Abstract

Trans fatty acids (t-FA) are geometrical isomers of unsaturated fatty acids that assume a saturated fatty acid-like configuration. Human diets contain t-FA derived from animal sources (e.g., dairy products and ruminant meats), but most are supplied by products containing industrially hydrogenated vegetable oils (e.g., margarines, shortenings and baked goods). Typical intake of t-FA in American diets has been estimated to be between 8-15 g/day, although wide variation exists between individuals. Human clinical studies since 1990 have revealed that relative to cis-monounsaturated fatty acids (i.e., oleic acid), t-FA increase total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C), and tend to decrease high density lipoprotein cholesterol (HDL-C) concentrations. Additionally, t-FA tend to increase the atherogenic lipoprotein (a). Thus, t-FA induce an adverse plasma lipid profile (increased ratios of TC/LDL-C and LDL-C/HDL-C), which represents increased risk for coronary heart disease. The effects of t-FA on LDL-C and HDL-C appear to be directly related to intake and clinically measurable above 3%en as t-FA. The cholesterol-raising ability of t-FA is analogous to that of the 12-16 carbon saturated fatty acids, possibly reflecting increased LDL production or delayed LDL clearance. By contrast, t-FA are unlike the saturated fatty acids in their depression of HDL-C. Preliminary evidence suggests that at least part of their impact on lipoproteins reflects increased serum cholesteryl ester transfer protein activity, i.e., increased transfer of cholesteryl esters from HDL to LDL. Since the adverse effects of t-FA on human plasma lipids may be confined to specific isomers, future studies delineating their effects are warranted.

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