Good Calories, Bad Calories (4 page)

I also search for other evidence in the scientific literature that wasn’t included in these discussions but might have shed light on the validity of the competing hypotheses. And, final y, I fol ow the evidence forward in time from the point at which a consensus was reached to the present, to see whether these competing hypotheses were confirmed or refuted by further research. This process also includes interview with clinical investigators and public-health authorities, those stil active in research and those retired, who might point me to research I might have missed or provide further information and details on experimental methods and interpretation of evidence.

Throughout this process, I necessarily made judgments about the quality of the research and about the researchers themselves. I tried to do so using what I consider the fundamental requirement of good science: a relentless honesty in describing precisely what was done in any particular work, and a similar honesty in interpreting the results without distorting them to reflect preconceived opinions or personal preferences. “If science is to progress,” as the Nobel Prize–winning physicist Richard Feynman wrote forty years ago, “what we need is the ability to experiment, honesty in reporting results—the results must be reported without somebody saying what they would like the results to have been—and final y—an important thing

—the intel igence to interpret the results. An important point about this intel igence is that it should not be sure ahead of time what must be.” This was the standard to which I held al relevant research and researchers. I hope that I, too, wil be judged by the same standard.

Because this book presents an unorthodox hypothesis as worthy of serious consideration, I want to make the reader aware of several additional details. The research for this book included interviews with over 600 clinicians, investigators, and administrators. When necessary, I cite or quote these individuals to add either credibility or a personal recol ection to the point under discussion. The appearance of their names in the text, however, does not imply that they agree with al or even part of the thesis set forth in this book. It implies solely that the attribution is accurate and reflects their beliefs about the relevant point in that context and no other.

Lastly, I often refer to articles and reports, for the sake of simplicity and narrative flow, as though they were authored by a single relevant individual, when that is not the case. A more complete list of authors can be found using the notes and bibliography.

THE FAT-CHOLESTEROL HYPOTHESIS

Men who have excessive faith in their theories or ideas are not only il prepared for making discoveries; they also make very poor observations. Of necessity, they observe with a preconceived idea, and when they devise an experiment, they can see, in its results, only a confirmation of their theory.

In this way they distort observation and often neglect very important facts because they do not further their aim…. But it happens further quite natural y that men who believe too firmly in their theories, do not believe enough in the theories of others. So the dominant idea of these despisers of their fel ows is to find others’ theories faulty and to try to contradict them. The difficulty, for science, is stil the same.

CLAUDE BERNARD, An Introduction to the Study of Experimental Medicine, 1865

THE EISENHOWER PARADOX

In medicine, we are often confronted with poorly observed and indefinite facts which form actual obstacles to science, in that men always bring them up, saying: it is a fact, it must be accepted.

CLAUDE BERNARD, An Introduction to the Study of Experimental Medicine, 1865

PRESIDENT DWIGHT D. EISENHOWER SUFFERED his first heart attack at the age of sixty-four. It took place in Denver, Colorado, where he kept a second home.

It may have started on Friday, September 23, 1955. Eisenhower had spent that morning playing golf and lunched on a hamburger with onions, which gave him what appeared to be indigestion. He was asleep by nine-thirty at night but awoke five hours later with “increasingly severe low substernal nonradiating pain,” as described by Dr. Howard Snyder, his personal physician, who arrived on the scene and injected Eisenhower with two doses of morphine. When it was clear by Saturday afternoon that his condition hadn’t improved, he was taken to the hospital. By midday Sunday, Dr. Paul Dudley White, the world-renowned Harvard cardiologist, had been flown in to consult.

For most Americans, Eisenhower’s heart attack constituted a learning experience on coronary heart disease. At a press conference that Monday morning, Dr. White gave a lucid and authoritative description of the disease itself. Over the next six weeks, twice-daily press conferences were held on the president’s condition. By the time Eisenhower’s health had returned, Americans, particularly middle-aged men, had learned to attend to their cholesterol and the fat in their diets. Eisenhower had learned the same lesson, albeit with counterintuitive results.

Eisenhower was assuredly among the best-chronicled heart-attack survivors in history. We know that he had no family history of heart disease, and no obvious risk factors after he quit smoking in 1949. He exercised regularly; his weight remained close to the 172 pounds considered optimal for his height.

His blood pressure was only occasional y elevated. His cholesterol was below normal: his last measurement before the attack, according to George Mann, who worked with White at Harvard, was 165 mg/dl (mil igrams/deciliter), a level that heart-disease specialists today consider safe.

After his heart attack, Eisenhower dieted religiously and had his cholesterol measured ten times a year. He ate little fat and less cholesterol; his meals were cooked in either soybean oil or a newly developed polyunsaturated margarine, which appeared on the market in 1958 as a nutritional pal iative for high cholesterol.

The more Eisenhower dieted, however, the greater his frustration (meticulously documented by Dr. Snyder). In November 1958, when the president’s weight had floated upward to 176, he renounced his breakfast of oatmeal and skimmed milk and switched to melba toast and fruit. When his weight remained high, he renounced breakfast altogether. Snyder was mystified how a man could eat so little, exercise regularly, and not lose weight. In March 1959, Eisenhower read about a group of middle-aged New Yorkers attempting to lower their cholesterol by renouncing butter, margarine, lard, and cream and replacing them with corn oil. Eisenhower did the same. His cholesterol continued to rise. Eisenhower managed to stabilize his weight, but not happily.

“He eats nothing for breakfast, nothing for lunch, and therefore is irritable during the noon hour,” Snyder wrote in February 1960.

By April 1960, Snyder was lying to Eisenhower about his cholesterol. “He was fussing like the devil about cholesterol,” Snyder wrote. “I told him it was 217 on yesterday’s [test] (actual y it was 223). He has eaten only one egg in the last four weeks; only one piece of cheese. For breakfast he has skim milk, fruit and Sanka. Lunch is practical y without cholesterol, unless it would be a piece of cold meat occasional y.” Eisenhower’s last cholesterol test as president came January 19, 1961, his final day in office. “I told him that the cholesterol was 209,” Snyder noted, “when it actual y was 259,” a level that physicians would come to consider dangerously high.

Eisenhower’s cholesterol hit 259 just six days after University of Minnesota physiologist Ancel Keys made the cover of Time magazine, championing precisely the kind of supposedly heart-healthy diet on which Eisenhower had been losing his battle with cholesterol for five years. It was two weeks later that the American Heart Association—prompted by Keys’s force of wil —published its first official endorsement of low-fat, low-cholesterol diets as a means to prevent heart disease. Only on such a diet, Keys insisted, could we lower our cholesterol and our weight and forestal a premature death.

“People should know the facts,” Keys told Time. “Then if they want to eat themselves to death, let them.”

Scientists justifiably dislike anecdotal evidence—the experience of a single individual like Eisenhower. Nonetheless, such cases can raise interesting issues. Eisenhower died of heart disease in 1969, age seventy-eight. By then, he’d had another half-dozen heart attacks or, technical y speaking, myocardial infarctions. Whether his diet extended his life wil never be known. It certainly didn’t lower his cholesterol, and so Eisenhower’s experience raises important questions.

Establishing the dangers of cholesterol in our blood and the benefits of low-fat diets has always been portrayed as a struggle between science and corporate interests. And although it’s true that corporate interests have been potent forces in the public debates over the definition of a healthy diet, the essence of the diet-heart controversy has always been scientific. It took the AHA ten years to give public support to Keys’s hypothesis that heart disease was caused by dietary fat, and closer to thirty years for the rest of the world to fol ow. There was a time lag because the evidence in support of the hypothesis was ambiguous, and the researchers in the field adamantly disagreed about how to interpret it.

From the inception of the diet-heart hypothesis in the early 1950s, those who argued that dietary fat caused heart disease accumulated the evidential equivalent of a mythology to support their belief. These myths are stil passed on faithful y to the present day. Two in particular provided the foundation on which the national policy of low-fat diets was constructed. One was Paul Dudley White’s declaration that a “great epidemic” of heart disease had ravaged the country since World War I . The other could be cal ed the story of the changing American diet. Together they told of how a nation turned away from cereals and grains to fat and red meat and paid the price in heart disease. The facts did not support these claims, but the myths served a purpose, and so they remained unquestioned.

The heart-disease epidemic vanishes upon closer inspection. It’s based on the proposition that coronary heart disease was uncommon until it emerged in the 1920s and grew to become the nation’s number-one kil er. The epidemic was a “drastic development—paral eled only by the arrival of bubonic plague in fourteenth-century Europe, syphilis from the New World at the end of the fifteenth century and pulmonary tuberculosis at the beginning of the nineteenth century,” the Harvard nutritionist Jean Mayer noted in 1975. When deaths from coronary heart disease appeared to decline after peaking in the late 1960s, authorities said it was due, at least in part, to the preventive benefits of eating less fat and lowering cholesterol.

The disease itself is a condition in which the arteries that supply blood and oxygen to the heart—known as coronary arteries because they descend on the heart like a crown—are no longer able to do so. If they’re blocked entirely, the result is a heart attack. Partial blocks wil starve the heart of oxygen, a condition known as ischemia. In atherosclerosis, the coronary arteries are lined by plaques or lesions, known as atheromas, the root of which comes from a Greek word meaning “porridge”—what they vaguely look like. A heart attack is caused most often by a blood clot—a thrombosis—typical y where the arteries are already narrowed by atherosclerosis.

The belief that coronary heart disease was rare before the 1920s is based on the accounts of physicians like Wil iam Osler, who wrote in 1910 that he spent a decade at Montreal General Hospital without seeing a single case. In his 1971 memoirs, Paul Dudley White remarked that, of the first hundred papers he published, only two were on coronary heart disease. “If it had been common I would certainly have been aware of it, and would have published more than two papers on the subject.” But even White original y considered the disease “part and parcel of the process of growing old,” which is what he wrote in his 1929 textbook Heart Disease, while noting that “it also cripples and kil s often in the prime of life and sometimes even in youth.” So the salient question is whether the increasing awareness of the disease beginning in the 1920s coincided with the budding of an epidemic or simply better technology for diagnosis.

In 1912, the Chicago physician James Herrick published a seminal paper on the diagnosis of coronary heart disease—fol owing up on the work of two Russian clinicians in Kiev—but only after Herrick used the newly invented electrocardiogram in 1918 to augment the diagnosis was his work taken seriously. This helped launch cardiology as a medical specialty, and it blossomed in the 1920s. White and other practitioners may have mistaken the new understanding of coronary heart disease for the emergence of the disease itself. “Medical diagnosis depends, in large measure, on fashion,” observed the New York heart specialist R. L. Levy in 1932. Between 1920 and 1930, Levy reported, physicians at New York’s Presbyterian Hospital increased their diagnosis of coronary disease by 400 percent, whereas the hospital’s pathology records indicated that the disease incidence remained constant during that period. “It was after the publication of the papers of Herrick,” Levy observed, that “clinicians became more alert in recognizing the disturbances in the coronary circulation and recorded them more frequently.”