Abstract
In recent years the association between dietary saturated fat, hypercholesterolemia, and coronary artery disease has been re-explored. Prompted largely by the notion that dietary fats, and their attendant fatty acids, can specifically influence the distribution of the plasma cholesterol between low density (LDL) and high density (HDL) lipoprotein cholesterol, the focus of the original research has shifted from total cholesterol to lipoproteins. Several new, sometimes controversial, concepts have arisen that challenge underlying assumptions of the Keys-Hegsted regression equations. First, although saturated fats as a class raise LDL, they also appear to have primary responsibility among dietary fatty acids for raising HDL, possibly depending on a balanced intake of polyunsaturated fats. Second, not all saturated fatty acids are equally responsible for changes in LDL or HDL. Only natural triglycerides (TG) rich in lauric (12:0) and myristic (14:0) acids are especially cholesterolemic, whereas 16:0-rich fats can be neutral or cholesterol-raising depending on the metabolic circumstances (lipoprotein setpoint) of the host. In normolipemic individuals with normal lipoprotein metabolism, dietary palmitic acid (16:0) typically appears neutral. When lipoprotein metabolism is impaired, eg, if LDL receptor activity is depressed by the presence of dietary cholesterol, consumption of 16:0-rich TGs can contribute to hypercholesterolemia. Although stearic acid (18:0) is typically considered neutral, exaggerated consumption of 18:0-rich fat (cocoa butter) lowers both LDL and HDL. Third, the saturated fat effect is related both to the dietary cholesterol load and the lipoprotein setpoint of the host, eg, 16:0 becomes progressively cholesterolemic as dietary cholesterol raises the setpoint.