Good Calories, Bad Calories

Chapter Six

DIABETES AND THE CARBOHYDRATE HYPOTHESIS

The consumption of sugar is undoubtedly increasing. It is generally recognized that diabetes is increasing, and to a considerable extent, its incidence is greatest among the races and the classes of society that consume most sugar. There is a frequently discussed, still unsettled, question regarding the possible role of sugar in the etiology of diabetes. The general attitude of the medical profession is doubtful or negative as regards statements in words…. But the practice of the medical profession is wholly affirmative.

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 technically, glucose or serum glucose. This glucose accumulates in the bloodstream, effectively overflows the kidneys, and spills over into the urine, causing a condition referred to as glycosuria. One symptom is a constant hunger, specifically for sugar and other easily digestible carbohydrates. Another is frequent urination, and the urine not only smells 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 Allen 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 still mitigate the symptoms of the disease by restricting the starches and sugar in their diet. And yet diabetologists would come to reject categorically 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 will 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 Allen remarked, that “large quantities of sweet foods and the maltose of beer” favored the disease onset; and unequivocal believers (Raphael Lepine 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 Allen, “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 will 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,” Allen 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 well-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 colleague 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