Department of Nutrition Faculty of MedicineUniversitas Indonesia

*Handbook of Clinical Nutrition 4th ed., 2006 ---- D. C. Heimburger & J. A. Ard

Krauses Nutrition & Diet Therapy 12th ed., 2008 ---- L. K. Mahan & S. Escott-Stump

Modern Nutrition in Health and Disease 10th ed., 2006 ---- M. E. Shils et al

Nutrition and Diagnosis-Related Care 6th ed., 2008 ---- S. Escott-Stump

*Coronary heart disease

Hypertension

Congestive heart failure

*Nutrients for the heart:

Macronutrient

Micronutrient

*Nutrients for (contd) Macronutrient

Carbohydrate: Glucose

Lipid: Fatty acids

Protein Energy Cells structure Contractile protein Cells regeneration- Enzymes

*Nutrients for (contd) Micronutrient

Vitamins:Thiamin, riboflavin, & niacin coenzymes in energy metabolismVitamin B6 amino acids metabolism

Minerals:Na, K, & Ca cardiac muscle contractionMg, Mn, Fe, & Cu energy metabolism

The most common cause of coronary heart disease (CHD) is atherosclerosis

The process begins with the accumulation of plaque in large & medium coronary arteries*

*The structure of mature, stable, & unstable plaque

composed of:

Low-density lipoprotein (LDL)CalciumFibrin *

*Natural progression of atherosclerosis

*

*Fatty acids & cholesterolSoluble fiberSoy proteinAlcoholHomocysteine, folic acid, and vitamins B6 & B12AntioxidantsPlant stanols & sterolsObesityNutritional factors effects on serum lipids & coronary heart disease (CHD):

*Fatty Acids & CholesterolDietary saturated fatty acids (SFAs) & cholesterol serum total cholesterol (TC) & LDL-cholesterol (LDL-C) levels

Monounsaturated fatty acids (MUFAs)

Polyunsaturated fatty acids (PUFAs) TC levelsLDL-C levelsTriglyceride levels

*Fatty Acids & (cont.)MUFAs: oleic acid is the most prevalent MUFA in the diet

Food sources: olive oil, canola oil, peanut oil, avocado

*Fatty Acids & (cont.)Types of dietary PUFAs: n-6 (omega-6) & n-3 (omega-3) fatty acidsn-6 fatty acids:

Linoleic acid (18:2) the major n-6 fatty acid in the diet Sources: plant oils

*Fatty Acids & (cont.)n-3 fatty acids:

-Linolenic acid (18:3) Food sources: plant oils, plankton

Eicosapentaenoic acid (EPA) Docosahexaenoic acid (DHA)fish & fish oilFood sources:

*DIET: Saturated Fat, Cholesterol Polyunsaturated Fat Serum CholesterolAtheromatous PlaqueCoronary Artery NarrowingMyocardial InfarctionClassic diet-heart hypothesis

*Several prospective studies:Zutphen (Netherland) & Chicago (USA): consumption of fish was associated with reduced CHD mortality

Other studies:a risk reduction in sudden cardiac death in persons who consumed fish more than once a week statistically significant inverse trendsbetween fish intake and CHD mortality

*Oleic acidElaidic acidCis formTrans form

*Trans-fatty acids: isomers of the normal cis fatty acids produced when unsaturated fatty acids are hydrogenated in the production of margarine & vegetable shortening (cooking fats)

*Point of unsaturationSaturated fatty acidTrans fatty acidcis shapetrans shapeConversion of unsaturated fatty acid (FA) to saturated FA & trans FA caused by frying & hydrogenation liquid vegetable oilsOxidationIsomerization

*Trans-fatty acids: serum LDL-C & HDL-cholesterol (HDL-C) levels

Evidence: high intake of trans fatty acids the risk of CHD

*The reduction in serum TC levels by water soluble fiber range from 0.52% per g of dietary fiber intake

Health Professionals Follow-Up Study: dietary fiber the risk of fatal CHD

Recommendation: 1013 g fiber/1000 kcal with 25% as soluble fiber

*Meta-analysis of 38 studies:Replacement of animal protein with soy protein ( 47 g/day) without changing dietary saturated fat or cholesterol, resulted in - 1012% in serum TC & LDL-C levels - has no adverse effect on HDL-C

Consuming 25 g soy protein/day could serum TC by 9 mg/dL

* Epidemiologic studies:moderate alcohol drinkers (12 drinks/day) have approximately 3040% lower CHD mortality risk & 10% lower total mortality risk than nondrinkersMechanism:

HDL-cholesterol levels Antithrombotic effectRecommendation: red wine,: 2 drinks/day: 1 drink/day1 drink 150 mL

*Homocysteine, Folic Acid, and Vitamins B6 & B12 Homocysteine: an amino acid metabolite of methionine

Recycling homocysteine methionine requires:Folic acidVitamin B6Vitamin B12

Marginal deficiencies of folic acid, vitamins B6 & B12 homocysteine levels

*Homocysteine, (cont.)Metabolism of homocysteineSAM: S-Adenosyl methionineFH4: tetrahydrofolatePLP: pyridoxal phosphate (vitamin B6 coenzyme)

*Homocysteine, (cont.)High levels of homocysteine adversely affect endothelial cells & produce abnormal clotting CHD risk

Folic acid has the most potent influence on homocysteine levels. Doses of 0.41 mg especially when combined with vitamins B6 & B12 serum homocysteine levels

*Homocysteine, (cont.)Diet: vegetables & legumes (source of folic acid) intake can often plasma homocysteine levels

delay & LDL oxidation*The oxidative modification on LDL is important in atherogenesis

Antioxidant vitamins:Vitamin E -carotene Vitamin C

*

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Epidemiologic evidence: an inverse relation between antioxidant vitamins especially vitamin E and CHD

Two trials of vitamin E supplementation have not shown benefit for prevention of CHD Antioxidant supplements are notrecommended for prevention of CHDAntioxidants (cont.)

*

* Inhibit absorption of dietary cholesterol

Lower serum TC levels

Adult Treatment Panel (ATP) III recommendation: 23 g/day for lowering LDL-cholesterol levelsFood source:

soybean oils

*BMI = BW (kg)

H (m)2BMI: body mass index, BW: body weight; H: heightFor clinical practice classification of weight is by measuring the body mass index (BMI)

*Proposed classification of weight by body mass index in adult AsiansObesity (cont.)The International Diabetes Institute, 2000

ClassificationBMI (kg/m2)Underweight

Normal range

Overweight At risk Obese I Obese II

*Obesity (cont.)BMI & CHD are positively related; BMI the risk of CHD also

In , higher BMIs are associated with higher triglyceride & lower HDL-C levels than average

*Serum LDL-cholesterol (LDL-C) levels has been the focus of much research since it is conclusively linked to:AtherosclerosisCHD developmentMyocardial infarctionStroke

LDL-C is the primary target for intervention efforts

*Nutritional factors that affect LDL-C LDL-CSaturated & trans- fatty acids

Dietary cholesterol

Excess body weight LDL-CPUFAsViscous fibrePlant stanols & sterolsWeight lossSoy protein

* Diet

Physical activitytherapeutic lifestyle changes (TLC) diet recommendations

*Nutrient Composition of the TLC DietFrom Third Report of the National Cholesterol Education Program (NCEP) ExpertPanel on Detection, Evaluation, and Treatment on High Blood Cholesterol inAdults [Adult Treatment Panel (ATP) III]

NutrientRecommended intakeSaturated fat*Polyunsaturared fatMonounsaturated fatTotal fatCarbohydrateFiberProteinCholesterolTotal calories (energy)

*Nutrient composition of (cont.)*Trans-fatty acids are another LDL-raising fat that should be kept at a low intake Carbohydrate should be derived predominantly from foods rich in complex carbohydrates, including grains, especially whole grains, fruits, and vegetablesDaily energy expenditure should include at least moderate physical activity (contributing approximately 200 kcal/day)

*Sodium chloridePotassiumCalciumMagnesiumAlcohol LipidsObesity

*The Seventh Report of the Joint National Committee (JNC 7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, 2004

* Evidence for an association between NaCl intake and blood pressure (BP) is provided by both observational & intervention studies Two meta-analyses: of BP by NaCl restrictions more prominent in hypertensive than in normotensive persons

*Sodium (cont.)Mechanisms of BP induced by NaCl Fluids retention plasma volume stroke volume cardiac output arterial pressure

vascular reactivity to norepinephrineDietary NaCl loading may cause:

*Potassium (K) loading prevents or alleviates development of hypertension in animal modelsIn society with high K intakes, mean BP & the prevalence of hypertension tend to be lowerHowever, not all surveys showed inverse correlation between K intakes and BP

*Proposed mechanisms a high dietary K intake may BP include:

Natriuretic effect of K

Direct vasodilatationPotassium (cont.)

*Two meta-analyses: weak but statistically significant inverse correlation between dietary calcium (Ca) and both systolic & diastolic BPPutative mechanisms dietary Ca may BP:

Natriuretic effect of Ca

Ca influx into vascular smooth muscle cells & capacity of these cells to extrude Ca

Direct vasodilatation

*Evidence suggests an association between lower dietary magnesium (Mg) and higher BPLimited information is available about the effects of Mg supplementation on BP in hypertensive personsA recent meta-analysis (2002):dose-dependent of BP reduction from Mg supplementation

*Magnesium (cont.)Plausible physiologic rationale for effects of Mg on BP:

Mg vascular tone & contractility

*57% of hypertension is attributed to consuming >2 drinks of alcohol (ethanol) per dayThe mechanisms by which alcohol may affect BP has not been establishedAlcohol: sympathetic nervous system activity

Stimulates cortisol secretion

(1 drink of red wine 150 ml)

* LipidsLimited epidemiologic evidence: direct association between diets high in SFAs and BP, and people with low mean BP levels consume diets low in total fat & SFAsDiet high in n-3 fatty acids may be associated with lower BPA recent meta-analysis (2002):High intake of fish oil BP Effect n-6 PUFAs on BP (?)

*Data from cross-sectional studies: direct linear correlation between BW or BMI and BP60% of hypertensive adults are >20% overweightMechanisms of obesity-related hypertension: Obesity hypervolemia cardiac output, without an appropriate reduction of peripheral resistance

Insulin resistance

* modificationWeight reductionProper dietSodium restrictionExerciseModeration of alcohol consumptionRecommendation for Preventing and Treating Hypertension

*The Seventh Report of the Joint National Committee (JNC 7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, 2004

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*Some studies have shown that the DASH diet can significantly reduce high BPThe DASH eating plan is low in salt (2.4 g Na = 6 g NaCl) by using:Less table salt

processed foods & high-sodium snacks

*Symptoms:

FatigueShortness of breathEdemaCongestion

*Risk factors:

HypertensionCoronary heart diseaseValvular diseaseDiabetes mellitus (contd)

*Poor DietHypertensionLipid AbnormalitiesAtherosclerotic Heart DiseaseMyocardial IschemiaHeart FailureStrokeHeart FailureStrokeMyocardial Infarction

* Energy

Energy needs depend on current dry weight, activity restrictions, and the severity of the heart failure Overweight: caloric reduction must be carefully monitoredMalnourished: 32 kcal/kg BW & 1.4 g of protein/kg BWNormal nutritional status: 28 kcal/kg BW & 1.1 g of protein/kg BW

* SodiumNa to be restricted to

* Calcium & Vitamin DCongestive heart failure (CHF) patients are at risk of developing osteoporosis

Magnesium Mg deficiency caused by poor intake & the use of diuretics Mg supplementation small improvements in arterial compliance Medical Nutrition (cont.)

* Thiamin Supplementation

Loop diuretics can deplete body thiamin & cause acidosis

Thiamin supplementation can improve left ventricular ejection fraction & symptomMedical Nutrition (cont.)

*Medical Nutrition (cont.) Avoid foods producing gas: beans, cabbage, onions, & cauliflower

Small frequent feedingslarger, infrequent meals are more tiring to consume can contribute to abdominal distention & O2 consumption

Use soft textures food

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