The media, as ever, jumped on the news of Ike’s heart attack and recovery. Because of the media’s uninformed sensationalism around the event, and the medical profession’s activism, Americans began to believe the government should play a role in individuals’ health. After all, if the president’s diet was a matter of public record and could be manipulated to improve his health, shouldn’t the same dietary guidelines be available to everyone? And if they were good for everyone, shouldn’t the government require Americans to follow these guidelines? More important, if government could now determine what made a diet healthy, did that not place incredible power in the hands of those who defined healthy diets? Ultimately, the events on that Denver golf course started a long, but uninterrupted, march toward dietary nannyism. But the more frightening problem came when the government—never heralded as a bastion of scientific knowledge—began to take advice from so-called experts based on preliminary and incomplete studies and to give the public potentially dangerous and very unhealthy guidelines.
In twice-daily press conferences, the news media eagerly followed the president’s recovery, in the process instructing Americans on the dangers of coronary disease. A new word crept into the everyday vocabulary: cholesterol. It had dark, evil overtones. Cholesterol. This was the monster Americans must defeat! A healthy person must keep his or her cholesterol low! High cholesterol portended to be the new polio, and Americans quickly embraced any maxim to lower cholesterol: quit smoking, exercise, and eat right. Ike had quit smoking in 1949, exercised, kept an optimal weight, and his cholesterol was below normal just prior to his attack. Afterward, Eisenhower began a strict, low-fat diet. . . and his weight began to rise. He cut out breakfast entirely, after first switching from oatmeal and skim milk to melba toast and fruit, but his weight still inched up. At that point Dr. Snyder was mystified: how can a man eat so little, exercise regularly, and still gain weight? After the president read about a group of New Yorkers who were battling cholesterol by cutting margarine, lard, cream, and butter out of their diets (and replacing them with corn oil), he followed suit.
Finally, his weight stabilized . . . but his cholesterol rose. Snyder grew so conscious of Ike’s fretting—his obsessing—about cholesterol that he began lying to him about the real cholesterol levels, understating them so Ike wouldn’t worry. Despite the fact that Eisenhower had essentially eliminated all supposedly high-cholesterol foods from his diet, his readings dramatically soared to what some physicians would call dangerous levels. History has a way of shining the spotlight on the ironic: at the very moment Ike’s physician was concealing cholesterol reports from his patient under the assumption that cholesterol caused heart ailments, Time magazine heralded Ancel Keys, a physiologist from the University of Minnesota whose research “proved” that a low-fat, low-cholesterol, carb-heavy diet would prevent heart disease.3 Two weeks later, the American Heart Association endorsed the Keys analysis, calling for low-fat/low-cholesterol diets. “Diet Linked to Cut in Heart Attacks,” proclaimed The New York Times in May 1962. And Ike? He lived for another fourteen years after his first heart attack.
Eisenhower’s own cardiologist bought into the dietary fat hypothesis, claiming a “great epidemic” of cardiovascular disease had struck America in the post-World War II period.4 Similarly, Jean Mayer of Harvard claimed in 1975 that the rise of heart disease was an epidemic as dire as the “arrival of bubonic plague . . . in fourteenth-century Europe, syphilis . . . at the end of the fifteenth century, and . . . tuberculosis at the beginning of the nineteenth century.”5 At the same time, medical “experts” and government officials began claiming that Americans had changed their diets to eat more red meat and fats in the twentieth century. In fact, both claims were false, and, as in the case of AIDs some thirty years later, one could make or break an “epidemic” simply by fiddling with definitions. And, as would be the case with global warming fifty years later, one could prove virtually anything based on where one started the trend line.
It is true that coronary cases seemed to increase dramatically between 1940 and 1970—but this was entirely because other diseases were being conquered and thus were not as rampant. A quarter of all men died of coronary disease in 1910, for example, and another quarter died from infections, parasites, flu, pneumonia, bronchitis, or tuberculosis, virtually all of which were eliminated or greatly suppressed by 1970. Cancer, meanwhile, went from eighth on the list to number two, and the rate of heart disease “doubled.”6 Simply put, modern medicine had conquered so many diseases over the previous century that people lived long enough to encounter (and die from) new or rare diseases.7 Cancer and heart disease, which took longer to manifest themselves than, say, smallpox, became the leading killers.
At the same time, improvements in technology made it possible to more accurately diagnose the cause of death, hence, unexplained or sudden deaths that had once been mysterious were finally, correctly, attributed to heart disease or cancer.8 Even the American Heart Association admitted that the “new” classification of arteriosclerotic heart disease in 1949 made a “great difference,” and that the “remarkable increase in the reported number of cases of this condition” lay almost entirely in the use of the electrocardiogram in confirming clinical diagnoses (emphasis in original).9 Predictably, when the International Classification of Diseases (ICD) added a second heart disease category (ischemic heart disease), the percentage of heart-disease deaths shot up dramatically. Even the World Health Organization acknowledged that “much of the apparent increase in [heart disease] mortality may simply be due to improvements in the quality of certification and more accurate diagnoses. . . .”10
Around the same time, the false notion that the United States used to be a vegan society began to gain traction, thus further contributing to misconceptions about meat. Proponents of this myth argued that the late 1800s had been some “idyllic era free of chronic disease,” which was ruined after the rise of meat and fat consumption consigned Americans to heart attacks.11 Americans, according to this legend, got away from eating as they did in the old days, when they consumed more cereals. Jane Brody’s 1985 Good Food Book claimed 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 and potatoes, and other vegetables and fruits and toward foods derived from animals. . . .”12 Two factors contributed to this perception. First, the publication of The Jungle by Upton Sinclair in 1906, which demonized the meat industry, cut American meat sales by half, and by the time of the Great Crash in 1929, meat packers had still not recovered.13 Second, there were flawed estimates by the United States Food and Drug Administration, which used “food disappearance” methods to calculate what people ate. Not only did the data go back no farther than the 1920s—one scholar described the data as “lousy” and said “you can prove anything you want to prove”—but most historical records show that Americans were voracious meat eaters in the 1800s.14 Some studies show that nineteenth-century Americans ate forty to sixty pounds of meat more per capita per year than in the twentieth century—but such evidence did not fit the “meat-makes-us-unhealthy” argument so it was largely ignored.15 Moreover, the farther back one goes, the clearer it becomes that hunter-gatherer (i.e., heavy meat-eating) societies were healthier than farmer societies (whose diets were high in carbohydrates—grains, corn, and rice). Tom Standage, in his Edible History of Humanity, noted thatfarmers suffered from various diseases of malnutrition that were rare or absent in hunter-gatherers. . . . Farmers were also more susceptible to infectious diseases such as leprosy, tuberculosis, and malaria as a result of their settled lifestyles. . . . As the farming groups settle down and grow larger, the incidence of malnutrition, parasitic diseases, and infectious diseases increases.16
None of this concerned Ancel Keys, however. He had a powerful personality and an apparently novel argument, namely, that fats and meat were linked to cholesterol, and cholesterol to heart disease. His theory dated to a visit to Italy in 1951, whe
re on the basis of noncontrolled (that is to say, unscientific) blood-serum measurements taken on a few hundred workers and Rotary Club members, he concluded that rich people had more heart disease simply because they ate more meat.17 Even then, he had to admit, “Direct evidence on the effect of the diet on human arteriosclerosis is very little. . . .”18 Over the next decade, Keys assembled his famous “six countries” study (later expanded to seven), claiming a consistent relationship between fat calories in the diet and heart disease. When other researchers examined his work, however, they found he had left out sixteen other countries, whose inclusion would disprove his hypothesis.19 Similarly, in 1957 the American Heart Association sharply criticized Keys’s findings as “uncompromising stands based on evidence that does not stand up under critical examination,” and concluded that there wasn’t enough evidence to link food, especially fat, and heart disease.20 Only four years later, in 1961, the AHA made a U-turn, directed by a six-man committee including Keys and his chief supporter, Jeremiah Stamler, by issuing a report that contained only half a page of “recent scientific references,” many of which actually contradicted the 1957 report’s conclusions. The new AHA report cited the “best scientific evidence of the time” to link dietary fat and heart disease. Time quickly enshrined Keys as the heart guru of the age.
From 1961 to 1977, a tidal wave of research appeared on the causes of heart disease, diet, and cholesterol, yet none of it arrived at any clear conclusions. At best, two camps appeared—the Keys school, arguing that a high-fat diet led to heart disease, and a completely opposite school of thought comprising researchers who claimed that, in fact, fats and meat were not the problem, carbohydrates and insulin were. One protégé of Keys at Minnesota, Henry Blackburn, observed in 1975 that two “strikingly polar attitudes persist” while Thomas Dawber, who pioneered the Framingham Heart Study, flipped back and forth, admitting in 1978 that “the diet-heart relation is an unproved hypothesis,” then in 1980 insisting that the Framingham Heart Study proved the Keys hypothesis, before adding the caveat, “many physicians and investigators of considerable renown still doubt the validity of the fat hypothesis . . . [and] some even question the relationship of blood cholesterol level to disease.”21 Research was showing fairly consistently that low-carbohydrate diets were optimal for losing weight, at which point the arguments usually shifted to the impact of high-fat diets on cholesterol, not weight.22
Despite the debate, the science was never settled. But there was a difference: the dietary-fat-equals-death group became utterly convinced of its certitude and acted like activists, while the other half of the researchers continued to act like scientists by suggesting nothing was proven on either side. Claude Bernard, in his Introduction to the Study of Experimental Medicine in 1865, warned thatmen who have excessive faith in their theories or ideas are not only ill prepared for making discoveries; they also make very poor observations [because] they observe with a preconceived idea, and when they devise an experiment, they can see, in its results, only a confirmation of their theory. . . . it happens further quite naturally that men who believe too firmly in their theories, do not believe enough in the theories of others. So the dominant idea of these [men] is to find others’ theories faulty and to try to contradict them.23
Meyer Friedman, in 1969, labeled this tendency the “tyranny [of a] hypothesis once formulated,” noting that “to enthuse about one’s own theory or hypothesis is legitimate and even beneficial, but if presentation gives way to evangelistic fervor, emphasis to special pleading, and enthusiasm to bias, then progress is stopped dead.”24 Thomas Jefferson said it only slightly differently: “He who knows best knows how little he knows.”
Even as massive studies by the National Institutes of Health and the American Heart Association involving fifty thousand test subjects were being prepared in 1961—studies that would provide abundant evidence when the conclusions came in—the AHA was already preparing booklets emphasizing the importance of lowering cholesterol. Some of the researchers were already spinning the results in favor of the Keys hypothesis before the study was even under way. It made good press to say that fat caused heart disease, reinforcing the “truth” of the original hypothesis. Albert Einstein had categorically dismissed such an approach when, in 1919, two of his required three experiments proved his theory of relativity, saying only that until the “redshift” condition had been met, “the whole theory would have to be abandoned.”25 After the redshift was in fact confirmed empirically, philosopher Karl Popper remarked, “What impressed me most was Einstein’s own clear statement that he would regard his theory as untenable if it should fail in certain tests.”26 This was merely the theory of the universe, not a minor point about dietary fat—and yet Einstein was anything but dogmatic or proselytizing. Forty years later, not only did a large segment of heart researchers fail to wait for the results of a dietary /cholesterol version of a redshift, but there was no acknowledgment that the absence of such data would matter anyway!
Data that didn’t fit the Keys hypothesis was arbitrarily dismissed. This included evidence of Japanese men in California who had low cholesterol levels and still had higher rates of heart disease than relatives living in Japan. As the insightful historian of the diet debate Gary Taubes noted:Any research that did not support their hypothesis was said to be misinterpreted, irrelevant, or based on untrustworthy data. Studies of Navajo Indians, Irish immigrants to Boston, African nomads, Swiss Alpine farmers, and Benedictine and Trappist monks all suggested that dietary fat seemed unrelated to heart disease. These were explained away or rejected by Keys.27
Among the various subgroups that began to stand out as more studies were conducted, the Masai nomads of Kenya had incredibly low blood-cholesterol levels, despite an almost exclusively fat/meat/milk diet; and other African tribes disproved the Keys hypothesis, despite his claims that they supported his conclusions.28
Supposedly, the Framingham Heart Study would provide definitive answers. Begun in 1952 in Framingham, Massachusetts, with 5,100 volunteers who were subjected to regular physicals and blood work—then reexamined every two years—the study initially included cholesterol among its risk factors, but as the evidence unfolded and as the participants in the study aged, low cholesterol was more closely linked to heart problems than high cholesterol! 29 More important still, the Framingham dietary research disproved Keys, yet it was not published with the rest of the Framingham data until researchers dug it out in the late 1960s and it was finally included in the twenty-fourth volume of the study released in 1968. This data found no difference at all between the diets of high-cholesterol men and low-cholesterol men.30 In short, there was a significant amount of evidence that the fatcholesterol-heart disease links either did not exist or, in fact, were the opposite of what was being sold to the public by the American Heart Association and the government.
Over the next few years, studies examining the amount of fat consumed and correlating it with either cholesterol or heart disease proved remarkably unsupportive of the Keys hypothesis. (Within particular populations in Puerto Rico, Honolulu, Chicago, Michigan, and Israel the results were the same, which is to say that there was no correlation.31) Then came the 5,400-strong Western Electric study in which, out of the 88 coronary cases, 14 were in the high-fat-intake group, 16 in the low-fat group. In 1977, researchers revisited the subjects and examined the cause of death, discovering that the “amount of saturated fatty acids in the diet was not significantly associated with the risk” of heart disease, and found no significant association of fatty acids in the diet with coronary disease.32 Despite a serpentine rationalization, the authors admitted that “most attempts to document the relation of dietary cholesterol, saturated fatty acids, and polyunsaturated fatty acids to serum cholesterol concentration . . . have been unsuccessful.”33
What followed is a case study in how data can be manipulated, regurgitated uncritically by the press, and turned into public policy. The update of the Western Electric study provided contrary evidence to t
he fat-heart disease hypothesis, so the authors of the study included four other studies whose evidence seemed to disprove their own results. Thus, they concluded that in fact a fatty diet affected serum cholesterol and long-term risk of death, and published this result in the New England Journal of Medicine in 1981. Jane Brody in The New York Times and The Washington Post slavishly reported these findings, which were then echoed in a report by the American Heart Association. To repeat: the Western Electric study did not show a correlation between risk of heart disease and a high-fat diet—it showed the opposite. Yet within four years after the publication of the study, virtually every major heart-related association had endorsed the false position.34
In fact, the only reliable method of arriving at medically and scientifically valid conclusions is to conduct double-blind, placebo-controlled clinical trials, and in fact, such trials are virtually impossible with food. Meat, butter, and cream, for example, have certain tastes that cannot be faked. Moreover, changing one aspect of a diet—fats—tends to change overall calories as well. Between 1950 and 1975, only about a dozen truly scientific trials of diet and heart disease were conducted. Only two of these actually examined low-fat diets and heart disease as opposed to cholesterol-lowering diets; and the two studies arrived at completely contradictory results.35 Or how about the New York Anti-Coronary Club, which examined 1,100 males beginning in the late 1950s? The researchers were so convinced that the fat/ heart disease link existed that as early as 1962 they leaked the interim results to The New York Times, which dutifully ran the headline “Diet Linked to Cut in Heart Attacks.”36 But there was a problem. The longer the study went, the more the data disproved the fat/heart disease link. In November 1966, another interim article appeared showing that 26 men on the low-fat diet had died, compared to only 6 on the high-fat diet. Seymour Dayton, in 1969, gave half of his test group a cholesterol-lowering diet and the other half a placebo: while only 66 of the lower-cholesterol group died from heart disease (compared to 96 in the placebo diet), the low-cholesterol group had higher death rates from cancer! A large study in Minnesota (the Minnesota Coronary Study) in 1968 found a cholesterol-lowering diet increased the risk of heart disease—but the results went unpublished for sixteen years, because, as one of the researchers said, “We were just disappointed in the way it came out.”37 In other words, the researchers were convinced that the science was “settled,” so their own results could not be valid.
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