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RESEARCH REPORT Cholesterol – A Review: Part I

by William R. Ware, PhD


“An almost endless number of observations and experiments have effectively falsified the hypothesis that dietary cholesterol and fats, and a high cholesterol level play a role in the causation of atherosclerosis and cardiovascular disease. The hypothesis is maintained because allegedly supportive, but insignificant findings are inflated, and because most contradictory results are misinterpreted, misquoted or ignored.” U. Ravnskov, M.D., Ph.D.

INTRODUCTION Cholesterol causes atherosclerosis and coronary heart disease, or put another but not equivalent way, there is a positive association between cholesterol levels and development and extent of atherosclerosis and thus coronary heart disease. Everyone knows this. This hypothesis has the status of an unquestionable belief, a self- evident truth. It is important, however, to distinguish between atherosclerosis and symptomatic or actual coronary heart disease (CHD). The latter generally includes angina or a history of one or more fatal or non-fatal heart attacks. Thus when CHD is an endpoint in a study, this generally includes clinical manifestations and actual adverse events, whereas if atherosclerosis is the subject of study, merely its presence and extent are at issue. Nevertheless, there is of course a close connection between the two. If an individual has no coronary atherosclerosis at all, the risk of an adverse coronary event is very small, and risk of symptomatic CHD or CHD adverse events increases with the extent of atherosclerosis. Also, the observation of atherosclerotic deposits in the coronary arteries leads to the diagnosis of coronary heart disease which makes itself evident by both symptoms (angina) and events (heart attacks). However, if one restricts their attention to the heart attack event itself, then the situation is somewhat more complex, given what in general is a multi-step process.

One might have thought that the cholesterol hypothesis would have met with resistance. After all, it seems a bit curious that a substance alleged to cause atherosclerosis and thus heart disease in fact comprises 5% of cell membrane lipids and plays a key role in maintaining cell wall structure. It is also the starting point for the synthesis of several groups of very important biochemicals, including male and female sex hormones, vitamin D (via photochemical action in the skin) and bile acids. Cholesterol is also used by the body in natural healing processes and tissue repair. The absorption through the gut of dietary cholesterol is poor, and the body is generally able to compensate for dietary intake by adjusting the endogenous synthesis which occurs mainly in the liver, and thus for most individuals, the serum levels are only very weakly related to dietary intake. Also, cholesterol molecules are never found free in blood since they are insoluble and are transported mainly by so- called lipoproteins of which the high and low density varieties (LDL and HDL) are regarded as bad and good according to the conventional wisdom, in spite of the fact that transport of cholesterol is essential to life. Given the vital functions of this molecule and its lipoprotein transporters, is it not a bit surprising that cholesterol is a cause of atherosclerosis?

International Health News

November 2007

Page 9

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