In Part Eight of Professor Tim Noakes’ ‘Ancel Keys’ Cholesterol Con’ series, Noakes kicked off in 1970 and recounted events and studies cemented by careerists whose future academic prospects would be enhanced by any findings that supported the Diet-Heart and Lipid hypotheses, all of whom were firmly convinced that Keys’ Twin Hypothesis were divinely ordained. In Part Nine, Noakes continues with the foreshadowing account of the greatest scam in the history of modern medicine, picking up in 1976. Noakes chronicles how circumstances driven by politics and profit led to the development of the first United States Department of Agriculture (USDA) Dietary Goals for the US in 1977, which were based specifically on Keys’ unproven Diet-Heart hypothesis. Despite severe criticism of the USDA Dietary Guidelines by many, they continue to reign supreme to this day. – Nadya Swart
Ancel Keys’ Cholesterol Con. Part 9 – 1976–1977
By Professor Tim Noakes
1976–1977. The McGovern US Senate Select Committee on Nutrition and Human Needs releases its Dietary Goals for the United States.
A key event that drove the global adoption of the Diet-Heart hypothesis was the 1972 US Presidential election in which the incumbent Richard Nixon was confronted by a losing war in Vietnam, rising food prices, unhappy housewives and a disgruntled farming community (1). He appointed Earl Butz as Secretary of Agriculture with two orders: increase the wealth of US farmers and bring down the price of food (2). Butz decided that the production of corn on an industrial scale by farmers receiving large government subsidies to cultivate all their available land was the solution to both “problems”. Butz’s actions would have momentous effects on global health.
The industrialisation of corn production would be of little value if all the newly grown corn was not eaten, either by US citizens or the rest of the world. The challenge was to convince the world that grains and cereals are healthier than the foods high in animal fat and protein on which Americans had built their nation.
The key player in driving this would be Senator George McGovern whose Senate Select Committee on Nutrition and Human Needs developed the first United States Department of Agriculture (USDA) Dietary Goals for the US in 1977. These novel guidelines (3) were based specifically on Keys’ unproven Diet-Heart hypothesis because they advocated replacing fat in the diet with carbohydrate-rich grains.
Recall that Jeremiah Stamler’s 1970 Committee (4) had proposed that US citizens needed to eat less fat, especially saturated fat. In 1970, the presumption was that the fat calories removed from the diet would be replaced by an increased protein intake (4). Yet in the seven years between these two events, the political landscape in the US had changed dramatically. With Butz in charge of US Agriculture, any fat removed from the diet would now have to be replaced with cheap grains, not by expensive proteins.
At the time, Senator McGovern was facing a number of personal and political challenges. He had suffered a humiliating defeat at the hands of Richard Nixon in the 1972 US Presidential Election and was losing the support of the Democratic Party leadership. It was becoming so bad that he and his wife even considered emigrating to England at the end of 1972.
His Senate Select Committee had been formed in July 1968 with the express purpose of investigating “hunger in America”. But by 1976, Democratic Senator Adlai Stevenson was saying the McGovern committee had served its purpose and he recommended that it be disbanded (5). Under his proposed reorganisation, the committee would be turned into a nutrition subcommittee under the Senate Committee on Agriculture. This would result in a dramatic reduction in the committee’s annual $450,000 budget and its staff of 16.
But before Congress could vote on this reorganisation, McGovern’s committee “announced with great fanfare, the proposal to make changes in the American diet in hope of avoiding the ‘epidemic of killer diseases’. The timing of the release had led many to believe that the publication was politically motivated” (5, p.1176).
As Cortez Enloe, then editor of Nutrition Today, would write: “They were fighting for their life. Their tenure was up. But Congress said, no, sorry George, you’re going to have to go over and live in the agriculture committee. So to prove that they were really doing something, they got out all their old hearings and pasted up all the things that looked alike, and put their flossy name on it, Dietary Goals for the United States. They had a big press conference. No hearing, just a press conference. This was supposed to impress Congress. But Congress wasn’t impressed. They blasted him out of business anyway” (5 p.1177). Support for McGovern’s committee was reduced to two staffers.
The irony is that even without Congressional support, McGovern’s committee would have a massive global influence, unfortunately, not for the better.
So McGovern decided to fight back by shifting the focus of his Committee to the role of diet in “health” and, specifically, the emerging problem of obesity and CHD in the US.
A key idea driving Senator McGovern’s thinking was that the US diet had changed radically in the years immediately preceding the beginning of the CHD “epidemic”, usually considered to have begun in the mid- to late 1920s. Keys and others argued without evidence that it was this dangerous dietary transformation that was driving the “epidemic” of heart disease in the US.
For example, Jane Brody, a popular writer of the day on topics of nutrition, would write in 1985 that: “Within this century the diet of the average American has undergone a radical shift away from plant-based foods such as grains, beans and peas, nuts, potatoes, and other vegetables and fruits and toward foods derived from animals – meat, fish, poultry, eggs and dairy products” (6, p.2).
Accordingly, on Tuesday, 27 July 27 1976 at 9:30am in room 1114 of the Dirksen Senate Office Building, McGovern together with Senators Edward Kennedy, Hubert Humphrey, Charles Percy, Robert Dole, Henry Bellmon, Kingsley Taft and Mark Hatfield listened to a presentation from Dr Theodore Cooper (7). Cooper was then the Assistant Secretary for Health in the Department of Health, Education, Art and Welfare. Cooper had trained as a heart surgeon and at the time was serving as a Director of the NIH Artificial Heart Programme. It is not certain that his surgical training made Cooper the ideal expert to speak to the Committee on this topic. Cooper would talk for two and a half hours; the meeting ending just in time for lunch at 12 noon.
Predictably, some of the Senators felt it necessary to have their say before Cooper began his address.
Senator Charles Perry was the first: “…experts have found enough incriminating evidence to conclude that our super-rich, fat-loaded, additive and sugar-filled American diet is sending many of us to early graves unnecessarily” (7, p.2) so that: “This is what the hearings are all about – to increase our understanding about the relationship between diet and preventive health care and to promote public awareness of the need for good nutritional habits in the maintenance of health” (p.3).
Thus the Commission began with the assumption that changing the US diet would prevent specific diseases; an assumption that was no more than an assumption. There was no evidence then that this assumption was correct.
Dr Cooper began by arguing that studies currently being funded by the NIH aimed to provide “more solid scientific information about confirming (my added emphasis) the fact of the relationship of diet to heart disease” (p.7). He predicted that it was “within the realm of possibility” that these still-to-be-completed studies would show that dietary changes would “help us achieve a 25-percent reduction in incidence (of CHD) and 20 percent in savings (on medical costs)” (p.7). This would be achieved by paying attention to the role of nutrients “particularly lipids, in the diet” (p.7).
In discussing the role of diet in obesity, especially in the poorer communities, Cooper expressed an opinion that was then common knowledge: “But it is true that the consumption of high carbohydrate sources with the induction of obesity constitutes a very serious public health problem in the underprivileged and economically disadvantaged” (p.10).
He then launched into a faithful description of Keys’ Twin Hypotheses: “In recent decades a body of suggestive (my added emphasis) research evidence indicates that the nature and extent of fat intake, as well as fat transport and metabolism, are involved in atherogenesis in some as yet unclarified fashion. Patients with known advanced atherosclerosis or with established coronary heart disease very often exhibit elevated blood lipid and cholesterol levels. A relationship exists between the quantity of dietary fat and its qualitative makeup and the blood lipids. The isocaloric substitution of unsaturated fats in the diet for saturated fats results in a marked lowering of the previously elevated plasma cholesterol levels. Even more striking results are obtained if pure polyunsaturated fatty acid esters are administered. Conversely, plasma lipids arise when a diet rich in saturated fats is given” (p.12). He continued: “…experimental evidence has been emerging during the last decade which seems (my added emphasis) to establish that maintaining a low serum cholesterol and low serum triglyceride level with controlled diets for five to 10 years or more results in a reduced incidence of deaths from coronary heart disease” (p.13). This latter statement was false, as Dr Cooper must have known when he made it.
He continued: “Even if what I said was completely unsubstantiated by future research (which it would be – my addition), there is nothing that I know of the recommendation to reduce fat intake, to reduce obesity and maintain an optimal body weight with an appropriate level of physical activity would in any sense be harmful. In fact, I’m quite aware that it will be beneficial for the prevention of other diseases as well” (p.13).
But hold on there, Dr Cooper. You’ve already warned that high carbohydrate diets cause obesity in poorer communities. What happens then if you replace dietary fats with an increased carbohydrate intake. Won’t obesity rates increase especially in those living in the poorer communities? Didn’t consider that, did you now?
Cooper was clearly aware of the social costs of obesity: “I know of no condition where the elimination of obesity wouldn’t be a beneficial public health preventive action. That goes for heart disease; it goes for cancer; it goes for arthritis; it goes for diabetes; it goes for any of the modern killer diseases in America” (p.14).
When asked by Senator McGovern to leave the Committee with a “general rule of thumb” about what diet they should be eating, Cooper responded: “Well, my first advice would be to eat less. As a general rule, I think the American public eats too much … In order to accomplish this, I think what we need to consider doing is to reduce our total fat intake. The American diet has a rather high content of fat when compared to many worldwide … Fat adds a caloric substance almost twice as much – nine kilocalories per gram – as compared to sugar. I think in order to have an effective reduction of weight … we have to focus on reducing fat intake” (p.19-20).
“I personally believe there is some benefit to reducing our preoccupation with sweet things … I would recommend an appropriate amount of protein intake … A healthy intake of fresh fruits and vegetables with substantial fibre content … It is very attractive for me to say stop eating commercially prepared foods” (p.20).
Interestingly Cooper also expressed his opinion about the role of exercise in weight control: “Exercise, unless you are into quite heavy labour where your total energy expenditure is in the several thousands of calories like three-chopping or lumber workers, is really not the main determinant of weight loss” (p.33).
In other words, you can’t outrun a bad diet (8).
Interestingly, in response to direct questioning from Senator Percy, Dr Cooper acknowledged that he is carbohydrate-sensitive, that is, insulin-resistant. He acknowledged that “if I have a problem, it is a tendency to put on weight” (p.37). He also acknowledged that he suffers from Fredrickson Type IV hyperlipidemia, which is essentially carbohydrate-sensitive hypertriglyceridemia (Table 1 in reference 8): “I am classified as (Fredrickson) type IV. As a type IV, my lipid levels are much more subject to elevation if I consume large amounts of carbohydrate or alcohol. I have no real problem in consuming a reasonable amount of cholesterol. I assume four eggs a week is quite suitable for me. I like them, and am not trying to have people not eat eggs…” (p.37).
In summary, the first person to speak to Senator McGovern’s Select Committee probing the role of diet in the development of CHD, provided a body of unsubstantiated evidence that removing fat from the diet would improve the health of all Americans. Yet he recognised he was personally carbohydrate-intolerant and understood carbohydrates posed a greater risk to his health than did dietary cholesterol and perhaps dietary fat.
Critically Dr Cooper failed to ask the single most important question: what if a majority of Americans are like me? That failure would have profound implications for the future health of the world, not just for the US.
A year later on 11 January 11 1977 in the very same Senate room, Senator McGovern announced the outcome of his Committee’s deliberations: the publication of the Dietary Goals for the United States (9).
In his prepared statement, Senator McGovern began: “The simple fact is that our diets have changed radically within the last 50 years, with great and often very harmful effects on our health. These dietary changes, represent as great a threat to public health as smoking. Too much fat, too much sugar or salt, can be and are linked directly to heart disease, cancer, obesity and stroke, among other killer diseases. In all, six of the 10 leading causes of death in the United States have been linked to our diet”.
“Those of us within Government have an obligation to acknowledge this. The public wants some guidance, wants to know the truth, and hopefully today we can lay the cornerstone for the building of better health for all Americans, through better nutrition”.
“Last year, every man, woman and child in the United States consumed 125 pounds of fat, and 100 pounds of sugar. As you can see from our displays, that’s a formidable quantity of fat and sugar”.
“The consumption of soft drinks has more than doubled since 1960 displacing milk as the second most consumed beverage. In 1975, we drank on the average of 295, 12 oz. cans of soda”.
“In the early 1900s, almost 40 percent of our caloric intake came from fruit, vegetables and grain products. Today, only a little more than 20 percent of calories comes from these sources” (9, p.1).
McGovern indicated that his Committee would “set forth” the necessary plan of action.
- Six basic goals are set for changes in our national diet;
- Simple buying guides are recommended to help consumers attain these goals; and
- Recommendations are also made for action within Government and industry to better maximise nutritional health” (9, p.1).
The six basic goals were the following:
Goal 1: Increase carbohydrate consumption to account for approximately 55 to 60 percent of the total (caloric) intake.
Goal 2: Reduce overall fat consumption from approximately 40 to 30 percent of energy intake.
Goal 3: Reduce saturated fat consumption to account for about 10 percent of total energy intake; and balance that with polyunsaturated and monounsaturated fats, which should account for about 10 percent of energy intake each.
Goal 4: Reduce cholesterol consumption to about 300mg a day.
Goal 5: Reduce sugar consumption by about 40 percent to account for about 15 percent of total energy.
Goal 6: Reduce salt consumption by about 50 to 85 percent to about 3g/day”.
The outcome was that the Dietary Goals advised Americans to restrict their intake of especially saturated fats by eating 8–12 servings of grain and cereals per day. Grains and cereals replaced the butter, lard, cheese, eggs and meat that had been the American staples until then (10).
The truth is that the 1977 USDA Dietary Goals for the US were compiled by a vegetarian Nick Mottern who had no formal training in nutrition science (10; 11, p.45) and who was ably assisted by an equally uninformed committee of “lawyers and ex-journalists”. “We were totally naïve,” said the staff director Marshall Matz, “a bunch of kids, who just thought, ‘Hell, we should say something on this subject before we go out of business’” (11, p.45).
The Dietary Goals were severely criticised by many, beginning with Dr Philip Handler, then President of the National Science Academy (NSA). Handler posed the question: “What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?” He added: “… resolution of this dilemma turns on a value judgement. The dilemma so posed is not a scientific question; it is a question of ethics, morals, politics. Those who argue either position strongly are expressing their values; they are not making scientific judgments” (11, p.51).
Similarly, Pete Ahrens (12) noted that: “…a trial of the low fat diet recommended by the McGovern Committee and the American Heart Association has never been carried out. It seems that the proponents of this dietary change are willing to advocate an untested diet to the nation on the basis of suggestive evidence obtained in tests of a different diet. This illogic is presumably justified by the belief that benefits will be obtained, vis-à-vis CHD prevention, by any diet that causes a reduction in plasma lipid levels” (12, p.1346).
His criticisms covered four topics:
- There has been no previous test of the “prudent diet”.
- The “prudent diet” will have only a small effect on plasma lipid levels.
- Any one diet produces different results in different people.
- Crucial questions remain to be resolved. These related specifically to the nature of the dietary fats that should be prescribed and their differential effects on the blood lipoproteins: chylomicrons, VLDL-, HDL- and LDL-cholesterol.
He concluded: “I believe it is anything but a service to the public to postulate one dietary solution for hyperlipidemia, no matter how well-meaning one is in advocating it. Let us address the unanswered questions and demand the means to solve them quickly” (p.1348).
Other dissenters included Eliot Corday MD: “New investigations indicate that the lipid hypothesis has not yet been proven to be completely correct (13, p.13) so that before a change of dietary goals is applied to the nation to prevent arteriosclerosis, it behoves the health planners to test the hypothesis of alterations in nutritional risks with the diets advocated by their health advisers” (13, p.13). He also noted that “less than 20 percent of patients” with CHD have an “abnormal lipid pattern” (p.13).
AE Harper, PhD, commented: “The assumption that cardiovascular diseases may be delayed by adoption of the dietary goals is speculation” (13, p.20) so that “proposals for action that are based on speculation and conjecture rather than on critical analysis are distressing under any circumstances. They are especially distressing when they are proposed by a senate committee for adoption as the basis for Federal policy” (p.20).
Gilbert A. Leveille, PhD, argued that the “committee’s report failed to consider all of the available evidence” and that “There is equally compelling evidence suggesting that the recommended dietary changes would make little or no difference as to the incidence and severity of cardiovascular disease or cancer” (13, p.22).
George V Mann, MD, who had resigned as Director of the Framingham Diet Heart Study when he realised that politics had trumped science, complained that: “The level of fat in the diet has not been related causally to any disease and in particular not to either obesity or to cancer. Those who contend this are adventurists” because “the amount of saturated fat in the diet has not been shown causal for any disease” (13, p.23). He concluded that: “The release of this document is a nutritional debacle.”
Robert E Olson, MD, concurred: “I think the proposal is disastrous … (as) there is no evidence at present to justify such a drastic change in the American diet” (13, p.23). He argued that the new guidelines are “not based on scientific evidence” and that: “There is no evidence from 10 intervention studies of coronary disease involving 5,000 men and 36,000 man years of study of the effect of the prudent diet that diet modification will change the mortality rate of this disease” (13, p.23).
Alexander M Schmidt, MD, warned: “For anyone to say, ‘Let’s change the nation’s dietary habits even though we don’t know doing so will do any good – it can’t do any harm’ is naïve. One doesn’t know, and can’t predict, what harm may result. But experience teaches us that we often learn late even a generation late of harm that no one could or did predict” (13, p.24) (my added emphasis).
Others argued that “The data demonstrating the concept that the risk of coronary heart disease is a function of serum lipids at any level is no longer valid” (14, p.865). Reisser continued: “ (The dietary advice)… on the grounds that it can do no harm, is not only specious but it is fatuous as well. It is both misleading and paternalistic. The advice deprives the majority of people their most desirable, traditional and protective foods: eggs, dairy products, liver, beef and pork” (14, p.865).
“There is an inference that everyone has the potential for the disease (CHD) and all he has to do to get it is to eat eggs, meat and butterfat. The fact that there are individual variations in the blood lipid response to diet variables is well known but ignored in diet recommendations, especially those by food advertisers” (14, p.867).
“The manufacturers of margarine, egg and meat substitutes, and other segments of the food industry have taken full advantage of the AHA campaign and, in fact, have taken over the burden of indiscriminately weaning the public away from eggs, beef, pork and dairy products containing butterfat. By constant repetition in all advertising media they have made it appear as a truism that anyone who consumes animal products, including meat, eggs, and dairy dishes, is in danger of CHD, and that substitution of their products will prevent the disease. They have made cholesterol appear to be a toxic substance similar to dangerous additives” (14, p.866).
A second edition of the Dietary Guidelines was subsequently published, which included an addition statement from Senator Percy (15) who now clearly had significant concerns about the scientific credibility of the Guidelines: “…I have become increasingly aware of the lack of consensus among nutrition scientists and other health professionals regarding (1) the question of whether advocating a specific restriction of dietary cholesterol intake to the general public is warranted at this time, (2) the question of what would be the demonstrable benefits to the individual and the general public, especially in regard to coronary heart disease, from implementing the dietary practices recommended in this report and (3) the accuracy of some of the goals and recommendations given the inadequacy of current food intake data.”
With regard to the evidence supporting efforts to reduce dietary cholesterol intake he wrote: “…in October 1977, the Canadian Department of National Health and Welfare reversed its earlier position and concluded in a National Dietary Position that:
“Evidence is mounting that dietary cholesterol may not be important to the great majority of people … Thus, a diet restricted in cholesterol would not be necessary for the general population.”
A similar conclusion was drawn in 1974 by the Committee on Medical Aspects of Food in its report to Great Britain’s Department of Health and Social Security.
Because of these divergent viewpoints, it is clear science has not progressed to the point where we can recommend to the general public that cholesterol intake be limited to a specified amount. The variances between different individuals are simply too great.
He next tackled the quality of the scientific evidence supposedly establishing a causative link between a specific diet and increased risk of CHD: “A similar divergence of scientific opinion on the question of whether dietary change can help the heart illustrates that science cannot yet verify with any certainty that coronary heart disease will be prevented or delayed by the diet recommended in this report.”
For example, Dr Jeremiah Stamler, Chairman of the Department of Preventive Medicine, Northwestern School of Medicine, strongly believes thousands of premature coronary heart disease deaths can ‘probably be prevented annually through dietary change’. However, Dr EH Ahrens, Jr, Professor of Medicine at Rockefeller University, told the Select Committee in March:
“Advice to the public on changing its dietary habits in hope of reducing the rate of new events of coronary heart disease is premature, hence unwise,”
He continued by highlighting the different opinions of those who either supported or opposed Keys’ hypotheses: “The same polarity is evidenced when one compares the view of William Kannel, Framington (sic) Heart Study’s Director, the Dietary Goals, ‘could have a substantial effect in reducing’ coronary heart disease, with the opinion of Vanderbilt University’s Dr George Mann that ‘no diet therapy has been shown effective for the prevention or treatment’ of that disease.”
Next, he called in the support of the American Medical Association who, in an 18 April 1977 letter to the Nutrition Committee had stated:
“The evidence for assuming that benefits to be derived from the adoption of such universal dietary goals as set forth in the report is not conclusive and … potential for harmful effects … would occur through adoption of the proposed national goals.”
So he continued: “This impressive lack of agreement among scientists on the efficacy of dietary change was also noted by the National Heart, Blood and Lung Institute’s Dr Robert Levy, when he observed that there are ‘bona fide scientific people coming out on both sides of the issue’ and by Health Undersecretary Theodore Cooper’s remarks last year to the Committee that a ‘great deal more nutrition work (is needed) … before one can speak with greater certainty concerning large-scale application’ of dietary change. Because of this continuing debate, I feel great care must be taken to accurately inform the public about the benefits of the diet proposed in this report.
“I feel the American public would be in a better position to exercise freedom of dietary choice if it were stated in bold print on the Goals and Food Selection pages that the value of dietary change remains controversial and that science cannot at this time insure (sic) that an altered diet will provide improved protection from certain killer diseases such as heart disease and cancer.
“In conclusion, I recognise the desirability of providing dietary guidance to the public and in helping the consumer become more responsible for every day health status. In my judgement, however, the best way to do this is to fully inform the public not only about what is known, but also about what remains controversial regarding cholesterol, the benefits of dietary change, and the reliability of current food intake data. Only then, will it be possible for the individual consumer to respond optimally to the Dietary Goals in this report.”
The second edition of the Dietary Goals also included some significant modifications of the original guidelines. Some suggest the cattle industry in McGovern’s home state of South Dakota was particularly unimpressed with his committee’s recommendations. So the second edition no longer advised consumers to eat less meat. Instead, consumers were advised to reduce their intake of animal fat “and choose meats, poultry, and fish, which will reduce saturated fat intake” (5, p.1177).
The new edition also removed any reference to restricting whole milk and egg consumption by young children and increased the suggested limit for adults’ salt intake from 3 –5g/day. This excluded “non-discretionary” salt in processed foods. As a result the limit on salt intake was effectively increased to 8 grams/day (5, p.1177).
Perhaps under pressure from the fast food industry, the second edition included the suggestion that “on the whole, quick foods are a nutritious addition to a balanced diet” (5, p.1177).
Interestingly, the Department of Health, Education and Welfare and the NIH were originally against these dietary guidelines becoming government policy, saying that “they don’t know enough to cast presumptions into federal policy” (p.1175).
To garner more support for their guidelines, the Department of Agriculture originally invited the National Academy of Sciences (NAS) to evaluate them. But before the contract could be signed, the then chairman of the NAS Food and Nutrition Board expressed his personal opinion: “The American diet has been referred to as ‘pathogenic’ (sic) by some and as ‘disastrous’ by others, implying that our national diet has deteriorated in the past 50 years. I submit that such a conclusion is erroneous and misleading. The American diet today is, in my opinion, better than ever before and is one of the best, if not the best, in the world today” (p. 1175).
Another to express his personal concerns about making these guidelines government policy, was Donald Fredrickson MD, the originator of the Fredrickson Classification of Hyperlipidemias (16) and who, at the time, was director of the NIH. Addressing a different House Committee he said: “I have been concerned about this question as director of the NIH and the Heart Institute and as a scientist in the field for 25 years. I feel that the problem we still have is that we can’t bring you proof that changing the diet for the average American will lengthen his life or reduce his likelihood of having a coronary….We’ve more or less become adjusted to the fact that we probably will never be able to get the ideal proof that we want…The weight of the evidence seems to be strong enough so that we can now direct people toward a kind of set of guidelines” (p.1178).
In July 1978, the American Society for Clinical Nutrition (ASCN) convened its own task force to evaluate the scientific validity of the proposed dietary interventions. Their concern was that the advice that scientists provide to government officials frequently “takes the form of advocacy” in which those scientists “put forth those elements of the total body of data that support the change in public policy that they favour” (17, p.2627).
In other words, the concern was that the scientists were cherry-picking only the data that supported their particular biases. What was needed was an independent panel of experts with a wider range of opinions (and biases).
The result was that the ASCN Task Force sampled the opinions of nine panellists who, on the basis of all the evidence – epidemiological, randomised controlled trials, animal studies and proposed biological explanation – rated, out of a possible score of 100, 10 specific issues relating specific nutrients as causative agents for specific diseases (Table 1).
Table 1: ASCN Panellists’ Assessment of the evidence available in 1977 linking specific dietary factors as the cause of specific diseases.
Panellists considered that the best evidence was that there were only two nutrient-disease relationships for which the evidence was conclusive. These were specific proven relationships between alcohol and liver disease, and carbohydrates and dental caries. The evidence the panellists considered was also detailed in a series of peer-reviewed articles (18-29).
Henry C McGill MD reviewed the evidence linking specifically dietary cholesterol intake and the development of atherosclerosis (18,24) whereas Charles J Glueck MD reviewed the evidence then available that linked dietary fat intake with atherosclerosis (19,25).
McGill concluded it was virtually impossible to detect an independent effect of dietary cholesterol on either blood cholesterol concentrations or on the development of coronary atherosclerosis. His reasoning was that, in population studies, “the intake of cholesterol is always associated with the intake of fat (especially saturated fat) (18, p.2632). He was also wary of conclusions drawn from population studies when applied to individuals: “…associations between two variables based on group means do not permit inferences to be drawn about the corresponding associations among individuals within a single group” (p.2633). In other words, all individuals respond in their own peculiar ways to different interventions. And that individual response cannot be predicted from observational studies of large populations.
He concluded that a reduction in dietary cholesterol intake might produce a modest reduction in total atherosclerotic disease without causing “any other known deleterious effects” (p.3635), a conclusion which, in retrospect, is conveniently simplistic. Because taking cholesterol out of the diet requires the removal of all animal produce including eggs, a move which would be detrimental especially in more deprived communities at risk of nutritional deficiencies. McGill recognised this problem: “The implementation of a low-cholesterol diet carries with it some degree of risk, however small, due to changes of food processing or food purchasing, or to unforeseeable hazards for individuals with marginally adequate diets” (p.3636).
One “unforeseeable” hazard was the manner in which the food processing industry would wilfully exploit this invitation to replace fat in the diet. Instead of filling this nutritional gap with an increased protein intake as Stamler and others had assumed would happen (3,4), it filled the taste gap with sugar, unleashing a global pandemic of sugar-driven, addictive eating behaviours (30).
In his extensive review of the literature, McGill made a few important points.
First, controlled experiments in humans “(dietary) cholesterol did influence serum cholesterol concentration but to a lesser degree than saturation of dietary fatty acids” (24, p.2685). This had been acknowledged even by Keys himself who had written: “for all practical purposes the dietary cholesterol variable can be disregarded…” (31). Ahrens had said essentially the same: “serum cholesterol levels ordinarily are independent of dietary cholesterol in man” (32, p.939). As a result, Stewart Truswell MD, another Keys’ acolyte, concluded that lowering dietary cholesterol intake by reducing weekly egg intake from 5–2 eggs/week, would be so small that it would not be advisable (33). Truswell also emphasised the nutritional value of eggs.
Second, association studies cannot prove causation but can serve only “as suggestive evidence for a causal relationship” (p.2697). However, “numerous cross-sectional studies have failed to find a significant independent association of dietary cholesterol with either serum cholesterol levels or with risk of arteriosclerotic heart disease” (p.2697).
Third, any attempt to lower blood cholesterol concentrations by simply lowering dietary cholesterol intake would be ineffective. Rather this would be accomplished only by “changes in a variety of dietary components” (p.2698).
In his submissions (19,25), Glueck concluded that studies of dietary fat intakes within population groups (i.e. by comparing individuals rather than population groups) “have usually failed to show a correlation between (dietary fat) intake levels, plasma cholesterol levels, and incidence of atherosclerotic disease” (19, p.2639). He also noted that “there are few precedents for use of diets high in polyunsaturated fats” (p.2642) and that “the benefits that might accrue from the ingestion of a low-fat, low-saturated fat, low-cholesterol diet has never been adequately tested except in terms of reduction in plasma lipid levels” (p.2642).
Despite his inability to find any solid evidence to support Keys’ Twin Hypotheses, yet Glueck’s personal bias was clearly evident in his second paper (25). Thus the failure of studies to support the Lipid Hypothesis were because the studies “began in adults whose atherosclerosis was advanced and potentially irreversible” (p.2706). The reality is that none of those studies provided any evidence to support this conclusion.
In relation to the MRFIT, described in detail elsewhere (34), Glueck wrote: “If MRFIT ends in a favourable conclusion we will be able to move ahead with confidence to improve the prognosis for a group of high risk patients, perhaps with a significant improvement in overall national vital statistics” (p.2708).
The corollary of this logic should have been that if the MRFIT failed to show any benefit of these interventions, then the opposite must apply. Specifically, the NIH/AHA alliance should have declared that interventions it tested were completely ineffective so no more taxpayers’ money should be wasted exploring that blind alley.
But when the MRFIT failed miserably to show any benefit of reducing multiple coronary “risk factors” (34), the alliance remained silent. Instead, it continued to explore the blind alley with yet more expensive experiments, most notably the hubristically labelled Women’s Health Initiative Randomised Controlled Dietary Modification Trial (WHIRCDMT) (35) that would cost $700 million.
Their logic adopted by the alliance was presumably that described by Glueck: “If the MRFIT does not succeed in achieving a significant reduction in events, despite a reduction in risk, the most likely explanation will be that the period of intervention was too short, and the degree of cholesterol lowering too small” (p.2708).
Actually, no, Dr Glueck. If a scientific experiment fails to support the tested hypothesis, then the hypothesis must be declared invalid and retired. To be replaced by a novel hypothesis that aims to advance knowledge by recognising that the previous, now disproved hypothesis, was wrong.
Instead, Glueck was proposing the classic post-hoc justification of why the study “failed”. This would soon become the standard operating procedure for the NIH and the AHA, also to explain, for example, why the failed $700 million WHIRCDMT was not actually a failure (35).
Glueck even extended his argument to include the yet-to-be-released results of the Lipid Research Clinics trial (34). Here, his conclusion was: “If the Lipid Research Clinics trial should end in a negative or equivocal result, the lipid hypothesis will not have been dealt a fatal blow. The atherosclerotic disease process may already have progressed too far to be arrested in these severely hypercholesterolemic subjects” (p.2708).
So, instead of accepting the findings from trials showing the low-fat diet does not improve all-cause mortality, the NIH/AHA alliance would simply ignore the findings from their previous studies and soldier on manfully, secure in the knowledge that someday, somehow, they would still prove that Keys’ Hypotheses are correct. Despite the mountain of contrary evidence.
Edward L Bierman MD reviewed the evidence for links between sugar intake and T2DM, CHD and dental caries (20,26). He concluded that there was strong evidence linking sugar and dental caries but there was no good evidence linking sugar intake with T2DM or obesity. Rather “adiposity appears to be the major determinant of the emergence of glucose intolerance and adult-onset diabetes, not carbohydrate and particularly not sucrose intake” (20, p.2644). Bierman’s opinion reflects the popular idea that obesity is the cause of insulin resistance, rather than the opposite. The possibility of reverse causation had yet to be considered.
He continued: “There is no known biological basis for the hypothesis that would relate higher sucrose or carbohydrate intakes to the causation of diabetes. On the contrary, a low-fat, high-carbohydrate diet, by leading to less obesity, may cause a reduced prevalence of diabetes” (p.2646). Clearly Dr Bierman did not foresee the global explosion in obesity and T2DM that would be unleashed by the low-fat high-carbohydrate dietary guidelines of McGovern’s Committee (1).
With regard to carbohydrates and CHD, Bierman acknowledged concerns that a high-carbohydrate diet increases blood triglyceride concentrations which “may well represent a risk factor for the development of coronary disease in the United States population (36)” (26, p.2713). But he discounted the importance of this effect of high-carbohydrate diets concluding that the “atherogenic potential of these dietary manipulations has yet to be explored” (p.2713). Any possibility that a low-fat high-carbohydrate diet might be harmful was simply implausible, given the strength of the belief in Keys’ unproven hypotheses.
Theodore van Itallie reviewed the role of excess calorie consumption as a cause of chronic disease. He argued that there is “no evidence that obese individuals develop increased fat storage (i.e. obesity) owing to a high consumption of carbohydrate as compared with fat or protein” (21, p.2648). In contrast, “…man and experimental animals more readily become obese on diets low in carbohydrates and high in fat, but this can be explained in terms of differences in palatability and a somewhat greater heat loss from carbohydrate. There is no evidence that the higher caloric density of fat … is itself responsible for undue weight gain” (p.2648).
He concluded that obesity was strongly and likely causally related to a number of chronic diseases, most especially what he termed “carbohydrate intolerance”: “The temporal association between obesity, carbohydrate intolerance and adult-onset diabetes mellitus is very close. The association with carbohydrate intolerance is only a few weeks” (p.2651-2652).
His biological explanation for these relationships was the following: “Increased storage of triglycerides in adipose tissue is invariably accompanied by adipocyte hypertrophy; this, in turn, leads to carbohydrate intolerance, insulin insensitivity and hyperinsulinemia. The insulin insensitivity of hypertrophic adipose tissue as well as of other tissues of the obese has been demonstrated in various in vitro preparations. The tissue changes engendered by obesity are presumably related to the exacerbation of carbohydrate intolerance and diabetes that is observed clinically” (p.2652). Again, the possibility of reverse causation was not mentioned, reflecting the popular beliefs of the day.
What is especially interesting, in retrospect, is that Van Italie includes no mention of the nature of the diet he believes will prevent or reverse obesity. By his reckoning, it must be a low-fat high-carbohydrate diet. But he cites no evidence to support what would logically be his advice. Yet, he understands that hyperinsulinemia is a feature of obesity. Surely he might have asked: if obesity is associated with hyperinsulinemia, how can a high-carbohydrate diet that promotes yet more hyperinsulinemia, ever be considered a wise dietary option?
The reviews of the relationship between alcohol and liver disease (22,28) concluded that there is strong evidence excessive alcohol consumption causes chronic liver disease but that there is no good evidence alcohol plays a role in coronary atherosclerosis.
In his review of any possible relationship between dietary salt and the development of arterial hypertension, Tobian (23,29) concluded that 80–91% of the US population are resistant to the development of hypertension and so have no need to lower their daily salt intake. However, for those who are “genetically susceptible to hypertension” (29, p.2745), “a life-long modest restriction of NaCl intake to levels less than 60mEq/day in adults will probably prevent the onset of hypertension indefinitely, and also prevent all subsequent hypertensive complications” (p.2745). The key, according to Tobian, is to identify those at risk for the development of hypertension.
The American Medical Association also produced its own response to the Dietary Goals (37). It began by stating that “it would be inappropriate at this time to adopt the proposed national dietary goals as…the evidence for assuming that benefits to be derived from adoption of such universal dietary goals…is not conclusive and there is a potential for harmful effects from a radical long term dietary change as would occur through the adoption of the proposed national goals” (37, p.576).
It presented the opinion that the evidence linking the American diet with a variety of different diseases including CHD, is “suggestive, fragmentary, and even conflicting” (p.577) so that “It is not proven that dietary modifications can prevent atherosclerotic heart disease in man (sic). It is not known that the demonstration of such a proof could or would find general applicability in our society” (p. 578). As a result: “In the absence of conclusive proof on the Diet-Heart question any dietary advice to the American public will always lack authenticity and authority, will be conducive to half-measures and will meet opposition which cannot be effectively countered” (p. 578).
The AMA Committee was equally unimpressed by the evidence linking high dietary fat intakes and cancer of the colon: “Whilst epidemiological data show a correlation between high fat intake and cancer of the colon, the case against high fat intake is weak because there are populations that have a high fat intake but little bowel cancer” (p. 579). The Committee also rejected any proven links between high fat diets and cancer of the breast.
Similarly, the Committee found no evidence to support the reduction in salt intake to reduce the prevalence of hypertension. It argued that dietary management of type 2 diabetes mellitus and obesity should both focus on calorie restriction on an individualised basis. Thus: “Adoption of national dietary goals is not an answer to obesity and could prove detrimental if followed by individuals properly requiring medical supervision for their particular condition” (p.580).
So their final conclusion was that the AMA “does not consider it appropriate for the government to adopt national goals that specify such matters as the amount and proportions of total fat, type of fat, sugar, cholesterol or salt content in the diets of the general public as these national goals advocate” (p.580). Rather, persons should be treated in individual programs that promote decreased caloric intake and increased physical activity for those with obesity or at risk of its development. “…(this) would be the most effective means of improving the health of our American citizens” (p.580).
As a result “…we (the AMA Committee) urge that the Report not be adopted” (p.581).
A final opinion was that of DM Hegsted, PhD, then Professor of Nutrition at Harvard School of Public Health and whose actions were so partial to the sugar industry (38,39): “The question to be asked, therefore, is not why should we change our diet but why not? What are the risks associated with eating less meat, less fat, less saturated fat, less cholesterol, less salt, and more fruits, vegetables, unsaturated fat and cereal products – especially whole grain cereals. There are none that can be identified and important benefits can be expected” (5, p.1176). One wonders whether, if he were still alive today, Hegsted would still hold this position.
For already in June 1979, Cortez Enloe had warned: “Suppose that, having accepted the McGovern promises and made the sacrifices, it turns out that the incidence of cancer does not go down. What then will happen to the public’s confidence in the health profession? What will unfulfilled promises do to the science of nutrition? No one seems to have considered these questions’” (5, p.1176).
These Dietary Goals continue to be modified every five years. However, the advice to eat less animal fat and protein and more carbohydrate in the form of grains and cereals remains immutable. Typically, the majority of the committee members writing the guidelines have significant conflicts of interest as do those currently preparing the 2020 guidelines. Indeed, 11 of the 20 members of 2020 Dietary Guidelines Advisory Committee, including the committee chair and vice-chair, have links to the International Life Sciences Institute (ILSI) (40-42), an organisation that serves as a front organisation for the food and drug industry (figure 1) and which has captured an inordinate influence on the development of global dietary guidelines (41,43-45).
Legend to figure 1. The ILSI connections. Reproduced from figure on page 5 of reference 41.
That the Dietary Guidelines Advisory Committee has little interest in producing dietary guidelines that reflect the totality of the modern evidence (46–48) continues to be an abiding concern.
In summary, the 1977 US Dietary Goals for the US were not based on hard evidence but, as a number of authors testified, rather on the assumption that Keys’ Diet-Heart hypothesis was correct and would be proven in the fullness of time by the expensive clinical trials then being considered by the NIH.
It is interesting that Dr Theodore Cooper, a cardiac surgeon then working for the NIH, played such an influential role in directing the initial thinking of the Senators on McGovern’s Commission (6).
Since the NIH had already bought into Keys’ certainty, it was predictable that the US Government Agency would also be enticed to embrace Keys’ solution for reversing the CHD epidemic.
As we would learn over the next 43 years, once the US Government had officially endorsed Keys’ unproven hypotheses, it would be extremely difficult, perhaps impossible for that certainty to be challenged.
The unproven, indeed disproven, fear that saturated fats are harmful, is alive, well and kicking vigorously in 2020 (48).
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