Gary Taubes

There is no such ambiguity, however, on the subject of carbohydrates. The most dramatic alterations in human diets in the past two million years, unequivocally, are (1) the transition from carbohydrate-poor to carbohydrate-rich diets that came with the invention of agriculture—the addition of grains and easily digestible starches to the diets of hunter-gatherers; (2) the increasing refinement of those carbohydrates over the past few hundred years; and (3) the dramatic increases in fructose consumption that came as the per-capita consumption of sugars—sucrose and now high-fructose corn syrup—increased from less than ten or twenty pounds a year in the mid-eighteenth century to the nearly 150 pounds it is today. Why would a dietary that excludes these foods specifically be expected to do anything other than return us to “biological normality”?

Since none of this research is particularly controversial, it’s hard to imagine why obesity researchers would not take seriously the hypothesis that carbohydrates have a unique ability to fatten humans—or, as Thomas Hawkes Tanner put it in The Practice of Medicine almost 140 years ago, that “farinaceous and vegetable foods are fattening, and saccharine matters are especially so.” Researchers who study carbohydrate metabolism have found this science compelling. In 1991, the Belgian physiologist Henri-Géry Hers, an authority on what are known as glycogen-storage diseases, one of which is named after him, put it this way: “Eating carbohydrates will stimulate insulin secretion and cause obesity. That looks obvious to me.…” but this simple chain of cause and effect has nonetheless been rejected out of hand by authority figures in the field of human obesity, who believe that the cause of the condition is manifestly obvious and beyond dispute, that the law of energy conservation dictates that obesity has to be caused by eating too much or moving too little.

Evolution should be our best guide for what constitutes a healthy diet.

This is how functioning science works. Outstanding questions are identified or hypotheses proposed; experimental tests are then established either to answer the questions or to refute the hypotheses, regardless of how obviously true they might appear to be. If assertions are made without the empirical evidence to defend them, they are vigorously rebuked…. Each new claim to knowledge, therefore, has to be picked apart and appraised….

This institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.

It’s not so much that fat fills us up as that carbohydrates prevent satiety, and so we remain hungry.

Diet Revolution may have been, as its publisher claimed, the fastest-selling book in history. Nonetheless, its “chief consequence,” as John Yudkin noted in 1974, may have been “to antagonize the medical and nutritional establishment.” In fact, Atkins had to antagonize only a very small and select group of men to have a profound and lasting affect on how we think about obesity and weight regulation. In obesity research, particularly in the United States in the 1970s, the established wisdom was determined not by any testing of hypotheses or even establishing of consensus but by the judgment of fewer than a dozen men who dominated the field.

Rats can be easily addicted to sugar, according to Hoebel, and will demonstrate the physical symptoms of opiate withdrawal when forced to abstain.

This era began with a handful of naïve assumptions…The forty years of research that followed would overturn them all—but it would have effectively no influence on the mainstream thinking about human obesity.

Practical considerations of what is to loosely defined as the “public health” have consistently been allowed to take precedence over the dispassionate, critical evaluation of evidence and the rigorous and meticulous experimentation that are required to establish reliable knowledge. The urge to simplify a complex scientific situation so that physicians can apply it and their patients and the public embrace it has taken precedence over the scientific obligation of presenting the evidence with relentless honesty. The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

Von Noorden’s focus on metabolic expenditure set the science of obesity on the path we still find it. The evolution of this research, however, proceeded like a magician’s sleight-of-hand. By the 1940s, common sense, logic, and science had parted ways.

It’s hard to avoid the observation that at least some individuals lose weight on carbohydrate-restricted diets while eating considerably more calories then would normally be consumed in a semi-starvation diet.… Something else is going on here, and it has nothing to do with calories.

“It appears that efforts to promote the use of low-calorie and low-fat food products have been highly successful,” Weinsier noted, but the reduction in fat intake did “not appear to have prevented the progression of obesity in the population.”