When a spanish-speaking friend
wants to wish you the very best that life can offer, he will often lift his glass with the following toast:
"To health and wealth — and time to enjoy both."
Embodied in this simple salute are the three basic desires common to people everywhere in all ages.
Why can't we live longer? Everyone wants to live longer. It is one of the most deeply rooted instincts of mankind. Everyone wants to live a life of usefulness and abundance, free of disease and unhappiness. As we grow older, we look forward even more anxiously to increasing our lifespan. We want time to enjoy our achievements, time still to make plans. By the time we reach 60 we realize with the great French painter Gauguin that "life is a split second." We begin to think about all the things we still want to do before we reach our seventieth year. If we are fortunate enough to pass our seventieth birthday, we wonder whether we can't live even longer—perhaps to be 80.
Well, why can't we? We are living much longer than did our ancestors a century ago. We have added 20 years to the average life expectancy in America since 1900.
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Advances in medical science have outlawed many dis-eases* These golden years are ours because of advances made by tireless research in medical science. They represent a decisive victory over the contagious and infectious diseases which sometimes wiped out whole sections of our population a generation ago.
Thanks to the new knowledge provided by recent research, we no longer need fear the ravages of such diseases as diphtheria, scarlet and typhoid fever, syphilis and—to a great extent— tuberculosis. All these pestilences, however, were caused by those invisible but ever-present enemies of health—germs.
Today the picture has changed. With the victory over deadly microorganisms, a new threat has emerged in clearer and more frightening perspective.
The 20th Century epidemic. A single, fundamental disease of the human body can now be held accountable for much of the illness and more than half of all deaths occurring each year in the United States It is a disorder known by the general term of "arteriosclerosis," which means a hardening and thickening of the arteries.
It is now so widespread that Dr. Paul Dudley White, the noted heart specialist, recently described it as "a modern epidemic."
As the disease progresses—sometimes over a long period of time—the vessels that carry the blood from the heart to the body's tissues become stiff, and their inner surfaces roughened and thick. These conditions lay the groundwork for the three most common causes of death and disablement in America: heart attack, heart failure, and stroke.
Is there anything that can be done to vanquish this number one killer, whose favorite victims are men in their middle span of life, and even the very young, sometimes those in their twenties? The answer is "yes"—provided you will take the time and the trouble now to learn a few simple rules.
Much of the exact nature of arteriosclerosis is still unknown.
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But during the past 10 years we have learned a great deal in the fields of pathology, chemistry, biology, and nutrition that has provided us with clues to the mystery, and a practical approach to treatment for the first time.
Widespread popular interest in the heart and in the aging process has helped immeasurably in the conquest of disease. But at the same time, it has been responsible for a good deal of fear and confusion among lay people. Some of these misconceptions are reflected in the questions my patients ask after reading articles of the kind that now appear in many newspapers and magazines.
Take diseases of the heart and blood vessels, for example. Terms such as atherosclerosis, coronary thrombosis, and cholesterol are today fairly commonplace, even in publications for the general reader. But few non-medical people know exactly what these words mean.
What is the cause of this new epidemic? Before taking up our discussion of ways to forestall a heart attack, it might therefore be well to understand more clearly the basic physiology involved.
Let us start with a closer look at the arteries, the vessels that carry fresh blood from the heart to the billions of cells in our bodies that are in constant need of nourishment. Upon careful examination, we find that the arteries are not the simple tubes we have pictured them to be. Viewing them in cross section, we see that their structure is more like that of a garden hose, containing three layers of tissue in the walls.
The inside layer or lining of the artery, which doctors call the intima9 consists of a slippery membrane somewhat similar to the mucous membrane on the inside of your mouth. The in-between layer, known as the media, is formed of muscle fiber. This enables the blood vessel to expand and contract with the heartbeat, to facilitate the flow of blood through it. The outer layer, called the adventitia, is composed of coarse strong fiber& which provide added strength to the artery.
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In both the outer and the intermediate layers, there are tiny intrinsic blood vessels which nourish the artery itself. The thickness and exact composition of the three layers vary, depending upon an artery's size and location.
Of the changes that may occur in the arteries as a result of disease, there are two types which concern us here. Both kinds have traditionally been known by the general term, "arteriosclerosis," which means hardening or thickening of the arteries.
Actually, however, there are two kinds of hardening of the arteries. One occurs when calcium deposits in the middle layer of the artery cause it to become brittle and hard. For this reason, it is sometimes called a "pipestem" artery. Such calcification does not necessarily obstruct the blood flow, and is usually harmless from a clinical point of view.
The other type of change, on the other hand—and it is the more frequent one—has serious consequences. It consists of a thickening of the inner wall of the artery by deposits of fats: cholesterol (a fatty alcohol), fatty acids, and the like, together with calcium.
As these deposits grow, the passageways or canals of the arteries become narrower, much in the same way as the drain from your kitchen sink becomes clogged with grease deposits. The result is that less and less blood can flow through the narrowed opening to the tissues or organs that depend on it for life. Your "pipes" have become clogged.
At the same time, the swelling of the lining cells and roughening of the inner surface provide sites for formation of blood clots inside the narrowed artery. If the blockage is complete in vital arteries that feed the heart muscle, a heart attack—or as we physicians call it, a coronary thrombosis—occurs. If this disaster occurs in the cerebral arteries of the brain, a "stroke," sometimes called a heart attack in the head, results. When the small arteries of the kidneys are affected, Bright's disease, formerly called "dropsy," and other diseases ensue.
But whether the thickening and blocking process takes place
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in the heart, head, or kidneys, it is essentially the same disease. Doctors refer to it as atherosclerosis.
About a century ago, during an autopsy, a German pathologist named Rudolph Virchow laid open an artery to examine its interior wall. Along the lining he observed deposits of mushy fat that he called atheromata, a Greek work meaning "porridge." It was from this word that we derived our term, atherosclerosis.
Embedded among the cells of the artery wall along with the fat, Virchow observed some glistening crystals. These turned out to be cholesterol. But how did these fats get into the artery walls? This question has puzzled scientists for the past 100 years, and it is still being pursued in various fields of research. The first theory advanced by researchers was that of "imbibition," which held that fat droplets were absorbed directly from the blood stream through the lining of the artery walls. When a weakening of the "ground" substance or actual structure of the artery wall occurred, cholesterol—the main offender—and its related fats were deposited in the artery wall. This theory has been supported by the recent discovery that these fatty deposits, especially cholesterol, exist in the same proportion in the artery wall as in the bloodstream itself.
Another theory that seeks to explain the way in which the fatty deposits get into the artery walls held that they did not come from the blood stream primarily, but were manufactured within the cells of the vessel wall.
It has also been claimed that fat molecules are normally absorbed by the artery wall without leaving a harmful residue of acid crystals. But some abnormal condition, such as high blood pressure, may force an excessive amount of the fat molecules into the wall. Then the artery cannot absorb the full amount, and deposits gradually build up.
Other researchers have believed that the fat droplets find their way into the artery wall through the tiny vessels that supply blood to the artery itself. According to this theory, a hemorrhage or series of small hemorrhages may occur in these tiny vessels.
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A clot is formed, which deposits fat particles in the artery wall when the small vessels break down.
My own conclusion, based upon years of animal, laboratory, and human research, plus experience with innumerable patients, is this: Atherosclerosis results from an impairment of the body's ability to utilize (or metabolize) normally not only the fats eaten in the diet, but also those that are in the body itself. This impairment is further aggravated by the body's inability to withstand stress or tension; and by deficiencies in the supply of hormones from vital glands such as the thyroid, the adrenals, and the sex glands.
In addition, there are other factors that influence the individual's susceptibility to atherosclerosis, or death from a heart attack or stroke. These include such things as inherited or constitutional factors, and the coagulability of the blood.
It is easy to see how complex the problem really is. The danger of oversimplification is great. However, one causative factor that stands out continuously above and beyond all others, important as they are, is fat in the diet. And it is this factor that we can control.
These fats from our foods enter our blood stream where, like sharks cruising about, they seek out the weak or vulnerable spots in the arteries. Here they attack, enter, and deposit or nest themselves. These fatty deposits then acquire calcium, and the hardening process begins in the arteries. Each particle becomes a captain around which rally the silent "Men of Death," who wage a relentless struggle. Soon they begin to throttle our life flow.
Our blood vessels then engage in a vain effort to halt the armada of killers we now harbor within our arteries. Special fat-eating cells are rushed to these spots, where the fats and cholesterol have breached the barrier or wall and entered the artery. In the life-and-death struggle that ensues, the fat-eating cells try to engulf the cholesterol and fat particles, and may succeed temporarily in the "counter-attack."
Dr. Timothy Leary, the distinguished Boston pathologist, in
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1933 first devised ingenious methods of lighting up, refracting, and photographing this deadly drama. It was seen that inevitably the special fat-fighting cells are themselves engulfed by the repeated tidal waves of cholesterol and fats washed into the blood and artery walls by fat-containing foods such as butter, eggs, cream, milk, meat fats, and other animal fats in our diet.
Why is the epidemic particularly strong in the U.S.A.? If you are a typical American, whether you know it or not you consume an unbalanced, obesity-producing diet. Drs. Louis Katz and J. Stamler, prominent researchers in this field, called it "a pernicious combination of overnutrition and undernutrition —excessive in calories, carbohydrates, lipids and salt; and frequently substandard in certain critically important amino acids, minerals and vitamins."
It is not surprising that this situation exists. The science of nutrition, a comparative newcomer to the medical field, has up until recently been concerned almost exclusively with undernutrition. People have been urged to "eat the right foods" and to provide plently of meat, eggs, milk, and cheese for their children.
In most areas of the world, this problem of getting enough nourishing food to eat is still of primary importance. But it is not the problem in America. Our problem is somewhat the opposite: "living too high on the hog." Our diet is too rich in fat as well as calories, refined sugars, starches, and oils. At the same time, it is low in essential nutriments, minerals and other vital requirements.
The exact relationship between the amount of fat you eat and the production of cholesterol in your body is still a very complex question. Investigators differ on some points.
Concerning one aspect of the problem, though, we are all agreed: the cholesterol found in the blood is made largely in the liver from fats in the diet.
It is also believed that cholesterol is produced in the arterial walls themselves.
But the main source and the one that we can to a great extent control is fat in our food.
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What is the situation in other countries of the world?
We have evidence that a prime factor for the great difference between Americans and peoples in various other countries is diet.
For example, let us see what happened in Norway during the war years of 1940-1945. Consumption of butter, milk, cheese and eggs (all of them high in fats) had to be sharply curtailed. Did the reduction of fat content in the national diet have any effect on the number of deaths from heart attack? The Norwegian Ministry of Health, which kept accurate records, answered that question with an emphatic "yes." With the reduction in fat consumption, the death rate from coronary attacks declined also. The Norwegians reported that heart deaths were reduced by 31 percent during each year among the urban population. At the same time, there was a 22 per cent drop in heart deaths among the rural population.
France, which also had to tighten its belt during the war years, had similar evidence to offer. Mr. Marcel Moine, of the French Ministry of Health, reported to me that from 1941 to 1945, when Frenchmen were on a low-fat diet, the death rate from heart disease was reduced to 20.6 for each 100,000 persons. In the postwar years, when normal fat consumption was resumed, the death rate rose to 25.5 per 100,000 population, or a return to the old, prewar death rate.
Italy provides another example. There studies were made recently in two neighboring provinces. In one area, where the daily diet included pork products rich in fats, the incidence of coronary and generalized artery disease was found to be much higher than in the adjoining province where the population followed the comparatively low-fat pattern of the country as a whole.
Similar studies have been made in various parts of the world—countries such as Finland, Denmark, South Africa, China, and Japan. Statistically the results all point in the same direction: high-fat diet means a high rate of heart deaths.
Figures, as Mark Twain and Marilyn Monroe have shown,
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sometimes have a way of misleading us. This is admittedly true of interpreting cause and effect relationships where the health of whole populations are concerned. The long arm of coincidence can sometimes reach around corners or do a juggling act. For example, you might claim, an the basis of statistics, that since the use of soap was also sharply reduced in some countries during the war, with a corresponding drop in death rate from cardiovascular disease, it was the soap (which is a fat) that caused the disease. In a more scientific view, however, the evidence weighs heavily on the side of fat as a prime factor in causing atherosclerosis.
Is the epidemic confined to older people? What has happened to our way of life to make men between 30 and 45 the preferred victims of the "silent killer" that strikes without warning? And why are more and more young women, long believed to be virtually immune to this disease until after menopause, now falling prey to it?
We do not know the entire answer to this enigma, or even whether there is a single answer. But research that has been carried on by my colleagues throughout the world, and by myself during the past 10 years, has provided some valuable clues.
Only recently, we discovered to our amazement that over 90 per cent of our adult population has, to a greater or less degree, a degenerative disease of the arteries that doctors call atherosclerosis. That, as you know, is the term meaning the thickening and narrowing of certain vital blood vessels. It is the way in which the stage is set for heart attacks and strokes.
Medical people once thought that it was a result of aging, but the disease is now being found in infants and children. As children, however, we have the power of absorbing the fatty deposits that attach themselves to the artery walls. As we grow older, we seem to lose this power of absorption. That is when the real trouble begins. At what age does this happen? Much earlier than we might expect.
For example, my associates and I made a study of the arteries of 600 patients who had died of various diseases. About 100 of
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them had met sudden death from accidents or acute illness. To our amazement we found that atherosclerosis, a disease of the arteries, was present in many of the young people before they had reached their thirtieth year.
By the time they were 40 to 50 years of age, the fatty deposits and embedded crystals of cholesterol were inside the artery walls. Such thickening and narrowing of the blood vessels interfered with the nourishment and vitality of the tissues in the heart, brain, or kidney.
Striking evidence of how widespread the disease is among our younger people today came also from Korea. There Army doctors autopsied 300 American soldiers who had died while serving in Korea. It was the first time such a study had been made of a cross section of the country's youth; their average age was only 22. A report of the mass autopsies contained startling information that 77 per cent of the young U.S. servicemen already had atherosclerosis! Balanced against this shocking total was a mere 11 per cent incidence of the same disease among Koreans and Orientals who had died on the same battlefield under the same conditions.
Does heredity have anything to do with the problem? At this point you are probably wondering: why do some people have more cholesterol in their blood than others? At present we do not know the whole answer to that question. We do, however, know some of the predisposing factors.
One of them is heredity. Some families are affected by what physicians call hereditary familial hyper-(excessive) cholester-emia. In such a family the tendency to high levels of cholesterol in the blood is passed on for several generations. Among members of such families we usually find a large number of individuals who suffer heart attack and strokes. If no heart attacks or strokes have occurred in your own family line, you have at least one protective factor in your favor from the beginning.
The second factor is one that is pretty much up to you. It concerns what you eat and how much you eat.
Unfortunately, it is too late for us to choose our parents.
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But it is not too late to choose our diet. By learning how to avoid food excessive in fat and cholesterol content, we can help minimize the effect of heredity.
Women have better natural protection against atherosclerosis. If you are a woman, you are less likely to suffer from a heart attack or stroke until well after you pass the half century mark. That is when your protective female hormones give out, and you become as susceptible to the disease as men.
Can't men take female hormones to protect themselves? They can, but if they do, they will "cross the border" and develop a high voice, full enlarged breasts, and other feminine characteristics. So that approach to the problem is not practical.
Anything else? Yes, there is something everyone can do without great inconvenience, and with the added reward of improved health in general. It is this: select a diet that will keep your blood fats down to normal levels.
Can you reverse damage done to your arteries by excessive fat? Only within the last few years have medical research teams produced reliable evidence showing that excessive fat in our diets may lay the groundwork for heart disease. If you are already past 30, it naturally occurs to you to wonder whether the damage done to your arteries is permanent, or whether it is reversible.
At the present stage of our research, we doctors cannot answer the question with certainty. We can cite the hopeful fact that experiments with animals have shown that the condition is reversible in animals. We have evidence that the cholesterol in the arteries is absorbed in children, as shown by Dr. Russell Holman and others. However, this metabolic gift seems to be lost as we grow up. There are many authorities in the field who do believe that since atherosclerosis is reversible in animals, it can also be eliminated even after it is established in humans as well. However, we must proceed cautiously in basing our conclusions solely upon studies of laboratory animals, because their metabolism is different from that of humans.
Another question that patients often ask me is: "Can you
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tell me whether I am already a victim of degenerative artery disease?" Unfortunately, we do not as yet have a test that can predict with certainty whether you are susceptible to coronary disease, or are likely to have a heart attack.
One fact, however, is certain: if laboratory tests show that you have an excessive amount of cholesterol in your blood, your chances of avoiding heart and blood vessel disease, which can lead to heart attack or stroke, are much smaller. You are then much more susceptible. If you are over 30 years of age, you ought to have your physician include such a measurement of cholesterol level in your routine check-up.
Too many men in the dangerous middle years are so busy playing for high stakes in the fast-moving game of life, that they forget that "hearts are trumps."
What is the solution for us? The many studies that have been made do not prove conclusively that heart disease is caused solely by diet. But they do heavily underscore much of the information that I have gathered from my own quarter of a century of practice and laboratory research.
Taken together, the evidence points strongly to this fact: If everyone in the United States would reduce his fat intake by 25 per cent, we would cut the number of heart deaths in half within another 20 years. Moreover, the low-fat diet will add immeasurably to your general health and well-being.
"But," you ask, "how can I go about reducing the fat in my diet? Where do I begin?" In the following pages you will find a safe guide; it includes low-fat menus and directions for using simple and inexpensive nutritional supplements that I employ in my own practice to help my patients forestall heart attack, and to treat those who have already had one or more.
If you follow these directions carefully, you will not only add years to your life, but life to your years.
