Maternal mortality rates are highest where mothers are poor and ill‐​fed and where, in consequence, their fetuses are malnourished. And a malnourished fetus is a fetus under metabolic pressure, so it must make a choice: which organs will it protect? Will it allow all its organs to be malnourished equally, or will it protect some organs at the expense of others? It appears a malnourished fetus chooses to protect its brain (these responses are little different from an adult’s: when adult mammals are starved, most of their organs shrink, the exceptions being the brain and, in the case of male mice, the testicles).39

So, on being starved, the fetus will deprive its other organs of nourishment, and in consequence it will grow into a short adult; and to help achieve that smallness, it will induce its muscles and other major organs to become resistant to insulin. The role of insulin is to direct the glucose we absorb from our food into our muscles and other major organs, so when we become insulin‐​resistant, their glucose uptake will be suppressed, thus sparing it for the brain.40 And, unexpectedly perhaps, it transpires that insulin resistance contributes to atherosclerosis.

Malnourished or poor mothers, therefore, produce children who are prone to developing strokes. But well‐​nourished or rich mothers do not. Hence the slope of the line in Figure 1: as mothers in the West have grown increasingly well‐​nourished, so their babies have been ever‐​less prone to developing strokes.

Understanding the Incidence of Heart Attacks in the 20th Century: Summarizing What We Know

From the divergences between the two lines in Figure 1 we can see that the causes of strokes and heart attacks must be different. Although both are caused by atherosclerosis, this condition must affect the arteries of the brain and heart in subtly different ways. All, therefore, we can currently state with certainty is that atherosclerosis is an inflammation of the arteries of which there are many possible causes, including the insulin‐​resistance of the metabolic syndrome and raised levels of sLDL, but also including smoking, stress, hypertension, diabetes, and aging, as well as a range of inflammatory diseases including arthritis, lupus, chronic infections, and inflammations of unknown cause. Another inflammatory disease that can apparently cause heart attacks is peptic ulceration, which is caused primarily by infection with Helicobacter pylori, because it transpires there is an association between H. pylori infection and atherosclerosis.41 Importantly, therefore, we still cannot know with certainty what accounted for the epidemiology of heart deaths in the 20th century, which must weaken the confidence with which we can pronounce on any putative causative factor.

Shattering the Cholesterol Story

Fifty years after Keys had captured the Senate Select Committee’s imagination, the failings of the cholesterol hypothesis had become so obvious that in 2007 Gary Taubes, a science journalist, could publish a book Good Calories, Bad Calories, which became a bestseller. In the book he claimed that carbohydrates in general, and sugar in particular, were the dietary hazards; natural fats were healthful.42

As we have seen above, there was already a long scientific tradition led by such professors as Yudkin, Mann, and Ahrens arguing for carbohydrates/​sugar, not fats, being the cardiac killers, but Taubes also had a populist predecessor, Robert Atkins (1930–2003), who in 1972 had published Dr. Atkins’ Diet Revolution. Atkins was a New York cardiologist who found that, for slimming, a diet low in carbohydrates and high in fat and protein worked.43

While Yudkin, Mann, and Ahrens had focused on sugar/​carbohydrates as the cause of heart attacks, Atkins had focused on sugar/​carbohydrates as the cause of obesity. And Taubes continued in Atkins’s wake, noting that the epidemic of obesity (and type 2 diabetes) accelerated when fat in food was being replaced by carbohydrate (see Figure 4). Thus, between 1960 and 2000 the incidence of obesity more than doubled, from 13.4 percent of the population to 30.9 percent, while the incidence of type 2 diabetes rose even more markedly, from 2.6 percent to 6 percent of the population. Since 2000 it has continued to rise, and it reaches nearly 10 percent today.44

Yet we should eschew easy myth‐​making. Thus Jennie Brand‐​Miller at the University of Sydney, Australia, has shown that in Australia and the United Kingdom, sugar consumption fell between 1980 and 2003 even as obesity rose, which suggests that obesity cannot be attributed to any single nutrient.45 Moreover, a recent massive study of the literature (data on 68.5 million people) found that while overweight (body mass index [BMI] over 25) and obesity (BMI over 30) are — as is widely known — associated with cardiovascular and other diseases, the impact may be less important than is widely feared, and the authors of the study noted that “the rate of this increase has been attenuated owing to decreases in underlying rates of death from cardiovascular disease.”46 Indeed, life expectancies in the United States have continued to rise (as they have continued to rise among industrialized countries since 1840) by three months for every year lived, or six hours for every day lived, which is truly extraordinary.47 Moreover, the so‐​called “obesity paradox” reveals how, under some circumstances, being overweight can apparently be healthful, and we should remember that as early as 1955 the WHO symposium noted that the Western diet had dual effects in both stimulating and damaging our health.48 We are still trying to understand these effects, and it must be premature to confidently dictate our diet.

There is nonetheless currently a scientific consensus on health and diet, which has been summarized by the American Heart Association:

Dietary saturated fat does increase the rate of cardiovascular disease significantly (Keys got that right), but

replacing it with refined carbohydrates and sugars does not reduce the rate of cardiovascular disease (Keys got that wrong, whereas his critics, including Yudkin, Mann, and Ahrens, got that right), but

replacing saturated (animal) fat with unsaturated (vegetable) fat does reduce the rate of cardiovascular disease significantly (as effectively as does treatment with statins) as long as those unsaturated fats are not trans fats.49

But this consensus has not yet deeply penetrated the public debate, and while most popular commentators now follow the Taubes anti‐​carbohydrate/​anti‐​sugar story, the federal government and leading medical authorities still follow the traditional anti‐​fat story.50 This divergence of opinion is both unnecessary and unhelpful.

A Nutritional Note

Reducing food to its constituent chemicals such as carbohydrate or fat is now increasingly criticized as “nutritionism,” because such reductionism may mislead by ignoring the complex and generally unknown interactions between the different chemicals in food.51 So, for example, the data may mean that meat is dangerous not because of its fat content but because of its protein or haem content (haem being the iron‐​containing chemical in meat that gives it a red color).52 Equally, a Harvard group has identified that plant‐​based diets that are rich in sugars, starch, or refined carbohydrates may be unhealthful.53

The current American Heart Association advice, therefore, seeks to avoid the nutritionist error by recommending a “Mediterranean” diet (rich in olive oil, vegetables, fruit, nuts, and legumes such as peas, beans, lentils, and chickpeas; moderate in fish, poultry, alcohol, and wholegrain cereals; and low in red meat, processed meat, and sweet foods such as cakes or jams). The similar DASH (Dietary Approaches to Stop Hypertension) diet is also recommended by the association.54

A Biochemical Note

Taubes suggested that, calorie for calorie, carbohydrates in the diet may promote obesity more than fat does because they stimulate the secretion of insulin, which in turn stimulates adipocytes (fat cells) to store fat: just as a pubertal girl puts on weight around her hips and at her breasts because of the local actions on fat cells by certain female hormones (not because she’s suddenly started to overeat), so someone who swaps fats for carbohydrates may start to put on weight because of the generalized effect on fat cells of insulin. Further, insulin drives down blood sugar levels, which in turn promotes the secretion of hunger hormones such as ghrelin, which therefore stimulates further eating.55

Conclusion

The central question remains: Why, in 1977, did the Senate Select Committee on Nutrition and Human Needs publish its Dietary Goals for the United States when so many credible authorities, including Yudkin, Atkins, Ahrens, Mann, and the American Medical Association, had anticipated, at least in part, today’s understanding of carbohydrates and other saturated fat substitutes as dangerous?

One problem is that scientists are much less scientific than is popularly supposed. John Ioannidis of Stanford University has shown in his 2005 paper “Why Most Published Research Findings Are False” (which has been cited nearly 5,000 times) that the poor application of statistics allows most published research findings to indeed be false, while Brian Nosek of the University of Virginia recently reported — again in large part because of the poor application of statistics — that fewer than half of published studies in psychology can be reproduced.56 Although Nosek’s findings have been challenged, it is now commonplace to describe a “crisis of reproducibility” in science, and mainstream scholars now write articles with such titles as “Saving Science.”57 Too many research papers, in short, cannot be trusted. Why not?

There is a perverse reason that scientists use poor statistics: career progression. In a paper entitled “The Natural Selection of Bad Science,” Paul Smaldino and Richard McElreath of the University of California, Merced, and the Max Planck Institute, Leipzig, found that scientists select “methods of analysis … to further publication rather than discovery.”58 Smaldino and McElreath report how entire scientific disciplines — despite isolated protests from whistleblowers — have, for more than half a century, selected statistical methods precisely because they will yield publishable rather than true results. The popular view is that scientists are falsifiers, but in practice they are generally verifiers, and they will use statistics to extract data that support their hypotheses. Keys, for example, was not a dishonest man, he was merely a typical scientist who had formulated a theory, which — by using poor statistics — he was able over the course of a long career and many publications to appear to verify.

Aggravating the problem of poor science is that research operates a version of public‐​choice theory: in his 1965 Logic of Collective Action, Mancur Olsen showed how small interest groups can capture public policy, and publicly funded science is no exception. Once armed with power over government‐​funded research grants, access to peer‐​reviewed journals, and appointments to university positions, Keys and his fellow elite researchers could enforce their paradigm on the whole field. Which was why the successful paradigm‐​shifter emerged not as a mainstream scientist but as a journalist — Taubes — who was spared the pressure to conform. And this public‐​choice aspect of science was aggravated by the Senate Select Committee’s endorsement of the fat paradigm, which fueled it, literally, with public money.

The federal government’s failings were further aggravated by lobbying. When McGovern’s committee reported, the reaction from the meat, egg, and other food lobbyists was so vitriolic that the committee was forced to hold additional public hearings. Following those, a second edition of Dietary Goals for the United States was hurriedly released in late 1977, retracting some of its strongest earlier claims. For example, the committee added this sentence: “science [cannot] at this time insure that an altered diet [will] provide improved protection from killer diseases such as heart disease.”59 As it happened, the meat and egg lobbyists were not wrong in all their objections, but they influenced the committee not because of their superior science, but because of their electoral power.

Because of the controversy, the reputation of the Select Committee suffered, and its mandate was allowed to lapse. The issuance of further federal dietary advice was then charged to the Department of Health and Human Services (HHS) and the Department of Agriculture (USDA), which have since jointly published, every five years, their Dietary Guidelines for Americans (the most recent was in 2015), which have, however, only reinforced the anti‐​fat, pro‐​carbohydrate message of the original 1977 Dietary Goals. This message was to be popularized in the USDA’s Food Guide Pyramid (1992), MyPyramid (2005), and MyPlate (2011).

The USDA was so empowered specifically to help protect agricultural interests, which inevitably has distorted its advice. Marion Nestle, for example, professor of nutrition at New York University, reports that when she was hired to edit the 1988 Surgeon General’s Report on Nutrition and Health,