Good Calories, Bad Calories (6 page)

The changing-American-diet argument is invariably used to support the proposition that Americans should eat more grain, less fat, and particularly less saturated fat, from red meat and dairy products. But the same food-disappearance reports used to bolster this low-fat, high-carbohydrate diet also provided trends for vegetables, fruits, dairy products, and the various fats themselves. These numbers tel a different story and might have suggested a different definition entirely of a healthy diet, if they had been taken into account. During the decades of the heart-disease “epidemic,” vegetable consumption increased dramatical y, as consumption of flour and grain products decreased. Americans nearly doubled (according to these USDA data) their consumption of leafy green and yel ow vegetables, tomatoes, and citrus fruit.

This change in the American diet was attributed to nutritionists’ emphasizing the need for vitamins from the fruits and green vegetables that were conspicuously lacking in our diets in the nineteenth century. “The preponderance of meat and farinaceous foods on my grandfather’s table over fresh vegetables and fruits would be most unwelcome to modern palates,” wrote the University of Kansas professor of medicine Logan Clendening in The Balanced Diet in 1936. “I doubt if he ever ate an orange. I know he never ate grapefruit, or broccoli or cantaloup or asparagus. Spinach, carrots, lettuce, tomatoes, celery, endive, mushrooms, lima beans, corn, green beans and peas—were entirely unknown, or rarities…. The staple vegetables were potatoes, cabbage, onions, radishes and the fruits—apples, pears, peaches, plums and grapes and some of the berries—in season.”

From the end of World War I , when the USDA statistics become more reliable, to the late 1960s, while coronary heart-disease mortality rates supposedly soared, per-capita consumption of whole milk dropped steadily, and the use of cream was cut by half. We ate dramatical y less lard(13

pounds per person per year, compared with 7 pounds) and less butter(8.5 pounds versus 4) and more margarine (4.5 pounds versus 9 pounds), vegetable shortening (9.5 pounds versus 17 pounds), and salad and cooking oils (7 pounds versus 18 pounds). As a result, during the worst decades of the heart-disease “epidemic,” vegetable-fat consumption per capitain America doubled (from 28 pounds in the years 1947–49 to 55 pounds in 1976), while the average consumption of al animal fat (including the fat in meat, eggs, and dairy products) dropped from 84 pounds to 71. And so the increase in total fat consumption, to which Ancel Keys and others attributed the “epidemic” of heart disease, paral eled not only increased consumption of vegetables and citrus fruit, but of vegetable fats, which were considered heart-healthy, and a decreased consumption of animal fats.

In the years after World War I , when the newspapers began talking up a heart-disease epidemic, the proposition that cholesterol was responsible—the

“medical vil ain cholesterol,” as it would be cal ed by the Chicago cardiologist Jeremiah Stamler, one of the most outspoken proponents of the diet-heart hypothesis—was considered hypothetical at best. Cholesterol itself is a pearly-white fatty substance that can be found in al body tissues, an essential component of cel membranes and a constituent of a range of physiologic processes, including the metabolism of human sex hormones.

Cholesterol is also a primary component of atherosclerotic plaques, so it was a natural assumption that the disease might begin with the abnormal accumulation of cholesterol. Proponents of the hypothesis then envisioned the human circulatory system as a kind of plumbing system. Stamler referred to the accumulation of cholesterol in lesions on the artery wal s as “biological rust” that can “spread to choke off the flow [of blood], or slow it just like rust inside a water pipe so that only a dribble comes from your faucet.” This imagery is so compel ing that we stil talk and read about artery-clogging fats and cholesterol, as though the fat of a greasy hamburger were transported directly from stomach to artery lining.

The evidence initial y cited in support of the hypothesis came almost exclusively from animal research—particularly in rabbits. In 1913, the Russian pathologist Nikolaj Anitschkow reported that he could induce atherosclerotic-type lesions in rabbits by feeding them olive oil and cholesterol. Rabbits, though, are herbivores and would never consume such high-cholesterol diets natural y. And though the rabbits did develop cholesterol-fil ed lesions in their arteries, they developed them in their tendons and connective tissues, too, suggesting that theirs was a kind of storage disease; they had no way to metabolize the cholesterol they were force-fed. “The condition produced in the animal was referred to, often contemptuously, as the ‘cholesterol disease of rabbits,’” wrote the Harvard clinician Timothy Leary in 1935.

The rabbit research spawned countless experiments in which researchers tried to induce lesions and heart attacks in other animals. Stamler, for instance, took credit for first inducing atherosclerotic-type lesions in chickens, although whether chickens are any better than rabbits as a model of human disease is debatable. Humanlike atherosclerotic lesions could be induced in pigeons, for instance, fed on corn and corn oil, and atherosclerotic lesions were observed occurring natural y in wild sea lions and seals, in pigs, cats, dogs, sheep, cattle, horses, reptiles, and rats, and even in baboons on diets that were almost exclusively vegetarian. None of these studies did much to implicate either animal fat or cholesterol.

What kept the cholesterol hypothesis particularly viable through the prewar years was that any physician could measure cholesterol levels in human subjects. Correctly interpreting the measurements was more difficult. A host of phenomena wil influence cholesterol levels, some of which wil also influence our risk of heart disease: exercise, for instance, lowers total cholesterol. Weight gain appears to raise it; weight loss, to lower it. Cholesterol levels wil fluctuate seasonal y and change with body position. Stress wil raise cholesterol. Male and female hormones wil affect cholesterol levels, as wil diuretics, sedatives, tranquilizers, and alcohol. For these reasons alone, our cholesterol levels can change by 20 to 30 percent over the course of weeks (as Eisenhower’s did in the last summer of his presidency).

Despite myriad attempts, researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream

than those who didn’t. “Some works claim a significant elevation in blood cholesterol level for a majority of patients with atherosclerosis,” the medical physicist John Gofman wrote in Science in 1950, “whereas others debate this finding vigorously. Certainly a tremendous number of people who suffer from the consequences of atherosclerosis show blood cholesterols in the accepted normal range.”

The condition of having very high cholesterol—say, above 300 mg/dl—is known as hypercholesterolemia. If the cholesterol hypothesis is right, then most hypercholesterolemics should get atherosclerosis and die of heart attacks. But that doesn’t seem to be the case. In the genetic disorder familial hypercholesterolemia, cholesterol is over 300 mg/dl for those who inherit one copy of the defective gene, and as high as 1,500 mg/dl for those who inherit two. One out of every two men and one out of every three women with this condition are likely to have a heart attack by age sixty, an observation that is often evoked as a cornerstone of the cholesterol hypothesis. But certain thyroid and kidney disorders wil also cause hypercholesterolemia; autopsy examinations of individuals with these maladies have often revealed severe atherosclerosis, but these individuals rarely die of heart attacks.

Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol. In 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death, and so they autopsied more than a hundred very recently deceased New Yorkers, al of whom had died violently, measuring the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic il ness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.”

This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. And even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.

Ancel Keys deserves the lion’s share of credit for convincing us that cholesterol levels predict heart disease and that dietary fat is a kil er. Keys ran the Laboratory of Physiological Hygiene at the University of Minnesota and considered it his franchise, as he would tel Time magazine, “to find out why people get sick before they got sick.” He became famous during World War I by developing the K ration for combat troops—the “K,” it is said, stood for

“Keys.” He spent the later war years doing the seminal study of human starvation, using conscientious objectors as his subjects. He then documented the experience, along with the world’s accumulated knowledge on starvation, in The Biology of Human Starvation, a fourteen-hundred-page tome that cemented Keys’s reputation. (I’l talk more about Keys’s remarkable starvation study in chapter 15.)

Keys’s abilities as a scientist are arguable—he was more often wrong than right—but his force of wil was indomitable. Henry Blackburn, his longtime col aborator at Minnesota, described him as “frank to the point of bluntness, and critical to the point of sharpness.” David Kritchevsky, who studied cholesterol metabolism at the Wistar Institute in Philadelphia and was a competitor, described Keys as “pretty ruthless” and not a likely winner of any “Mr.

Congeniality” awards. Certainly, Keys was a relentless defender of his own hypotheses; he minced few words when he disagreed with a competitor’s interpretation of the evidence, which was inevitably when the evidence disagreed with his hypothesis.

When Keys launched his crusade against heart disease in the late 1940s, most physicians who believed that heart disease was caused by diet implicated dietary cholesterol as the culprit. We ate too much cholesterol-laden food—meat and eggs, mostly—and that, it was said, elevated our blood cholesterol. Keys was the first to discredit this belief publicly, which had required, in any case, ignoring a certain amount of the evidence. In 1937, two Columbia University biochemists, David Rittenberg and Rudolph Schoenheimer, demonstrated that the cholesterol we eat has very little effect on the amount of cholesterol in our blood. When Keys fed men for months at a time on diets either high or low in cholesterol, it made no difference to their cholesterol levels. As a result, Keys insisted that dietary cholesterol had little relevance to heart disease. In this case, most researchers agreed.

In 1951, Keys had an epiphany while attending a conference in Rome on nutrition and disease, which focused exclusively, as Keys later recal ed, on malnutrition. There he was told by a physiologist from Naples that heart disease was not a problem in his city. Keys found this comment remarkable, so he and his wife, Margaret, a medical technician whose specialty was fast becoming cholesterol measurements, visited Naples to see for themselves. They concluded that the general population was indeed heart-disease-free—but the rich were not. Margaret took blood-cholesterol readings on several hundred workers and found that they had relatively low cholesterol. They asked “a few questions about their diet,” Keys recal ed, and concluded that these workers ate little meat and that this explained the low cholesterol. As for the rich, “I was taken to dine with members of the Rotary Club,” Keys wrote. “The pasta was loaded with meat sauce and everyone added heaps of parmesan cheese. Roast beef was the main course. Dessert was a choice of ice cream or pastry. I persuaded a few of the diners to come for examination, and Margaret found their cholesterol levels were much higher than in the workmen.” Keys found “a similar picture” when he visited Madrid. Rich people had more heart disease than poor people, and rich people ate more fat.

This convinced Keys that the crucial difference between those with heart disease and those without it was the fat in the diet. A few months later, he aired his hypothesis at a nutrition conference in Amsterdam—“fatty diet, raised serum cholesterol, atherosclerosis, myocardial infarction.” Almost no one in the audience, he said, took him seriously. By 1952, Keys was arguing that Americans should reduce their fat consumption by a third, though simultaneously acknowledging that his hypothesis was based more on speculation than on data: “Direct evidence on the effect of the diet on human arteriosclerosis is very little,” he wrote, “and likely to remain so for some time.”