Some years ago authorities thought that they were beginning to see daylight when they discovered that persons who were suffering from hardening of the arteries accumulated an excessive amount of cholesterol, a substance of fatty origin, in their blood, and that when this substance was deposited within the confines of the arteries it caused sores or lesions, which were followed by hardening of the arteries.
Cholesterol is found in large quantities in the fatty foods of animal origin such as eggs, milk, butter, cream, as well as the fatty meats and fish. It seemed logical to assume that by controlling the intake of these foods hardening of the arteries could be eliminated or greatly lessened.
However, many of our authorities were not satisfied with this assumption. Although they were aware that a restriction in the intake of the cholesterol-rich foods benefited their patients, they were still confronted by questions that seemed baffling. For one thing, they noticed that many persons who consumed large quantities of the cholesterol-rich foods did not suffer from hardening of the arteries; for another, further research disclosed that not all types of cholesterol, but only a special type, giant cell cholesterol, caused damage.
Finally, they began to realise that hardening of the arteries does not develop merely from an intake of cholesterol-rich foods, but from a faulty utilisation of them.
Research at many of our institutions confirmed this fact. The US. News & World Report14 reported on the work done by scientists in different institutions, including the Heart Institute of the National Institute of Health in Washington, which proved that certain key substances (hormones) that normally break up our fat foods are lacking in persons suffering from these diseases. It further stated that our scientists are now working feverishly in the hope of discovering the missing element or elements so that where necessary they could be supplied to sufferers from these
We wish it were as simple as that! An examination of the results of hormone therapy in other metabolic diseases such as diabetes and arthritis will reveal how ineffective this type of treatment can be.
William S. Gailmor, discussing this subject, referred to the work of Dr. Wm. D. Kountz of the Washington University of Medicine, St. Louis, Mo., who based his work on the fundamental research of Dr. Timothy Leary of Tufts University and the so-called anoxemia (lack of oxygen) theory of Dr. Wilhelm C. Hueper, President of the American Society of Arteriosclerosis. Dr. Kountz demonstrated conclusively that A thyroid hormone deficiency, by preventing metabolism or absorption of a fatty substance (cholesterol) into the tissues, allows it to accumulate in the arteries, ultimately causing the characteristic âœhardening.â 15
Stephen M. Spencer in an article in The Saturday Evening Tost referred to the work of Dr. John Gofman, who demonstrated that just as diabetics cannot handle sugar, so according to this theory, certain people cannot handle their butter and eggs as efficiently as the rest of us can.16
That the excessive accumulation of cholesterol in the blood is due to an impairment of metabolism, and that it is only one of the many changes which occur in the body as a result of this impairment, is now being recognised to an ever greater extent.
Waldemar D. Kaempffert, former science editor of The New York Times, referring to the work of Drs. Alfred Steiner, Forest E. Kendall, and James Q. L. Mathers of the Department of Medicine, Columbia University, says that the relative level of phospholipids and cholesterol may be as important in the development of arteriosclerosis as the increase in the level of cholesterol itself.17
Dr. Meyer Friedman, Dr. Ray Rosenman, and Dr. Sanford Byers of the Harold Brunn Institute of Mt. Zion Hospital, also challenging the idea that cholesterol is the sole cause of arteriosclerosis, mentioned that while it was thought that cholesterol caused an increase in phospholipids, research at the Brunn Institute disclosed that the increase in phospholipids precedes and causes an increase in cholesterol and as such cholesterol is an effect, not a cause.18
Deposits of cholesterol, a fatty alcohol, on the walls of the arteries, are not the primary cause of hardening of the arteries. First come mucoid proteins, then cholesterol, and large globules of fatâ”sometimes. This is another report by Waldemar D. Kaempffert. It is based on the work of Drs. Henry D. Moon and James F. Rinehart of the University of California School of Medicine. Moon and Rinehart saw cases of arteriosclerosis where there were no cholesterol deposits at allâ”only these mucoid proteins, Kaempffert continues.
Drs. Moon and Rinehart19 did not overlook the presence of cholesterol deposits in these cases; they were merely not convinced that cholesterol was the primary cause of the hardening. They came to this conclusion by checking parts of arteries of persons who died suddenly, some from heart attacks, other from other causes. They checked samples of arteries of 250 persons ranging in age from four months to ninety years. They observed that the early changes in arteriosclerosis, especially in the coronary vessels of youngsters, showed slight thickenings of the innermost layer of the arteries, marked by an increase in the deposits of mucoprotein, by fibrous growths, and by breaks in the elastic tissue fibers, but not by deposits of cholesterol.
The second or later stage showed further accumulation of mucoprotein, the formation of hard, fibrous plaques in the walls of the arteries, and the presence of fatâ”but only sometimes cholesterol.
In the more advanced stages of arteriosclerosis parts of the arteries were hard and glossy looking, and deposits of large globules of fat (including cholesterol), and frequent deposits of calcium existed, causing narroVing of the arterial tubes and slowing down the flow of blood, which exposed the patients to the danger of the formation of fatal clots.
From all this, Drs. Moon and Rinehart concluded that fat metabolism becomes important only in the later stages of the disease and that the original trouble probably lies in how the body uses protein.
That a diet rich in starches and sugars can lead to the accumulation of fats in the blood and predispose to hardening of the arteries and to heart disease is another point also reported recently by Dr. Edward H. Ahrens of the Rockefeller Institute. Appearing at a meeting of the Association of American Physicians he made it amply clear that dietary carbohydrate, not fat, is the thing to watch in guarding against those conditions.20
We are stressing all this to show that by pinpointing only one of the many changes that occur as part of the metabolic disorder we fail to obtain a true picture of what actually takes place.
It should not be difficult for us to agree with Dr. Herman T. Blumenthal21 of the St. Louis Jewish Hospital, who concluded that hardening of the arteries may not be one disease but many and that even the metabolic changes which have received so much attention, may be the result rather than the cause of the aging and hardening of the arteries.
The primary objective should be to obtain a clear picture of the many facets that contribute to the breakdown in metabolism and lead to the onset of these diseases; only in this way can we understand how this condition can be counteracted or prevented.
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