Atherogenesis. An epidemiological model based on the presence of unnatural trans and cis isomers of unsaturated fatty acids in the maternal diet and in mothers milk.

The hypothesis that the presence of unnatural trans and cis isomers of unsaturated fatty acids in the maternal diet and in human mothers milk could be responsible for initiating atherosclerosis in utero or in infants is proposed. It is suggested that the key etiological factor involved in the formation of atherosclerotic plaques could be uncontrolled division of smooth muscle cells of the intima resulting from the intracellular excess of linoleic acid and deficiency of its metabolites gamma-linolenic acid and dihomogamma-linolenic acid. This imbalance is brought about by competitive inhibition of the enzyme delta-6-desaturase by unnatural trans and cis unsaturated fatty acids. Delta-6-desaturase is the enzyme responsible for converting linoleic acid to dihomogamma-linolenic acid. The cellular presence of unnatural trans and cis isomers of unsaturated fatty acids would therefore enhance increased levels of linoleic acid and deficiency of its metabolites gamma-linolenic acid and dihomogamma-linolenic acid. It is proposed that prophylaxis against the effects of delta-6-desaturase inhibition could be achieved by the adoption of an Eskimo-like diet containing the essential fatty acid metabolites gamma-linolenic acid and/or dihomogamma-linolenic acid and eicosapentaenoic acid per se in high concentrations.