Abstract

It is not a new concept that nutrition is one of the causal factors for coronary heart disease (CHD), nor that diet plays a role in its prevention. That this is so follows from extensive epidemiological data, from animal studies in which atherosclerosis can be induced, and can be caused to regress, by dietary manipulation of plasma cholesterol levels, from controlled clinical trials of plasma lipid lowering diets and drugs and from growing understanding of mechanisms underlying the interactions between diet, plasma lipid transport, atherogenesis and arterial thrombosis.4.9 This paper is concerned with how, rather than whether, nutritional patterns should be modd in some, reduction of dietary cholesterol is specifically advocaw and increasingly in recent reports an increase in complex carbohydrate sources containing soluble fibre is advised. Recommendations to increase intake of polyunsaturated fat are usually made, though the extent of change varies considerably and the type of fatty acid is seldom specified. In small metabolic trials, fat-modified diets reduce plasma cholesterol by M-15%, though most larger field studies are associated with a smaIIer change. In evaluating the extent and nature of dietary modification necessary to reduce CHD incidence materially, it is important to recognize that a dose-response relationship exists between the fall in plasma cholesterol and the fall in CHD incidence. This is borne out by comparisons of different trials and is evident from the LRC trial of cholestyramine in which varying compliance with the drug led to differing cholesterol levels and to parallel changes in incidence. It follows that a substantial change in diet, with concordant major change in the distribution of plasma cholesterol levels, will reduce the rate of CHD in the population more effectively than a more modest intervention. The feasibility of achieving a considerable lowering of mean plasma cholesterol is enhanced by the demonstration. that the effects on cholesterol level of certain changes in nutrient intake are additive. A pronounced effect on cholesterol level, and particularly on that of low density lipoprotein (LDL) cholesterol, has been shown when the diet provides 9% energy each from saturated fatty acids and polyunsaturated (chiefly linoleic) acids, supplemented with fruit and vegetable sources of fibre, and restricted in dietary cholesterol. In an institutional study, this diet reduced plasma cholesterol by 29%, LDL cholesterol by 34.5%.S These considerations should be taken into account in designing an optimal diet for high CHD-risk populations. As a rational basis for selecting a recommended nutrient intake, it is suggested that the goal should be to achieve an optimal distribution of plasma cholesterol concentrations. . The target in designing a diet that is to be recommended for population use is to achieve such a distribution, so that a large majority of the population maintains levels associated with low CHD risk. Selection of optimal distributions .has been the subject of multidisciplinary discussion;’ in adults, a population mean of 4.7 mmol/l (180 mg/dl) was proposed. A WHO Expert Committee has referred to a mean of 5.2 mmol/l (200 mg/dl) or less.” These levels were selected on the basis of cross-cultural and prospective epidemiological studies, clinical findings, observations on lipid levels in human neonates, studies of lipoprotein transfer from plasma into the arterial wall and knowledge of LDL interaction with the high-affinity ceil surface receptor for this lipoprotein.

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