Good Calories, Bad Calories

diabetes became ever more common in hospitals and life-insurance exams, and as life insurance itself became popular, physicians increasingly diagnosed mild diabetes in outwardly healthy individuals, so the incidence numbers rose. As with coronary heart disease, the diagnostic definition of diabetes changed over the years, as did the relevant statistical analyses, so no conclusions can be considered definitive.

Nonetheless, the numbers were compelling. In 1892, according to William Osler in Principles and Practice of Medicine, only ten diabetics had been diagnosed among the thirty-five thousand patients treated at Johns Hopkins Hospital. At Massachusetts General Hospital in Boston, only 172 patients had been diagnosed as diabetic out of nearly fifty thousand admitted between 1824 and 1898; only eighteen of those were under twenty years old, and only three under ten, suggesting that childhood diabetes was an extremely rare diagnosis. Between 1900 and 1920, according to Haven Emerson, director of the Institute of Public Health at Columbia University, the death rate from diabetes, despite improved treatment of the disease, had increased by as much as 400 percent in American cities. It had increased fifteen-fold since the end of the Civil War. Emerson reported proportional increases in diabetes mortality in Great Britain and France and suggested they were due to the increased consumption of sugar, combined with an increasingly sedentary lifestyle. Moreover, diabetes rates had dropped precipitously during World War I in populations that had faced food shortages or rationing. “It is apparent,” wrote Emerson in 1924, “that rises and falls in the sugar consumption are followed with fair regularity within a few months by similar rises and falls in the death rates from diabetes.”

The hypothesis that sugar and refined carbohydrates were responsible might have survived past the 1930s, but Elliott Joslin refused to believe it, and Joslin’s name was by then “synonymous” with diabetes in the United States. Joslin may once have ranked beneath Frederick Allen in the hierarchy of American diabetologists, but Allen’s reputation had been built on his starvation cure for diabetes, which was only marginally effective, and rendered unnecessary once insulin was discovered in 1921. Joslin achieved lasting fame by pioneering the use of insulin as a treatment. From the 1920s onward, Joslin’s textbook The Treatment of Diabetes Mellitus and his Diabetic Manual were the bibles of diabetology.

When Emerson presented his evidence that rising sugar consumption was the best explanation for the rise in diabetes incidence, Joslin rejected it. He said that increased sugar consumption had been offset in America by decreasing apple consumption, and that the carbohydrates in apples were effectively identical to table sugar as far as diabetics were concerned. (This wasn’t the case, but Joslin had little reason to believe otherwise in the 1920s.) Emerson countered with U.S. Department of Agriculture data reporting an actual increase in apple consumption in the relevant decades, but Joslin was unyielding.

Joslin found it inconceivable that sugar or any other refined starch could have a unique property that other carbohydrates did not. They all broke down to glucose after digestion, or glucose and fructose, in the case of table sugar. The insulin-releasing cells of the pancreas (known as ? cells), which are dysfunctional in diabetes, respond only to the glucose. Early on in his career, Joslin, like Ancel Keys thirty years later, found the Japanese diet to be compelling evidence for the salubrious nature of carbohydrate-rich diets. “A high percentage of carbohydrate in the diet does not appear to predispose to diabetes,” he wrote in 1923, since the Japanese ate such a diet and had an extremely low incidence of diabetes. He acknowledged that the rising death rate from diabetes in the United States coincided with rising sugar consumption, and that diabetes mortality and sugar consumption “must stand in some relation,” but the Japanese experience argued against causality. He considered a rising incidence of obesity to be one factor in the increasing prevalence of diabetes, and decreasing physical activity, caused by the increasing mechanization of American life, to be another. A third factor, as the Japanese experience suggested, was a diet that was fat-rich and carbohydrate-poor.

Joslin effectively based his belief primarily on the work of a single researcher: Harold Himsworth of University College Hospital, London. To Joslin, Himsworth’s “painstakingly accumulated” data constituted compelling evidence that a deficiency of carbohydrates and an excess of fat bring on diabetes. It was Himsworth’s research and Joslin’s faith in it that led a half-century of diabetologists to believe unconditionally that diabetes is not caused by the consumption of sugar and refined carbohydrates.

The two scientists effectively piggybacked on one another. In the post–World War II editions of Joslin’s textbook, he cited a 1935 article by Himsworth as the support for the statement that increased fat consumption explained the rising incidence of diabetes.^*31 Himsworth’s article, in turn, rejected the hypothesis that sugar caused diabetes by citing a 1934 article by Joslin and a 1930 article by C. A. Mills of the University of Cincinnati. Joslin’s 1934 article also depended almost entirely on Mills’s article. Mills’s article had stated “that there is no evidence in support” of the sugar-diabetes hypothesis; he had based this statement almost entirely on the observation that in Norway, Australia, and elsewhere sugar consumption rose from 1922 through the end of that decade but diabetes mortality did not. Other investigators, however, Joslin included, noted that the discovery of insulin in 1921 naturally led to a temporary leveling off of the otherwise rising tide of diabetes mortality. (On the other hand, as Mills noted, “of the thirteen countries highest in consumption of sugar, eleven are found among the thirteen highest in death rate from diabetes.”)

Himsworth’s achievements in clinical research were notable. He may have been the first researcher to differentiate between juvenile diabetes, caused by the inability of the pancreas to produce sufficient insulin and now known as insulin-dependent or Type 1 diabetes, and non-insulin-dependent diabetes, or Type 2, primarily a disease of adults, linked to excess weight and characterized by an insensitivity to insulin. Himsworth would later be knighted for his research contributions. Regrettably, his epidemiology was not as good as his clinical research.

Himsworth had first become convinced that diabetes was caused by fatty diets after asking his patients about their eating habits prior to their diabetes diagnosis and being told they had consumed “a smaller proportion of carbohydrate and a greater proportion of fat” than did healthy individuals.

Like Joslin, Himsworth considered all carbohydrates to be equivalent, sugar included; they could all be treated under one nutritional category when comparing diet and disease trends in populations. So Himsworth’s strongest argument was also the Japanese/American comparison. Whereas Joslin used it to exonerate sugar and high- carbohydrate diets, Himsworth used it to implicate fat and low-carbohydrate diets. Himsworth found the correlation between trends in diabetes mortality and the rising tide of fat consumption in England and Wales to be “striking” (the same word that Emerson had used to describe the correlation between trends in diabetes mortality and sugar consumption in the United States). “The progressive rise in diabetic mortality in Western countries during the last fifty years coincides with a gradual change towards higher fat and lower carbohydrate diets,” Himsworth wrote. “The diabetic mortality rate is high in countries whose diets tend to be high in fat and poor in carbohydrate; and low where the opposite tendency prevails. The fall in diabetic mortality in World War I was related to a fall in fat and rise in carbohydrate intake…. Diabetic mortality rises with economic position and, simultaneously, dietary habits change so that a greater proportion of fat and less carbohydrate is taken.” All of these observations, however, could also have been explained by variations in the consumption of sugar and white flour.

To defend his theory, Himsworth had to render irrelevant the conflicting evidence—the experience of isolated populations, for example, eating their traditional diets. “There appears to be unanimous agreement,” he wrote, “that the incidence of diabetes mellitus is very low in the lower social grades of coloured races resident in their native lands, but there is evidence that when these races are transplanted to westernized countries the diabetic mortality rate rapidly rises.” Himsworth’s interpretation was that the original diets of these populations were fat- poor and carbohydrate-rich and became higher in fat when these people moved into urban environments. Himsworth acknowledged that the Masai ate a diet that “contained the highest proportion of fat of any recorded diet” and did not appear to suffer from diabetes, but he considered this evidence “so scanty that no opinion can be expressed.”