The Science of life," wrote the 19th Century French physiologist Claude Bernard, "is a superb and dazzlingly lighted hall which may be reached only by passing through a long and ghastly kitchen."
In the United States of the 20th Century we are, as Bernard predicted, spending a lot of time in the kitchen, trying to determine what in our diet might be killing us. This search has followed some unique paths: Charcoaled steaks were once believed to cause cancer and the suggestion that saccharin does the same has sent dieters, scientists and politicians into a frantic scramble for data to support or refute the association.
Through all these years of controversy, new discoveries, warnings and public skepticism, however, one theory has been steadily increasing in popularity and, as announced last week by the National Institutes of Health (NIH), has produced major changes in the American diet. The villain is cholesterol, and the theory that a diet loaded with saturated fats and cholesterol increases the risk of heart disease has encouraged many persons to cut in half their intake of cholesterol-rich foods. The result is 5-to-10 per cent drop in our average cholesterol level over the last 10 years.
This dramatic change in diet is the result of intense publicity by private interest in groups, especially the American Heart Association, combined with growing pressure from food companies which now offer a wide variety of cholesterol-free food.
These findings also raise the question of what role the federal government should assume in regard to dietary cholesterol, for the NIH survey demonstrated that the dietary change is not uniform. The drop in cholesterol is largely confined to the well-educated, higher-income portion of our population, the same group currently thought to be the major benefactor of a progressive decline in the proportions of the coronary heart disease epidemic.
In 1976, the death rate from coronary heart disease fell below 200 deaths per 100,000 population -- its lowest level in 35 years. But heart disease, formerly "an affliction of the wealthy," is becoming relatively more common within the poorer segments of our population.
To date, Washington has taken a cautious attitude toward this problem. The first official condemnation of cholesterol by any branch of the federal government didn't occur until last January, when the Senate Select Committee on Nutrition included the recommendation that our daily intake of cholesterol be reduced to 300 mg (about 1 1/4 eggs) as one of its six "Dietary Goals of the United States." One reason behind this government reluctance, which also could have major implications for future public health decisions, can be seen in the reactions to the committee's report.
On March 24, in special hearings called by the Nutrition Committee chairman, Sen. George McGovern, and attended by an unusually large and powerful group of senators including committee members Kennedy, Dole, Percy and Schweicker, an angry group of representatives from the nation's beef producers and feeders criticized "Dietary Goals of the United States" -- especially the one concerning cholesterol -- as based on insufficient evidence and potentially harmful to their industry.
In April, the American Medical Association issued a statement saying it was "inappropriate to recommend radical dietary changes" and suggested that the committee's recommendation that low cholesterol dietary instruction be instituted in all public schools not be adopted.
The Government Printing Office has been instructed to stop publication and distribution of "Dietary Goals for the United States," and the committee has reopened the already lengthy hearing record with testimony scheduled for July 26 from the AMA and the American Egg Board.
What eventually happens to the committee's six dietary goals, -- which, in addition to recommending limits on the amount of cholesterol and saturated fat eaten, suggest cutbacks in the daily consumption of salt and sugar -- will provide a unique picture of the balancing of public health, economic and political considerations.
It also will be a barometer of exactly how much scientific information is needed before a branch of the federal government will voluntarily endorse preventive measures affecting large portions of the population. For, unlike saccharin, whose continued use is potentially harmful to an estimated 400 persons per year -- the number of bladder cancer cases believed caused by saccharin -- coronary heart disease is still this nation's most common cause of death, with 647,000 victims recorded in 1976. And, unlike the one or two studies relating saccharin to cancer, there is extensive and detailed scientific information with which to judge the current status of the cholesterol controversy.
Persons who believe excess cholesterol is hurting us point to dozens of epidemiologic or population surveys that establish a direct statistical association between the level of blood cholesterol and the death rate from coronary heart disease.
Since the original study in 1916 performed by a Dutch physician, C.D. DeLangen, practicing in Java, population surveys have been done in such diverse places as Framingham, Mass., Chicago, Tel Aviv and Johannesburg. From these surveys a monotonous and frightening pattern emerges. People who eat large amounts of meat, butter and saturated fat have higher levels of cholesterol than people who don't and the higher a person's cholesterol level the greater the risk he or she will develop heart disease.
Further, persons with familial hypercholesterolemia, a rare genetic disease whose unfortunate victims have extremely high levels of blood cholesterol because their cells lack cholesterol receptors, usually die before age 20 of heart disease. In one case, a heart attack occurred in a 1 1/2-year-old South African girl.
The milder form of this same genetic deficiency, where each cell has only half the normal number of cholesterol receptors, is one of the most common genetic or inherited diseases in this country, affecting 1 out of every 500 Americans. These persons also develop heart attacks, usually in their mid 30s and 40s, and account for a large number of persons with early or "premature" death from coronary heart disease.
Still, statistical associations and the behavior of a genetic disorder do not provide proof that cholesterol causes heart disease and certainly don't account for the size of the problem in this country. Causing Atherosclerosis
A Therosclerosis is the pathologic or disease process responsible for heart attacks and other coronary heart problems. The name is derived, in part, from the Greek word athera, meaning gruel. It refers to the thick, sticky, yellow substance that oozes out of arteries affected by atherosclerosis when cut at autopsy. This yellow gruel is pure cholesterol.
Our coronary arteries, five pencil-sized tubes beginning at the base of our aorta, the main artery of the body, and supplying our heart muscle with blood, are believed to be so frequently affected by atherosclerosis because of their strategic location.
Each coronary artery begins its path at sharp right angles to the main flow of blood pumping out of the heart. This bend makes the initial stream of blood flowing into the artery rough and turbulent, like water gushing out of an open fire hydrant. The harsh stream of blood pounding on the delicate inner lining of the coronary artery 60 times each minute will occasionally cause a tear in its surface. And, once this tear occurs, it's believed that cholesterol finds its way into the arteries' wall.
Then, like a fallen tree in rapidly flowing water, this collection of cholesterol attracts passing cells and other debris that make up an atherosclerotic plaque. The plaque grows and can eventually block an artery, producing a heart attack.
Therefore, accepting this theory of injury followed by cholesterol collection, there appear to be two ways to prevent atherosclerosis and thereby reduce heart disease. One is to reduce the chance of injury to the artery. The best way currently known to reduce turbulence and injury is to control abnormally high blood pressure. The other approach is to lower the level of cholesterol.
The amount of cholesterol in our blood is a delicate balance depending on four factors: what we eat, how much our cells use, how much is broken down and excreted in the stool and how much our body makes. Seventy-five per cent of our cholesterol is made in our liver and, to date, we have no control over it. But through diet and, occassionally, drugs, we can change the other factors.
Much of our current knowledge describing the way cholesterol is metabolized comes from the results of meticulous work performed in the laboratory of E. H. Ahrens Jr., professor of medicine at Rockeller University.
"The main reason working with cholesterol is so difficult," Ahrens explains, "is being it stays in the body for such a long time."
Two months after giving a patient a test dose of cholesterol, half of it is still present. To complete a project, Ahrens and his colleagues have to study their subjects for three months, checking their bowel movements for cholesterol loss.
From such experiments we know that dietary cholesterol cannot be absorbed alone into our intestinal wall. It must first be combined with bile, proteins and other fats into a small transferrable package called a micelle. The formation of micelles depends on the amount of fat in our diets and, using this pickup system, a person will absorb from 30 to 80 per cent of the cholesterol eaten. Where in this range each of us falls and what happens to our cholesterol levels as a result of our diet is a very indidual matter. Transporting Fats
ONCE ABSORBED, cholesterol, along with other fats and proteins, is combined into a tiny milky white droplet called a chylomicron for its passage from our intestine to our bloodstream. Following an especially fatty meal, thousands of these chylomicrons shower our bloodstream like drops of milky oil poured into water. But the cholesterol contained in chylomicrons does not contribute to the slow, gradual growth of the underlying atherosclerotic plaque. Chylomicrons stay in our blood-stream but a few hours following a meal. The body has a separate system to carry out the day-to-day transport of fats, proteins and cholesterol. Like a fleet of trucks, this internal transport system is classified by weight.
There are the light pickups known as very low-density lipoproteins (LDL) which, along with their other freight, carry cholesterol manufactured in our liver to other parts of the body. Then there are the heavier low-density lipoproteins which move cholesterol from cell to cell and serve as the keys to unlock the cell's cholesterol receptors. Finally, there are the garbage trucks, high density lipoproteins (HDL) which pick up excess cholesterol and return it to the intestine where it is disposed of.
The cholesterol traveling with the LDL is the portion that gets trapped inside arteries. Therefore, the amount of a person's total cholesterol contained in the LDL carrier is of crucial importance in the development of atherosclerosis. LDL cholesterol can be decreased by a diet high in polyunsaturated fats.
Likewise, the higher levels of HDL found in marathon runners and premenopausal women are thought to protect these groups by clearing cholesterol out of their systems more efficiently. The exact meaning of the HDL cholesterol transport vehicle still needs to be fully explained but, for once, a high level of something appears to be good.
Therefore, as viewed from the limited perspective of our internal anatomy, it appears our current faith in the cholesterol theory is well founded. We know cholesterol is the main substance found inside atherosclerotic plaques. We know our bodies need far lower levels of cholesterol than most of us have. We have shown that, although there are large individual differences, many of us can reduce the amount of cholesterol in our blood-stream by changing our diet. And, finally, there is early but encouraging evidence that exercise, by increasing the amount of HDL, may decrease the risk of heart disease by changing the form in which cholesterol is transported.
The only thing left to prove is that, by lowering cholesterol, you save lives.
In the past four years, three separate studies using clofibrate, a cholesterol-lowering drug, have tried to prove this. The studies involved 5,106 men and women, each of whom had suffered at least one heart attack. All three studies had failed to show any difference in the number of new heart attacks or deaths.
Despite these negative results, cholesterol-lowering drug sales reached $38 million last year with Atromid-S (the brand name for clofibrate) accounting for $27 million. Clofibrate has recently been critized by Ralph Nader's Health Research Group for causing gallstones, although this has long been recognized as a complication of its cholesterol-lowering effect.
Of greater importance than clofibrate's potential toxicity, however, is the question of why all those studies failed to show any benefit. Is the drug worthless? Some scientists believe the failures are not drug-related but because we've given cholesterol too much importance. Like many of the experimental animals used in cholesterol testing, rabbits don't normally eat the stuff. When it's forced into their stomach, however, they can absorb four times more of it per pound than humans. They are literally drowning in cholesterol.
Most researchers still believe that the relationship of cholesterol to heart disease is to strong not to test it more thoroughly before discarding it. They attribute the failure of the clofibrate studies to the fact that cholesterol was only slightly reduced (generally from 5 to 10 per cent) and that the patients were too old and had already developed heart disease.
Through a group of 12 cholesterol research clinics, one located at George Washington University, and at a cost of $100 million, the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health hopes to determine whether further lowering of cholesterol in a younger population will help. In this study, 3,800 men between the ages of 30 and 50 who have never had heart disease but whose cholesterol lovels put them in the upper 5 per cent of the U.S. population (a level above 265 mg with most of it in the LDL form) will be placed on a low-cholesterol, high-polyunsaturated diet.
In addition, half the 3,800 will be given another drug, choleystramine, which interferes with the formation of micelles and thereby reduces the amount of dietary cholesterol absorbed. All the men will be followed for five years and, if the study's goal of a 25 per cent reduction in blood cholesterol is achieved with enough of the participants, it will be the most vigorous test of the cholesterol hypothesis to date. Other Factors
THE RESULTS of this Lipid Research Clinic study will not be available for a number of years, definitely not in time to influence the committee's decision this summer. Most researchers, however, are not waiting for these results. A recent survey of 182 scientists around the world found that 92 per cent of them had already changed to a low-cholesterol diet.
The just released NIH survey found that, over the past 10 years, the average amount of cholesterol Americans eat dropped from 800 mg to 400 mg and the ratio of saturated to unsaturated fat has decreased from 3:1 to 1:1, the American Heart Association's recommended level. Another study has discovered a simultaneous drop in the average level of cholesterol in our blood from 226 mg to 221 mg.
But does this drop in cholesterol levels and the change in our diet account for the gradual but persistent decline in our death rate from coronary heart disease?
"No way to tell," Dr. Robert Levy, director of the NHLBI, admits. "In addition to the dietary changes, we also know that middle-aged white males, the ones most often affected by coronary disease, are smoking 25 per cent less and exercising more than they did 10 years ago. It could be any one or all these factors," the NIH official concludes, "or none of them."
Despite this uncertainty, Dr. Levy does observe that the greatest decrease in the coronary death rate has occurred within the affluent portion of our population, the same fraction that is thought to be most closely observing the dietary and exercise recommendations. Nevertheless, despite all this encouraging evidence, don't expect the NIH to join the Senate Nutrition Committee in an official condemnation of cholesterol.
"The scientific jury is still out on the cholesterol question," says Dr. Levy, "and the public has already been placed in the middle too often by scientists supporting one theory or the other.
"No, this time the choice should be up to the individual, not the government."
Dr. Levy is not scheduled to testify at the Senate hearings this month; he presented testimony on the cholesterol issue last year. Indeed, the committee heard extensive scientific evidence pro and con on the cholesterol question before it published its dietary goals.
Despite scientific caution, the guidelines finally were issued, according to a nutrition committee staff member, "because the American people need this type of dietary information to offset the tremendous influence of food advertising and pricing practices. Without this report, the consumer has nowhere to turn for help. We're just trying to balance the situation."
In light of the NIH findings, a better balance in regard to individual dietary information appears needed. Nevertheless, since its January report, the committee has had no response from other branches of the federal government, while the staff and members of the committee, which is scheduled to go out of existence on Dec. 31, have spent their time listening to the disquieting voices of industries at risk if further dietary change occurs.
among those scheduled to testify on July 26 is G. C. Bookey, vice president of the American Egg Board, an organization established in 1974 under the Egg Research and Consumer Information Act. Last year, the board spent $5 million advertising its product, "the incredible edible egg," attempting to reverse what has been a steady decline in the number of eggs eaten in this country since 1950. The egg board also supports research to support preliminary findings demonstrating that a diet high in eggs does not automatically increase the level of cholesterol in a person's blood.
The reception accorded Bookey, if it is anything like that given last March to Wray Finney, president of the American National Cattlemen's Association, will be friendly. In his opening remarks to that hearings. Sen. McGovern acknowledged that 75 per cent of his state's agricultural income results from the sale of live animals. In response, he and other committee members were told that the beef industry is having a difficult time. Although beef consumption per capita is up, the nationwide prices are at or below their cost of production and, since domestic consumption accounts for 90 per cent of all meat sales, any decrease in consumer demand would be damaging.
But judged from the other perspective, the stakes are also high. There are 4 million persons in the United States today affected by coronary heart disease. Their total medical bill is estimated to be $40 billion per year.
A recent survey of a school district in Massachusetts discovered that 13 per cent of the children had higher than average cholesterol levels. Considering what we now know about cholesterol, at least some of these children could have their levels lowered by an appropriate diet and, if the cholesterol-heart disease association is later demonstrated to be true, perhaps spared the effects of heart disease as adults.