Low-Fat Way to Health
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 to enjoy due to the discoveries made by advances made by countless hours research in the medical field. If it were not for the contagious and infectious diseases which sometimes crippled and killed large portions of our population decades ago, we can live longer, healthier, and happier. Thanks to the cures and vaccines devised from extensive studies and trials, we no longer need fear such diseases as diphtheria, scarlet and typhoid fever, syphilis and-to a great extent- tuberculosis. All these diseases were caused by those invisible but ever-present germs, but today the picture has changed. With ways to deal with deadly microorganisms, a new danger has arrived and 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 accepting our discussion of ways to prevent a heart attack, we should explain the basic physiology involved. We will begin with the arteries, the vessels that carry fresh blood from the heart to the rest of our whole body, that are in constant need of nourishment. Upon careful examination, you will discover that the arteries are not simply tubes as we have often 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. Intima, or the interior lining of the artery, consists of a slippery membrane somewhat similar to the one inside of your mouth. The middle layer, known as the media, is made up of muscle fiber. This allows 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 built of coarse strong fiber, which provides a strong structure 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.
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. 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, and experience with innumerable patients, is this: Atherosclerosis happens when a body is unable to normally metabolize not only the fats eaten in the diet, but also those that are produced naturally by the body itself. This inability is made worse since the body cannot withstand stress or tension, as well as deficiencies in the supply of hormones from vital glands such as the thyroid, the adrenals, and the sex glands. Furthermore, there are other factors that can affect an individual’s vulnerability to atherosclerosis, heart attack or stroke, such as inherited or constitutional factors, and the ability of blood to clot. As you can see, this disease can be very sophisticated, and the danger of underestimating it can be very costly. However, one main factor that plays a substantial role is the amount of fat in the diet, which is something 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 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.
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