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American Journal of Clinical Nutrition, Vol 62, 655S-708S, Copyright © 1995 by The American Society for Clinical Nutrition, Inc
REVIEW ARTICLES |
Expert Panel: David B Allison, Margo A Denke, John M Dietschy, Edward A Emken, Penny M Kris-Etherton, and Robert J Nicolosi
This review critically evaluates the scientific data on trans fatty acids and coronary heart disease (CHD) risk. Trans fatty acids are present in a variety of foods but they contribute only 4-12% of total dietary fat intake (2-4% of total energy intake) in the United States. The physical properties of trans fatty acids are intermediate between cis and saturated fatty acids, but a trans double bond is chemically less reactive than a cis double bond. Biochemical data indicate that trans fatty acids are subject to the same metabolic control mechanisms that regulate the metabolism of saturated and cis-isomeric fatty acids. Equivocal results have been reported in observational studies of trans fatty acid intake and CHD because of numerous methodologic limitations, including the difficulties inherent in quantifying trans fatty acid intake. Studies in hamsters indicate that trans fatty acids have a neutral effect on low-density-lipoprotein (LDL)-receptor activity, LDL- cholesterol production rate, and plasma LDL-cholesterol concentration. Other animal studies show no differences in atherosclerosis incidence or severity between diets containing hydrogenated and native vegetable oils. In clinical studies partially hydrogenated oils lower total and LDL-cholesterol concentrations when substituted for animal or vegetable fats rich in saturates but raise total and LDL-cholesterol concentrations when substituted for the unhydrogenated native oil. The effects of trans fatty acids on high-density lipoprotein cholesterol and lipoprotein(a) concentrations are unclear because of limited and conflicting clinical data. Data supporting a relation between trans fatty acid intake and CHD risk are equivocal compared with extensive data from studies in animals and humans linking saturated fat intake to CHD. Additional research is needed to resolve questions about the independent effects of trans fatty acids on plasma lipoproteins and their mechanisms of action.
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