“The urgency of finding means of prevention is sharpest for men in middle age for it is in that group that the social cost of CHD is greatest... Starting with men aged 40 through 59, the follow-up would show CHD causing close to 40% of all deaths in five years. It is understandable, then, that most work on the epidemiology of CHD begins with men of those ages” (p.I-1) .
The first part of the diet-heart hypothesis, that serum cholesterol was related to coronary heart disease (CHD), originated from the work of Russian pathologists in the early twentieth century. Having observed fatty deposits in arteries during post mortems, a number of researchers sought to understand if dietary cholesterol determined serum cholesterol [58-60 62 64 65 67 68 70]. The summary of findings from the original animal studies was that: rabbits (herbivores) fed animal foods developed fatty deposits/changes in the aortas; rats (omnivores) fed animal foods produced no observable changes in the aortas; and rabbits fed cholesterol in plant food showed no arterial damage.
In the 1950s, Keys undertook several experiments with human subjects and concluded “that the cholesterol content, per se, of all natural diets has no significant effect on either the serum cholesterol level or the development of atherosclerosis in man" (p.182) .
The logic that only animal foods contain cholesterol and thus, if animal foods consumed to administer dietary cholesterol had no impact on serum cholesterol then animal foods per se had no impact on serum cholesterol, was overlooked. Attention turned to dietary fat in food when non-animal foods would have been more logical to examine.
In the early 1950s, literature referred to animal and vegetable fat and not the degree of saturation of fat [86 97 99]. Interventions with vegetable fat were extrapolated to conclusions about animal fat, without animal fat having been tested [86 97].
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