What dietary factors may decrease risk for atherosclerosis

Dietary factors may decrease risk for atherosclerosis are being discussed.Lipids, primarily free and esterified cholesterol, constitute a prominent part of early atherosclerotic plaques. In current models of atherogenesis, lipids are thought to be transported into the artery wall by plasma lipoproteins. These lipoproteins include low density lipoproteins (LDL), intermediate density lipoproteins (IDL), and, perhaps to a lesser extent, very low density lipoproteins (VLDL). More extensive descriptions of these lipoproteins and of their metabolism are given in Ch. 183. Elevated levels of LDL and IDL are strongly associated epidemiologically with accelerated atherogenesis.

For instance, the risk of coronary heart disease in the United States, where the average level of serum cholesterol in an adult male is approximately 230 mg per deciliter, is several fold higher than in rural Japan, where the average is about 160 mg per deciliter. The atherogenicity of VLDL is not so strongly supported as that of LDL and IDL in large population studies. Impaired centnpetal transport of cholesterol has recently been found in some patients with hypertriglyceridemia, however, suggesting that altered properties of VLDL may indeed contribute to atherogenesis in some individuals. An impressive inverse relationship exists between plasma levels of high density lipoprotein (HDL) cholesterol and risk of coronary heart disease. This presumably reflects the importance of the retrieval mechanisms for cholesterol, which depend upon certain subspecies of HDL.

The risk of coronary heart disease has been shown to correlate with levels of cholesterol in plasma as low as 180 mg per deciliter. The majority of individuals in industrialized western nations would therefore be expected to benefit from reduction of levels of serum cholesterol, reflecting primarily changes in the content of LDL in plasma. The results of several intervention studies tend to support this contention. Increasing the levels of HDL in plasma in order to increase the mobilization and retrieval of cholesterol might be equally attractive, but no studies of the effect of such an intervention on heart disease have yet appeared.

What is the best diet for Human atherosclerosis And dietary factors may decrease risk for atherosclerosis.

A single pattern of dietary modification is appropriate for individuals with nearly all types of primary hyperlipidemia (excepting only primary chylomicronemia), as well as for those individuals in the population at large who have less sinking elevations of levels of atherogenic lipoproteins. The elements of this “universal” diet will be considered individually.

1. Reduce body weight to the ideal.

This manipulation primarily induces a marked reduction in elevated VLDL levels. It also effects some reduction in LDL cholesterol levels and may increase HDL cholesterol levels slightly.

2. Decrease the intake of saturated fat.

This change effects a potent and uniform lowering of LDL cholesterol. The typical American diet contains approximately 40 per cent or more of calories as fat (15 per cent saturated fat). Levels of 30 per cent of calories as fat (8 per cent saturated fat) can be achieved easily, and 20 per cent (5 per cent saturated) is attainable with major modifications of food selection. To achieve the 30 per cent level of dietary fat, fat-rich meats, dairy products, and items such as certain baked goods must be restricted. To achieve the 20 per cent level, major substitution of vegetable protein sources for meats must be made.

When the intake of saturated fats is decreased, there are several possible sources of replacement calories, polyunsaturated fats, monounsaturated fats, or carbohydrates. Major substitution with polyunsaturated fat may result in lower levels of HDL cholesterol and of the principal HDL protein, apolipopro-tein A-I. Furthermore, polyunsaturated fatty acids are susceptible to hydroperoxidation, which could theoretically lead to generation of free radical chains and perhaps to an enhanced carcinogenesis. Such an effect is probably small if present at all. Since some epidemiologic evidence links total fat intake to cancer (see below), however, substitution of carbohydrates for fat may be more judicious.

Monounsaturated fats, abundant in certain vegetable oils such as olive oil, have little effect on LDL levels. Major substitution of carbohydrate for fat is associated with modest elevations of plasma triglyceride levels in the short term, but these levels return to normal after a period of several months. Strict vegetarians tend to have lower levels of both LDL and HDL than individuals on a typical Amencan diet, but the changes in LDL levels are of much greater magnitude. Furthermore, potentially important differences in composition of HDL are seen, with an increased ratio of phospholipid to cholesterol.

3. Decrease the intake of cholesterol.

Reduction of dietary saturated fats automatically eliminates much cholesterol; however, rich sources such as organ meats and egg yolks should be restricted specifically. The effect of restriction of cholesterol on LDL levels varies widely among individuals. This variation appears to reflect two factors: (a) There is an approximately four fold difference among individuals in the fraction of dietary cholesterol that is absorbed, (b) There are differences in the degree to which dietary cholesterol is capable of suppressing endogenous cholesterogenesis. Lacking metabolic ward studies on a given patient, it must be presumed that reduction of dietary cholesterol is likely to be of benefit. The typical American diet provides 500 mg or more of cholesterol per day, but an intake of 300 mg per day is relatively easily achieved, and intakes of 100 mg per day can be achieved with more rigorous mixed diets. Strict vegetarian diets contain no cholesterol.

4. Restrict alcohol Alcohol should be limited in all cases to maintain ideal body weight.

VLDL secretion is increased dramatically by even limited use of alcohol. Therefore, alcohol should always be eliminated in the diet of individuals with elevated serum triglycerides. Increased alcohol intake may be associated with elevated levels of HDL cholesterol, but it is not yet clear whether this change represents subspecies of HDL that participate in centripetal cholesterol transport. No categorical presumption of beneficial effects of alcohol on HDL can yet be made.

5. Other factors.

Increased dietary fiber appears to have marginal effect on serum lipoprotein levels. The ingestion of lecithin, which is widely suggested by health food advocates, also lacks significant effect, as do a number of vitamins and minerals that have been similarly recommended.

Individuals following this judicious dietary regimen usually show reductions of 10 to 15 per cent in plasma cholesterol levels on the basis of reduction of saturated fats. An additional reduction of up to 10 per cent may be achieved by restriction of cholesterol. Based on large epidemiologic studies, it can be roughly estimated that at least a two-fold reduction in risk of coronary disease would be expected in the Amencan population if such modifications of lipid levels were uniformly achieved.

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