Abstract
The correlation of fat consumption with coronary heart disease (CHD) mortality in six countries specifically selected by Keys [1] and the introduction of the risk concept in the Framingham Study [2] triggered an upsurge in CHD epidemiology. These studies established the prevailing view that a high dietary intake of saturated fats and cholesterol results in an elevation of blood cholesterol or in low density lipoprotein levels which, aided at times by other risk factors, are primarily responsible for an enhanced tendency to severe atherosclerosis and CHD. Despite enormous expenditure of time, finance, and animals, controversy over the etiology, pathogenesis, and preventive management persists unabated. Serious criticisms of the consensus concept of atherosclerosis [3, 4] and possible deleterious effects associated with dietary changes recommended for whole populations reinforce the need for review of the evidence. At the crux of the issue is the use and meaning of cause in medicine.
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