Good Calories, Bad Calories

For the past quarter century, Americans have become progressively heavier and more diabetic. By 2004, one in three Americans was considered clinically 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 Gillman of Harvard reported last year, the prevalence of excessively fat infants increased dramatically 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 technically 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 will respond to this stimulus by overproducing insulin-secreting cells. “The baby is not diabetic,” explains Boyd Metzger, who studies diabetes and pregnancy at Northwestern University, “but the insulin- producing cells 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 tells 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 potentially a lifetime of weight problems.” Gillman and his colleagues 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 well-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 will feel the effect, and perhaps their children’s children as well. 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 II increase in Type 2 diabetes among the Pima, and may also “be a factor in the alarming rise of this disease nationally.”

The question we now face is whether the same vicious cycle may also be a factor in the alarming rise of obesity nationally, as well as internationally. There’s no reason to think that the hormonal and metabolic consequences of high blood sugar—from what James Neel in 1982 called 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 clinically 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. BUTTERFIELD, later vice-chancellor 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 million 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 Illinois (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 Campbell 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 fellow congressmen found the testimony compelling, 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, Campbell, 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 still, 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 fellow congressmen, however, wanted to tell the American public something more definitive, so