Abstract
A series of studies in monkeys and hamsters, and reevaluation of published human data, indicate that dietary saturated fatty acids exert a dissimilar metabolic impact on cholesterol metabolism. Myristic acid(14 : 0) appears to have a major cholesterol-raising effect by means of decreasing LDL receptor activity and by increasing the direct production of LDL (from sources other than VLDL-catabolism) Palmitic acid (16 : 0) appears neutral in most cases (plasma cholesterol<200mg/dl) or until the LDL receptor is down-regulated, as with high cholesterol intake or obesity. In such cases. the down-regulated LDL receptors coupled with an increased VLDL production (induced by 16 : 0 and 18 : 1) can divert VLDL remnants to LDL and expand the LDL pool. Furthermore. the cholesterolemic impact of any saturated fatty acid can be countered up to a saturable 'threshold' level by dietary linoleic acid (18 : 2) which up-regulates the LDL receptor. Once above this 'threshold' the major fatty acids (16 : 0, 18 : 0, 18 : 1, 18 : 2, 18 : 3) appear to exert an equal impact on the circulating cholesterol concentration.