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“Someday We’ll Have to Get Smarter”
WHEN I RETURNED IN 1968 from duty as an Army surgeon in Vietnam, I was offered a position in the Department of General Surgery at the Cleveland Clinic in Cleveland, Ohio. My major specialties were thyroid, parathyroid, gastrointestinal, and breast surgery, but I was always interested in vascular medicine, and made a point of taking extra training in the subject.
Medicine ran in the family. My father, Caldwell B. Esselstyn, was a distinguished physician, a great innovator in group practice in upstate New York. It was his idea to bring to a rural county all the best in medicine—from dentistry and psychiatry to obstetrics-gynecology and pediatrics—using a rotating roster of specialists. My father-in-law, the late Dr. George Crile, Jr., had been a breast cancer pioneer at the Cleveland Clinic, which had been founded by his father. When he started practicing medicine, radical mastectomies were still the order of the day; it was his vision that the surgery did not always have to be so extensive, and he devoted much of his professional life to developing less radical operations.
But something besides medicine also ran in the family. Both my father and my father-in-law were living examples of the toxic American diet. Between them, they had diabetes; strokes; prostate, colon, and lung cancer; and coronary artery disease. About three years before my father died of heart disease in 1975, he said something that has stayed with me ever since: “Someday, we’re just going to have to get smarter about showing people how to live healthier lives.”
Everything in my professional experience underscored the importance of that declaration. Despite my father-in-law’s pioneering work, for example, by the time I arrived at the Cleveland Clinic, many women were still losing breasts or being disfigured by surgery for breast cancer. And although I enjoyed my work as a surgeon—I take great pride in surgery that is well performed, that achieves a positive result, and relieves suffering—I was increasingly disillusioned by what I was not doing: never curing the underlying disease, never doing anything to help prevent it in the next victim. I was distressed by the general lack of interest among physicians in preventing cancer and heart disease, rather than intervening mechanically once they had struck.
I began reading a great deal of medical literature, with a particular emphasis on epidemiology. There was a beautiful simplicity to the evidence. You looked at a map of the world, and almost all the chronic ailments like coronary disease were crowded into the western countries. Then there were all these other countries, especially in Asia and Africa, where those diseases hardly showed up at all.
For example, women in the United States were twenty times more likely than women in Kenya to develop breast cancer.1 And in the early 1950s, breast cancer was almost unknown in Japan (later, the rates began to rise as the Japanese adopted lifestyles—and eating habits—more like those of affluent Westerners). A close look at the cultures with low rates of breast cancer showed an obvious common denominator: a low intake of dietary fat and correspondingly low cholesterol levels. The same was true for cancers of the colon, prostate, and ovary, and for diabetes and obesity.2
The more I read, the more convinced I became that the connection between nutrition and disease was critical. The correlation seemed most vivid in coronary artery disease, the leading killer of men and women in the United States. It has become clearer in the past decade or so, but even twenty years ago, the general reading was that the connection between cholesterol and heart disease was paramount. The epidemiological evidence seemed incontrovertible. In those parts of the world where coronary artery disease is rare, diets are low in fat and serum cholesterol levels are consistently below 150 mg/dL. In the United States, where vascular disease is the leading killer, the average citizen eats sixty-five pounds of fat per year—consuming two tons of suet by the age of sixty—and average cholesterol levels hover around 200 mg/dL.3
Autopsies of soldiers during the Korean and Vietnam wars showed the effects of America’s artery-clogging diet even on the very young. The arteries of Asian soldiers were largely clean, free of fatty deposits. But almost 80 percent of American battlefield casualties showed gross evidence of coronary artery disease—clogging and damage that, had the soldiers lived, would have grown worse with every passing decade.4 What’s more, in recent years, researchers have observed that as residents of areas with a low incidence of cardiovascular disease begin to adopt a more Western style of life and diet, the incidence of disease—especially coronary disease—rises dramatically.
It may be years before we understand each step and every nuance of the process by which dietary fat and cholesterol destroy coronary arteries. But we are well aware of the general outlines. Simply stated, just as you need stone to build a stone wall, you need a specific level of fat and cholesterol in your bloodstream to narrow and clog your arteries with atherosclerosis.
When the cholesterol carried in the bloodstream reaches unsafe levels—levels I will discuss in Chapter 4—fat and cholesterol are deposited on the linings of the blood vessels. These deposits are called plaques. Old plaques may contain scar tissue and calcium and can steadily enlarge, severely narrowing and sometimes blocking the arteries. A significantly narrowed artery cannot supply the heart muscle with adequate blood. Heart muscle deprived of normal blood supply causes chest pain, or angina (see Figure 2 in insert).
Most people think that it is the vessel’s finally closing off, completely blocked by a large old plaque, that causes a heart attack, or myocardial infarction. Wrong. That process actually accounts for only about 12 percent of deaths from heart attacks. The most recent scientific evidence shows that most heart attacks are caused by younger fatty plaques—plaques too small to cause the overt symptoms that ordinarily bring on mechanical interventions like angioplasty.
Here’s what happens: the lining that covers such plaques ruptures, and the fatty deposits inside leach out into the bloodstream. The body responds by rushing its clotting forces to repair the injury. When the clotting process succeeds, the entire artery may clot and close, thus completely depriving an area of heart muscle of its blood supply, causing it to die (see Figure 3).
If a person survives such an attack, the dead portion of heart muscle scars. Multiple heart attacks and widespread scarring weaken the heart, sometimes causing it to fail, a condition called congestive heart failure. If a heart attack is extensive, if it disrupts rhythmical contraction, or if congestive heart failure is prolonged, the victim may die.
My research shows that this entire process is preventable—and that through nutrition (plus, in some cases, low doses of cholesterol-lowering drugs) the risk of heart attack and heart failure can be eliminated. Scientists and physicians have been slow to recognize the connection between nutrition and coronary disease. In part, that’s because the development of the disease is not like, say, a bee sting, in which the relationship between cause and effect is quite obvious. It may require decades of self-injury from a high-fat diet before clinical symptoms develop.
But truth to tell, when scientists peer too deeply into the most minute details of a problem, they sometimes miss the obvious solution. Sometimes, intuition and logic point strongly to an answer that has not yet been proven through the scientific method. There are some classic examples in medical history. In the mid-nineteenth century, for instance, an English physician named John Snow removed the handle from the Broad Street pump in London because he was convinced that somehow the shared water was causing a devastating cholera epidemic. He was right. It was many decades later that science identified the waterborne organism that causes cholera, but Dr. Snow intuited what the problem was, and he saved the town.
Similarly, we do not know even today precisely how insulin does its job of escorting blood sugar into the body’s cells to be converted to energy. Nevertheless, doctors have been using insulin to save the lives of diabetics for more than eighty years. We know the connection is crucial even though we do not understand exactly how.
 
 
By the late 1970s, I was certain that there was a strong connection between nutrition and many diseases. The connection with heart disease seemed most obvious. First, there was the compelling fact that in nations where blood levels of cholesterol were customarily below 150 mg/dL, coronary artery disease was rare, while in places where the levels were higher, so was the incidence of heart disease. In addition, the earliest scientific studies—which have been consistently confirmed by the most recent research—showed that a diet high in fat and cholesterol causes coronary artery disease in animals and humans.
My own logic and intuition strongly suggested that the converse might also be true: reducing fat in the diet might make coronary artery disease cease to progress—and even partially reverse. In fact, this had been demonstrated in monkeys. They had acquired the disease after being fed a diet deliberately loaded with fat; when the dietary fat was reduced, their disease had reversed.5 There was no doubt in my mind that further research into the nutrition-disease connection was well worth the effort.
Our local dietitians were skeptical about my theory, and several senior cardiologists at the Cleveland Clinic did not believe there was a connection between diet and coronary disease. Nonetheless, I pursued my studies.
Then, in April 1984, I had a personal epiphany—and in effect became the first subject of my own experiment. I was with my wife, Ann, at a meeting of the Eastern Surgical Society in New Haven, Connecticut. It was pouring rain. I was wet and uncomfortable—thoroughly disgusted with the day. And then a waitress served me a plate containing a huge, bloody slice of roast beef. Suddenly, I was repelled by the meat along with everything else. At that moment, I gave it all up—decided never to consume meat again.
Ann ate every bite of that meal in New Haven. But it was not long before she, too, adopted a plant-based diet. Her mother had died of breast cancer at the age of fifty-two. And one day, at an aunt’s house, just as lunch was about to begin at the aunt’s eighty-fifth birthday party, Ann’s sister called. She, too, had been diagnosed with breast cancer, at the age of forty-eight. Ann sat down and didn’t eat a bit of that lunch. And she joined me in my dietary experiment.
Between April and June 1984, my cholesterol level fell from 185 mg/dL to 155. This still was not acceptable. Next, I omitted from my diet every possible source of oil and dairy fat (milk, butter, ice cream, cheese). Before long, my blood cholesterol was 119 mg/dL—without the use of any cholesterol-lowering medication. This was especially reassuring, since my late father, who had his first heart attack at age forty-three, had a total cholesterol as high as 300 mg/dL.
I was convinced that I could help others achieve similar results, and that the effects on their health would be nothing short of dramatic.