Scientists aren’t sure how it works but many are convinced the fat in your blood is the real villain behind most heart attacks. Its name is cholesterol and it comes in the best foods you eatALAN PHILLIPS December 10 1955
Scientists aren’t sure how it works but many are convinced the fat in your blood is the real villain behind most heart attacks. Its name is cholesterol and it comes in the best foods you eatALAN PHILLIPS December 10 1955
ON THE morning of September 23, the president of the United States ate a hearty breakfast of sausage, bacon and eggs, spent a couple of hours at his desk, then played eighteen holes of golf. The president, vacationing in Colorado, was feeling fit and relaxed. He ate a heavy lunch then went back on the course. On the eighth hole he complained of a pain in his chest which he put down to indigestion. Next day the world learned the stunning truth: the president’s supposed “indigestion” was due to coronary thrombosis.
As stock-market shares dropped fourteen billion dollars in their total paper value and statesmen mourned what many took to be a lessened chance for peace, middle-aged men rushed to doctors’ offices in numbers that a heart specialist in New York termed “fantastic.” Lying in a hospital bed, Dwight D. Eisenhower drew the whole world’s attention to a health problem that badly needed it.
Heart disease is now the No. 1 killer in Canada, the United States, Britain, northern Europe, Australia and New Zealand. “Increasingly,” says Dr. Ancel Keys, world-famous researcher and a director of the American Heart Association, “heart disease dominates the total health and mortality picture among adults in the Western world . . . particularly,” he adds, “in the more prosperous countries and the more prosperous classes.”
This is a curious qualification. What does it mean? Simply, that the more we earn the more we spend on food. We tend especially to gratify our taste for fatty foods. And fat, more and more scientists are coming to believe, is a lure that delivers us up to heart disease.
In this, the latest theory about increasing heart disease, it isn’t the fat we store on our bones that abets the great assassin, it’s the fat we store in our arteries. President Eisenhower weighed no more on the day of his heart attack than in the days when he was a West Point cadet. He kept a vigilant eye on his total calories, but like most of us —according to this theory—he let the percentage of fat in his food rise too high. In time, this caused the percentage of fat in his blood to rise. Gradually it settled in his arteries and eventually blocked the flow of blood to his heart.
One of the first signs of this condition is that the blood shows an increase of a type of fat called cholesterol. “Its concentration in the blood,” says Dr. Keys, “is affected by genetic factors, by hormones, and possibly by physical activity, but the largest factor, and most clearly demonstrated in man, is the diet. The main item of influence in the diet identified so far is the total fat content, or the proportion of all calories provided by fats.”
This theory is not accepted by all heart specialists. Many continue to place the emphasis on overweight, lack of exercise, or on emotional turmoil, tension and overwork, sometimes lumped together under the one label, stress. But others are turning to the theory that fat in the blood stream is the villain, or at least the biggest single villain yet unmasked. “I do not think anyone even superficially versed on the subject,” says Dr. Thaddeus Labecki of the Mississippi State Board of Health, “would deny that the lipoprotein particles (fats) which enter the lining of the arteries do come from the blood stream, and they find themselves in the blood stream because they are ingested with our food.”
Although some doctors consider it dubious, the theory seems to be supported, statistically at least, by postwar prosperity. Studies made in China, Japan, Ceylon and Okinawa show that heart disease is rare among people in countries so poor. It is higher among the laboring classes of Spain and Italy, whose standard of living is also higher. But it is nowhere near as high as in the richer nations. For as national incomes rise, so, too, does heart disease, till it reaches a peak in the United States, with Canada just below.
The latest figures from the Dominion Bureau of Statistics show that deaths from all causes in Canada in 1954 were 124,520. Deaths from heart disease were 41,297. This means that one of every three Canadians now living can expect to die from a damaged heart.
There are twenty-one different disorders of the heart. All except one are rare or on the wane. But this one exception accounts for eighty percent of the heart-disease death rate. It is the cause of most heart attacks. Yet, primarily, it is not a disease of the heart. As a prominent British doctor, J. N. Morris, told the World Congress of Cardiology last year in Washington, the heart attack is only “the visible tip of the iceberg.” Behind it—the secret cause said Morris, “is a mass disorder on a scale of the epidemics of history”—a mysterious malady known as atherosclerosis.
Atherosclerosis is by far the more dangerous of two kinds of hardening of the arteries. In one, a relatively innocent type called arteriosclerosis, the flexible artery wall grows hard and brittle, but usually the tube stays fairly open and smooth on the inside. In atherosclerosis, named from the Creek for “porridge,” sometimes referred to as a “soft hardening,” molecules of fat penetrate the artery’s inner lining, thin as the membrane of the mouth. Gradually the fat accumulates, narrowing the bore and roughening it so that the slowed-down blood clings and clots more easily.
These lesions may block the arteries to any organ in the body. They are the hidden cause of much senility, kidney disease, high blood pressure and the stoppage of blood to the brain which we call a stroke. But atherosclerosis wreaks its greatest havoc in the arteries of the heart.
The heart is a light, hollow, tough and tireless muscle that can take an amazing amount of strain without slackening a moment in its job of pumping five quarts of blood around the body. Beating more than 100,000 times a day, it drives the blood down great arteries that branch like tree trunks and branch again, growing smaller till the blood reaches the tiniest twigs, the capillaries, so narrow that the red corpuscles must squeeze through one at a time before beginning their long trip through the veins.
Of all the body tissues fed through this intricate supply line—62,000 miles long, two and a half times around the world none needs the blood food more vitally than the heart. If the flow of blood to any part of the heart fails for a moment the laboring cells cry out for rest. These are the pains that President Eisenhower thought was indigestion. In one of the arteries that bring blood to his heart, called coronaries because they curve above the heart like a crown, a yellowish bulge of fat and fibre had slowed the blood to a trickle. Later it clotted. The pain became suffocating. A patch of heart cells, cut off completely from nourishment, were dying. At this point the president’s artery disease had become heart disease.
These two disorders, so closely linked, cause much confusion in terms. Often, when doctors speak of the causes of heart disease, they are talking about the things that bring on a heart attack-—emotional upset, shock or fatigue. But the angina pains that sometimes warn of the danger are actually the first symptoms of atherosclerosis. So when scientists speak of the causes of heart disease, they are usually referring to the things that cause artery disease, which is really the underlying condition.
"Everyone over twenty has some atherosclerosis,” says Dr. Lyman Duff, dean of medicine at McGill University and an outstanding Canadian researcher. "We can halt it to some extent. But we can’t reverse it. We even have difficulty diagnosing it in the coronaries—until it has gone so far that it causes a heart attack or angina.”
This difficulty frustrates both physicians and researchers. They can take X-ray pictures of most arteries in the body, but coronaries cannot be seen in X-rays because they are similar in substance to the heart. They can see the disease in the tiny arteries that cross the back of the eyeball by looking into the round hole in the centre of the eye through the magnifying lens of an ophthalmoscope. If fat has misshapen these arteries, or if it is bad in the legs, where a skilful doctor can feel it, the chances are it is also bad in the coronaries. The reverse, unfortunately, isn’t true. "It’s queer,” says Duff "You’d think the fat in the arteries would deposit at the same rate all over the body, but it may be very moderate in all the other arteries and be extreme in the coronaries. We won’t know why until we know the cause.”
Many doctors would say that our stepped-up pace of life is to blame, that Eisenhower simply paid the price of being president. And there is some evidence that stress will hasten a heart attack in persons with fat-clogged arteries. There are, for example, recent reports from Helsinki of six heart patients in hospital who died of excitement brought on by the scheduled visit of their doctor. And a fifty-year-old Montreal streetcar driver keeled over dead in October during a heated exchange with two women passengers who wouldn’t move back in the car.
But when stress is broached as a cause of atherosclerosis, some research men shrug and say that proof is lacking. The eminent British pathologist, W. Melville Arnott, calls the stress theory of atherosclerosis "absurd.” It "implies that the laboring classes . . . and the great majority of the . . . inhabitants of the Orient live some sort of idyllic existence . . . securely insulated from the fierce competitive, intellectual, and emotional burdens which grind the life out of those unfortunates whose lot it is to think, direct, and govern . . . All available evidence is to the contrary.”
However, he says, "The ready acceptance of this stress-and-strain concept is understandable. ... It places . . . heart disease in the position of being the unjust reward of virtue. How much nicer it is when stricken with coronary thrombosis (closure) to be told that it is all due to hard work, laudable ambition and selfless devotion to duty than to be told it is due to gluttony ...”
Some insurance companies say that the large number of attacks are due to changes in listing the causes of death, to improved diagnosis, and most of all, to the fact we’re living longer. But hospital and coroners’ records examined by the British researcher, J. N. Morris, indicate, that the absolute increase in heart disease since the turn of the century is at least twofold.
Even our vaunted long life span is illusory for middle-aged adults. For example, the old-age figures show that an average baby born in this country can expect to live to a riper age than an average baby born in Italy. They do not show that when Italian men reach fifty they have an even chance of living as long as Canadians, and that, from then on, their chances of surviving get better, until, at seventy, they have roughly twice the life expectancy of a North American.
The premise that our ageing population explains the rising toll from heart disease presupposes that degenerating arteries are as inevitable a part of ageing as wrinkles. This opinion does not explain why, in three hundred autopsies by U. S. doctors on soldiers killed in Korea, atherosclerosis was much more advanced in young Americans than in Orientals the same age. Or why heart disease in Ontario, for years our richest province, is two and a third times as common as in Newfoundland, our poorest.
The beginning of the cholesterol or blood-fat theory of heart disease occurred a hundred years ago when a German pathologist, Rudolf Virchow, was slicing open a hardened artery to study it under a microscope. He saw a patch of fibrous tissue, dead cells, lumps of soft fat, and glittering scaly layers of a pearly white substance, a crystalline fat called cholesterol. Cholesterol, a common but little-known body fat that all our tissues seem to need, made up more than half the lesion.
In Russia, some fifty-five years later, Dr. N. H. Anitschkow dissolved cholesterol in seed oil and fed it to rabbits. In a few weeks the fatal lesions appeared in their arteries and Anitschkow was sure that cholesterol produced the same thing in humans.
Other Russian scientists took issue with Anitschkow and cholesterol became a fighting word among pathologists all over the world. This long dispute was kindled afresh in the 1930s by a New York doctor, Irvine Page, now the president of the American Heart Association. Analyzing the fats in artery lesions, Page noticed that they had a chemical make-up like that of the fats in the blood. And the more cholesterol he force-fed into the blood of his rabbits, the more showed up in their arteries.
Page and others also noted that most heart patients had a higher-than-average blood cholesterol. And those who didn’t live through an attack had higher levels than those who did. A large percentage of fat men had high blood cholesterol and overweight persons were prone to heart disease. Disorders such as diabetes, gout and nephrosis (a kidney ailment) pushed up the cholesterol in the blood, and it had long been remarked that when patients survived these illnesses it was very frequently to die of a blocked coronary artery.
And then some researchers felt that heredity had a weird metabolic effect. People whose parents both had heart disease had high blood cholesterol, and they frequently suffered their first angina pains in their teens. When one parent had heart trouble, the blood cholesterol was often above normal.
This held out hope that atherosclerosis could be detected by the level of cholesterol in the blood, a simple test any doctor can make. But, often enough to kill this hope, there were people with heart disease whose blood cholesterol was not above normal. Statistically, working with averages, blood cholesterol levels had significance. Individually, it was not a reliable test. It was even hard to judge what a "normal” level was in a given individual.
The evidence was confusing and contradictory. And most baffling of all were the early experiments with humans. When the researchers fed cholesterol-rich foods to humans with or without heart disease, the cholesterol in the blood didn’t rise. It didn’t drop when they cut the food cholesterol. Later, they found that the human liver manufactures so much cholesterol that the relatively small amount in a normal diet seems to have no effect on the blood level, which the liver normally regulates.
Some doctors cited this as proof that diet had no effect on blood cholesterol and thus on artery disease. The experiment with rabbits, they said, proved nothing about human beings. They scoffed at colleagues who went on low-cholesterol diets or put their heart patients on one. Their main point was that doctors, on such inconsistent evidence, had no right to ask people to give up foods abundant in cholesterol. For these are the great protective foods—butter, cream, cheese, poultry, eggs, liver and all other organ meats— the most nourishing staples of our diet.
Then, in the late Forties, a young doctor named John Gofman, head of a research team at the University of California, wondered if perhaps the answer to the riddle was that only some, not all, of the blood cholesterol was guilty of abetting heart disease. Gofman was also a chemist, co-discoverer of a new element, Uranium 233. By spinning the blood in a whirligig called an ultracentrifuge, he separated its molecules as we separate milk and cream. He discovered that cholesterol was carried in the blood, along with other globules of fat, on stringy molecules known as lipo-proteins. Gofman called them "giant molecules.”
Rabbits with the most damaged arteries, Gofman found, had the most giant molecules in their blood. He later took blood samples from 1,500 Californians. After fatty meals he observed an acute rise in the level of such molecules. In normal people they soon broke down but in people with atherosclerosis the blood stayed cloudy for a long time.
Many such experiments led Gofman to declare flatly: "We can identify people early in life, before any symptoms, and give them a quantitative rating as to their chances of surviving one year, five years, ten years or twenty years with respect to coronary disease. Further, I would publicly challenge any doubter to find scientific flaws in the evidence that leads to these predictions.”
Nevertheless, Gofman has his doubters. They agree that his tests, together with total cholesterol, have a high predictive value among groups, but they feel that this claim to be able to diagnose individuals is too sweeping. By now most researchers share his conviction that atherosclerosis is caused by faulty fat metabolism. In the same way that diabetics have lost the power to use sugar, many people cannot handle fats.
Meanwhile, another scientist was approaching the same opinion by another route. Dr. Ancel Keys, of the University of Minnesota, head of the laboratory of physiological hygiene, felt that "in human diets there must be something which influences the blood but that this is not cholesterol though it is often associated with it.”
Experimenting with humans in 1951, Keys raised their blood cholesterol, which could not be raised by cholesterol-rich foods alone, by foods containing cholesterol plus other fats. He was certain that his "something” was "plain fat, the total of all the fats and oils, visible and invisible, in the diet.”
If diet was the cause, heart disease could be prevented. But the theory needed testing over many years, and there wasn’t time for such long-range studies. Keys looked for answers in what he calls "experiments of nature.” One such set of experiments had come out of World War II. Whole populations had been forced to cut down on fats. In Britain the cut had been small, about fourteen percent. Studying Britain’s death rates from coronary disease, Keys noted from 1941 on "a small but significant decline.” At the end of the war, with diet back to normal, the death rate from heart disease resumed its upward climb. If emotional stress or overwork had been primary factors it should certainly have been the other way around, he reasoned.
The same pattern showed in figures from Germany. The Netherlands was the same. It was even more marked in Sweden, where fats had also been rationed. Before the Germans marched into Norway in 1940, the average Norwegian had 3,470 calories a day and thirty-seven percent of his food was fat. The Germans cut his calories to 2,850 and his fat to twenty percent. Within a few weeks the death rate from heart disease dropped sharply. With equal abruptness it rose again in 1945 when the Germans quit the country.
Such crude correlations, of course, proved little. Keys had no information on changes in weight or blood, no way of judging if anything other than food had had any effect. He sought further evidence abroad.
In the spring of 1952, Keys studied forty-eight middle-aged men employed in the factories of Slough, near London.
He compared them with several hundred men of similar age from Minnesota. The Englishmen ate thirty-five percent of their food as fat, the Americans forty-two percent. And the Englishmen’s blood cholesterol levels were lower by ten percent than the Minnesota men’s, a difference that also tallied with the lower English death rate.
Later that year, in Madrid, Keys studied two groups of Spaniards. One group was poor, the other made up of rich professional men whose diet was high in fats. Keys couldn’t get accurate figures for heart disease, although many doctors told him it was common among the wealthy and rare among the poor. He found that at fifty years of age upper-class Spaniards averaged thirty percent more cholesterol in their blood than the poor men.
Neither of these surveys was very satisfying. Last year, accompanied by a whole battery of experts, including the famous heart specialist, Paul Dudley White, who attended Eisenhower, Keys set sail for Naples. He picked four groups of healthy men: steelworkers, firemen, clerks, and some wealthy volunteers from the Naples Rotary Club. He measured their height, weight, fat folds and food, took blood samples, blood pressures and electrocardiograms. An expert insurance actuary, Ernest H. Klepetar, checked the accuracy of Italian statistics, while White and his fellow specialists, in a sweeping survey, found no evidence that Italian doctors diagnosed heart disease any differently than they did.
For breakfast, the working men ate a plain bread roll with coffee. For lunch they had bread, pasta (spaghetti or macaroni), local vegetables, fruit and a little cheese. They ate very little sugar or potatoes, and no butter. Meat, fish, cheese, milk and eggs were luxuries. The fat content of their diet was only twenty percent, yet they weren’t undernourished.
The Lunch Was Full of Fat
The findings showed the young men were not much different from their North American counterparts. Their blood cholesterol rose with age until they were thirty-four. "Thereafter,” Keys reports, "in sharp contrast with the Minnesotans, the Italians showed no further age trend,” so that by fifty they had seventeen to twenty-four percent less blood cholesterol than the Americans. And, says Keys, for Americans in their fifties, who eat twice as much fat as an average Italian, "our death rate from arteriosclerotic heart disease is . . . almost four times that of Italy.”
The prosperous Naples businessmen presented a different picture. "Attendance at their luncheons,” says Keys, "was like being back home except that the banter and speeches were in Italian. There were big servings of fat meat, rich gravies, butter with the bread, ice cream, and pastry full of shortening. These men had blood cholesterol levels similar to Americans.”
Two professors at the University of Bologna then suggested that Keys might clinch his point by taking his team to Bologna. In Bologna, they said, bread is baked with olive oil and lard. In Naples the bread contains no shortening. In Bologna, the pasta is apt to he fettucine, tagliatelle, or tortellini—all made with eggs and fats and served with much oil and rich sauce. In Naples the pasta is made without fat and served with only a dash of oil and sauce. Keys selected a group of Bologna policemen. Their blood cholesterol at fifty was twenty-one percent higher than that of the working men of Naples, about the same as that of the wealthy Neapolitans.
These studies seemed to throw unexpected light on the problem of overweight. Recent insurance figures have shown that overweight people have more heart disease than people of normal weight, who, in turn, have more than the lightweights. Keys found that the English workers at Slough were thinner than North Americans and had less heart disease. The Naples working men, however, were fatter than North Americans and had the least of the lot.
"Clearly,” says Keys, "obesity is not the controlling factor.” He thinks that the high death rate among overweight people is not so much because they are carrying extra body weight as because they are probably eating too many high-fat foods. All doctors, though, warn that once heart disease has developed, overweight—not the muscular overweight of athletes, but overfat -puts an added and dangerous burden on t he heart.
Surveys like Keys’ are now being made by doctors in nine countries. So far, their data agree. A study last year of autopsies made on the adult Bantus of South Africa shows that these natives seldom have artery disease. Their blood contains little cholesterol and their food contains little fat, only ten percent.
The case against fat has other witnesses. Recent British experiments have indicated that our blood clots more readily after a high-fat meal. And at Harvard University, Frederick J. Stare has produced atherosclerosis for the first time in a monkey, the most manlike animal, "purely by dietary means a diet high in cholesterol and fat and poor in protein” (the italics are his).
Some scientists think that lack of certain proteins in our food may weaken the artery wall and allow the fat to enter more easily. Or that certain proteins may help disperse the fat; a newly discovered vitamin in the B group, called choline, present in lean meat, liver and eggs, has this power. Or lack of proteins may weaken the glands whose job is to make the hormones which help control the fat in the blood.
There are many indications that the level of fat in the blood, including cholesterol, is regulated by hormones. When the thyroid gland is sluggish the fat is a long time breaking down. And small doses of a hormone-like substance named heparin clear the blood and also relieve heart pains.
Relief has also been obtained for three out of four heart patients by slowing down the adrenal glands with Roentgen rays. And, conversely, adrenalin injected into heart patients brings on angina pains. Adrenalin is a hormone that our adrenal glands secrete when we overexercise, get too cold or have an emotional upset added evidence that stress, though perhaps not a first cause of heart disease, may often be the last.
Sex is another ambiguous piece of the puzzle. Men are twenty times more liable than women to die of a heart attack—until the menopause, when this sex difference disappears. Dr. Louis Katz, of Chicago’s Michael Reese Hospital, has halted atherosclerosis by injecting male patients with female hormones.
All these discoveries and theories offer some hope of eventual control, perhaps the kind we have now with diabetes, perhaps even a cure that will dissolve the fat already coating our arteries. But today we can only try to stop the disease from developing. Out of all the findings in Europe, out of all the research, only one theory of practical import emerges: when we eat too much fat consistently it may eventually clog our blood, end up in our arteries, block them and cripple our heart.
How can we reduce the fat and cholesterol in our blood?
Beginning in 1951 and for the next four years, Keys made seven experiments on 104 men. He kept their calories, proteins and activity the same, and juggled their fats and carbohydrates. When the fat in their food was cut from forty to twenty-four percent, their blood cholesterol dropped sixteen percent. He reduced their fat to eighteen percent. Blood cholesterol fell twenty-four percent. And when all but four percent of the fat was taken out of their diet, the men lost forty-six percent of their blood cholesterol.
Also, he found, the blood cholesterol level went down when the total calorie intake was less than the body needed for fuel. It rose when the calorie intake was more than was needed. When the weight leveled off again, so did the blood cholesterol. So the process of gaining or losing weight, not the state of overweight, is important, he has concluded.
Is there reason to stop eating foods rich in cholesterol—mineral-rich, vitamin - loaded, body - building protein foods such as cheese, milk and liver?
Keys thinks not. Here is an experiment he made with a group of people: he cut from their diet all egg yolks and butter, and made up the calories in vegetable oils and animal fats. He was cutting their cholesterol intake nearly in half, yet it made no significant change in their blood cholesterol. Then he added a couple of egg yolks—the richest source of cholesterol—and cut down on butter, margarine, salad and cooking oils, shortening in bread and pastry, and all kinds of fat meat. He made up these calories with cottage cheese, sugar and potatoes. He had increased the food cholesterol yet the blood cholesterol fell. He concluded that the regulation of our blood cholesterol can safely be entrusted to our liver—as long as we aren’t eating too many fats with our cheese, milk, eggs, liver and poultry.
How much is too much?
This is a ticklish question. The amount of fat one person can handle with ease may be far too much for someone else. This is one reason why doctors talk so cautiously about diet. But there is no scarcity of facts and opinions.
There are three main classes of food: carbohydrate (sugar and starch), protein and fat. Since the turn of the century, while eating about the same amount of protein, we have been steadily substituting fats for carbohydrates. In 1935, for example, the average Canadian was getting thirty-four percent of his calories from fats. Today, it is close to thirty-eight percent and headed upward — along with atherosclerosis. Dr. L. B. Pett, the Canadian government’s chief nutritionist, thinks we should roll this figure back to about twenty-four percent.
How to Fry Your Food
Food experts sort fats, roughly, into two groups: "visible” and "invisible.” Invisible fat is the fat in such protein foods as eggs and oysters, and milk products like cocoa and ice cream. It is packed between the cells of most meats and many kinds of fish. But also, we know now, many of these foods contain fat-dispersing vitamin choline, and this may be nature’s way of safeguarding these important foods. In any case, in Dr. Pett’s opinion, "The amount of fat in these foods isn’t dangerous. The real problem is 'visible’ fat—butter, margarine, lard, all the kinds of shortening used in baking and cooking.”
We are using more and more butter and margarine. We fry potatoes, doughnuts, pancakes, fritters, chicken and fish in a manner that soaks up fat. Over the years Dr. Pett’s division has noticed a steady increase in the amount of shortening commercial companies call for in their recipes. Even the trend toward cake mixes boosts our fat consumption.
What can we do about it?
"Use more skim milk,” Pett advises. If you deep-fry foods properly you use a lot less fat. You don’t have to cut off everything you like. We’ve found that we can produce just as good a baked product with half the fats that are usually recommended in the recipes. If people are aroused to the thought that the villain of the piece is simply too much fat, they can play it safe without much sacrifice.”
But will we? The insurance actuary who accompanied Keys in Italy, Ernest Klepetar, is skeptical. "Past epidemics, such as tuberculosis,” he says, "were fought by uncovering and bringing to the attention of the public poverty and slums ... It will be difficult to persuade the more successful exponents of our way of life that the best thing they can do to live longer is to lower their standard of living.” ★