Good Calories, Bad Calories

A good diet,” Mayer wrote, “high in fruits and vegetables and with a reasonable amount of undermilled cereals—will give all you need of useful fiber.” The assumption that it would lead to long life and good health, however, was based more on faith and intuition than on science.

concluded that at least 75 to 80 percent of cancers in the United States might be avoidable with appropriate changes in diet and lifestyle.

even low levels of insulin, far below those considered the clinical symptom of hyperinsulinemia (chronically high levels of insulin), will shut down the flow of fatty acids from the fat cells. Elevating insulin even slightly will increase the accumulation of fat in the cells. The longer insulin remains elevated, the longer the fat cells will accumulate fat, and the longer they’ll go without releasing it.

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.

For every 5 percent of saturated-fat calories that replaced carbohydrates in the diet, the risk of breast cancer decreased by 9 percent. This certainly argued against the hypothesis that excessive fat consumption caused breast cancer.

If blood-sugar levels increase—say, after a meal containing carbohydrates—then more glucose is transported into the fat cells, which increases the use of this glucose for fuel, and so increases the production of glycerol phosphate. This is turn increases the conversion of fatty acids into triglycerides, so that they’re unable to escape into the bloodstream at a time when they’re not needed. Thus, elevating blood sugar serves to decrease the concentration of fatty acids in the blood, and to increase the accumulated fat in the fat cells.

If this hypothesis of hunger, satiety, and weight regulation is correct, it means that obesity is caused by a hormonal environment—increased insulin secretion or increased sensitivity to insulin—that tilts the balance of fat storage and fat burning. This hypothesis also implies that the only way to lose body fat successfully is to reverse the process; to create a hormonal environment in which fatty acids are mobilized and oxidized in excess of the amount stored. A further implication is that any therapy that succeeds at inducing long-term fat loss—not including toxic substances and disease—has to work through these local regulatory factors on the adipose tissue.

In fat tissue, insulin increases LPL activity; in muscle tissue, it decreases activity. As a result, when insulin is secreted, fat is deposited in the fat tissue, and the muscles have to burn glucose for energy. When insulin levels drop, the LPL activity on the fat cells decreases and the LPL activity on the muscle cells increases—the fat cells release fatty acids, and the muscle cells take them up and burn them.

influenced her suspicion that carbohydrates would also cause chronic disease in humans through their effect on insulin and insulin-like growth factor.

In retrospect, the influential figures in the clinical investigation of human obesity in the 1970s can be divided into two groups. There were those who believed carbohydrate-restricted diets were the only efficacious means of weight control—Denis Craddock, Robert Kemp, John Yudkin, Alan Howard, and Ian McLean Baird in England, and Bruce Bistrian and George Blackburn in the U.S.—and wrote books to that effect, or developed variations on these diets with which they could treat patients. These men invariably struggled to maintain credibility. Then there were those who refused to accept that carbohydrate restriction offered anything more than calorie restriction in disguise—Bray, Van Itallie, Cahill, Hirsch, and their fellow club members. These men rarely if ever treated obese patients themselves, and they repeatedly suggested that since no diet worked nothing was to be learned by studying diets.

Making LDL the “bad cholesterol” oversimplified the science considerably, but it managed to salvage two decades’ worth of research, and to justify why physicians had bothered to measure total cholesterol in their patients.

Our brains, for instance, are 70 percent fat, mostly in the form of a substance known as myelin that insulates nerve cells and, for that matter, all nerve endings in the body. Fat is the primary component of all cell membranes. Changing the proportion of saturated to unsaturated fats in the diet, as proponents of Keys’s hypothesis recommended, might well change the composition of the fats in the cell membranes. This could alter the permeability of cell membranes, which determines how easily they transport, among other things, blood sugar, proteins, hormones, bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of these membrane fats could affect the aging of cells and the likelihood that blood cells will clot in vessels and cause heart attacks.

Over the course of nine weeks, she reported, “weight loss, fat loss, and percent weight loss as fat appeared to be inversely related to the level of carbohydrate in the diets”—in other words, the fewer carbohydrates and the more fat in the diet, the greater the weight loss and the greater the fat loss.

pressure in school-age children. The NIH has funded subsequent

(Saturated fats, in particular, the ACS added, “may have an effect on increasing cancer risk,” a statement that seemed to be based solely on the belief that if saturated fat causes heart disease it probably causes cancer as well.)

The evidence suggests that nicotine induces weight loss by working on fat cells to increase their insulin resistance, while also decreasing the lipoprotein-lipase activity on these cells, both of which serve to inhibit the accumulation of fat and promote its mobilization over storage, as we discussed earlier

The first principle is that you must not fool yourself—and you are the easiest person to fool.

The gist of Dr. Atkins’ Diet Revolution can be distilled down to three assertions. The first is that weight could be lost on his diet without hunger, and perhaps without even restricting calories.

The laboratory evidence that carbohydrate-rich diets can cause the body to reain water and so raise blood pressure, just as salt consumption is supposed to do, dates back well over a century

there is no scientifically justifiable reason—or evidence—to assume that the obese are any more defective in character or behavior

[T]he salient question is whether the increasing awareness of [heart] disease beginning in the 1920s coincided with the budding of an epidemic or simply better technology for diagnosis.

The scientific obligation is first to establish the cause of the disease beyond reasonable doubt.

This research supports the hypothesis that elevations of insulin and IGF will increase the risk of disease and shorten life, and so any diet or lifestyle that elevates insulin and makes IGF more available to the cells and tissues is likely to be detrimental.

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.

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.

When researchers have measured seasonal variations in insulin levels in humans, they have invariably reported that insulin is highest in late fall and early winter—twice as high, according to one 1984 study—and lowest in late spring and early summer. Moreover, as the University of Colorado’s Robert Eckel has reported, lipoprotein-lipase activity in fat tissue elevates in late fall and decreases in spring and summer; its activity in skeletal muscle follows an opposite pattern. This would stimulate weight loss in the spring and weight gain in the fall, whether we consciously desire either or not, and would certainly make it easier to lose weight in the spring and gain it in the fall.

White flour and sugar were singled out as particularly noxious, because these had been increasing dramatically in Western diets during the latter half of the nineteenth century, coincident with the reported increase in cancer mortality.

Wishful science eventually devolves to the point where it is kept alive simply by the natural reluctance of its advocates to recognize or acknowledge error, rather than compelling evidence that it is right.

Yudkin also fed high-sugar diets to college students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cells became stickier, which he believed could explain the blood clots that seemed to precipitate heart attacks.

Yudkin blamed heart disease exclusively on sugar, and he was equally adamant that neither saturated fat nor cholesterol played a role. He explained how carbohydrates and specifically sugar in the diet could induce both diabetes and heart disease, through their effect on insulin secretion and the blood fats known as triglycerides.