The treatment of atherosclerosis has for many years centered around attempts to lower the serum cholesterol level. The rationale for such therapy rests entirely on the statistically significant correlation which exists between coronary atherosclerosis and elevated serum cholesterol levels.1 However, it has yet to be shown that reduction of serum cholesterol significantly modifies the course of coronary atherosclerosis. In fact, there is evidence that the serum cholesterol is not a true reflection of tissue cholesterol levels, and, therefore, definitive evaluation of any therapy can only be obtained from long-term clinical studies based on the incidence of myocardial infarction and on survival. Nevertheless, because of our almost total ignorance of the etiology of atherosclerosis, the best available field for the clinical investigation of atherosclerosis remains the experimental reduction of the total cholesterol stores of the body.
The cholesterol content of the body can be lowered in three ways: