The Diet Delusion: Challenging the Conventional Wisdom on Diet, Weight Loss and Disease
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The Diet Delusion sets out to review the published research in the field of nutrition and weight management and explores the perceived wisdom of why there is an obesity and diabetes epidemic in much of the developed world, especially in the USA.
suggested, would be triggered by the “composition of the diet, and more specifically the use of highly refined carbohydrates.” It wasn’t until the late 1970s, just a few years before Neel himself publicly rejected his hypothesis, that obesity researchers began invoking thrifty genes as the reason why putting on weight seems so much easier than losing it. Jules Hirsch of Rockefeller University was among the first to do so, and his logic is noteworthy, because his primary goal was to establish
weight as those who were semi-starved on the balanced diet. Between 1963 and 1973, Robert Kemp, a physician at Walton Hospital in Liverpool, published three articles reporting his clinical experience with a low-carbohydrate, unrestricted-calorie diet. Kemp reported that his obese patients craved carbohydrates and were invariably puzzled and frustrated by two aspects of their condition: “that other28 people can eat just the same diet and remain thin,” and “that they themselves in earlier life may
of insulin as a fattening hormone would become a long-running controversy. Those physicians who believed, as Louis Newburgh did without reservation, that obesity was an eating disorder, rejected the idea that insulin could fatten humans, if for no other reason than that this suggested the existence of a defective hormonal mechanism that could lead to obesity. The evidence, however, suggested exactly that. When insulin was injected into diabetic dogs in the laboratory, or diabetic human patients
more insulin secreted in the days after the surgery, the greater the ensuing obesity. Obesity in these lesioned animals could be prevented by short-circuiting the exaggerated insulin response—by severing the vagus nerve, for example, that links the hypothalamus with the pancreas.fn10 Similarly, the hypersecretion of insulin was reported to be the earliest detectable abnormality in genetic strains of obesity-prone mice and rats. By the mid-1970s, it was clear that Stephen Ranson’s insights into
populations6 for us to draw reliable conclusions. He also insisted that in many of these populations—particularly the Inuit—relatively few individuals were likely to live long enough to develop chronic disease, so little could be learned. This argument, too, has taken on the aura of undisputed truth. This could be called the “nasty, brutish, and short7” caveat, after Thomas Hobbes’s pithy interpretation of the state of primitive lives. But earlier generations of physicians had the advantage of