Good Calories, Bad Calories (21 page)

FREDERICK ALLEN, Studies Concerning Glycosuria and Diabetes, 1913

Sugar and candies do not cause diabetes, but contribute to the burden on the pancreas and so should be used sparingly…. Carbohydrates are best taken in starchy forms: fruits, vegetables and cereals. The absorption is slower and the functional strain minimal.

GARFIELD DUNCAN, Diabetes Mellitus and Obesity, 1935

OF ALL THE DISEASES OF CIVILIZATION that may have been linked to the consumption of sugar and the refining of carbohydrates, diabetes was certainly a prime suspect. Here is a disease in which a conspicuous manifestation is the body’s inability to use for fuel the carbohydrates in the circulation—known as blood sugar or, more technical y, glucose or serum glucose. This glucose accumulates in the bloodstream, effectively overflows the kidneys, and spil s over into the urine, causing a condition referred to as glycosuria. One symptom is a constant hunger, specifical y for sugar and other easily digestible carbohydrates. Another is frequent urination, and the urine not only smel s like sugar but tastes like it. For this reason, diabetes was often known as the sugar sickness. Hindu physicians two thousand years ago suggested it was a disease of the rich, caused by indulgence in sugar, which had only recently arrived from New Guinea, as had flour and rice.

“This ancient belief has a point in its favor,” noted the American diabetologist Frederick Al en in his 1913 textbook Studies Concerning Glycosuria and Diabetes. “It originated before the time of organic chemistry, and there was no way for its authors to know that flour and rice are largely carbohydrate, and that carbohydrate in digestion is converted into the sugar which appears in the urine. This definite incrimination of the principal carbohydrate foods is, therefore, free from preconceived chemical ideas, and is based, if not on pure accident, on pure clinical observation.”

By the end of the nineteenth century, researchers had established that the pancreas was responsible for the disease. By the 1920s, insulin was discovered and found to be essential for the utilization of carbohydrates for energy. Without insulin, diabetic patients could stil mitigate the symptoms of the disease by restricting the starches and sugar in their diet. And yet diabetologists would come to reject categorical y the notion that sugar and refined carbohydrates could somehow be responsible for the disease—another example of powerful authority figures winning out over science.

In the era that predated the discovery of insulin—a hormone that plays the crucial role in the carbohydrate hypothesis we wil be discussing—the leading authorities on the treatment of diabetes could be divided into three groups: those firmly convinced that sugar and other carbohydrates played no causative role (among them Carl von Noorden, the pre-eminent German authority); those who thought the evidence ambiguous (including the German internist Bernhard Naunyn) and wouldn’t put the blame on sugar itself but would concede, as Al en remarked, that “large quantities of sweet foods and the maltose of beer” favored the disease onset; and unequivocal believers (Raphaël Lépine of France was one), who would also note that vegetarian, beer-drinking Trappist monks frequently became diabetic, as did laborers in sugar factories.

Those diabetologists who believed that a connection existed argued that the glucose resulting from the digestion of sugar and refined carbohydrates passed with exceptional ease into the blood, and so it was easy to imagine that it might tax the body’s ability to use it. Add sugar to the diet of someone whose ability to assimilate carbohydrates is already borderline or damaged in some way, and that person might pass from an apparently healthy condition to one that is pathological. In such cases, explained Al en, “in the absence of any radical difference between diabetes and nondiabetic conditions, the assumption of a possible production by sugar is logical…. A sufficiently excessive indulgence may presumably weaken the assimilative power of individuals in whom this power is normal or slightly reduced.”

This scenario seemed to explain the fact that glycosuria wil often vanish when mild diabetics fast or refrain from eating sugar and other high-carbohydrate foods. It also explained why some individuals could eat sugar, flour, and white rice for a lifetime and never get diabetes, but others, less able to assimilate glucose, would become diabetic when they consumed too many refined carbohydrates. Anything that slowed the digestion of these carbohydrates (like eating carbohydrates in unrefined forms) and so reduced the strain on the pancreas, the organ that secretes insulin in response to rising blood sugar, or anything that increased the assimilation of glucose without the need for insulin (excessive physical activity), might help prevent the disease itself. “If he is a poor laborer he may eat freely of starch,” Al en wrote, “and dispose safely of the glucose arising from it, because of the slower process of digestion and assimilation of starch as compared with free sugar, and because of the greater efficiency of combustion in the muscles due to exercise. If he is wel -to-do, sedentary, and fond of sweet food, he may, with no greater predisposition, become openly diabetic.”

Diabetes seemed very much to be a disease of civilization, absent in isolated populations eating their traditional diets and comparatively common among the privileged classes in those nations in which the rich ate European diets: Sri Lanka (then Ceylon), Thailand, Tunisia, and the Portuguese island of Madeira, among others.*29 In China, diabetes was reportedly absent among the poor, but “the rich ones, who eat European food and drink sweet wine, suffer from it fairly often.”

To British investigators, it was the disparate rates of diabetes among the different sects, castes, and races of India that particularly implicated sugar and starches in the disease. In 1907, when the British Medical Association held a symposium on diabetes in the tropics at its annual conference, Sir Havelock Charles, surgeon general and president of the Medical Board of India, described diabetes among “the lazy and indolent rich” of India as a

“scourge.” “There is not the slightest shadow of a doubt,” said Charles’s col eague Rai Koilas Chunder Bose of the University of Calcutta, “that with the progress of civilization, of high education, and increased wealth and prosperity of the people under the British rule, the number of diabetic cases has enormously increased.” The British and Indian physicians working in India agreed that the Hindus, who were vegetarians, suffered more than the Christians or the Muslims, who weren’t. And it was the Bengali, who had taken on the most trappings of the European lifestyle, and whose daily sustenance, noted Charles, was “chiefly rice, flour, pulses*30 and sugars,” who suffered the most—10 percent of “Bengali gentlemen” were reportedly diabetic. (In comparison, noted Charles, only eight cases of diabetes had been diagnosed among the seventy-six thousand British officials and soldiers working in India at the time—an incidence rate of .01 percent.)

Sugar and white flour were also obvious suspects in the etiology of diabetes, because the dramatic increase in consumption of these foodstuffs in the latter decades of the nineteenth century in the United States and Europe coincided with dramatic increases in diabetes incidence and mortality. Unlike heart disease, diabetes was a relatively straightforward diagnosis. After the introduction of a test for sugar in the urine in the 1850s, testing for 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 compel ing. In 1892, according to Wil iam 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 fal s in the sugar consumption are fol owed with fair regularity within a few months by similar rises and fal s in the death rates from diabetes.”

The hypothesis that sugar and refined carbohydrates were responsible might have survived past the 1930s, but El iott 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 Al en in the hierarchy of American diabetologists, but Al en’s reputation had been built on his starvation cure for diabetes, which was only marginal y 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 al broke down to glucose after digestion, or glucose and fructose, in the case of table sugar. The insulin-releasing cel s of the pancreas (known as ß cel s), 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 compel ing 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 Col ege Hospital, London. To Joslin, Himsworth’s “painstakingly accumulated” data constituted compel ing 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 unconditional y 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 I 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. Mil s of the University of Cincinnati. Joslin’s 1934

article also depended almost entirely on Mil s’s article. Mil s’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 natural y led to a temporary leveling off of the otherwise rising tide of diabetes mortality. (On the other hand, as Mil s 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 smal er proportion of carbohydrate and a greater proportion of fat” than did healthy individuals.

Like Joslin, Himsworth considered al carbohydrates to be equivalent, sugar included; they could al 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 fal in diabetic mortality in World War I was related to a fal 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.” Al of these observations, however, could also have been explained by variations in the consumption of sugar and white flour.