Good Calories, Bad Calories (23 page)

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—constituted 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 Institute 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 Japanese 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 naïve 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 assumption, 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 prone 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 cluster of diseases so intimately associated 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 assessed 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 appetite-control apparatus by the density of the carbohydrates. He contrasted the “eating of a smal quantity of sugar, say roughly a teaspoonful,” with the same quantity 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 quantity 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. “Assume 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] mass 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 analyses, 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 analyses. 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 Japanese in the late 1950s to the extremely low incidence of heart disease, he paid no attention to sugar consumption. Fat consumption in Japan 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 Japan was very low, too—less than forty pounds per person per year in 1963, and stil under fifty pounds in 1980