Diet and coronary heart disease.Hum Nutr Clin Nutr. 1982; 36(6):413-27.HN
There is a moderately good correlation between dietary saturated fatty acids and coronary heart disease (CHD) when populations in different parts of the world are compared but not within the same cultural community or for individuals. Total energy, essential fatty acids (EFA), dietary fibre, alcohol and salt also contribute to the relationship of diet to CHD. Saturated fatty acids exert their pathogenic role mostly through altering the homoeostasis of lipoprotein metabolism, leading to an increase in cholesterol-rich low-density lipoproteins, and influencing adversely the balance between the accumulation in and clearance of cholesterol esters from the arterial wall. Polyunsaturated fatty acids (PUFA) alter lipoprotein metabolism directly by decreasing synthesis and increasing catabolism and excretion and indirectly by being substitutes for saturated fatty acids, which are therefore consumed in smaller quantities. PUFA have an important additional role, because of their EFA content. A deficiency of the EFA, linoleic and arachidonic acids, relative to the saturated fatty acid intake, can be correlated with CHD mortality. The pathogenic pathways of a relative EFA deficiency leading to CHD are as likely to be related to intravascular coagulation and myocardial metabolism as to lipoprotein metabolism. EFA requirements may not be met in communities having a high intake of saturated fatty acids if there is also a dietary deficiency of antioxidants particularly vitamin E. Two large primary prevention trials of diets enriched with PUFA showed, under institutional circumstances, that it is possible to reduce serum cholesterol by 10-15 per cent. There was in each a reduction in the total incidence of cardiovascular diseases, and the greatest effect was on the incidence of non-fatal myocardial infarction. In both trials there was an increase in non-cardiovascular mortality. The significance of this finding is evaluated in conjunction with a similar finding derived from the only long-term primary prevention trial using a drug. The possibility that gradual depletion of membrane cholesterol over many years might have an adverse effect on the function of ageing cells cannot be dismissed. In communities where there is a high incidence of CHD, the aim should be to reduce plasma cholesterol concentrations to the region of 210 mg/dl. The evidence that it is necessary, practicable or even desirable to reduce plasma cholesterol to lower levels in order to reduce CHD incidence further is not impressive. To achieve this aim by dietary measures there should be a reduction of energy from fats to a level of 35 per cent or below and reduction of the contributions from saturated fats to about 10 per cent. In addition, there is a sound basis for recommending reduction of total energy intake to that actually needed, an increase in dietary cereal fibre and a reduction in alcohol.