Nutrition for Diabetes Mellitus

Chapter 19
Role in Wellness
Physical health dimension
Long-term serious physical health complications may be
avoided if hyperglycemia is controlled through dietary
and lifestyle modifications
Intellectual health dimension
Ability to understand diabetes; to regularly be compliant
regarding insulin injections, if required; and to follow
dietary and exercise recommendations may depend on
intellectual health
Emotional health dimension
Dealing with chronic lifelong condition and changes in
dietary intake may necessitate loss of symbolic foods,
which may be emotionally upsetting
Social health dimension
Support, especially from family members and friends
crucial and pivotal in adjustment
Spiritual health dimension
Eating special diets based on religious or spiritual
beliefs may need adaptations to maintain blood glucose
control
Diabetes mellitus (DM)
Group of conditions characterized by:
Relative or complete lack of insulin secretion by beta
cells of pancreas or defects of cell insulin receptors
Results in disturbances of carbohydrate, protein, and
lipid metabolism and hyperglycemia
Usually characterized by:
Elevated fasting blood glucose (126 mg/dL if found on
at least two occasions)
Hyperglycemia
Associated with disability and premature death
Main goal of treatment maintenance of
insulin/glucose homeostasis
Complications
Macrovascular complications

Coronary artery disease

Peripheral vascular disease

Cerebrovascular accidents
Microvascular complications

Nephropathy
Approximately half of individuals with
type 1 diabetes mellitus (T1DM) develop
chronic renal failure and chronic kidney
disease (CKD)
Decreased sensations in extremities
Injury may occur without patients
awareness
Impaired healing may lead to gangrene
and amputations

Retinopathy
Leading cause of blindness in North
America

Autonomic effects

Orthostatic hypotension

Persistent tachycardia
Gastroparesis
Neurogenic bladder
Impotence
Impaired visceral pain sensation

Symptoms of angina pectoris

or myocardial infarction may
be obscured

Glucose intolerance
Primary categories

T1DM: 5% to 10% all cases

T2DM: >90% all cases

-

Other types

Latent autoimmune diabetes of adults (LADA)

Gestational diabetes mellitus (GDM)

Impaired glucose tolerance (IGT)

Other forms of diabetes

Type 1 diabetes mellitus

Symptoms:

Onset usually sudden

Excess hunger

Hyperglycemia

Weight loss while consuming large food

quantities (polyphagia)

Polyuria and polydipsia

Usually diagnosed at 20 years of age or less

Autoimmune disease

Autoimmune destruction of beta cells not

clearly understood
Multiple genetic predispositions and
unidentified environmental factors
appear to contribute
One or more autoantibodies present in
85% to 89% of individuals diagnosed
with T1DM
Idiopathic diabetes

Some forms no known cause

No insulin produced

Prone to ketoacidosis

No evidence of autoimmunity
Insulin
Type 1 DM

Exogenous insulin required to maintain normal

blood glucose levels and to survive
Type 2 DM

Some individuals may require insulin to

optimize blood glucose control
Goal of insulin therapy, in conjunction with nutrition
therapy and physical activity

Mimic physiologic insulin delivery

Types of insulin

Rapid or short acting

Intermediate acting

Long acting

Types of insulin administration

CSII

Fixed (conventional or standard

therapy)

Flexible (intensive insulin therapy)

Continuous subcutaneous insulin

infusion (CSII)
Conventional or standard insulin therapy

A mixed dose is constant dose of

intermediate-acting insulin combined
with short- or rapid-acting insulin

Administration of insulin and food intake

must be synchronized to avoid
hypoglycemia
Flexible or intensive insulin therapy

Multiple daily injections (MDIs) of shortor rapid-acting insulin before meals as

well as intermediate insulin once or
twice daily

Insulin adjusted to correspond with food

intake
Doses also adjusted to treat:

Hyperglycemia

Inconsistent carbohydrate
intake

Modification in usual physical

activity

Intensive insulin therapy postpones

onset and slows development of
retinopathy, nephropathy, and
neuropathy in patients with T1DM

Form of intensive therapy

Rapid- or short-acting insulin pumped
continuously in micro amounts through
subcutaneous catheter

Monitored 24 hours a day

Boluses or rapid- or short-acting insulin given

before meals
Exercise

Lowers blood glucose levels

Assists in maintaining normal lipid levels

Increases circulation

Consistent and individualized exercise may

reduce therapeutic dose of insulin

Patients with T1DM

Exercise when blood glucose levels

between 100 and 200 mg/dL or about
30 to 60 minutes after meals

Avoid exercising when blood glucose is

>250 mg/dL and ketones present in the
urine or when insulin at peak action

Glucose control compromised if proper

adjustments not made in food intake or
insulin administration

Patients with T2DM who take oral hypoglycemic

agents may be at risk of postexercise
hypoglycemia

Type 2 diabetes mellitus

Rarely present with classic diabetes

symptoms
First symptoms often complications of
T2DM:

Heart attack

Stroke

Neuropathic problems

Primary metabolic problem

Insulin resistance or

Failure of cells to respond to insulin

produced by body

Pancreas loses ability to

produce insulin

Two strongest risk factors

Family history

Obesity

Obesity produces insulinresistant state, causing beta

cells to produce excessive
amounts of insulin

Upper body obesity even

greater risk factor for diabetes
than degree of obesity

Waist-to-hip ratio >

0.8 for women; 0.95
to 1 for men
Oral glucose-lowering medications

Used to treat T2DM when diet and physical

activity alone cannot control hyperglycemia
Blood glucose monitoring

Blood glucose levels cornerstone of diabetes

management

Improved glycemic control correlated with

reduced rates of:

Retinopathy

Nephropathy

Neuropathy

Blood glucose levels can be monitored several

ways

Glycosylated hemoglobin (A1C)

Self-monitoring

Glycosylated hemoglobin (A1C)

Formed through irreversible process

Hemoglobin combines with

glucose, forming
glycohemoglobin

Amount of A1C reflects average blood

glucose level for 100- to 120-day period
before test

More glucose RBC exposed to,

greater value

Blood sample can be drawn at any time

Not affected by short-term

factors such as food intake,
exercise, or stress

Self-monitoring

Performed in individuals home with

blood glucose meters

Droplet of blood obtained through

fingerstick on regular basis to monitor

glucose levels

Before and after meals

Bedtime

Self-monitoring and charting

Particularly useful in evaluating

Glycemic control

Physical activity

Effectiveness of meal
plan
Diabetes Mellitus, contd

Self-monitoring of blood glucose (SMBG)

Records of blood glucose levels review

by health care team to determine food,
insulin, and exercise needs

Allows for individualized

treatment especially with meal
plans

SMBG recommended three or more

times daily for:

T1DM

Pregnant women taking insulin

Individuals with T2DM taking insulin

Usually need to perform SMBG

more often than those who do
not take insulin
Hypoglycemia

Below normal values of blood glucose levels

Can result from:

Too much insulin

Skipping meals

Too much exercise without concomitant

increase in food intake

Onset sudden

Fatal if left untreated

Hypoglycemia symptoms occur when:

Blood glucose drops below 50 mg/dL or

Relatively significant drop in blood glucose

Diabetic ketoacidosis

Life-threatening condition caused by insulin

deficiency

Body breaks down fats and proteins for energy

Can cause ketosis, an abnormal

accumulation of ketones

Ketoacidosis may
result
Diabetic ketoacidosis (DKA)

Hyperglycemia

Causes osmotic diuresis

Leads to dehydration

Precipitates lactic acidosis

Stimulates respiratory center

Produces deep, rapid

respirations known as
Kussmauls respirations

Large amounts of ketone bodies present

Produces fruity or acetone odor on

breath

If not recognized and treated promptly:

Acidosis and dehydration may lead to

loss of consciousness

Possibly coma and death

Common conditions that precipitate DKA

Insufficient or interrupted insulin therapy

Too much food

Infection

Other stresses

Trauma

Surgery

Emotional stress

Myocardial infarction
Hyperglycemic hyperosmolar nonketotic syndrome
(HHNS)

Life-threatening emergency

Relative or actual insulin deficiency

Results in severe hyperglycemia

Triggered by stress (trauma, infection) that

increases bodys demand for insulin

Enough insulin may be present in plasma to

prevent formation of ketones

Prevents acidosis but hyperglycemia

may occur

If hyperglycemia left untreated

Serum becomes hyperosmolar

Produces osmotic diuresis

Simultaneous significant loss of

electrolytes via urine

Mortality 10% to 25%

Nutrition Therapy
Nutrition therapy

Essential element of glycemic control and

diabetes self-management education (DSME)

Individualized nutrition therapy required to

achieve treatment goals
Basis for nutrition therapy and DSME

Comprehensive nutrition assessment

Self-care treatment plan

Clients health status, learning ability, readiness

to change, and current lifestyle
Nutrition recommendations same for individuals with
diabetes as for the general population
Carbohydrate recommendations

Based on eating habits, blood glucose, lipid

goals

Blood glucose control not impaired by use of

sucrose in the meal plan, but sucrosecontaining foods should be substituted for other
carbohydrates and foods, and should not be
eaten in addition to a meal plan
Protein intake can range from 15% to 20% of daily kcal
from animal and vegetable protein sources
If diabetes well controlled, blood glucose levels not
affected by moderate alcohol intake

Considered as additional kcal

Consume with food to reduce risk of

hypoglycemia

Nutritive and nonnutritive sweeteners

Fructose creates smaller rise in plasma glucose

than sucrose and other carbohydrates

Large amounts of fructose (up to 20% of

daily kcal intake) provide no advantage
as a sweetener

Negative effects on serum cholesterol

and LDL cholesterol levels

Corn sweeteners, fruit juice or juice concentrate,

honey, molasses, dextrose, and maltose

Affect glycemic response and caloric

content similar to sucrose

Sugar alcohols: sorbitol, mannitol, and xylitol

Lower glycemic responses than other

simple and complex carbohydrates

Ingesting large amounts may have

laxative effect
Nonnutritive sweeteners

Approved for use, considered safe for

consumption by individuals with diabetes

Saccharin

Aspartame

Acesulfame K
Special Considerations
Illness

Blood glucose levels may become elevated and

diabetes control may worsen

Caused by an increase in hepatic

production of glucose stimulated by
infection, illness, injury, or stress

Specifically, by the release of

epinephrine, norepinephrine,
glucagon, and cortisol

Increases insulin requirements

Gastroparesis

Delayed gastric emptying can manifest with:

Heartburn

Nausea

Abdominal pain

Vomiting

Early satiety

Weight loss

Affects approximately 20% to 30% of individuals

with diabetes

Result of vagal autonomic neuropathy

More often in T1DM

Dietary treatment of gastroparesis

Monitor intake carefully

Carbohydrates replaced with soft or

liquid consistency foods

Six small meals may be better tolerated

Constipation or diarrhea

Fiber intake altered to patients

needs
Special Considerations, contd

Dry mouth eased by increasing fluids

and moistening food with broth

Low-fat (40 g) soft or liquid diet may

prevent delay in gastric emptying

Metoclopramide (Reglan) may increase
gastric contractions and relax pyloric
sphincter

Insulin should be matched with meals to

regulate delayed absorption and
glucose changes
Management Through the Life Span
Pregnancy

Women with preexisting diabetes

Vulnerable to fetal complications

Maternal health can be compromised

when complications of diabetes occur

Ideally excellent glycemic control should

be achieved 3 months before
conception

Gestational diabetes mellitus (GDM) may be

induced by stress of pregnancy

Form of glucose intolerance

Onset during pregnancy

Resolves on parturition

Risk of fetal abnormalities and mortality

increases in presence of hyperglycemia

During pregnancy, some hormones and

enzymes produced by placenta antagonistic to
insulin

Maternal insulin does not cross the

placenta, but glucose does

If blood glucose levels get too

high, causes pancreas of fetus
to increase insulin production,
leading to macrosomia

Newborns may also have other problems

Respiratory difficulties

Hypocalcemia

Hypoglycemia

Hypokalemia

Jaundice

Nutrition therapy during pregnancy

Individualization of nutrition therapy

contingent on maternal weight and
height

Include provision of adequate

kcal and nutrients to meet
pregnancy needs consistent
with established maternal
blood glucose goals
Management Through the Life Span, contd

SMBG presents important information

about effect of food on blood glucose
levels

Minimal daily SMBG should be

planned four times a day

Fasting

1 or 2 hours after
each meal
Gestational diabetes mellitus (GDM)

Develops in about 5% to 10% of all pregnancies

More frequent among Native American African

American, and Hispanic/Latino American
women

Women who develop GDM often obese

Good glucose control usually accomplished by

individualization of intake and graphing of
weight gain

To reduce risks of fetal macrosomia, neonatal

hyperglycemia, and perinatal mortality, insulin
may be prescribed in addition to nutrition
therapy

Glucose levels usually revert to normal following

delivery

20% to 50% eventually

develop T2DM
Type 2 DM in children

Incidence and prevalence

Increased 30-fold over past 20 years,

especially ethnic minority populations

Obesity most prominent clinical risk factor

About 30% children with T2DM, BMI

>40, morbid obesity

17% have BMIs >45

Clinical signs of risk for T2DM

Acanthosis nigricans

Reflects chronic
hyperinsulinemia

Polycystic ovarian syndrome (PCOS)

Associated with insulin

resistance and obesity

Hypertension

Occurs in 20% to 30% of

patients with T2DM

Girls appear more susceptible than

boys to T2DM

Female-to-male ratio of 1.7:1

regardless of race

Nutrition therapy and exercise first-line

treatments

Most children with T2DM require drug

therapy

Ideal treatment goal normalization of blood

glucose values and A1c

Important to successfully control

associated comorbidities

Hypertension and
hyperlipidemia

Ultimate goal decrease risk of acute and

chronic complications

All children with T2DM should receive:

Comprehensive self-management
education including SMBG

Referral to RD with expertise in

nutritional management of children with
diabetes

Behavior modification strategies for

lifestyle changes

Increased daily physical activity

-----------NOTES FROM LECTURE---------Nutrition for Diabetes Mellitus

3 Cardinal Signs: Polyphagia, Polydipsia, Polyuria
Diabetes Mellitus: condition characterized by either relatvie or
complete lack of insulin by the beta-cells of the pancreas or by
defects of insulin cell receptors which result in disturbances in
CHO, CHON, and lipid metabolism and elevated blood glucose
level.
Coal Stove Analogy
- Body cells (mitochondria)= coal stove
- Carbohydrate coal
- insulin: coal stove
Type 1: destruction of the pancreatic beta cells causing
impairement in insulin production
Type 2
- insulin resistance to cell receptors
- abnormal insulin secretion
- inappropriate hepatic gluconeogenesis
Gestational Diabetes
0 occurs during pregnancy after placenta is formed and is
caused by placental hormones working in opposition to insulin
Hormones involved in Blood Glucose Management
- Insulin: lowers blood glucose by allowing cell uptake
- Counter- Regulatory hormones: "STRESS HORMONES":
raise BG levels by allowing stored glycogen to be released as
BG
Glucagon: first hormone released to raise BG; in excess can
cause nausea and vomiting
Epinepherin e or adrenalin: causes increased heart rate,
physical tremors
Cortisol: causes warm, sweaty feeling
Growth hormone
BG Issues
Dawn Phenomenon: increasd release of counterregulatory
hormones (cortisol and growth hormone) decrease insulin's
effectiveness
- occurs at dawn for normal nighttime sleep pattern; FBG will
rise naturally as a result of release of glycogen stores from
cortisol and or growth hormone production
Somogyi effect: a high BG always follows a low BG because of
release of glycogen stores from liver
- Since this is temporary rise of BG, avoid overcorrection of
hyperglycemia to inhibit a continued cycle of low and high BG
readings ( will only occur if insulin injection is used)
Diagnosing DM
- FBS (Fasting Blood Sugar)
- HBA1c Glycosylated Hemoglobin
- Opthalmoscopic Examination
- Urinalysis
- Pre-Diabetes: intermediate state between normal glucose
metabolism and diabtes
2 forms
Impaired Fasting Glucose (IFG): FBS of 100 to 125 mg/dl
Impaired glucose tolerance (IGT)= 140 to 199 mg/dl 2 hours
after ingestion of 75g glucose
What to Look For?
- Polyphagia
- Polyuria
- Polydipsia
- Fatigue

- Weakness
- Vision changes
- cool skin

Dieatary Management
Energy intake matches energy requirements
Energy Balance: Glucose Homeostasis

If not manage
- DKA (Diabetes Keto-Acidosis)
- HHNS (Hyperosmolar, Hyperglycemic, Non-Ketotic
Syndrome)
- Hypoglycemia
Long Term complications
- cardiovascular conditions
Peripheral Vascular Disease
Retinopathy
Neuropathy (Peripheral and Autonomic)
Dermopathy

Glycemic Response
After meals: glucose rises followed bby an increase in insulin
levels
Insulin: promotes glucose uptake and utilization. As a result,
glucose levels decrease
Fats: raises insulin secretion
Glycemic Index: predicts the effect of carbohydrate containing
food on postprandial glycemia

GOAL
- to normalize blood glucose levels and decrease
complications
- improve health through healthy food choices and physical
activity
- Address individual nutritional needs takin into consideration
personal and cultural preferences
Type 1 Medications
Insulin
- Long Acting: Lente or cloudy insulin with peak action of
variable time with peakless long acting clear insulin
Lantus
- short Acting Insulin:
Regular R insulin: last 4 to 8 hous must be taken 30 minutes
before meals
Lispro insulin: works within 5 minutes of injection and has
shorter duration
Type 2 Medication
- Sulfonylureas
- Metformin
- Alpha-glucosidae inhibitors
Lifestyle Modification
Exercise
Type 1: doesnt improve glycemic control but prevents CV
Type 2: stop exerising if hypoglycemia signs or symptoms
occur
Treatment of Acute Complications
DKA or HHNK
- insulin administration
- IV fluid administration
- Correction of electrolyte imbalance
Hypoglycemia
- if unconcious glucagon is injected
- if concsius oral hypoglycemics
RULE of 15

Preventing Long Term complications

For CV diseases
- control BP
For Retinopathy
- annual eye exam
Nephropathy
- Keep BG level under control
Dermopathy
- check skin daily for cuts or irritated areas
Neuropathy: proper foot care

Meal Planning
Carbohydrate counting
- emphasizes eating a consistent amount of CHO rather than
restricting type of CHO
- All forms of CHO basically affects BG levels similarly when
eaten in the same amount
Exchange List
- system of grouping foods into categories of CHO, Meat, and
meat substitutes and Fats contianing
General Guidelines
CHO: 45-65% kcal
- the amount of CHO is important
- Best choices: vegetables, fruits, beans, and whole grains
Fats: 25-35%kcal
- monounsaturated
- omega03 polyunsaturated fats
Limit Saturated Fat
- choose non-fat or low-fat dairy instead of whole milk products
- Limit trans-fats (hydrogenate fat found in snack food, fried
foods, commercially baked goods) to less than 1% of total
calorie
CHON: 12-20%
- best choice: fish soy poultry than red meat
Limit cholesterol intake to 300 mg/day
All bitter vegetables are excellent in reducing blood sugar
Sour foods containing high vitamin C ae good in dissolving
excess fats and bringing down in blood glucose levels
Eat before hunger sets in
Choose fresh fruit