Alpha-linolenic acid and metabolism of cholesterol and long-chain fatty acids.

Animal studies have demonstrated that dietary 18:3n-3 reduces 20:4n-6 content in plasma and tissue lipids. At megadose levels of 18:3n-3, the reduction in phospholipid 20:4n-6 is brought about by a combination of inhibition of desaturase activities and redistribution of 20:4n-6 from phospholipids to neutral lipid pools. The shifting phenomenon is not apparent when the dietary level of 18:3n-3 is low. Dietary 18:3n-3 reduces cholesterol levels in blood and liver tissue; however, the mechanism by which this effect is mediated is not known. Further studies are warranted to investigate the role of dietary 18:3n-3 on cholesterol biosynthesis, storage, and mobilization into and from the tissues and on the secretion of cholesterol into bile. The effect of the ratio of dietary 18:2n-6 to SFA as a determinant of 20:4n-6 and lipid-lowering effects should be further explored in human subjects. It is important to elucidate whether dietary 18:3n-3 interacts with other nutrients to modulate the parameters implicated in the pathogenic processes. The optimum level of dietary 18:3n-3 required to obtain health beneficial effects needs to be determined. Specific effects of dietary 18:3n-3 on low- and high-density lipoprotein cholesterol levels also deserves further investigation before any recommendation to achieve health benefits can be made.