi:10.1016/j.yfrne.2012.01.002 [PubMed]
Grosshans, M., Vollmert, C., Vollstadt-Klein, S., Tost, H.,
Leber, S., Bach, P., ...Kiefer, F. (2012). Association of leptin
with food cue-induced activation in human reward pathways.
Archives of General Psychiatry, 69(5), 529-537. [PubMed]
Kalra, S. P. (2012). Leptin gene therapy for hyperphagia,
obesity, metabolic diseases, and addiction. In Brownell, K. D.,
& Gold, M. S., Food and addiction (131-137). New York, NY:
Oxford University Press.
Dagher, A (2012). Hunger, hunger, and food addiction. In
Brownell, K. D., & Gold, M. S., Food and addiction (131-137).
New York, NY: Oxford University Press.
Schussler, P., Kluge, M., Yassouridis, A., Dresler, M., Uhr, M.,
& Steiger, A. (2012). Ghrelin levels increases after pictures
doi:10.1038/oby.2011.385 [PubMed]
English, P. J., Ghatei, M. A., Malik, I. A., Bloom, S. R., &
Wilding, J. P. H. (2002). Food fails to suppress ghrelin levels in
obese humans. The Journal of Clinical Endocrinology and
Metabolism, 87(6), 2984-2987. [PubMed]
Naleid, A. M., Grace, M. K., Cummings, D. E., & Levine, A.
S. (2005). Ghrelin induces feeding in the mesolimbic reward
pathways between the ventral tegmental area and the nucleus
doi:10.1016/j.peptides.2005.04.025 [PubMed]
Skibicka, K. P., Hansson, C., Alvarez-Crespo, M., Friberg, P.
A., & Dickson, S. L. (2011). Ghrelin directly targets the ventral
tegmental area to increase food motivation. Neuroscience, 180,
129-137. doi:10.1016/j.neuroscience.2011.02.016 [PubMed]
Disse, E., Bussier, A., Veyray-Durebex, C., Deblon, N.,
Pfluger, P. T., Tschop, M. H., ...Rohner-Jeanrenaud, F. (2010).
Peripheral ghrelin enhances sweet taste food consumption and
preference, regardless of its caloric content. Physiology and

[Back to Contents]

Page 8














Behavior, 101, 277-281. doi:10.1016/j.physbeh.2010.05.017

Dickson, S. L., Egecioglu, E., Landgren S., Skibicka, K. P.,
Engel, J. A., & Jerlhag (2011). The role of central ghrelin
system in reward from food and chemical drugs. Molecular and
doi:10.1016/j.mce.2011.02.017 [PubMed]
Kawahara, Y., Kaneko, F., Yamada, M., Kishikawa, Y.,
Kawahara, H., & Nishi, A. (2013). Food reward-sensitive
interaction of ghrelin and opioid receptor pathways in
mesolimbic dopamine system. Neuropharmacology, 67, 395402. doi:10.1016/j.neuropharm.2012.11.022 [PubMed]
Overduin, J., Figlewicz, D. P., Bennet-Jay, J., Kittleson, S., &
Cummings, D. E. (2012). Ghrelin increases motivation to eat,
but does not alter food palatability. The American Journal of
Physiology - Regulatory, Integrative and Comparative
Physiology, 303, R259-R269. doi:10.1152/ajpregu.00488.2011
Vengeliene, V. (2013). The role of ghrelin in drug and natural
doi:10.1111/adb.12114 [PubMed]
Leggio, L., Ferrulli, A., Cardone, S., Nesci, A., Miceli, A.,
Malandrino, N., ... Addolorato, G. (2011). Ghrelin system in
alcohol-dependent subjects: Role of plasma ghrelin levels in
alcohol drinking and craving. Addiction Biology, 17, 452-464.
doi:10.1111/j.1369-1600.2010.00308.x [PubMed]
Raspopow, K., Abizaid, A., Matheson, K., & Anisman, H.
(2010). Psychosocial stressor effects on cortisol and ghrelin in
emotional and non-emotional eaters: Influence of anger and
doi:10.1016/j.yhbeh.2010.06.003 [PubMed]
Skibicka, K. P., Hansson, C., Egecioglu, E., & Dickson, S. L.
(2011). Role of ghrelin in food reward: Impact of ghrelin on
sucrose self-administration and mesolimbic dopamine and
acetylcholine receptor gene expression. Addiction Biology, 17,
95-107. doi:10.1111/j.1369-1600.2010.00294.x [PubMed]
Mebel, D. M., Wong, J. C. Y., Dong, Y. J., & Borgland, S. L.
(2012). Insulin in the ventral tegmental area reduces hedonic
feeding and suppresses dopamine concentration via increased
reuptake. Behavioral Neuroscience, 36,
doi:10.111/j.1460-9568.2012.08168.x [PubMed]
Broglio, F., Arvat, E., Benso, A., Gottero, C., Mucciolo, G.,
Papotti, M., ... Ghigo, E. (2001). Ghrelin, a natural GH
secretatogue produced by the stomach, induces hyperglycemia
and reduces insulin secretion in humans. The Journal of
Clinical Endocrinology and Metabolism, 86(10), 5083-5086.
Broglio, F., Gottero, C., Prodam, F., Destesfanis, S., Gauna, C.,
Me, E., ... Ghigo, E. (2004). Ghrelin secretion is inhibited by
glucose load and insulin-induced hypoglycaemia but unaffected
by glucagon and arginine in humans. Clinical Endocrinology,
61, 503-509. doi:10.1111/j.1365-2265.2004.02121.x [PubMed]
Kellerer, M., Lammers, R., Fritsche, A., Strack, V., Machicao,
F., Borboni, P., Ullrich, A., & Haring, H. U. (2001). Insulin
inhibits leptin receptor signaling in HEK293 cells at the level
mechanism for
hyperinsulinaemia-associated leptin resistance. Diabetologia,
44, 1125-1132. [PubMed]
Lustig, R. H. (2013, October). Sugar, hormones and addiction.
Symposium conducted at The Lifestyle Intervention
Conference, Las Vegas, NV.
Jastreboff, A. M., Sinha, R., Lacadie, C., Small, D. M.,
Sherwin, R. S., & Potenza, M. N. (2013), Neural correlates of

Alan Aragons Research Review February/March 2014














stress- and food cue-induced food craving in obesity. Diabetes

Care, 36, 394-402. doi:10.2337/dc12-1112 [PubMed]
Daws, L. C., Avison, M. J., Robertson, S. D., Niswender, K.
D., Galli, A., & Saunders, C. (2011). Insulin signaling and
doi:10.1016/j.neuropharm.2011.02.028 [PubMed]
Zimmerman, U. S., Buchmann, A., Steffin, B., Dieterle, C. &
Uhr, M. (2006). Alcohol administration acutely inhibits ghrelin
secretion in an experiment involving psychosocial stress.
doi:10.1111/j.13691600.2006.00026.x [PubMed]
Kraus, T., Reulbach, U., Bayerlein, K., Mugele, B.,
Hillemacher, T., Sperling, W., ... Bleich, S. (2004). Leptin is
associated with craving in females with alcoholism. Addiction
Biology, 9, 213-219. doi:10.1080/13556210412331292541
Rojdmark, S., Calissendorff, J., & Brismar, K. (2001). Alcohol
ingestion decreases both diurnal and nocturnal secretion of
leptin in healthy individuals. Clinical Endorcrinology, 55, 639647. [PubMed]
Lenz, B., Schopp, E., Muller, C. P., Bleich, S., Hillemacher, T.,
& Kornhuber, J. (2012). Assocaition of V89L SRD5A2
polymorphism with craving and serum leptin levels in male
alcohol addicts. Psychopharmacology, 224, 421-429.
doi:10.1007/s00213-012-2770-5 [PubMed]
Grucza, R. A., Krueger, R. F., Racette, S. B., Norberg, K .E.,
Hipp, P. R., & Bierut, L. J. (2010). The emerging link between
alcoholism risk and obesity in the United States. Archives of
doi:10.1001/archgenpsychiatry.2010.155 [PubMed]
Ceylan-Isik, A. F., McBride, S. M., & Ren, J. (2010). Sex
difference in alcoholism: Who is at greater risk for
development of alcoholic complication? Life Sciences, 87, 133138. doi:10.1016/j.lfs.2010.06.002 [PubMed]
Jerlhag, E., Egecloglu, E., Landgren, S., Salome, N., Hellg, M.,
Moechars, D., ... Engel, J. A. (2009). Requirement of central
ghrelin signaling for alcohol reward. Proceedings of the
National Academy of Sciences, 106(27), 11318-11323.
Umhau, J. C., Petrulis, S. G., Diaz, R., Riggs ,P. A., Biddison,
J. R., & George, D. T. (2002). Long-term abstinent alcoholics
have a blunted blood glucose response to 2-deoxy-d-glucose.
Alcohol and Alcoholism, 37(6), 586-90. [PubMed]
Krahn, D., Grossman, J., Henk, H., Mussey, M., Crosby, R., &
Gosnell, B. (2006). Sweet intake, sweet-liking, urges to eat, and
weight change: Relationship to alcohol dependence and
doi:10/1016/j.addbeh.2005.05.056 [PubMed]
Blum, K., Sheridan, P. J., Wood, R. C., Braverman, E. R.,
Chen, T. J. H., Cull, J. G., & Comings, D. E. (1996). The D2
dopamine receptor gene as a determinant of reward deficiency
syndrome. Journal of the Royal Society of Medicine, 89, 396400. [PubMed]
Dumesnil, C., Dauchet, L., Ruidavets, J. B., Bingham, A.,
Arveiler, D., Ferrieres, J., ... Dallongeville, J. (2013). Alcohol
consumption patterns and body weight. Annals of Nutrition and
Metabolism, 62, 91-97. doi:10.1159/000342839 [PubMed]
Neale, A., Abraham, S., & Russell, J. (2008). "Ice" use and
eating disorders: A report of three cases. International Journal
of Eating Disorders, 42, 188-191. doi:10.1002/eat.20587

[Back to Contents]

Page 9

68. Cabeza de Vaca, S., & Carr, K. D. (1998). Food restriction

enhances the central rewarding effect of abused drugs. The
Journal of Neuroscience, 18(8), 7502-7510. [PubMed]
69. Jerlhag, E., Egecioglu, E., Dickson, S. L., & Engel, J. A.
(2010). Ghrelin receptor antagonism attenuates cocaine- and
amphetamine-induced locomotor stimulation, accumbal
dopamine release, and conditioned place preference.
Psychopharmacology, 211, 415-422. doi:10.1007/s00213-0101907-7 [PubMed]
70. Clifford, P. S., Rodriguez, J., Schul, D., Hughes, S., Kniffin, T.,
Hart, N., ... Martinez, J. (2012). Attenuation of cocaine-induced
locomotor sensitization in rats sustaining genetic or
pharmacologic antagonism of ghrelin receptors. Addiction
doi:10.1111/j.13691600.2011.00339.x [PubMed]
71. Janowsky, D. S., Pucilowski, O., & Buyinza, M. (2003).
Preference for higher sucrose concentrations in cocaine
abusing-dependent patients. Journal of Psychiatric Research,
37, 35-41. [PubMed]
72. Levandowski, M. T., Viola, T. W., Tractenberg, S. G.,
Teixeira, A. L., Brietzke, E., Bauer, M. E., & Grassi-Oliveira,
R. (2013). Adipokines during early abstinence of crack cocaine
in dependent women reporting childhood maltreatment.
doi:10.1016/j.psychres.2013.07.007 [PubMed]
73. Fox, H. C., D'Sa, C., Kimmerling, A., Siedlarz, K. M., Tuit, K.
L., Stowe, R., & Sinha, R. (2012). Immune system
inflammation in cocaine dependent individuals: implications
for medications development. Human Psychopharmacology:
Clinical and Experimental, 27, 156-166. doi:10.1002/hup.1251
74. Wiss, D. A., & Waterhous, T. S. (2013). Nutrition therapy for
eating disorders, substance use disorders, and addictions. In
Brewerton, T. D., & Dennis, A. B., Eating disorders, substance
use disorders, and addictions. (In Press). Springer Publishing.
75. Curran, H. V., & Robjant, K. (2006). Eating attitudes, weight
concerns and beliefs about drug effects in women who use
ecstasy. Journal of Psychopharmacology, 20(3), 425-431.
doi:10.1177/0269881106060584 [PubMed]
76. Kobeissy, F. H., Jeung, J. A., Warren, M. W., Geier, J. E., &
Gold, M. S. (2007). Changes in leptin, ghrelin, growth
hormone and neuropeptide-Y after an acute model of MDMA
and methamphetamine exposure in rats. Addcition Biology, 13,
15-25. doi:10.1111/j.1369-1600.2007.00083.x [PubMed]
77. Shalev, U., Yap, J., & Shaham, Y. (2001). Leptin attenuates
acute food deprivation-induced relapse to heroin seeking. The
Journal of Neuroscience, 21(4):RC129. [PubMed]
78. Nolan, L. J., & Scagnelli, L. M. (2007). Preference for sweet
foods and higher body mass index in patients being treated in
long-term methadone maintenance. Substance Use and Misuse,
42, 1555-1566. doi:10.1080/10826080701517727 [PubMed]
79. Housova, J., Wilczek, H., Haluzik, M. M., Kremen, J., Krizova,
J., & Haluzik, M. (2005). Adipocyte-derived hormones in
heroin addicts: The influence of methadone maintenance
treatment. Physiological Research, 54, 73-78. [PubMed]
80. D'Cunha, T. M., Sedki, F., Macri, J., Casola, C., & Shalev
(2013). The effects of chronic food restriction on cue-induced
heroin seeking in abstinent male rats. Psychopharmacology,
225, 241-250. doi:10.1007/s00213-012-2810-1 [PubMed]
81. Maric, T., Sedki, F., Ronfard, B., Chafetz, D., Shalev, U.
(2012). A limited role for ghrelin in heroin self-administration
and food deprivation-induced reinstatement of heroin seeking
Alan Aragons Research Review February/March 2014














in rats. Addiction Biology, 17(3), 613-622. doi:10.1111/j.13691600.2011.00396.x [PubMed]

Krahn, D. D. (1991). The relationship of eating disorders and
substance abuse. Journal of Substance Abuse, 3(2), 239-253.
Munn-Chernoff, M. A., Duncan, A. E., Grant, J. D., Wade, T.
D., Agrawal, A., Bucholz, K. K., ... Heath, A. C. (2013). A
twin study of alcohol dependence, binge eating, and
compensatory behaviors. Journal of Studies on Alcohol and
Drugs, 74, 664-673. [PubMed]
Robinson, C., & McCreary, C. (2011, July). The relationship
between a history of substance use disorders and weight loss
success: A program evaluation of WLA MOVE! level 2.
Hodgkins, C., Frost-Pineda, K., & Gold, M. S. (2007). Weight
gain during substance abuse treatment: The dual problem of
addiction and overeating in an adolescent population. Journal
doi:10.1300/j069v26s01_05 [PubMed]
Levine, A. S., Kotz, C. M., & Gosnell, B. A. (2003). Sugar and
fats: The neurobiology of preference [Special section]. Journal
of Nutrition, 831S-834S.
Kozak, A. T., & Fought, A. (2011). Beyond alcohol and drug
addiction. Does the negative trait of low distress tolerance have
an association with overeating? Appetite, 57, 578-581.
doi:10.1016/j.appet.2011.07.008 [PubMed]
Fischer, S., Anderson, K. G., & Smith, G. T. (2004). Coping
with distress by eating or drinking: Role of trait urgency and
expectancies. Psychology of Addictive Behaviors, 18(3), 269274. doi:10.1037/0893-164X.18.3.269 [PubMed]
Czarlinksi, J. A., Aase, D. M., & Jason, L. A. (2012). Eating
disorders, normative eating self-efficacy and body image selfefficacy: Women in recovery homes. European Eating
Disorders Review, 20, 190-195. [PubMed]
Cowan, J., & Devine, C. (2008). Food, eating, and weight
concerns of men in recovery from substance addiction.
Appetite, 50, 33-42. doi:10.1016/j.appet.2007.05.006 [PubMed]
Grant, L. P., Haughton, B., & Sachan, D. S. (2004). Nutrition
education is positively associated with substance abuse
treatment program outcomes. Journal of the American Dietetic
Association, 104, 604-610. doi:10.1016/j.jada.2004.01.008
Barbadoro, P., Ponzio, E., Pertosa, M. E., Aliotta, F., DErrico,
M. M., Prospero, E., & Minelli, A. (2010). The effects of
educational intervention on nutritional behaviour in alcoholdependent patients. Alcohol and Alcoholism, 46(1), 77-79.
doi:10.1093/alcalc/agq075 [PubMed]
Curd, P., Ohlmann, K., & Bush, H. (2013). Effectiveness of a
voluntary nutrition education workshop in a state prison.
Journal of Corrective Health Care, 19(2), 144-150.
doi:10.1177/107/1078345812474645 [PubMed]
Sandwell, H, & Wheatley, M. (2009). Healthy eating advice as
part of drug treatment in prisons. Prison Service Journal, 182,
15-26. [Full PDF]

[Back to Contents]

Page 10

Structural balance theory: does your butt care about

your biceps?
by Menno Henselmans
Everything that sucks is good for you. Thats what our intuition
tells us. Give someone a piece of food that tastes disgusting and
tell them its really good for them. Theyll take your word for it.
Give someone a piece of this cheesecake and afterwards tell
them its healthy and theyll go Yeah, right. Even worse, if you
tell them beforehand, theyll enjoy the cheesecake less.1 We
readily believe that stretching is good for us because it hurts and
its boring, even though stretching often doesnt help at all.
Bodybuilders take this masochistic no pain no gain outlook on
life to extremes. Unseasoned chicken with sauceless rice and
plain broccoli, anyone? One particular fitness concept that has
completely escaped scientific scrutiny because of its inherent
plausibility is structural balance theory. To show that nothing
escapes the truth, I will hereby shine the light of science on this
Structural balance theory 101
I was going to call this structural balance theory for dummies,
but this didnt seem applicable, because structural balance theory
doesnt seem to have any advanced version. In fact, it has no
operational definition at all.* Structural balance theory was
popularized by Charles Poliquin in the 90s and it has since
spread like a hookers legs in the fitness community. The theory
in its currently most common form is that your body tries to
maintain a certain balance between muscular strength in every
part of the body or in every movement pattern (as I said, the
definition varies depending on who you ask). If any body part or
movement pattern becomes overdeveloped, the nervous system
shuts it down to prevent further imbalance. For example, a weak
rotator cuff is often said to limit bench press strength.
Specifically, Poliquin proposed the following strength ratios for
perfect structural balance in the upper body.
[Footnote]*: According to Poppers falsifiability criterion, this
alone would make it pseudoscience.

Before analyzing this theory, I should say that although I have

previously also reviewed Poliquins BioSignature Modulation, I
am only interested ideas, not their creators. As president
Roosevelt said with equal arrogance and eloquence, Great
minds discuss ideas; average minds discuss events; small minds
discuss people. The fact that Poliquin is the man behind both
theories is simply an unfortunate coincidence of his ability to
come up with plausible theories without supporting them with
evidence. Whats the point of discussing theories that do not at
least seem to make sense? You dont see me criticize CrossFits
use in bodybuilding, for example. That is like taking candy from
a child. (CrossFit, like circuit training, was designed as a bit-ofeverything social workout, not an optimal bodybuilding or
powerlifting program.)
Back to the interesting stuff: does your body care about
structural balance? Ill look at structural balance from 7
1. Antagonist inhibition for strength
Structural balance theory says that if the biceps gets stronger and
the triceps doesnt, biceps activity will be restrained by the
nervous system. Like one of the horses pulling a carriage being
reined back by the driver because it was trying to run faster than
the other horses. Sounds plausible, right?
Plausible but deceptive. A more valid analogy would be a
carriage being pulled by 2 horses in opposite directions. Horse
Triceps wants to move to the dumbbell rack to do overhead
extensions, but horse Biceps wants to move to the mirror to look
at his guns. This situation is regulated by antagonist coactivation. Antagonist co-activation is the activity of muscles
with the opposite function of the prime movers (the agonists).
For example, during a biceps curl the triceps is an antagonist.
Antagonist co-activation is required to stabilize movement. The
triceps basically corrects for overenthusiastic actions of the
biceps. Now heres where the research gets interesting. When
the prime movers become stronger, it is not their activity that is
restrained by the nervous system but that of the antagonists.2 So
during a curl, the stronger your biceps gets, the weaker your
triceps contracts. The motor cortex, the part of your brain that
controls movement, learns to maximally contract the biceps
during a curl with minimal interference from the triceps.
This makes evolutionary sense. It is an efficient adaptation. A
limitation on prime mover activity would be highly unadaptive.
Since nature only cares about function and adaptivity, we see
extreme structural imbalance between antagonists in nature in
various animals. A good example is the jaws of a crocodile.
Some crocodiles have a bite force of 3,700 pounds per square
inch (psi).18 Thats the equivalent of 16,460 newtons, roughly
the force needed to lift 3691 pounds (1677 kg). You may be able
to clench your teeth into a piece of unseasoned chicken with 150
to 200 psi (890 newtons). Yet you can easily hold a crocs jaws
shut because the muscles that open instead of close the jaw are
extremely weak. In humans, we see this in a less extreme form
in the weakness of the tibialis anterior on your shins compared to
the strength of the calves. Opposite function, opposite strength

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 11

2. European weightlifting secrets

The original idea of using strength ratios for various exercises
came from European weightlifters. They used ratios between the
Olympic lifts and accessory movements like the squat to assess
how to improve the Olympic lifts. If a lifter didnt progress in
the Clean & Jerk and her front squat was comparatively weak,
getting stronger in the front squat became a priority.
This may seem like structural balance training, but its not. The
accessory exercises chosen were highly specific to the
corresponding Olympic lift. Front squats build the Clean & Jerk,
because the catching position of the C&J is essentially a front
In this case, its a matter of using different exercises to cause
morphological and neural adaptations in the same muscle groups
(muscle growth and power). It has nothing to do with structural
balance with other parts of the body. Front squats are a better
exercise choice to gain muscle and strength, but the Olympic
lifts themselves are required for the nervous system to master the
Snatch and the Clean & Jerk. Front squats build the foundation
and the Olympic lifts convert this potential into exercise specific
In fact, Olympic weightlifters are an excellent example of
athletes who are not structurally balanced. Many of them do
nothing but squats and Olympic lifts. That means almost all of
their training is in the frontal plane: the bar only goes up or
down vertically. Imagine that, decades of Olympic weightlifters
held back because they didnt know their performance in the
Scott barbell curl wasnt structurally balanced.
3. A muscle is just a dumb piece of meat.
Thats what my friend and colleague Brge Fagerli says in our
seminars together to explain that muscle growth is mostly a local
process. The stimulus for muscle growth tension, muscle
damage or metabolic stress occurs in the muscle and the
subsequent adaptation follows in the same place. Almost
everything we know about the mechanisms of muscle growth
happens within the muscle. The following is a rough overview of
how muscle grows.3-5





When you put tension on a muscle, its muscle fibers

The muscle fibers release growth factors like insulinlike growth factor 1 (IGF-1) and myokines like IL-6 to
signal the need for repair (myogenic signaling).
The mTOR master enzyme integrates all the signals for
muscle growth, such as amino acid availability and the
presence of growth factors, and then translates this
information for your genes (translation initiation).
Your genes are located within muscle cell nuclei that
function as command centers in their region of a muscle
fiber. They contain the blueprint to create new proteins.
Nearby satellite cells are activated and fuse to the
muscle fibers to enlarge them (myonuclear addition)
and aid in the creation of more new muscle proteins.

Alan Aragons Research Review February/March 2014

As such, there is no plausible physiological mechanism by

which one body part could limit growth in another (which is
what structural balance theory claims).
4. Does training your legs make your upper body bigger?
Strength training newbies are often told to exercise their legs.
When they protest that they dont really care about leg muscle
growth, theyre told that training their legs will make their upper
body larger too. The arguments are:
A) Heavy compound leg work like squats increases the
production of anabolic hormones. The increases in
circulating testosterone, growth hormone and IGF-1
then amplify the training effect in other body parts.
B) The body grows best in proportion. Your body wont
build a Schwarzeneggerian torso on chicken legs. AKA
structural balance theory.
The research in support of argument A, the effect of hormones,
is methodologically weak and inconsistent.3,6-8 In the only 2
studies in which training the lower body increased the effect of
training the upper body (or the other way around), the
participants performed squats immediately before training their
biceps.9,10 The authors concluded that this timing is ideal, since
the biceps is trained exactly when anabolic hormone
concentrations are at their peak. So, if theres any validity at all
to the idea that training your legs makes your upper body bigger
(or the other way around), the mechanism is hormonal and it has
nothing to do with structural balance theory.
In other words, your body does not care about structural balance
between the upper and lower body. You only need to look
around you to see that upper and lower body growth are only
proportionate in people who train their whole body equally.
Look at how top-heavy some ring gymnasts are.
Look at the freakily large quads of sprint cyclists.
Look at the amazing physiques of wheelchair
bodybuilders and the performance of wheelchair
Also, compare chicken leg syndrome to Brazilian booty
syndrome (nature, how I love thee).
5. The cross-training effect
If you only train your right biceps, your left biceps will become
stronger too. Not only that, your triceps gets stronger too, even
on the untrained side.13 This is called the cross-training effect. Is
this finally proof of structural balance theory? How can crosstraining occur if muscle is just dumb meat?
Cross-training has nothing to do with muscular adaptations.
Researchers have used every measurement technique known to
mananthropometric measurements, imaging techniques,
analysis of the muscle cross-sectional area, etc.to see if the
untrained limb gets bigger. It doesnt.11,12
The mastermind behind the cross-training effect is your nervous
system, mainly your brain (specifically the motor cortex). Many
parts of your body are operated by some of the same parts of
[Back to Contents]

Page 12

your nervous system. So when the nervous system learns how to

recruit your muscles on one side of your body, some of these
neural adaptations can also be used by the other side. Thats why
some researchers now call it the cross-education effect.11,12
This is a form of structural balance, but it is in fact the complete
opposite of structural balance theory. Structural balance theory
says that when your right biceps gets too strong relative to your
triceps or your other arm, it is shut down. What the crosseducation effect and antagonist co-activation both show is that
this doesnt happen. Instead, the triceps, even the other arm,
adapts along with the biceps. Basically, your body automatically
maintains structural balance, although putting it this way is
misleading. A better way to put it is that your body cares about
strength symmetry both within a limb (e.g. triceps/biceps) and
across limbs (e.g. right arm/left arm).
6. Sports injuries
Why does your body care about strength symmetry but not
structural balance? Because strength asymmetry puts you at risk
for injury, at least outside of the gym in uncontrolled settings
like sports.14-17 The body doesnt care about aesthetics, but
160,000+ years of human evolution sure taught it to care about
injuries.21 Balance in the actual structures of your body, like
proportionate muscle development, is irrelevant as long as
everything is functional. If you never use your legs, having
chicken legs is not dysfunctional. Yet if you use your legs and
one leg is stronger than the other, the stronger leg is at risk for
overuse injuries and the weaker leg is not adapted to cope with
the forces generated by both legs.
Thus, the relevance of strength symmetry depends on the type of
exercise you do. Arm wrestlers specializing in only 1 arm are a
good example of how extreme strength asymmetry can still be
functional. Physique athletes should care about symmetry and
proportion in body parts, but strength asymmetry is rarely a
cause for concern. Strength athletes mostly use a barbell or other
type of symmetric implement like rings, kegs or bars. As long as
these movements remain symmetric, correcting strength
asymmetry is rarely needed. Other athletes involved in sports
that do not automatically lead to symmetric strength
development have to pay attention to thisespecially in
uncontrolled and high impact sports.

muscle with the same function or even a division (head) of the

same muscle, what is left becomes stronger. Compensatory
hypertrophy occurs in the remaining muscle. This again makes
no sense from a structural balance perspective, which would
require that the remaining body part becomes weaker to retain
structural balance. But it makes perfect sense from an
evolutionary perspective. The body adapts without concern for
anything but function. Lost half of your calves? Better learn to
walk on the other half.
Structural balance theory is good broscience: plausible at a
glance, but ill-defined and completely lacking in scientific study.
Closer inspection reveals that it has no plausible neural or
physiological mechanism, it makes no evolutionary sense, it
cannot explain the wide display of structural imbalance in nature
and sports, and it does not correspond with any empirical
evidence. . .except an anecdote from Charles Poliquin.
It is the power of a well-told story. From childhood onwards, we
like to believe stories. They make things real for us. Like a
poison to our judgment, they make us forget context and forego
reason. Let science be the antidote to anecdote, and reject
structural balance theory.
More of Mennos articles are
accessible at his website,
Mennos ideas on everything
related to fat loss and muscle
hypertrophy can be seen in his
course on optimal program
design and his upcoming
seminar in Miami with Brge
Fagerli, who I interviewed in
the August 2012 issue of


7. Removing body parts

If youre not convinced of the bodys disregard for structural
balance, lets look at an extreme example. Weve looked at how
the body responds to muscle growth of muscles with opposing
functions, muscles on the other limb and muscles on the upper
vs. lower half of the body. But what happens when there is
extreme structural imbalance between muscles with the same
function (synergists)? This scenario rarely occurs in humans
because these muscles will be activated together, and will
therefore grow together. Fortunately (?), we can do much more
extreme experiments on animals.


Researchers have looked at what happens when you surgically

remove body parts (ablation) or cut them off from the nervous
system (denervation) in various animals.19,20 When you remove a


Alan Aragons Research Review February/March 2014



Raghunathan R, Walker Naylor R, Hoyer WD. The Unhealthy

= Tasty Intuition and Its Effects on Taste Inferences,
Enjoyment, and Choice of Food Products. Journal of
Marketing: October 2006, Vol. 70, No. 4, pp. 170-184. [AMA]
. Dal Maso F, Longcamp M, Amarantini D. Training-related
decrease in antagonist muscles activation is associated with
increased motor cortex activation: evidence of central
mechanisms for control of antagonist muscles. Exp Brain Res.
2012 Aug;220(3-4):287-95. [PubMed]
Mitchell CJ, Churchward-Venne TA, Bellamy L, Parise G,
Baker SK, Phillips SM. Muscular and systemic correlates of
resistance training-induced muscle hypertrophy. PLoS One.
2013 Oct 9;8(10):e78636. [PubMed]
Schoenfeld BJ. The mechanisms of muscle hypertrophy and
their application to resistance training. J Strength Cond Res.
2010 Oct;24(10):2857-72. [PubMed]
West DW, Burd NA, Staples AW, Phillips SM. Human
exercise-mediated skeletal muscle hypertrophy is an intrinsic
process. Int J Biochem Cell Biol. 2010 Sep;42(9):1371-5.

[Back to Contents]

Page 13















Phillips SM. Strength and hypertrophy with resistance training:

chasing a hormonal ghost. Eur J Appl Physiol. 2012
May;112(5):1981-3; author reply 1985-7. [PubMed]
West DW, Burd NA, Tang JE, Moore DR, Staples AW,
Holwerda AM, Baker SK, Phillips SM. Elevations in ostensibly
anabolic hormones with resistance exercise enhance neither
training-induced muscle hypertrophy nor strength of the elbow
flexors. J Appl Physiol (1985). 2010 Jan;108(1):60-7.
West DW, Kujbida GW, Moore DR, Atherton P, Burd NA,
Padzik JP, De Lisio M, Tang JE, Parise G, Rennie MJ, Baker
SK, Phillips SM. Resistance exercise-induced increases in
putative anabolic hormones do not enhance muscle protein
synthesis or intracellular signalling in young men. J Physiol.
2009 Nov 1;587(Pt 21):5239-47. [PubMed]
Hansen S, Kvorning T, Kjaer M, Sjgaard G. The effect of
short-term strength training on human skeletal muscle: the
importance of physiologically elevated hormone levels. Scand J
Med Sci Sports. 2001 Dec;11(6):347-54. [PubMed]
Rnnestad BR, Nygaard H, Raastad T. Physiological elevation
of endogenous hormones results in superior strength training
adaptation. Eur J Appl Physiol. 2011 Sep;111(9):2249-59.
Farthing JP, Borowsky R, Chilibeck PD, Binsted G, Sarty GE.
Neuro-physiological adaptations associated with crosseducation of strength. Brain Topogr. 2007 Winter;20(2):77-88.
Epub 2007 Oct 12. [PubMed]
Carroll TJ, Herbert RD, Munn J, Lee M, Gandevia SC.
Contralateral effects of unilateral strength training: evidence
and possible mechanisms. J Appl Physiol (1985). 2006
Nov;101(5):1514-22. [PubMed]
Sariyildiz M, Karacan I, Rezvani A, Ergin O, Cidem M. Crosseducation of muscle strength: cross-training effects are not
confined to untrained contralateral homologous muscle. Scand
J Med Sci Sports. 2011 Dec;21(6):e359-64. [PubMed]
Knapik JJ, Bauman CL, Jones BH, Harris JM, Vaughan L.
Preseason strength and flexibility imbalances associated with
athletic injuries in female collegiate athletes. Am J Sports Med.
1991 Jan-Feb;19(1):76-81. [PubMed]
Nadler SF, Malanga GA, DePrince M, Stitik TP, Feinberg JH.
The relationship between lower extremity injury, low back
pain, and hip muscle strength in male and female collegiate
athletes. Clin J Sport Med. 2000 Apr;10(2):89-97. [PubMed]
Devan MR, Pescatello LS, Faghri P, Anderson J. A Prospective
Study of Overuse Knee Injuries Among Female Athletes With
Muscle Imbalances and Structural Abnormalities. J Athl Train.
2004 Sep;39(3):263-267. [PubMed]
Burnham RS, May L, Nelson E, Steadward R, Reid DC.
Shoulder pain in wheelchair athletes. The role of muscle
imbalance. Am J Sports Med. 1993 Mar-Apr;21(2):238-42.
Erickson GM, Gignac PM, Steppan SJ, Lappin AK, Vliet KA,
Brueggen JD, Inouye BD, Kledzik D, Webb GJ. Insights into
the ecology and evolutionary success of crocodilians revealed
through bite-force and tooth-pressure experimentation. PLoS
One. 2012;7(3):e31781. [PubMed]
Snow MH. Satellite cell response in rat soleus muscle
undergoing hypertrophy due to surgical ablation of synergists.
Anat Rec. 1990 Aug;227(4):437-46. [PubMed]
Walsh JV Jr, Burke RE, Rymer WZ, Tsairis P. Effect of
compensatory hypertrophy studied in individual motor units in
medial gastrocnemius muscle of the cat. J Neurophysiol. 1978
Mar;41(2):496-508. [PubMed]
Wells JC, Stock JT. The biology of the colonizing ape. Am J
Phys Anthropol. 2007;Suppl 45:191-222. [PubMed]

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 14

Overfeeding polyunsaturated and saturated fat causes
distinct effects on liver and visceral fat accumulation
in humans.
Rosqvist F, Iggman D, Kullberg J, Jonathan Cedernaes J,
Johansson HE, Larsson A, Johansson L, Ahlstrm H, Arner P,
Dahlman I, Risrus U. Diabetes. 2014 Feb 18. [Epub ahead of
print] [PubMed]
BACKGROUND: Excess ectopic fat storage is linked to type 2
diabetes. The importance of dietary fat composition for ectopic
fat storage in humans is unknown. PURPOSE: We investigated
liver fat accumulation and body composition during overfeeding
saturated (SFA) or polyunsaturated (PUFA) fat. DESIGN:
LIPOGAIN was a double-blind, parallel-group, randomized trial.
Thirty-nine young and normal-weight individuals were overfed
muffins high in SFA (palm oil) or n-6 PUFA (sunflower oil) for
7 weeks. Liver fat, visceral (VAT), subcutaneous abdominal
(SAT), and total adipose tissue (TAT), pancreatic fat, and lean
tissue was assessed by MRI. Transcriptomics were performed in
SAT. RESULTS: Both groups gained similar weight. SFA
however markedly increased liver fat compared with PUFA and
caused 2-fold larger increase in VAT than PUFA. Conversely,
PUFA caused a nearly 3-fold larger increase in lean tissue than
SFA. Increase in liver fat directly correlated with changes in
plasma SFA and inversely with PUFA. Genes involved in
regulating energy dissipation, insulin resistance, body
composition and fat cell differentiation in SAT were
differentially regulated between diets, and associated with
increased PUFA in SAT. CONCLUSION: In conclusion,
overeating SFA promotes hepatic and visceral fat storage
whereas excess energy from PUFA may instead promote lean
tissue in healthy humans. SPONSORSHIP: The sponsors had
no role in the design and conduct of the study; collection,
management, analysis, and interpretation of the data; or
preparation, review, or approval of the manuscript.
Study strengths
The question of dietary fatty acids on health is huge and largely
unsolved. This study is innovative since its the first to compare
the overfeeding effects of the major source of omega-6 PUFA in
the diet (linoleic acid) with the major source of SFA (palmitic
acid). The study was meticulously blinded. Quality control was
bolstered by subjects receiving dietary counseling from a
Registered Dietitian (RD) every two weeks, and maintaining a
daily food diary. Erythrocyte membrane fatty acid composition
objectively assessed compliance to the treatment protocols.

As depicted above, the main findings were unanimously more

favorable changes in the PUFA overfeeding compared to SFA.
Despite similar gains in total bodyweight (1.6 kg, accomplished
by consuming an additional 750 kcal/day from fat-fortified
muffins). The ratio of lean:fat tissue gained in the PUFA group
was 1:1, whereas it was 1:4 in SFA, indicating an overall better
lean-partitioning effect of surplus energy from PUFA.
Furthermore, liver fat and visceral fat deposition was
significantly greater in SFA. Its notable that physical activity
did not change or differ between groups through throughout the
trial, which strengthens the validity of the other outcomes.

The authors acknowledged several limitations. First off, the

results might be limited to the subject profile (healthy, young
relatively lean lacto-ovo vegetarians with low baseline levels of
hepatic and visceral fat). The authors conceded that their results
still need confirmation in older populations and individuals with
type 2 diabetes or non-alcoholic fatty liver disease (NAFLD).
The short study duration (7 weeks) leaves open questions about
the long-term. Fixed spectrum models examined by the MRI
methods used do not cover the full range of lipids.

It was a diligent decision to use palmitic acid in the SFA

condition since its the most common SFA in the food supply,
including plant foods. However, the effects seen in this study
cannot necessarily be generalized to all SFAs. Palm oil was used
in the SFA overfeeding arm. Palm oils track record in the
literature on markers of cardiovascular health has generally been
neutral to positive.1-7 However, the present study clearly shows
superior results of omega-6 PUFA-rich sunflower oil in the
context of overfeeding. The authors speculate that this could be
due in part to the greater ease of oxidation, thus potentially
lowering the production of non-esterified fatty acids, which in
turn would lower triacylglycerol synthesis in the liver. Despite
the interesting results seen in the present study, I would caution
against generalizing this comparison to all SFA vs PUFA
sources. There could be other constituents within foods that can
differently influence outcomes. More comparisons are needed.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Study limitations

Page 15

Can we say what diet is best for health?

Katz DL, Meller S. Annu Rev Public Health. 2014 Mar
18;35:83-103. [PubMed]
ABSTRACT: Diet is established among the most important
influences on health in modern societies. Injudicious diet
figures among the leading causes of premature death and
chronic disease. Optimal eating is associated with increased life
expectancy, dramatic reduction in lifetime risk of all chronic
disease, and amelioration of gene expression. In this context,
claims abound for the competitive merits of various diets
relative to one another. Whereas such claims, particularly when
attached to commercial interests, emphasize distinctions, the
fundamentals of virtually all eating patterns associated with
meaningful evidence of health benefit overlap substantially.
There have been no rigorous, long-term studies comparing
contenders for best diet laurels using methodology that
precludes bias and confounding, and for many reasons such
studies are unlikely. In the absence of such direct comparisons,
claims for the established superiority of any one specific diet
over others are exaggerated. The weight of evidence strongly
supports a theme of healthful eating while allowing for
variations on that theme. A diet of minimally processed foods
close to nature, predominantly plants, is decisively associated
with health promotion and disease prevention and is consistent
with the salient components of seemingly distinct dietary
approaches. Efforts to improve public health through diet are
forestalled not for want of knowledge about the optimal feeding
of Homo sapiens but for distractions associated with
exaggerated claims, and our failure to convert what we reliably
know into what we routinely do. Knowledge in this case is not,
as of yet, power; would that it were so. SPONSORSHIP: None
My commentary
Since this is a review paper, its not conducive to my normal
assessment of methodological strengths & weaknesses. What Ill
do is offer my commentary. The cool thing is that the full text of
this article is available here, so you have the freedom to dig into
it on your own. Before I comment on the sections that jumped
out at me, let me first mention the general structure of the paper.
A summary of several major diet types is given: low-carb, lowfat, low-glycemic, Mediterranean, mixed/balanced such as
DASH & DPP, Paleolithic, vegan, & other (table here). After
these summaries, an attempt is made to elucidate commonalities
among the diets that lead to better health.
In their assessment, the authors take an impressively rigorous
look at each of the dietary regimes. The thorough-ness of the
paper makes it quite refreshing. When discussing low-carb diet,
they mentioned the interesting angle of an Eco-Atkins
approach (reviewed in the August 2010 AARR), which
essentially is a vegetarian version of the Atkins diet.8
Interestinglyat least in my viewthis foreshadowed a
potential bias in the authors perspective. Funny enough, the bias
I initially detected dropped down like a hammer in their final
analysis (Ill get to that).

economics by stating that, An emphasis on meat is an

inefficient basis for feeding a global population now in excess of
seven billion. Ethical concerns have been raised about meateating in general and in particular with regard to the treatment
of animals associated with feeding multitudes, along with
concerns about the environmental costs of heavily animal-based
diets. While this statement is still defensible, it certainly
borders on irrelevance given the specific topic of human health
effects of the various diets.
In contrast to the authors reaching outside of the nutritional
box to challenge low-carb, the diets they virtually exempt the
mixed, balanced diets (DASH & DPP) from any significant
criticism aside from an odd couple of oddly placed references to
the potential link between dairy intake and cancer9,10 when
discussing the DASH diet. Once again, this set off my bias
sensors. The DASH diet is rife with all of the trappings of
1980s saturated fat phobia (maximum of 6% of calories) and
cholesterol phobia (150 mg max). Challenging this, a recent
systematic review and meta-analysis by Chowdhury et al that
examined 32 observational studies (n=512,420) and 27
randomized controlled trials ( n=105,085) found no clear support
for the traditional recommendation to increase poly-unsaturated
fat intake and decrease saturated fat intake.11 In another recent
meta-analysis, Ramsden et al had similar findings, that no
lowering of cardiovascular risk factors was evident from
substituting unsaturated fats in place of saturated fats.12
The DASH diet is rooted in the attempt to lower blood pressure,
and in addition to its other restrictions, it aims to cap sodium at
2300 mg/day, with a footnote that 1500 mg was found to be even
better at lowering blood pressure in those with pre-existent
hypertension. Of course, this may be perfectly appropriatefor
hypertensives. However, there are adjacent clinical consequences
to consider. Graudal et al recently analyzed 167 intervention
studies and found that alongside decreased blood pressure,
sodium restriction also caused a 2.5% increase in cholesterol,
and a 7% increase in triglyceride.13
Moving toward the final analysis, the authors of the present
paper summed up the compatible elements of each of the diets
reviewed as: Limited refined starches, added sugars, processed
foods; limited intake of certain fats; emphasis on whole plant
foods, with or without lean meats, fish, poultry, seafood. This is
where I feel they should have halted the progression of their
conclusions and recommendations. However, they continue
onward and end up paying tribute to journalist Michael Pollans
famous saying by relaying, nearly verbatim, his recommendation
to eat food, not too much, mostly plants.14

Keep in mind that Im seeing a very subtle and delicate bias, but
a bias nonetheless. The authors step outside of the
health/nutrition realm per se, and delve into the realm of ethico-

Theres a certain degree of eloquence in that conclusion, but its

an oversimplification. At best, its too vague (at what point in
processing is food not food?). At worst, its misleading and
dismissive of the delicate contingencies of individual dietary
needs driven by preference, tolerance, and various physiological
demands. Given the broad gamut of diet types (from plant to
animal-dominant) that have shown similar clinical effectiveness
for various parameters, the mostly plants clause remains
speculative. Its not definitively supported by the current
evidence, especially when the rule is applied to percentage of
total energy. So, can we say what diet is best for health? On an
individual basis, yes we can. On a universal basis, we cannot.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 16

Study limitations
Effects of supplementing n-3 fatty acid enriched eggs
and walnuts on cardiovascular disease risk markers in
randomized, crossover, free-living intervention study.
Burns-Whitmore B, Haddad E, Sabat J, Rajaram S. Nutr J
2014, 13:29 [Epub ahead of print] [PubMed]
BACKGROUND: Plant and marine n-3 fatty acids (FA) may
favorably modify select markers of cardiovascular disease risk.
Whether supplementing the habitual diet of lacto-ovovegetarians (LOV) with walnuts (containing alpha-linolenic
acid, ALA) and n-3 FA enriched eggs (containing primarily
docosahexaenoic acid, DHA and ALA) would have equivalent
effects on CVD risk factors is explored in this study.
METHODS: In this study, 20 healthy free-living LOVs
following their habitual diet were randomly assigned in a
crossover design to receive one of three supplements: n-3 FA
enriched egg (6/week), walnuts (28.4 g, 6/week) or a standard
egg, 6/week (control) for 8 weeks each with 4-wk
membrane fatty acids, serum lipids and
inflammatory markers were measured at the end of
each treatment. RESULTS: Dietary compliance
was observed by an expected increase in
erythrocyte membrane ALA following the walnut
treatment and in DHA following the n-3 FA
enriched egg treatment. Walnut treatment lowered
serum triacylglycerol, total cholesterol and Apo B
(p < 0.05) compared to the standard egg but not the
n-3 FA enriched egg treatment. However, walnut
treatment significantly reduced total: HDL
cholesterol ratio compared to both egg treatments.
There were no differences between treatments for
CONCLUSION: For LOV, a direct source of
DHA such as n-3 FA enriched eggs seems
necessary to increase membrane levels of DHA.
However for producing an overall favorable blood
lipid profile, daily consumption of a handful of
walnuts rich in ALA may be a preferred option for
lacto-ovo vegetarian. SPONSORSHIP: This work
was supported by the American Egg Board
Fellowship; Agriculture Research Institute (Grant)
from California
Polytechnic University, Pomona;
California Walnut Commission (in-kind donation of walnuts);
Chino Valley Ranchers (in-kind donation of eggs).

This was a free-living study, which is beneficial for testing realworld conditions, but the trade-off is that it also allows for a
higher degree of inter-individual dietary variation, and thus less
control. Nevertheless, it was reported (according to recall data)
that energy, carbohydrate, fiber, total fat, saturated fat, and
monounsaturated fat were not significantly different between the
three treatments, which lessens this concern. However, a
potential confounder was the higher protein intake in the
supplemental egg conditions. Specific data regarding habitual
physical activity levels were missing, and would have provided
some useful insight. A final limitation is that the results might be
limited to the subject profile (healthy, normolipidemic). The
authors further acknowledge that, ...caution must be used in
interpretation of the results for people with chronic diseases,
people that consume other animal products and people that may
exhibit sensitivity to dietary cholesterol.

This study is the first to ever compare the blood lipid-altering

effects of walnuts with that of n-3 fatty acid-enriched eggs and
regular eggs. This investigation is highly relevant to lacto-ovo
vegetarians, who comprise a large segment of the vegetarian
population, and who could benefit from fortification and
supplement tactics to optimize their diets further. A crossover
design helped alleviate the compromised statistical power of the
relatively small subject number (n=20). Participants received
diet counseling and their intervention foods from a Registered
Dietitian (RD) every two weeks during the treatment periods,
which bolstered compliance with the experimental protocols.

As seen above, one of the main findings of this study was that
the walnut treatment showed a significant decrease in total
cholesterol, triglyceride, and apo B compared to the standard
eggs but not the n-3 FA-enriched eggs. However, the total-C:
HDL-C ratio was lower in the walnut treatment compared to
both the egg treatments. In this sense, it can be said that walnuts
have more favorable effects on blood lipids than both the
standard and the n-3 eggs. Notably, that the n-3 eggs caused
lower cholesterol levels than the standard eggs but not to a
statistically significant degree. The other main finding was that
n-3 eggs were more effective at increasing membrane levels of
DHA, which has implications for cardiovascular disease
prevention.15 The ALA content of walnuts was insufficient at
causing a similar effect via endogenous conversion to DHA. The
practical application suggested by these outcomesat least for
lacto-ovo vegetariansis to cover the bases by consuming both
walnuts as well as a direct DHA source like n-3-enriched eggs.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Study strengths

Page 17

Resistance training in overweight women on a

ketogenic diet conserved lean body mass while
reducing body fat.
Jabekk PT, Moe IA, Meen HD, Tomten SE, Hstmark AT. Nutr
Metab (Lond). 2010 Mar 2;7:17. [PubMed]
BACKGROUND: The aim of the present study was to compare the
effects of 10 weeks resistance training in combination with either a
regular diet (Ex) or a low carbohydrate, ketogenic diet (Lc+Ex) in
overweight women on body weight and body composition.
METHODS: 18 untrained women between 20 and 40 years with
BMI >/= 25 kg*m-2 were randomly assigned into the Ex or Lc+Ex
group. Both groups performed 60-100 min of varied resistance
exercise twice weekly. Dietary estimates were based on two 4-day
weighed records. Body composition was estimated using Dual
Energy X-ray Absorptiometry. Fasting blood samples were
analyzed for total-, HDL- and LDL-cholesterol, triacylglycerols,
and glucose. RESULTS: 16 subjects were included in the analyses.
Percentage of energy (En%) from carbohydrates, fat and protein
was 6, 66, and 22 respectively in the (Lc+Ex) group and 41, 34, 17
in the Ex group. Mean weight change (pre-post) was -5.6 +/- 2.6 kg
in Lc+Ex; (p < 0.001) and 0.8 +/- 1.5 kg in Ex; (p = 0.175). The
Lc+Ex group lost 5.6 +/- 2.9 kg of fat mass (p = 0.001) with no
significant change in lean body mass (LBM), while the Ex group
gained 1.6 +/- 1.8 kg of LBM (p = 0.045) with no significant change
in fat mass (p = 0.059). Fasting blood lipids and blood glucose were
not significantly affected by the interventions. CONCLUSION:
Resistance exercise in combination with a ketogenic diet may
reduce body fat without significantly changing LBM, while
resistance exercise on a regular diet may increase LBM in without
significantly affecting fat mass. Fasting blood lipids do not seem to
be negatively influenced by the combination of resistance exercise
and a low carbohydrate diet. SPONSORSHIP: Ketolyse AS,

Study strengths
This study is innovative since its the first and still the only one
to compare the chronic effect of a ketogenic diet with a
conventional diet in subjects undergoing progressive resistance
training. Every exercise session was supervised by research
personnel. Body composition was assessed via dual X-ray
absorptiometry (DXA). Urine reagent strips were used to
objectively assessed the adherence of the ketogenic diet group.
4-day weighed food records were taken at the 4th and 7th week
of the intervention in order to analyze dietary intake.
Study limitations
The authors gave a detailed description of the ketogenic groups
diet programming (specific carbohydrate restriction with ad
libitum intake of protein and fat-rich foods, dietary guide book,
use of reagent strips to detect ketosis). Surprisingly, they
completely omitted any of the programming details of the
regular/control diet or whether or not the subjects were issued
any interventional instructions at all. Several limitations are
acknowledged by the authors: small study sample (16 subjects
completed), insulin sensitivity not measured, neither was
albumin bound fatty acids, plasma lipoprotein distribution or
fatty acid distribution. They further acknowledged that only
fasting values were assessed and that they did not measure sex or
Alan Aragons Research Review February/March 2014

thyroid hormones, catecholamines, glucagon, or corticosteroids

all of which could have played roles in the metabolic effects of
the diets. A final acknowledged limitation was that menstrual
cycle was not coordinated with blood collection. I would add
that the use of untrained subjects leaves question about how
trained subjects might respond in a similar comparison.

Above is the breakdown of the diets in all of their disparate

glory, and as we go over the results, it will help to refer to how
these differences played in. The ketogenic group lost a
significant amount of total bodyweight (5.6 kg), while the
control group slightly gained (0.8 kg). The weight lost in the
ketogenic group was almost exclusively body fat, while no
significant change in fat mass was seen in the control group.
Interestingly, the control group gained a significant amount of
lean body mass (1.8 kg), while the ketogenic group had no
significant lean mass change.

The greater drop in total bodyweight in the ketogenic group can

at least partially be attributed to the discrepancy in total caloric
intake (217 kcals more in the control condition). However, this
was not a statistically significant difference. Nevertheless, it
would explain about 2 kg of the 5.6 kg fat mass lost in the
ketogenic group. Regarding the greater fat loss in the ketogenic
group, the authors speculate that greater satiety, increased
lipolysis (via decreased insulin and increased catecholamines
and glucagon), decreased carbohydrate-mediated de novo
lipogenesis, and decreased glucose-driven triacylglycerol
formation in the fat cell.
Interestingly (and perhaps due to bias), they dont include the
lower energy intake in their speculation of the ketogenic diets
greater fat loss, but they point to the higher energy intake of the
control group in their speculation about the latters increase in
lean mass (which was not seen in the ketogenic group). A
second speculation they made about this lack of increased LBM
was that the state of ketosis could have driven a higher use of
amino acids for glucose production. This is far-fetched
compared to the simpler explanation that glycogen is a
component of lean mass, and a higher carbohydrate intake
results in greater glycogen storage.
Interestingly, the authors did not discuss the fat loss advantage
of the ketogenic groups higher protein intake. A recent metaanalysis by Clifton et al noted that a three-fold greater effect on
fat mass was found in studies where a difference between the
diets of only 5% energy from protein was maintained.16 This
happens to be the exact protein intake difference between the
diets in the present study.
[Back to Contents]

Page 18








Chong YH, Ng TK. Effects of palm oil on cardiovascular

risk. Med J Malaysia. 1991 Mar;46(1):41-50. [PubMed]
Elson CE. Tropical oils: nutritional and scientific issues.
Crit Rev Food Sci Nutr. 1992;31(1-2):79-102. [PubMed]
Ebong PE, Owu DU, Isong EU. Influence of palm oil
(Elaesis guineensis) on health. Plant Foods Hum Nutr.
1999;53(3):209-22. [PubMed]
Edem DO. Palm oil: biochemical, physiological, nutritional,
hematological, and toxicological aspects: a review. Plant
Foods Hum Nutr. 2002 Fall;57(3-4):319-41. [PubMed]
Sundram K, Sambanthamurthi R, Tan YA. Palm fruit
chemistry and nutrition. Asia Pac J Clin Nutr.
2003;12(3):355-62. [PubMed]
Hayes KC, Pronczuk A. Replacing trans fat: the argument
for palm oil with a cautionary note on interesterification. J
Am Coll Nutr. 2010 Jun;29(3 Suppl):253S-284S. [PubMed]
Oyewole OE, Amosu AM. Public health nutrition concerns
on consumption of red palm-oil (RPO): the scientific facts
from literature. Afr J Med Med Sci. 2010 Dec;39(4):255-62;
discussion 263-5. [PubMed]
Jenkins DJ, Wong JM, Kendall CW, Esfahani A, Ng VW,
Leong TC, Faulkner DA, Vidgen E, Greaves KA, Paul G,
Singer W. The effect of a plant-based low-carbohydrate
("Eco-Atkins") diet on body weight and blood lipid
concentrations in hyperlipidemic subjects. Arch Intern Med.
2009 Jun 8;169(11):1046-54. [PubMed]
Lampe JW. Dairy products and cancer. J Am Coll Nutr.
2011 Oct;30(5 Suppl 1):464S-70S. [PubMed]
Song Y, Chavarro JE, Cao Y, Qiu W, Mucci L, Sesso HD,
Stampfer MJ, Giovannucci E, Pollak M, Liu S, Ma J.Whole
milk intake is associated with prostate cancer-specific
mortality among U.S. male physicians. J Nutr. 2013
Feb;143(2):189-96. [PubMed]
Chowdhury R, et al. Association of Dietary, Circulating,
and Supplement Fatty Acids With Coronary Risk: A
Systematic Review and Meta-analysis. Ann Intern Med.
2014 Mar;160(6):398-406. [AIM]
Ramsden CE1, Zamora D, Leelarthaepin B, MajchrzakHong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM,
Hibbeln JR. Use of dietary linoleic acid for secondary
prevention of coronary heart disease and death: evaluation
of recovered data from the Sydney Diet Heart Study and
updated meta-analysis. BMJ. 2013 Feb 4;346:e8707.
Graudal NA, Hubeck-Graudal T, Jrgens G. Effects of lowsodium diet vs. high-sodium diet on blood pressure, renin,
aldosterone, catecholamines, cholesterol, and triglyceride
(Cochrane Review). Am J Hypertens. 2012 Jan;25(1):1-15.
Pollan M. 2007. Unhappy meals. New York Times Mag.,
Jan. 28. [NYT]
Holub BJ. Docosahexaenoic acid (DHA) and cardiovascular
disease risk factors. Prostaglandins Leukot Essent Fatty
Acids. 2009 Aug-Sep;81(2-3):199-204. [PubMed]
Clifton PM, Condo D, Keogh JB. Long term weight
maintenance after advice to consume low carbohydrate,
higher protein diets - A systematic review and meta
analysis. Nutr Metab Cardiovasc Dis. Nutr Metab
Cardiovasc Dis. 2014 Mar;24(3):224-35 [PubMed]

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 19

In defense of the bros.

Bryan Krahn, CSCS
They say the first step towards recovery is admitting you have a
problem. So here goes: Im Bryan and Im a bro.
In my defense, I cant help my bro-styling ways. My muscle
building teeth were cut in the late 80s and 90s, the salad days
of bro bodybuilding. This era was also pre-internet, when a
muscle-heads only resources were ghostwritten Weider
magazines and the occasional re-run of ESPNs American
That left a huge void for muscle building information so we
looked to our only legitimate source for guidance and inspiration
-- other bodybuilders.
Now theres nothing wrong with a little observational evidence.
In fact, were a law suddenly passed that young bodybuilders
couldnt read about training and nutrition online anymore and
could only copy what the top natural pros are doing -- no
questions asked -- hypertrophy rates across the country would
double, and internet memes like Do You Even Lift would cease
to exist.
Problem is, throw steroids into the mix and suddenly things get
dicey. Its because almost everything works -- if you take
enough gear. The most cockamamie training schemes will
produce pumps and big PRs, while asinine tilapia and MCT
oil type-diets will shred fat with negligible lean mass lost.
Its not surprising (and a little depressing) that some bros go
their whole lives believing that training and diet play second
fiddle to the type and quantity of gear they take.
Its also not surprising that the most ridiculous bro-isms happen
to be contest prep related. Take a bodybuilder on a long, hard
prep, when each pound of weight lost is accompanied by a 10%
increase in anxiety, and now throw in an extra-healthy dose of
anabolics -- forget the braintrust at Weider University, this is the
true source of much bro science.
Everyones heard that higher reps with lighter weights when
dieting etches in the cuts and brings out striations. Yes, its
those 30-rep sets of cable flyes thats bringing out Mongos
coveted pectoral-deltoid separation, not the Draconian diet hes
been following for 16-weeks, the hours of cardio, or the
pharmaceutical cocktail from his life extension doc.

cardio and only a half-cup of water -- a day. His argument:

Hes a redhead, and gingers hold water more. Im not sure if
his client won his show. Im more surprised he even survived.
Of course, those are extreme examples, but evidence-based guys
all say the real problem with broscience is that when it trickles
down into the mainstream it holds the maturation of the entire
industry back.
For example, spiking insulin with a big dose of high glycemic
carbs post workout became a thing in gym culture to halt
catabolism in its tracks and kickstart anabolism. Forget that the
practice is really only necessary for high intensity athletes
performing multiple exercise bouts in a day (or that many
bodybuilders doing it are also injecting insulin), now Mrs. Jones
thinks she needs a massive sugar bomb after her Zumba class so
she can recover.
Then theres clean eating, a nice bro-ism in theory for making
better food choices thats been twisted and perverted by
misinformed zealots and unleashed upon the mainstream diet
Yes, cut enough sugary or fatty foods from your menu and
youll lose weight. If labeling the ones you cut out dirty helps
keep you on track, fine. However, we now have an entire
generation of bros swearing off dairy, wheat, and all forms of
white death (sugar) because its dirty or toxic. As a result,
destructive behaviors like binge eating and orthorexia are
reportedly on the rise in seemingly healthy fitness populations.
I realize youve heard all this before. I couldve easily saved
1000 words and wrote, So yeah, broscience is bad, mkay?
Heres the thing. I kinda like broscience.
Okay, let me re-phrase, cause saying I like broscience is
basically saying I accept pseudo science or bad science. Even
when broscience has proven to be true -- like weight trainers
needing more protein -- you cant turn a blind eye to the many
times its been flat-out wrong. As they say, even a broken clock
is correct twice a day.
I just have a soft spot for broscientists. Not the marketing
hucksters cherry picking data to convince me I can eat all the
carbs I want after 9 pm (EDT) and not gain fat. The real bros -the guys in the gym experimenting, inventing techniques, and
tweaking exercises. Those bros are my peeps.

Sometimes though, the pre-contest broscience goes beyond

amusing and into dangerous. How many bodybuilders have
missed pre-judging in favor of the hospital because some gym
scientist had them cut water too soon, or were told to channel
their inner wrestler and wear garbage bags in the sauna to lose
that last bit of water theyre holding.

Broscientists like that are who got me excited about lifting

weights. I remember the day I befriended my first real-life
bodybuilder and convinced (begged) him to let me train with
him. I didnt receive a sterile lecture about loading parameters
and the importance of activation drills -- we did wide grip pullups for a wide back, 21s to make the biceps more vascular, and
heavy dumbbell pullovers to expand the rib cage while
developing a serratus three fingers deep.

I remember a guru telling me (with a straight face) that his

prized competitors peak weak would include two hours of

It mightve been wrong or gym science but it also spoke to

my teenage mind and motivated me. And years later, long after

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 20

Ive abandoned many of my bro-isms, I still see the things I did - even the incorrect things -- as essential to my development.
After all, I started as an ADHD-afflicted teenager and yet here I
am, still training, in my fourth decade of life. Had those first
workouts been less experiential and more sterile and educational,
I doubt I wouldve continued past age 20.
To that end, even as the industry matures (thanks in part to the
people involved in this Research Review) and evidence-based
practices supplant outdated or erroneous ones, I still hold onto a
few bro-isms. I even champion a few of my own that Ive come
up with.
Im convinced that weak bodyparts are usually the bodyparts
you have trouble getting a pump in, while strong bodyparts
typically need just a set or two.
Im convinced that calves grow best when you train them daily
and when you throw the kitchen sink at them -- at least until that
stops working.
Im convinced that if youre not experiencing any hunger or loss
of energy on a diet after the first few weeks then you need to cut
your calories. (Or at least cut back on your stimulants. Meh, do
what you want.)
Those are some of my bro-isms. If any evidence for them exists,
I havent seen it, but until the likes of Schoenfeld or Aragon
decide to torpedo them, Ill consider them bro-true.
Which should be the metric for all good broscience -- its what
you believe based on experience and intuition and good old
observation. If one day science validates your beliefs, great! But
if what you believe turns out to be wrong, then its incumbent on
you to revise your theories. Trust me, it doesnt make you less of
a bro.
So train hard, keep records, and make adjustments to your
approach till you find what works for your body, all the while
keeping a close eye on the objective science.
And go easy on the bros! Cause even the most buttoned-up, lab
coat wearing, evidence-based guy will tell you that bodybuilding
is a beautiful amalgam of art and science. The bros are the
artistic side of our muscle-building pursuit, and without them,
what we do would be a lot less colorful.
Bryan Krahn, BA, CSCS, is a
fitness consultant, writer,
editor, and online coach. He's
been published like, a lot,
under his own name and has
ghost written for many
prominent figures in the
fitness scene. He blogs about
training, eating, and New York
City at bryankrahn.com. And
yes, he even lifts.


Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 21

Should you stop counting calories and macros?

By Armi Legge

behaviors like preparing healthy meals than hitting specific

numbers, are generally able to lose more weight and keep it off
longer than people who are motivated by external rewards or
If youve ever counted calories and gone over, its easy to feel
like youve failed, which is a kind of self punishment. While Im
stretching a bit, most evidence indicates that more rigid control
techniques, like counting calories, arent as effective in the longrun. They also tend to increase your risk of binge eating and
other eating disorders.1
From an anecdotal standpoint, many of the people Ive worked
with have had similar experiences. They dont necessarily feel
like failures if they go over their calories, but theyre so sick of
being constrained by their calorie and macronutrient targets that
overeating is almost like a screw you, to their diet.
Obviously this isnt true for everyone, but it can happen.
2) It can be painfully inconvenient.
Say youre at a friends house, a restaurant, or a camping trip.
Suddenly you dont have a nice kitchen anymore to weigh your
food, or a handy app or spreadsheet to count calories and


Or, maybe youre out with friends, and they decide to go to a

restaurant. You already have a meal planned, but you also dont
want to be the Oh, I have to get up early, have fun without me,
person. That sucks.

You know that calories count if you want to lose fat. (If not, go
to the AARR index and search for calorie. Read for an hour
and come back).You also know that your macronutrient intake is
extremely important if you want to build muscle, lose fat, or be

Maybe you went out with your friends and sat awkwardly while
everyone else ordered food. Or, you get 50 calories worth of
tomato soup, so you can go home and eat broccoli and chicken
breasts to hit your macros.

The logical conclusion, therefore, is to start counting calories. If

calories in versus calories out is true, then you should strictly
control your calorie intake, right? That can work well, but not
for everyone or forever.

Yes, you can always eyeball your portions and estimate your
macros while eating out. However, if youre kind of obsessive,
like me, its hard to make yourself do that in the real world. It
also makes eating more complicated, which brings us back to
problem number 1.

Here are 4 reasons even obsessive bodybuilders and athletes

should consider not counting calories or macros, at least for a

This becomes even more of an issue while traveling.

1) It can drive you to overeat.

As odd as this might sound, this is a common problem. Its basic
economics. When something is in short supply, you value it
more. If you have a very specific limit on how many calories
you can eat, that number becomes increasingly more important
throughout the day. Often, this gets to the point you cant stop
thinking about your diet.

3. Its extremely difficult while traveling.

If you like traveling, like me, counting calories and macros can
be hard. Its almost as bad as dealing with TSA employees.
Youll probably encounter new foods which you cant identify,
or even pronounce. Try estimating the macros of Gai Pad Med
Ma Muang, a Thai chicken dish with cashews, honey, peppers,
and other vegetables. Good luck.

On one hand, thats a good thing. Calories should be a little

scarcer while youre dieting. On the other hand, this can drive
you a little nuts.

Another problem is that you have less time while traveling, and
your normal routine is shattered, which makes it even harder to
stick to your meal plan and thus calories and macros.

There is some indirect evidence this is true, too. People who are
intrinsically motivated to lose weight, who focus more on

You can generally find simpler foods while traveling if you

know where to look, but thats not always possible or fun.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 22

If you use an app like MyFitnessPal to count calories and it runs

out of battery (damn iPhone), then youre really screwed.

There are all kinds of methods you can use to accomplish that,
which dont involve counting calories or macros.

If youre traveling for more than about two weeks, youll

probably need a different system for dieting.

If youre sick of meticulously tracking your food, look at this as

a wakeup call. Try something new.

If youre traveling less than two weeks, you can generally make
calorie counting work, not that youd want to.

Heres your challenge.

4. It can be stressful and distracting.

If youve been counting calories and macros, go one week

without it. Yes, if youre a OCD like me, this will be a little
scary. All the more reason to do it.

Theres a concept in economics called externality, where one

action has unintended consequences in another area.
While calorie counting might seem to only take a few minutes
per day, youll often spend a significant amount of time thinking
about food and what youll eat to hit your macros.
There have been times when Im out with friends, got a little
hungry, and immediately started thinking about how I was going
to hit my calories and macros if we got food. These thoughts can
creep into almost every other aspect of your life such as work,
time with family, etc.
Instead of being able to enjoy your food, you cant stop thinking
about how many grams of carbs, protein, and fat you still need to
eat, or if youve eaten too much.
Its exhausting.
At this point, you may think that you dont need to ever count
calories or macros. Or you think Im an idiot, so let me explain.
Calorie Counting Also Works, so be Flexible
Counting calories and macros works extremely well for some
people. I have friends whove been doing it with no problem for
years. Some of them weigh their food every day, too.

Assuming you dont enter a speed eating contest, its hard to

gain much of any fat in one week. The benefits on the other
hand, can be huge.
If you find that you enjoy your new style of eating, try it for
another week. Keep doing it as long as you can while improving
or maintaining your physique and performance.
If you feel anxious on the first day, dont wuss out. Give the
system at least a week.
After going at least a week without tracking, and youd still
rather count calories and macros, go for it. Just make sure the
benefits are worth the added effort and inconvenience, and dont
give up on a more relaxed approach completely.
Theres also nothing wrong with using a hybrid approach -counting calories and macros some days, and freestyling it on
others. Thats what I do while cutting.
Ultimately, youll get lean and stay that way using the system
thats easiest for you to maintain. Or you can just go Paleo.2
Armi Legge is the editor of Evidence
Magazine, a monthly publication that
helps you automate your diet and training,
so you can have the body you want and
move on with your life. Learn more about it

Theyre happy with their system, and its helped them stay
extremely lean.
In other cases, you might have to count calories. If youre
getting extremely lean for a bodybuilding competition or a photo
shoot, it might be worth the inconvenience and stress to count
calories for a few weeks or months.
However, there are others who get sick of counting calories and
macros, and run into all of the problems listed above. When that
happens, if they dont have a system in place to stay on track,
they often gain weight or feel so out of control theyre a nervous
If the only way you know to control your diet and stay lean is
through counting calories and macros, and that stops working for
you, youre screwed.

1. Pelletier L, Dion S, Slovinec-D'Angelo M, Reid R. Why Do
You Regulate What You Eat? Relationships Between Forms
of Regulation, Eating Behaviors, Sustained Dietary Behavior
Change, and Psychological Adjustment. Motivation and
Emotion. 2004;28(3):245277.
2. LOL

Your new goal is to become comfortable with multiple kinds of

dieting. As long as youre in a calorie deficit, youll lose fat.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 23

Does reverse dieting build metabolic capacity?

By Alan Aragon

I have received numerous incarnations of the question titling this
section. It relates to the transition period into caloric
maintenance or surplus after prolonged dieting for several weeks
or months. To the best of my knowledge, the term reverse
dieting has its origins in competitive bodybuilding, where the
post-contest period is commonly treacherous ground when it
comes to the ravenous gorging of foods that were avoided during
prep. One of two unfavorable outcomes can occur.
The lesser of the evils is that the competitor ends up filling
glycogen stores and looking fuller and tighter the next day,
wishing this was the look that made it to the stage the day
before. The competitor then returns to the scheduled
maintenance or off-season intake, and hums right along,
accepting the eventual reality of not being contest-lean, but also
enjoying the lack of severe restriction in terms of food type
and/or amount.
The more brutal scenario is when this post-contest feeding
frenzy continues for the next few days (or weeks), resulting in
rapid fat gains that boomerang the competitor to pre-competition
level body fat levels and beyond. The adverse psychological
impact is a discussion thats beyond the scope of this article, but
for now, suffice it to say that it aint a good thing.
In my observations, the latter scenario is far more common after
prep periods, especially preps that are very severe in their caloric
deficit and/or the limits placed on the range of foods allowed
to be consumed. Diets based on a narrow set of supposedly
clean foods often fail to benefit prep beyond more flexible
approaches emphasizing macronutrient targets. An underrecognized downside is that they can also create a devastating
aftermath by accumulated feelings of deprivation, triggering a
vicious backlash against the pre-contest diet.

carb increment, it would take nearly 1-2 months to hit

maintenance carb levels. Ironically, the reverse dieting period
has been described as being as difficult or even more so than the
dieting period in terms of the willpower and self-control required
to not binge everything back. Its also ironic that instead of
phasing into a more psychologically relaxed off-season phase,
reverse dieting can have a tendency to perpetuate the
obsessiveness inherent in the pre-contest phase. Therefore, for
some competitors, there really is no actual break from dietary
micromanagement, regardless of season.
Observations, claims, & perspectives
One of the most obvious and concrete benefits of reverse dieting
is that it draws a hard line protecting against the post-contest
binge, which in severe cases can put back most or all of the
competitors body fat in a matter of a few days. Along with that
comes the physical discomfort of bloating and edema, not to
mention the psychological stress of the rapid disappearance of
the hard-fought aesthetics. However, beyond this, the benefits of
reverse dieting are more subtle. In some cases, the claimed
benefits tread well into speculative/hypothetical ground, despite
being asserted as factual.
One of the popular claims is that reverse dieting builds
metabolic capacity. In other words, it increases the amount you
can eat (emphasis on carbs) as a matter of maintenance intake. In
light of the starvation-level carb & total kcal intakes common
among pre-contest diets, this increased maintenance carb intake
is seen as a godsend. It allows competitors to begin their contest
prep at a higher carb intake, and end off at a higher intake as
well. This avoidance of starvation-level intake has also been
claimed to prevent so-called metabolic damage, characterized by
stalled weight loss despite continued efforts to reduce caloric
intake or increase exercise output. So, before I answer the
question about building metabolic capacity, lets take a closer
look at the opposite phenomenon.

The broad definition of reverse dieting is a gradual, incremental

re-introduction of calories (mostly from carbohydrate) into the
diet for a prolonged period after the dieting phase. There is no
universal or official set of reverse dieting rules, but the general
incarnation in coaching circles is to increase carbohydrate (and
to a lesser degree, fat and protein) on a weekly basis, to the order
of roughly 5-10 g carbs/week (Ive also heard of figures like 1020 g thrown around) until maintenance levels are hit, at which
point a decision is made to either hold steady or continue into a
bulking or surplus phase.

Its important that the metabolic damage concept be viewed in

an objective/critical light, since it has a tendency to lend itself to
fairy tales. Metabolic damage is actually a dramatized version of
what researchers know as adaptive thermogenesis (AT), defined
as the margin of decrease in resting energy expenditure (REE)
that cannot be accounted for by losses in lean/metabolically
active tissue. The highest margin of AT was seen recently in
Johanssen et al reported 29.4% drop in resting metabolic rate
after massive weight loss in obese subjects in a nationally
televised competition.1 Significant AT was apparent since this
metabolic rate drop was 504 kcal greater than what the loss of
lean mass would have predicted; it amounted to an AT of 18.8%.
Keep in mind that this is after a mean weight loss of 57.6 kg
(126.7 lb) in 6 months. Its not likely that physique competitors
will significantly exceed that degree of metabolic slowing. In a
more typical example, Liebel et al showed that in obese subjects,
a 10% or greater weight loss resulted in a 15% greater REE
reduction than predicted by body composition change. 2

Given a scenario where someones daily maintenance carb target

is 300 g, using the lower incremental range of 5-10 g/week, if a
contest diet ended someone off at, say, 150 g/day, then it could
take 15-30 weeks (almost 4-8 months) to arrive at maintenancelevel carb intake. Using the higher range of a 10-20 g weekly

It should also be noted that none of the subjects in Liebel et als

or Johanssen et als research were on an optimally designed
progressive resistance training program with optimized
macronutrient targets, so it's entirely possible for AT in welldesigned programs to be significantly less than what has been

Alan Aragons Research Review February/March 2014

[Back to Contents]

Enter reverse dieting

Page 24

reported in the literature. Another thing Id like to point out

about metabolic damage-related claims is the unreliability of
self-reported intake and output. For example, Lichtman et al
found that obese subjects with a reported history of diet
resistance under-reported food intake by an average of 47%,
and over-reported physical activity by 51%.3 Furthermore,
under-reporting intake might be greater among women than men
(especially in overweight women).4 At this point I would
encourage the reader to refer back to the April/May 2013 issue
of AARR for further insight by Lyle McDonald on perception
versus realities of metabolic damage.

and ending up at a higher maintenance caloric requirement at the

end of a reverse dieting cycle.

Raising metabolic capacity

A recent comprehensive case study by Rossow et al examined

the 6-month prep and 6-month recovery period of a professional
drug-free bodybuilder.8 During the prep phase, markers of
metabolic stress were substantially elevated. Increases in cortisol
and ghrelin were seen with consurrent decreases were seen in
leptin, testosterone, red blood cell count, hematocrit, thyroid (T3
& T4), and resting energy expenditure. Its reasonable to
postulate that that reverse dieting variants that are too gradual
result in keeping the trainee at a subpar recovery rate. The
sooner a trainee can fully alleviate this physiologically insulted
state, the betterof course without sabotaging it all by binging.

Aside from preventing post-contest binging, the reported

benefits of reverse dieting center around higher caloric
(especially carb) intakes for maintenance. There are also reports
of maintaining impressive levels of leanness during the reverse
dieting period, despite the incremental intake hikes. There are at
least five factors explaining these intriguing phenomena.
One would be that the gradual increases in carbohydrate
facilitate increases in resistance training performance, which can
translate to an increased training energy expenditure. In support
of this, Paoli et al recently saw an unprecedented 22.6% increase
in REE in a 22-hour post-exercise period as a result of a protocol
involving a rest-pause-type of technique where heavy loads were
taken to failure.5 This results would be reflective of trainees who
are able to train progressively while maintaining a high intensity
of effort.
A second possibility is an increase in non-exercise activity
thermogenesis (NEAT) occurring alongside the graduated
increases in energy intake. A memorable example supporting
this possibility is research by Levine et al, who fed non-obese
adults 1000 kcal above their maintenance needs for 8 weeks.6 On
average, 432 kcal was stored, and 531 kcal was burned. Nearly
two-thirds of the latter (336 kcal) was attributable to NEAT.
Now heres the interesting finding that warrants special attention
within the context of this discussion: the metabolic responses to
the caloric surplus was highly variable, ranging from a 89 kcal
decrease to a 692 kcal increase. Its the latter occurrence that
would explain the maintenance of leanness during reverse
dieting, but its the former that should also caution against
assuming it will work spectacularly for everyone.
A third explanation for increased metabolic capacity is the
increased REE associated with gains in fat-free mass, which are
inevitable alongside progressive training combined with
increasing energy intake.
A fourth factor is the return of the metabolic rate-regulating
hormonal milieu towards normal. Most notably in this aspect is
thyroid activity, which is suppressed under prolonged
hypocaloric conditions, especially those involving carbohydrate
restriction. Classic research by Pasquali et al showed that
carbohydrate intake can be a thyroid-regulating factor
independent of total caloric intake.7
A fifth and very likely explanation is simply a combination of
the previous factors, where the collective result appears to be the
metabolic miracle of staying lean while increasing calories-in,
Alan Aragons Research Review February/March 2014

So, to answer the question, does reverse dieting increase
metabolic capacity? Yes it canbut not by magic, not as
effectively for some as for others, and not necessarily by virtue
of its gradual nature. While a regimented, gradual transition to
maintenance or surplus can prevent binging, dragging out this
process by making it too gradual is not necessarily optimal from
a recovery and progression standpoint.

Since theres a lack of objective research to lean on in this area,

Ill offer my opinion. I personally would not recommend taking
more than a 2-week period to transition from deficit to
maintenance, and I would not recommend taking more than 4
weeks to go from deficit to surplus. The objective would be to
transition as quickly as possible, and not let shifts in scale
weight or body fat regain mess with your head. So, if you can
transition even more quickly than the aforementioned
timeframesgreat. That means more time in recovery, and a
faster track toward growth. Physique competitors need to come
to grips with the reality that the vast majority cannot stay within
spitting distance of contest-leanness without compromising
muscle gains in the off-season.




Johannsen DL, Knuth ND, Huizenga R, Rood JC, Ravussin E, Hall KD.
Metabolic slowing with massive weight loss despite preservation of fat-free
mass. J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96. [PubMed]
Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure
resulting from altered body weight. N Engl J Med. 1995 Mar
9;332(10):621-8. [PubMed]
Lichtman SW1, Pisarska K, Berman ER, Pestone M, Dowling H,
Offenbacher E, Weisel H, Heshka S, Matthews DE, Heymsfield SB.
Discrepancy between self-reported and actual caloric intake and exercise in
obese subjects. N Engl J Med. 1992 Dec 31;327(27):1893-8. [PubMed]
Garriguet D. Under-reporting of energy intake in the Canadian Community
Health Survey. Health Rep. 2008 Dec;19(4):37-45. [PubMed]
Paoli A, Moro T, Marcolin G, Neri M, Bianco A, Palma A, Grimaldi K.
High-Intensity Interval Resistance Training (HIRT) influences resting
energy expenditure and respiratory ratio in non-dieting individuals. J Transl
Med. 2012 Nov 24;10:237. [PubMed]
Levine JA, et al. Role of nonexercise activity thermogenesis in resistance to
fat gain in humans. Science. 1999 Jan 8;283(5399):212-4. [Pubmed]
Pasquali R, Parenti M, Mattioli L, Capelli M, Cavazzini G, Baraldi G,
Sorrenti G, De Benedettis G, Biso P, Melchionda N. Effect of dietary
carbohydrates during hypocaloric treatment of obesity on peripheral
thyroid hormone metabolism. J Endocrinol Invest. 1982 Jan-Feb;5(1):4752. [Pubmed]
Rossow LM1, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural
bodybuilding competition preparation and recovery: a 12-month case study.
Int J Sports Physiol Perform. 2013 Sep;8(5):582-92. [Pubmed]

[Back to Contents]

Page 25

Interview with Tom Venuto.

Tom is one of the true legends of the industry, and has earned a
reputation as one of the rare few guys who you cant say
anything bad about. Ive known Tom personally since 2008
when he began his subscription to AARR. Its a special honor to
have him here for a one-on-one interview about a topic he
probably has more knowledge about than anyone else:
Tom The Icon! First off I want to thank you for agreeing to
do this interview, I realize that you are a busy international
man of mystery & intrigue, and donating your insight &
expertise here is much appreciated. The first thing I'd like to
ask is how the transformation 'games' originated in your
audience, and what has it developed into today, in terms of
scope, size, & magnitude. You mentioned playing somewhat
of a Bill Phillips role (for those who can recall the earlier
days of EAS & Body for Life), and I think that's a really
noble and challenging position to have a foot in.
Thanks for the flattering, if not embellished intro Alan, and its a
privilege to contribute to AARR again. Through the 1990s and
into the 2000s I was deep into natural bodybuilding competition
and busy establishing myself in the fitness business. That was
indeed the Phillips / EAS / Muscle Media era. Everyone in the
industry noticed the conspicuous success of the Body For Life
challenge back then, and that definitely planted the seeds as
inspiration for our future Burn the Fat Challenge. Originally,
however, our first body transformation contest was born by
In November of 2008 I wrote a motivational call to action type
of article that urged my readers to get in better shape over the
thanksgiving and Christmas holidays rather than let themselves
go, and to start right away, not procrastinate until the new year.
That article produced a huge response but then everyone went on
their merry way. Then in January, having almost forgotten about
the challenge I laid down 7 weeks earlier, I was again deluged
with messages like this one: Hey Tom, I accepted your holiday
fitness challenge and I just wanted to say thank you for the
motivation. This was the first time ever I actually lost fat over
the holidays I even ate cookies and pie without guilt this year
I was just careful to keep it in moderation and fit it into my
calorie budget like you told me to. Thanks again. Some people
even sent me their progress pictures.

was 49 days (7 weeks) simply because that was the length of

time from thanksgiving week into the new year. In the summer,
we launched a second event because so many people said they
needed the motivation again. We made it 98 days assuming that
twice the time would allow twice the transformation
(surprisingly that was not always the case). More than 2000
people entered that event. Weve been sponsoring the challenges
with steady participation ever since and have started new
performance-based fitness challenges as well.
Performance-based fitness challenges as well? That's a great
idea. Do you run these alongside the regular body comp
transformations? I'd love to hear some memorable examples
of both a) the physical transformations, and b) the
performance transformations. What makes these particular
cases stand out to you?
Today we run performance-based challenges alongside the
before and after photo / body comp transformation contests to
appeal to people with different motivations. We discovered from
earlier events that some people wont post half-naked pictures
online no matter how big the incentives are. We also found that
even though we judged our contests based on personal
improvement and not the absolute best physique, some people
got demotivated if they felt like they never had a chance to win.
Photos-optional fitness performance challenges got those people
Weve done the usual thing you see on a lot of gamified sites,
like push ups, pull ups, plank time, deadlifts and other workout
challenges, but the real success for us was the fitness habits
challenge. We made a list of what actions and behavior
changes would create lasting success if they became habits. We
kept score and awarded points every day for things like writing
goals, posting nutrition in a journal, tracking the training
sessions and reporting results every week for accountability.
Then we started events like our Mt Everest Challenge which
requires 2903 floors to the summit and our 1 million step
challenge, which involves taking just over 10,000 steps in 98
days, as tracked with a pedometer. We used a leaderboard and
have a group at Fitbit as well. The combination of an attainable
goal, prizes, accountability and friendly competition made this a
huge success and we got thousands of people off the couch. We
had three people do over 3 million steps and none were
endurance athletes. One of them, Marc Chabot, age 55, dropped
52 pounds in 98 days. These contests made me a big fan of
gadgets or apps that make you accountable for your activity,
training and nutrition.

Critics said we were crazy to run a transformation contest at that

time of year, but it was a hit. More than 1000 people entered. It

For the before and after transformations, we have hundreds of

case studies from every age group and background. Two types
stand out the most. First, the success stories from real people
who have either overcome serious adversities like injury or just
ordinary life challenges like being busy that most people use as
excuses. Cynthia Cardenas for example, won one of our 49-day
events while being a stay at home mom of 5 kids all under the
age of 8, including homeschooling 2 of them. Because dropout
rates are so high for all kinds of diets as well as fitness contests,
the second group that really stands out is the long-term
maintainers, not just the big losers at the end of each
contest. Brian Nordberg is like the poster man for this. He
dropped 122 lbs, kept it off more than 4 years and since gained

Alan Aragons Research Review February/March 2014

[Back to Contents]

Thats when I knew we were on to something. So the following

year, we formalized it, created a competition structure and
announced our first Burn the Fat Holiday challenge. We offered
great prizes, including a trip for two to Maui for the male and
female winners. Each contestant took progress photos, set goals,
tracked their weight and body composition, recorded progress in
a journal every week and wrote an essay at the end. Doing it in
an online forum with thousands of members turned out to be
fantastic for accountability and community support.

Page 26

over 20 pounds of muscle. Hes now a participant in the

National Weight Control Registry. You can see both of them at
Burn the Fat Blog or on the back cover of my book.
Fascinating & impressive cases, Tom. Are there key qualities
(work ethic, approach, habits, etc) you find as common
threads among folks who are able to successfully transform?
Or, are there really no consistently common threads at all
among the long-term success stories (I'm not discounting
that possibility).
Ive seen people with big differences in dietary approaches
food choices (vegetarian or carnivore), meal schedules (three
meals or six meals), macronutrients (high-carb, low-carb and
everywhere in between) and so on all become equally
successful, as long as they adhered to the big picture principles,
such as maintain a calorie deficit for fat loss, get optimal protein
levels and so on. But there are definitely common threads among
all the success stories.
First, absolutely, work ethic is high on the list. Ive never heard a
transformation contest finalist or winner say, That was easy.
More often, Ive heard the polar opposite: I worked harder than
I ever have in my life for this event.
Second is using mental training strategies: visualization or
mental rehearsal, self-image modification, goal setting,
relaxation or meditation, affirmations or motivational scripting,
self-talk, working on belief systems, and so on. Some type of
conscious work on mindset is always there.
Third is doing nutrition by the numbers. Not everyone tracks
calories and macronutrients, especially long-term, so I wouldnt
say this is mandatory, but it correlates highly with success. In
our contests, Id estimate at least 90% of the top finishers and
winners logged nutrition with spreadsheets, software or apps.
Fourth is accountability through tracking and self-monitoring.
Its like the classic business management and sports coaching
maxims: what gets measured gets improved and if you dont
measure it, you cant manage it. In the best transformations we
see people consistently tracking actions and performance,
including training and nutrition journals. They also track
outcomes such as weight, body composition, measurements and
progress photos. Collecting progress data weekly also provides a
feedback loop system to help with course corrections.
Fifth is a social support system, which in our case, is built into
the challenge because we host our contest in an online forum
with thousands of members. We usually also see a strong
personal support system from friends or family, but in the cases
where someone doesnt get the kind of support they need from
their immediate social circle, they always say their online
support system made all the difference

diet, high physical activity, supportive environment, good

coping mechanisms (for handling stress, etc), self monitoring
progress, journaling food and training, less sedentary leisure
time, consistent eating patterns and more home cooking/less
eating at restaurants.
If someone is following these guidelines, youd think theyd be a
sure thing for making it into the long-term maintainer group. But
its not always that easy to predict who sticks with it and who
relapses. Knowing about these strategies and doing them are two
different things. Long-term weight control is a huge challenge
for a lot of people and its always complicated with a lot of
distractions, obstacles or bumps in the road. The phrase I hear a
lot is, Life got in the way. The real question is what makes
people follow through with these maintenance behaviors without
getting derailed.
I believe one reason is that maintainers expect problems and
accept adversity as part of the process and have mental and
physical strategies to get through it and forge onward. In a word,
theyre resilient. The maintainers get knocked down and get
back up quickly, over and over again. The relapsers get knocked
down and stay down. The difference is in the way each person
thinks about and explains adversity. I could go on and on about
this, but to keep this brief, Id highly recommend looking up
Martin Seligmans work in positive psychology on learned
helplessness and explanatory style if you want to learn more. I
think he nailed it.
Another difference between the maintainers and the relapsers is
in whether the motivation is purely extrinsic and temporary or
its also intrinsic and long-term. Purely external rewards like a
trip to Hawaii can be incredible short-term motivators. Ive
heard people say they worked harder, specifically hoping to
win that vacation, than theyve ever worked for anything in their
lives and they did it they won. Unfortunately, Ive seen some
of those overall winners regain the fat they lost afterwards,
because when the contest and vacation were over, they had
nothing else to keep them going. Short-term win, long-term fail.
On the other hand, weve seen people enter our contest, and
agree that a trip to Hawaii would be amazing, but they said their
biggest motivator was getting healthy for their family. After a
recent checkup, their doctor said, Youre not going to live long
enough to see your kids (or grandkids) grow up if you dont
change your ways. That was the turning point. Staying healthy
for family isnt a short-term goal with an end date its an
intrinsic and long-term motivation a value and thats what
keeps them going.
Tom Venuto is a natural bodybuilder
and the author of Burn the Fat, Feed the
Muscle. Tom received his degree in
exercise science and has been involved
in the fitness industry since 1989,
including 15 years as a personal trainer
before he became a full-time writer,
publisher and online coach. You can
visit Tom at www.BurnTheFatBlog.com
or learn more about the new 2014
hardcover edition of his book at

Final question: Any interesting motivational lessons you've

learned from these long-term success cases? Can you speak
about the unpredictability of which people (even contest
winners) relapse and which make their transformations last?
Most of our contest winners whove also kept the fat off longterm are succeeding by using the same best practices youd see
in the research on long-term maintainers, like what comes out of
the National Weight Control Registry studies; calorie controlled
Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 27

Here is an interesting VICE episode (20:38) documenting a

strongman training facility in Iceland.

If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.

Alan Aragons Research Review February/March 2014

[Back to Contents]

Page 28