Atherosclerosis is a major cause of death in the United States. Epidemiological studies have discovered an inverse risk-factor relationship between HDL and atherosclerosis as well as a positive correlation between LDL and atherosclerosis. Recent studies in animals and man indicate that substantial quantities of high density lipoprotein precursers including lecithin and A-1 are synthesized in the intestine and may enter the lymph on chylomicrons. Lecithin (phosphotidylcholine) is a major component of the surface chylomicrons acting as a major emulsifier of the chylomicron neutral lipid. In HDL lecithin is one of the two substrates for the lecithin-cholesterol acyltransferase (LCAT) reaction which converts free cholesterol and lecithin into cholesterol ester and lysolecithin. It is known that HDL can remove cholesterol from cells and LCAT may facilitate this process by converting free to esterified cholesterol. While the source(s) of the HDL components (particularly lecithin) is not completely known, a good working hypothesis is that some, perhaps a major portion, come from the surface of chylomicrons. Chylomicrons are synthesized and assembled in intestinal epithelial cells. Much of the lipid in chylomicrons comes from lipid in the intestinal lumen (e.g. largely from dietary and bile sources). Dietary and biliary lecithin is largely hydrolyzed to lysolecithin and fatty acid in the intestine. However, with an increase in intraluminal lecithin concentration, a greater percentage of chylomicron lecithin is derived from the absorbed lysolecithin moiety. The question is, what is the ultimate effect of pure dietary lecithin given in the presence of a normal diet on the composition and concentration of high density lipoprotiens and their precursors? Or more simply can a dietary supplement of pure lecithin increase HDL concentration and/or alter HDL distribution, composition and physical properties? To answer these questions we will feed large amounts of pure plant derived lecithin rich in linoleic acid, to normal subjects and measure the quantities, composition and physical properties of the HDL fractions appearing in the serum after both short and long term lecithin ingestion. Further, since dietary supplementation of polyunsaturated lecithin may also effect other lipoprotein levels, composition and properties (for instance the cholesterol ester composition and thermal transitions) V (Text Truncated - Exceeds Capacity)