Part 15 (1/2)

George Cahil , a former professor at the Harvard Medical School, is a pedagogical example. Cahil had done some of the earliest research on the regulation of fat-cel metabolism by insulin in the late 1950s, and had coedited the 1965 Handbook of Physiology on adipose-tissue metabolism. In 1971, when Cahil gave the Banting Memorial Lecture at the annual meeting of the American Diabetes a.s.sociation, he described insulin as ”the overal fuel control in mammals.” ”The concentration of circulating insulin,” he explained, ”serves to coordinate fuel storage and fuel mobilization into and out of the various depots with the needs of the organism, and with the availability or lack of availability of fuel in the environment.” When I interviewed Cahil in 2005, he told me it was true that ”carbohydrate is driving insulin is driving fat.” But Cahil did not consider this chain of cause and effect to be a sufficient reason to speculate that carbohydrates drive obesity. Nor did he consider it a possibility that avoiding carbohydrates might reverse the process. Rather, he believed unconditional y that positive caloric balance was the critical factor. When it came to weight regulation, Cahil repeatedly told me, ”a calorie is a calorie is a calorie.” He acknowledged that the obese ate no more, on average, than the lean, and this is why he believed that the obese must be fundamental y lazy and this was the proximate cause of their obesity.*121 There was no reason to test competing hypotheses, Cahil said, because any competing hypothesis would contradict the laws of physics as he understood them.

When clinical investigators tried to unravel the connection between diet, insulin, and obesity in human subjects, as the University of Was.h.i.+ngton endocrinologist David Kipnis did in the early 1970s, the results were invariably a.n.a.lyzed in light of this same preconception. Kipnis had fed ten ”grossly obese” women a series of three-and four-week diets that were either high or low in calories, and high or low in carbohydrates. The fat-rich diets lowered insulin levels, Kipnis reported in The New England Journal of Medicine in 1971, and the carbohydrate-rich diets raised them, regardless of how many calories were being consumed. Even when these women were semi-starved on fifteen hundred calories a day, a high-carbohydrate content (72 percent carbohydrates and only 1 percent fat) stil increased their insulin levels, even compared with the hyperinsulinemia of these obese women on their normal diets.

One interpretation of these results is that we could remove the carbohydrates from the diet and replace them with fat, and weight would be lost, perhaps without hunger, because insulin levels would drop, even if the total calories consumed did not. Kipnis's results, as the University of Heidelberg clinicians Gotthard Schettler and Guenter Schlierf wrote in 1974, underlined the ”necessity of restricting carbohydrates in obesity in order to restore insulin levels to normal, thus hopeful y decreasing appet.i.te and fat deposition....”

Kipnis, however, refused to believe that carbohydrates might cause obesity, or that avoiding carbohydrates might ameliorate the problem. When I interviewed him over thirty years later, he described the findings of his research as ”very obvious.” ”You manipulate the amount of carbohydrates you give a human,” he said, ”you can manipulate his or her basal insulin level.” He also said that ”insulin causes deposition of fat in fat cel s.” But when it came to the cause of human obesity or weight gain, Kipnis rejected the relevance of these physiological phenomena. ”Most people are obese because they eat more than they need to sustain the energy requirements that they have,” he said. ”They eat too d.a.m.n much.”

For the past quarter century, Americans have become progressively heavier and more diabetic. By 2004, one in three Americans was considered clinical y obese; two in three were overweight. One in ten adult Americans had Type 2 diabetes-one in five over the age of sixty. It is now clear that the roots of this epidemic are evident even in infants and in the birth weights of newborns. Among middle-income families in Ma.s.sachusetts, for example, as a team of researchers led by Matthew Gil man of Harvard reported last year, the prevalence of excessively fat infants increased dramatical y between 1980 and 2001. This increase was most conspicuous among children younger than six months of age.

The probable explanation is that as women of childbearing age get heavier and more of them become diabetic, they pa.s.s the metabolic consequences on to their children through what is known technical y as the intrauterine environment. The nutrient supply from mother to developing child pa.s.ses across the placenta in proportion to the nutrient concentration in the mother's bloodstream. If the mother has high blood sugar, then the developing pancreas in the fetus wil respond to this stimulus by overproducing insulin-secreting cel s. ”The baby is not diabetic,” explains Boyd Metzger, who studies diabetes and pregnancy at Northwestern University, ”but the insulin-producing cel s in the pancreas are stimulated to function and grow in size and number by the environment they're in. So they start over functioning. That in turn leads to a baby laying down more fat, which is why the baby of a diabetic mother is typified by being a fat baby.”

This is also the most likely explanation for why children born to women who gain excessive weight during pregnancy also tend to be fatter. As Laura Riley, medical director of labor and delivery at Ma.s.sachusetts General Hospital, told the Boston Globe in response to the Harvard study, she now tel s her patients, ”If you overdo it during pregnancy, you're setting yourself up for a bigger baby,” and that, in turn, means ”you are setting your baby up for potential y a lifetime of weight problems.” Gil man and his col eagues described the problem this way: ”Our observation of a trend of increasing weight among young infants may portend continued increase in childhood and adult obesity.”

But if fatter mothers are more likely to make fatter babies, and fatter babies are more likely to make fatter mothers, which is also a wel -doc.u.mented observation, then this is another vicious cycle. It suggests that, once a generation of adolescents and adults start eating the highly refined carbohydrates and sugars now ubiquitous in our diets, even their children wil feel the effect, and perhaps their children's children as wel . The extreme instance of this phenomenon today is the Pima Indians, whose incidence of diabetes is among the highest of any population in the world. In 2000, NIH investigators reported that Pima born to mothers who were diabetic have a two-to threefold increased risk themselves of becoming diabetic as adults, and so have a two-to threefold increased risk of pa.s.sing diabetes on to their own children-of ”perpetuating the cycle,” as the NIH investigators explained. The ”vicious cycle” of the ”diabetic intrauterine environment,” they wrote, can explain much of the postWorld War I increase in Type 2 diabetes among the Pima, and may also ”be a factor in the alarming rise of this disease national y.”

The question we now face is whether the same vicious cycle may also be a factor in the alarming rise of obesity national y, as wel as international y.

There's no reason to think that the hormonal and metabolic consequences of high blood sugar-from what James Neel in 1982 cal ed the ”excessive glucose pulses that result from the refined carbohydrates/ over-alimentation of many civilized diets”-do not pa.s.s from mother to child through the intrauterine environment, whether the mother is clinical y diabetic or not. If so, the longer the obesity epidemic continues, and the longer we go without unambiguously identifying the causes of obesity, metabolic syndrome, and diabetes, the worse this vicious cycle is likely to get.

Chapter Twenty-three.

THE FATTENING CARBOHYDRATE DISAPPEARS.

We need the help of the psychosocial scientists in finding better ways of communicating with our patients, in explaining to them that obesity is dangerous, that weight is lost slowly, that carbohydrates make fat and so on.

W.J.H. b.u.t.tERFIELD, later vice-chancel or of the University of Cambridge, introductory remarks to the first Symposium of the Obesity a.s.sociation of Great Britain, October 1968 It is incredible that in twentieth-century America a conscientious physician should have his hard-won professional reputation placed on the line for daring to suggest that an obesity victim might achieve some relief by cutting out sugars and starches.

ROBERT ATKINS, author of Dr. Atkins' Diet Revolution, testifying before Congress, April 12, 1973 THERE ARE TWO MOMENTS IN THE HISTORY OF George McGovern's Senate Select Committee on Nutrition and Human Needs when the competing paradigms of nutrition and obesity can be captured in the act of s.h.i.+fting-one coming, one going. The first was in April 1973, during a hearing that the committee held on the subject of obesity and fad diets. Appearing that day to testify were Robert Atkins-author of Dr. Atkins' Diet Revolution, a book that had already sold almost one mil ion copies in the six months since its publication-and three authorities in nutrition and health, who would testify that Atkins's severely carbohydrate-restricted diet was neither revolutionary, effective, nor safe. The tenor of the hearing was inquisitorial, and a pithy condemnation of Atkins and his diet by the Harvard nutritionist Fred Stare was read into the record by Senator Charles Percy of Il inois (Stare did not attend). ”The Atkins diet is nonsense,” Stare declared. ”Any book that recommends unlimited amounts of meat, b.u.t.ter and eggs, as this does, in my opinion is dangerous. The author who makes the suggestion is guilty of malpractice.”

A few weeks later, McGovern's committee hosted hearings on ”Sugar in the Diet, Diabetes, and Heart Disease.” Testimony came from an international panel of authorities, including Peter Cleave, Aharon Cohen of Hada.s.sah University in Jerusalem, George Campbel of the Durban Diabetes Study Program in South Africa, Peter Bennett of the NIH, and Walter Mertz of the U.S. Department of Agriculture. These investigators discussed the potential dangers of refined carbohydrates in the diet, and John Yudkin testified to the particular dangers of sugar. McGovern and his fel ow congressmen found the testimony compel ing, although difficult to reconcile with the growing acceptance, their own included, of the notion that it was fatty foods that caused heart disease, and carbohydrates that would prevent it.

Those on the committee saw no connection between the two sets of hearings. They believed Atkins was peddling dietary nonsense, whereas Cleave, Campbel , and the others were promoting reasonable science, albeit a minority viewpoint. The congressmen did not comprehend that both sets of hearings were about the role of refined and easily digestible carbohydrates and the damage they might cause. ”We weren't thinking of those two things,”

said the committee staff director, Kenneth Schlossberg, looking back from a perspective of three decades, ”which was not very bright.”

Three years later, in July 1976, McGovern's committee returned to the subject of diet and disease in the hearings that would lead, a half year later stil , to the publication of Dietary Goals for the United States. The first witness was a.s.sistant Secretary of Health Theodore Cooper, who repeatedly emphasized the need for further research to establish reliable knowledge about the diet-disease connection. McGovern and his fel ow congressmen, however, wanted to tel the American public something more definitive, so McGovern asked Cooper if he could, at least, agree with the proposition that ”overconsumption may be as serious a problem of nutrition as under-consumption.”

”Particularly overconsumption of the wrong things,” Cooper replied. ”Very often in the poor we see people who are plump who might be cal ed obese, and people would then conclude that they do not have a deficiency because they look rotund, healthy in one sense of the word. But it is true that the consumption of high carbohydrate sources with the induction of obesity const.i.tutes a very serious public health problem in the underprivileged and economical y disadvantaged. I would agree with that.”

This response seems clear enough: the overconsumption of ”high carbohydrate sources”-a phrase used to describe carbohydrate-dense starches and refined carbohydrates rather than leafy green vegetables and fruits-was a.s.sociated with obesity in the poor, and perhaps even the cause.

McGovern then asked Cooper to provide a ”general rule of thumb” about eating habits that would help prevent disease and lengthen our lives, and Cooper reluctantly agreed to do so.

”What kinds of foods in general should we be consuming less of and what should we be eating more of?” McGovern asked.

”I think what we need to consider doing is to reduce our total fat intake,” Cooper replied. ”Fat adds a caloric substance-almost twice as much-nine calories per gram-as compared to sugar. I think in order to have an effective reduction in weight and realignment of our composition we have to focus on reducing fat intake.”

With that answer, Cooper had contradicted himself, and the conventional wisdom on diet and health in America had s.h.i.+fted. The problem was no longer overconsumption of high-carbohydrate sources, but the overconsumption of fatty foods. And if Cooper realized that reducing our total fat intake meant increasing our consumption of carbohydrates, he neglected to say so.

Between 1973 and the mid-1980s, the notion of the fattening carbohydrate, which had persisted in clinical and popular literature for wel over a century, was replaced with the belief that it is dietary fat, with its particularly dense calories, that is responsible for overweight and obesity. The prescription of reducing diets that restricted starches and sugars, and perhaps oils and b.u.t.ter as wel , was replaced with diets that targeted fat alone-restricting not just b.u.t.ter and oils but meat, eggs, and dairy products-thereby increasing carbohydrate consumption. Obesity was conceptual y transformed from a condition commonly a.s.sociated with the excessive consumption of carbohydrates and carbohydrate craving to one that would be described by prominent nutritionists as a ”carbohydrate-deficiency syndrome,” which in turn explained why ”an increase in dietary carbohydrate content at the expense of fat is the appropriate dietary part of a therapeutical strategy.”

What makes this s.h.i.+ft al the more perplexing is that it occurred immediately after the science of fat metabolism evolved to explain why carbohydrates were uniquely fattening, and it fol owed a six-year period in which carbohydrate-restricted diets achieved unprecedented credibility among clinicians. The latter coincided precisely with the genesis of obesity research as what would be considered a legitimate field of scientific study, a transformation marked by the increasingly frequent appearance of conferences and symposiums dedicated to reporting the latest findings in obesity research, al of which, through 1973, had been dominated by discussions of the peculiar efficacy of carbohydrate-restricted diets.

The first was hosted by the University of California, San Francisco, in December 1967. Among the dozen speakers was the veteran UC Berkeley nutritionist Samuel Lepkovsky, who used exactly the same logic as Alfred Pennington had in the 1950s to argue the biological rationale of carbohydrate restriction. ”Positive caloric balance may be a result rather than a cause of the [obese] condition,” Lepkovsky said. ”It seems desirable in the treatment of obesity to direct efforts toward an increased utilization of fat. This effort can be made by restricting the intake of carbohydrates and increasing the ingestion of fat.” The one presentation at the conference that was specifical y on the dietary treatment of obesity came from a team of U.S. Navy physicians, who had been prescribing an eight-hundred-to-one-thousand calorie ”ketogenic” diet to overweight naval personnel. Their diet was 70 percent fat, 20 percent protein, and 10 percent carbohydrate, and it induced ”significant weight loss” in al their patients. ”Uniformly and without exception,” they added, ”patients who underwent dieting found that the satiety value of the ketogenic diet was far superior to that of a mixed or high-carbohydrate diet, even though the food selection was minimal....”

In 1968, the newly founded Obesity a.s.sociation of Great Britain hosted in London its first symposium on obesity. The presentations were dominated by investigators who believed in the fattening nature of carbohydrates and the efficacy of carbohydrate-restricted diets. These included John Yudkin and his col eague Stephen Szanto; W.J.H. b.u.t.terfield, who would later become vice-chancel or of the University of Cambridge; Alan Kekwick and Gaston Pawan of the University of London, who were primarily responsible for reviving the concept of Banting's diet in the U.K.; and Denis Craddock, a general pract.i.tioner and author of Obesity and Its Management, which would be published in 1969 and was one of at most two or three clinical guides to obesity treatment published in the U.K. in the 1960s or 1970s. As Craddock reported at the conference, he had recently completed a survey of a hundred pregnant patients, sixty of whom had begun to fatten excessively during the early months of their pregnancy. ”This weight gain was control ed in most cases”-fifty-seven of the sixty-”simply by restricting carbohydrates in the diet,” he said.

The conference had been organized by Alan Howard and his col eague Ian McLean Baird. Howard was a biochemist and pathologist at the University of Cambridge who would later become the founding editor, with George Bray, of the International Journal of Obesity. Howard had become interested in carbohydrate restriction because he had been twenty pounds overweight, had unsuccessful y dieted for years, then final y lost the weight and kept it off by avoiding flour, starches, and sweets. At the London conference, Howard reviewed the literature on carbohydrate restriction dating back to Banting and concluded that this was the only effective method to induce and maintain weight loss. ”A common feature of al who have written on the subject,” he said, is ”that the patient's hunger is satisfied whilst on a diet high in carbohydrate of the same caloric value, patients complain of hunger.”

After the London meeting, obesity conferences evolved from local to international affairs. The first was in Paris in 1971, hosted by European nutrition and dietetics a.s.sociations. Here the sole presentation on the dietary treatment of obesity was by a col aboration from the French National Inst.i.tute on Health and Medical Research (INSERM), which is the local counterpart of the NIH in the United States and the Medical Research Council in the United Kingdom. These INSERM investigators had prescribed diets of twelve to eighteen hundred calories to over a hundred obese patients, in either three or seven meals a day, and with varying amounts of carbohydrates. Weight loss increased, they reported, when the subjects divided their calories among seven meals, which served to moderate the insulin response. Moreover, ”lowering the carbohydrate content of the diet increased the weight loss at both meal frequencies.”

The next conference was hosted by the NIH in Bethesda, Maryland, in October 1973. Six of the presentations at this meeting discussed the treatment of obesity by methods other than drugs or surgery. Two were on physical activity, and neither reported any significant effect of exercise on body weight. Two addressed the benefits of behavioral modification on weight loss, and neither reported any significant benefit. Of the two remaining presentations, one was by Ernst Drenick of UCLA on prolonged fasting to treat obesity-”our experiences are disappointing,” said Drenick-and the other was by Charlotte Young of Cornel on dietary treatments.

As Howard had in London, Young reviewed the hundred-year history of carbohydrate-restricted diets, including the research of Pennington and that of Margaret Ohlson and her own trials in the 1950s. Young then discussed her recent studies, in which she had put obese young men on eighteen-hundred-calorie diets with the protein content fixed at 460 calories (26 percent), but with varying proportions of fat and carbohydrates. 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. ”No adequate explanation could be given for the differences in weight losses,” she said. Al of the carbohydrate-restricted diets, she said, ”gave excel ent clinical results as measured by freedom from hunger, al aying of excessive fatigue, satisfactory weight loss, suitability for long term weight reduction and subsequent weight control.”

The last of these conferences to be held before the nutritional wisdom began to s.h.i.+ft definitively was in London in December 1973, just two months after the NIH meeting. This one was organized by Yudkin, and many of those giving presentations had also attended the NIH conference. Their presentations were similar, but here there was more of a tendency to implicate carbohydrates specifical y as the cause of obesity. Lester Salans and Edward Horton, both col aborators of Ethan Sims on his experimental obesity studies, discussed the effect of carbohydrates on hyperinsulinemia and the role of hyperinsulinemia in obesity. ”It is clear that in both lean and obese subjects the carbohydrate content of the diet influences...insulin and glucose concentrations,” Horton reported. He added that it was probably hyperinsulinemia that induced both obesity and insulin resistance. Yudkin then gave the only talk on dietary therapy, ent.i.tled ”The Low-Carbohydrate Diet,” noting that these diets are higher in vitamins and minerals than calorie-restricted diets, simply because the foods restricted-starches and sugars-have few or no vitamins and minerals. The diet wil ”reduce superfluous adiposity,” Yudkin said, ”but it wil not need to be changed when this has been done.... The diet is intended as anew but permanent pattern of eating and not simply as a cure for obesity, to be abandoned when an acceptable loss of weight is achieved.” Harry Keen, who was then at Guy's Hospital Medical School and would become one of the most influential diabetologists in the U.K.,*122 said the critical issue wasn't just obesity, but the chronic diseases that accompanied it. ”With the chronical y failed case of obesity we are dealing with the wreckage of the situation,” he said, so it was necessary to set ”new patterns of body weight and body size, if we are going to make a serious attempt to reduce the frequency, for example, of atherosclerosis, of diabetes mel itus and of a number of other conditions.” Keen and his col eagues had tested the viability of this goal, he reported, on a group of ”ostensibly normal men in whom obesity is represented no more frequently than in the population at large.” These men were instructed to restrict their carbohydrate intake to less than five hundred calories a day, but to continue eating protein and fat as desired. The result was an average weight loss of fourteen pounds, impressive because these individuals were not necessarily overweight to begin with. That weight loss had been maintained for almost five years. To those who might be pessimistic about the prevention of obesity and overweight in the public at large, Keen said, this result should be taken as ”a word of rea.s.surance and optimism.”

By 1972, The New York Times Natural Foods Dieting Book was offering both a low-calorie weight-loss plan, at a thousand calories a day, and a low-carbohydrate method. ”You strictly curtail the amount of carbohydrates you eat daily,” the book explained. ”You eat, instead, foods in which the carbohydrate content is very low or nonexistent. Meat...fish, poultry, fats, b.u.t.ter, most cheeses and eggs are equal y low in that fattening substance, and these are the foods that form the basis for your diet...for without carbohydrates you cannot gain weight!”

Two years later, when the nonprofit organization Consumer Guide published its first edition of Rating the Diets, a 380-page compendium of the pros and cons of popular diets, carbohydrate restriction seemed firmly established in the canon. Rating the Diets, which obesity authorities would repeatedly recommend as a valuable review of the evidence, concluded that a diet including less than sixty grams of carbohydrates each day had ”much to recommend it” and so was ”helpful and beneficial” for weight loss. It also quoted a medical textbook to the effect that ”the difficult-to-treat obese patient,”

which effectively means every obese patient, ”appears to suffer from some defect in dealing with carbohydrate which leads to an unnatural conversion of it to fat and to storage of the fat. Avoidance of too much dietary carbohydrate reduces this tendency.” The only caveat with these diets, according to Rating the Diets, was that they ”pay little attention to the kinds of fats you eat” and so might increase heart-disease risk.

The s.h.i.+ft in the nutritional wisdom was now taking place, driven by the contagious effect of Ancel Keys's dietary-fat/heart-disease hypothesis on the closely related field of obesity. Any diet that al owed liberal fat consumption was to be considered unhealthy. Clinical investigators working on the problem of human obesity concurred.

Through the 1950s, the carbohydrate-restricted diet had chal enged only the positive-caloric-balance hypothesis of obesity. Yudkin had managed to reconcile carbohydrate restriction with this conventional wisdom by insisting that low-carbohydrate diets were low-calorie diets in disguise. By doing so, Yudkin made the diets political y acceptable, although he also directed attention away from the underlying science. In the same 1960 Lancet article in which Yudkin proclaimed what he cal ed ”the inevitability of calories,” he had made the point that if the diet was indeed low in calories, then its fat content would also be comparatively low, reconciling his diet with Keys's dietary-fat hypothesis. This was Yudkin's ”no bread, no b.u.t.ter” argument. If carbohydrate calories are restricted, fat calories are, too. Though the proportion of fat in the diet increases if carbohydrates are avoided, the absolute quant.i.ty of fat may actual y decrease. This is why Yudkin insisted that the correct terminology for these diets should be ”low-carbohydrate” rather than ”high-fat.” ”It is highly implausible,” Yudkin wrote in 1974, ”that a given amount of fat that is harmless when energy intake is excessive becomes harmful when this excess is corrected by a reduction in the intake of sugar and starch.”

As a result of Yudkin's conciliatory efforts, the only carbohydrate-restricted diets that elicited a backlash from nutritionists were those promoted by clinicians whose interpretation of the science disagreed with Yudkin's. This situation was exacerbated by the fact that it was these physicians, without university affiliations, who adopted the diet quickly and then wrote books for the lay public that sold exceptional y wel . Because their claims sounded like quackery-The High-Calorie Way to Stay Thin Forever , as Dr. Atkins' Diet Revolution was subt.i.tled-they were treated as such, and particularly so after the medical and public-health authorities decided that dietary fat might cause heart disease.

The smal contingent of influential nutritionists from Fred Stare's department at Harvard provide an example of how this process of entrenchment evolved. In 1952, when Alfred Pennington lectured at Harvard on the benefits of carbohydrate restriction and Keys was only beginning his crusade against dietary fat, Mark Hegsted had suggested, ”Dr. Pennington may be on the right track in the practical treatment of obesity.” A decade later, and a year after the American Heart a.s.sociation had official y sided with Keys, the Brooklyn obstetrician Herman Tal er published his best-sel er, Calories Don't Count, based on Pennington's work and Tal er's clinical experiences with the diet. Stare cal ed the book ”trash,” and Jean Mayer described the high-fat aspect of the diet as ”potential y dangerous.” Philip White, who received his doctorate in nutrition from Stare's department, then wrote a review of Calories Don't Count for JAMA, accusing Tal er of perpetrating ”nutrition nonsense and food quackery.” In 1973, in response to the publication of Dr. Atkins' Diet Revolution, based on Atkins's clinical experience with overweight patients and another decade of science, White edited a critique of carbohydrate-restricted diets in JAMA-the first draft of which was written by Ted Van Ital ie, another veteran of Stare's nutrition department-that now dismissed the diets as ”bizarre concepts of nutrition and dieting [that] should not be promoted to the public as if they were established scientific principles.”

Meanwhile, these nutritionists would readily admit that they didn't know what caused obesity (why some people ate too much and others didn't) and that calorie restriction conspicuously failed to cure it. After nearly twenty years in the field, as Jean Mayer wrote in the introduction to his 1968 monograph, Overweight, he was ”as aware as any man of the gigantic gaps in our knowledge-and of the likelihood that many of our present concepts may be erroneous.” He also noted, in his discussion of hormonal influences on obesity, that insulin ”favors fat synthesis” and that someone who over-secretes insulin could ”tend to become hungry as a result.” But when a physician suggested publicly, as Atkins did, that carbohydrates raised insulin levels, that insulin favors fat synthesis, and that a diet lacking carbohydrates might reverse this process, these nutritionists would denounce it, as Mayer himself did in 1973, as ”biochemical mumbo-jumbo.”