by Ernest N. Curtis M.D. ( Internal Medicine and Cardiology )
A delusion is a false belief held with conviction despite incontrovertible evidence to the contrary. In the medical field no delusion has had wider acceptance and a longer run than the belief that cholesterol levels in the blood are a major factor in the causation of atherosclerosis and its two chief complications - heart attack and stroke.
Known as the Lipid Hypothesis or Cholesterol Theory, the seeds of this delusion were sown in the late 19th century by a German pathologist named Rudolph Virchow. He performed chemical analyses on arterial plaques taken from corpses and discovered that they contained large amounts of cholesterol. He theorized that cholesterol from the blood infiltrated the walls of the arteries and thus caused the plaques he found there. He called this process lipid insudation.
Further credence was given to this theory when researchers in the early 1900s fed rabbits and chickens a pure cholesterol diet and reported deposits on the arterial walls that they thought were atherosclerotic plaques.
At this point it was thought that all the cholesterol in the blood came from the diet. But in 1925 it was found that the human body produces 80-90% of its own cholesterol and that diet is relatively unimportant. This caused some to raise questions about the validity of the Cholesterol Theory.
Unfortunately it took many years for scientific technology to advance to the point where investigators could tell that the arterial lesions found in the cholesterol-fed chickens and rabbits were different from those in true atherosclerotic plaques. In fact they more closely resembled the arterial deposits seen in people afflicted with a rare type of genetic cholesterol storage disorder. Moreover, these lesions did not progress on to ulcerate or fissure and cause thrombotic complications such as heart attack and stroke.
The delusion was further reinforced by publication of results from the Framingham Study in the 1960s. Initiated in 1948 under the auspices of the NIH, this study sought to enroll as many healthy people as they could between the ages of 30 and 62 in the town of Framingham, Massachusetts.
These subjects filled out detailed questionnaires regarding their dietary patterns, levels of exercise, numbers of cigarettes smoked daily, etc. They were then closely followed to see who died, had heart attacks, or other symptoms of CHD. The collected data were then analyzed to see if there were correlations between certain factors and the subsequent development of CHD.
After about 20 years the investigators felt they had enough data to say that there were significant correlations between high blood pressure, cigarette smoking, and elevated cholesterol levels with the later development of CHD. Thus the concept of "risk factors" for heart disease was established.
But in fact the correlations were quite weak and subsequent analysis has shown that none of the relationships for dietary fat or cholesterol are significantly related to the later development of heart disease.
By this time researchers and academics who were convinced that diet and elevated blood cholesterol were major causes of CHD were firmly in control of the National Heart, Lung, and Blood Institute (NHLBI - a branch of the NIH) and the American Heart Association - the two organizations responsible for the bulk of the funding for heart related research. They felt the time was then ripe for clinical trials to confirm the idea that lowering cholesterol would serve to reduce the incidence of CHD.
The Coronary Drug Project enrolled about 8000 men with a history of heart attack. They were divided into five groups of about 1000 each and a control group of about 3000. Each of the five treatment groups took a different drug and the control group a placebo.
Two of the five treatment groups took different doses of estrogen and the other three thyroid hormone, clofibrate, and niacin. Estrogen was given on the theory that it might be what afforded relative "protection" against heart attack to women while the other three all worked to lower cholesterol by different mechanisms.
Unfortunately, so many excess deaths occurred in the two estrogen groups and the thyroid group that the double-blinded coding had to be broken and the trial stopped prematurely. The clofibrate and niacin treatment groups showed no significant benefit when compared to the control group.
The next major undertaking was the Multiple Risk Factor Intervention Trial (MR.FIT). Over 360,000 healthy middle-aged men were screened and about 12,000 with the highest risk factor profile were selected. Most were heavy smokers, hypertensive, and had elevated cholesterol levels.
The treatment group was given intensive dietary education and advice designed to reduce fat and cholesterol consumption and increase the intake of polyunsaturated fats. Their blood pressures were aggressively treated and they were subjected to a number of interventions to reduce or eliminate cigarette smoking. The control group merely remained on their normal diet and continued their same level of smoking and blood pressure control.
The study was successful in the sense that the treatment group achieved and maintained significant reductions in fat and cholesterol in the diet, cut way down or eliminated smoking, and reduced their blood pressure readings considerably. But after 10 years of followup, there was no significant difference between the two groups in either CHD mortality or total mortality.
After a Residency in Internal Medicine and a Fellowship in Cardiology, he entered private practice in Long Beach, California.