Good Calories, Bad Calories Part 4

Hrdli ka considered the possibility, which Keys would raise fifty years later, that these Native Americans were unaffected by chronic disease because their life expectancy was relatively short; he rejected it because the evidence suggested that they lived as long as or longer than the local whites.

In 1910, Hrdli ka's field observations on cancer were confirmed by Isaac Levin, a Columbia University pathologist, who surveyed physicians working for the Indian Affairs Bureau on reservations throughout the Midwestern and Western states. Levin's report, ent.i.tled "Cancer Among the North American Indians and Its Bearing upon the Ethnological Distribution of the Disease," discussed the observations of 107 physicians who had responded to his survey, with their names, locations, size of practice, duration of practice, and number of cancers diagnosed: Chas. M. Buchannan, for instance, practiced fifteen years among two thousand Indians with an average life expectancy of fifty-five to sixty years and saw only one case of cancer; Henry E. Goodrich, practicing for thirteen years among thirty-five hundred Indians, saw not a single case. Levin's survey covered over 115,000 Native Americans treated by agency doctors for anywhere from a few months to two decades and produced a total of twenty-nine doc.u.mented cases of malignant tumors.

The two most comprehensive attempts to deal with the question of cancer in isolated populations were in The Natural History of Cancer, with Special Reference to Its Causation and Prevention, published in 1908 by W. Roger Wil iams, a fel ow of the British Royal Col ege of Surgeons, and The Mortality from Cancer Throughout the World, published in 1915 by the American statistician Fredrick Hoffman. In The Natural History of Cancer, Wil iams marched from continent to continent, region to region. In Fiji, for instance, in 1900, among 120,000 aborigines, Melanesians, Polynesians, and "Indian coolies," there were only two recorded deaths from malignant tumors. In Borneo, a Dr. Pagel wrote that he had been in practice for ten years and had never seen a case. Wil iams also doc.u.mented the rising mortality from cancer that Tanchou had reported in the developed nations. In the United States, the proportional number of cancer deaths rose dramatical y in the latter part of the nineteenth century: in New York, from thirty-two per thousand deaths in 1864 to sixty-seven in 1900; in Philadelphia, from thirty-one in 1861 to seventy in 1904.

Hoffman dedicated the better part of his career to making sense of these observations. He began his cancer studies as chief statistician of the Prudential Insurance Company and continued them as part of an investigation of the Committee on Statistics of the American Society for the Control of Cancer (a predecessor of the American Cancer Society, of which Hoffman was a founder). In The Mortality from Cancer Throughout the World and then again in Cancer and Diet, his 1937, seven-hundred-plus-page update of the evidence, Hoffman concluded that cancer mortality was increasing "at a more or less alarming rate throughout the entire world," and this could only partial y be explained by new diagnostic practices and the aging of the population.

Hoffman could not explain away the observations that physicians like Schweitzer and Hutton had made around the world and that both he and Wil iams had doc.u.mented so comprehensively. In 1914, Hoffman himself had surveyed physicians working for the Bureau of Indian Affairs. "Among some 63,000 Indians of al tribes," he reported, "there occurred only 2 deaths from cancer as medical y observed during the year 1914."

"There are no known reasons why cancer should not occasional y occur among any race or people, even though it be of the lowest degree of savagery or barbarism," Hoffman wrote.

Granting the practical difficulties of determining with accuracy the causes of death among non-civilized races, it is nevertheless a safe a.s.sumption that the large number of medical missionaries and other trained medical observers, living for years among native races throughout the world, would long ago have provided a more substantial basis of fact regarding the frequency of occurrence of malignant disease among the so-cal ed "uncivilized" races, if cancer were met with among them to anything like the degree common to practical y al civilized countries. Quite to the contrary, the negative evidence is convincing that in the opinion of qualified medical observers cancer is exceptional y rare among primitive peoples.

Through the 1930s, this evidence continued to acc.u.mulate, virtual y without counterargument. By the 1950s, malignancies among the Inuit were stil considered sufficiently uncommon that local physicians, as in Africa earlier in the century, would publish single-case reports when they did appear. One 1952 article, written by three physicians from Queen's University in Ontario, begins with the comment "It is commonly stated that cancer does not occur in the Eskimos, and to our knowledge no case has so far been reported." In 1975, a team of Canadian physicians published an a.n.a.lysis of a quarter-century of cancer incidence among Inuit in the western and central Arctic. Though lung and cervical cancer had "dramatical y increased" since 1949, they reported, the incidence of breast cancer was stil "surprisingly low." They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1974.

These missionary and colonial physicians did often diagnose tumors and other diseases of civilization in local whites, and among natives who were working for European households and industries. In August 1923, for instance, A. J. Orenstein reported in the British Medical Journal on his experience as a superintendent of sanitation for the Rand mines in South Africa: "In a series of one hundred consecutive necropsies on native mine laborers conducted by myself in the latter part of 1922 and the first two months of 1923, two cases of carcinoma were observed-one was carcinoma of the pancreas and glands of the neck in a native male of the Shangaan race, age about 40, the other was a case of carcinoma involving practical y the whole of the liver, in a native male of the same race, age about 25." The reports from these physicians were a reminder of how dramatic the course of the disease could be, and evidence against the argument that sophisticated diagnostic technology, unavailable in these outposts, was required to diagnose cancer. In 1923, George Prentice, who worked in Nyasaland, in southern central Africa, described one native patient with an inoperable breast tumor in the British Medical Journal: "It ran an uninterrupted course," Prentice wrote, "completely destroyed the breast, then the soft structure of the chest wal , and then ate through the ribs; when I last saw the negress in her vil age, I could see the heart pulsating. That was just before her death."

The absence of malignant cancer in isolated populations prompted questions about why cancer did develop elsewhere. One early hypothesis was that meat-eating was the problem, and that primitive populations were protected from cancer by eating mostly vegetarian diets. But this failed to explain why malignancies were prevalent among Hindus in India-"to whom the fleshpot is an abomination"-and rare to absent in the Inuit, Masai, and other decidedly carnivorous populations. (This hypothesis "hardly holds good in regard to the [American] Indians," as Isaac Levin wrote in 1910. "They consume a great deal of food [rich in nitrogen-i.e., meat], frequently to excess.") By the late 1920s, the meat-eating hypothesis had given way to the notion that it was overnutrition in general, in conjunction with modern processed foods, lacking the vital elements necessary for health, that were to blame. These were those foods, as Hoffman put it, "demanding conservation or refrigeration, artificial preservation and coloring, or processing otherwise to an astonishing degree." As a result of these modern processed foods, noted Hoffman, "far-reaching changes in bodily functioning and metabolism are introduced which, extending over many years, are the causes or conditions predisposing to the development of malignant new growths, and in part at least explain the observed increase in the cancer death rate of practical y al civilized and highly urbanized countries."

White flour and sugar were singled out as particularly noxious, because these had been increasing dramatical y in Western diets during the latter half of the nineteenth century, coincident with the reported increase in cancer mortality. (They would also be implicated in the growing incidence of diabetes, as we'l discuss, and appendicitis.) Moreover, arguments over the nutritive value and appeal of white flour and sugar had been raging since the early nineteenth century.

Flour is made by separating the outer layers of the grain, containing the fiber-the indigestible carbohydrates-and virtual y al of the vitamins and protein, from the starch, which is composed of long chains of glucose molecules. White sugar is made by removing the juice containing sucrose from the surrounding cel s and husk of the cane plant or sugar beet. In both cases, the more the refining, the whiter the product, and the lower the vitamin, mineral, protein, and fiber content. The same is true for white rice, which goes through a similar refining process.

This might seem obviously disadvantageous, but white flour had its proponents. It was traditional y considered "more attractive to the eye," as Sir Stanley Davidson and Reginald Pa.s.smore observed in their textbook Human Nutrition and Dietetics (1963). It was preferred by bakers for its baking properties, and because it contains less fat than wholemeal flour it is less likely to go rancid and is more easily preserved. Mil ers preferred it because the leftover bran from refining rice and wheat (as with the mola.s.ses left over from refining sugar) could be sold profitably for livestock feed and industrial uses.

Nutritionists also argued that white flour had better "digestibility" than whole-meal, because the presence of fiber in the latter prevented the complete digestion of any protein or carbohydrates that were attached. White flour's low protein, vitamin, and mineral content also made it "less liable than whole meal flour to infestation by beetles and the depredation of rodents," as Davidson and Pa.s.smore wrote.

It wasn't until the mid-nineteenth century that white flour became suitably inexpensive for popular consumption, with the invention of rol er mil s for grinding the grain. Until then, only the privileged cla.s.ses ate white flour, and the poor ate wholemeal. Sugar was also a luxury until the mid-nineteenth century, when sugar-beet cultivation spread throughout the civilized world. In 1874, with the removal of tariffs on sugar importation in Britain, sugar consumption skyrocketed and led to the eventual development of the biscuit, cake, chocolate, confectionery, and soft-drink industries. By the beginning of World War I, the English were already eating more than ninety pounds of sugar per capita per year-a 500-percent increase in a single century-and Americans more than eighty pounds. Not until the mid-twentieth century did mechanical rol ers begin replacing hand-pounding of rice in Asian nations, so that the poor could eat polished white rice instead of brown.

Explorers would carry enormous quant.i.ties of white flour, rice, and sugar on their travels and would trade them or give them away to the natives they met along the way.*27 In The Voyage of the Beagle, Darwin tel s how the expedition's members persuaded Aborigines in Australia to hold a dancing party with "the offer of some tubs of rice and sugar." As early as 1892, the Barrow Eskimos were already described as having "acquired a fondness for many kinds of civilized food, especial y bread of any kind, flour, sugar, and mola.s.ses." These foods remained primary items of trade and commerce with isolated populations wel into the twentieth century.28 Until the last few decades, the nutritional debate over the excessive refining of flour and sugar had always been about whether the benefits of digestibility and the pleasing white color outweighed any potential disadvantages of removing the protein, vitamins, and minerals. In late-nineteenth-century England, the physician Thomas Al inson, head of the Bread and Food Reform League, wrote: "The true staff of life is whole meal bread." Al inson was among the first to suggest a relationship between refined carbohydrates and disease. "One great curse of this country," wrote Al inson, "is constipation of the bowel which is caused in great measure by white bread. From this constipation come piles, varicose veins, headaches, miserable feelings, dul ness and other ailments.... As a consequence pil factories are now an almost necessary part of the state." Al inson's chain of cause and effect from white bread to constipation to chronic disease was given credibility in the late 1920s by the innovative and eccentric Scottish surgeon Sir Arbuthnot Lane in a book ent.i.tled The Prevention of the Diseases Peculiar to Civilization. The hypothesis would hold a tight grasp on a school of British medical researchers for decades to come.

The preferred explanation for how sugar, white flour, and white rice might perpetrate disease emerged from a great era of nutritional research in the early twentieth century. In 1912, the Polish-born biochemist Casimir Funk coined the term "vitamine" (the "e" was later dropped) and speculated that vitamins B1, B2, C, and D were necessary for human health. During the next quarter-century, researchers continued to discover new vitamins essential to health and identified a host of diseases-such as beriberi, pel agra, rickets, and scurvy-as caused by specific vitamin deficiencies. Beriberi results from a deficiency in thiamine (vitamin B1), which is lost in the refining of polished rice and white flour. This led to the suggestion that even a disease like cancer could be a kind of deficiency disease, caused by vitamin starvation, as the journalist (and future homeopath) J. El is Barker cal ed it in his book Cancer: How It Is Caused, How It Can Be Prevented (1924).

The Scottish nutritionist Robert McCarrison was perhaps the leading proponent of the hypothesis that the chronic il nesses of civilization could be attributed to "the extensive use of vitamin-poor white flour and to the inordinate use of vitamin-less sugar." McCarrison had founded a laboratory in India that would later become the National Inst.i.tute of Nutrition and had spent nine years working in the Himalayas, "amongst isolated races far removed from the refinements of civilization," as he explained in a 1921 lecture at the University of Pittsburgh. "During the period of my a.s.sociation with these peoples,"

he wrote, "I never saw a case of asthenic dyspepsia, of gastric or duodenal ulcer, of appendicitis, of mucous colitis, or of cancer, although my operating list averaged over 400 operations a year." McCarrison attributed their good health to several factors, including a diet of "the unsophisticated foods of Nature." "I don't suppose that...as much sugar is imported into their country in a year as is used in a moderately sized hotel of this city in a single day," he said.

McCarrison's research included a comparative study of the diets and physiques of the disparate populations and religious groups on the Indian subcontinent. The "physique of northern races of India," McCarrison wrote, "is strikingly superior to that of the southern, eastern, and western races." Once again, he attributed the difference to the vitamins and nutrients present in the northern-Indian diet but not elsewhere. They ate wel -balanced diets, with milk, b.u.t.ter, vegetables, fruit, and meat-and ate their wheat ground course as wholemeal flour, which "preserves al the nutrients with which Nature has endowed it." "White flour, when used as the staple article of diet," wrote McCarrison, "places its users on the same level as the rice-eaters of the south and east of India. They are faced with the same problem; they start to build up their dietaries with a staple of relatively low nutritive value." He also fed rats and mice in his laboratory on diets of these different populations and reported that the rats fared best on those diets containing "in abundance every element and complex for normal nutrition" and fared worst on those "excessively rich in carbohydrates, and deficient in suitable protein, mineral salts and vitamins."

By World War I , this rising tide of research on essential vitamins led the United States to decree that mil ers had to enrich white flour with vitamin B, iron, and nicotinic acid. In England, the government acted in similar fashion a decade later. The concept of "protective foods," containing the requisite protein, vitamins, and minerals for a healthy diet-fresh meat, fish, eggs, milk, fruits, and vegetables-now became the orthodox wisdom. During a century of debate, no one seems to have considered whether the properties of these refined foods-flour, sugar, and white rice-could have an impact on human health other than through the protein, fiber, vitamins, and minerals removed. Thirty years later, that would turn out to be the case, but by that time much of this original research on diseases of civilization would have been forgotten.

Chapter Six.

DIABETES AND THE CARBOHYDRATE HYPOTHESIS.

The consumption of sugar is undoubtedly increasing. It is general y recognized that diabetes is increasing, and to a considerable extent, its incidence is greatest among the races and the cla.s.ses of society that consume most sugar. There is a frequently discussed, stil unsettled, question regarding the possible role of sugar in the etiology of diabetes. The general att.i.tude of the medical profession is doubtful or negative as regards statements in words.... But the practice of the medical profession is whol y 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 technical y, glucose or serum glucose. This glucose acc.u.mulates 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 princ.i.p.al 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 quant.i.ties 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 pa.s.sed 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 a.s.similate carbohydrates is already borderline or damaged in some way, and that person might pa.s.s 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 a.s.sumption of a possible production by sugar is logical.... A sufficiently excessive indulgence may presumably weaken the a.s.similative 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 a.s.similate 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 a.s.similation 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 a.s.similation 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 cla.s.ses 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 a.s.sociation 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 a.n.a.lyses, 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 Ma.s.sachusetts 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 Inst.i.tute 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 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 j.a.panese 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 j.a.panese 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 j.a.panese 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 j.a.panese 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 acc.u.mulated" data const.i.tuted 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 postWorld 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 j.a.panese/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.

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 mel itus 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."

Final y, Himsworth had to deal with the reported absence of diabetes among the Inuit. He acknowledged that his hypothesis implied that the Inuit should have an extremely high incidence of diabetes, which they did not. (There were three reported cases of confirmed diabetes among a population of sixteen thousand Alaskan Eskimos in 1956.) Rather than suggest that the Inuit died too young to get diabetes-Ancel Keys used the early-death rationale a quarter-century later to explain away their reported freedom from heart disease and cancer-Himsworth suggested they did not actually eat high-fat diets, despite al reports to the contrary. He cited two journal articles. One, he wrote, implied that the Inuit on Baffin Island ate a diet of only 48 percent fat calories, not that much higher than the average Englishman. The other, from 1930, reported that the "fisherfolk" of Labrador and northern Newfoundland subsisted on a diet of 21 percent fat calories and 70 percent carbohydrates, which meant a diet only slightly higher in fat than those eaten in Southeast Asian countries. (Himsworth did both these authors a disservice by suggesting that they believed that the Eskimo diets were carbohydrate-rich rather than fat-rich. The former article noted that the Eskimo "in his natural state eats practical y only flesh," of which "in cold weather...one-third to one-half [by serving, not calories] may be taken as fat." The "fisherfolk" discussed in the latter article were not Eskimos, as Himsworth a.s.sumed, but those "of English and Scotch descent." Half of their daily calories came from white flour purchased at the local trading post, the author reported. Another quarter came from hard bread, rol ed oats, mola.s.ses, and sugar.) "It would thus appear," Himsworth concluded, "that the most efficient way to reduce the incidence of diabetes mel itus amongst individuals predisposed to develop this disease would be to encourage the consumption of a diet rich in carbohydrate and to discourage them from satisfying their appet.i.te with other types of food."

Once Joslin embraced Himsworth's fat hypothesis, it became the conventional wisdom among diabetologists and the mainstream medical community in the United States. In the 1946 and 1959 editions of his textbook, Joslin al otted the suggestion that sugar and refined carbohydrates play a role in diabetes less than a page and a half. In the 1971 edition, edited by Joslin's col eagues a decade after his death and renamed Joslin's Diabetes Mellitus, the subject had vanished entirely.

Oddly, Himsworth himself acknowledged that his own hypothesis was difficult to defend. In a 1949 lecture to the British Royal Col ege of Physicians, Himsworth described the "paradox" of his fat hypothesis: "Though the consumption of fat has no deleterious influence on [the ability to metabolize glucose], and fat diets actual y reduce the susceptibility of animals to diabetogenic agents, the incidence of human diabetes is correlated with the amount of fat consumed." Himsworth even suggested that dietary fat might not be the culprit after al , or that perhaps "other, more important, contingent variables"

tracked with fat in the diet. He suggested that total calories played a role, because of the intimate a.s.sociation of diabetes and obesity, and because "in the individual diet, though not necessarily in national food statistics, fat and calories tend to change together." He did not mention sugar, which tends to change together with fat in both national food statistics and individual diets.

Despite Joslin's unconditional rejection of the hypothesis, investigators outside the United States continued to publish reports that implicated sugar specifical y in the etiology of diabetes. In 1961, the Israeli diabetologist Aharon Cohen of Hada.s.sah University reported that this was the best explanation for the pattern of diabetes seen in Jews who had immigrated to Israel from Yemen. In 1954, Cohen had spoken with Joslin, who had argued that diabetes was primarily caused by an inherited predisposition. Cohen, however, had spent the preceding years studying the dramatic differences in diabetes incidence among Native American tribes, and also treating diabetes among the refugees who had flooded into Israel with the end of World War I , and believed otherwise. As Cohen recal ed the conversation, Joslin had effectively chal enged him to test his belief by systematical y examining the Israeli immigrant populations, and that's what Cohen did. Over the next five years, Cohen and his col aborators examined fifteen thousand Israelis living in a belt from Jerusalem to Beersheba. He concentrated on Yemenite Jews, because he had two distinct, contrasting populations to work with. One had arrived in 1949, fifty-thousand strong, flown in a legendary yearlong airlift known as Operation Magic Carpet. The other had lived in Israel since the early 1930s.

Cohen was "astonished" that he found only three cases of diabetes in his examinations of five thousand Yemenites who had come in 1949. The incidence of diabetes was nearly fifty times as great in the earlier arrivals, and comparable to other populations in Israel, New York, and elsewhere. Other studies had also demonstrated, as Cohen put it, "a significantly greater prevalence" of coronary heart disease, hypertension, and high cholesterol among the Yemenites who had been in Israel for a quarter-century or more.

Cohen and his col aborators interviewed the more recent immigrants about their diets, both in Israel and in Yemen. They concluded that sugar consumption was the one noteworthy difference that might explain the increased incidence of diabetes, and perhaps the coronary heart disease, hypertension, and high cholesterol, too. "The quant.i.ty of sugar used in the Yemen had been negligible," Cohen wrote; "almost no sugar was consumed. In Israel there is a striking increase in sugar consumption, though little increase in total carbohydrates."

In New Zealand, Ian Prior, a young cardiologist who would later become the nation's most renowned epidemiologist, studied a population of five hundred Maoris living in an isolated val ey of the North Island, thirty-five miles from the nearest town. Despite a physical y active life-certainly by the standards of modern-day Europe or the United States-the Maoris, as Prior reported in 1964, had a remarkably high incidence of diabetes, heart disease, obesity, and gout. Sixty percent of the middle-aged women were overweight; over a third were obese. Sixteen percent had heart disease, and 11 percent had diabetes. Six percent of the men had diabetes. The staples of the Maori diet, Prior reported, were bread, flour, biscuits, breakfast cereals, sugar (over seventy pounds per person a year), and potatoes. There was also "beer, ice-cream, soft drinks, and sweets." Tea was the common beverage, "taken with large amounts of sugar by the majority."

In South Africa, George Campbel , who began his career as a general pract.i.tioner in Natal and then ran the diabetic clinic at the King Edward VI I Hospital in Durban, focused on a population of Indian immigrants living in the Natal region and on the local Zulu population. In the early 1950s, according to Campbel , his patients fel into two distinct categories of disease. The local whites suffered from diabetes, coronary thrombosis, hypertension, appendicitis, gal -bladder disease, and other diseases of civilization. The rural Zulus did not. In 1956, Campbel spent a year working at the Hospital of the University of Pennsylvania in Philadelphia and was "absolutely staggered by the difference in disease spectrum" between the black population in Philadelphia and the rural Zulus. Among the blacks of Philadelphia, he saw the same disorders that characterized his white patients in Durban.

After returning to South Africa, Campbel went to work at the King Edward VI I Hospital, which served exclusively the "non-white" population, and admitted some sixty thousand patients a year while administering to six hundred thousand outpatients. Once again, says Campbel , he was struck by the "remarkable difference in the spectrum of disease," in this instance between the urbanized Zulus, who were appearing with the same spectrum of diseases he had seen among the blacks of Philadelphia, and what he cal ed their "country cousins" who stil lived in rural areas. The Natal Indian population became the primary subject of Campbel 's research when he realized that four out of every five of his diabetic patients came from that impoverished Indian community.

The ancestors of these Natal Indians had arrived in South Africa in the latter half of the nineteenth century to work as indentured laborers on the local sugar plantations. When Campbel began studying them in the late 1950s, over 70 percent lived below the poverty line, and many stil worked for the sugar industry. Campbel and other researchers carried out half a dozen health surveys of this Natal Indian population. The incidence of diabetes among middle-aged men in some of the vil ages ran as high as 33 percent. It was nearly 60 percent among the ward patients and outpatients at the King Edward VI I Hospital. In ten years of operation, Campbel 's clinic treated sixty-two hundred Indian diabetics, out of a local Indian population of only 250,000. A "veritable explosion of diabetes is taking place in these people," Campbel wrote, "in whom the incidence of the disease is now almost certainly the highest in the world." Campbel contrasted this with the numbers in India itself, where the average incidence of diabetes across the entire country was approximately 1 percent. This disparity between the incidence of diabetes in India and the incidence among the Indians of Natal ruled out a genetic predisposition to diabetes as a meaningful explanation.

For the Natal Indians, working primarily in and around sugar plantations, Campbel considered sugar the obvious suspect for their diabetes. He reported that the per-capita consumption of sugar in India was around twelve pounds yearly, compared with nearly eighty pounds for these working-cla.s.s Natal Indians. The fat content of the diet in Natal was also very low, which seemed to rule out fat as the culpable nutrient. Excessive calorie consumption couldn't be to blame, according to Campbel , because some of these impoverished Natal Indians were living on as little as sixteen hundred calories a day-"a figure in many countries which would be regarded almost as a starvation wage"-and yet they "were enormously fat and suffered from undoubted diabetes proven by blood tests."

Campbel also found the disparities in diabetes prevalence and sugar consumption between urban and rural Zulus to be tel ing. The urban Zulu population, as hospital records demonstrated, was beset by diabetes. But in "thousands" of physical examinations performed on rural Zulus, Campbel wrote, "no case of diabetes has ever been discovered in any of them." Studies of a rural Zulu population in 1953 and an urban population in Durban in 1957, wrote Campbel , concluded that the former were eating six pounds of sugar a year each, compared with more than eighty pounds for the latter. The fat content of the diet in both populations was very low-less than 20 percent of the total calories-which again seemed to rule out fat as the culpable nutrient. By 1963, according to the South African Cane Growers a.s.sociation, the urban Zulus were eating almost ninety pounds of sugar per person annual y, while the rural Zulus were eating forty pounds each (a sixfold increase in a decade).

"In the last few years sugar intake has risen drastical y in Natal," wrote Campbel , "because of very efficient advertising and because sugar has obviously reached as high an addictive status in our non-White people as in the Whites.... Al [sugar]cane workers get a weekly ration of 1 lb. Andit is estimated that they can augment this by chewing sugar cane to the extent of 1 lb. daily!"

These sugarcane cutters, in whom, as Campbel noted, "diabetes is virtual y absent," turned out to be pivotal, in that later generations of diabetologists would cite them as compel ing evidence that diabetes was not caused by eating sugar. Campbel , however, believed it was the refining of the sugar, which al owed for its quick consumption and metabolism, that did the damage; chewing sugarcane resulted in a slow intake of sugar that he believed would be relatively benign. Moreover, cane cutters would cut and move by hand as much as seven tons of sugarcane each day, which required an extraordinary effort that suggested to Campbel -as it had to Frederick Al en a half-century before-that a physical y active lifestyle might ward off the danger of excessive sugar consumption, perhaps by burning the sugar as fuel to maintain the necessary "huge output of energy" before it could do its damage. "There are few occupations in the world," Campbel wrote, "which entail such hard physical exertion as that involved in the cutting, moving, and stacking of sugar cane."

Campbel also believed that diabetes required time to manifest itself. The cane cutters had been receiving their refined-sugar ration for only a decade at most. From his medical histories of the diabetic Zulus at his clinic, Campbel found what he cal ed a "remarkably constant period in years of exposure to town life" before rural Zulus who had moved permanently into Durban developed diabetes. "The peak 'incubation period' in 80 such diabetics," he wrote, "lay between 18 and 22 years." Thus, Campbel suggested that diabetes would appear in a population to any extent only after roughly two decades of excessive sugar consumption, just as lung cancer from cigarettes appears on average after two decades of smoking. He also suggested that, if international statistics were any indication, the kind of diabetes epidemic they were experiencing among Natal Indians-or, for that matter, most Westernized nations-required a consumption of sugar greater than seventy pounds per person each year.

Campbel appears to be the first diabetologist to propose seriously an incubation period for diabetes. Joslin's textbooks suggest he believed that if sugar consumption caused diabetes the damage could be done quickly-in a single night of "acute excess." In arguing against the sugar theory of diabetes, Joslin said that no one to his knowledge had ever developed the disease after drinking the sugar solution used in a type of diabetes test known as a glucose-tolerance test.*32 By the same logic, you could imagine that smoking a pack of cigarettes in an evening might cause lung cancer within the next few weeks in the rare unfortunate first-time smoker. That it has not been known to happen does not imply that tobacco is not a potent carcinogen.

In the early 1960s, Campbel began corresponding with a retired physician of the British Royal Navy, Surgeon Captain Thomas Latimore "Peter" Cleave.

In 1966, they published Diabetes, Coronary Thrombosis and the Saccharine Disease, a book in which they argued that al the common chronic diseases of Western societies-including heart disease, obesity, diabetes, peptic ulcers, and appendicitis-const.i.tuted the manifestations of a single, primary disorder that could be cal ed "refined-carbohydrate disease." Because sugar was the primary carbohydrate involved, and the starch in white flour and rice is converted into blood sugar in the body, they opted for the name saccharine disease ("saccharine," in this instance, meant "related to sugar"

and rhymes with "wine," in their usage, not "win," as the artificial sweetener does).

After the book was published, Campbel returned to working exclusively on diabetes. Cleave tried to convince the medical establishment of the strength of evidence linking chronic diseases to the refining of carbohydrates, with little success. One biostatistician who insisted the idea should be taken seriously was Sir Richard Dol , director of the Statistical Research Unit of Britain's Medical Research Council, who wrote the introduction to Diabetes, Coronary Thrombosis and the Saccharine Disease. In the early 1950s, Dol had published the seminal studies linking cigarettes to lung cancer. Dol later said of Cleave's research, "His ideas deserved a lot more attention than they got."

The primary obstacle to the acceptance of Cleave's work was that he was an outsider, with no recognizable pedigree. He had spent his entire career with the British Royal Navy, retiring in 1962, after spending the last decade directing medical research at the Inst.i.tute of Naval Medicine. Much of Cleave's early career was spent in British naval hospitals in Singapore, Malta, and elsewhere, which gave him firsthand experience of how chronic-disease incidence could differ between nations.

Cleave's nutritional education was furthered by the experience of his brother, Surgeon Captain H. L. Cleave, who spent the war years imprisoned by the j.a.panese in Hong Kong and then Tokyo. In the Hong Kong prison, peptic ulcers were a plague. The diets in these camps were predominantly white rice.

Until vitamin-B supplements were distributed, beriberi was also a problem. After two years, many of the prisoners, including Cleave's brother, were transferred to a camp outside Tokyo, where the ulcers vanished. In the Tokyo POW camps, the rice was brown, lightly mil ed, with unmil ed barley and mil et added.

In the decades after the war, Cleave became an obsessive letter-writer, corresponding with hundreds of physicians around the world, requesting information on disease rates and the occurrence and appearance of specific diseases. His 1962 book on peptic ulcers contained page after page of testimony from physicians reporting the relative absence of ulcers in those populations where sugar, white flour, and white rice were hard to come by.

Cleave's intuition was to reduce the problem of nutrition and chronic disease to its most elementary form. If the primary change in traditional diets with Westernization was the addition of sugar, flour, and white rice, and this in turn occurred shortly before the appearance of chronic disease, then the most likely explanation was that those processed, refined carbohydrates were the cause of the disease. Maybe if these carbohydrates were added to any diet, no matter how replete with the essential protein, vitamins, minerals, and fatty acids, it would lead to chronic diseases of civilization. This would explain why the same diseases appeared after Westernization in cultures that lived almost exclusively on animal products-the Inuit, the Masai, and Samburu nomads, Australian Aborigines, or Native Americans of the Great Plains-as wel as in primarily agrarian cultures like the Hunza in the Himalayas or the Kikuyu in Kenya.

Cleave would later be disparaged for suggesting that al chronic diseases of civilization have a single primary cause, but he insisted that it was naive to think otherwise. Though it may seem odd, he considered dental cavities the chronic-disease equivalent of the canary in the mine. If cavities are caused primarily by eating sugar and white flour, and cavities appear first in a population no longer eating its traditional diet, fol owed by obesity, diabetes, and heart disease, then the a.s.sumption, until proved otherwise, should be that the other diseases were also caused by these carbohydrates.

Diabetes, obesity, coronary heart disease, gal stones and gal -bladder disease, and cavities and periodontal disease are intimately linked. As early as 1929, physicians were reporting that a fourth of their coronary-heart-disease patients also had diabetes. Diabetics, as Joslin noted, were especial y p.r.o.ne to atherosclerosis, which became increasingly clear after the discovery of insulin. Studies in the late 1940s revealed that diabetic men were twice as likely to die of heart disease as nondiabetics; diabetic women were three times more likely. Moreover, diabetics had an exceptional y high rate of gal stones; and the obese had an exceptional y high rate of gal -bladder disease. As Joslin's textbook also observed, "The destruction of teeth and the supporting structures is very active just prior to the onset of diabetes," connecting cavities to the disease.

Cleave's desire for simplicity led him to theorize that any cl.u.s.ter of diseases so intimately a.s.sociated must have a single underlying cause. Darwin's theory of evolution led Cleave to believe that endemic chronic disease must be caused by a relatively rapid change in our environment to which we had not yet adapted. He cal ed this idea "The Law of Adaptation": species require "an adequate period of time for adaptation to take place to any unnatural (i.e., new) feature in the environment," he wrote, "so that any danger in the feature should be a.s.sessed by how long it has been there." The refining of carbohydrates represented the most dramatic change in human nutrition since the introduction of agriculture. "Whereas cooking has been going on in the human race for probably 200,000 years," Cleave said, "there is no question yet of our being adapted to the concentration of carbohydrates.... Such processes have been in existence little more than a century for the ordinary man and from an evolutionary point of view this counts as nothing at al ."

Cleave believed the concentration of carbohydrates in the refining process did its damage in three ways.

First, it led to overconsumption, because of what he cal ed the deception of the appet.i.te-control apparatus by the density of the carbohydrates. He contrasted the "eating of a smal quant.i.ty of sugar, say roughly a teaspoonful," with the same quant.i.ty in its original form-a single apple, for instance. "A person can take down teaspoonfuls of sugar fast enough, whether in tea or any other vehicle, but he wil soon slow up on the equivalent number of apples.... The argument can be extended to contrasting the 5 oz. of sugar consumed, on the average, per head per day in [the United Kingdom] with up to a score of average-sized apples.... Who would consume that quant.i.ty daily of the natural food? Or if he did, what else would he be eating?"

Second, this would be exacerbated by the removal of protein from the original product. Cleave believed (incorrectly) that peptic ulcers were caused by the lack of protein necessary to buffer the gastric acid in the stomach.

Final y, the refining process increased the rate of digestion of carbohydrates, and so the onrush of blood sugar on the pancreas, which would explain diabetes. "a.s.sume that what strains the pancreas is what strains any other piece of apparatus," wrote Cleave and Campbel , "not so much the total amount of work it is cal ed upon to do, but the rate at which it is cal ed upon to do it. In the case of eating potatoes, for example, the conversion of the starch into sugar, and the absorption of this sugar into the blood-stream, is a slower and gentler process than the violent one that fol ows the eating of [any] ma.s.s of concentrated sugar."

The link between refined carbohydrates and disease had been obscured over the years, Cleave and Campbel explained, by the "insufficient appreciation of the distinction" between carbohydrate foods in their natural state and the unnatural refined carbohydrates-treating sugar and white flour as equivalent to raw fruit, vegetables, and wholemeal flour. When researchers looked at trends between diet and disease, as Himsworth and Joslin had done with diabetes and Keys and a later generation of researchers would do with heart disease and even cancer, they would measure only fat, protein, and total carbohydrate consumption and fail to account for any potential effect of refined carbohydrates. Occasional y, they might include sugar consumption in their a.n.a.lyses, but they would rarely make a distinction between wholemeal bread and white flour, between brown rice and white. In most cases, cereal grains, tubers, vegetables, and fruits, and white sugar, flour, rice, and beer, were al included under the single category of carbohydrate.

"While the consumption of al carbohydrates may not be moving appreciably with the rise or fal in the incidence of a condition," Cleave and Campbel explained, "the consumption of the refined carbohydrates may be moving decisively."

Cleave first made this point in 1956, when he published his hypothesis in an article that also contested Joslin's belief that the increased incidence of diabetes in the twentieth century was unrelated to sugar consumption. Had Joslin or Himsworth charted sugar consumption separately from that of al carbohydrates, Cleave wrote, "what was the opposite of a relationship between diabetes mortality and carbohydrate consumption would become a very close relationship."*33 (See chart on fol owing page.) Cleave had identified one of the fundamental flaws of modern nutrition and chronic-disease epidemiology. Greater affluence inevitably takes populations through a nutrition transition that represents a congruence of fundamental changes in diet. Meat consumption tends to increase, and so saturated fat increases as wel . Grain consumption decreases, and so carbohydrate consumption as a whole decreases. But the carbohydrates consumed are more highly refined: white rice replaces brown, white flour replaces wholemeal; sugared beverages and candy spark a dramatic increase in sugar consumption. As a result, whenever investigators tested the hypothesis that chronic disease was caused by high fat intake or even high animal-fat intake or low carbohydrate intake, the refinement of the carbohydrates would confound the results. The changing-American-diet story led Ancel Keys and others to insist that fat caused heart disease and to advise eating low-fat, high-carbohydrate diets because, as the diagnosis of coronary heart disease increased over the century, carbohydrate consumption apparently decreased, while the total fat available for each American increased from 100 pounds per person per year to almost 130 pounds.*34 But the greatest single change in the American diet was in fact the spectacular increase in sugar consumption from the mid-nineteenth century onward, from less than 15 pounds a person yearly in the 1830s to 100 pounds by the 1920s and 150 pounds (including high-fructose corn syrup) by the end of the century. In effect, Americans replaced a good portion of the whole grains they ate in the nineteenth century with refined carbohydrates.

Peter Cleave's chart showing the relationship between diabetic mortality rate (with the 1938 rate equal to 1) and the amount of sugar consumed per capita in England and Wales. The dotted line is sugar consumption. The solid line is diabetes mortality.

Despite the century of debate in the United Kingdom on the merits of white flour and wholemeal flour and the potential evils of sugar, it wouldn't be until the 1990s that epidemiologists began to delineate between refined and unrefined carbohydrates in their dietary a.n.a.lyses. Even in 1989, when the National Academy of Sciences published its seven-hundred-page Diet and Health report, the authors made little attempt to differentiate refined carbohydrates from unrefined, other than occasional y to note studies in which sugar intake by itself was studied.

When Keys linked the low-fat, high-carbohydrate diet of the j.a.panese in the late 1950s to the extremely low incidence of heart disease, he paid no attention to sugar consumption. Fat consumption in j.a.pan was extremely low, as were heart-disease rates, and so he concluded that the lower the fat the better. But the consumption of sugars in j.a.pan was very low, too-less than forty pounds per person per year in 1963, and stil under fifty pounds in 1980 -equivalent to the yearly per-capita consumption recorded in the United States or in the United Kingdom a century earlier.

The remarkable health of the islanders of Crete and Corfu in Keys's Seven Countries Study-and thus the supposedly salubrious effects of the Mediterranean diet itself-could also be explained by the lack of sugar and white flour. Despite the popularity of the Mediterranean diet today, our understanding of what exactly such a diet is-particularly in Crete and Corfu, where Keys's study had doc.u.mented such remarkably low mortality rates -is based on only two dietary surveys: Keys's study itself, which a.n.a.lyzed the Cretan diet in 1960, and a Rockefel er Foundation study in 1947.

According to the Seven Countries Study, the Cretan diet circa 1960 included a total of only sixteen pounds a year of sugar, honey, pastries, and ice cream. According to the Rockefel er study, the Cretan diet included only ten pounds a year of sugar and sweets, and the considerable bread consumed was all wholemeal. The reported benefits of the Mediterranean diet, therefore, could be attributed to the fish, olive oil, and vegetables consumed, as it is today, but they could also be due to the minimal quant.i.ties of sugar and the absence of white flour.

This lack of concern for any potential health-related difference between vegetables and starches, on the one hand, and refined starches and sugars, on the other, has haunted cancer research as wel . Speculation that dietary fat caused breast, colon, and prostate cancer began in the 1970s, with the same international comparisons that led to the heart-disease hypothesis in the 1950s. Cancer epidemiologists simply compared carbohydrate, protein, and fat contents of diets in different countries with the mortality from various cancers. And these investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between j.a.pan and the United States. They did not serve science wel by ignoring sugar consumption and the difference between refined and unrefined carbohydrates.

These preliminary studies then prompted hundreds of mil ions of dol ars of studies that failed to confirm the initial hypot