Good Calories, Bad 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

[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.

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

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

(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.)

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.

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

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.

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.

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.

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.

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

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.

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

The deposition of fat in men and women is distinctly different. Men tend to store fat above the waist—hence the beer belly—and women below it. Women put on fat in puberty, at least in the breasts and hips, and men lose it. Women gain weight (particularly fat) in pregnancy and after menopause. This suggests that sex hormones are involved, as much as or more than eating behavior and physical activity. “The energy conception can certainly not be applied to this realm,” as the German clinician Erich Grafe observed in 1933 about this anatomical distribution of fat deposits and how it differs by sex.

The “remarkable sodium and water retaining effect of concentrated carbohydrate food,” as the University of Wisconsin endocrinologist Edward Gordon called it, was then explained physiologically in the mid-1960s by Walter Bloom, who was studying fasting as an obesity treatment at Atlanta’s Piedmont Hospital, where he was director of research. As Bloom reported in the Archives of Internal Medicine and The American Journal of Clinical Nutrition, the water lost on carbohydrate-restricted diets is caused by a reversal of the sodium retention that takes place routinely when we eat carbohydrates. 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. 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. This

According to this hypothesis, the fundamental difference between the lean and the obese is the amount of fat stores that the hypothalamus is set to defend—the set point—not the manner or vigor with which it is defended.

It’s possible that obesity, diabetes, heart disease, hypertension, and the other associated diseases of civilization all have independent causes, as the conventional wisdom suggests, but that they serve as risk factors for each other, because once we get one of these diseases we become more susceptible to the others.

Once these authorities insist that a consensus exists, they no longer have motivation to pursue further research. Indeed, to fund further studies is to imply that there is still uncertainty.

Ironically, some of the most reliable facts about the diet-heart hypothesis have been consistently ignored by public-health authorities because they complicated the message, and the least reliable findings were adopted because they didn’t.

Over the years, compelling arguments dismissing a heart-disease epidemic, like the 1957 AHA report, have been published repeatedly in medical journals. They were ignored, however, not refuted.

There is always an easy solution to every human problem,” H. L. Mencken once said—“neat, plausible, and wrong.

The refining of carbohydrates represented the most dramatic change in human nutrition since the introduction of agriculture.

Atkins wanted “a revolution, not just a diet.” “Martin Luther King had a dream,” Atkins wrote. “I, too, have one. I dream of a world where no one has to diet. A world where the fattening refined carbohydrates have been excluded from the diet.” Atkins deliberately portrayed his diet as diametrically opposed to the growing orthodoxy on the nature of a healthy diet.

The fact that insulin increases the formation of fat has been obvious ever since the first emaciated dog or diabetic patient demonstrated a fine pad of adipose tissue, made as a result of treatment with the hormone. REGINALD HAIST AND CHARLES BEST, The Physiological Basis of Medical Practice, 1966

It is better to know nothing,” wrote Claude Bernard in An Introduction to the Study of Experimental Medicine, “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek, neglecting meanwhile everything that fails to agree with them.

considering the half century of experimental observations on these diets. It leaves us with two seemingly paradoxical observations. The first is that weight loss can be largely independent of calories. The second is that hunger can also be.

These researchers simply never confronted the possibility that the nutrient composition of the diet might have a fundamental effect on eating behavior and energy expenditure, and thus on the long-term regulation of weight.

The first law of thermodynamics dictates that weight gain—the increase in energy stored as fat and lean-tissue mass—will be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance—by “a plethora of calories,” as Russell Cecil and Robert Loeb’s 1951 Textbook of Medicine put it.

what should be the salient question in all obesity research: why wasn’t intake adjusted downward to match expenditure, or vice versa? Nor does it explain why reversing this caloric imbalance fails to reverse the weight gain reliably.*

Von Noorden’s proposition, which still obtains today, is the equivalent of saying that “alcoholism is caused by chronic overdrinking” or “chronic fatigue syndrome is caused by excessive lethargy and/ or deficient energy.” These propositions are true, but meaningless. And they confuse an association with cause and effect. They tell us nothing about why one person becomes obese (or alcoholic or chronically fatigued) and another person doesn’t.

If eating behavior did not produce deposits of body fat we could not call it overeating,” is how this phenomenon was phrased in 1986 by William Bennett, then editor of the Harvard Medical School Health Letter and one of the rare investigators interested in obesity ever to make this point publicly.