An Examination of the Evidence Supporting the Association of Dietary Cholesterol and Saturated Fats with Serum Cholesterol and Development of Coronary Heart Disease

Marion G. Volk

Abstract

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.

(Altern Med Rev 2007;12(3):228-245)

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