When a Spanish-speaking friend wants to wish you the best, he will often lift his glass with the following toast: “To health and wealth – and time to enjoy both.” In this toast there are three basic wishes that everyone has at some point in their lives. Why can’t we live longer? Everyone wants to live longer. Everyone wants to enjoy a life of purpose and fulfillment, without disease or unhappiness. As we grow older, we worry even more about increasing our lifespan, even if by just a little. We want to have time to still make plans, to enjoy what we’ve done in our lives, and whatever else life has to offer. By the time we reach 60, we realize that, in the words of the great French painter Gauguin, “life is a split second.” We begin to think about all the things we still want to do before the next ten years pass us by. If we are fortunate enough to get there, we wonder why we can’t live even longer-perhaps to be 80, or even to 100. Well, why can’t we? Actually, we indeed are living much longer than we did a century ago, increasing the average life expectancy by 20 years in America since 1900. How have we achieved this?

Advances in medical science have outlawed many diseases. 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 considered the source of more than half of all deaths occurring each year in the United States. This disorder is known to doctors as “arteriosclerosis,” which means a hardening and thickening of the arteries. It is now so widespread that Dr. Paul Dudley White, the renowned 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 hard, and the inside tubes become roughened and thick. The conditions pave the way for the three most common causes of death and disability in America: heart attack, heart failure, and stroke. Is there any way to avoid this disease, whose most common victims are middle-aged men, and sometimes even the younger ones, sometimes those in their twenties? The answer is yes, provided you will take the time and give some effort now to learn a few simple methods on how to prevent it.

Much of the exact nature of arteriosclerosis is still unknown. 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 intima 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.

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.

To make matters worse, the swelling of the lining cells and roughening of the inner surface allows for blood clots to form inside the narrowed artery. If the flow is completely blocked off in vital arteries that feed blood to the heart muscle, the result is a heart attack, or as we physicians call it, a coronary thrombosis. If this condition occurs in the cerebral arteries of the brain, a “stroke,” which is sometimes referred to as a heart attack in the head, results. When this happens in kidney area, Bright’s disease, formerly called “dropsy,” among other diseases, will strike. Regardless, whether this process of narrowing and blockage of the arteries takes place in the heart, head, or kidneys, it is fundamentally the same disease. Doctors call it atherosclerosis. About a century ago, during an autopsy, a German pathologist named Rudolph Virchow opened up an artery to examine its interior wall. Along the lining he observed deposits of mushy fat that he called atheromata, a Greek word meaning “porridge.” Thus, this was the root word from which we derived the term atherosclerosis. Fixed among the cells of the artery wall along with the fat, Virchow observed some shiny crystals, which turned out to be cholesterol. The question that remains is how these fats got into the walls of the arteries, which has puzzled doctors for the past century.

It is currently being researched by various scientist, with many different specialties. The first theory proposed by researchers was a process called “imbibition,” supposing that the fat droplets were absorbed directly from the blood stream through the lining of the artery walls. When the actual structure of the artery wall started to deteriorate, cholesterol and other similar 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 ratio in the artery wall as in the bloodstream. Another theory argues that they did not come from the blood stream, but were made within the cells of the vessel wall. There are other claims that fat molecules are normally absorbed by the artery wall without ever leaving damaging remains of acid crystals. However, conditions such as high blood pressure, may force too many the fat molecules into the wall, so that the artery cannot absorb such an amount, causing deposits to build up. Others have thought that the fat droplets find their way into the artery wall through the vessels that supply the artery with blood. According to this idea, a hemorrhage or series of small hemorrhages may occur in these tiny vessels. As a result, a clot is formed, which dumps 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.

When we consume fatty foods, the fat enters our blood stream, searching for the weak spots in the arteries. These fats deposit themselves into the weak spots, and then absorb calcium, which initiates the hardening process, and soon it begins to reduce our blood flow. Our body tries to deal with these dangerous deposits: special fat-eating cells are sent where the fats and cholesterol have breached the lining and broken into the artery. The fat-eating cells try to swallow up the cholesterol and fat particles, trying to digest them and reduce the damage temporarily. Dr. Timothy Leary, the distinguished Boston pathologist, in 1933 first invented creative ways of illuminating, refracting, and photographing this process. It was observed that these special fat-fighting cells would be overwhelmed by the substantial amounts of cholesterol and fats continually entering blood and artery walls through the consumption of high-fat foods such as butter, eggs, cream, milk, and fatty meats.

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