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.
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 pipes 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 inside layer 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 ease the flow of blood through it. The outer layer, called the adventitia, is built of coarse strong fiber, which provides some 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. 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 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 word 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.
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, and experience with innumerable patients, is this: Atherosclerosis is the outcome 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 further aggravated 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 effect an individual’s vulnerability to atherosclerosis, heart attack or stroke, such as inherited or constitutional factors, and the coagulability of the blood. As you can see, this disease can be very complex, and the danger of oversimplification can be very costly. However, one contributing factor that is extremely prominent is the amount of fat in the diet, which is something 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 narrow and 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 barrier or wall and broken into the artery. The fat-eating cells try to swallow up the cholesterol and fat particles, trying to digest them and counter their destructive properties 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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categories: Fat,Nutrition,Dieting,Weight Loss