Fat On Trial. Part 1

In 1911, in Moscow, Russia, a scientist named Anitschkow made the first discovery that later led to the identification of fat as the killer in cases of hardening of the arteries. He gave us the first clue to the role that fat in the blood vessels plays in causing heart attacks and strokes. Professor Anitschkow, now a vigorous 86, fed animals with cholesterol, one of the purest of fats. He found that the arteries of these animals became blocked with fatty deposits, in a manner indistinguishable from the blocking found in human arteries. The experiment also brought about premature aging in the animals; they grew old and suffered a loss of health and general vitality long before their time. It was only after a gap of more than a generation that scientists got on the track of the killer fat, but now the pursuit is highly active all over the world. The culprit is now on trial, and evidence for his conviction is steadily mounting.

Here is how I entered the race. Some 20 years ago, with research assistance from the American Medical Association, I was working on the development of a new treatment for cirrhosis of the liver caused by alcoholism. I was feeding fats, including cholesterol, to experimental animals for the purpose of producing cirrhosis in them. New chemicals were than to be tested, to see whether one of them might be useful in curing this disease. To my amazement, I found that in feeding the fat, I not only produced the liver condition, but that the heart blood vessels of the animals became plugged with fat, mostly cholesterol. Within a short time, the animals developed heart disease, just as it occurs in humans, and suffered changes common to human beings with atherosclerosis. This was a fascinating discovery. It excited my interest in the challenging problem of fat and its effect on the heart, and stimulated me to continue searching for clues and answers to this universal illness, which causes more deaths than any other disease. My co-workers and I decided to carry the hunt still further. We wanted to track down this killer and to discover, if we could, how to ward off his devastating attack. This is how we went about it. First, we looked for the answer to this question:

Is cholesterol and excess fat present in the blood of everyone with atherosclerosis? The answer came to us after two years of work. We studied 200 patients who had had heart attacks and discovered that the great majority, and particularly those under 60, suffered from an excess of fats in their blood. Other patients who showed a normal level of cholesterol had other blood fat abnormalities. For it soon became clear that cholesterol was not the only important heralding factor announcing the approach or actual presence of atherosclerosis. Several other fat components were involved as described in Chapter 2: beta lipoproteins, fat enzymes (see Chapter 2) called cholesterol esterases, large fat globules circulating in the blood after a meal, called chylomicrons, and special large complexes of fat molecules discovered by Dr. John Gofman and his team of biophysicists. At present we now know that excesses or abnormalities in any one or more of these five "public enemies" are directly connected with the production of a heart attack, a stroke, or other complication of atherosclerosis. It is therefore perfectly possible to have a normal cholesterol blood level and yet have some of the other above abnormalities in the fat chemistry of the blood that help produce a heart attack or stroke. To date, in two study groups of atherosclerosis, the cholesterol factor has been found to be the predominant one. This is due to the fact that it is a very frequent finding in atherosclerosis, and also because of the great difficulties encountered, both by physicians and scientists, in measuring the other four culprits mentioned above in the development of atherosclerosis.

What about the factor of heredity? As research information piled up, another fact became clear. Of the 200 people studied, a substantial number had a family history of heart attacks or strokes. That is, members of their families were particularly susceptible to these two diseases. The patients we were working with seemed to be unfortunate links in an heredity chain. Later, Dr. David Adlersberg and Dr. Charles Wilkinson, Jr., discovered that in some cases an excess of cholesterol in the blood was an inborn error of fat metabolism. Inability of some people to handle fat in their systems made them especially prone to atherosclerosis. This hereditary tendency could sometimes be traced accurately through the family of a patient; in those cases where the tendency was strong, deposits of fats in the arteries and skin could be predetermined, according to Mendelian, or genetic laws of inheritance. One unforgettable case that is an example of the hereditary factor was that of Mrs. S. She was admitted to my teaching ward service in the hospital 10 years ago in a state of shock and coma from an excruciating chest pain. This young woman, only 29 years old, had been ironing clothes in her home when she apparently was seized by a sudden, lightning-like pain. In a fainting condition, Mrs. S. had collapsed to the floor. She fell with a cry, and her little girl, aged 5, also cried out and summoned the neighbors. After only a few minutes in the hospital the patient expired, despite heroic efforts by our interne and resident, as well as physicians and nurses who were on duty at that moment.

Examination of the heart following death revealed to our surprise that Mrs. S. had a coronary thrombosis from extensive atherosclerosis. This was a rare cause of death in so young a woman, but one nevertheless that is occurring with greater frequency. We immediately suspected a hereditary cause in her death and questioned the family, with the following results: The mother of Mrs. S. was in good health as late as age 56. However, the father had died at age 40 of a heart attack while driving an automobile. His only other brother had also died of a heart attack at age 52. Mrs. S.'s paternal grandfather had died of a heart condition in his fifties and his own brother had died of a "stroke." Mrs. S. had no sisters and only one older brother, who was 32 years old and suffering from angina pectoris. (This is a heart condition caused, in most cases, by atherosclerosis of the coronary arteries.) This strong family trend towards the incidence of a coronary artery disease and atherosclerosis is a striking example in the case of Mrs. S., although in this case at an unusually young age. At least one-third of the usual cases that I see in private practice, as well as those seen by other physicians of heart disease, are found to have a history of either heart attacks or "strokes" in the family. When this atherosclerotic coat of arms has been handed down in a family, it is vitally necessary that double precautions be followed in strict adherence to the nutritional program set forth in this book. Still another characteristic example of the powerful influence of inheritance in the development of atherosclerosis is the case of Mr. J., aged 39. This patient suffered from pains in both calves of the legs whenever he walked for distances more than a block. He would have to stop and rest until the pains would subside, before he could continue again. We found a typical advanced degree of atherosclerosis of the arteries affecting both legs. The father of Mr. J., a bank official, had already suffered a coronary thrombosis when he was 56. His two older brothers, in turn, had each died of the complications of atherosclerosis - one from a heart attack, and the other from a "stroke." Mr. J. had one sister, age 52, who was troubled greatly by swellings in the ankles of both legs, which were discovered to be caused by Bright's disease* This condition, sometimes called "dropsy" in the old days, is caused by atherosclerosis or "hardening of the arteries," in the kidneys. This is still a very widespread condition and one that accounts for much sickness and death throughout the world, although it is an insidious process, like its fellow "assassins" in the heart and brain.

Mr. J.'s case was so advanced that nutritional care, diet, and weight reduction were of no avail and surgery had to be resorted to. By an ingenious technique, a team of four vascular surgeons who were experts in blood vessel surgery, grafted or transplanted two sets of new arteries in both legs, taken from blood vessel "banks." These storage "banks" keep normal healthy blood vessels available for operations and emergencies in the same way that blood is stored in blood banks for blood transfusions. Mr. J. almost lost his life during the eight-hour operation but is now fully recovered and walking normally again. However, he does follow the low-fat diet and nutritional program that apparently has arrested the progress of his former atherosclerosis and is well and vigorous once more.