From Ignatowski's demonstration1 in 1908 that a milk-egg-yolk diet produced aortic atheromatous changes in rabbits to Windaus' finding2 in 1910 of a high concentration of cholesterol and especially of cholesterol esters in the atheromatous plaques was a short step. Progress in control of cholesterol atheromatosis has, on the other hand, been painfully slow.
The logical first step of decreasing exogenous cholesterol intake fails in man because of rapidly increased synthesis in the liver and probably elsewhere. Whether saturated fats are rigidly restricted or replaced by unsaturated fats, whether cholesterol absorption is prevented (e.g. β-sitostěrol) or its turnover increased with excessive fecal loss of the bile acids (e.g. thyroid), compensating endogenous synthesis again soon opposes the hypocholesterolemic effects of these measures. Possible reduction of elevated plasma triglycerides by heparin (?) has an uncertain hypocholesterolemic effect subject to the same compensatory adjustments. At present there are no direct means of preventing