The original fake medical news story – Prof Noakes on Ancel Keys’ Cholesterol Con

In the previous series by Professor Tim Noakes, ‘It’s the insulin resistance, stupid’, Noakes’ focus came down to the apparent loss of interest by Ancel Keys in hard science and the consequences of the global update of his inaccurate hypothesis ‘proving’ an epidemiological link between cholesterol and cardiovascular disease. In Part 1 of this next series by Noakes, ‘Ancel Keys’ Cholesterol Con’, Noakes points out that “Keys’ religious certainty made him the immaculate disciple for the promotion of what would soon become a politically and commercially-driven agenda, the consequences of which have been so catastrophic for global health. In a world where, particularly relating to Covid-19, previous information presented with the same ‘religious certainty’ is being overturned on an ever-increasing basis, there appears to be a lot to learn from the global oversight in respect of the biggest medical con artist to date, Ancel Keys. – Nadya Swart

Ancel Keys’ Cholesterol Con, Part 1. How an insecure and unproven hypothesis became a global unchallenged dogma

By Prof Tim Noakes

“THE METHOD OF SCIENCE IS THE METHOD OF BOLD CONJECTURES AND INGENIOUS AND SEVERE ATTEMPTS TO REFUTE THEM,’ SAID KARL POPPER, THE DEAN OF THE PHILOSOPHY OF SCIENCE. POPPER ALSO NOTED THAT AN INFINITE NUMBER OF POSSIBLE WRONG CONJECTURES EXIST FOR EVERY ONE THAT HAPPENS TO BE RIGHT. THIS IS WHY THE PRACTICE OF SCIENCE REQUIRES AN EXQUISITE BALANCE BETWEEN A FIERCE AMBITION TO DISCOVER THE TRUTH AND A RUTHLESS SCEPTICISM TOWARD YOUR OWN WORK. THIS, TOO, IS THE IDEAL, ALBEIT NOT THE REALITY, OF RESEARCH IN MEDICINE AND PUBLIC HEALTH.” 

In the previous column (2) I showed how Ancel Keys first stole the ideas of the Diet-Heart and Lipid Hypotheses from Dr John Gofman MD. To conceal his own grave academic limitations – in particular, his absence of training in medicine, cardiology and lipidology (the study of blood fats) – he found the perfect diversion in the discipline of nutritional epidemiology for which he required no special skills or training. Masquerading behind this covert scientific pretence, he promoted weak associational data from that freshly discovered academic discipline as if it were definitive proof for his, actually Gofman’s, hypotheses. Yet he was fully aware that associational data cannot prove causation except under a few exceptional circumstances; circumstances that Keys’ especially weak associational data could never establish. 

Only ever in passing did Keys acknowledge this fatal weakness in his false claims. It was as if he believed that in every other case, associational data do not prove causation. But his claim was different. Since they were his ideas (even if purloined), then they had to be correct. Even when his proof failed all accepted scientific canons. His truth, he knew, was so absolute, so perfect, it required no human proof. It was biblical. With time he would collect a bevy of disciples who would faithfully spread his false prophecy to all corners of the Earth.

Keys’ goal was not to use science to discover an ultimate truth for the benefit of humankind. He was rather more mercenary. His fancy was to become the global nutritional megastar, “Mr Cholesterol”. Or, as Nina Teicholz describes, his personal goal to be “by far, the Greatest Man (in nutrition)” (3, p.46). Especially as all this was happening in the heady post-war 1950s; when coronary heart disease (CHD) was supposedly reaching “epidemic” proportions in the US and elsewhere. At the exact time when the premier focus of medical research in the US and the western world had become the need to find an urgent solution to the CHD “crisis”.  Keys’ proposed solution was particularly appealing because it was really so very simple. So everyone could easily understand it: Remove saturated fat from the diet. Do this and Keys’ prediction was that the CHD “problem” will disappear: “(If) mankind stopped eating eggs, dairy produce, meat and all visible fats…(coronary heart disease would) become very rare” (4, p. 99). 

For the record, Keys’ solution at the time (January 1952) was the following: “I would recommend a sharp reduction in all dietary fats without paying any special attention to the cholesterol content of the diet. I would allow the use of an ordinary amount of eggs and milk in cooking, the use of skim milk for cereals and as a beverage, a good daily serving of lean meat or fish, and a boiled or poached whole egg for Sunday; but no butter, cream, oleomargarine, salad oil, mayonnaise, fried foods, gravy, ice cream, chocolate, or pastries made with shortening. Periodic measurements of serum cholesterol may help to judge the severity with which such restrictions should be maintained” (4, p. 99). 

Keys confidently provided this advice despite an absolute absence of any evidence at the time to support his developing dogma. Clearly he just “knew” what was going to save the world from the scourge of coronary heart disease.

In contrast to Keys’ absolute certainty, one of the world’s leading cardiologists of the day, Louis Katz MD, warned that he would prescribe this low-fat low-cholesterol diet only: “When a patient has had two or more attacks of coronary insufficiency and/or myocardial infarction attributable to coronary atherosclerosis, and if that patient has a cholesterol level in the upper limits of normal, or above… Otherwise, I would not, because I am a firm believer in the view that prohibitions should not be carelessly advocated until such time as it is clearly revealed that the prohibition has a great chance of being beneficial to the patient” (4, p. 99)). Importantly Katz was a world-leading cardiologist who actually treated patients with heart disease. He also had a penchant for asking difficult (and relevant) questions (5) whilst Keys had no training in either medicine or cardiology. Yet remarkably Keys’ unproven opinions would ultimately win the argument over more qualified clinicians like Katz. For Keys had effectively positioned himself as the right man in the right place at exactly the right time. And with the certainty that only he had the most conclusively correct solution. 

So when, in the late 1960s, Keys became one of the original beneficiaries of research funding from the newly formed National Heart, Lung, and Blood Institute (NHLBI), he discovered, to his utter dismay (and perhaps horror) that, far from supporting his claims, his brilliantly designed and perfectly executed test – The Minnesota Coronary Experiment  (MCE) (6) – comprehensively disproved both his hypotheses. According to Popper’s description that a real scientist is someone imbued with a “ruthless scepticism toward your own work”, had Keys been just such a scientist, this should have been the end of his hypotheses. For the MCE established that the replacement of dietary saturated fat with the polyunsaturated fatty acid (PUFA), linoleic acid, which lowered average blood cholesterol concentrations by 15%, to the apparently “safe” level of 175mg/dL (4.6mmol/L), had absolutely no effect on heart disease outcomes. Instead “no differences between the treatment and control groups were observed for cardiovascular events, cardiovascular deaths or total mortality” (6, p.129).  This finding fatally dispatched Keys’ hypotheses because the MCE established that when tested in a rigorous and essentially flawless trial, lowering blood cholesterol concentrations to ‘safe’ levels with the precise dietary changes that Keys promised would prevent CHD, no such outcomes were achieved. But instead of declaring this inconvenient truth, as all honest scientists must and will do (or, at least, they once used to do), the authors (7) invented two novel explanations that have since become the go-to excuse for nutritional scientists whose experiments disprove their deeply held biases. 

First, they declared that it is not their theory that is wrong. How could that possibly be? “Although the study did not show a statistically significant reduction in cardiovascular events or total deaths from the treatment, the authors suspect (my added emphasis) that it might have shown such a reduction if the period of treatment had been longer in persons in the age range likely to benefit” (6, p.134). 

In other words, in breach of the Popper Principle, the authors know (beforehand) that their ideas are correct; the scientists cannot be wrong and so their ideas cannot be questioned. If the experiment failed to produce the expected results in line with their predictions, then it is not they, the scientists, who could possibly be wrong. Instead it is clearly the experiment that has failed. And it is in error for the very obvious reason that it failed to prove that the authors’ utterly brilliant theory is wholly correct. When they did not find the result they wanted, the MCE authors simply buried the findings as if the study had never been done. The tragedy was that, hidden in the data, was the evidence that the diet caused harm (8). That re-analysis by independent scientists established that removing saturated fat from the diet to lower the blood cholesterol concentrations, caused measurable harm. The effect was especially marked in those over 65 years of age (see Figure 10 in reference 9). 

Had those data been properly analysed and published in 1976 when they became available, the dietary advice that developed subsequently, in particular the 1977 US Dietary Guidelines developed by Senator George McGovern’s hopelessly under-qualified committee (as I discuss subsequently (10)) could not have happened. For the reason that it is not ethical to prescribe to a single individual, let alone to an entire nation, an intervention that is known beforehand to cause harm, even if that harm occurs to only a tiny minority. This is the foundation for ethical medical practice: First do not harm. This same post-hoc rationalization would be used by the Directors of the $700 million Women’s Health Initiative Randomized Controlled Dietary Modification Trial (WHIRCDMT), discussed subsequently (11), which also failed to show any benefit of replacing dietary saturated fat with polyunsaturated fatty acids (PUFAs), even though that dietary intervention also lowered blood cholesterol concentrations (12).  

I suspect that the NHI was absolutely certain that the WHIRCDMT would  provide the ultimate Nobel Prize-winning proof of Keys’ hypotheses (13, p.60-62). They were certain that their deluxe trial, for which no cost had been spared, would finally provide the definitive proof for the benefit of a low-fat, cholesterol-lowering diet in the prevention of coronary heart disease (CHD). Evidence that a host of studies (to be described) pursued over 30 years at a cost of hundreds of millions of dollars of US taxpayers’ money, had stubbornly refused to provide. 

In the end the WHIRCDMT found, as had the Recovered MCE, that the replacement of dietary saturated fat causes harm especially to those with pre-existing heart diseases or type 2 diabetes mellitus (11). The third study in what should now be referred to as this nutritional holy trinity is the Recovered Sydney Diet Heart (Recovered SDHS) Study (14). In that study subjects with a previously documented heart attack were randomized to either a group that continued eating as they always had, or to one in which dietary saturated fat was replaced with the polyunsaturated fat (PUFA), linoleic, acid extracted from safflower. Whilst the original study (15) reported that the diet was neither harmful nor helpful, when the original data were recovered and re-analysed by independent scientists (14), it became clear that the diet had caused harm, as I discuss more fully in a subsequently column (16).

I argue that these three RCTs – the WHIRCDMT, the Recovered MCE and the Recovered SDHS costing a total close to $1 billion – have unequivocally established that removing saturated fat from the diet causes harm. So powerful is this evidence that, in my opinion, it should be the end of the debate.

So any one of these studies should, by itself, have brought to an end, the idea pioneered by Ancel Keys, that humans should avoid eating saturated fat since saturated fat is the driver of coronary heart disease. For the simple reason that those three studies prove once and for all, that any dietary advice based on Keys’ false hypotheses is not just wrong; it is unethical. It is unethical because advising anyone, on supposedly medical grounds, to adopt a practice that has been shown to cause harm in some, breaches the first rule of ethical medical care. Which is: First do no harm.

Worse, it is not as if we had not been warned.

The first trial of the low fat diet enriched with polyunsaturated fats was the Diet and Coronary Heart Disease Study Project, popularly referred to as the Anti-Coronary Club Program in New York City. The study (17) reviewed in detail subsequently (18) began in 1957 and continued until 1972. Unfortunately in 1961, during the trial, its principal investigator Dr Norman Jolliffe died suddenly of a heart attack. And whilst the clinicians who continued the trial after Jolliffe’s death claimed that his Prudent Diet reduced the number of coronary events, hidden in their data was one very inconvenient fact: There were more deaths in the group that followed the Anti-Coronary Diet. Clearly the Prudent Diet had not helped the Anti-Coronary Club members to live any longer. 

The next published clinical trial of a modified diet to treat patients after heart attack was conducted at a group of Middlesex hospitals in the United Kingdom (19). The tested diet had a reduced fat content – there was no substitution of fat with polyunsaturated fats. Subjects in the intervention group were restricted to 40 grams of fat each day provided by 14 grams of butter, 84 grams of meat, I egg, 56g of cottage cheese and skimmed milk. The diet was not popular: “The diet was often unpleasant…The main objections were to the skimmed milk, and to the small butter ration…and to the restriction on biscuits and cakes” (19, p.501). Patients eating this “unpleasant” diet lost more weight and showed greater reductions in blood cholesterol concentrations. But the incidence of new cardiac events was not different between diet groups. Thus the authors concluded prophetically: “A low fat diet had no place in the treatment of myocardial infarction (heart attack)” (19, p.504). If that conclusion had been accepted in 1965, the world would have been saved 55 years of futile efforts by the NHI and the AHA to prove the opposite. The third relevant study was the second to evaluate the replacement of dietary saturated fat with PUFAs in patients who had recently suffered a heart attack (20). It found that “the patients receiving the key treatment (corn oil) fared worse than those in the other two groups: two years from start of treatment, infarction or death had occurred in one-quarter more of the corn-oil than of the control group. This difference closely approaches the conventional significance level (0.1>P>0.05)” (20, p.1533). 

The authors warned: “It is concluded that under the circumstances of this trial, corn oil cannot be recommended in the treatment of ischaemic heart disease” (20, p.1533). Thus already by 1965 three trials of low fat diets in real heart attack patients living in the real world had found no evidence for benefit to cardiovascular health and only indications of harm. Then another eight-year study (21) reported a higher incidence of cancers in a group of men who had replaced saturated fat with “vegetable” (seed) oils. Thus whereas the number of fatal CHD deaths were higher in the control group, deaths from cancer were increased (31 vs 17) in the intervention group. As a result, all-cause mortality was the same in both groups, again confirming no benefit and the potential for harm when dietary saturated fat is removed from the diet and replaced by “vegetable” oils. 

The potential link between cancer and diets high in PUFAs or in individuals with low blood cholesterol concentrations (22-40) – not necessarily because they had been prescribed cholesterol-lowering diets (or drugs) – became a problem for the NHLBI in the 1980s and continues today (41-43).  As does the evidence for an association between low blood cholesterol concentrations and a range of other medical and behavioural conditions (44-62). Predictably this relationship is never raised by those promoting the AHA/NHI position that “the lower the blood cholesterol concentration, the better”.  

To investigate the matter or, perhaps more accurately, to scotch any speculation that low fat dietary advice could ever do anything other than good – by preventing and reversing CHD – the NHLBI convened 3 workshops between 1980 and 1982 (1, p. 54). The NHLBI faithfully concluded that “the evidence didn’t imply cause and effect. They believed that high cholesterol caused heart disease and that low cholesterol was only a sign of people who might be cancer-prone because of a genetic predisposition” (I, p.55). As a result, and very conveniently, “the data do not preclude, countermand, or contradict the current public health message which recommends that those with elevated cholesterol levels seek to lower them through diets lower in saturated fat and cholesterol” (41; 42, p.2503S).

In a further NHLBI Conference in October 1990, any possibility that adverse outcomes were the direct result of low blood cholesterol concentrations was once more fudged: “Conclusions. Definitive interpretation of the association observed was not possible, although most participants considered it likely that many of the statistical associations of low or lowered total cholesterol level are explainable by confounding in one form or the other. The conference focused on the apparent existence and nature of these associations and on the need to understand the source rather than on any pertinence of the findings for public policy” (43, p.1046). 

In other words, the Conference participants all of whom derived substantial benefit from the status quo – which is dependent on Keys’ Twin Hypotheses being correct – reached a consensus based on nothing better than their personal biases, that a low blood cholesterol concentration is not a direct cause of any adverse health outcome. And because of their certainty that this is true, the general public should not be informed that this is even an issue of concern. Case closed even in the absence of definitive proof. 

Recall, of course, that then as now, the NHLBI had no evidence whatsoever that lowering “elevated” blood cholesterol concentrations with diets low in saturated fat and cholesterol provided any benefits.  But any possibility that this dietary intervention might cause harm was simply ignored. As remains the case today. This is a remarkable achievement for this small group of medical scientists. 

As a result, any possibility that interventions that lower blood cholesterol concentrations might also increase risk of death from cancer or be linked to other serious medical or abnormal behavioural conditions, has been conveniently written out of the scientific record. It is a forbidden subject in all medical schools across the globe. It is quite simply unmentionable.

How and why did Keys and his cronies bury the negative findings from the MCE?

So why did Keys and his cronies ignore what should have been very worrying findings from the SDHS and the MCE?  And why did they fail to uncover and report, as was their scientific duty, the clear evidence for harm in the MCE subsequently detected by Ramsden et al. (8)? Or the evidence for harm that was clearly apparent in the SDHS, also to be subsequently uncovered by Ramsden and his colleagues (14)? The son of the first author of the original MCE paper, Dr Ivan Franz, suggested the following: “My feeling is, when the overall objective of decreasing deaths by decreasing cholesterol wasn’t met, everything else seemed less compelling. I suspect there was a lot of consternation about why (they couldn’t find a benefit). The idea that there might be something adverse about lowering cholesterol (via vegetable oils) was really antithetical to the dogma of the day” (63). Or in the words of Steven Broste whose 1981 MSc thesis analysed the original MCE data: “The results flew in the face of what people believed at the time. Everyone thought cholesterol was the culprit. This theory was so widely held and so firmly believed – and then it wasn’t borne out by the data. The question then became: Was it a bad theory? Or was it bad data?…My perception is that they were hung up trying to understand the results” (64). 

A lead author of the Recovered MCE, Daisy Zamora, concluded that: “Had this research been published 40 years ago, it might have changed the trajectory of diet-heart research and recommendations” (64), a chilling thought. All this invites the obvious question: If scientists can’t accept the evidence of their own experiments, especially when that evidence runs contrary to their firmly-held beliefs, then why do they bother to conduct experiments in the first place? These actions show that they are not disinterested scientists searching for an ultimate truth. They were pursuing some other purpose. Had Keys demanded that those data be thoroughly scrutinized and published in the 1970s instead of 46 years later as was his ethical responsibility – after all he was spending public money and the public have the right to hear the whole truth not the “truth” the scientists want them to believe – there would have had one significant consequence that, to my knowledge, no modern ethicist has yet identified.  They would have forced the termination of all future clinical trials of diets that aimed to lower blood cholesterol concentrations by removing saturated fat from the diet. 

For the very simple reason that I have already described: The overriding medical tenet is: First do no harm. 

Armed with the evidence from the MCE and the SDHS (and later the WHIRCDMT) that removing saturated fat from the diet causes harm, it would have been unethical for any medically-trained research scientist to participate in a trial that was known to put the health of even a single trial participant at risk. No future study would have received ethical approval for a University Review Board. Instead, as a result of Keys’ inaction, based on his scientific solipsism that his was the only opinion that mattered, and strengthened by his religious certainty that he was correct (and, besides, his career had to be protected), the future health of the entire world has been harmed. As Andrew Mente PhD, senior scientist of the Prospective Urban Rural Epidemiology (PURE) studies (65), which produced results that are the polar opposite of those from Keys’ Seven Countries Study (11), posted recently on his Twitter account (@andrewmente): “The basis of science is scepticism; the basis of religion is faith”.

Keys and his acolytes had long since crossed the slender boundary dividing scepticism from faith – demarcating science from religion.  For already in June 1953 at the Annual Health Conference of New York held at Lake Placid, and well before he had conducted a single test of his hypotheses, Keys confirmed his religious certainty: “Many factors are probably involved in the clinical appearance of coronary heart disease, but 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 (4, 66-69). No other etiological factor of comparable importance is as yet identified” (70, p.1399-1400).

But the references cited by Keys are mainly personal opinions and none provide definitive support for Keys’ contention. In fact William Dock MD, then Professor of Medicine at the Long Island College of Medicine had a somewhat different opinion: “Today, over most of the earth, want is the rule, and atherosclerosis is being prevented by chill penury. Where a luxus diet prevails, diabetes and atherosclerosis flourish” (71, p.188). Subsequently he wrote: “…by the time thrombosis and clinical disease occur, cholesterol or beta-lipoprotein levels in many populations are relatively less elevated in coronary cases than are the plasma triglyceride levels (my added emphasis). The latter affect platelet stickiness, fibrinolysin, and plasma clotting times more than do the beta-lipoproteins” (71, p. 794). So unlike Keys, Dock recognized that dietary carbohydrates and fats had different effects on blood cholesterol and triglyceride concentrations since he cited the study of MacDonald and Braithwaite (72) which showed this. We turn later to the evidence that MacDonald somehow forgot about the importance of this finding when he became the leading modern Professorial apologist for sugar and dietary carbohydrates (73).

Gary Taubes neatly describes the trap into which Keys would fall: “Believing that your hypothesis must  be correct before all the evidence is gathered encourages you to interpret the evidence selectively. This is human nature. It is also precisely what the scientific method tries to avoid. It does so by requiring that scientists not just test their hypotheses, but try to prove them false. ‘The method of science is the method of bold conjectures and ingenious and severe attempts to refute them,’ said Karl Popper, the dean of the philosophy of science. Popper also noted that an infinite number of possible wrong conjectures exist for every one that happens to be right. This is why the practice of science requires an exquisite balance between a fierce ambition to discover the truth and a ruthless scepticism toward your own work. This, too, is the ideal, albeit not the reality, of research in medicine and public health” (1, p.24-25). But for Keys and his acolytes there was no place for scepticism. Instead Keys insisted that “each new research adds detail, reduces areas of uncertainty, and, so far, provides further reasons to believe” (1, p.25).

Einstein, who discovered an ultimate Universal truth, wrote the exact opposite: “No amount of experimentation can ever prove me right; a single experiment can at any time prove me wrong”. But Keys and his cronies pioneered an opposite belief. They believed that a single experiment could prove them right. And no amount of contrary findings could ever prove them wrong. So they always searched for the single study they could market as the definitive proof of their speculative hypotheses. Every other study was irrelevant and, in their minds, could legitimately be suppressed. The sadness is that their attitude still dominates the disciplines of medicine and nutrition today.

So it was that Keys’ religious certainty made him the immaculate disciple for the promotion of what would soon become a politically- and commercially-driven agenda. The consequences of which have been so catastrophic for global health.

It wasn’t just Ancel Keys. He needed a host of influential fellow travellers.

The reality is that, on his own, Keys could not have bullied the disciplines of nutrition and medicine into abandoning scientific scepticism for religious certainty, beginning in 1953 and continuing essentially unchallenged to the present day. To achieve that fundamental transformation, he needed the active support of many powerful and influential persons and institutions. Those who would also invest billions of dollars to undertake a specific brand of research designed to promote, not falsify, this new dogma.

For the first 40 years of my professional career I, probably like almost all medical doctors, was completely blind to the magnitude of this deception and the nature of the forces directing it. Only when I read and re-read the game-changing books by the pathfinders for truth in this matter – Russell L. Smith and Edward R. Pinckney (74), Thomas J. Moore (75), Gary Taubes (1) and Nina Teicholz (3) – did I being to understand the truth, even if at first only dimly. 

In the remaining columns in this series, I will highlight the key scientific events over the past 100 years that produced what is the original fake medical news story – the adoption of Keys’ Diet-Heart and Lipid Hypotheses as indisputable medical dogmas. This happened not just in the absence of definitive supportive evidence. But rather in the face of an irrefutable body of evidence that definitively proves and continues to prove more resolutely every new day, that both are false (74,76-80). My aim is to show how this scam unfolded and why a greater public understanding of exactly how we have been lied to for more than 100 years, is the sole antidote to reverse the massive harm to global health that these untruths have caused.

 References 

  1. Taubes G. Good calories bad calories. Fats, carbs, and the controversial science of diet and health. Anchor Books, New York, NY. 2008.
  2. Noakes TD. It’s the insulin resistance, stupid: Part 6. Crossfit Essentials
  3. Teicholz N. The Big Fat Surprise. Why butter, meat and cheese belong in a heathy diet. Simon and Schuster, New York, NY. 2014. 
  4. Allen EV, Katz LN, Keys A, Gofman JW. Atherosclerosis: A symposium. Circulation 1952;5;99-100.
  5. Weisse AB. Re
    membering Louis N. Katz, MD (1897-1973). Circulation 1998;97:1338-1339.
  6. Frantz ID, Dawson EA, Ashman PL, et al. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey. Arteriosclerosis 1989;9:129-135.
  7. What is particularly interesting about the MCE is that Keys was the senior researcher, the Principal Investigator, on the project. But when the first paper describing the results was published in 1989 (6), Keys’ name is not included as an author. Perhaps once it failed to support his hypothesis, he no longer wanted to be associated with the study?
  8. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016;353:i1246.
  9. Noakes TD. It’s the insulin resistance, stupid: Part 8. Crossfit Essentials
  10. Noakes TD. It’s the insulin resistance, stupid: Part 19. Crossfit Essentials
  11. Noakes TD. It’s the insulin resistance, stupid: Part 22. Crossfit Essentials
  12. Howard BV, Van Horn L, Manson JE et al. Low-fat dietary pattern and risk of cardiovascular disease. The Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006;295:655-666.
  13. Noakes TD, Sboros M. Real Food on Trial. Columbus Publishing, UK. 2019. 
  14. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death. Evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013 Feb 4;346:e8707.
  15. Woodhill JM, Palmer AJ, Leelarthaepin B, et al. Low fat, low cholesterol diet in secondary prevention of coronary hear
  16. t disease. Adv Exper Med Biol 1978; 109:317-31
  17. Noakes TD. It’s the insulin resistance, stupid: Part 23. Crossfit Essentials. PLEASE COMPLETE
  18. Singman HS, Berman SN, Cowell C, et al. The Anti-Coronary Club: 1957-1972. Am J Clin Nutr 1980;33:1183-1191.
  19. Noakes TD. It’s the insulin resistance, stupid: Part 15. Crossfit Essentials
  20. Research Committee. Low-fat diet in myocardial infarction. A controlled trial. Lancet 1965;7411:501-504.
  21. Rose GA, Thomson WB, Williams RT. Corn oil in treatment of ischaemic heart disease. BMJ 1965;1;1531-1533.
  22. Pearce ML, Dayton S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1971;297:464-467. 
  23. Nydegger UE, Butler RE. Serum lipoprotein levels in patients with cancer. Cancer Res 1972;32:1756-1760.
  24. Kark JD, Smith AH, Harmes CG. The relationship of serum cholesterol to the incidence of cancer in Evans County, Georgia. J Clin Epidemiol 1980;33:311-322.
  25. Williams RR, Sorlie PD, Feinleib M, et al. Cancer incidence by level of cholesterol. JAMA 1981;245:247-252.
  26. Kagan A, McGee DL, Yano K, et al. Serum cholesterol and mortality in a Japanese-American population. The Honolulu Heart Program. Am J Epidemiol 1981;114:11-20.
  27. Kozarevic Dj, McGee D, Vojvodic N, et al. Serum cholesterol and mortality. The Yugoslavia Cardiovascular Disease Study. Am J Epidemiol 1981;114:21-28.
  28. Dyer AR, Stamler J, Paul O, et al. Serum cholesterol and risk of death from cancer and other causes in three Chicago epidemiological studies. J Clin Epidemiol 1981;34:249-260.
  29. Garcia-Palmer MR, Sorlie PD, Costas R, et al. An apparent inverse relationship between serum cholesterol and cancer mortality in Puerto Rico. Am J Epidemiol 1981;114:29-40.
  30. Miller SR, Tartier PI, Papatestas AE, et al. Serum cholesterol and human colon cancer. J Nat Cancer Inst 1981;67:297-300.
  31. Stemmerman GN, Nomura AMY, Hellbrun LK, et al. Serum cholesterol and colon cancer incidence in Hawaiian Japanese men. J Nat Cancer Inst 1981;67:1179-1182.
  32. Williams RR, Sorlie PD, Feinleib M, et al. Cancer incidence by level of cholesterol. JAMA 1981;245:247-252.
  33. Kark JD, Smith AH, Hames CG. Serum retinol and the inverse relationship between serum cholesterol and cancer. BMJ 1982;284:152-154.
  34. Stemmerman GN, Nomura AMY, Hellbrun LK. Dietary fat and the risk of colorectal cancer. Cancer Res 1984;44:4633-4637.
  35. Salmond CE, Beaglehole R, Prior IAM. Are low cholesterol values associated with excess mortality. BMJ 1985;290:422-424.
  36. Schatzkin A, Taylor PR, Carter C, et al. Serum cholesterol and cancer in the NHANES 1 epidemiologic followup study. Lancet 1987;330:298-301.
  37. Stemmerman GN, Chyou P-H, Kagan A, et al. Serum cholesterol and mortality among Japanese-American Men. The Honolul
  38. u (Hawaii) Heart Program. Arch Intern Med 1991;151:969-972.
  39. Weverling-Rinjsburger AWE, Blauw GJ, Lagaay AM, et al. Total cholesterol and risk of mortality in the oldest old. Lancet 1997;350:1119-1123.
  40. Lavinge PM, Jafri H, Karas R. The association between lower levels of low-density lipoprotein cholesterol and cancer predates the diagnosis of cancer by 18 years. J Am Coll Cardiol 2012;59(13):E1622.
  41. Sung K-C, Huh JH, Ryu S, et al. Low levels of low-density lipoprotein cholesterol and mortality outcomes in non-statin users. J Clin Med 2019;8:1571.
  42. Nago N, Ishikawa S, Goto T, Kayaba K. Low cholesterol is associated with mortality from stroke, heart disease, and cancer. The Jichi Medical School Cohort Study. J Epidemiol 2011;21:67-74.
  43. Feinleib M. Summary of a workshop on cholesterol and noncardiovascular disease mortality. Prev Med 1982;11:360-367.
  44. Feinleib M. Review of the epidemiological evidence for a possible relationship between hypocholesterolemia and cancer. Cancer Res 1983;43(5 Suppl):2503s-2507s. 
  45. Jacobs D, Blackburn H, Higgins M, et al. Report of the conference on low blood cholesterol: mortality associations. Circulation 1992;86:1046-1060.
  46. Schupf N, Costa R, Lushsinger J, et al. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219-226.
  47. Bathum L, Christensen RD, Perdersen LE, et al. Association of lipoprotein level with mortality in subjects aged 50+ without previous diabetes or cardiovascular disease: A population-based register study. Scand J Prim Health Care 2013;31:172-180.
  48. Claxton AJ, Jacobs DR, Welles IC, et al. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. J Acq Immune Def Syndr Hum Retrovirol 1998;17:51-57.
  49. Mufti RM, Balon R, Arfken CL. Low cholesterol and violence. Psychiatr Serv 1998;49:221-224.
  50. Neaton JD, Wentworth DN. Low serum cholesterol and risk of death from AIDS. AIDS 1997;11:929-930.
  51. Iribarren C, Jacobs DR, Sidney S, et al. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiol Infect 1998;121:335-347.
  52. Iribarren C, Jacobs DR, Sidney S, et al. Serum total cholesterol and risk of hospitalization, and death from respiratory disease. Int J Epidemiol 1997;26:1191-1202.
  53. Ellison LE, Morrison HI. Low serum cholesterol concentration and risk of suicide. Epidemiol 2001;12:168-172.
  54. Horwich TB, Hamilton MA, Maclellan WR, et al. Low serum total cholesterol is associated with marked increases in mortality in advanced heart failure. J Card Fail 2002;8:216-224.
  55. Charach G, Argov O, Nochomovitz H, et al. A longitudinal 20 years of follow up showed a decrease in the survival of heart failure patients who maintained low LDL cholesterol levels. Quart J Med 2018;111:319-325.
  56. Roquer J, Cuadrado-Godia E, Rodriquez-Campello A, et al. Serum cholesterol levels and survival after rtPA treatment in 
  57. acute stroke. Eur J Neurol 2012;19:648-654.
  58. De Lau LML, Koudstaal PJ, Hofman A, et al. Serum cholesterol levels and the risk of Parkinson’s Disease. Am J Epidemiol 2006;164:998-1002.
  59. Huang X, Chen H, Miller WC, et al. Lower low-density lipoprotein cholesterol levels are associated with Parkinson’s disease. Movement Disorders 2007;22:377-381.
  60. Zuliana G, Cavalieri M, Galvani M, et al. Relationship between low levels of high-density lipoprotein cholesterol and dementia in the elderly. The InChianti Study. J Gerontol 2010;65A;559-564.
  61. Tuikkala P, Hartikainen S, Korhonen MJ, et al. Serum total cholesterol and all-cause mortality in a home-dwelling elderly population: a six-year follow up. Scand J Prim Health Care 2010;28:121-127.
  62. Newson RS, Felix JF, Heeringa J, et al. Association between serum cholesterol and noncardiovascular mortality in older age. J Am Geriatr Soc 2011;59:1779-1785.
  63. Takata Y, Ansai T, Soh I, et al. Serum total cholesterol concentration and 10-year mortality in an 85-year-old population. Clin Interv Aging 2014;9:293-300.
  64. Maihofer AX, Shadyab AH, Wild RA, et al. Associations between serum levels of cholesterol and survival at age 90 in postmenopausal women. J Am Geriatr Soc 2020;68:288-296. 
  65. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6:e010401.
  66. Begley S. Records found in dusty basement undermine decades of dietary advice. Raw data from a 40-year-old study raises new questions about fats. Sci Amer April 19th 2017.
  67. Whoriskey P. This study 40 years ago could have reshaped the American diet. But it was never published. The Washington Post April 12th 2016.
  68. Dehghan M, Mente A, Zhang X, et al. Association of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet 2017;390:2050-2062; Mente A, Dehghan M, Rangarajan S, et al. Association of dietary nutrients with blood lipids and blood pressure in 18 countries: a cross-sectional analysis from the PURE study. Lancet 2017;390:774-787; Miller V, Mente A, Dehghan M, et al. Fruit, vegetable, and legume intake, and cardiovascular disease and deaths in 18 countries (PURE): a prospective cohort study. Lancet 2017;390:2037-2049; Dehghan M, Mente A, Rangarajan S, et al. Association of dairy intake with cardiovascular disease and mortality in 21 countries from five countries (PURE): a prospective cohort study. Lancet 2018;392:2288-2297.
  69. Morrison LM, Hall L, Chaney AL. Cholesterol Metabolism: Blood Serum Cholesterol and Ester Levels in 200 Cases of Acute Coronary Thrombosis. Am J Med Sci 1948; 216:32-38. 
  70. Dock W. Causes of arteriosclerosis. Bull New York Acad Med 1950;26:182-188.
  71. Gubner R, Ungerleider HE. Arterio-sclerosis: A Statement of the Problem. Am J Med 1949;6:60-83.
  72. Duff GL, McMillan GC. Pathology of atherosclerosis. Am J Med 1951;11:92-108.
  73. Keys A. Prediction and possible prevention of coronary disease. Am J Publ Health 1953;43:1399-1407. 
  74. Dock W. Ather
  75. osclerosis: The facts and the mysteries. Bull NY Acad Med 1967;43:792-797.
  76. MacDonald I, Braithwaite DM. The influence of dietary carbohydrate on the lipid pattern in serum and in adipose tissue. Clin Sci 1964;27:23-30.
  77. Noakes TD. It’s the insulin resistance, stupid: Part 17. Crossfit Essentials
  78. Smith RL, Pinckney ER. The Cholesterol Conspiracy. Warren H Green Inc; St Louis MI, 1991.
  79. Moore TJ. Heart Failure: A Critical Inquiry into American Medicine and the Revolution in Heart Care. New York, NY: Simon and Schuster, 1989. [Also Moore TJ. The cholesterol myth. The Atlantic. 1989;264(September):37].
  80.  Ravnskov U. The Cholesterol Myths. Exposing the fallacy that saturated fat and cholesterol cause heart disease. New Trends Publishing, Washington, DC. 2000.
  81. Colpo A. The Great Cholesterol Con.  LULU publishers, 2007. 
  82. Kendrick M. The Great Cholesterol Con. The truth about what really causes heart disease and how to avoid it. John Blake, London, UK. 2007.
  83. Ravnskov U. Fat and cholesterol are good for you. GB Publishing, Sweden. 2009.
  84. Rosch PJ. Fat and cholesterol don’t cause heart attacks. And statins are not the solution. Columbia Publishing, UK. 2016.

Read Also:

(Visited 1,788 times, 254 visits today)