Low-Fat Approach to Health
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.
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.
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?
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, 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 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.
Carl Juneau teaches men how to get six pack abs using a special mix of carefully sequenced abs exercises. Visit his site to discover powerful abs workouts that help to tone and define your abs.
Did you enjoy this post? Why not leave a comment below and continue the conversation, or subscribe to my feed and get articles like this delivered automatically to your feed reader.
I need some advice for my blog….I like your layout. Can you help me?