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Ancel Keys' Cholesterol Con, Part 2

ByProf. Timothy NoakesMay 17, 2020

The Greatest Scam in the History of Modern Medicine

A sequence of 70 events was critical in advancing the global acceptance of Keys’ unproven diet-heart and lipid hypotheses and then subsequently disproving them. In Table 1, I outline each event in its barest detail. In the coming columns, I expose the meaning of each scientific event and how the most damaging of the scientific findings were skillfully managed by a core of like-thinking scientists to ensure the truth could not emerge.

The ideas and arguments I present are not original in that I am not their original source. Rather, they have been covered in compelling detail in four iconic books (1-4) and a number of other sources that address what has become known as the “Cholesterol Scam” or “Cholesterol Con” (5-9). This list is not exhaustive.

Rereading the books by Russell Smith and Edward Pinckney, Thomas Moore, Gary Taubes, and Nina Teicholz brings home to me just how brilliantly exceptional these texts are. If this series drives yet more to read any or all of those books, the series will have been successful.

My goal here is perhaps twofold: first, to introduce and direct the diligent reader to the original sources of all this material, and second, to bring into focus the comprehensive nature of the ingenious scam to which we have all been exposed — at great cost. Included is my interpretation of the reasons why that scam has succeeded so far.

My real hope is that by once more retelling the story of how this scam unfolded over the past century, we may come a little closer to the day when medical and nutrition professions will be forced to finally acknowledge what is now obvious: that this has been the greatest scam in the history of modern medicine.

Who knows? One day they might even apologize.

Table 1: Historical sequence of the significant events leading to the global adoption of the diet-heart and lipid hypotheses, despite an absence of definitive proof and in the face of multiple disproofs

Date Event Relevence
1910 Future Nobel laureate German chemist Adolf Windaus detects the presence of cholesterol in arterial plaque (atherosclerosis). The assumption becomes that the cholesterol in the arterial plaque originated from the bloodstream and crossed into the arterial wall to cause “artery clogging” — i.e., the lipid hypothesis.
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1910 With the help of German chemist E.C. Kayser, soap and candle makers in Cincinnati, Ohio, William Procter and James Gamble produce a hydrogenated oil from cottonseed. They subsequently form the company Procter & Gamble (P&G). The commercial product Crisco, produced by this hydrogenation process, is promoted to U.S. housewives as a healthier and cheaper alternative to usual animal fats used in cooking. Cleverly promoted as a superior substitute for butter, lard, and tallow, Crisco sales increase 40-fold in four years. The false perception is created that industrially produced foods are much healthier than are the foods our ancestors have eaten for millions of years — foods such as meat, fish, eggs, animal fats including lard and tallow as well as those from brains and bone marrow, and, more recently, dairy.
1913 Russian scientist Nikolai Anichkov feeds herbivorous rabbits a mixture of cholesterol and sunflower oil, and produces a form of atherosclerosis, not unlike that found in humans. The logical conclusion becomes that, provided the blood cholesterol concentration is sufficiently high, the same outcome will be apparent in all creatures, including humans. Eminent Ancel Keys lipid hypothesis acolyte Daniel Steinberg, MD, concludes Anichkov’s finding is the equal of William Harvey’s 1628 discovery of the circulation. He argues that Anichkov should have been awarded the Nobel Prize in medicine/physiology.
1939-1945 Mortality from coronary heart disease (CHD) falls sharply in a number of European countries during World War II. There is no such effect in the U.S. Since consumption of animal-based products was dramatically reduced over the same time period in the affected European countries, the logical conclusion becomes that animal foods are the direct cause of coronary atherosclerosis and CHD.
1945 U.S. President Franklin Delano Roosevelt dies suddenly from a cerebral stroke at age 63. Roosevelt had suffered from malignant hypertension (high blood pressure) for some years, but the medical treatment then available was ineffective. U.S. national pride is challenged to better understand heart disease so that, in the future, the disease can be treated more effectively, and in the long-term, hopefully prevented.
1948 U.S. President Roosevelt’s successor, President Harry Truman, signs the National Heart Act into law. The National Heart Act creates the National Institutes of Health, including the National Heart Institute (NHI), and makes available substantial funding for heart disease research in the U.S. The first $500,000 is provided for what becomes known as the Framingham Heart Study.
1948 Procter & Gamble donates all the funds it raises from its “Truth or Consequences” radio program to the American Heart Association (AHA). The amount is $1.74 million (or $17 million in 2014 dollars). As a result, the AHA creates its first professional initiative “to raise money and let Americans know that heart disease was the country’s number one killer” (4, p. 48). The AHA soon becomes the largest not-for-profit group of any kind in the U.S., “investing hundreds of millions of dollars in research” by 1960 (4, p. 48). Essentially, all this money would be spent promoting Keys’ twin hypotheses.
1948 The Framingham Heart Study (FHS) is launched. The goal of the FHS is to “determine the factors predisposing to the development of the disease through clinical and laboratory examination and long-term follow-up.” These factors will become known as “risk factors.” The management of these supposed risk factors makes every person a potential “at-risk” patient and will have a major influence on the manner in which medicine is practiced, not just in the U.S. but globally. These developments provide the opportunity for the discovery and marketing of a new class of pharmaceutical agents to treat risk factors, at the same time exposing humans to the potential for harm produced by new chemical agents.
1950 John Gofman, MD, uses an ultracentrifuge technique to separate and identify the different blood lipoprotein particles. He becomes the first to propose the diet-heart and lipid hypotheses. Keys will ultimately steal Gofman’s ideas and present them as his own. Gofman identifies himself as the scientist best equipped to lead future research of factors causing the heart disease “epidemic” then developing in the U.S. and elsewhere. Most importantly, he understands high-carbohydrate diets raise lipoproteins in the Sf o 20-400 lipoprotein band in ultracentrifuge results, and elevations of this lipoprotein band are associated with CHD. He warns, “Neglect of [the carbohydrate factor] can lead to rather serious consequences … by allowing certain individuals sensitive to the carbohydrate action to take too much carbohydrate as a replacement for some of the animal fats” (3, p. 156-157). But Gofman is too great a threat to Keys and his acolytes, so he is muscled out of the discussion. He changes his research direction and moves on. In the end, his contribution has been written out of history.
1952 Laurance W. Kinsell, MD, discovers the substitution of animal fats with vegetable fats lowers blood cholesterol concentrations. The importance of this study, which antedates the formulation of Keys’ twin hypotheses, is that it establishes a dietary change that reliably lowers blood cholesterol concentrations. Indirectly, it supports Keys’ eventual hypothesis that eating animal products raises the blood cholesterol concentration, which must then be the direct cause of increased rates of coronary heart disease (CHD). The supposition is that replacing dietary animal fats with a more plant-based diet and liberally substituting all saturated fats with processed hydrogenated polyunsaturated fats in “vegetable” oils will guarantee the opposite outcome.
1953 Autopsies of young U.S. soldiers killed in the Korean War reveal 77% exhibit advanced (“gross”) coronary atherosclerosis. The finding is overstated; the truth is not as dire as the article suggests. Yet the article reinforces the importance of searching for coronary risk factors, initiated by the Framingham Heart Study. The article also suggests these factors can be detected ante-mortem and can predict who is at greater risk of developing CHD in the future. The assumption is that reversal of these factors will prevent the development of symptomatic CHD in middle age. The MRFIT, MONICA, Look AHEAD, and Helsinki Businessmen studies, among many others, effectively prove this is, at best, wishful thinking. Nevertheless, this fact will be successfully hidden from succeeding generations of medical students and doctors.
1953 Searching for a new research direction, Keys discovers a World Health Organization (WHO) document showing an association between dietary fat intake and CHD mortality rates in 22 countries. The U.S. is the worst affected country, Japan the least. Keys publishes his original paper, an exercise in armchair science based on the data from just six of the 22 countries for which the WHO data were available. Scientists will subsequently accuse Keys of “cherry-picking” only the most convenient data that supported his evolving hypotheses. Although Keys knows that such associational epidemiological studies cannot prove causation, he never deviates from actively promoting his diet-heart and lipid hypotheses as if they are already proven. The problem is evidently Keys’ personality, for he begins his “scientific” quest certain of his correctness. He writes in 1953, “No other variable in the mode of life besides the fat calories in the diet is known which shows anything like such a consistent relationship to the mortality rate from coronary or degenerative heart disease.” He claims, “There is no longer any doubt that one central item is the concentration, over time, of cholesterol and related lipids, and lipoproteins in the blood serum. No other etiological influence of comparable importance is as yet identified” (10, pp. 1399-1400). Keys and his equally solipsistic acolytes will spend the rest of their lives convincing the world that they alone are correct.
1955 President Dwight Eisenhower suffers his first heart attack during the final year of his first term of office in the White House. Dr. Paul Dudley White is one of the cardiologists who assists in the medical management of the president. Eisenhower recovers and is reelected for a second term. He becomes a staunch advocate of Keys’ unproven dietary theories and a formidable ally of the AHA and NHI research programs. The main aim of these research programs is to “prove” Keys’ hypotheses are correct. With White’s approval, Keys places Eisenhower on his experimental “heart-healthy, low-fat, prudent diet.” The outcomes are not good, as Eisenhower develops Type 2 diabetes mellitus (T2DM), suffers a stroke, has multiple heart attacks, and dies from intractable heart failure in 1969. The autopsy shows he has advanced obstructive coronary artery disease, the very condition Keys’ unproven, experimental diet is meant to prevent or reverse. We now know incorrectly treated T2DM is a key determinant of chronic heart failure. Thus, Keys’ “heart-healthy” diet contributes significantly to the death of President Eisenhower, but this connection is never made public.
1955 A seminar is held by the WHO Study Group on Atherosclerosis and Ischemic Heart Disease. During the seminar, Keys’ presentation of his 1953 WHO epidemiological associational data is heavily criticized by Jacob Yerushalmy, MD, and Herman Hilleboe, MD, who point out associational studies cannot prove causation except in exceptional circumstances. Keys takes this criticism as a form of public humiliation and vows to prove to the world that he is correct. His solution is to begin planning the Seven Countries Study (SCS), but the SCS is just another associational study. Most importantly, the SCS begins with the pre-conceived biases of its principal investigator. It is designed and run as an experiment to vindicate Keys. That is how the study eventually is marketed to the scientific and medical communities, even though it ultimately fails to provide much support for any of Keys’ biases. The key measurement in the study — the diets of persons living in the different countries — is so poorly conducted that meaningful conclusions cannot be drawn. But this fact is skillfully hidden by Keys and his colleagues.
1956 The U.S. Public Health Service funds Keys’ Seven Countries Study. Using his growing national and international status as the diet doctor for President Eisenhower, Keys manages to convince key members of the U.S. Public Health Service to fund the study that will become known as the Seven Countries Study.
1957 A nutrition committee representing the AHA rejects Keys’ diet-heart and lipid hypotheses and concludes, “Perhaps the best that can be said [about Keys’ evidence] is that there is an association that has statistical value, but that it is not an obligatory association either in small groups or, and much less so, in an individual” (11, p. 174, my addition). The AHA rules that Keys’ hypotheses are not supported by hard scientific evidence and thus cannot be used to mandate specific dietary changes: “The evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease (11, p. 175). The review authors write, “There is not enough evidence available to permit a rigid stance on what the relationship is between nutrition, particularly the fat content of the diet, and atherosclerosis and coronary heart disease. We are certain of one thing: the evidence now in existence justifies the most thorough investigation. This should be done soon, thoroughly, and uncompromisingly” (11, p. 164).
1957 Edward “Pete” Ahrens, MD, publishes a review of dietary factors, especially different dietary fats, that influence blood cholesterol concentrations. Even though he remains a Keys skeptic all his life — at one point writing, “It has not been demonstrated in man that lowered levels of serum lipids will alter his susceptibility to atherosclerosis” (12, p. 1911) — he concludes the review by observing that “patients with existent or threatening atherosclerosis may be justifiably advised to eat high portions of unsaturated fats” (12, p. 1911). This statement is not evidence-based (then or now) but indicates the extent to which the low-fat dietary bias has already infected even the most skeptical thinkers of the day.
1957-1972 The New York Diet and Coronary Heart Disease Study of Norman Jolliffe, MD, subsequently known as the Anti-Coronary Club Program, is initiated. This is perhaps the first study to evaluate the effects of the “prudent diet” that limited the consumption of animal fats, especially replacing saturated fats with polyunsaturated fatty-acid-enriched margarines and “vegetable” oils in the dietary management of persons who had suffered a heart attack. Although the study is marketed as proof that this diet improves long-term health outcomes in persons with heart attack, hidden in the data is evidence that there were more deaths in the group randomized to the test diet. The authors do their best to hide this inconvenient evidence. Also, most unfortunately, during the trial, the principal investigator, Dr. Jolliffe, dies suddenly from a heart attack.
1957 The initial results from the Framingham Heart Study (FHS) are reported. Although the FHS finds elevated blood cholesterol concentrations are weakly predictive of future CHD risk, its key but hidden findings are that the nature of the diet predicts neither the blood cholesterol concentration nor the risk of death from CHD. These findings disprove Keys’ diet-heart hypothesis. As a result, the report of the finding has to be hidden. The report is consigned to a vault in the NHI buildings in Washington, D.C. This subterfuge is ultimately revealed by a former director of the FHS, George Mann, MD, who resigns from the study group when he realizes those controlling the FHS will not allow all its true findings to be disclosed. The finding that an elevated blood HDL cholesterol concentration is a better predictor of a (reduced) future CHD risk than is an elevated total or LDL cholesterol concentration for an (increased) CHD risk is also written out of history because it conflicts with the diet-heart hypothesis. Ultimately, the finding that an elevated HDL cholesterol concentration is protective against CHD leads to the finding that insulin resistance, high blood triglyceride levels, and low HDL cholesterol concentrations are the more important predictors of CHD risk. The FHS also finds, inconveniently, that those with low blood cholesterol concentrations are at increased risk for developing cancer.
1958 The Oslo Secondary Prevention Trial (OSPT) is initiated. CHD death rates dropped steeply in Norway during the latter years of WWII but increased again in the post-war years. The increase was associated with an increased consumption of trans-fat-laden margarines, which were government subsidized. The OSPT studies the effects of a diet high in polyunsaturated fats on the recurrence of CHD in men who had suffered a first heart attack. It is therefore similar to New York’s Anti-Coronary Club Program.
1959-1965 Margaret Albrink, MD, and Evelyn Man, Ph.D., report blood triglyceride concentrations are more likely than blood cholesterol concentrations to be elevated in persons with CHD and those with T2DM. Albrink and Man also note that in persons with T2DM, the main dietary change in the previous 30 years had been an increased dietary carbohydrate intake and reduced dietary fat intake. These changes were associated with increased blood triglyceride concentrations but without noticeable change in blood cholesterol concentrations. In a historically important editorial in the Annals of Internal Medicine in June 1965, Albrink concludes humans evolved as hunters eating high-fat, high-protein diets with relatively little carbohydrate. As a result, she argues, human metabolism evolved in a low-carbohydrate state: “The habitual diet of prehistoric man would have been low in carbohydrate and high in fat and protein and as such would promote his ability to conserve carbohydrate” (13, p. 1331). She suggests exposing humans that had evolved in this way — a way that causes them to conserve any ingested carbohydrates — to high-carbohydrate diets could be harmful: “The common modern diseases of diabetes, atherosclerosis, and obesity and associated hyper(tri)glyceridemia may be the present day manifestations of the effect of affluence on a once useful genetic trait, the ability to conserve carbohydrate” (13, p. 1332).
1960 The NIH establishes an executive committee on diet and heart disease. The committee proposes a National Diet Heart Study (NDHS). The resulting pilot study establishes (i) that it is not possible to complete a double-blind dietary intervention in which foods are provided to the subjects, and (ii) that a long-term study of the effects of a low-fat dietary intervention on CHD outcomes would be too expensive to undertake. Nina Teicholz concludes the pilot NDHS “could reasonably be viewed in part as an industry-driven effort to broaden the market for its commodity oil.” She writes, “Companies contributing to the study included nearly every major food corporation in the country including the vegetable oil giant Anderson, Clayton & Company, Carnation, The Corn Products Company, Frito-Lay, General Mills, H. J. Heinz, the Pacific Vegetable Oil Corporation, Pillsbury, and Quaker Oats, among others” (4, p. 91).
1961 A new AHA committee, now including Keys’ principal acolyte Jeremiah Stamler, MD, reverses its 1957 decision that there is no strong evidence demonstrating dietary fat, especially saturated fat intake, is a key driver of the evolving CHD epidemic. Instead, it puts its financial, scientific, and academic weight behind Keys’ hypotheses, which it endorses as the sole scientific option it is prepared to support. This acceptance is not based on any new scientific evidence from long-term randomized controlled trials. Rather, it is more likely influenced by a generous $1.74-million “gift” from P&G to the AHA in 1948. The evidence is the conclusion in a 1961 AHA publication that lowering the blood cholesterol concentration “may lessen the development or extension of atherosclerosis and hence the risk of heart attacks or strokes” (14, p. 389). As a result, “the reduction or control of fat consumption under medical supervision with reasonable substitution of poly-unsaturated fats for saturated fats, is recommended as a possible means of preventing atherosclerosis and decreasing the risk of heart attacks and strokes” (14, p. 390).
1962-1989 The NHI provides funding for the Minnesota Coronary Experiment (MCE). Keys is promoted to principal investigator. With the MCE, Keys initiates the first randomized controlled trial of his diet-heart and lipid hypotheses. Subjects partially replace dietary saturated fat with linoleic acid from corn oil. The study is extremely well controlled so that subjects in the intervention and control groups are provided with foods exactly according to the experimental protocol. Although the original findings are available in 1976, the final results are reported only in 1989. The reasons for the delay become apparent when the data are recovered, re-analyzed, and republished by independent scientists in the Recovered Minnesota Coronary Experiment (RMCE). The findings of the RMCE disprove Keys’ hypotheses, and so once more, they are buried. The main conclusion from the study is that removing saturated fat from the diet causes harm so that it is unethical to prescribe this dietary approach to any patient.
1965 On July 1, 1965, the Sugar Research Foundation sends its Director of Research, John Hickson, on a covert mission to the Harvard University School of Public Health. There, he meets with Professor Mark Hegsted, MD, of Harvard to discuss ways in which the Harvard Medical School might be able to assist the sugar industry in deflecting attention from an accumulating body of evidence clearly documenting the negative health consequences of sugar consumption. Hickson’s mandate is to limit the potential damage resulting from four scientific papers published in the June 1965 issue of the Annals of Internal Medicine. All four articles provide evidence that either sugar or carbohydrates likely play a significant role in the causation of CHD. Hickson contracts Professor Frederick Stare, MD, and Hegsted to write an editorial in the New England Journal of Medicine (NEJM). To ensure they convey the “correct” message, he pays the duo the equivalent of $50,000 in today’s money. Two years later, the editorial appears in the NEJM. It presents the false argument that there is no evidence linking sugar to CHD. It concludes, “Increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit [in the prevention of CHD]” (15, p. 246, my addition). The editorial essentially ends any future interest in (or reference to) the possibility that carbohydrate-sensitive hypertriglyceridemia is a significant cause of CHD, thereby burying the novel work conducted by Albrink and Man in the 1950s. Thus, whereas until 1965 there were two competing theories about which dietary macronutrient — carbohydrate or fat — is the more likely cause of CHD, after the publication of the editorial, there remains only one — fat, and especially saturated fat from the consumption of animal products. Key’s diet-heart hypothesis wins the argument, even in the absence of a trace of definitive proof. Future research and teaching on this topic in medicine and in the nutrition sciences is made to reflect this industry-directed, false messaging.
1965 The World Health Organization (WHO) funds the Co-operative Trial in the Primary Prevention of Ischaemic Heart Disease using the drug clofibrate. This is the first study to evaluate the effects of a drug that lowers blood cholesterol concentrations on CHD outcomes. The trial randomizes 15,745 men aged 30-59 in three European cities to intervention and control groups and follows them for five years. The intervention group receives the cholesterol-lowering drug clofibrate. Although the study finds a significant reduction in the number of non-fatal heart attacks in the intervention group taking clofibrate, the total number of deaths in that group is significantly increased. The study establishes the principle that it cannot be assumed that a drug intervention, however well intended, is without risk to those in the intervention group. It is a rule that will be frequently ignored in the pursuit of developing novel drugs such as statins, which are prescribed to healthy people in the hope that some benefit might develop in the long term.
1966 The National Heart, Lung, and Blood Institute (NHLBI) initiates the Coronary Drug Project. This study evaluates the effects of five different drugs — including niacin and clofibrate — that mostly lower blood cholesterol concentrations on CHD outcomes in 8,341 U.S. men aged 30-64. None of the drugs is effective and all produce worrying side effects. The study confirms the results of the 1965 WHO Co-operative Trial using clofibrate: No drug that effectively lowers the blood cholesterol concentrations is without potentially harmful side effects.
1966-2013 The Sydney Diet Heart Study is initiated. The study randomizes 458 men who have suffered a recent heart attack to control and dietary intervention groups. Those in the dietary intervention group replace some dietary saturated fat with the polyunsaturated fatty acid linoleic acid from safflower and sunflower oil. The first outcomes reported in the 1970s show an excess of deaths in the dietary intervention group, but this finding is hidden in the original publication and the data are essentially lost. The full extent of the harm caused by the replacement of dietary saturated fat with linoleic acid is only revealed in 2013 with the publication of the Recovered Sydney Diet Heart Study.
1967 Peter Kuo, MD, identifies carbohydrate-sensitive hypertriglyceridemia (CSHT) as the most common lipid abnormality in patients with CHD. Albrink and Man’s finding that hypertriglyceridemia, not hypercholesterolemia, appears to be the most common abnormality in persons with CHD is confirmed by Kuo. He also confirms their speculative conclusion that the hypertriglyceridemia is caused by dietary carbohydrates, not dietary fats. The effect of this finding is essentially nullified, like Albrink and Man’s work, by the editorial that appears in the November 1967 issue of the NEJM. From that moment, any potential role of CSHT in the causation of CHD is effectively written out of the medical literature. The effect has been so long lasting that even today the potential role of hypertriglyceridemia and carbohydrates in the causation of CHD is fastidiously ignored by many in the teaching and practice of medicine.
1967 Donald Fredrickson, MD, and his colleagues Robert Levy, MD, and Robert Lees, MD, develop a novel classification of blood lipid abnormalities that predispose one to CHD. Fredrickson and his colleagues perform electrophoresis on blood samples and develop a simpler classification of the common blood lipid abnormalities found in persons with CHD: the Fredrickson Classification. Since electrophoresis is a laboratory method more widely available than the ultracentrifugation technique necessary for the Gofman classification, this classification soon begins to enjoy widespread support. The classification includes a Type IV pattern that is essentially carbohydrate-sensitive hypertriglyceridemia. Thus, the Fredrickson Classification clearly identifies dietary carbohydrate as one potential driver of CHD. However, with time, the Fredrickson Classification falls out of favor, replaced by a simplistic model in which only blood cholesterol concentrations are considered important. Fredrickson’s concerns about the role of carbohydrates in the genesis of CHD are progressively forgotten, and his contribution — like those of Gofman, Albrink, Man, and Kuo — are written out of history.
1968 The first results from the Oslo Secondary Prevention Trial are reported. The study finds that while there are fewer fatal heart attacks in the dietary intervention group, overall mortality is unaffected. Thus, the study finds that while lowering the blood cholesterol concentration might reduce the clinical expression of one form of CHD, it must be causing increased deaths from other causes (since total mortality is not reduced). This becomes a recurring theme in studies of blood cholesterol-lowering interventions. Although all-cause mortality should be the most important measure of any intervention aimed at improving health outcomes, this critical point continues to be ignored.
1968 The first findings are reported for the Los Angeles Veterans Trial of the “effects of a diet high in unsaturated fat in preventing complications of atherosclerosis.” The trial randomly assigns 846 men living in a Los Angeles Veterans Administration Hospital to control and diet intervention groups. The diet replaces saturated fats with a diet high in polyunsaturated fats. The intervention fails to reduce all-cause mortality and increases deaths from cancer, but it is sold to the world as proof that a low-fat diet high in polyunsaturated fatty acids can prevent CHD. It becomes one of four such studies — the Anti-Coronary Club Trial, the LA Veterans Hospital Study, the Finnish Mental Health Study, and the Oslo Secondary Prevention Trial — which show no benefit of the diet but which are marketed for the next 50 years as proof of the value of replacing dietary saturated fat with polyunsaturated fats from hydrogenated vegetable oils high in trans fats (and other manufactured chemicals, the long-term effects of which remain unknown).
1969 The NIH establishes a review panel to determine whether it is practical to initiate a trial of the diet-heart hypothesis. This committee, under the leadership of Edward “Pete” Ahrens, concludes a test of the diet-heart hypothesis would be too expensive and too impractical to be undertaken. This, however, does not hinder either the AHA or the NHI from continuing to promote, in the absence of any reasonable evidence, dietary interventions to lower blood cholesterol concentrations as if these interventions have already been proven beneficial and without risk of harm. The evidence for potential harm has already been clearly established by the LA Veterans Hospital Study.
1970 The results from Keys’ Seven Countries Study (SCS) are reported. The study has significant problems that are seldom mentioned. First, it is an associational study that cannot prove causation. Second, the selection of the seven countries for study is not performed randomly. Third, many of the studied countries are recovering from the debilitating effects of WWII. Fourth, the collection of the dietary data is hopelessly inept. The singular finding is a significant linear relationship between the median blood cholesterol concentrations in the different study populations and 10-year coronary deaths in those communities. While there is a significant relationship between the percentage of calories from saturated fat and 10-year coronary death rates, there are a host of unexplained anomalies in death rates between communities eating either quite different or quite similar diets. Most importantly, as in the Framingham Heart Study, differences in blood cholesterol concentrations between individuals cannot be explained by any single dietary factor, including the amount of saturated fat in the diets. A host of other studies have since confirmed that, compared to still unidentified factors, diet has a very marginal effect on blood cholesterol concentrations. Thus, like the Framingham study, the SCS disproves the foundational prediction of Keys’ diet-heart hypothesis, which is that dietary animal fat consumption is the sole determinant of the blood cholesterol concentration. Once again, this inconvenient finding is neglected in the teaching of medicine or nutrition/dietetics.
1970 The NHLBI forms its Expert Panel on Hyperlipidemia and Atherosclerosis. This later becomes the 1971 NIH Task Force on Atherosclerosis. The NIH Task Force concludes definitive testing of Keys’ diet-heart hypothesis would be too expensive, as it would cost upward of $1 billion. Instead, the NIH agrees to spend $250 million on two trials — the Lipid Research Clinics Coronary Prevention Trial (LRC-CPPT) and the Multiple Risk Factor Intervention Trial (MRFIT) — neither of which tests the role of diet in CHD. Thus, by 1970, the NHLBI clearly has no intention of evaluating the effects of Keys’ low-fat diet on long-term health outcomes. Nevertheless, this does not stop its hubristic promotion of that diet as the key component of its strategy to prevent CHD. The point, perhaps, is that the NHLBI had long since decided this strategy was appropriate, and the organization did not require any scientific proof to justify its promotion of that preventive approach.
1971 The WHO initiates the European Collaborative Trial of Multifactorial Prevention of Coronary Heart Disease. The trial recruits 60,881 men aged 40-59 from 80 factories in the U.K., Belgium, Italy, and Poland. One half receives advice on physical activity, eating a cholesterol-lowering diet, smoking cessation, and controlling body weight and blood pressure. The control group is left to its own devices. At the time, it is the largest randomized trial of CHD prevention ever attempted. The trial outcomes are first reported in 1980.
1971 The Multiple Risk Factor Intervention Trial (MRFIT) is initiated. The trials recruits 12,888 persons presumed to be at the very highest risk for future CHD from a population of 361,662 screened individuals. The group is then split in two. The control group continues to follow its usual behaviors; the intervention group is exposed to intensive educational and behavioral interventions, unmatched in scope before or since. The initial findings from the study are first published in 1982.
1971 The Helsinki Policeman Study of the role of glucose intolerance/insulin resistance/T2DM in the development of CHD is initiated. The study recruits 1,259 of the original participants in a 1966 study of Helsinki and National Police Force members to evaluate the role of glucose intolerance in the development of CHD. This is the first study that specifically investigates the role of insulin resistance (with or without T2DM) on the future development of CHD. It therefore addresses the relationship first suggested by Albrink and Man in 1959 and Kuo in 1967. The initial results are reported in 1979.
1972 The results of the AHA National Cooperative Pooling Project are reported. The AHA organizes the directors of five major U.S. studies, pooling their data to evaluate any possible relationships between supposed CHD risk factors and the subsequent development of CHD. The data shows a “strong relationship” between risk factors and subsequent CHD development. However, the predictive value of an elevated blood cholesterol concentration is, at very best, marginal. Thus, an elevated blood cholesterol concentration above 249 mg/dL (6.4 mmol/L) increases risk of a first coronary event/sudden death for any individual from 0.0045/year to 0.0067/year. According to the data, knowing one’s blood cholesterol concentration offers no value in predicting the probability of suffering a heart attack in the near future.
1973 Plans for the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT) get underway. The trial randomizes 3,810 men to control and intervention groups, both of which are placed on a cholesterol-lowering diet. The intervention group is treated with the cholesterol-lowering drug cholestyramine and followed for seven years. The results of the study are first reported in 1984.
1973 The first results of the Nagasaki-Hiroshima/Honolulu/San Francisco Japanese Ancestry Study (Ni-Hon-San) are reported. One of the unsolved paradoxes confronting the diet-heart hypothesis is that persons of Japanese ancestry living in Japan have very low CHD rates but higher rates of stroke than persons living in the U.S. The diet-heart hypothesis alone cannot explain this finding. The Ni-Hon-San Study seeks to determine the role of environmental factors in explaining different CHD and stroke rates in persons of Japanese ancestry, resident in either Japan or in two cities in the U.S. The clearest finding from the Ni-Hon-San Study is that differences in the health of Japanese persons living in different parts of the world cannot be explained solely by lower or higher intakes of saturated fat and lower or higher blood cholesterol concentrations. Instead, the key measure of overall health — total mortality — is (once more) not different between any of these groups despite many lifestyle differences and differences in blood cholesterol concentrations. In short, the Ni-Hon-San Study fails to support Keys’ hypotheses.
1974 The Helsinki Businessmen Study is initiated. The study randomizes 1,222 healthy middle-aged men who exhibit coronary risk factors into intervention and control groups. The study lasts five years, during which the intervention group receives multiple interventions aimed at lowering risk of future development of CHD. The intervention group participants are advised to stop smoking, to achieve a normal body weight with the adoption of a prescribed diet, and to moderate alcohol intake. In addition, those with hypertension or hypercholesterolemia are treated with appropriate prescription drugs. The initial results are reported in 1991.
1977 The McGovern Senate Select Committee on Nutrition and Human Needs releases its Dietary Goals for the U.S. Senator George McGovern’s senate committee, faced with the threat of redundancy and loss of funding, decides it will dictate to the U.S., and subsequently the world, the foods everyone should be eating to remain healthy. At the time, McGovern is himself experimenting with the zero-fat Pritikin diet. The committee is later described as “a bunch of kids, who just thought, Hell, we should say something on this subject before we go out of business” (3, p. 45). The final report is compiled by a vegetarian named Nick Mottern, who has no formal training in the nutritional sciences. The report is heavily criticized for not being evidence-based. In response to the request from concerned senior scientists that the committee should wait for more research “before we make announcements to the American public,” McGovern famously responds, “Senators don’t have the luxury that the research scientist does of waiting until every last shred of evidence is in.” By refusing to wait for that “every last shred of evidence,” McGovern’s committee inadvertently pushes the world into the global obesity/diabetes epidemic. It will be perhaps the single greatest medical/scientific failure of the past century. Today, 43 years later, the scientific world is still awaiting the publication of “every last shred of evidence” that proves the value of the low-fat diet.
1978 Dietary trans fats are first identified as being uniquely damaging to human health. When P&G promoted the development of Crisco after 1913, it was unaware that the hydrogenation of seed oils produces a novel group of fatty acids known as trans fatty acids. By the 1960s, trans fatty acids contributed as much as 50% of the fatty acid content of products containing these hydrogenated fatty acids. Two scientists in the U.S., Drs. Mary Enig and Fred Kummerow, are the first to propose that trans fats are uniquely unhealthy. Enig suggests trans fatty acids might be linked to the development of cancers, while Kummerow presents evidence that trans fats may be uniquely involved in the causation of atherosclerosis. Thus, the ultimate irony: Polyunsaturated fats in vegetable oils promoted by Keys and his acolytes as the key method for lowering blood cholesterol concentrations to prevent CHD might have contributed to the dramatic rise in CHD, which began in the 1920s exactly when hydrogenated polyunsaturated fatty acids full of trans fats were first developed and marketed by P&G.
1979 The Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Project is initiated. A group of European epidemiologists led by Professor Hugh Tunstall-Pedoe, MD, senses a research opportunity in the 1970s when it becomes clear that rates of CHD are falling rapidly in many countries across the globe. They propose a research project involving 21 countries spanning four continents to determine whether the falling CHD and stroke rates in these countries could be explained by changes in CHD risk factors. The results are reported in 1994.
1979 The first results from the Helsinki Policemen Study of insulin resistance as a predictor of CHD risk are reported. The results find that five-year incidence of CHD deaths and non-fatal heart attacks is significantly related to elevated blood glucose concentrations measured one hour post-glucose ingestion. Ten-year mortality as well as CHD deaths and non-fatal heart attacks are also higher in those with the highest fasting, one hour, and two hours post-glucose-ingestion blood glucose concentrations. The authors conclude the area-under-the-curve blood insulin concentrations post-glucose ingestion are at least as strong a predictor of future CHD risk as is the blood cholesterol concentration. Subsequently, a number of studies propose “insulin resistance is the most important single cause of coronary artery disease” (16, p. 1449).
1980 The inconvenient results of the WHO European Collaborative Trial of Multifactorial Prevention of Coronary Heart Disease are released. This study of 60,881 middle-aged men employed in 80 factories in the U.K., Belgium, Italy, and Poland finds reducing key risk factors reduces — but not significantly — total mortality, non-fatal heart attacks, and fatal CHD. The reduction in all these outcomes is statistically significant in only one country: Belgium. The study is often touted as further evidence that coronary risk factor intervention trials significantly reduce future CHD risk, but this study, like many others (MRFIT, Helsinki Businessmen Study, and the Women’s Health Initiative Randomized Controlled Dietary Modification Trial (WHIRCDMT)), fails to achieve that outcome.
1980 The Food and Nutrition Board of the National Academy of Sciences releases “Toward Healthful Diets.” The publication of the U.S. Department of Agriculture Dietary Goals for Americans (USDADGA) is heavily criticized by many members of the National Academy of Sciences, most especially its president, Philip Handler. The organization’s response is to publish a contrary and more conservative opinion entitled “Toward Healthful Diets” (17). The review argues the USDADGA is extending its recommendations in the absence of any scientific evidence that those guidelines will be beneficial while presenting no risk of harm. The review makes six dietary recommendations, none of which promote the low-fat, high-carbohydrate diet for disease prevention. It states: “Select a nutritionally adequate diet from the foods available, by consuming each day appropriate servings of dairy products, meats or legumes, vegetables and fruits, and cereal and breads” (17, p. 16).
1982 The inconvenient findings of the MRFIT study are published. This large study of more than 12,000 subjects provides the gold standard for an intervention that radically improves the health behaviors of those in the intervention group. Subjects in that group greatly reduced their dietary fat and cholesterol intakes; their blood cholesterol concentrations fell by 5-7%; their smoking rates fell by 50%; and 67% of subjects with hypertension normalized their elevated blood pressures. These changes were sustained for seven years. Nevertheless, the trial failed miserably. There were no measurable health benefits from these favorable reductions in “risk factors.” Thus, after spending $115 million in a trial that lasted 10 years, the researchers have conclusively proved multiple interventions that substantially modify what are considered to be the most important CHD risk factors (smoking, high blood pressure, and elevated blood cholesterol concentrations) have absolutely no effect on the measured health outcomes. This study is never mentioned by the advocates of the diet-heart hypothesis. Nor is it mentioned that T2DM is clearly the strongest risk factor for future CHD events in this population. One possibility is that the change to a low-fat diet negated the expected benefits of reduced rates of smoking and hypertension in the intervention group. This, too, is never mentioned. Nor is it mentioned that the incidence of lung cancer increased in the intervention group.
1984 The results of the LRC-CPPT are published. The LRC-CPPT tested the effects of the cholesterol-lowering drug cholestyramine on CHD outcomes during seven years of follow-up. Prior to the start of the experiment, the researchers agreed that, because of the extraordinary importance of the study (it would establish for the first time whether lowering the blood cholesterol concentration was harmful or helpful), they would accept as significant only a finding that demonstrated the study had a less than 1% probability of any positive findings being the result of chance alone. But when they find the results are not significant at the 1% level, they simply move the statistical goal posts. This allows them to claim the study has produced a statistically important finding. In fact, the only “significant” finding is that the annual risk of heart attack falls by 0.2% in the intervention group. Once again, however, the truly important measurement — total all-cause mortality — is not different between groups. In a classic example of scientific fraud, this failed study is then used as the definitive proof that lowering blood cholesterol concentrations with a low-fat dietary intervention will also reduce CHD risk. When the chief investigator is asked how he could possibly justify this clearly fraudulent interpretation, he responds: “It’s an imperfect world. The data that would be definitive is ungettable, so you do your best with what is available” (3, p. 58). In other words, when the data do not support your preconceived biases, you simply bury the evidence by lying to the world. So much for the need for an independent, impartial body of scientific evidence.
1984 The 1984 NIH organizes the National Consensus Development Meeting. Once Keys’ acolytes at the NIH decide the LRC-CPPT study provided the definitive evidence that lowering blood cholesterol concentrations by whatever means — by drugs or diet — will reverse the CHD epidemic, they need to ensure the fake findings of that study will never be questioned. Thus, they convene a National Consensus Development Meeting, run over three days. The reality is that the goal of all consensus meetings is to present the illusion of consensus when it is clear no such consensus exists. The meeting is chaired by one of Keys’ most stalwart supporters, Dr. Daniel Steinberg, MD, who has written the consensus document even before the meeting begins. The meeting simply endorses his personal biases and resolves that “saturated fat increases LDL cholesterol, a major cause of atherosclerosis and CHD, and replacing it with polyunsaturated or monounsaturated fat decreases LDL cholesterol.” As a logical extension, during the meeting, they come up with “a simple set of numbers that satisfied everyone. We proposed ‘desirable’ (blood cholesterol) levels of <200 (mg/dL) for persons younger than 20 years; <220 for those 30 to 39 years; and <240 for those older than 40 years, and we proposed the same guidelines for men and women” (18, p. 10). Thirty-six years later and still without definitive supportive evidence, these guidelines remain entrenched in the teaching of medical practice around the globe. At the time, the consensus is vigorously opposed by a number of senior scientists. Today, such scientists would simply be dismissed as “cholesterol skeptics.”
1987 The National Cholesterol Education Program (NCEP) is launched in the U.S. The NIH National Consensus Development Meeting, actually the Steinberg Consensus, entrenched elevated blood cholesterol concentrations as the major driver of CHD and established the (urgent) need for all to lower their elevated blood cholesterol concentrations. But in 1984, the majority (61%) of U.S. physicians did not share this perspective; they did not believe cholesterol was the key driver of CHD. The NIH therefore decides this will have to change. The goal of the NCEP is to give scientific credibility to a nationwide program of blood cholesterol testing in all but infants, so those with elevated blood cholesterol concentrations can receive appropriate management to reduce their future risk for developing CHD. In their zeal to promote this program, few question the extraordinary costs such a program will entail. Also hidden is the fact that the major beneficiaries of the NCEP will not be the U.S. public. Rather, the key beneficiaries will be the pharmaceutical industry, which will provide medications to lower elevated blood cholesterol concentrations; the laboratories involved in measuring blood cholesterol levels in hundreds of millions of U.S. citizens; and the tens of thousands of medical practitioners involved in sampling their patients’ blood for cholesterol testing. In reality, the NCEP is little more than a targeted intervention by the U.S. pharmaceutical industry to prepare the U.S. public and their physicians for the introduction of a novel group of prescription drugs — the cholesterol-lowering statin drugs then still in development — that it hopes will provide the industry with an unprecedented financial windfall. In the end, the strategy works perfectly, as the statin drugs, first marketed a few years later, become one of the most financially lucrative drugs ever produced. This ushers in an era of unmatched profits for the pharmaceutical industry.
1989 The initial results of Keys’ Minnesota Coronary Experiment (MCE) are reported. Thirteen years after the results of the MCE first become available to the study scientists, they are finally published in a relatively obscure medical journal. This initial (1989) report claims the replacement of dietary saturated fat with the polyunsaturated fatty acid linoleic acid is neither beneficial nor harmful. The reality is that when Keys’ acolytes discover their original MCE data does not support Keys’ diet-heart hypothesis, in their embarrassment, they choose to bury the data. The later publication of the Recovered MCE results shows the low-fat dietary intervention not only failed to produce any benefits; in reality, it caused harm. Had these findings been honestly reported in 1976, they would likely have prevented the publication of the USDA Dietary Guidelines of Senator McGovern’s committee in 1977 and would have forestalled the global damage caused by the acceptance of those guidelines.
1989 The results of Dr. Robert Knoop’s Dietary Alternatives Study and the Boeing Employees Fat Intervention Trial (BeFIT) are published. By 1977, it had become clear to the Framingham Heart Study (FHS) researchers (and others) that an elevated blood cholesterol concentration is a very weak predictor of future CHD risk. For a brief period (1977-1979), those researchers published a series of papers showing that a low blood HDL cholesterol concentration is a much better predictor of CHD risk. However, after 1979, those same researchers, perhaps warned that this “unorthodox” opinion will harm their careers and future funding prospects should they persist, just as quickly reverted to their original opinion by embracing the conventional AHA/NIH party line: “Serum total cholesterol makes ‘a significant contribution to … coronary heart disease in persons older than 50 and practically up into the eighties’” (19).
1991 The results of the Helsinki Businessmen Study are reported. The goal of this study was to determine whether lifestyle modifications — in particular stopping smoking, achieving an ideal weight through the adoption of a “healthy” diet, moderation of alcohol use, and active drug treatment of those with hypertension or hyperlipidemia that did not respond to diet — would reduce the subsequent development of CHD. The study, like MRFIT, produces a seriously inconvenient finding. Although those in the intervention group succeed in reducing their CHD risk factors by 46%, their rates of CHD events during the follow-up are significantly higher than in the control group that had made no special attempt to modify risk factors. This paper has also been forgotten by history since it refutes what would otherwise appear to be common sense: Reversing coronary risk factors must reduce coronary risk.
1993 The Women’s Health Initiative Randomized Controlled Dietary Modification Trial (WHIRCDMT) is initiated. The goal of the WHIRCDMT is to determine whether a population of older women who adopted the USDA Dietary Guidelines for Americans would exhibit reduced risk of colorectal and breast cancers and suffer less from coronary heart disease. For the study, 48,835 post-menopausal women are randomized to one of two groups. Those in the control group are encouraged to continue eating their usual diet, whereas the intervention group adopts the USDA Dietary Guidelines by reducing fat intake and eating more vegetables and grains. Women in the intervention group also receive an “intensive behavioural modification program,” comprising 18 group sessions in the first year followed by quarterly maintenance sessions for the next seven years. The control group receives only a copy of Dietary Guidelines for Americans. As a result, any positive outcomes in the intervention group cannot be ascribed purely to dietary change, since the intervention group receives additional interventions not shared by the control group. The first results of the study are reported in 2005.
1993 Professor Walter Willett, MD, of Harvard University invents the Mediterranean Diet. In the 1980s, scientists in the three nations that produce much of the world’s olive oil — Greece, Italy, and Spain — began to wonder if perhaps it was olive oil in the diet of the Cretans that explains their low rates of CHD (as identified by Keys’ Seven Countries Study). Funded in part by support from those three governments between 1993 and 2004, about 50 olive-oil-sponsored conferences are held around the world, promoting the idea that the “Mediterranean Diet,” especially if it contained liberal amounts of olive oil, is especially healthy. At the very first conference, Willett presents his Mediterranean Diet Pyramid. The key differences from the food pyramid promoted by the 1977 U.S. Dietary Guidelines for Americans are that beans and legumes are the main source of protein, with fish, poultry, and eggs to be eaten only once weekly and red meat at most monthly. This conforms to Willett’s personal choice as someone who eats a predominantly plant-based diet. Paradoxically, over the past 30 years, meat consumption in France, Italy, Spain, and even among the Cretans, the Swiss, and the Japanese, has increased substantially. Despite this, heart disease rates have continued to fall in all those countries, even though average blood cholesterol concentrations, especially in Japan, have increased. These findings do not support Willett’s interpretation that the Mediterranean Diet is uniquely healthy because it limits the consumption of animal products.
1994 The findings of the Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Study are reported. The MONICA Study was initiated in 1974 with the goal of measuring trends in cardiovascular mortality and coronary heart disease and stroke morbidity in 21 countries, and assessing the extent to which these trends could be explained by changes in known risk factors, daily living habits, health care, or major socioeconomic features measured at the same time in those participating countries. The assumption was that falling rates of CHD in those countries would be explained by changes in the “classical” risk factors. The findings of the study are that perhaps as little as 15% of the variance in coronary event rates in women and 40% in men could be explained by trends in the classic coronary risk factors, indicating the so-called classic risk factors explain less than one half to three-quarters of the real factors explaining CHD. The findings are therefore in line with those from MRFIT, the WHO European Collaborative, the HBS, and the WHIRCDMT.
2003 The Look AHEAD (Action for Health in Diabetes) Trial is planned. The primary objective of the Look AHEAD clinical trial is to assess the long-term effects (up to 11.5 years) of an intensive weight loss program conducted over four years with overweight and obese individuals with T2DM. Approximately 5,000 male and female participants with T2DM, aged 45-74 years, with elevated body mass indexes, are randomized into one of two groups: an intensive lifestyle intervention group or the control group. The goal of the intensive lifestyle intervention is to produce sustainable weight loss through decreased caloric intake and increased physical activity. The control group receives diabetes support and education alone. The primary study outcome is the time to the development of the first major cardiovascular disease (CVD) event. The first results are reported in 2014.
2003-2013 The Prospective Urban Rural Epidemiology (PURE) Study is initiated. Between January 1, 2003, and March 31, 2013, the PURE Study enrolls and finally studies 135,335 individuals aged 35-70 years living in 628 urban and rural communities in 18 countries on five continents. The study includes three high-income countries (Canada, Sweden, and the United Arab Emirates), 11 middle-income countries (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, and Turkey), and four low-income countries (Bangladesh, India, Pakistan, and Zimbabwe). Upon entry to the study, participants complete standardized questionnaires that collect information about their socioeconomic status, lifestyle, health history, medication use, and physical activity. Food intake is assessed using validated, country-specific food frequency questionnaires. Follow-up occurs at three, six, and nine years. The initial goal of the study is to determine whether the burden of risk factors and the incidence of cardiovascular disease is “higher in low- and middle-income countries than in high-income countries, whether mortality after a cardiovascular event is higher in low- and middle-income countries than in high-income countries, or whether both are true.” In time, the study evolves into the most thorough epidemiological evaluation of the diet-heart and lipid hypotheses ever undertaken, dwarfing everything that had come before and most especially Keys’ error-ridden Seven Countries Study.
2005 The inconvenient results of the WHIRCDMT are reported. The published results of the WHIRCDMT show the low-fat “heart-healthy” diet fails to reduce risk for developing cancers of the colon, rectum, or breast; the diet also fails to influence CHD outcomes. In fact, the sole significant finding of the study, and the one the original scientific publication fails to hide, is that the health of postmenopausal women who began the trial with either CHD or T2DM worsened if they ate the low-fat diet. The study becomes the first in the trinity of studies (the WHIRCDMT, the Recovered MCE, and the Recovered SDHS) that establish the removal of saturated fat from the diet causes harm, thus revealing the prescription of low-fat diets that remove saturated fat is unethical. The study also finds the risk for developing T2DM is increased in women who are prescribed cholesterol-lowering statin drugs, and the low-fat diet did not increase weight loss compared to the usual American diet. All these findings are particularly inconvenient for the diet-heart hypothesis. This explains why the true findings of this study are conveniently buried.
2008 Results for the Weight Loss on Low-Carbohydrate, Mediterranean, or Low-Fat Diets Study are published. For this two-year trial, 322 moderately obese subjects with an average age of 52 years were randomly assigned to one of three diets: a low-fat, restricted-calorie diet; a Mediterranean, restricted-calorie diet “rich in vegetables and low in red meat, with poultry and fish replacing beef and lamb”; or a low-carbohydrate, non-restricted-calorie diet including 25 grams of carbohydrate/day for the first two months with a gradual increase to 120 g/day. Intake of total calories, protein, and fat were not limited in the latter diet, which is that described by Dr. Robert Atkins. The study establishes two irrefutable facts. First, it establishes that the AHA-prescribed low-fat diet performs dismally and is substantially worse than the Atkins low-carbohydrate diet. This has since been shown repeatedly, which is important since in defending its disproven diet, the AHA has wasted much effort vilifying the Atkins Diet. Second, the study establishes that the Mediterranean Diet is no better and in some cases is not as effective as the Atkins diet. This key fact has also been rigorously suppressed since the new but still unproven dogma is that the Mediterranean Diet is the optimum diet to lower CHD risk. However, in all relevant measures in this study, the Atkins Diet outperforms the Mediterranean Diet.
2012 The Look AHEAD Trial is terminated prematurely. This trial sought to use the conventional calories in, calories out (CICO) model of weight control to reverse obesity in persons with T2DM and so reduce the development of T2DM complications. In October 2012, the planned 11.5-year study is terminated as “futile” after 9.6 years when it is established that these interventions are no more effective in slowing the progression of arterial damage than doing nothing.
2013 The results of the Recovered Sydney Diet Heart Study (SDHS) are published. The original findings of the SDHS, which began in 1966, were reported in 1978 as the following: “Survival was slightly better in the second (dietary intervention) group. Multivariate analysis showed that none of the dietary factors were significantly related to survival.” But even then, the data did not support that conclusion. Rather, the data showed the intervention group that had replaced dietary saturated fats with an increased ingestion of polyunsaturated fatty acids actually did worse. But the extent of that outcome was buried as the results were incompletely analyzed and published in a relatively obscure medical journal. But when the original data are recovered and subjected to independent analysis 35 years later, a rather different result emerged. Thus: “The intervention group had (significantly) higher rates of death than controls” (20). These higher death rates in the intervention group occurred in all important categories: all cause, cardiovascular disease, and coronary heart disease. Had these findings been properly analyzed and honestly reported in 1978, they would have been accepted as disproof of Keys’ hypothesis and the world would not have been subjected to dietary guidelines based on a false and now frequently disproven hypothesis.
2016 The results of the Recovered Minnesota Coronary Experiment (RMCE) are published. On the death Ivan Franz II, the principal investigator of the MCE, his son, Ivan Franz III, discovers the original data for the MCE Trial. He submits the recovered computer files for analysis to those who had reported the Recovered Sydney Diet Heart Study (RSDHS). The recovered data confirm the original MCE report had misrepresented and significantly underplayed the true findings of the study by implying there were no differences in CHD outcomes between the control and intervention groups. In contrast, the RMCE establishes no age group benefitted from the intervention, but survival was significantly worsened in those over 65 who were placed on the intervention “heart-healthy” prudent diet. In addition, “there was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol (concentration)” (21). Thus, the evidence from the WHIRCDMT, the Recovered MCE, and the Recovered SDHS is unequivocal: Removing saturated fat from the diet causes harm to both men and women. It is therefore unethical ever to advise anyone to follow this dietary practice.
2017 A report is published on the association of food consumption, blood cholesterol concentrations, and cardiovascular disease in 42 European countries. A group of scientists from the Czech Republic uses international statistics to search for associational (non-causal) relationships between nutritional factors and the prevalence of cardiovascular disease in 42 European countries. The mortality data are derived from the European Cardiovascular Disease Statistics, whereas the nutritional information comes from the FAOSTAT website, which reports the “total quantity of foodstuffs produced in a country added to the total quantity imported and adjusted to any change in stocks that may have occurred during the reference period” (22). The overall conclusion from these associational relationships is eating more animal fat and protein and less carbohydrate is associated with higher blood cholesterol concentrations and a lower prevalence of hypertension and cardiovascular disease. While associational studies cannot prove causation, they can perhaps show what is unlikely to be true. The clearest evidence to refute Keys’ lipid hypothesis is the data showing an inverse relationship between actual CVD mortality rates in the 42 countries and the prevalence of raised blood cholesterol concentrations in those countries. The authors conclude: “Our results do not support the association between cardiovascular disease (CVDs) and saturated fat which is still contained in official dietary guidelines. Instead, they argue with data accumulated from recent studies that link CVD risk with the high glycemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered” (22, p. 1).
2017 The first results from the PURE Study are published. The key findings from this large study are that those living in countries with high carbohydrate intakes have higher rates of total mortality, whereas total fat and individual types of fat intake are associated with lower total mortality. Total fat intake and types of fat eaten are also not associated with cardiovascular disease, heart attack, or death from cardiovascular disease, but saturated fat intake predicts lower rates of stroke. The authors conclude: “Our data are at odds with current recommendations to reduce total fat and saturated fats. Reducing saturated fatty acid intake and replacing it with carbohydrate has an adverse effect on blood lipids. Substituting saturated fatty acids with unsaturated fats might improve some risk markers, but might worsen others. Simulations suggest that ApoB-to-ApoA1 ratio probably provides the best overall indication of the effect of saturated fatty acids on cardiovascular disease risk among the markers tested. Focusing on a single lipid marker such as LDL cholesterol alone does not capture the net clinical effects of nutrients on cardiovascular risk” (23, p. 776). The principal investigator in this study is Professor Salim Yusuf, Ph.D., who is one of the world’s most respected medical scientists. Yusuf was one of the few who were critical of the recommendations of the 1984 National Cholesterol Consensus Development Conference. In 2011, he was rated the world’s second-most-cited researcher, in part for his work on large-scale clinical trials that have had a significant impact on the treatment and prevention of cardiovascular and cerebrovascular disease. From 2015-16, he served as President of the World Heart Federation, and during this time, he dropped the findings of the PURE Study on an unsuspecting world. Predictably, his apparent desertion of the Keys’ diet-heart hypothesis is not universally appreciated by those medical and scientific colleagues who saw little value in the tentative conclusion he and his team had drawn from an epidemiological associational study. However, they apparently had few qualms about the fact that Keys’ hypotheses are also based on epidemiological associational studies of much poorer quality. In particular, the dietary analyses in the PURE Study were exceptionally well conducted.
2017 The first results of the Virta Health Study are reported. In 2014, Finnish entrepreneur Sami Inkinen teamed up with two of the original and most respected low-carbohydrate diet investigators, Stephen Phinney, MD, and Jeff Volek, Ph.D., to form Virta Health. The goal was to advance the work of Atkins, Westman, Phinney, and Volek, and to determine whether T2DM might be “reversed” by a ketogenic low-carbohydrate diet. Inkinen’s genius was to realize T2DM is ultimately a behavioral disease caused by poor dietary choices in those with insulin resistance. He realized its reversal cannot be achieved by the prescription of therapeutic drugs and occasional visits to medical specialists. Instead, it requires that the patient with T2DM receive continuous feedback, advice, and encouragement on a moment-to-moment basis. Inkinen and his team appreciated that this could only be achieved through a radical new medical model: the Virta Health Clinic model, which “has reinvented the diabetes care model by providing patients with continuous, technology-enabled remote care from Virta medical providers who are experts in safely reducing and eliminating diabetes medications.” The remote care Virta Clinic was developed in 2015; shortly thereafter, 262 subjects with T2DM, aged between 21-65 years, were recruited to participate in a five-year study of the effects of the intervention on multiple health markers. To date, outcome results have been reported at three, 12, and 24 months. After one year, 60% of subjects had “reversed” their T2DM by lowering their HbA1c values to below 6.5%, representing an average 1.3% reduction in HbA1c values (despite reduced medication use). Furthermore, 94% had either reduced or eliminated insulin use. Subjects also lost an average of 12% of body weight, equivalent to 14 pounds. Changes in conventional metabolic risk factors for coronary heart disease were also dramatic. When compared to subjects receiving conventional management for T2DM, those receiving the Virta intervention showed significantly greater benefits in the form of increased ApoA1 and HDL-C concentrations; reduced high sensitivity CRP values (a measure of inflammation); reduced triglyceride/HDL-C ratios; reduced ApoB/ApoA1 ratios; reduced total LDL particle numbers and especially reduced in small, dense LDL particle numbers; reduced large VLDL particle numbers; reduced blood pressure and reduced anti-hypertensive medication use; and reduced white blood cell counts. As a result, 10-year atherosclerotic cardiovascular disease (ASCVD) risk had decreased 12%. Thus, the study establishes that T2DM is a reversible medical condition. However, its reversal requires the prescription of a high-fat, low-carbohydrate ketogenic diet — the opposite of Keys’ low-fat, high-carbohydrate diet. The study also confirms that the prescription of a high-fat diet reverses all established metabolic risk factors for CHD with the exception of LDL cholesterol, which might increase modestly in some. The Virta Study provides the ultimate repudiation of Keys’ diet-heart hypothesis.
2019 Professor John Ioannidis, MD and Ph.D., declares nutritional epidemiology is a scandal: “It should just go in the waste bin.” Ioannidis is one of the world’s most influential medical scientists whose special interest is the quality of the evidence used to make medical decisions. In the 1990s, he turned his attention for the first time to nutritional epidemiological science. He showed the nutritional sciences are especially weak because they lack hard evidence and have an overreliance on epidemiological associational studies with statistically weak outcomes that cannot prove causation. Thus, he argued, “thousands of spuriously significant associations have already been produced and translated in heavily opinionated, debated recommendations. Getting another significant result in a field that is already saturated with so many significant results offers no information gain: we still (think we) know what (we thought) we knew. Conversely, ‘negative’ results offer high information gain, because they change our probably false beliefs about potentially effective interventions … we should hope to get more ‘negative’ results in the future” (24, p. 1386). Essentially, he suggests the need for a revolution in how nutritional research is conducted and how the results are interpreted. Most of that which has been done before needs to be thrown “in the waste bin,” he says.
2019 A collection of six articles published in the Annals of Internal Medicine exonerates the consumption of red and processed meats as a significant cause of ill health in humans. The fundamental basis for Keys’ hypotheses was that the U.S. diet had changed radically in the years before the outbreak of the CHD epidemic, beginning in the 1920s. The primary change, according to this logic, was that U.S. citizens had exchanged a diet high in cereals and grains for one full of animal fats, especially saturated fats. But actual data of what U.S. citizens were eating in the 18th, 19th and early 20th centuries simply does not show that. Meat consumption had dropped progressively before beginning to rise again in the mid-20th century. Thus, Keys’ hypotheses were based on a fundamental flaw in logic. These studies confirm that replacing meat in the diet is not associated with measurable health benefits.

Conclusion

On the basis of all this information, it is extremely difficult — in fact impossible — to make any credible case supporting Keys’ hypotheses.

In the following 11 columns, I provide the details behind each of these 70 events before providing a final summary of exactly what the multibillion-dollar research effort to find support for Keys’ hypotheses actually revealed.

It is finally time to expose this evidence more widely, but especially to the medical and nutrition/dietetics professions, so that in 2020, we can give humans the appropriate dietary advice that will return us all to a state of optimum metabolic health.


Additional Reading


References

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