The Presence of Cholesterol In The Lesion Led To Cholesterol-Feeding Experiments.
The cholesterol/lipid saga began with Anitschkow (1913) inducing atherosclerotic lesions by overfeeding rabbits cholesterol (egg yolks) mixed with lipids (sunflower oil).
The high cholesterol blood and tissue levels thus induced in
rabbits was interpreted to be the key factor in the atherosclerotic lesions which developed.
Dietary Cholesterol Does Not Cause Hypercholesterolemia
The assumption was that dietary cholesterol and cholesterol in the lesions were one and the same is in retrospect altogether too simplicit and should have been discarded years ago for cholesterol feeding in humans does not result in hypercholesterolemia like that which occurs in animal studies.
Cholesterol Injected Into Animals Causes Nothing
Strangely, the observation made by Anitschkow himself, that if the cholesterol was administered by injection there was no induction of hypercholesterolemia or of atherosclerotic lesions, has been completely ignored by all researchers conducting cholesterol-fed animal experiments. The animal feeders must use a stomach tube in order to instill the exact amount of cholesterol into the animal. It certainly would have been much more exacting and scientific to have used the parenteral use of cholesterol if it could have produced the desired results.
The Site of Action of Cholesterol Is In The Intestinal Stream
Obviously, the target zone of the cholesterol feedings is the intestinal stream, not the enterocirculation, and not the intestinal stream of all of the animals in the same experiment nor in different experiments. The differences in the diverse and constantly changing microbial population of the gut offers a most logical explanation of the differences, particularly since all of the agents effective in the prevention and/or in the treatment of atherosclerosis possess antifungal and/or antimycotoxicty modes of action.
We must then add to the confusion the fact that cholesterol alone was usually ineffective unless animal lard or oil was added to the experiment.
Schoental (1981) has suggested that it was the variable presence of mycotoxins in high fat diets which were responsible for the marked variations in the results of atherosclerosis dietary experiments.
Finally, cholesterol and lipids are both fungal growth promoters; excessive intake would enhance the growth of mycotoxin-producing fungi normally present in the gut of both animals and humans.
The Failure of Cholesterol to Induce Atherosclerosis
Anitschkow and the dietary researchers have all ignored studies which have shown that cholesterol feedings do not cause atherosclerosis by Weltmann and Biach (1913), van Leersum (1914) and Knack (1915) who fed rabbits cholesterol or cholesterol-rich foods and did not induce atheroslcerotic lesions. They proved conclusively that cholesterol per se was not the cause of atherosclerosis.
Many experiments have been conducted which conclusively prove that neither fats per se nor cholesterol per se induce atherosclerosis. It should be noted that in one primate study, cynomolgus monkeys fed longterm high fat diets did not develop atherosclerosis lesions.
Keys (1963) pointed out that dietary cholesterol has no adverse effect in humans.
Altschule (1974) stated "The interpretation...that diet-induced hypercholesterolemia causes atherosclerosis has been demolished by the observation that intimal changes occur within days after cholesterol feeding has begun, weeks before the serum cholesterol rises."
The Lack Of Lipids In Spontaneously-Occurring Atheroslcerotic Lesions In Animals
Atherosclerosis was found in a signifcant number of over 400 autopsies performed on l62 species of birds and mammals.As was the case, birds were most often involved.No correlation was found between atherosclerosis and diet in either wild or captive birds. Equally significant was the observation that the atherosclerosis lesion in sea lions and seals consisted of fibrous intimal plaques which contained no stainable lipid whatsoever.This suggests that the basic atherosclerosis lesion is not due to lipids; a suggestion which would appear to be confirmed by the fact that in giant anteaters and aardvaks, necrosis of the fibrous plaque has been found to precede lipid deposition.
Anitschkow and his followers up to this very day, have not known that
mycotoxins can be found in eggs and that sunflowers are heavily contaminated
by mycotoxin-producing fungi and their toxins. The major seeds and grains
used in the production of oils are well documented to contain mycotoxins,
particularly corn and peanuts. It is not surprising that corn and peanut
oils have been found to be consistently most atherogenic in animal models.
On the other hand soya beans are fairly free of mycotoxins and soya oil
is not too atherogenic.