Prudent Diet and Preventive Nutrition From Pediatrics to Geriatrics: Current Knowledge and Practical Recommendations

(Part I of a Multipart Series)

Enas A Enas, A Senthilkumar, Hancy Chennikkara, Marc A Bjurlin

Coronary Artery Disease in Asian Indians (CADI) Research Foundation, and University of Illinois, Chicago, USA

 

"A man is what he eats" (German proverb). Food provides not only the essential nutrients for life but also other bioactive compounds for the promotion of health and the prevention of disease.1–3 The results of 50 years of intensive worldwide research support the conclusion that diet is the major environmental cause of atherosclerosis and cardiovascular diseases (CVD), especially in genetically susceptible individuals.4 A high-caloric diet, combined with limited physical activity, contributes to dyslipidemia, insulin resistance, diabetes, and obesity. All these abnormalities increase the risk of CVD. Over the past few decades, the prevalence of obesity has doubled in adults, and quadrupled in teenagers in the USA. A similar pattern is emerging in India, where an epidemic of coronary artery disease (CAD) and diabetes is under way, with no signs of a downturn. Whereas the rates of CAD have declined by 60% in the US, the rates have increased by 300% in India over the past 30 years.5 The public and physicians are constantly bombarded with confusing and conflicting dietary advice. This review analyzes the important recent developments in the fields of diet and nutrition for the prevention and treatment of CVD and diabetes, with particular attention to Asian Indians.

Facts and Myths about Cholesterol, Fats, and Meats

The modern understanding of the role of nutrition in heart disease began in 1903 when Anitschkow and Chalatow found that a diet of meat, milk, and egg produced atherosclerosis in rabbits. A decade later, serum total cholesterol (TC) level was found to be the agent responsible. Contrary to common belief, the contribution of dietary cholesterol to serum TC is small (<10 mg/dl). The average adult on a western diet consumes about 300 mg of cholesterol daily, which is about the size of 3 toothpicks, and hardly 3 cal. Nonetheless, high intakes of dietary cholesterol increase the number of circulating low-density lipoprotein (LDL) particles.6 Dietary cholesterol is found only in the animal kingdom; 3 oz of beef, lamb, or pork contains 75 mg of cholesterol. Most of the cholesterol in poultry is in the skin, and some in dark meat. One cup of milk has 33 mg, 2 egg yolks have 560 mg, and 100 g of brain has 2000 mg of cholesterol. One hundred grams of shrimp contain about 150 mg of cholesterol but <1 g of saturated fat. The recommended dietary intake of cholesterol and various types of fat is given in Table 1.1,6–12 The contribution of dietary saturated fat to serum TC is very large—10 times greater than that of dietary cholesterol. Fats are substances consisting of a combination of fatty acids, which are classified as saturated (SAFA), monounsaturated (MUFA), polyunsaturated (PUFA), and transunsaturated (TRAFA), depending on the location and number of double bonds.13 It is not often appreciated that the quality of the fat is more important than the quantity of fat consumed. The National Cholesterol Education Program (NCEP) recommends an intake of total fat of 25%– 35%, MUFA up to 20%, PUFA up to 10%, and SAFA <7% of the total energy14 (Table 1). Although many affluent Asian Indians consume 50% of energy from fat, the average consumption is about half this amount (20%–25% of the energy). Increasing the MUFA intake to 20%, and total fat intake to 35% of the energy appears to be appropriate for Asian Indians because of the beneficial effects on highdensity lipoprotein (HDL) and triglycerides (TG) . The NCEP dietary guidelines for PUFA and SAFA seem appropriate for Asian Indians without any modification.

Saturated fatty acids, the arch villain of atherosclerosis: Excessive consumption of SAFA is the principal dietary culprit contributing to elevated serum TC level, which is the primary determinant of atherosclerosis.15,16 Differences in CAD mortality worldwide are explained by differences in SAFA intake and the resulting serum TC levels in 40 countries, except for France, Finland, and India.16–18 Intake of SAFA suppresses the LDL receptor activity and decreases the clearance of LDL from the circulation, resulting in a marked elevation of its level.19 SAFA raises the serum TC level thrice as much as PUFA, and MUFA lowers it. For example, substitution of 20% of the daily energy intake of carbohydrate by SAFA increases the TC level by 30 mg/dl, whereas PUFA and MUFA lower it by 10 mg/dl.13 Most of this increase is due to an increase in LDL. Although some increase in HDL also occurs, it is not sufficient to offset the atherogenicity and thrombogenicity resulting from marked elevation of LDL.6,20

Our diet contains SAFA of different chain lengths with varying atherogenic properties. According to their chain lengths, SAFA can be classified as short chain (4:0–6:0), medium chain (8:0–10:0), long chain (12:0–18:0), and very long chain (20:0–24:0) fatty acids. Stearic acid (C18:0) is desaturated to oleic acid soon after its absorption, and hence does not raise the TC level.21,22 Therefore, its use need not be restricted and, in fact, it can be recommended.23 SAFA with chain lengths of 12–16 have the most cholesterol-raising properties.24 These are lauric acid (C12:0), myristic acid (C14:0), and palmitic acid (C16:0). These 3 fatty acids account for only 25%–30% of the total dietary fat but 60%–70% of SAFAs in western diets.24 Palmitic acid is the most common fatty acid in the human diet, and the principal SAFA in both animal fats and palm oil. In a study conducted in a metabolic ward, 40% of energy as palmitic acid raised the TC by 25 mg/dl v. 15 mg/ dl with lauric acid.21 Myristic acid is the most powerful cholesterol-raising SAFA, and increases the TC level 50% more than palmitic acid. Replacement of 20% of energy from carbohydrate with myristic acid raises the blood TC level by 46 mg/dl, compared to 30 mg/dl with palmitic acid, and 20 mg/dl with lauric acid.25 Most of the rise in the TC level is due to an increase in LDL, the respective contribution from HDL being 16 mg/dl, 8 mg/d and 12 mg/dl.25 The major sources of myristic acid are butter and tropical oils (Table 2).6,20–25 The TC-raising potential of lauric acid is 33% less than that of palmitic acid, and it is the principal SAFA in coconut and palm kernel oils, both containing 48%.23–25 Coconut and palm oils are also high in myristic acid (18%), and this explains why the consumption of these oils raises the LDL level in a fashion similar to that of butter (Fig. 1).25,26 Studies in laboratory animals indicate that coconut oil increases both TG and LDL levels;6,27,28 the claim that lauric acid does not raise TC is not supported by scientific data.21,23 Recent studies have shown that caprylic acid (C:8) and capric acid (C:10) raise the LDL level to about 50% that of palmitic acid, and raise the TG level.6,23–25 Coconut oil contains 14% of these two cholesterol-raising SAFA.

Replacing 5% of the daily energy intake of SAFA with MUFA and PUFA could reduce the risk of CAD by 42%.29 Therefore, substituting MUFA and PUFA for SAFA and TRAFA is more effective in lowering the risk of CAD than simply reducing the total amount of fat.30 Since 1970, the total fat intake decreased from 42% to 34%, and SAFA from 18% to 12% in the USA, as a result of nationwide changes in dietary habits.2,31 This change in dietary fat intake is primarily responsible for the decrease in serum TC level from 220 to 200 mg/dl in the US population. This decrease in TC level is principally responsible for the dramatic reduction in CAD, during a period when the rates of obesity and diabetes doubled in Americans.32

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Disclaimer: The views and opinions expressed in these columns are solely those of the interviewee(s) and do not necessarily represent those of the editor/publisher. 

 


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