in sucrose consumption.” This coincided with an almost immediate increase in weight and blood pressure, and a decrease in cholesterol levels—all 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 “exceptionally high incidence” of “diabetes, gout, and osteoarthritis, as well 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 atolls, 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 “substantially higher” than those of the atoll-dwellers 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.” Finally, 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 colleagues 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 well. The greater incidence of asthma could be explained by the presence of allergens 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 coincidentally 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 called 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 compelling evidence refuted it. This was Occam’s razor, and it should be the guiding principle of all 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, all, 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—chronically high levels of insulin (hyperinsulinemia), a condition known as
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
It wasn’t until the late 1990s that the evolving science of metabolic syndrome began to have any significant influence outside the field of diabetes, at which point the media finally began to take notice.†40 The potential implications of metabolic syndrome for heart disease and other chronic diseases have only just begun to be appreciated by the research community. As a result, a hypothesis that emerged from research in the 1950s as an alternative explanation for the high rates of heart disease in Western nations has been accepted by medical researchers and public-health authorities a half-century later as a minor modification to Keys’s dietary- fat/cholesterol hypothesis, even though this alternative hypothesis implies that Keys’s hypothesis is wrong. The bulk of the science is no longer controversial, but its potential significance has been minimized by the assumption that saturated fat is still the primary evil in modern diets.
The Tokelau experience stands as an example. The current accepted explanation for the pattern of disease among the Tokelauans is that the increased sugar and flour in their diets caused metabolic syndrome, and in turn heart disease and diabetes, at least according to Scott Grundy, who is a nutritionist and specialist in the metabolism of blood lipids at the University of Texas Southwestern Medical Center and the primary author of the 2003 cholesterol guidelines published by the National Cholesterol Education Program (NCEP). This does not mean, however, that Grundy believes that Cleave’s saccharine-disease hypothesis of chronic disease is correct, or that Keys was incorrect. Rather, as he explained it, in the United States the situation was less straightforward than in Tokelau. “What you’re faced with,” Grundy said, “is a historical change in people’s habits. Going back to the 1940s, ’50s, and ’60s, people ate huge amounts of butter and cheese and eggs, and they had very high LDL levels [the “bad cholesterol”] and they had severe heart disease early in life, because of such high cholesterol levels. What’s happened since then is, there has been a change in population behavior, and they don’t consume such high quantities of saturated fat and cholesterol anymore, and so LDL has come down a great deal as our diets have changed. But now…we have got obesity, and most of the problem is due to higher carbohydrate consumption or higher total calories. And so we’re switching more to metabolic syndrome.”
Grundy’s explanation is a modern version of the changing-American-diet story, in this case invoked as a rationale to explain how metabolic syndrome could be the primary cause of heart disease today, while Keys’s hypothesis could still be correct, but no longer particularly relevant to our twenty-first-century health problems.
