Good Calories, Bad Calories (27 page)

wrote Jane Brody after the publication of the Phoenix and NCI studies, “I would say you could safely abandon bran muffins, whole-grain cereals, beans and peas and fiber-rich fruits and vegetables and return to a pristine diet of pasty white bread. But dietary fiber…has myriads of health benefits.” After Stolberg’s 1999 report on the Nurses Health Study, the Times published an article by Brody entitled “Keep the Fiber Bandwagon Rol ing, for Heart and Health,” pointing out that fiber was certainly good for constipation and that earlier results from the Nurses Health Study had suggested that women who ate “a starchy diet that was low in fiber and drank a lot of soft drinks developed diabetes at a rate two and a half times greater than women who ate less of these foods.” This, according to Brody, constituted the motivation to keep fiber in a healthy diet.

Five days after Kolata’s article on the negative results from the Phoenix and NCI trials, the Times published an explanatory article by Kolata—“Health Advice: A Matter of Cause, Effect and Confusion”—in which she discussed why the public had come to be misled on the benefits of fiber. She suggested that one reason was the loose use of language: “Scientists and the public alike use words like ‘prevents’ and ‘protects against’ and ‘lowers the risk of’

when they are discussing evidence that is suggestive, and hypothesis-generating, as wel as when they are discussing evidence that is as firm as science can make it.” Burkitt’s fiber hypothesis, she said, had been based on hypothesis-generating data—international comparisons, in particular—and had then been refuted by the best studies science could do. “Yet even in the aftermath of the high-fiber diet studies,” Kolata noted, “researchers were speaking confidently about other measures people could take to ‘prevent’ colon cancer, like exercising and staying thin. And they were saying that there were reasons to keep eating fiber because it could ‘reduce the risk’ of heart disease. When asked about the evidence for these statements, the researchers confessed that it was, of course, the lower level hypothesis-generating kind.”

The very next day, the Times ran an article by Burros entitled “Plenty of Reasons to Say, ‘Please Pass the Fiber,’” in which she suggested, based on what Kolata would have cal ed “hypothesis-generating data,” that eating fiber “significantly” lowers the risk of heart attack in women, and that “fiber is also useful in preventing the development of diabetes,” “helps control obesity,” and “may also be useful in reducing hypertension.” Less than a month later, Brody fol owed with an article entitled “Vindication for the Maligned Fiber Diet,” noting that, although fiber had “been knocked around a bit lately, after three disappointing studies failed to find that a high-fiber diet helped to prevent colon cancer,” a recent study published in the New England Journal of Medicine of thirteen subjects fol owed for six weeks suggested it helped them to better control their diabetes and so should be eaten on that basis.

“Since diabetes greatly increases a person’s risk of developing heart disease and other disorders caused by fat-clogged arteries,” Brody wrote, “the results of this study are highly significant to the 14 mil ion Americans with Type 2 diabetes.” By 2004, Brody was advocating high-fiber diets solely for their al eged ability, untested, to induce long-term weight loss and weight maintenance. In effect, fiber had now detached itself from its original hypothesis and existed in a realm always a step beyond what had been tested. Cleave’s hypothesis that refined carbohydrates and sugars were the problem, the single best explanation for the original data, had been forgotten entirely.

THE SCIENCE OF THE CARBOHYDRATE HYPOTHESIS

Forming hypotheses is one of the most precious faculties of the human mind and is necessary for the development of science. Sometimes, however, hypotheses grow like weeds and lead to confusion instead of clarification. Then one has to clear the field, so that the operational concepts can grow and function. Concepts should relate as directly as possible to observation and measurements, and be distorted as little as possible by explanatory elements.

MAX KLEIBER, The Fire of Life:

An Introduction to Animal Energetics, 1961

AFTER THE UNITED STATES EXPLORATION EXPEDITION under Captain Charles Wilkes visited the Polynesian atols of Tokelau in January 1841, the expedition’s scientists reported finding no evidence of cultivation on the atols, and confessed their surprise that the islanders could thrive on a diet composed primarily of coconuts and fish. Tokelau came under the administration of New Zealand in the mid-1920s, but the atol s remained isolated, visited only by occasional trading ships from Samoa, three hundred miles to the north. As a result, Tokelau lingered on the fringes of Western influence. The staples of the diet remained coconuts, fish, and a starchy melon known as breadfruit (introduced in the late nineteenth century) wel into the 1970s. More than 70 percent of the calories in the Tokelau diet came from coconut; more than 50 percent came from fat, and 90 percent of that was saturated.

By the mid-1960s, the population of Tokelau had grown to almost two thousand and the New Zealand government, concerned about the threat of overpopulation, initiated a voluntary migration program during which more than half the Tokelauans moved to the mainland. From 1968 to 1982, a team of New Zealand anthropologists, physicians, and epidemiologists led by Ian Prior took the opportunity to study the health and diet of the emigrants as they resettled, as wel as those who remained behind on the islands as their diets were progressively Westernized. This Tokelau Island Migration Study (TIMS) was a remarkably complete survey of the health and diet of al men, women, and children of Tokelauan ancestry. It was also quite likely the most comprehensive migration study ever carried out in the history of nutrition-and-chronic-disease research.

On Tokelau, the primary changes during the course of the study came in the mid-1970s, with the establishment of a cash economy and trading posts on the atol s. The year-round availability of imported foods led to a decrease in coconut consumption to roughly half of al calories. This was offset by a sevenfold increase in sugar consumption*38 and a nearly sixfold increase in flour consumed—from twelve pounds per person annual y to seventy pounds. The islanders also began eating canned meats and frozen foods, which they stored in freezers donated by the United Nations; by 1980, six pounds of mutton per capita, three pounds of chicken backs, and five pounds of tinned corned beef had been consumed. (In comparison, 270 pounds of fish were caught per islander in 1981.) By then, the trading ships were also delivering annual y some eighteen pounds per person of crackers, biscuits, and Twisties, a cheese-flavored corn snack. Smoking increased dramatical y, as did alcohol consumption.

Through the 1960s, the only noteworthy health problems on the islands had been skin diseases, asthma, and infectious diseases such as chicken pox, measles, and leprosy. (Modern medical services and a trained physician had been available in Tokelau since 1917.) In the decades that fol owed, diabetes, hypertension, heart disease, gout, and cancer appeared. This coincided with a decrease in cholesterol levels, consistent with the decrease in saturated-fat consumption. Average weights increased by twenty to thirty pounds in men and women. A similar, albeit smal er, trend was seen in Tokelauan children. The only conspicuous departure from these trends was in 1979, when the chartered passenger-and-cargo ship Cenpac Rounder ran aground and the islanders went five months without a food or fuel delivery. “There was no sugar, flour, tobacco and starch foods,” reported the New Zealand Herald, “and the atol hospitals reported a shortage of business during the enforced isolation. It was reported that the Tokelauans had been very healthy during that time and had returned to the pre-European diet of coconut and fish. Many people lost weight and felt very much better including some of the diabetics.”

As for the migrants to New Zealand, the move brought “immediate and extensive changes” in diet: bread and potatoes replaced breadfruit, meat replaced fish, and coconuts virtual y vanished from the diet. Fat and saturated-fat consumption dropped, to be replaced once again by carbohydrates, “the difference being due to the big increase in sucrose consumption.” This coincided with an almost immediate increase in weight and blood pressure, and a decrease in cholesterol levels

—al more pronounced than the increases witnessed on Tokelau. Hypertension was twice as common among the migrants as among the Tokelauans who remained on the islands. The migrants also had an “exceptional y high incidence” of

“diabetes, gout, and osteoarthritis, as wel as hypertension.” Electrocardio-graphic evidence suggested that the “migrants were at higher risk for coronary heart disease than were non-migrants.”

A number of factors combined to make this higher disease incidence among the migrants difficult to explain. For one thing, the Tokelauans who emigrated smoked fewer cigarettes than those who remained on the atol s, so tobacco was unlikely to explain this pattern of disease. The migrants tended to be younger, too, which should have led to the appearance of less chronic disease on the mainland. And though the weights of the Tokelauan migrants were “substantial y higher” than those of the atol -dwel ers and, “in fact, obesity became a problem for some,” the migrant lifestyle was definitively the more rigorous of the two. The men worked in the forest service and casting shops of the railway; the women worked in electrical-assembly plants or clothing factories, or they cleaned offices during the evening hours, and they walked “some distance to and from the shops with their purchases.” Final y, the original Tokelauan diet had been remarkably high in fat and saturated fat, but the migrants consumed considerably less of both. If Keys’s hypothesis was correct, the migrants should have manifested less evidence of heart disease, not more.

In fact, the migrant experience had led to an increased incidence over the entire spectrum of chronic diseases. Prior and his col eagues acknowledged that their data made this difficult to explain in any simple manner. They suggested “that a different set of relevant variables might account for observed differences in incidence.” Excess weight, whatever the cause, could explain at least part of the increased incidence of hypertension, diabetes, coronary heart disease, and gout among the migrants. They appeared to get more salt in their diets than the islanders did, so that might also explain the increased incidence of hypertension, as might the stress of assimilating to a new culture. The red meat consumed on the mainland might have contributed to the increased incidence of gout as wel . The greater incidence of asthma could be explained by the presence of al ergens in New Zealand that were absent in Tokelau.

As in the Tokelau study, the dominant approach over the past fifty years toward understanding the chronic diseases of civilization has been to assume that they are only coincidental y related, that each disease has its unique causal factors associated with the Western diet and lifestyle, although dietary fat, saturated fat, serum cholesterol, and excess weight invariably remain prime suspects.

The less common approach to this synchronicity of diseases has been to assume, as Peter Cleave did, that related diseases have related or common causes; that they are manifestations of a single underlying disorder. Cleave cal ed it the saccharine disease because he believed sugar and other refined carbohydrates were responsible. By this philosophy, if diabetes, coronary heart disease, obesity, gout, and hypertension appear simultaneously in populations, as they did in the Tokelauan experience, and are frequently found together in the same patients, then they are very likely to be manifestations of a single underlying pathology. If nothing else, Cleave argued, this common-cause hypothesis was the simplest possible explanation for the evidence, and thus the one that should be presumed true until compel ing evidence refuted it. This was Occam’s razor, and it should be the guiding principle of al scientific endeavors.

In the early 1950s, clinical investigators began to characterize the physiological mechanisms that would underlie Cleave’s saccharine-disease hypothesis of chronic disease, and that could explain the appearance of diseases of civilization going back over a century—the basis, in effect, of this carbohydrate hypothesis. The research evolved in multiple threads that resulted in some of the most fundamental discoveries in heart-disease and diabetes research. Only in the late 1980s did they begin to come together, when the Stanford diabetologist Gerald Reaven proposed the name Syndrome X to describe the metabolic abnormalities common to obesity, diabetes, and heart disease, al , at the very least, exacerbated by the consumption of sugar, flour, and other easily digestible carbohydrates. Syndrome X included elevated levels of the blood fats known as triglycerides; low levels of HDL cholesterol, now known as the good cholesterol; it included hypertension, and three phenomena that are considered precursors of adult-onset diabetes—chronical y high levels of insulin (hyperinsulinemia), a condition known as insulin resistance (a relative insensitivity of cel s to insulin), and the related condition of glucose intolerance (an inability to metabolize glucose properly). Over the years, other abnormalities have been added to this list: the presence of predominantly smal , dense LDL particles, and high levels of a protein cal ed fibrinogen that increases the likelihood of blood-clot formation. Elevated uric-acid concentrations in the blood, a precursor of gout, have been linked to Syndrome X, as has a state of chronic inflammation, marked by a high concentration in the blood of a protein known as C-reactive protein.

In the last decade, Syndrome X has taken on a variety of names as authorities, institutions, and associations have slowly come to accept its validity. It is often referred to as insulin resistance syndrome. The National Heart, Lung, and Blood Institute belatedly recognized the existence of Syndrome X in 2001, cal ing it metabolic syndrome. It has even been referred to as insulin resistance/metabolic syndrome X, or MSX, by those investigators attempting to cover al bases.*39 By any name, this metabolic syndrome is as much a disorder of carbohydrate metabolism as is adult-onset diabetes, and is certainly a consequence of the carbohydrate content of the diet, particularly, as Cleave would have predicted, such refined, easily digestible carbohydrates as sugar and white flour.