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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.

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