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Nutrition
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The Fasting State
1. Energy and ATP:
a. Fuels are oxidized to generate ATP.
b. ATP releases energy that is used to drive body processes
c. Some energy released from ATP is lost as heat.
d. Intake of food does not meet the minute to minute needs for ATP and so body needs energy
stores.
e. Meals can meet body’s need for energy for period of hrs, blood can meet the body’s need for
energy for the period of minutes and ATP for seconds. However, energy stores can provide
energy for periods of months.
f. In general teenagers require more energy b/c growing requires additional energy.
g. Old people require less energy b/c their REE goes down.
2. Components of Energy Expenditures:
a. Resting Energy Expenditure (REE):
 Energy required for maintenance of vital processes
 Main determinant of REE  Lean body mass
 Technique of measurement  indirect calorimetry, to assess O2 consumption.
 Estimation equations e.g. Harris-Benedict Equation
 Energy from main classes of fuel:
Carbos  4 kcal/g
Fat  9 kcal/g
Protein  4 kcal/g
Alcohol  7 kcal/g
1 kcal  4.18 kj
b. Thermic Effect of Food (TEF):
 Energy required for digestion, transportation and metabolizing the nutrients in the
meal and also anabolism
 Goes up for few hrs following meals.
c. Thermic Effect of Exercise (TEE):
 Energy required for muscular exercise
 Highly variable
d. Adaptations (Adaptive thermogenesis, AT):
 Chronic low energy  adaptation in the energy expenditure  energy expenditure goes
down  survival response
e. Fat stores the most energy and releases the most energy so fat is used to supply the body w/
energy b/w the meals. (Protein sparing)
 Carbos can provide energy for 1 day
 TAGs can provide energy for 111 days
 Proteins can provide energy for 18 days
f. Muscle stores water along with energy (in the form of glycogen) and adepocyte stores energy in
the form of TAGs w/o water and so adepocyte is 10X caloric dense than muscle.
3. Fuel Fluxes:
a. Consumer organs:
 Brain will use ketoacids if available as their first choice for energy, but ketoacids are
not usually available so most of the time they use glucose as the source of energy. It
doesn’t use fatty acids as the source of energy.
 Muscle uses fatty acid as the source of the energy but if FAs are not present they the
next choice is ketoacids and only when both of the FAs and ketoacids are not present it
would use glucose.
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b. Maintainer Organs:
 Maintain supplies to consumer organs either by releasing their own stored fuels or from
other organs.
 Kidney can produce and release glucose in chronic acidosis conditions.
c. Liver:
 Uses AAs during meals to generate ATP
 Uses FAs b/w meals to generate ATP
 Stores carbos as glycogen and small amounts of TAGs
 Converts glycogen and AAs to glucose
 Converts FAs to ketoacids to supply FAs for liver (?)
d. Adipose Tissue:
 Uses glucose during meals to generate ATP
 Uses FAs b/w meals to generate ATP
 Stores energy as TAGs
 Converts TAGs to FAs to supply liver w/ FAs
e. Prolonged Fasted State Adaptation:
 The key to adaptation is the production of sufficient keton bodies form free fatty acids
in the liver, to displace the brain’s need for glucose. Once the glycogen supplies are
depleted, gluconeogenensis from protein is the only source of glucose for the brain and
that would deplete body protein rapidly.
 Glucose and Insulin levels go down and then stabilizes at lower levers which is required
for the metabolic adaptation.
 Glucagon levels are only of importance in controlling hepatic glucose production and
doesn’t change.
 Free FA mobilization and plasma levers of FFAs increases  get converted to keton
bodies by liver  increased keton bodies in blood and urine  body protein
conservation and mild ketoacidosis.
 Levels of urea nitrogen shows catabolism of protein by liver and levels of ammonia
nitrogen shows catabolism of protein by kidney and as the fasting time goes up the
levels of urea nitrogen goes down and ammonia nitrogen goes up.
The Fed State
1. General:
a. Any excess energy over REE, TEE and exercise is stored as fat once glycogen stores are replete.
b. Insulin is major fed state anabolic hormone.
c. High insulin is not absolute necessity for anabolism to take place. It depends upon what energy
substrates are provided.
2. The Intermittently Fed State:
a. Although breakfast is the smallest meal the glycemic rise is higher and longer than that
following lunch and supper. Insulin follows the glucose response.
b. Over night insulin levels go really low to maintain plasma glucose levels so in the morning
when food is introduced, body has to adjust to the incoming food the most and so glucose and
insulin rise the most when c/w other meals of the day.
c. At night lypolysis goes up b/c insulin levels are low at night. Since insulin is the potent
suppressor of lyposysis in the morning/during the day when insulin levels goes up lypolysis
goes down and so FFAs levels stay low thought out the day.
3. Fuel Homeostasis in Uncontrolled Diabetes:
a. Diabetes represents the inability to efficiently respond to the fed state.
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b. If insulin is the main fed-state “anabolic” signal, and the individual either cannot secret it or
secretes it late and in insufficient amounts to overcome tissue insulin resistance, then
homeostasis is disrupted  Superfasted state – exogenous and endogenous fuels are secreted at
the same time in to the circulation and their clearance is impaired.
4. Fuel Homeostasis in Hypoenergetic State:
a. Very low energy all protein diet for obesity  low insulin, low glucose, high FFAs and keton
bodies – Protein loss is prevented here by providing about 1 g/kg/ day of protein (protein
sparing)
 Circulating protein stimulates less insulin secretion than carbohydrates  Low
insulin  Lypolysis  ketogenesis
b. Fat can be added as a source of dietary energy in the cases of refractory childhood epilepsy.
5. Fuel Homeostasis in Continuous Parenteral Feeding:
a. Isocaloric (Isoenergetic):
 Continuous IV feeding providing constant amount of protein (1 g/kg/day), full
calories at 40 kcal/kg/day.
 Energy can be provided in three different mixtures: N balance - same in all 3 cases
I.
Only as Glucose: Higher insulin, Higher glucagons, Higher lactate
II.
Only as Lipid: Higher FFA, Higher ketones
III.
½ Glucose + ½ Lipid
b. Hypoenergetic (Hypocaloric):
 w/o full calories, protein sparing
 When person is ill for shorter periods e.g. postoperative period
 3 different types:
I.
Glucose alone w/o Protein: (-)ve N balance
II.
P1 – Small amount of protein, + glucose or + lipid: Improvement in N
balance
III.
P2 – Much higher amount of Protein: N equilibrium
 4 Things to be learned:
I.
Exogenous protein spares protein vs. glucose alone
II.
Dose response: more protein sparing w/ more protein provided
III.
In short interval (only 3 days) hypocaloric feeding gives no extra benefit
over P1 alone
IV.
Mix of substrate determines production of anabolism
 N balance:
I.
Better N balance w/ higher protein inputs w/o increasing energy inputs
II.
At any protein intake, adding extra energy improves N balance
III.
Improvement in N balance is seen after input has been maintained for many
days b/c adaptations occur w/ time.
Nutrition & the Kidney
1. Effects of Nutrition on the Normal Kidney:
a. 3 Primary Fx of Kidney:
I.
Excretion: involves water, minerals and organic compounds
II.
Endocrine: 1,25-dihydroxycholecalciferol and erythropoeitin
III.
Metabolic
b. Kidney also excretes or degrades other hormones that is influenced by nutrients like insulin
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c. Kidneys are required to respond to major changes in intake of water, sodium, potassium, acids
and bases, calcium and phosphorus, magnesium and trace elements in order to maintain
homeostasis.
d. Protein Effects:
 Increase in renal blood flow starting 2 hrs after a protein meal and lasting about 1 hr
 RBF and GFR also increases following IV AA infusion
 These effects are seen b/c of glucagons, GH and Insulin like Growth Factor I.
e. Malnutrition Effects:
 Transient or permanent
 Decreased protein intakes  Decreased RBF and GFR
 Low protein diet  Decreased urea production Decreased plasma urea filtration
Decreased medullary hypertonicity  Impaired capacity to concentrate urine (capacity
to dilute urine is not affected)
 Decreased capacity to acidify the urine/Impaired excretion of an acid load b/c of insufficient
phosphate intake and that leads to renal conservation of H2PO4 and so less availability of
H2PO4 for excretion. Also, synthesis and excretion of ammonia also goes down in
malnutrition.
2. Effects of Nutrients on the Progression of Renal Insufficiency:
a. Loss of functioning nephrones to the point of mild renal insufficiency  adaptation in
remaining nephrones like increased Glomerular plasma flow and GFR, nephorne hypertrophy
 alteration in chemical, electrical and pore size barriers  increased gradient across the
Glomerular capillaries  injury to remaining nephrones  Progression of renal failure.
b. Nutrients that contribute to the progression of renal failure:
 Protein:
o High protein increases pressure and flow  damage to Glomerular BM  permeability
to large molecules  deposition in mesangium mesangial expension  inflammation
 scarring
o Low protein intake can prevent these changes
o Low protein intake is advised in mil to moderate renal failure
 Phosphorous & Calcium:
o Low phosphorous intake  decreases the deposition of calcium phosphate in kidney
tissue  prevents progression of renal failure
o Low protein diet are usually low in phosphorous too
c. Causes of Progressive Renal Failure:
 Continued activity of the underlying renal failure
 Systemic hypertension
 High protein diet
 High phosphorous diet
 Vitamin D overdose: causes hypercalcemia
 Hyperuricemia
 Acidemia
d. Mechanisms of Progressive Renal Failure:
 Intraglomerular capillary pressure and capillary blood flow
 Intraglomerular transcapillary hydraulic pressure
 Glomerular hypertrophy
 Calcium phosphate or calcium oxalate deposition in kidney
 Urate deposition in kidney
3. Nutritional and Metabolic Consequences of Chronic Renal Failure:
a. Clinical changes seen in CRF:
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 Weakness
 Feeling of ill health
 Insomnia
 Fatigue
 Anorexia
 N/V
 Diarrhea
 Itching
 Muscle cramps
 Hiccups
 Twitching of extremities
 Tremors
 Irritability
 Decreased mentation
b. Inability to excrete fluid and electrolyte loads  CHF and Hypertension
c. Altered electrolyte concentrations  arrhythmias, seizures, metabolic acidosis
d. Dietary therapy and dialysis are helpful
e. Consequences of CRF:
 Accumulation of products of protein and AA metabolism – urea, creatinine etc
 Inability to excrete salt loads
 Impaired ability to excrete water, K, Ca, Mg, PO4, SO4, H+
 Impaired intestinal absorption of Ca
 High risk of vitamin deficiencies: B6, C, folic acid, 1,25-dihdroxyD
 Retention of toxic chemicals like Al
 Increased secretion of some hormones like insulin
 Decreased secretion of erythropoietin and 1,25-dihydroxyD
 Resistance to insulin
 Increased sensitization to glucagons
 Impaired renal metabolism of glutamine, alanine and glycine
 Accumulation of metabolic end products like urea, creatinine etc
 Hyperparathyroidism as consequence of low 1,25-dihydroxyD, ass w/ osteodystrophy
 Hyperlipidemia
 Accelerated CVD
 Wasting syndrome w/ loss of muscle, fat and multiple functional consequences of these
4. Dietary Management of CRF:
a. Goals of diet therapy:
 Stop the rate of progression of renal failure
 Maintain good nutritional status
 Prevent or minimize those aspect of uremic toxicity that may be influenced by diet (like
eating food containing of purins ??)
 Moderate the metabolic derangements as much as possible
b. Management:
 Monitoring the diet and change w/ worsening renal function
 Major changes are required when dialysis is begun
c. Recommended nutrient intakes for nondialyzed patients w/ CRF and for patients undergoing
maintenance hemodialysis or chronic peritoneal dialysis:
 Protein:
o Recommended protein intake for normal adult person is 0.8 g/kg/day
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o
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Protein intake should be restricted in person w/ CRF
However, if the person is on dialysis then don’t have to restrict protein that much b/c
dialysis can remove undesirable end products of protein and AA metabolism.
o In DM, the efficiency of body protein metabolism is impaired and there may be risk to
restriction
 Energy:
o W/ low protein intake, the body protein metabolism is compromised if energy intake is
less than requirements especially when insulin is insufficient or its action is decreased
as in renal insufficiency.
 Lipids:
o Renal insufficiency  high incidence of hyperlipidemia  elevated TAG, LDL, VLDL
and low HDL  atherogenic
o Recommended to take 30% of calories as fat w/ < 10% as saturated fat and < 300 mg/d
of cholesterol
 Phosphorous and Calcium:
o Low diet phosphorous recommended in CRF and phosphate binder (calcium or
aluminum salts) can be used also
o Dairy products have high phosphorous
 Magnesium:
o Mg levels increase w/ renal failure so intake of Mg should be restricted
o Pt should avoid Mg containing antacids and laxatives
 Sodium and Water:
o Decreased ability to excrete sodium and water
o Diuretics can be used
o Restriction in Na intake
 Potassium:
o K retention is almost the rule in renal failure and so it’s intake must be very strictly
restricted
o (“40-40-40” diet for severe renal failure: 40 g protein, 40 meq Na and 40 meq K)
 Vitamins:
o Mild-moderate risk of deficiency of water soluble vitamins b/c decreased intake (of
water ?) , altered metabolism and use of a number of medications that may interfere w/
absorption, metabolism an action of certain of them. Most likely to be deficient are B6,
C and folic acid and should be prescribed prophylactically
o Vit A is elevated in uremia and so it should not be given (risk of bone toxicity if high)
o Vit K should be given if antibiotics are to be administered
o Vit E doesn’t have to be supplemented
o Vit D can be given if needed w/ Ca levels monitored
 Acidosis:
o Alkali supplements when blood pH is < 7.35 or serum bicarbonate is < 20 meq/l
o Calcium carbonate is an alkali supplement that can be given - advantage: will lower
phosphorus levels
o Sodium carbonate is another alkali supplement and can be given as long as can handle
Na levels
5. Dietary Management of Acute Renal Failure:
a. The most common causes:
 Shock
 Severe infection
 Trauma
 Medications
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 Obstruction
 GN
b. Patients will have fluid and electrolyte disorders, acid-base disturbances, uremic toxicity and
will develop very rapid tissue wasting
c. Nutrients will be provided parenterally at the start of the tx
6. Nutrition Alterations in Renal Stone Diseases:
a. A high urine volume is desirable – achieved by increasing fluid intake
b. In the cases of those types of stones that are more soluble in alkaline urine, oral alkalization
supplements are given
c. In the presence of intestinal disorders such as the short bowel syndrome that predisposes to
oxalate hyperabsorption, high oxalate containing foods are to be avoided. If there is high
oxalate then high Ca should be given, which will lower the hyperabsorption of oxalate
d. Uric acid stones: Alkaline urine, avoid alcohol, avoid food w/ high purine
e. Calcium Nephrolitiasis ass w/ decreased citrate excretion in distal RTA – sodium or potassium
citrate supplementation can be used
f. W/ cystinuria and cystine stones the dietary interventions are to increase urine volume and
alkalize the urine.
Nutrition & Cardiovascular Disease:
1. Background:
a. Number of LDL particles is reflected by the levels of apoprotein B, b/c LDL particles have a
relatively fixed number of apoprotien B. Therefore the level of apoprotein B is a strong
predictor of coronary heart disease b/c it reflects LDL level.
b. The uptake of LDL particles by macrophages is not receptor dependent.
2. Definition / Prevalence of Hypercholestrolemia:
a. Total serum cholesterol of 5.2 mmol/L (200 mg/dl) or less is considered desirable.
b. Total Cholesterol of 6.2 mmol/L (240 mg/dl) or more is considered to be elevated.
c. Total cholesterol levels b/w 5.2 and 6.2 mmol/L are borderline
d. Serum cholesterol are considered to be elevated in pt w/ 2 or > risk factors.
e. Risk factors for Coronary Artery Disease:
 Modifiable:
- Smoking
- Hypercholesterolemia
- Low HDL cholesterol
- Hypertension
- DM
- Obesity
 Non Modifiable:
- Age
- Family Hx of premature coronary artery disease
- MI or sudden death in 1st degree relative < 55 yr of age
f. Friedewald Equation:
 LDL Cholesterol = [total cholesterol] – [HDL cholesterol] – [TAG]/5
g. The decision to Tx hyperlipidemia should be made on at least 2 measurements in the fasting
state, taken 2-3 months apart. The decision to use drug therapy should be based on hither LDL
cholesterol values that stay high despite 6 months of diet therapy.
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W/O CHD and w/ < 2 RF
W/O CHD and w/ 2 or > RF
W/ CHD
Dietary Therapy initiation
Levels
160 mg/dL
130 mg/dL
> 100 mg/dL
Drug Therapy Consideration
Levels
190 mg/dL
160 mg/dL
130mg/dL
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LDL Goal
<160 mg/dL
<130 mg/dL
</= 100 mg/dL
3. Diet Components:
a. Dietary Cholesterol:
 Cholesterol is found as integral component of cell membrane of all animals, birds and fish
but is absent in plants, nuts and seeds.
 Saturated fat diet  high LDL
 High dietary cholesterol  high circulation cholesterol
b. Fatty Acids:
 All saturated fatty acids are not as potent.
 Saturated fatty acids can be found in red meat, whole milk products and plant sources like
coconut and palm oils, cocoa butter and hydrogenated vegetable oils (Hydrogenation make
unsaturated FAs  Saturated FAs.
 Monosaturated FAs (oleic acid) are considered good to replace saturated FAs b/c they lower
LDL a little and don’t decrease HDL levels.
 Polyunasaturated FAs are divided into two groups:
- Omega 6 = Linoleic acid: found in vegetable oil  decreases LDL and may
decrease HDL
- Omega 3 = Linolenic acid: Found in fatty fish and shellfish  Lowers TAGs,
VLDL and apoprotein B production
 AE: Contamination w/ mercury or pesticide, excessive
bleeding and fat-soluble vitamin toxicity
 Dietary trans-FAs  atherogenesis: Found in animal fats and hydrogenated vegetable oils
c. Plasma Homocysteine:
 Cardiovascular Disease RF
 Atherosclerosis and thromboembolism seen in people w/ high homocystine levels
 Homocystine levels increase w/ age, male, smoking and some medications.
 Homocystine levels can be lowered w/ Vitamins B6, B12 and folate.
d. Fibers:
 Non digestible carbohydrates from the cell walls of plant foods
 Insoluble fibers are useful in constipation but have no effect on hyperlipidemia
 Soluble fibers (gum, pectins and mucilages) have antihyperlipidemic effect
- Sources: citrus fruits, barley, oats, dry beans and peas
- AE: Eructation, abdominal bloating and flatus
- MOA: similar to bile acid binding resins
e. Alcohol:
 Raises A-I and A-II and HDL3
 Controversy about use of moderate alcohol for protection against coronary heart disease
f. Carbohydrates:
 Carbohydrates like vegetables, fruits and grains should be used to replace saturated FAs
 Natural foods are high in complex carbohydrates and are usually low in caloric density and
contain a variety of vitamins and minerals.
g. The indication for medication is based on LDL and not on cholesterol
4. Diet Prescription:
a. The dietary management of hypercholesterolemia is based on 3 major components:
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 Restoration of normal body weight
 Reduction of intake of saturated fatty acids and dietary cholesterol
 Increase in fiber intake
b. Two steps of the dietary changes:
 A reduction of the major and obvious sources of saturated FAs and cholesterol in the diet
(can be prescribed by physician)
 Careful attention to whole diet  to reduce the intake of saturated FAs and cholesterol to a
minimal levels compatible w/ an acceptable and nutritious diet (requires help of a dietician)
- Replacement of saturated FAs w/ carbohydrates and polysaturated FAs
c. Control DM, HTN
d. Stop smoking
5. Diet and HTN:
a. Causal Factors:
 Genetic
 Emotional: Chronic tension  Increases sympathetic tone  elevated levels of
catecholamines in circulation
 Diet:
- Overweight, obesity
- High Na intake
- Low K
- Low Ca and Mg
- Low PUFA or EFA consumption
- Alcohol
b. Dietary influence on BP:
 HTN is 2x higher in obese people
 Loosing little weight will lower BP
 High Na intake  high BP
 Lowering Na intake lowers BP
 Diuretics  increase urinary Na  reduce BP
 Urinary excretion is the main route of Na loss but sweat glands modulate Na loss and low
Na intake results in low sweat Na content.
c. Current Recommendations:
 Lower Na content in food
 High K lowers BP so K content in food should be increased
 Lower the processed food in diet and increase natural food in diet
 Too little Ca is ass. w/ HTN, so shouldn’t reduce the Ca intake
 Alcohol may rise BP
 Lacto-ovo-vegetarian diet: reduces BP (may b/c of increased K intake)
 Should replace saturated FAs w/ PUFA  Fall in BP (may be b/c of increased synthesis of
vasodilator prostaglandins)
 Increased plasma insulin is ass w/ elevated catecholammines independent of plasma
glucose. Also, insulin promotes renal tubular reabsorption of Na and thus high
carbohydrate diets promote Na retention.
6. Summary of Prescription:
a. For the overweight – Weight reduction by diet and exercise
b. Restrict Na to 2 g/day or 5 g of salt
c. Maintain consumption of low fat, low Na milk and cheese products to maintain Ca levels
d. More fibers
e. Less saturated fat
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f.
g.
h.
i.
j.
k.
l.
More polyunsaturated fats
Alcohol should be limited to 2 oz/day
Regular isotonic exe
K intake should not be increased b/c it rises w/ low Na intake
Supplement Ca and Mg to people who are deficient of these
Relaxation therapy
Avoid smoking
Geriatric Nutrition
1. definitions:
a. Aging: Progressive and generalized impairment of function w/ time resulting in a loss of
adaptive responses to stress and in an increasing risk of age-related diseases.
b. Geriatric: Persons 65 yrs of age and older
2. Demographics:
a. Gain in the life expectancy is due to changes in environmental factors such as hygiene, better
nutrition and medical care.
b. Nutrition is cornerstone of keeping elderly people in the community, enjoying a healthy active
life.
3. Physiological Concomitants of Aging:
a. Successful vs. Usual Aging:
 Usual Aging: Disease free aging but accompanied bye multiple decremental
evidences of disuse. (disuse +/- disease)
 Successful Aging: Functioning optimal physical, emotional and cultural levels.
 Fragile Aging: Aging w/ incremental loss of function and more severe diseases.
b. Body Composition:
 Body Weight:
- continue to gain weight till mid 40’s in males and mid 50’s in females
- Stable weight from then till 70’s
- Loose some weight then after.
 Lean Body Mass:
- Reaches a peak value b/w 20-30 yr of age
- Progressively decreases by 6% per decade then after
- May be in part due to decrease in physical activity
 Fat Mass:
- % of body fat increases by about 50% from age 20-65 and then stabilizes
- In very old people > 85 yr of age may have decrease in fat mass
 Fat Distribution:
- The adipose tissue changes distribution w/ aging: increasing visceral w/
corresponding decreasing subcutaneous fat depots
- This altered ration of water and lipid compartments affects drug half-lives, may
influence glucose and lipid metabolism and makes the dx of obesity and
undernutrition by clinical assessment more difficult.
 Bone Density:
- Peak bone mass is reached around 30 yrs and depends on heredity, race, sex and
Ca intake early in life
- In female: type I osteoporosis – estrogen dependent
- In males: type II osteoporosis – less clinical consequences
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c. Metabolism:
 Resting Metabolic Rate:
- Decreases by 20% from 30-90 yrs
- Thus energy requirement decreases w/ age following the decline in RMR and
physical activity
 Glucose Intolerance:
- Decrease in glucose tolerance w/ aging b/c of insulin resistance that develops b/c
of obesity, lack of activity and diet composition
- Hyperlipidemia can cause HTN and CVD
 Protein:
- Total rates of turnover of both visceral and muscle protein decreases w/ aging
- This can diminish the capacity of the elderly to respond to restricted diet intake or
to stressful conditions that require mobilization of AAs from the myocytes for
protein synthesis in vital organs, including cells of immune system
4. Nutritional Status of Elderly:
a. It’s difficulty to differentiate disease related changes from those due to aging or inadequate
intake, and the negative impacts of poverty and sedentary lifestyles
b. Surveys:
 High prevalence of obesity and protein-energy malnutrition
 Low intakes of micronutrients vitamins A, D, B6, B12, folic acid, Ca and Zn
 Overdoses of vitamins
 Undernutrition in hospitalized pt due to acute disorders like stroke, CHF, COPD and
infections (their investigations and tx can also lead to undernutrition)
c. Criteria for Presence of Malnutrition:
 Good hx taking, Clinical judgment and Biochemistry profile can be used to find out if
the person is malnourished
 Presence of a catabolic or malabsorptive state
 Inadequate food intake
 Unambiguous emaciation or obesity – obese person can have protein and other
nutrient deficiencies
 Involuntary weight loss of 4-5 kg over past 6 months
 Serum albumin < 34 g/L
 Lymphocyte count < 1.2 x 10^9/L
 Hemoglobin: Male < 120 g/L, female < 115 g/L
 Pressure ulcers – bedsores
 Anorexia from any cause if prolonged can result in protein-calorie malnutrition
d. Factors Contributing to Malnutrition:
 Social Factors:
- Isolation
- Economic
- Institutionalization
 Neurosensory Factors:
- Vision
- Taste
- Smell
- Hearing  social isolation
- Thirst
- The sum of the above factors interact to decrease the pleasurable aspects of eating
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
Pahophysiological Factors:
- Functional status and motor impairment
- Mechanism of eating: poor dentition/dentures
- Gastro-intestinal: atrophic gastritis affects folate, iron, calcium absorption and
B12 bioavailability. Constipation due to decreased colonic motility
- Health status: chronic and acute illness
 Psychological Factors:
- Major life events: death of spouse, relatives, contemporaries
- Depression
- Dementia
- Food beliefs
 Other Factors:
- Anorexia: decreased feeding drive, early satiety
- Alcohol intake: empty calories, memory deficits
- Medications: drug-nutrient interactions
e. Drug-Nutrition Interactions:
 Aging changes affects drug metabolism and thereby affects nutrition indirectly
 Volume of Distribution:
- Increase in proportion of fat and decreases in water compartments reduces the
volume of distribution of water soluble drugs w/ initial higher plasma [ ] and
accumulation in the CNS e.g. ethanol, cimentidine, digoxine
- Increase in proportion of fat augments the volume of distribution of the lipid
soluble drug resulting in prolonged action due to longer elimination ½ lives e.g.
benzodiazepines
- In PEM the protein binding goes down b/c of low albumin  increase in plasma
free drug [ ] e.g. NSAIDs
 Hepatic Metabolism: Reduced clearance b/c of decreased hepatic mass and blood
flow e.g. theophylline, benzodiazpines, antidepressants
 Renal Excretion: Reduction in the rate of elimination of drug by the kidney due to fall
in GFR and renal plasma flow  accumulation of digoxin, antibiotics, lithium and
cimetidine
 Drug Use and Dialysis: Adeverse drug reaction b/c elderly people usually take lot of
drug
5. Nutrients Needs of Elderly:
a. 2 differences b/w dietary intakes b/w younger and older adult:
 Vit D intake is doubled from age 50 to 70 and tripled after age 70
 Ca intake is increased from 1000 mg to 1200 mg/day from age 50 onwards
b. Energy:
 Decrease in RMR and activity as age
 Requirements/day for 65-74 yr old: Males = 2300 kcal, Females = 1800 kcal
 Requirements/day for 75+ yrs: Males = 2000 kcal, Females = 1500 kcal
 Obesity tend to increase w/ age and so inter-individual variability is the rule
 On such a limited energy allowance, all food must be nutrient dense w/ little leeway
for empty-calorie foods such as sweets, fats, oils or alcohol
 RNI Ca intakes are same for both sexes
 RNI Phosphorus is slightly in excess of Ca and are higher in men than in women
 The RNI for iron declines for females following menopause and becomes the same
for both sexes
c. Water: 6-8 glasses/day – reduces osmotic work of kidney and prevents stone formation and
ameliorates constipation
Nutrition 13
d. Vitamin Supplementation: If energy intake is less than 1500 kcal supplementation w/ a multiple
vitamin is indicated
Nutrition & DM
1. Background:
a. DM causes macroangiopathy (atherosclerosis), microangiopathy (retinopathy, nephropathy and
mononeuropathies) and polyneuropathy and autonomic neuropathy
b. Types:
 Type I: total insulin deficiency (autoimmune)
 Type II: Combination of insulin resistance and insulin insufficiency (Early/Mild
Cases  hyperinsulinemic, Severe Cases  hypoinsulinemic)
2. Goals of Diet Therapy:
a. Achieve optimal nutrition including special needs for children and pregnancy
b. To achieve and/or maintain reasonable weight (not same as ideal body weight)
c. Maintain plasma glucose and lipids as close to physiological levels as possible in order to
decrease long term diabetic complications and atherosclerosis
3. Strategy:
a. Individualizing dietary prescriptions
b. Clinical end point is normalizing glycemia and its excursions after ingestion of meals and
snacks  self-monitor own blood glucose and adjust behavior accordingly
c. Require knowledgeable and committed physician, dietitian, teaching nurse (2 out of 3)
d. Dietitian intervention becomes keystone to success b/c well-informed and motivated type 1
diabetic can achieve near normoglycemia and obese type 2 diabetes can achieve cure w/ weight
loss
e. Note: Excessive calorie intake can be responsible for the causing type 2 diabetes
4. Diet Principles:
a. Energy Intake: In obese type 2 diabetes the primary aim is to restrict total calories to achieve
weight reduction, but in non-obese patient calories are not restricted and rather the weight
should be maintained.
b. Composition of the Diet:
 DM is a RF for CHD
 Hyperglycemia is ass w/ decreased HDL, increased LDL and increased TAG
 Saturated FAs increase plasma cholesterol and so intake of these should be reduced
 Polyunsaturated FAs should be maintained
 Monosaturated FAs decrease LDL slightly but don’t decrease HDL and do not raise
TAG  safe
 < 10% calories should be from saturated FAs and up to 10% calories should be
from polyunsaturated FAs and dietary cholesterol should be restricted to < 300
mg/day, 50-60% of calories from carbohydrates
 Protein is usually not restricted but if nephropathy is present then should be
restricted to lower levels of recommended amounts
 Complex carbos are recommended and simple sugars (not sucrose ?) should be
restricted b/c simple sugars are digested and absorbed faster than complex carbos
like starch and so aggravates hyperglycemia
 High carbos diet can increase TAGs and decrease HDL
 Raw fruits and vegetables maximize the fiber effects
 Alcohol increases TAGs and so should be avoided in hyperlipidemia and promotes
obesity. Also alcohol exacerbate hypoglycemia
Nutrition 14

Salt is restricted to < 4 g/day if hypertensive, however it can be harmful in some
individuals w/ poorly controlled diabetes, postural hypotension and fluid imbalance
 The optimal composition  b/w high carbohydrate and high monounsaturated fat
diets
c. Artificial Sweetners and Sugar Substitutes:
 Approved Sweetners:
- Cyclomate and Saccharin – Table top use, prohibited in manufactured food b/c
they are carcinogenic in animals
- Aspartame – Made by joining 2 AAs phenylalanine and aspartic acid w/ methanol
and so metabolized like protein. Loss of sweetness w/ baking
- Sucralose – Stays stable when heated, secreted unchanged in feces
- Bulking Agents: Polydextrose, Maltodextrins, sorbitol and hydrogenated starch
hydrolysate
 Not Yet Approved Sweentners:
- Caloric Sweenterns:
 Fructose
 Mannitol
 Sorbitol
 Xylitol
d. Glycemic Index:
 Definition: The incremental plasma glucose responses to a reference food (gluclose)
 Factors determining glycemic response to foods:
- The amount of carbs
- The chemical form of the carbos
- The physical form of the carbos (cooked vs. raw)
- Concurrent nutrition ingested (fat slows gastric emptying, protein stimulates
insulin secretion, fiber slows intestinal transit)
- Presence of gastrointestinal abnormality like gastroparesis
 Self monitoring is the key to the glycemic control
5. Specific Requirements for Type I DM and Insulin-Treated Type II DM:
a. Timing and composition of meals in relation to insulin
b. Prevention of hypoglycemia
c. NPH w/ Regular Insulin twice a day  excess insulin b/w meals and less insulin at lunch time
 so requires snacks b/w meals and at the bed time, and fewer calories at lunchtime
d. Ultralente (or newer Ultralong-Acting) + Ultrarapid or Continuous Subcutaneous Insulin
Infusion w/ Pump:
 A base line insulin level can be obtained by Ultralente (or Glargine) Insulin
injections or by the continuous infusion of regular insulin and the level is adjusted
to keep the glucose level stable in the absence of meals
 Ultrarapid (or regular) insulin is given at each meal in amounts adjusted depending
on the content of the meal and the expected level of activity
e. B/W meal snakes are not required
6. Specific Requirements for Type 2 DM:
a. Obese:
 Avoid extreme energy restriction
 Avoid unrealistic targets
 Even a modest weight loss can be ass w/ a marked improvement in glucose control
 On Oral Hypoglycemic: Monitor hypoglycemia and adjust doses accordingly
rather than adding snacks
 On Insulin: same as in type 1
Nutrition 15
b. Non Obese:
 Not on Insulin: Weight maintaining energy intake, distribute food into 5-6 feedings
to decrease individual challenges to beta cells w/ limited secretory reserve
 On Insulin: same as in type 1
7. Exercise-Nutrition Interactions:
a. Aerobic exercise should be recommended
b. Exercise generally will lower glycemia in diabetics b/c glucose utilization by muscle cell
increases w/ exercise
c. Patients receiving insulin tx:
 Risk of late exercise or post exercise hypoglycemia: can take rapidly assimilated
CHO b/4 or just after the activity or if on multiple insulin injection then can adjust
the dose
 If pre-exercise glucose is too low then exercise can result in further hypoglycemia
 If the pre-exercise glucose is too high and there is insulin deficiency then exercise
can result in hyperglycemia and ketosis
8. Pregnancy and Lactation in the Diabetic Person:
a. Augmented ketogenesis b/c coupling of ketogenesis and gluconeogenesis to make glucose
necessary for conceptus and milk production
b. Marked changes in insulin sensitivity occur toward the end of gestation and in the neonatal
period  countered by altered insulin doses rather than dietary changes
9. Treatment of Hypoglycemia Reactions:
a. Insulin-treated patients should always carry a source of simple oral carbohydrates that can be
used in mild hypoglycemic reactions
b. Chocolate and Ice-cream should be avoided b/c fat will slow the absorption of available sugar
and they can also lead to obesity
c. When hypoglycemic reaction occurs in the evening or night  Carbohydrate should be
followed by longer acting carbohydrates and protein intake to prevent further hypoglycemia
during the night
d. Patients w/ impaired consciousness or an inability to swallow may aspirate and should not be
treated w/ oral carbohydrate and they require subcutaneous glucagon or intravenous glucose