Tradional diets

In the 1920’s, Kuczynski reported on the nomadic plainsmen of the Kirghiz and Dzungarian Steppes in Central Asia and estimated that they consumed an astonishing 20 liters of fermented mare’s milk, and between 10 to 20 pounds (4.5 to 9kg) of meat per day.1 2 Lack of systematically documented dietary data however suggests that these findings could have been slightly overestimated, as evidently has been the case for early researcher's estimates of the Masai's intake of milk, meat, cholesterol and total energy.3 Nevertheless, these nomadic plainsmen consumed enormous quantities of organic pasture raised animals foods, perhaps among the largest ever documented. 

Kuczynski noted that these nomads, evidently largely as a result of their diet experienced a high incidence of obesity, premature extensive atherosclerosis, contracted kidney, apoplexy, arcus senilis, and gout.4 5 In specific, Kuczynski asserted that:2

They get arteriosclerosis in an intense degree and often at an early age as shown by cardiac symptoms, nervous disordes, typical changes of the peripheral vessels, nephrosclerosis and, finally, apoplectic attacks. Even in men thirty-two years old I frequently observed arcus senilis.

The Nomadic Kirghiz Plainsmen

Kuczynski compared the diet and health of these nomadic plainsmen with Russian peasants, who had an apparent low incidence of these conditions while consuming a vastly different diet. Their diet was based on soup, bread, pickles, potatoes, with very little meat, but consumed large amounts of alcohol.5 In comparison to the nomadic plainsmen, Kuczynski asserted in regards to these Russian peasants that:2

Repeatedly I found at the age of about seventy years no signs of arteriosclerosis, no arcus senilis, etc.; they were men of youthful appearance, with no grey in their still abundant growth of hair, and with their sexual functions still intact.

For more information regarding the health of nomadic populations, Don Matesz has previously posted aninformative review addressing the high rates of obesity, cardiovascular disease and cancer among the modern, still largely nomadic Mongols consuming diets rich in organic pasture raised animal foods

In 1916, Cornelis D. de Langen observed that the native Javanese, the indigenous people of the Indonesian island of Java who consumed a diet which was 'mainly vegetarian with rice as the staple, that is very poor in cholesterol and other lipids', had very low levels of serum cholesterol and incidence of coronary heart disease.6 Conversely, de Langen observed that their Javanese counterparts who worked as stewards on Dutch passenger ships and consumed traditional cholesterol laden Dutch food had much higher levels of serum cholesterol and incidence of coronary heart disease.7 Blackburn noted in regards to de Langen's classical findings from Indonesian hospitals that:6 

Pursuing this clinical impression, he reviewed 10 years of admissions charts and found only 5 cases of acute gallbladder disease among many thousands of patients passing through the medical wards and only 1 case on the surgery service among 70,000 admissions surveyed. 

Following these observations, de Langen stated in regards to the rarity of vascular disease among the Javanese that:6 

thrombosis and emboli, so serious in Europe, are most exceptional here. This is not only true of internal medicine, but also on surgery, where the surgeon needs take no thought of these dreaded possibilities among his native patients. Out of 160 major laparotomies and 5,578 deliveries in the wards, not a single case of thrombosis or embolism was seen.

These findings closely resemble observations from over 15,000 operations carried out in Norway during the period around World War II, where the changes in incidence of post-operative thrombosis was consistent with changes in the availability of cholesterol laden foods [reviewed previously]. Blackburn also noted in regards to de Langen’s 1922 experiment, which is regarded as apparently the first ever systematic feeding experiment of diet in relation to serum cholesterol levels, that:6

…he found an average 40 mg/dl increase in cholesterol in 5 Javanese natives who were shifted from a rice-based vegetarian cuisine to a 6-week regimen high in meat, butter, and egg fats.

These findings were reproduced decades later in hundreds of tightly controlled feeding experiments, firmly establishing that dietary cholesterol and isocaloric replacement of complex carbohydrates and unsaturated fat by saturated fat raises LDL and total cholesterol in humans.8

In 1908, Williams noted in regards to the findings of early doctors who practiced in Indonesia and the rarity of cancer among the Javanese that:9

...a single example of a malignant tumour in a native being esteemed a great rarity.

In 1949, a government survey found that in Okinawa, known to have the highest concentration of centenarians in the world, the population consumed about 85% of their total energy intake from carbohydrates, with the staple at the time being the sweet potato. The dietary survey also showed that the Okinawans derived about 9% of their energy intake from protein and less than 4% of energy from all sources of animal foods combined (Table 1).10 These findings were largely consistent with previous dietary surveys dating back to 1879 and 1919.11

In 1946, Steiner examined autopsies of 150 Okinawans, of which 40 were between the age of 50 and 95. Steiner noted only seven cases of slight aortic atherosclerosis, all of which were found in those over the age of 66, and only one case of calcification in the coronary arteries. In 1946 Benjamin reported similar findings from a study of 200 autopsies on Okinawans.12

Even in 1995 the observed rates of coronary heart disease and dietary related cancers, including that of the colon, prostate, breast and ovarian in Okinawa were not only many fold lower than that of the United States, but even significantly lower than that of mainland Japan.10 This may be explained by the likelihood that these diseases are slowly progressive diseases and therefore the more traditional Okinawan diet consumed several decades prior would still have played a major role in the development and manifestation of these diseases.

The Papua New Guineans traditionally subsisted on a plant based diet, of which a number of varieties of sweet potatoes typically supplied over 90% of dietary intake. They also grew a number of other crops including corn, as well as sugar cane which was consumed as a delicacy. Pig feasts are organised a few times a year, but at which pork is not consumed in excess of 50 grams. A dietary survey on the Papua New Guineans highlanders estimated that carbohydrate accounted for 94.6% of total energy intake, among the highest recorded in the world. Total energy intake was adequate, however only 3% of energy intake was derived from protein (25g for men and 20g for women), yet there was no evidence of dietary induced protein deficiency or anemia. Furthermore, this surveyed population was described as being muscular and mostly very lean, physically fit and in good nutritional state.16 17 They also drank 'soft' water which is considered a risk factor for cardiovascular disease. It was estimated that tobacco was smoked by 73% of males and 20% females. Also, the highlanders spend up to twelve hours a day inside a smoke-filled house due to centrally placed open wood fires with little ventilation and no chimneys in their homes, resulting in a very high exposure to hazardous smoke in this population.16 

Despite cardiac risk factors including high exposure to smoke and soft drinking water, a number of authors observed a great rarity of incidence of atherosclerosis, coronary heart disease and stroke among the traditional Papua New Guineans, but also noted an increase in incidence paralleling the Westernization of the nation. In 1958, Blackhouse reported on autopsies of 724 individuals between 1923 and 1934 and found no evidence of heart attack incidence and only one case of slight narrowing of the coronary arteries. However, it has been suggested that this study was selective as only a small portion of the autopsies were performed on females or the elderly. In 1969, Magarey et al. published a report on the autopsy results of 217 aortas and found a great rarity of atherosclerosis. The authors noted that the prevalence and severity of atherosclerosis was less than had been reported in any previously investigated population.18 In 1973, Sinnett and Whyte published findings from a survey of 779 highlanders using electrocardiograms among other methods, and found little probable evidence of coronary heart disease, and no clinical evidence of diabetes, gout, Parkinson’s disease, or any previous incidence of stroke.16

For a population that consumed virtually the highest intake of carbohydrates out of any population to also have virtually the lowest incidence of atherosclerosis and diabetes ever recorded highlights the vital importance of the health properties of specific carbohydrate rich foods. These findings further question certain 'carbohydrate-induced dyslipidemia' hypotheses, emphasized by certain researchers, who perhaps intentionally do not always take the quality of carbohydrate rich foods into careful consideration.19

In 1900, Sir William MacGregor reported in the Lancet in regards to the observed rarity of cancer among the native Papua New Guineans, asserting that:20

For nine and a half years I never saw a case in British New Guinea ; but at the end of that time there occurred an example of sarcoma of the tibia in a Papuan, who had for seven or eight years lived practically a European life, eating tinned Australian meat daily.

In 1974, Clezy brought to attention the rarity of mortality from colorectal cancer among the Papua New Guineans, for which the observed annual rate per 100,000 was 0.6 for men and 0.2 for women. These rates were 100 fold lower than that of many developed nations during the same time period, although this could have been in part explained by underdiagnosis.17

Even in more recent statistics after modest changes towards a western diet, the Papua New Guineans still had among the lowest rates of hip fractures in the world, which Frassetto et al. observed was more than 50 fold lower than that of the Scandinavian nations.21 Although these researchers ascribed the worldwide differences in rates of hip fractures to the ratio of vegetable to animal protein, evidence from prospective cohort studies and randomized controlled trials, as well as experimental animal models suggests that saturated fat may be at least as great, if not an even greater contributor to poor bone health.22 23 24 25 26

In the video below, Plant Positive reviews the diet and health of the Tokelauans and Pupukans whose diet is rich in coconuts, as well as the diet and health of other South Pacific island populations.

The Tokelauns, and more on the Masai

In 1908, William Roger Williams published an extensive review of the medical literature and documentations from a large number of populations around the world before the widespread use of intensive farming practices. Williams observed that compared to the nations with carnivorous dietary patterns there was a significantly lower incidence of cancer among the nations subsisting predominantly on a plant-based diet. He also noted that groups within nations with carnivorous dietary patterns that largely abstained from animal foods, such as nuns, monks, slaves and prison inmates had a similar low incidence of cancer.9

Williams reported on the cancer rates of the area inhabited by the Gaucho of the Argentina Pampas, another nomadic population that subsisted predominantly on organic pasture raised animal foods, noting that:9

Cancer is commoner in Argentina which comprises the pampas region inhabited by the Gauchos, who for months subsist entirely on beef, and never touch salt than in other parts of South America. On the other hand, among the natives of Egypt, who are of vegetarian habits, and consume immense quantities of salt, cancer is almost unknown.

The Nomadic Argentinean Gaucho

These findings are largely consistent with modern reviews from prominent health authorities, including the report from the expert panel of the World Cancer Research Fund that produced convincing evidence that red meat is a major risk factor for cancer and that dietary fiber provides significant protection [reviewed previously]. However, these findings raise questions as to whether the Egyptians plant-based diet that is centered on wheat provides significant protection against salt sensitive cancers. In regards to the cancer incidence among the different ethnic groups of Egypt, Williams quoted from a 1902 publication in the British Medical Journal authored by Dr. F. C. Madden of Cairo that:9

The consensus of opinion among medical men in Egypt is, that cancer is never found either in male or female, among the black races of that country. These include the Berberines and the Sudanese, who are all Mussulmans, and live almost entirely upon vegetarian diet. Cancer is fairly common, however, among the Arabs and Copts, who live and eat somewhat after the manner of Europeans.

Williams also observed that the increases in incidence of cancer within populations coincided with increases in animal food intake. For example, in regards to the observed marked increase cancer incidence among the Native American’s after gaining easier means to hunt buffaloes, Williams asserted:9 

In this connexion it should be borne in mind, that in their primitive condition these savages had no horses and no firearms ; consequently it was no easy matter for them to kill the fleet buffaloes, on which they mainly depended for subsistence ; hence, in their primitive condition, they were generally less well nourished than when, after contact with whites, they had, by the acquirement of horses and firearms, become assured of a constant supply of their favourite food [coinciding with an increase in cancer incidence].

In 1903, John Harvey Kellogg, the founder of the Kellogg Company asserted:

Dr John Bell, who was, about a hundred years ago [now two hundred years ago], professor in a leading college in London, wrote that a careful adherence to a vegetarian dietary tended to prevent cancer. He also stated that in some cases persons who had already acquired cancer had been cured by adherence to a non-flesh dietary. When I first read this book, I did not agree with the author; I thought he was mistaken; but I have gradually come to believe that what he says on this subject is true. 

These findings are consistent with Dr. Dean Ornish’s on-going Prostate Cancer Lifestyle Trial which has already produced strong suggestive evidence of reversal of prostate cancer growth.27 These findings are also consistent with experiments showing that dietary restriction of methionine, typically found in higher quantity and bioavailability in protein rich animal foods compared to unprocessed plant foods can inhibit and even reverse human tumor growth in animal models and in culture [reviewed previously]. 

Publications producing evidence of regression of atherosclerosis in humans dates back to the periods following both the World Wars in Scandinavia and the low countries of Europe, where a number of researchers found a trend between changes in intake of cholesterol laden foods throughout periods of food scarcity in the war and changes in the severity of atherosclerosis at autopsy [reviewed previously]. Several decades later during the 1960's and 70's experiments involving modest dietary and lifestyle changes or drugs produced the first angiographic evidence of modest regression of atherosclerosis.28

In experimental animal models, the first suggestive evidence of regression of atherosclerosis came from rabbit models produced by Anichkov and colleagues during the 1920’s. Beginning from 1957 much more substantial evidence of regression was produced in rabbits and then later replicated in a number of other species, including non-human primates.29 30

In 1970, Armstrong et al. published the first study producing substantial evidence of regression of atherosclerosis in non-human primates. Armstrong et al. induced severe autopsy proven atherosclerosis in Rhesus monkeys resembling that of human atherosclerosis by feeding a diet with 40% of energy from egg yolks for 17 months. The egg yolks were then removed from the diet of the remaining monkey’s and replaced by either linoleic acid rich chow or sugar rich low fat chow for three years reducing serum cholesterol to 140 mg/dl and resulting in a marked regression of atherosclerosis.28 31 These results were later reproduced in well over a dozen experiments in various primate species in which severe atherosclerosis was induced typically by feeding diets rich in dietary cholesterol and saturated fat and then reversed the process either by removing these atherogenic components, or by other means which significantly reduce serum cholesterol.30

During the late 1980’s, Dr. Dean Ornish and Dr. Caldwell Esselstyn began reversing atherosclerosis, and more importantly greatly decreased the number of reoccurring cardiac events in participants who adhered to a plant-based diet and often other lifestyle modifications.32 33 34 35 More recently Dr. Esselstyn has replicated his initial findings in around 200 participants over the period of a decade, with publication pending results showing a phenomenal success rate of a 99.5% reduction in reoccurring cardiovascular events 

How food pyramid affects your body

A few years back, Denise Minger instantly rose to fame in the Low-Carb and Paleo diet circles shortly after publishing a blog post criticizing the chapter describing the findings from the China-Cornell-Oxford Project in the book, The China Study, written by Dr. T. Colin Campbell.1 This blog post was very welcomed by proponents of these diets as it provided them with a reference which they used to attempt to use refute much criticism they had been receiving for promoting a diet rich in animal foods.

One reason Minger’s critique likely received much attention, was that unlike other individuals who have attempted to criticize the China Study, rather than making her intention of defending a diet rich in animal foods obvious, Minger attempted to give readers a false impression that if anything she was bias towards a plant-based diet. Minger’s intentions became somewhat apparent when Paleo diet proponent Richard Nikoley posted an e-mail that he received from Minger on his blog.2 The contents of this e-mail made it obvious that Minger had been sending e-mails to proponents of Low-Carb and Paleo diets, suggesting that they cite her blog post as "ammo" to shoot down "vegans" who cite The China Study. The language used by Minger in the e-mail, such as the statement “Of course, they aren't”, in reference to whether animal foods are linked to chronic diseases, suggested the likelihood of confirmation bias in favor of downplaying the harms of animal foods. This raises the question as to whether it was her intention to simply downplay Dr. Campbell’s work, rather than producing an honest review.

As described previously by Plant Positive, and myself, there were a number of serious concerns with Minger’s interpretations of the data from the China Study which further casted doubt on her true intentions. One particular example was Minger's attempt to attribute the association between fat intake, a marker of animal food intake, and an increased risk of breast cancer mortality in the China Study to the consumption of "hormone-injected livestock".3The fact that the mortality data that Minger examined was from the early to mid-1970s, a time when the use of hormone injections was not exactly widely practiced throughout rural China casts serious doubt on this claim. Furthermore, it is important to consider that the time lag between exposure to a causal agent and when breast cancer becomes life threatening is more than often several decades. For example, the greatest risk of excess death from radiation-related solid cancers, such as breast cancer among the atomic bomb survivors of Hiroshima and Nagasaki was more than half a century after exposure.4 It is therefore likely that most of the dietary related deaths from breast cancer that occurred in the early 1970s would more likely to have been caused by the diets consumed several decades earlier, likely even before hormone injections was used to any meaningful extent in China. This provides further suggestive evidence that Minger was merely trying to downplay the evidence of the harms of animal foods, rather than producing an honest review.

Given Denise Minger’s misleading blog posts, naturally I was more concerned than interested to see what sort of take home message Minger would be attempting to provide readers of her recently published book, Death By Food Pyramid. I have therefore decided to review a number of the key sections of the book to help readers to decide whether to purchase and incorporate the dietary advice in this book.

The original USDA Food Pyramid from 1992

The title Death By Food Pyramid that Denise Minger and/or publisher chose for this book provides readers with the false impression that Americans (and people in other nations which share similar dietary guidelines) are complying with the federal guidelines, and, as a result more are dying prematurely of dietary related diseases. Evidence strongly casts doubt on such suggestions. For example, despite the tendency for people to over-report the intake of healthy food in food surveys, such surveys have nevertheless found that nearly the entire population of the United States does not adhere to the federal dietary recommendations.5

Although it may be fair to suggest that the federal dietary guidelines can be considered as a lost opportunity to save additional lives, evidence does not suggest that the Food Pyramid promoted a diet that would have increased the risk of dietary related deaths compared to the cholesterol-rich diet consumed by Americans in earlier decades. For example, numerous studies have found that in a number of nations, including the United States, large reductions in serum cholesterol, largely as the result of displacing the proportion of saturated fat in the diet with other sources of energy can explain a significant portion of the decline in coronary heart disease mortality. These large declines generally occurred in order of the nations that were earlier to embrace the lipid hypothesis and reduce the intake of animal fat. For example, this decline began in the late 1960s in the United States, Finland, Australia and New Zealand, but not until a decade later in the United Kingdom which had been distracted by John Yudkin's sugar hypothesis and much slower to embrace the lipid hypothesis.6 In the former communist nations of Eastern Europe, this decline did not occur until the 1990s, following the abolishment of communist subsidies on meat and animal fats after the collapse of the Soviet Union.6 

Although Minger notes this observed decline in mortality in the United States in her book, she suggests that it can more likely be explained by the reduction in smoking prevalence, rather than the displacement of saturated fat with other sources of energy, such as omega-6 polyunsaturated fats and carbohydrate. Minger however failed to provide any data demonstrating what portion of the decline in mortality could be attributed to changes in smoking prevalence and diet/serum lipids. The IMPACT CHD mortality model incorporates among the highest quality data available for risk factors and treatments to help determine how individual risk factors and treatments have contributed to changes in coronary heart disease mortality of a given population. The fact that the prediction of change in coronary heart disease mortality calculated by the IMPACT model has been demonstrated to be largely comparable with the actual change in mortality in nations throughout North America, Northern, Southern, Eastern and Western Europe, South-East Asia, Africa, Australasia and the Middle East provides confidence in the validity of this model.7 8 9 10 11 12 13 14 15 16 17 18 19 20 21

It should be noted that the use of the IMPACT model has made it clear that in those nations which experienced the most dramatic declines in heart disease mortality in the world, such as Finland and the former communist nations of Eastern Europe, large dietary induced declines in serum cholesterol has typically explained a very significant portion of the decline.8 9 10 22 23 The same can be said for the increases in serum cholesterol as the result of an increase in intake of cholesterol and saturated fat, and the surge in heart disease mortality among a number of populations, such as Beijing.17 19 These findings are also supported by earlier studies.6 For example, in 1989 Epstein examined the changes in coronary heart disease mortality in 27 countries during the previous 10 to 25 years, noting that:24

In almost all of the countries with major falls or rises in CHD mortality, there are, respectively, corresponding decreases or increases in animal fat consumption...

Epstein also noted that during this period the prevalence of smoking among women remained largely unchanged or increased in most nations, and that therefore changes in smoking prevalence was unable to explain the large differences in the rate of decline between countries and sexes.24

Figure 1. In the United States between 1980 and 2000, changes to serum cholesterol resulting from dietary changes had a greater impact on the decline in coronary heart disease mortality than any other factor, resulting in approximately 1.1 million years of life gained. 

The IMPACT model found that in the United States between the years of 1980 and 2000, a time at which coronary heart disease mortality was reduced by about half, the decline in serum cholesterol, largely due to changes in diet, could explain approximately 24% of this reduction, compared to only about 12% for the decline in smoking prevalence (Fig. 1).7 22 Considering that coronary heart disease has been the leading cause of death in the United States, as well as many other nations for the best part of a century, if anything, a more appropriate title for Minger's book would be "Saved By Food Pyramid".25

In the chapter Amber Waves of Shame, Denise Minger attempts to explain about the implementation of the Dietary Goals for the United States of 1977, also known as McGovern Report. This report has been considered by many as laying a cornerstone for the forthcoming USDA guidelines. In this chapter, Minger also describes how the egg, meat, milk, salt and sugar industries attempted to hijack the report due to the nature of the recommendations to limit these foods, referencing a video on this topic by Dr. Michael Greger which can be viewed below. It comes as no surprise that Minger cited this video but chose to neglect many of the hundreds of studies cited throughout Dr. Greger's series of videos that cast significant doubt on her own dietary recommendations.

Dr. Michael Greger on the McGovern Report

In an attempt to criticize the science supporting the McGovern Report, Minger focuses on a publication from the American Society for Clinical Nutrition (ASCN) expert committee, published in the American Journal of Clinical Nutrition in 1979, which critically examined the evidence for each of the foods and nutrients that the McGovern Report recommended limiting. Minger states that there was significant disagreement among the ASCN panel regarding the causal association between dietary cholesterol, saturated fat and heart disease. Nevertheless, the panel gave the strength of evidence of a causal association for dietary cholesterol and saturated fat combined a score of 73 out of 100, which was considered “rather high”. Because the score of each of the panelists contributed equally to the overall score, this rather high score suggests that very few of the panelists were in significant disagreement with the diet-heart hypothesis. For dietary cholesterol and saturated fat considered separately, the scores were a little lower, which was suggested to be due to the nature of these two nutrients being highly correlated, making it difficult to determine which contributes more to atherosclerotic heart disease.26 In comparison, virtually all of the panelists considered the evidence linking carbohydrate (ie. sugar) to heart disease as being “extremely weak”, scoring it only 11 out of 100.26 This fact is however largely neglected by Minger despite discussing the potential adverse effects of sugar on heart health in this book.

Minger quotes several selected sentences from the paper on dietary fat and heart disease by ASCN panelist Charles J. Glueck regarding the failure of several diet-heart trials to produce unequivocal supportive evidence, suggesting as if Glueck concluded that there was scant evidence supporting the diet-heart hypothesis. This however was not the case. Glueck actually indicated that while it can be considered that there may not have been unequivocal evidence supporting the diet-heart hypothesis, there was some strong suggestive evidence. In fact, in the paper Minger cites, Glueck described why the failure of the diet-heart trials to produce statistical significant findings does not necessarily negate the hypothesis:27

These failures could have been due to the short duration of the studies, the age of subjects at inception of the studies, or to the inadequacy of the changes in plasma lipids so produced.

In a different paper published in the same issue of the American Journal of Clinical Nutrition, Glueck cited several lines of strong suggestive evidence supporting the diet-heart hypothesis. Notably, Glueck stated:28

Animal studies, particularly in subhuman primates, reveal an unequivocal causal relation between dietary cholesterol or saturated fat, plasma cholesterol levels and development or regression of atherosclerosis

Considering that there is “unequivocal causal” evidence from experiments on nonhuman primates, naturally this would be of considerable concern for humans. If a similar harmful effect would to be shown for a food additive, especially at intakes even lower than that typically consumed in developed nations, there is little doubt that it would be banned almost immediately. Furthermore, in this same paper, without expressing significant disagreement, Glueck quoted the conclusions of a review of the epidemiological evidence by Jerimiah Stamler, one of the expert advisors for the McGovern Report:28

…there is every reason to conclude-based on all seven criterias set forth-that the epidemiologic associations among dietary lipids serum cholesterol and CHD incidence represent etiologically significant relationships. In the multifactorial causation of this disease at least four major factors are operative; diet high in cholesterol and saturated fat, hypercholesterolemia, hypertension and cigarette smoking. However, since the data from both animal and human studies indicate that high blood pressure and cigarette smoking are minimally significant in the absence of the nutritional metabolic prerequisites for atherogenesis, it is further reasonable and sound to designate ‘rich diet’ as a primary, essential, and necessary cause of the current epidemic of premature atherosclerotic disease ranging in the Western industrialized countries.

As has been the case for smoking, there has never been, and never will likely be a definitive trial which tests the diet-heart hypothesis. Indeed, the few smoking cessation trials that have been carried out have failed to produce statistically significant findings for lung cancer mortality. Some of these trails even produced paradoxical findings, including non-significant increased rates of mortality from lung cancer and other cancers in the cessation group.29 30 Similar to the diet-heart trials, there are however plausible explanations as to why these trials failed to demonstrate significant findings for the benefits of smoking cessation. Such explanations include an insufficient duration of study period, and only modest differences in risk factors, points that Glueck noted as limitations of the trails testing the diet-heart hypothesis.29 30 This illustrates why it is critical to consider the totality of evidence, as negative findings from certain lines of evidence, even when normally considered to be at the top of the hierarchy of evidence does not necessarily negate a hypothesis. In other words, the lack of unequivocal evidence should not necessarily prevent federal agencies from recommending lifestyle changes to the public. This point was made clear by Senator George McGovern when he responded to criticism of the report, asserting that:31

I would only argue that Senators don´t have the luxury that a research scientist does of waiting until every last shred of evidence is in.

Minger also attempts to downplay the McGovern Report by taking the statements made by members of the McGovern Committee out of context. For example, Minger focuses on the statements of McGovern Committee member Chris Hitt who believed that even in the worst case scenario, that at the very least "the goals were safe, that there were no risks". Minger then takes this statement out of context to suggest as if the committees opinion of the likely effectiveness of the guidelines had more or less became “at least this probably won’t kill everybody”[p.43]. This statement, which suggests that the guidelines are not only ineffective, but are potentially dangerous, is clearly not what Chris Hitt stated, and is a far stretch from the opinion of committee as a whole.

Although Minger would try to have readers believe that a significant portion of the experts at the time were not in favor of the diet-heart hypothesis, evidence strongly suggests otherwise. As pointed out by Plant Positive in his new series of videos, in December 1976, just before the publication of first edition of the dietary goals, Dr. Kaare R. Norum conducted a survey to confirm how supportive the experts in the field were of the validity of the diet-heart and lipid hypotheses. Out of 211 epidemiologists, nutritionists and geneticists who received the survey, 193 recipients from 23 different countries responded.32 The list of surveyed recipients was considered to have included virtually every prominent researcher in the field from the time.33 As a result of this survey, Norum asserted that:

Almost all agreed that there is a connection between diet and the development of CHD, between diet and plasma lipoprotein levels, and between plasma cholesterol and the development of CHD.

It is clear that Minger is trying to give the reader the false impression that the McGovern Committee, the ASCN expert committee, and a large portion of experts in this field felt that the guidelines of the McGovern Report, particularly the guidelines regarding the restriction of cholesterol and saturated fat were not evidence based by taking selected statements made by a number of these experts out of context. These tactics were perhaps used in order to give the reader the false impression that, even from the beginning, the federal guidelines have never been evidence based, providing momentum for the rest of her book. As can be seen from the table below based on Norum's survey, the impression that Minger attempts to provide the reader of the expert opinion of the time should be considered as misleading.

Cracking down on eggs for health

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. 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). 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.

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.

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.

Eggs vs. Cigarettes in Atherosclerosis

In the video below Plant Positive addresses various critiques of Spence and colleagues findings, as well as other relevant research on dietary cholesterol.

Cholesterol Confusion 6 Dietary Cholesterol (And the Magic Egg)

In addition to developing atherosclerosis and gangrene, the feeding of egg yolks and cholesterol to various species of nonhuman primates has also resulted in the development of xanthomatosis, a condition where deposits of cholesterol develop underneath the skin and is associated with chronically elevated serum cholesterol.1840 41 42 43 This condition has been shown to be cured in nonhuman primates upon the cessation of a cholesterol-rich diet.41 A case report found that a 30-year-old woman with a healthy body weight who had been following a carbohydrate restricted diet for three and a half years had developed xanthomas on her hands and a chronically elevated serum cholesterol level of 940 mg/dl.44 The composition of the woman’s diet was reported as follows:

Each day she had consumed eight to 12 eggs, one or two lean steaks or half a small chicken and, half to one litre of milk. Sometimes some cottage cheese or tomatoes enriched the menu and, on rare occasions, fruit. She completely avoided butter, bread, potatoes, rice, noodles, alcohol, or any other food or beverage containing carbohydrate. The daily cholesterol intake, which was mainly derived from the egg yolks, was about 3500 mg. The total calorie intake was about 8-4 MJ (2000 kcal) (35 % protein, 55 % fat, and 10 % carbohydrates, polyunsaturated fat:saturated fat (P:S) ratio=0 26).

The woman was advised to change her diet, and in particular to stop eating eggs. After 16 days her serum cholesterol dropped to 750 mg/dl, and after several years dropped to 188 mg/dl and the lipid deposits on her skin had cleared up. This woman’s diet induced xanthomas and chronically elevated cholesterol resemble the characteristics of people with homozygous familial hypercholesteromia, a rare genetic disorder that results in chronically elevated concentrations of predominantly large LDL cholesterol particles.45 People with this disorder are short lived and often experience heart attacks during childhood.46 Such unfavorable risk factors would normally be of great concern to any responsible physician. However, despite the overwhelming evidence of the danger of elevated serum total and LDL cholesterol,30 47 48 including for women,49 50 Sally Fallon and Mary Enig, the founders of the Weston A. Price Foundation claim that ‘For women, there is no greater risk for heart disease, even at levels as high as 1000 mg/d’.51 It is clear that this organization has little concern for the wellbeing of people.

It has been well established in rigorously controlled feeding experiments that adding dietary cholesterol to a diet that is low in cholesterol can significantly raise serum cholesterol in humans.52 An addition of 200 mg cholesterol per day to a cholesterol-free diet has been shown to raise serum cholesterol by as much as 20%.53 This may be largely explained by the strong evidence that dietary cholesterol down-regulates the LDL receptor.54 However, as Hopkins addressed in a meta-analysis of rigorously controlled feeding experiments, there exists a ceiling effect at which adding additional dietary cholesterol to a diet already rich in cholesterol has little appreciable effect on serum cholesterol (Fig. 3). Therefore, the fact that numerous studies carried out on populations with a relatively high baseline cholesterol intake failed to find a significant association between cholesterol intake and serum cholesterol does not negate the evidence that lowering intake to near zero will significantly lower serum cholesterol.

Figure 3. Effects of added dietary cholesterol on serum total cholesterol at different baseline levels of intake

Several controlled experiments have found that overweight compared to lean people, and insulin resistant compared to insulin sensitive people are less responsive to dietary cholesterol.55 56 This likely explains why researchers who have financial or personal connections with the egg industry have specifically selected overweight and insulin resistant participants with a modestly high baseline dietary cholesterol intake for controlled trials, as it can be pre-empted that this subgroup of the population will show little response when egg intake is increased.

It has been demonstrated in multiple meta-analyses of rigorously controlled feeding experiments that dietary cholesterol, including that from eggs yolks does have a modest adverse effect on the LDL:HDL cholesterol ratio.57 58 Furthermore, unlike for LDL cholesterol, there is limited causal evidence that simply raising HDL will lower the risk of coronary heart disease. For example, a meta-analysis of 108 randomized controlled trials found that while lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, modifying HDL had little appreciable effect after controlling for LDL cholesterol.47 In addition, a recent meta-analysis of mendelian randomization studies found that while genetically modified LDL significantly influenced the risk of coronary heart disease, genetically modified HDL had little appreciable influence.59 This evidence together with the evidence that dietary cholesterol adversely influences both concentrations of LDL as well as the LDL:HDL ratio, especially in healthy people reinforces the recommendations to limit egg and cholesterol intake.

Another contributor to confusion caused by studies typically influenced by the egg industry is the suggestion that dietary cholesterol does not increase the number of LDL particles, or only increases the concentration of large LDL particles, which is considered by some to be less atherogenic. However, as elaborated by Plant Positive, several studies not influenced by the egg industry have found that cholesterol intake does increase the total number of LDL particles in healthy people.60 61 In addition, a systematic review found that higher LDL particle number, but not other LDL subfractions was consistently associated with an increased risk for cardiovascular disease, independent of other lipid measurements.62 The National Lipid Association Expert Panel recently concluded that ‘All lipoprotein particles in the LDL fraction are atherogenic, independent of size’, and was unable to identify any patient subgroups in which LDL subfraction measurements are recommended. In specific, the panel provided the following evidence for these conclusions:63

Studies have linked large LDL particles to atherosclerosis in nonhuman primates, in patients with familial hypercholesterolemia (who have an elevated concentration of predominantly large LDL particles), in participants of the population-based MESA study, in normolipidemic men with CHD, and among patients after MI [heart attack] in the Cholesterol And Recurrent Events (CARE) study... Many studies document links between small dense LDL particles and atherosclerotic CVD. However, these statistical associations between small, dense LDL and CV [cardiovascular] outcomes are either significantly attenuated or abolished when the analyses are adjusted for the overall number of circulating LDL particles (LDL-P) either by adjustment for Apo B levels or by adjustment for nuclear magnetic resonance-derived LDL-P... To date, there is no evidence that the shift in LDL subfractions directly translates into change in disease progression or improved outcome.

More recently a meta-analysis of mendelian randomization studies with over 312,000 individuals found that inheriting any of nine studied genetic variants that modify lifelong LDL cholesterol concentrations, but not any other known risk factors predicted a 55% lower risk of coronary heart disease for each mmol/l (38.7 mg/dl) lower LDL cholesterol.48 Despite having significantly different effects on LDL particle sizes, all of the nine studied genetic variants predicted essentially the same decrease in coronary heart disease per unit lower LDL cholesterol, including the gene responsible for familial hypercholesterolemia which elevates predominantly large LDL particles.45 Therefore there is convincing evidence that large LDL particles promote atherosclerosis.

The elevation of LDL cholesterol is not the only adverse effect that increased intake of eggs and cholesterol confers. As Spence and colleagues also pointed out in regards to recent controversy surrounding dietary cholesterol:40 64

Focusing on fasting serum cholesterol levels misses the bulk of the problem. Even though serum cholesterol rises very little after a meal, dietary cholesterol increases the susceptibility of LDL-C to oxidation, vascular inflammation, oxidative stress, and postprandial hyperlipemia and potentiates the harmful effects of saturated fat, impairs endothelial function, and increases cardiovascular events.

Multiple international studies based on data from the World Health Organization have found the mean per capita dietary cholesterol levels are consistently associated with the rates of coronary heart disease mortality.39 65 This includes a large study of 40 countries.66 Similarly, it was found in the 25 year follow-up of the Seven Countries Study that dietary cholesterol was associated with a significantly increased risk of coronary heart disease across the 16 cohorts.67

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

The next post in this series will focus on findings from more recent prospective cohort studies that addressed the intake eggs and cholesterol and the risk of coronary heart disease, diabetes, heart failure, cardiovascular disease and all-cause mortality. Many of these important findings have gone unaddressed in recent reviews of the literature.