as well as saturated fat did.
By the early 1970s, Keys’s dietary-fat hypothesis of heart disease, despite the ambiguity of the evidence, was already being taught in textbooks and in medical schools as most likely true. After Yudkin retired in 1971, his hypothesis effectively retired with him. His university replaced him with Stewart Truswell, a South African nutritionist who was among the earliest to insist publicly that Keys’s fat theory of heart disease was assuredly correct and that it was time to move on to modifying the diets of the public at large accordingly. Truswell believed it was more important for the prevention of heart disease to convince the public to eat more onions, for their reported ability to alter the “tendency to thrombosis,” than to eat less sugar.
Yudkin spent his first year of retirement writing a book on his sugar theory, published in 1972 and entitled
FIBER
The thing is, it’s very dangerous to have a fixed idea. A person with a fixed idea will always find some way of convincing himself in the end that he is right.
ATLE SELBERG, winner of the 1950
Fields Medal in Mathematics
THE HYPOTHESIS THAT SUGAR AND refined carbohydrates cause chronic disease peaked as a subject of serious consideration in late April 1973, when George McGovern’s Senate Select Committee on Nutrition and Human Needs held its first hearing on diet and what the committee took to calling killer diseases. The testimony would have little impact on the content of McGovern’s
The committee had initially planned a series of hearings in 1972 on dietary fat, cholesterol, and heart disease, but the plans changed because McGovern ran for president. When the committee returned to the diet-and-chronic- disease issue after McGovern’s defeat, the subject that seemed most urgent—thanks in part to the publication of John Yudkin’s
The hearings were a surprisingly international affair. Aharon Cohen from Jerusalem testified on diabetes and heart disease among the Yemenite Jews. George Campbell testified on his studies of diabetes in Zulus and Natal Indians in South Africa. Peter Bennett, an NIH epidemiologist, testified on the Pima Indians of Arizona, who had the highest incidence of diabetes ever recorded at the time: half of the Pima over thirty-five years old were diabetic. “The only question that I would have,” Bennett said, “is whether we can implicate sugar specifically or whether the important factor is not calories in general, which in fact turns out to be really excessive amounts of carbohydrates.” Walter Mertz, chairman of the USDA Human Nutrition Institute, testified, as did his colleague Carol Berdanier, explaining that refined sugar seemed to play particular havoc with health, at least in laboratory rats. It elevated blood sugar and triglycerides, and caused subjects to become diabetic, Berdanier said, “and they die at a very early age.”
When the testimony focused on sugar and diabetes, the committee members found it compelling. They occasionally 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 Campbell 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 all 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 tells 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 equally adamant that neither saturated fat nor cholesterol played a role. He explained how carbohydrates and specifically 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?”
“Well, 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 William 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, all potential causes of heart disease, or potentially 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