24
" WHEN IT COMES TO THE CAUSE of chronic disease, as we discussed earlier, the carbohydrate hypothesis rests upon two simple propositions. First, if our likelihood of contracting a particular disease increases once we already have Type 2 diabetes or metabolic syndrome, then it’s a reasonable assumption that high blood sugar and/or insulin is involved in the disease process. Second, if blood sugar and insulin are involved, then we have to accept the possibility that refined and easily digestible carbohydrates are as well. "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
30
" A common feature of epidemiological data is that they are almost certain to be biased, of doubtful quality, or incomplete (and sometimes all three),” explained the epidemiologist John Bailar in The New England Journal of Medicine in 1980. “Problems do not disappear even if one has flawless data, since the statistical associations in almost any nontrivial set of observations are subject to many interpretations. This ambiguity exists because of the difficulty of sorting out causes, effects, concomitant variables, and random fluctuations when the causes are multiple or diffuse, the exposure levels low, irregular, or hard to measure, and the relevant biologic mechanisms poorly understood. Even when the data are generally accepted as accurate, there is much room for individual judgment, and the considered conclusions of the investigators on these matters determine what they will label ‘cause’… "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
34
" Though glucose is a primary fuel for the brain, it is not, however, the only fuel, and dietary carbohydrates are not the only source of that glucose. If the diet includes less than 130 grams of carbohydrates, the liver increases its synthesis of molecules called ketone bodies, and these supply the necessary fuel for the brain and central nervous system. If the diet includes no carbohydrates at all, ketone bodies supply three-quarters of the energy to the brain. The rest comes from glucose synthesized from the amino acids in protein, either from the diet or from the breakdown of muscle, and from a compound called glycerol that is released when triglycerides in the fat tissue are broken down into their component fatty acids. In these cases, the body is technically in a state called ketosis, and the diet is often referred to as a ketogenic diet. "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
35
" It also makes us question the admonitions that carbohydrate restriction cannot “generally be used safely,” as Theodore Van Itallie wrote in 1979, because it has “potential side effects,” including “weakness, apathy, fatigue, nausea, vomiting, dehydration, postural hypotension, and occasional exacerbation of preexisting gout.” The important clinical question is whether these are short-term effects of carbohydrate withdrawal, or chronic effects that might offset the benefits of weight loss. The same is true for the occasional elevation of cholesterol that will occur with fat loss—a condition known as transient hypercholesterolemia—and that is a consequence of the fact that we store cholesterol along with fat in our fat cells. When fatty acids are mobilized, the cholesterol is released as well, and thus serum levels of cholesterol can spike. The existing evidence suggests that this effect will vanish with successful weight loss, regardless of the saturated-fat content of the diet. Nonetheless, it’s often cited as another reason to avoid carbohydrate-restricted diets and to withdraw a patient immediately from the diet should such a thing be observed, under the mistaken impression that this is a chronic effect of a relatively fat-rich diet. In "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
37
" Fat Americans: They Don’t Know When They’re Hungry, They Don’t Know When They’re Full,” as a New York Times headline suggested in 1974. By that time, obesity, like anorexia, was categorized as an eating disorder, and the field of obesity therapy had become a subdiscipline of psychiatry and psychology. All these behavioral therapies, call them what you may, were in fact aimed at correcting failures of will. Every attempt to treat obesity by inducing the obese to eat less or exercise more is a behavioral treatment of obesity, and implies a behavioral-psychological cause of the condition. "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease
38
" What’s been clear for almost forty years is that the levels of circulating insulin in animals and humans will be proportional to body fat. “The leaner an individual, the lower his basal insulin, and vice versa,” as Stephen Woods, now director of the Obesity Research Center at the University of Cincinnati, and his colleague Dan Porte observed in 1976. “This relationship has also been shown to occur in every commonly used model of altered body weight, including…genetically obese rodents and overfed humans. In fact, the relationship is sufficiently robust that it exists in the presence of widespread metabolic disorder, such as diabetes mellitus, i.e., obese diabetics have elevated basal insulin levels in proportion to their body weight. "
― Gary Taubes , Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease