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Nutrition 1 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. Nutrition 2 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. Nutrition 3 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 Nutrition 4 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: Nutrition 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 5 Nutrition o o 6 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 Nutrition 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. 7 Nutrition 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 8 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: Nutrition 9 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 Nutrition 10 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 Nutrition 11 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 Nutrition 12 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