Good Calories, Bad Calories (17 page)

At the core of al such ongoing scientific controversies is the inability to measure accurately the phenomenon at issue—the effect of dietary fat, for instance, on heart disease or cancer—either because it is negligible or nonexistent, or because the epidemiological tools available lack sufficient resolution for the task. Even clinical trials, unless done with meticulous attention to detail, double-blind, and placebo-control ed, cannot do the job. And if fat consumption has no effect whatsoever on heart disease or breast cancer, the available clinical and epidemiological tools wil always be incapable of demonstrating such a fact, because it is impossible in science to prove the nonexistence of a phenomenon. So the effect of saturated fat on heart disease—or the benefit of replacing saturated fat in the diet with carbohydrates or unsaturated fats—wil remain beyond the realm of science to demonstrate unambiguously. Investigators and public-health authorities wil continue to base their conclusions on their personal assessment of the totality of the data or the consensus of opinion among their col eagues.

One chal enge in this kind of controversy is to determine whether those skeptical of the established wisdom are incapable of accepting reality, closed-minded, or self-serving, or whether their skepticism is wel founded. In other words, is the evidence invoked to support the established wisdom the product of sound scientific thinking and reasonably unambiguous, in which case the skeptics are wrong, or is it what Francis Bacon would have cal ed “wishful science,” based on fancies, opinions, and the exclusion of contrary evidence, in which case the skeptics are right to be so skeptical? Bacon offered one viable suggestion for differentiating. Good science, he observed, is rooted in reality, and so it grows and develops, and the evidence grows increasingly more compel ing, whereas wishful sciences remain “stuck fast in their tracks,” or “rather the reverse, flourishing most under their first authors before going downhil ever since.”

Wishful science eventual y devolves to the point where it is kept alive simply by the natural reluctance of its advocates to recognize or acknowledge error, rather than compel ing evidence that it is right. “These are cases where there is no dishonesty involved,” explained the Nobel Prize–winning chemist Irving Langmuir in a celebrated 1953 lecture, “but where people are tricked into false results by a lack of understanding about what human beings can do to themselves in the way of being led astray by subjective effects, wishful thinking or threshold interactions.” Whereas good science would blossom over time, Langmuir noted, this “pathological science” would not. The most concise statement of this philosophy may be an unwritten rule of experimental physics credited original y to Wolfgang Panofsky, a former Manhattan Project physicist and presidential science adviser. “If you throw money at an effect and it doesn’t get larger,” Panofsky said, “that means it is not real.”

That has certainly been the case with the dietary-fat/breast-cancer hypothesis. The relationship between dietary fat, cholesterol, and heart disease is more complicated, because the hypothesis constitutes three independent propositions: first, that lowering cholesterol prevents heart disease; second, that eating less fat or less saturated fat not only lowers cholesterol and prevents heart disease but, third, that it prolongs life.

Since 1984, the evidence that cholesterol-lowering drugs, particularly those known as statins, are beneficial—proposition number one—has certainly blossomed, particularly regarding people at high risk of heart attack. These drugs reduce serum-cholesterol levels dramatical y, and they seem to prevent heart attacks, although whether they actual y do so by lowering cholesterol levels or by other means as wel is stil an open question. (“Most drugs have multiple actions,” notes the University of Washington biostatistician Richard Kronmal. Saying that statins reduce heart-disease risk by lowering cholesterol, he adds, is like “saying that aspirin reduces heart-disease risk by reducing headaches.”) There is also a legitimate question as to whether they wil prolong the life of anyone who is not in imminent danger of having a heart attack, but new trials consistently seem to confirm their benefits. Al this may be irrelevant to the question of a healthy diet, however, because there is no compel ing reason we should believe that a drug and a diet wil have equivalent effects on our health, even if they both happen to lower cholesterol.

The evidence supporting the second and third propositions—that eating less fat, or less saturated fat, makes for a healthier and longer life—has remained stubbornly ambiguous. The message of the 1984 consensus conference and the ensuing expert reports was that the benefits of low-fat diets were effectively indisputable, and so pursuing further research on these questions was unnecessary. This in turn led to the ubiquitous belief in the validity of Keys’s hypothesis and the unwholesome nature of saturated fat, but the reality is that since the early 1980s the evidence has become progressively less compel ing.

Keys’s own experience stands as an example. In the early 1950s, Keys had based his dietary-fat hypothesis of heart disease to a great extent on the congruence between the changing-American-diet story and the appearance of a heart-disease epidemic. By the early 1970s, however, he had publicly acknowledged that the heart-disease epidemic may indeed have been a mirage. There was “no basis” to make the claim, he admitted, that trends in heart-disease mortality in the United States reflect changes in the consumption of any item in the diet.

In the late 1950s, Keys supported his fat hypothesis with the disparity in fat consumption, cholesterol levels, and heart-disease mortality he found among Japanese men living in Japan, Hawaii, and Los Angeles. This association was then confirmed, more or less, in his Seven Countries Study, in which the Japanese vil agers stil had remarkably little fat in their diets, low cholesterol levels, and fewer heart-disease deaths over ten years than any other population with the exceptions of those of the islands of Crete and Corfu and the vil age of Velika Krsna in what is now Serbia. By the mid-1990s, however, the Japanese contingent of the Seven Countries Study, led by Yoshinori Koga, reported that fat intake in Japan had increased from the 6

percent of calories they had measured in the farming vil age of Tanushimaru thirty-five years earlier, to 22 percent of calories. “There have been progressive increases in consumption of meats, fish and shel fish and milk,” they reported. Mean cholesterol levels rose in the community from 150 mg/dl to nearly 190 mg/dl, which is only 6 percent lower than the average American values (202 mg/dl as of 2004). Yet this change went along with a

“remarkable reduction” in the incidence of strokes and no change in the incidence of heart disease. In fact, the chance that a Japanese man of any particular age would die of heart disease had steadily diminished since 1970. “It is suggested that dietary changes in Tanushimaru in the last thirty years have contributed to the prevention of cardiovascular disease,” Koga and his col eagues concluded.

In the late 1950s, Keys had dismissed the possibility that misdiagnosis might have contributed to the extremely low heart-disease death rates in Japan they had observed initial y. In 1984, Keys reversed himself, saying that the Japanese cardiologists who had worked with his Seven Countries Study “might have been misled by the local physicians who signed the death certificates and provided details.”

Three years later, Keys acknowledged to the New York Times that he had re-evaluated his hypothesis. “I’ve come to think that cholesterol is not as important as we used to think it was,” he said, “Let’s reduce cholesterol by reasonable means, but let’s not get too excited about it.”

As in Japan, increases in fat consumption with coincident decreases in heart disease have occurred recently in Spain and Italy, which has prompted the observation that the French paradox—a nation that eats a high-fat diet and has little heart disease—has evolved into the French-Italian-Spanish paradox.*24 Through the mid-1990s, according to John Powles, an epidemiologist with the British Institute of Public Health, France and Italy both showed declines in death rates from stroke and heart disease that were greater than those in most European countries, while the decline in mortality in Spain lagged only slightly behind. And studies of Mediterranean immigrants to Australia suggest that the low heart-disease rates of these immigrants fal even lower in Australia, despite a considerable increase in their meat consumption.

In the late 1970s, the World Health Organization launched a research project known as MONICA, for “MONItoring CArdiovascular disease,” that was similar in concept to Keys’s Seven Countries Study but considerably larger. The study tracked heart disease and risk factors in thirty-eight populations in twenty-one countries—a total population of roughly six mil ion people, which unlike previous studies included both men and women. Hugh Tunstal -Pedoe, the MONICA spokesman, has described the project as “far and away the biggest international col aborative study of cardiovascular disease ever carried out” and noted that, “whatever the results, nobody else has better data.” By the late 1990s, MONICA had recorded 150,000 heart attacks and analyzed 180,000 risk-factor records. Its conclusion: heart-disease mortality was declining worldwide, but that decline was independent of cholesterol levels, blood pressure, or even smoking habits.

The MONICA investigators suggested reasons why their study might not have confirmed Keys’s hypothesis, among them the possibility, as Tunstal -

Pedoe noted, that with populations “the contribution of classical risk factors is swamped by that of other dietary, behavioral, environmental, or developmental factors.” He also discussed something that may have contributed initial y to the widespread belief in Keys’s hypothesis: the tendency to publish or pay attention to only that evidence that confirms the existing beliefs about heart disease and risk factors. “If you do a study in your population and you show a perfect correlation between risk factors and heart disease, you rush off and publish it. If you don’t, unless you have great confidence in yourself, you worry that perhaps you didn’t measure something properly, or perhaps you’d better keep quiet, or perhaps there’s something you haven’t thought about. And by doing this, there is a risk of myths’ becoming self-perpetuating.” “There are people,” Tunstal -Pedoe said, “who want to believe that if we find anything less than 100-percent correlation between traditional risk factors and trends in heart disease, we are somehow traitors to the cause of public health, and what we say should be suppressed, and we should be ashamed of ourselves. Whereas we are asking a perfectly reasonable question, and we came up with results. That is what science is about.”

In the two decades since the NIH, the surgeon general, and the National Academy of Sciences first declared that al Americans should consume low-fat diets, the research has also failed to support the most critical aspect of this recommendation: that such diets wil lead to a longer and healthier life. On the

contrary, it has consistently indicated that these diets may cause more harm than good. In 1986, the year before the National Cholesterol Education Program recommended cholesterol-lowering for every American with cholesterol over 200 mg/dl, the University of Minnesota epidemiologist David Jacobs visited Japan, where he learned that Japanese physicians were advising patients to raise their cholesterol, because low cholesterol levels were linked to hemorrhagic stroke. At the time, Japanese men were dying from stroke almost as frequently as American men were succumbing to heart disease. Jacobs looked for this inverse relationship between stroke and cholesterol in the MRFIT data and found it there, too. And the relationship transcended stroke: men with very low cholesterol seemed prone to premature death; below 160 mg/dl, the lower the cholesterol, the shorter the life.

In April 1987, the Framingham investigators provided more reason to worry when they final y published an analysis of the relationship between cholesterol and al mortality. After thirty years of observation, there was a significant association between high cholesterol and premature death for men under fifty. But for those over fifty, both men and women, life expectancy showed no association with cholesterol. This suggested, in turn, that if low cholesterol did prevent heart disease, then it must raise the risk of dying from other causes.