Good Calories, Bad Calories (7 page)

Over the next half-dozen years, Keys assembled a chain of observations that became the bedrock of his belief that fat caused heart disease. He fed high-fat and medium-fat diets to schizophrenic patients at a local mental hospital and reported that the fat content dramatical y raised cholesterol. He traveled to South Africa, Sardinia, and Bologna, where Margaret measured cholesterol and they assessed the fat content of the local diet. In Japan, they measured the cholesterol levels of rural fisherman and farmers; they did the same for Japanese immigrants living in Honolulu and Los Angeles. He concluded that the cholesterol/heart-disease association was not peculiar to race or nationality, not a genetic problem, but a dietary one. They visited a remote logging camp in Finland and learned that these hardworking men were plagued by heart disease. A local clinic had six patients, including three young men, who “suffered from myocardial infarction.” They shared a snack with the loggers: “slabs of cheese the size of a slice of bread on which they smeared butter,” Keys wrote; “they washed it down with beer. It was an object lesson for the coronary problem.”

Keys bolstered his hypothesis with a 1950 report from Sweden that heart disease deaths had virtual y disappeared there during the German occupation of World War I . Similar phenomena were reported in nations that had undergone severe food-rationing during the war—Finland, Norway, Great Britain, Hol and, the Soviet Union. Keys concluded that the dramatic reduction in coronary deaths was caused by decreased consumption of fat from meat, eggs, and dairy products. Skeptics observed, however, that these are among many deprivations and changes that accompany food rationing and occupation. Fewer calories are consumed, for instance, and weight is lost. Unavailability of gasoline leads to increased physical activity. Sugar and refined-flour consumption decreases. Any of these might explain the reduction in heart-disease mortality, these investigators noted.

Keys encountered similar skepticism in 1953, when he argued the same proposition, using comparisons of diet and heart-disease mortality in the United States, Canada, Australia, England and Wales, Italy, and Japan. The higher the fat intake, Keys said, the higher the heart-disease rates.

Americans ate the most fat and had the highest heart-disease mortality. This was a “remarkable relationship,” Keys wrote: “No other variable in the mode of life besides the fat calories in the diet is known which shows anything like such a consistent relationship to the mortality rate from coronary or degenerative heart disease.”

Many researchers wouldn’t buy it. Jacob Yerushalmy, who ran the biostatistics department at the University of California, Berkeley, and Herman Hil eboe, the New York State commissioner of health, co-authored a critique of Keys’s hypothesis, noting that Keys had chosen only six countries for his comparison though data were available for twenty-two countries. When al twenty-two were included in the analysis, the apparent link between fat and heart disease vanished. Keys had noted associations between heart-disease death rates and fat intake, Yerushalmy and Hil eboe pointed out, but they were just that. Associations do not imply cause and effect or represent (as Stephen Jay Gould later put it) any “magic method for the unambiguous identification of cause.”

This is an irrefutable fact of logical deduction, but confusion over the point was (and stil is) a recurring theme in nutrition research. George Mann, a former director of the famous Framingham Heart Study, cal ed this drawing of associations between disease and lifestyles “a popular but not very profitable game.” When the science of epidemiology was founded in 1662 by John Graunt, a London merchant who had undertaken to interpret the city’s mortality records, Mann noted, even Graunt realized the danger of confusing such associations with cause and effect. “This causality being so uncertain,”

Graunt wrote, “I shal not force myself to make any inference from the numbers.”

The problem is simply stated: we don’t know what other factors might be at work. Associations can be used to fuel speculation and establish hypotheses, but nothing more. Yet, as Yerushalmy and Hil eboe noted, researchers often treat such associations “uncritical y or even superficial y,” as Keys had: “Investigators must remember that evidence which is not inherently sound cannot serve even for partial support.” It “is worse than useless.”

Ironical y, some of the most reliable facts about the diet-heart hypothesis have been consistently ignored by public-health authorities because they complicated the message, and the least reliable findings were adopted because they didn’t. Dietary cholesterol, for instance, has an insignificant effect on blood cholesterol. It might elevate cholesterol levels in a smal percentage of highly sensitive individuals, but for most of us, it’s clinical y meaningless.*5

Nonetheless, the advice to eat less cholesterol—avoiding egg yolks, for instance—remains gospel. Tel ing people they should worry about cholesterol in their blood but not in their diet has been deemed too confusing.

The much more contentious issues were how the quantity and type of fat influenced cholesterol levels, and, ultimately more important, whether cholesterol is even the relevant factor in causing heart disease. Keys and his wife had measured only total cholesterol in the blood, and he was comparing this with the total amount of fat in the diet. Through the mid-1950s, Keys insisted that al fat—both vegetable and animal—elevated cholesterol.

And if al fat raised cholesterol, then one way to lower it was to eat less fat. This was the basis of our belief that a healthy diet is by definition a low-fat diet.

Keys, however, had oversimplified. Since the mid-1950s, researchers have known that the total amount of dietary fat has little effect on cholesterol levels.

In 1952, however, Laurance Kinsel , director of the Institute for Metabolic Research at the Highland–Alameda County Hospital in Oakland, California, demonstrated that vegetable oil wil decrease the amount of cholesterol circulating in our blood, and animal fats wil raise it. That same year, J. J. Groen of the Netherlands reported that cholesterol levels were independent of the total amount of fat consumed: cholesterol levels in his experimental subjects were lowest on a vegetarian diet with a high fat content, he noted, and highest on an animal-fat diet that had less total fat. Keys eventual y accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.

Kinsel and Edward “Pete” Ahrens of Rockefel er University then demonstrated that the crucial factor in control ing cholesterol was not whether the fat was from an animal or a vegetable, but its degree of “saturation,” as wel as what’s known as the chain length of the fats. This saturation factor is a measure of whether or not the molecules of fat—known as triglycerides—contain what can be considered a ful quotient of hydrogen atoms, as they do in saturated fats, which tend to raise cholesterol, or whether one or more are absent, as is the case with unsaturated fats, which tend, in comparison, to lower it. This kind of nutritional wisdom is now taught in high school, along with the erroneous idea that al animal fats are “bad” saturated fats, and al

“good” unsaturated fats are found in vegetables and maybe fish. As Ahrens suggested in 1957, this accepted wisdom was probably the greatest

“handicap to clear thinking” in the understanding of the relationship between diet and heart disease. The reality is that both animal and vegetable fats and oils are composed of many different kinds of fats, each with its own chain length and degree of saturation, and each with a different effect on cholesterol.

Half of the fat in beef, for instance, is unsaturated, and most of that fat is the same monounsaturated fat as in olive oil. Lard is 60 percent unsaturated; most of the fat in chicken fat is unsaturated as wel .

In 1957, the American Heart Association opposed Ancel Keys on the diet-heart issue. The AHA’s fifteen-page report castigated researchers—including Keys, presumably—for taking “uncompromising stands based on evidence that does not stand up under critical examination.” Its conclusion was unambiguous: “There is not enough evidence available to permit a rigid stand on what the relationship is between nutrition, particularly the fat content of the diet, and atherosclerosis and coronary heart disease.”

Less than four years later, the evidence hadn’t changed, but now a sixman ad-hoc committee, including Keys and Jeremiah Stamler, issued a new AHA report that reflected a change of heart. Released to the press in December 1960, the report was slightly over two pages long and had no references.*6

Whereas the 1957 report had concluded that the evidence was insufficient to authorize tel ing an entire nation to eat less fat, the new report argued the opposite—“the best scientific evidence of the time” strongly suggested that Americans would reduce their risk of heart disease by reducing the fat in their diets, and replacing saturated fats with polyunsaturated fats. This was the AHA’s first official support of Keys’s hypothesis, and it elevated high cholesterol to the leading heart-disease risk. Keys considered the report merely an “acceptable compromise,” one with “some undue pussy-footing” because it didn’t insist al Americans should eat less fat, only those at high risk of contracting heart disease (overweight middle-aged men, for instance, who smoke and have high cholesterol).

After the AHA report hit the press, Time quickly enshrined Keys on its cover as the face of dietary wisdom in America. As Time reported, Keys believed that the ideal heart-healthy diet would increase the percentage of carbohydrates from less than 50 percent of calories to almost 70 percent, and reduce fat consumption from 40 percent to 15 percent. The Time cover story, more than four pages long, contained only a single paragraph noting that Keys’s hypothesis was “stil questioned by some researchers with conflicting ideas of what causes coronary disease.”

THE INADEQUACY OF LESSER EVIDENCE

Another reason for the confusion and contradictions which abound in the literature concerning the etiology of coronary artery disease is the tyranny that a concept or hypothesis once formulated appears to exert upon some investigators in this field. Now to present, to emphasize, and even 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 in its tracks and controversy inevitably takes over. Unfortunately it must be admitted that in the quest to determine the causes of coronary artery disease, these latter deteriorations have taken place.

MEYER FRIEDMAN, Pathogenesis of Coronary Artery Disease, 1969

FROM THE 1950S ONWARD, researchers worldwide set out to test Ancel Keys’s hypothesis that coronary heart disease is strongly influenced by the fats in the diet. The resulting literature very quickly grew to what one Columbia University pathologist in 1977 described as “unmanageable proportions.” By that time, proponents of Keys’s hypothesis had amassed a body of evidence—a “totality of data,” in the words of the Chicago cardiologist Jeremiah Stamler

—that to them appeared unambiguously to support the hypothesis. Actual y, those data constituted only half the evidence at best, and the other half did not support the hypothesis. As a result, “two strikingly polar attitudes persist on this subject, with much talk from each and little listening between,” wrote Henry Blackburn, a protégé of Keys at the University of Minnesota, in 1975.

Confusion reigned. “It must stil be admitted that the diet-heart relation is an unproved hypothesis that needs much more investigation,” Thomas Dawber, the Boston University physician who founded the famous Framingham Heart Study, wrote in 1978. Two years later, however, he insisted the Framingham Study had provided “overwhelming evidence” that Keys’s hypothesis was correct. “Yet,” he noted, “many physicians and investigators of considerable renown stil doubt the validity of the fat hypothesis…. Some even question the relationship of blood cholesterol level to disease.”

Understanding this difference of opinion is crucial to understanding why we al came to believe that dietary fat, or at least saturated fat, causes heart disease. How could a proposition that incited such contention for the first twenty years of its existence become so quickly established as dogma? If two decades’ worth of research was unable to convince half the investigators involved in this controversy of the validity of the dietary-fat/cholesterol hypothesis of heart disease, why did it convince the other half that they were absolutely right?

One answer to this question is that the two sides of the controversy operated with antithetical philosophies. Those skeptical of Keys’s hypothesis tended to take a rigorously scientific attitude. They believed that reliable knowledge about the causes of heart disease could be gained only by meticulous experiments and relentlessly critical assessments of the evidence. Since this was a public-health issue, and any conclusions would have a very real impact on human lives, they believed that living by this scientific philosophy was even more critical than it might be if they were engaged in a more abstract pursuit. And the issue of disease prevention entailed an unprecedented need for the highest standards of scientific rigor. Preventive medicine, as the Canadian epidemiologist David Sackett had observed, targets those of us who believe ourselves to be healthy, only to tel us how we must live in order to remain healthy. It rests on the presumption that any recommendation is based on the “highest level” of evidence that the proposed intervention wil do more good than harm.

The proponents of Keys’s hypothesis agreed in principle, but felt they had an obligation to provide their patients with the latest medical wisdom. Though their patients might appear healthy at the moment, they could be inducing heart disease by the way they ate, which meant they should be treated as though they already had heart disease. So these doctors prescribed the diet that they believed was most likely to prevent it. They believed that withholding their medical wisdom from patients might be causing harm. Though Keys, Stamler, and like-minded physicians respected the philosophy of their skeptical peers, they considered it a luxury to wait for “final scientific proof.” Americans were dying from heart disease, so the physicians had to act, making leaps of faith in the process.