Abstract
Both 18:2n-6 and 18:3n-3 fatty acids contribute to lowering total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) if an individual is below their polyunsaturated fatty acid (PUFA) threshold requirement. Generally speaking, the appropriate intake of 18:2n-6 at or near the 18:2 requirement facilitates lipoprotein metabolism by reducing LDL and increasing high density lipoprotein (HDL), if either lipoprotein fraction was not being metabolized at maximal efficiency at the time of intervention. At high intakes of 18:2n-6 (>200% energy) HDL-C also becomes depressed as very low density lipoprotein (VLDL) output decreases and HDL-C removal increases via enhanced activity of hepatic triacylglycerol lipase (HTGL) and hepatic scavenger receptor-B1 (SR-B1) receptors. The main effect of n-3 high unsaturated fatty acids (HUFAs) at moderately high levels is to depress plasma triacylglycerols (TG) and postprandial lipemia via depressed output of VLDL and chylomicrons, respectively. In humans, n3-HUFAs typically increase LDL-C slightly, whereas HDL-C remains largely unchanged.