Cracking Down on Eggs and Cholesterol

Since the breakthrough led by Nikolai Anichkov a century ago, the feeding of cholesterol, and to an extent, dietary fat have been recognized as the sine qua nons for the dietary modification of experimental atherosclerosis, and have been used in thousands of experiments to successfully accelerate the development of atherosclerosis in mammalian, avian and fish species, not only of herbivorous, but also omnivorous and carnivorous nature.1 2 3 4 5 6 7 8 9 10 11 This includes the promotion of experimental atherosclerosis in over one dozen different species of nonhuman primates- New World monkeys, Old World monkeys, and great apes including the closest living relative to humans, the chimpanzee (Fig. 1).2 3 12 13 14 15 16 17 18 19 20 21 The atherosclerotic lesions induced by cholesterol feeding, including in the form of fresh eggs yolks in many opportunistic omnivores, such as various species of nonhuman primates, birds and pigs have been shown to closely resemble the disease in humans.1 2 3 4 22 23 24
Figure 1. Aortic atherosclerosis of a chimpanzee which died of a heart attack after long-term feeding of a diet rich in cholesterol and artery-clogging saturated fat
It has also been observed that the long-term feeding of cholesterol and saturated fat has resulted in heart attacks, sudden death, development of gangrene, softening on the bones and numerous other serious complications in nonhuman primates.2 3 25 26 27 28 For example, it has been shown that when diets rich in cholesterol and saturated fat are fed to monkeys of the genus Macaca, including the rhesus monkey and the crab-eating macaque, they experience heart attacks at approximately the same rate as high-risk populations living in developed nations.3
In species that are unlike humans, very resistant to dietary induced elevations in LDL cholesterol, such as the order of the carnivora, unless LDL-receptor deficient breeds are used atherosclerosis is typically induced by raising serum (blood) cholesterol with a diet with very large amounts of dietary cholesterol, and either containing thiouracil or deficient in essential fatty acids.9 10 29 As noted by Steinberg:30

The point is very clearly made: the arteries of virtually every animal species are susceptible to this disease if only the blood cholesterol level can be raised enough and maintained high enough a long enough period of time.

Long-term feeding of cholesterol in relatively small amounts has actually been shown to induce atherosclerosis in rabbits, chickens, pigeons and monkeys despite only small or insignificant increases in serum cholesterol.1 4 13 Armstrong and colleagues conducted an experiment ‘designed to demonstrate a null point of the effect of dietary cholesterol on the arterial intima’, by comparing a group of rhesus monkeys fed a cholesterol-free diet with a group fed cholesterol equivalent to that found in only half of a small egg in the average human diet of 2,000 calories per day (43µg/kcal). However, even when fed in very small amounts dietary cholesterol still had a significant adverse effect on these monkeys arteries after a period of only 18 months (Fig. 2).13 Armstrong and colleagues concluded:

No null point for the effect of dietary cholesterol on arterial intima was found even at an intake level far below that conventionally used for the induction of experimental atherosclerosis in the nonhuman primate. The intimal changes found in response to very low cholesterol intake imply that subtle qualitative alterations in lipoproteins are of critical importance to our understanding of lesion induction.

Figure 2. Subclavian artery from a rhesus monkey fed very small amounts of dietary cholesterol (43µg/kcal). Sudanophilia (black area) is intense in the area of major intimal thickening
It has also been demonstrated that the cessation of a cholesterol-rich diet and the subsequent lowering of serum cholesterol results in the regression of atherosclerosis in various mammalian and avian species, including herbivores, omnivores, carnivores and nonhuman primates.31 In one experiment Armstrong and colleagues induced severe atherosclerosis in rhesus monkeys by feeding a diet with 40% of calories from egg yolks for 17 months. The egg yolks were then removed from the monkeys diet and replaced with a cholesterol-free diet with either 40% of calories from corn oil or low-fat chow with 77% calories from sugar for three years, resulting in a reduction of serum cholesterol to <140 mg/dl and a marked regression of atherosclerosis.32 33
In a recently published study, Spence and colleagues observed that egg yolk consumption was associated with carotid plaque in high-risk patients.34 These findings should not come as a surprise considering the evidence accumulated from thousands of animal experiments over the last 100 years, which have demonstrated that the feeding of cholesterol and saturated fat accelerates the development of atherosclerosis in virtually every vertebrate that has been sufficiently challenged. These lines of evidence have been neglected by the egg industry and promoters of cholesterol laden diets (ie. Paleo, Primal and low-carb) who have attempted to discredit this study without considering the relevant evidence. As noted by Stamler:35

To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case. 

These findings from Spence and colleagues are not only supported by the findings from animal experiments, but also by numerous previous human studies that found a positive association between dietary cholesterol and the severity of atherosclerosis.36 37 38 39
In the video below Dr. Michael Greger addresses the completely unethical measures that the egg industry resorted to in order to confuse the general public about these findings from Spence and colleagues, including attempts to bribe researchers.