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121 " The most obvious difficulty with the notion that a retarded metabolism explains the idiosyncratic nature of fattening is that it never had any evidence to support it. Before von Noorden proposed his hypothesis, Magnus-Levy had reported that the metabolism of fat patients seemed to run as fast if not faster than anyone else’s. "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
122 " it’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations. Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. "
123 " Eating carbohydrates prompts the kidneys to hold on to salt, rather than excrete it. The body then retains extra water to keep the sodium concentration of the blood constant. So, rather than having water retention caused by taking in more sodium, which is what theoretically happens when we eat more salt, carbohydrates cause us to retain water by inhibiting the excretion of the sodium that is already there. "
124 " Exercise can and does increase thirst and appetite, in most persons, in most situations, and most people respond to these sensations accordingly! "
125 " Removing carbohydrates from the diet works, in effect, just like the antihypertensive drugs known as diuretics, which cause the kidneys to excrete sodium, and water along with it. "
126 " these studies were expensive, and one way to justify the expense was to generate evidence that supported the official advice to avoid fat. If the evidence didn’t support the recommendations, then the task was to interpret it so that it did.*16 "
127 " 1983, Jules Hirsch of Rockefeller University framed this enigma in the form of two alternative hypotheses. One was the common belief “that obesity is the result of a willful descent into self-gratification.” The other was the “alternative hypothesis that there is something ‘biologic’ about obesity, some alteration of hormones, enzymes or other biochemical control systems which leads to obesity.” Because no such biologic abnormality had been unambiguously identified, Hirsch believed, “it is perhaps better to maintain the illusion that obesity is not an illness. It is more pleasant to believe that it is no more than an error of good judgment and that better judgments and choices will eventually lead” to a better outcome. "
128 " Despite these commonsensical objections, Mayer’s hypothesis won out. It helped that Mayer—like Ancel Keys and Dennis Burkitt—perceived the process of convincing the public and the medical-research community to be akin to a crusade. This served to absolve him, apparently, of the obligation to remain strictly accurate about what the research, including his own, had or had not demonstrated. "
129 " energy balance must be regulated involuntarily, without conscious intent, and that the mechanisms that do so adapt both intake to expenditure and expenditure to intake. Our bodies work to minimize long-term fluctuations in energy reserves and maintain a stable body weight, and they do so, as with all our homeostatic systems, "
130 " the hypothesis simply failed to explain how the brain manages to monitor our fat stores, and then raise or lower food intake and energy expenditure in response. Saying that we’re all endowed with a lipostat that monitors our adiposity and then regulates hunger appropriately is just another way of saying that our weight remains remarkably stable, whether we’re lean or obese, and then assigning the cause to a mysterious mechanism in the brain whose function is to achieve this stability. "
131 " When researchers looked at trends between diet and disease, as Himsworth and Joslin had done with diabetes and Keys and a later generation of researchers would do with heart disease and even cancer, they would measure only fat, protein, and total carbohydrate consumption and fail to account for any potential effect of refined carbohydrates. "
132 " by the 1960s hypertension and high cholesterol were two of the three major risk factors associated with premature coronary heart disease (the third was smoking), so it was difficult to imagine that eating carbohydrates might be beneficial for one risk factor, cholesterol, while being detrimental for another, blood pressure. "
133 " Though the traditional response to the failure of semi-starvation diets to produce long-term weight loss has been to blame the fat person for a lack of willpower, Bruch, Rony, and others have argued that this failure is precisely the evidence that tells us positive caloric balance or overeating is not the underlying disorder in obesity. "
134 " If we consider the last forty years of research as a test of Mayer’s hypothesis that physical activity induces weight loss or even inhibits weight gain, it’s clear the hypothesis leads nowhere meaningful. What Mayer initially insisted had to be true, so much so that he publicly accused the “enemies of exercise” of propagating “pseudo-science,” had devolved over the intervening decades into an analysis of whether the prescription of an exercise program would inhibit weight gain by three ounces each month or accelerate it by two. "
135 " Obese patients who try to reduce their weight by semi-starvation, as Rony noted, will always be fighting what he called their “spontaneous impulses of eating and activity.” Once they give in to these impulses, which is effectively preordained, they will get fat again. "
136 " By 1980, this link between cancer and low cholesterol was appearing in study after study. The most consistent association was between colon cancer and low cholesterol in men. In the Framingham Study those men whose total cholesterol levels were below 190 mg/dl were more than three times as likely to get colon cancer as those men with cholesterol greater than 220; they were almost twice as likely to contract any kind of cancer than those with cholesterol over 280 mg/dl. "
137 " as this research had now made clear, the critical molecules determining the balance of storage and mobilization of fatty acids, of lipogenesis and lipolysis, are glucose and insulin—i.e., carbohydrates and the insulin response to those carbohydrates. "
138 " The obvious implication is that obesity and Type 2 diabetes are two sides of the same physiological coin, two consequences, occasionally concurrent, of the same underlying defects—hyperinsulinemia and insulin resistance. "
139 " Glucose goes directly into the bloodstream and is taken up by tissues and organs to use as energy; only 30–40 percent passes through the liver. Fructose passes directly to the liver, where it is metabolized almost exclusively. As a result, fructose “constitutes a metabolic load targeted on the liver,” the Israeli diabetologist Eleazar Shafrir says, and the liver responds by converting it into triglycerides—fat—and then shipping it out on lipoproteins for storage. The more fructose in the diet, the higher the subsequent triglyceride levels in the blood.*58 "
140 " A more rational form of treatment,” Pennington suggested, would be one that makes fat once again flow readily out of the fat cells, that directs “measures primarily toward an increased mobilization and utilization of fuel” by the muscles and organs. "