Gary Taubes

This is considered the fundamental principle underlying modern genetic research: once evolution comes upon a genetic mechanism that works, it reuses it again and again. Those genes that regulate the development and the existence of any single living organism will likely be used in some similar fashion in all of them. “When reduced to essentials,” as the cancer researcher J. Michael Bishop suggested in his 1989 Nobel prize lecture, “the fruit fly and Homo sapiens are not very different.”

But the greatest single change in the American diet was in fact the spectacular increase in sugar consumption from the mid-nineteenth century onward, from less than 15 pounds a person yearly in the 1830s to 100 pounds by the 1920s and 150 pounds (including high-fructose corn syrup) by the end of the century. In effect, Americans replaced a good portion of the whole grains they ate in the nineteenth century with refined carbohydrates.

We should not be surprised that dieting is difficult, as Keith Frayn of Oxford University says in his 1996 textbook, Metabolic Regulation. “It is a fight against mechanisms which have evolved over many millions of years precisely to minimize its effects.”

“Theories that diseases are caused by mental states and can be cured by will power,” as Susan Sontag observed in her 1978 essay Illness as Metaphor, “are always an index of how much is not understood about the physical terrain of a disease.” This is certainly the case with obesity.

The bulk of the science is no longer controversial, but its potential significance has been minimized by the assumption that saturated fat is still the primary evil in modern diets.

Whatever the accepted wisdom, making obesity a behavioral issue is endlessly problematic.

Men who have excessive faith in their theories or ideas are not only ill prepared for making discoveries; they also make very poor observations.

Skepticism, however, cannot be removed from the scientific process. Science does not function without it.

A colleague once defined an academic discipline as a group of scholars who had agreed not to ask certain embarrassing questions about key assumptions.

The most dramatic of these animal obesity models is known as hypothalamic obesity, and it served as the experimental obesity of choice for researchers from the 1930s onward. It also became another example of the propensity to attribute the cause of obesity to overeating even when the evidence argued otherwise. The interpretation of these experiments became one of a half-dozen critical turning points in obesity research, a point at which the individuals involved in this research chose to accept an interpretation of the evidence that fit their preconceptions rather than the evidence itself and, by so doing, further biased the perception of everything that came afterward.

Neither eating less nor exercising more will lead to long-term weight loss, as the body naturally compensates.

The reason for this book is straightforward: despite the depth and certainty of our faith that saturated fat is the nutritional bane of our lives and that obesity is caused by overeating and sedentary behavior, there has always been copious evidence to suggest that those assumptions are incorrect, and that evidence is continuing to mount.