The lipid hypothesis is the basis for much of the contemporary diet advice and drug therapy aimed at preventing coronary heart disease (CHD), and was developed from a sequential association of dietary lipids, cholesterol, and CHD nearly 100 years ago. The lipid hypothesis considers pathological changes that relate to the end stage of the complex chronic condition summarized as CHD, not to its genesis. Ongoing research provides only inconclusive evidence of the effects of modification of total, saturated, monounsaturated, or polyunsaturated fats on cardiovascular morbidity and mortality. 3-Hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors or statins, the highest selling drugs in medical history, may provide evidence that the lipid hypothesis is based on erroneous assumptions, since some of the mechanisms of action of statins seem to be independent of cholesterol reduction. This article assesses the methodology and assumptions underlying the early studies that gave rise to the current assumption of a causal relationship between dietary fat consumption and CHD. It argues that flaws in methodology have led to inaccurate and highly debatable conclusions. It assesses research supporting criticism of these early studies and considers other factors that may influence CHD. It offers alternative interpretations of the use of statins in controlling CHD. Finally, it provides an historical context suggesting different causes of CHD that have no relation to fat intake.
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