Good Calories, Bad Calories (25 page)

When the testimony focused on sugar and diabetes, the committee members found it compel ing. They occasional y solicited suggestions as to how Americans might reduce the 120-odd pounds of sugar they were eating on average in 1973, to the less than seventy pounds that Campbel said could be safely consumed without triggering an epidemic of diabetes and obesity.

With the subject of heart disease, however, controversy arrived. Cohen testified that there was no “direct relationship” linking heart disease to dietary fats, and that he had been able to induce the same blood-vessel complications seen in heart disease merely by feeding sugar to his laboratory rats. Peter Cleave testified to his belief that the problem extended to al refined carbohydrates. “I don’t hold the cholesterol view for a moment,” Cleave said, noting that mankind had been eating saturated fats for hundreds of thousands of years. “For a modern disease to be related to an old-fashioned food is one of the most ludicrous things I have ever heard in my life,” said Cleave. “If anybody tel s me that eating fat was the cause of coronary disease, I should look at them in amazement. But, when it comes to the dreadful sweet things that are served up…that is a very different proposition.” Yudkin blamed heart disease exclusively on sugar, and he was equal y adamant that neither saturated fat nor cholesterol played a role. He explained how carbohydrates and specifical y sugar in the diet could induce both diabetes and heart disease, through their effect on insulin secretion and the blood fats known as triglycerides. McGovern now struggled with the difficulty of getting some consensus on these matters.

“Are you saying that you don’t think a high fat intake produces the high cholesterol count?” McGovern asked Yudkin. “Or are you even saying that a person with high cholesterol count is not in great danger?”

“Wel , I would like to exclude those rare people who have probably a genetic condition in which there is an extremely high cholesterol,” Yudkin responded. “If we are talking about the general population, I believe both those things that you say. I believe that decreasing the fat in the diet is not the best way of combating a high blood cholesterol…. I believe that the high blood cholesterol in itself has nothing whatever to do with heart disease.”

“That is exactly opposite what my doctor told me,” said McGovern.

“If men define situations as real,” the sociologist Wil iam Isaac Thomas observed in the 1920s, “they are real in their consequences.” Embracing a hypothesis based on incomplete evidence or ideological beliefs is risk enough. But this also makes it extremely difficult to entertain alternative possibilities, unless we can reconcile them with what we have now convinced ourselves is indisputable.

By the early 1970s, al potential causes of heart disease, or potential y any chronic disease, had to be capable of coexisting with the belief that dietary fat was the primary cause of coronary heart disease. The notion that refined or easily digestible carbohydrates caused chronic disease could not be so reconciled.

The evidence that led Peter Cleave to propose this alternative theory—the disparity in disease rates among populations, the intimate relationship of atherosclerosis, hypertension, obesity, and diabetes, and the apparent absence of chronic disease in populations relatively free of Western influences

—had to be explained in other ways if they were to be consistent with Keys’s hypothesis. Fiber, the indigestible carbohydrates in vegetables, starches, and grains, now replaced refined carbohydrates and sugar in the debate about the nutritional causes of chronic diseases. The fiber hypothesis captured the public’s nutritional consciousness by virtue of the messianic efforts of a single investigator, a former missionary surgeon named Denis Burkitt, who proposed that this indigestible roughage was a requisite component of a healthy diet. The notion was consistent with Keys’s hypothesis, which was not the case with Cleave’s or Yudkin’s hypothesis, and it resonated also with the era’s countercultural leanings toward diets heavy in vegetables, legumes, and cereal grains.

Burkitt’s fiber hypothesis was based original y and in its entirety on Cleave’s saccharine-disease hypothesis, but simply inverted the causal agent.

Rather than proclaim, as Cleave did, that chronic disease was caused by the addition of sugar and refined carbohydrates to diets that we had evolved natural y to eat, Burkitt laid the blame on the subtraction of the fiber from those evolutionarily ideal diets, which in turn led to constipation and then, through a variety of mechanisms, al the chronic diseases of civilization. The fiber deficiency itself was caused either by the removal of fiber during the refining of carbohydrates or by the consumption of refined carbohydrates in lieu of the fibrous, bulky roughage we should be eating. The fiber hypothesis and the refined-carbohydrate hypothesis of chronic disease were photographic negatives of each other, and yet the fiber hypothesis caught on immediately upon appearing in the journals. The refined-carbohydrate hypothesis, which was the only one of the two that was capable of explaining the actual evidence, remained a fringe concept.

Denis Burkitt began his career as a missionary surgeon in Uganda in 1947. In the early 1960s, he earned his renown—“one of the world’s best-known medical detectives,” as the Washington Post would cal him—for his studies of a fatal childhood cancer that came to be known as Burkitt’s lymphoma and would be the first human cancer ever linked to a viral cause. That discovery alerted Burkitt to the lessons to be learned by tracking the geographical distribution of disease. Burkitt spent five years gathering information about the lymphoma from hundreds of African hospitals, and made a legendary ten-thousand-mile, sixty-hospital trek from Kampala to Johannesburg and back as part of his research.

In 1966, Burkitt returned to England, where he worked as a cancer epidemiologist for the Medical Research Council. There Richard Dol told him about Cleave and his saccharine-disease hypothesis. Burkitt met with Cleave and read Diabetes, Coronary Thrombosis and the Saccharine Disease, which he found revelatory. Cleave possessed “perceptive genius, persuasive argument and irrefutable logic,” Burkitt wrote.

What he was saying was that many of the common diseases in post-industrialized western countries are rare throughout the third world, were rare even in England or New York until about the First World War, are equal y common in black and white Americans, and therefore must be due not to our skin color or our genes, but to the way we live. Now, this made an enormous amount of sense to me because I knew from my experience in Africa that he was perfectly right saying this.

On a tour of the United States, Burkitt visited hospitals and observed, as George Campbel had a decade earlier, that African-American patients in these hospitals were often obese, diabetic, or atherosclerotic, conditions virtual y nonexistent among the black Ugandans Burkitt had treated.

Burkitt considered himself in the ideal position to test Cleave’s hypothesis on a wider scale. He had already established a network of 150 African hospitals, mostly missionary hospitals in rural areas, that mailed him monthly reports on their cancer cases: “I was able to ask them al : ‘Do you see gal stones, appendicitis, diverticular disease, coronary heart disease….’” Burkitt also sent his questionnaire to mission hospitals through out the world, and over eight hundred faithful y returned them. The results confirmed the basics of Cleave’s hypothesis. Whereas Cleave had anecdotal evidence, Burkitt recal ed, he now had “anecdotal multiplied by a thousand,” and it was al consistent. Moreover, he had the necessary reputation to be taken seriously, whereas Cleave did not. Cleave, Campbel , and others had been “written off as cranks,” Burkitt said. “Now, just because there happened to be a Burkitt’s lymphoma, when Burkitt said, ‘What about looking at this,’ people listened to me when they hadn’t listened to far better guys.”

Through the early 1970s, Burkitt published a series of articles expanding on Cleave’s hypothesis. “These ‘western’ diseases are certainly associated geographical y and in many instances tend to be related to one another in individual patients,” Burkitt wrote in the Journal of the National Cancer Institute in 1971. “My epidemiological studies in Africa and elsewhere substantiate Cleave’s basic hypothesis. Changes made in carbohydrate food may of course be only one of many etiological factors, but in some instances they would appear to be the major one.”

But Burkitt was beginning to revise Cleave’s hypothesis. Now Burkitt’s working assumption, as he explained in the JNCI, was that any dietary factors responsible for benign conditions such as appendicitis or diverticulitis were likely to be responsible as wel for related malignant conditions—in particular, colon and rectal cancer. Burkitt’s research had led him to Thomas Al inson, who in the 1880s argued that white flour caused constipation, hemorrhoids, and other il s of modern societies. It also led him to a 1920 article by the Bristol University surgeon Arthur Rendle Short, documenting a dramatic increase in the incidence of appendicitis that Rendle Short also blamed on white flour and the lack of fiber in modern diets. Burkitt believed he could draw a direct line of causation from the absence of fiber in refined carbohydrates to constipation, hemorrhoids, appendicitis, diverticulitis, polyps, and final y malignant colon and rectal cancer.

Burkitt’s African correspondents had reported that appendicitis increased dramatical y in urban populations—at Burkitt’s Mulago Hospital in Kampala, the number of yearly appendectomies had increased twenty-fold from 1952 to 1969—whereas polyps, diverticular disease, and colorectal cancer, al common in the United States and Europe, wrote Burkitt, were stil “very rare in Africa and almost unknown in rural communities.” Burkitt concluded that appendicitis, just as it appeared in Western nations typical y in children, appeared in Africans, both adults and children, within a few years of the adoption of Western diets.

Burkitt focused now on constipation. He theorized that removing the fiber from cereal grains would slow the “transit time” of the stool through the colon.

Not only would any carcinogens in the stool therefore have more time to inflict damage on the surrounding cel s, but it was conceivable that the overconsumption of refined carbohydrates would increase the bacterial flora of the stool, and that in turn could lead to carcinogens being metabolized by the bacteria out of “normal bowel constituents.” Burkitt could offer no explanation for why this might cause appendicitis, but he was confident that some combination of al these factors played a role.

In the summer of 1969, Burkitt began studying stool characteristics in available subjects. “Finished bowel transit tests on family,” he recorded in his diary on July 4. The fol owing month, he visited Alec Walker, who ran the human biology department at the South African Institute of Medical Research.

Walker had been studying the rising tide of chronic diseases in urban Bantus in South Africa since the late 1940s, and he was the rare investigator who shared with Burkitt an interest in human feces and constipation. Walker had done extensive studies linking the relative lack of constipation among black convicts in the local prison, as wel as the lack of appendicitis in the Bantus at large, to their traditional high-fiber diets. (Walker publicly dismissed the hypothesis that sugar or refined carbohydrates caused heart disease, but he also reported that the Bantus developed chronic disease only after they moved into the city and began consuming “more white bread, sugar, soft drinks and European liquor.”) Walker had also just submitted an article to the British Medical Journal linking the very low mortality rates from colon cancer among the Bantus to their bowel motility, a characteristic, he wrote, that was

“largely lost” among Western societies. Walker’s research gave Burkitt the confidence to devote his efforts to the study of stool characteristics and bowel behavior, hoping to associate in a scientific manner fiber deficiency, constipation, and the presence of chronic diseases.

It was precisely this work that led to the fiber hypothesis and its present place in our nutritional consciousness. In 1972, Burkitt and Walker published an article in The Lancet supporting their theory and discussing their measurements of transit time and stool characteristics in twelve hundred human subjects. In rural areas, unaffected by industrialization, they reported, “diets containing the natural amount of fiber are eaten and result in large, soft stools that traverse the intestine rapidly. By contrast, the refined low-fiber foods of the economical y-developed countries produce smal firm stools which pass through the gut very slowly.” Thus, the relative constipation endemic in the developed world, they suggested, appeared to play a causative role in bowel-related disorders: appendicitis, diverticulitis, and both benign and malignant tumors of the colon and rectum, al of which showed the classic distribution of diseases of civilizations. “Al these diseases are very closely associated epidemiological y,” Burkitt and Walker explained. “These diseases are stil rare in developing countries and in rural Japan, where eating habits have changed but little, but they are al seen increasingly in Japanese who live in Hawaii and California and are increasing in Japan in those who have changed to a Western diet. In no country or region is one of these diseases common and the others rare save that appendicitis, which afflicts the young, appears about a generation before the other conditions.”

Within two years, Burkitt had extended his hypothesis from appendicitis, diverticulitis, and colon cancer to al chronic diseases of civilization. In the process, Cleave’s refined-carbohydrate hypothesis of saccharine diseases was transformed into Burkitt’s fiber hypothesis of Western diseases. This transformation of the causal agent of disease from the presence of carbohydrates to the absence of fiber may have been influenced by factors other than science—Burkitt’s close association with Harold Himsworth in particular. Himsworth had been secretary of the Medical Research Council when Burkitt was hired, and he had been publicly effusive about Burkitt’s contributions to modern medicine. It was Himsworth’s research that had been responsible for convincing diabetologists that sugar and other carbohydrates were not the cause of diabetes. Indeed, Cleave and Campbel had presented their saccharine-disease theory in the context of diabetes as a refutation of Himsworth’s scholarship as much as Joslin’s. That Burkitt would find Cleave’s general thesis compel ing but the details unacceptable in light of Himsworth’s own work and beliefs is quite possible. Burkitt would often tel the story of how Himsworth had convinced him of the importance of paying attention to those factors that were absent in searching for the causative agents of disease. “Denis,” Burkitt recal ed Himsworth tel ing him, “do you remember the story in Sherlock Holmes when Holmes said to Watson: ‘The whole clue, as I see it, to this case lies in the behavior of the dog.’ And Watson said: ‘But, sir, the dog did nothing at al .’ ‘That,’ said Holmes, ‘is the whole point.’ And it often is in medicine…. The clue can lie in what is not there rather than what is there.” In this case, fiber was not there. Burkitt also seemed motivated by the simple expediency of emphasizing the positive benefits of fiber rather than the negative effects of sugar and flour, which seemed like a hopeless cause. “[Sugar] is simply an integral part of the daily diet and emphatical y is here to stay,” Burkitt’s col aborator Alec Walker said. Better to say Don’t Forget Fibre in Your Diet, which was the title of Burkitt’s 1979 diet book, than to say, Don’t eat sugar, flour, and white rice, and drink less beer.