Good Calories, Bad Calories

At the core of all 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-controlled, cannot do the job. And if fat consumption has no effect whatsoever on heart disease or breast cancer, the available clinical and epidemiological tools will 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—will remain beyond the realm of science to demonstrate unambiguously. Investigators and public-health authorities will continue to base their conclusions on their personal assessment of the totality of the data or the consensus of opinion among their colleagues.

One challenge 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 well 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 called “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 compelling, whereas wishful sciences remain “stuck fast in their tracks,” or “rather the reverse, flourishing most under their first authors before going downhill ever since.”

Wishful science eventually devolves to the point where it is kept alive simply by the natural reluctance of its advocates to recognize or acknowledge error, rather than compelling 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 originally 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 dramatically, and they seem to prevent heart attacks, although whether they actually do so by lowering cholesterol levels or by other means as well is still 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 will 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. All this may be irrelevant to the question of a healthy diet, however, because there is no compelling reason we should believe that a drug and a diet will have equivalent effects on our health, even if they both happen to lower cholesterol.