An Independent Critique of Low-carb Diets: Cracking Down on Eggs and Cholesterol
In the September and October 2012, and February 2013 McDougall newsletters, I presented readers with articles addressing the dangers of low-carbohydrate diets, which are also popularly known as Paleo and Primal diets and as Atkins-type diets. Please take this opportunity to read these articles.
This year marks the 100th year anniversary of when Nikolai Anichkov first used the rabbit model to show that the ingestion of dietary cholesterol alone is a primary cause of atherosclerosis. Since 1913 it has been demonstrated in thousands of animal experiments that the feeding of cholesterol, including in the form of fresh egg yolk accelerates the development of atherosclerosis in virtually every vertebrate species that has been sufficiently challenged. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates.
The experimental evidence showing that dietary cholesterol is a primary cause of atherosclerosis is so extensive that suggesting that it is somehow irrelevant to humans would require implying that the Darwinian foundation of biomedical research is invalid. As this is not likely considered a plausible approach for promoters of cholesterol laden diets, particularly of Paleo and Primal type diets who emphasize the importance of evolution, they have instead resorted to simply ignoring a century of research and often inaccurately claiming that cholesterol feeding has only successfully accelerated atherosclerosis in obligate herbivores, such as rabbits. These promoters have also resorted to using scapegoats such as sugar to blame as a primary cause of atherosclerosis, while ignoring the evidence that the development of atherosclerosis can actually be reversed in animals, including nonhuman primates even when the great majority of the diet is composed of pure sugar when fed in the context of a cholesterol free diet.
This article provides an overview of the large body of evidence from both human and animal studies which has served as a basis for the recommendations to restrict the intake of dietary cholesterol and eggs, and outlines the unethical tactics that the egg industry have used to confuse the general population.
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
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.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
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.1 413 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.
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 a review of the literature, Uffe Ravnskov, the spokesperson for The International Network of Cholesterol Skeptics reviewed 15 of the earliest prospective (longitudinal) cohort studies and inappropriately concluded that ‘Overall, longitudinal studies within population have found no difference between the diet of coronary patients and others’.68 Fourteen of these studies measured cholesterol intake, of which for the Chicago Western Electric Study Ravnskov inappropriately cited data from an earlier follow-up that found no association rather than the longer follow-up which found a significant association. Among the remaining thirteen studies, the participants who developed coronary heart disease actually had on average 13 mg/day greater intake of cholesterol for someone consuming on average 2,000 calories a day.
Considering the probable degree of measurement error dietary intake and the fact that these studies were carried out in largely homogenous populations where most people had similar diets, only relatively small differences in dietary composition would have been expected between participants with and without heart disease even if diet does play a major role in heart disease [reviewed previously]. Furthermore, Ravnskov failed to mention that four of the largest studies that he cited, including the Chicago Western Electric Study found on average that 200 mg/1,000 calories higher intake of cholesterol was associated with a 30% increased risk of coronary heart disease over and above the adverse effects it has on serum cholesterol.64
To learn more on this topic please visit my website and the Dr. McDougall archive on Heart Disease & Atherosclerosis.
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