Consider, for instance, that most reliable evidence suggests that Americans have indeed made a conscious effort to eat less fat, and particularly less saturated fat, since the 1960s. According to the USDA, we have been eating less red meat, fewer eggs, and more poultry and fish; our average fat intake has dropped from 45 percent of total calories to less than 35 percent, and National Institutes of Health surveys have documented a coincident fall in our cholesterol levels. Between 1976 and 1996, there was a 40-percent decline in hypertension in America, and a 28-percent decline in the number of individuals with chronically high cholesterol levels. But the evidence does not suggest that these decreases have improved our health. Heart-disease death rates have indeed dropped over those years. The risk of suffering a severe heart attack, what physicians call an acute myocardial infarction, may have diminished as well. But there is little evidence that the incidence of heart disease has declined, as would be expected if eating less fat made a difference. This was the conclusion, for instance, of a ten-year study of heart-disease mortality published in The New England Journal of Medicine in 1998, which suggested that the death rates are declining largely because doctors and emergency-medical-service personnel are treating the disease more successfully. American Heart Association statistics support this view: between 1979 and 2003, the number of inpatient medical procedures for heart disease increased 470 percent. In 2003 alone, more than a million Americans underwent cardiac catheterizations; more than a quarter-million had coronary-artery bypass surgery.
The percentage of Americans who smoke cigarettes has also dropped considerably over the years—from 33 percent of Americans over eighteen in 1979 to 25 percent fifteen years later. This should also have significantly reduced the incidence of heart disease. That it hasn’t, strongly suggests we’re doing something that counteracts the beneficial effect of giving up cigarettes. Indeed, if the last few decades were considered a test of the fat-cholesterol hypothesis of heart disease, the observation that the incidence of heart disease has not noticeably decreased could serve in any functioning scientific environment as compelling evidence that the hypothesis is wrong.
Throughout the world, on the other hand, the incidence of obesity and diabetes is increasing at an alarm in grate. Obesity levels in the United States remained relatively constant from the early 1960s through 1980, between 12 and 14 percent of the population; over the next twenty-five years, coincident with the official recommendations to eat less fat and so more carbohydrates, it surged to over 30 percent. By 2004, one in three Americans was considered clinically obese. Diabetes rates have increased apace. Both conditions are associated with an increased risk of heart disease, which could explain why the incidence of heart disease is not decreasing. It is also possible that obesity, diabetes, and heart disease all share a single, underlying cause. The surge in obesity and diabetes occurred as the population was being bombarded with the message that dietary fat is dangerous and that carbohydrates are good for the heart and for weight control. This suggests the possibility, however heretical, that this official embrace of carbohydrates might have had unintended consequences.
I first heard this notion in 1998, when I interviewed William Harlan, then associate director of the Office of Disease Prevention at the National Institutes of Health. Harlan told me that public-health experts like himself assumed that if they advised all Americans to eat less fat, with its densely packed calories, weights would go down. “What we see instead,” he said, “is actually weights have gone up, the portion sizes have gone up, the amount we eat has gone up…. Foods lower in fat became higher in carbohydrates and people ate more.”
The result has been a polarization on the subject of nutrition. Most people still believe that saturated fat, if not any and all fat, is the primary dietary evil—that butter, fat, cheese, and eggs will clog our arteries and put on weight—and have reduced their intakes. Public-health experts and many in the media insist that the obesity epidemic means the population doesn’t take their advice and continues to shun physical activity while eating fatty foods to excess. But a large number of people have turned to the message of Banting and one remarkably best-selling diet book after another: Eat Fat and Grow Slim (1958), Calories Don’t Count (1961), The Doctor’s Quick Weight Loss Diet (1968), Dr. Atkins’ Diet Revolution (1972), The Complete Scarsdale Medical Diet (1978), The Zone (1995), Protein Power (1996), Sugar Busters! (1998), and The South Beach Diet (2003). All advocate an alternative hypothesis: that carbohydrates are the problem, not fat, and if we eat less of them, we will weigh less and live longer. All have been summarily dismissed by the American Heart Association, the American Medical Association, and nutritional authorities as part of a misguided fad.
But is it? If 150 years of anecdotal evidence and observation suggest that carbohydrates are uniquely fattening, it would be unjustifiable scientifically to reject that hypothesis without compelling evidence to the contrary. Such evidence does not exist. My purpose here is to examine the data that do exist and to demonstrate how we have reached the conclusions we have and whether or not they are justified.
There is a more important issue here as well, and it extends far beyond the ideal weight-loss diet. Prior to the official acceptance of the low-fat-is-good-health dogma, clinical investigators, predominantly British, had proposed another hypothesis for the cause of heart disease, diabetes, colorectal and breast cancer, tooth decay, and half-dozen or so other chronic diseases, including obesity. The hypothesis was based on decades of eyewitness testimony from missionary and colonial physicians and two consistent observations: that these “diseases of civilization” were rare to nonexistent among isolated populations that lived traditional lifestyles and ate traditional diets, and that these diseases appeared in these populations only after they were exposed to Western foods—in particular, sugar, flour, white rice, and maybe beer. These are known technically as refined carbohydrates, which are those carbohydrate-containing foods—usually sugars and starches—that have been machine-processed to make them more easily digestible.
In the early 1970s, the hypothesis that refined carbohydrates cause heart disease and other chronic diseases competed directly with the dietary-fat hypothesis of heart disease. Carbohydrates could not cause heart disease, so the argument went, because fat seemed to cause heart disease. Moreover, any diet that contained a suitably low proportion of calories as fat would, by definition, be high in carbohydrates, and vice versa. The only caveat was that the fat hypothesis was, indeed, only a hypothesis, and the evidence to support it was ambiguous at best. By the mid-1970s, the carbohydrate theory of chronic disease had been transformed into a more politically and commercially acceptable version: it wasn’t the addition of refined and starchy carbohydrates to the diet that caused chronic disease, but the absence of fiber or roughage, removed in the refining process, that was responsible. This conclusion, however, has not been supported by clinical trials, which have shown that fiber has little or no effect on the incidence of any chronic disease.