

by Ernest N. Curtis M.D. (Internal Medicine and Cardiology)



The burden of proof in science always lies with those who propose a theory. In this case the claim is that cholesterol is one of the chief causative agents for atherosclerosis.



Since the burden of proof is on those making the claim, we need only rebut their arguments. We don’t have to prove anything or advance an alternative theory.

The claim that cholesterol causes atherosclerosis can be rebutted on many levels. I don’t give much credence to epidemiologic evidence, but even that doesn’t pass scientific muster when it comes to cholesterol.



The correlations between cholesterol and heart attacks (the chief complication of atherosclerosis) cited in the medical literature are not even high enough to suggest an association between the two, much less a significant correlation. Even a high degree of correlation would not prove causation but the figures are nowhere near that level.

Another fly in the epidemiological soup is the fact that the incidence of heart attacks is fairly evenly distributed throughout the entire range of blood cholesterol levels. In fact more than half occur in those with cholesterol levels in the low normal range.



Many people with very high cholesterol levels live long healthy lives with no signs of complications from atherosclerosis. Conversely, many people with relatively low levels of cholesterol suffer from severe atherosclerosis and its complications. Add to that the fact that women have, on average, significantly higher cholesterol levels than men yet suffer far fewer heart attacks and I think we can conclude that the so-called evidence from epidemiology is nonexistent.

Many proponents of the cholesterol theory cite some of the statin drug trials as proof of the significance of cholesterol as an important factor by showing that reduction of its blood level provides a small degree of protection against heart attacks.

But these studies all showed a lack of normal response/exposure. There was a total disconnection between the small degree of outcome improvement and both the initial cholesterol level and the degree of cholesterol lowering attained. That is, the same small amount of benefit (which was so small as to be of no practical significance) was seen in subjects whose cholesterol declined only slightly and those in whom it declined a lot.



The benefit was also the same for those with low initial cholesterol levels and those with high initial levels. In scientific studies, this disconnection means that the factor being studied is not a cause of the outcome in question and that some other factor is at work. In this case it is possible that the anti-thrombotic action of the drug is the cause since the degree of protection against heart attack was almost identical to that seen in similar studies using aspirin or other anti-platelet drugs.