Dietary Cholesterol and Heart Disease

Having decided that high levels of cholesterol in the blood was the major cause of the seemingly inexorable rise in heart disease, the first suggested cause was a high intake of cholesterol in the diet.

The dietary cholesterol hypothesis

In 1913 a Russian physiologist named Anitschkow conducted an experiment on rabbits that was to change the history of atherosclerosis for most of the following century.[1] The experiment consisted of feeding huge doses of cholesterol to rabbits, an animal which would never normally eat any food that contains cholesterol and whose liver is not equipped to excrete the excess. Not surprisingly, the rabbits' cholesterol shot up to very high levels and the concentrations proved toxic; some atherosclerosis of the blood vessels was discovered at autopsy. Anitschkow was no fool; he realised that this experiment had no practical significance for humans. Similar experiments on dogs, rats and humans showed that the rises of blood cholesterol and atherosclerosis didn't happen in them. This is because cholesterol is a natural part of their diets and their livers are equipped to cope with any excess.

In 1950, team led by Dr John Gofman, again hypothesised that blood cholesterol was to blame.[2] Quickly, trials were conducted on rabbits based on Anitschkow's 1913 study and rabbits fed a high-cholesterol diet again developed blockages in their arteries. Several scientists pointed out that the results were more likely to be an allergic reaction to the unnatural diet. One such, Ancel Keys, pointed out the error of the approach when he wrote in 1956: 'For many years there was argument as to whether cholesterol in the diet promotes atherosclerosis in man. One cause of the disagreement resided in the persistent error in attributing to man the same responses seen in rabbits and chicks fed large amounts of cholesterol. . . . It is now clear that dietary cholesterol per se, which is contained in almost all foods of animal origin, has little or no effect on the serum cholesterol concentration in man'.[3] (emphasis added)

Let the cholesterol trials begin

The longest running and most respected study is the Framingham Heart Study. It was set up in the town of Framingham, Massachusetts, in 1948 and is still going on today. It was this study that gave rise to other 'risk factors' with which we all are so familiar today: lack of exercise, smoking, and so on. The Framingham researchers thought that they knew exactly why some people had more cholesterol in their blood than others — they ate more in their diet. To prove the link, they measured cholesterol intake and compared it with blood cholesterol.

Table I: Cholesterol intake — The Framingham Heart Study
Blood Cholesterol in Those
Below Median
Above Median
704 ± 220.9
492 ± 170.0

As Table I shows, men ate 704 mg a day plus or minus 221 mg, so we are talking amounts from below 500 to getting on for 1000 — a two to one relationship. Yet although men consumed cholesterol over this wide range, there was no difference in the levels of cholesterol in their blood. With women there was again that two to one relationship in intake. And in their case, the women who ate the least cholesterol had the highest blood cholesterol levels! But the difference wasn't statistically significant. The important part, however, is that these figures showed clearly that there was no relationship between the amount of cholesterol eaten and levels of blood cholesterol in either sex.

After 22 years of intense expert study and analysis, the researchers concluded:

'There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group.'[4]

That was way back in 1970, and no finding since has changed that view. Indeed more recent studies have only confirmed it.

Dr William Castelli, Director of the Framingham Study, wrote in 1992: 'In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people's serum cholesterol. . .'

Because cholesterol is a major component in all animals' bodies, eggs have a very high cholesterol content. That is why we are still told to eat no more than about 3 a week. Dr Uffe Ravnskov did his own test of the theory by eating a total of 59 eggs over 9 days. Did his cholesterol level shoot up? No; it fell by more than 11% from 7.23 mmol/L to 6.39 mmol/L.[5]

Dr George V. Mann was involved with the Framingham Study and also conducted extensive studies of the Maasai, whose diet is very high in cholesterol but who do not suffer from CHD at all. His work led him to the conclusion that:

'The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons or pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.'[6]

The evidence is clear and unequivocal: Eating a diet high in cholesterol, does not increase blood levels of cholesterol or the numbers of heart attacks.


[1]. Anitschkow N. On variations in the rabbit aorta in experimental cholesterol feeding. Beitr Path Anat u allgem Path 1913; 56: 379.
[2]. Gofman JW, Lindgren F, Elliot H, et al. The role of lipids and lipoproteins in atherosclerosis. Science 1950; 111: 166-171, 186.
[3]. Keys A. Diet and The Development of Coronary Heart Disease. J Chron Dis 1956; 4: 364-380.
[4]. Kannel WB, Gordon T. The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24). Washington DC, Dept of Health, Education and Welfare, 1970.
[5]. Ravnskov U. The Cholesterol Myths. New Trends Publishing Inc, Washington DC, 2000. p 109.
[6]. Coronary Heart Disease: The Dietary Sense and Nonsense. George V. Mann, ed. Veritas Society; London, 1993.

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Last updated: December 9, 2011