Low-Fat Approach 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.” Hidden in this phrase are the three basic desires common to every person of every age. Why can’t we live longer? Everyone wants to live longer. Everyone wants to enjoy a life of purpose and abundance, without disease or unhappiness. As we grow older, we worry even more about lengthening our lifespan, even if by just a little bit. We want to have time to still make plans, to enjoy what we’ve accomplished, 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 we reach our seventieth birthday. If we are fortunate enough to pass our seventieth birth-day, 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.
Even worse, the behavior of arteriosclerosis is still rather unclear, but during the past 10 years we have made great advances in the fields of pathology, chemistry, biology, and nutrition which have allowed us to slowly inch towards understanding and creating a practical approach for a treatment. Due to popular interest in the heart and in the aging process, we have taken great steps towards the conquest of disease. However, this disease is still the source of fear and confusion among most people, as their misconceptions are revealed in questions patients ask after reading articles that are now seen in many newspapers and magazines. For example, people have heard of terms related to heart disease and blood vessels, such as atherosclerosis, coronary thrombosis, and cholesterol are quite familiar, 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 thinking and science behind it. 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 small blood vessels which naturally nourish the artery itself. How thick the layers are and how they are exactly structured is variable, depending on how large the artery is and where it is located. There are many occurrences where the artery can change due to the introduction of disease, but only two scenarios are of major concern to us. Both of them fall under the category of “arteriosclerosis,” which means hardening or thickening of the arteries. However, there are actually two kinds of this hardening of the arteries. The first type occurs when calcium deposits in the middle layer of the artery accumulate and make the artery become brittle and hard. Thus, this condition is sometimes associated with the term “pipe stem” artery. This calcification does not necessarily block the blood flow, and is usually harmless from the medical perspective. Unfortunately, I cannot the same for the other condition, as it is more common and has much more serious consequences. This condition involves the thickening of the inner wall of the artery by deposits of fats, cholesterol (a fatty alcohol) and fatty acids together with calcium. As these deposits build up, the passages of the arteries become much narrower, similar to the way the drain in a kitchen sink becomes clogged with grease deposits. As a result, less blood (that your body depends on for life) flows to your vital organs due to the constricted and narrowing openings, as 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 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?
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, 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.
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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