Good Calories, Bad Calories (73 page)

Since none of this research is particularly controversial, it’s hard to imagine why obesity researchers would not take seriously the hypothesis that carbohydrates have a unique ability to fatten humans—or, as Thomas Hawkes Tanner put it in The Practice of Medicine almost 140 years ago, that

“farinaceous and vegetable foods are fattening, and saccharine matters are especial y so.” Researchers who study carbohydrate metabolism have found this science compel ing. In 1991, the Belgian physiologist Henri-Géry Hers, an authority on what are known as glycogen-storage diseases, one of which is named after him, put it this way: “Eating carbohydrates wil stimulate insulin secretion and cause obesity. That looks obvious to me….” But this simple chain of cause and effect has nonetheless been rejected out of hand by authority figures in the field of human obesity, who believe that the cause of the condition is manifestly obvious and beyond dispute, that the law of energy conservation dictates that obesity has to be caused by eating too much or moving too little.

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 Association, 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 Washington endocrinologist David Kipnis did in the early 1970s, the results were invariably analyzed 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 appetite 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 damn 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 Massachusetts, 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 pass 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 passes 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 Massachusetts 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 -documented 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 passing 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 post–World 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 pass 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.

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. BUTTERFIELD, later vice-chancel or of the University of Cambridge, introductory remarks to the first Symposium of the Obesity Association 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 shifting—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, butter 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 Hadassah 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 Assistant 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 constitutes 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 associated 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 shifted. 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.