Professor The University of Texas At Austin Austin, TX, United States
Abstract: Linoleic acid (LA) has long been understood to be quantitatively the major omega-6 PUFA in the food supply. It is referred to as an, or “the” “essential fatty acid” though in the era of vitamin discovery arachidonic acid was the most efficacious dietary fatty acid for eliminating deficiency symptoms of fat-free diets.
At the whole animal/human, biochemical, and molecular levels, the competition of LA and all omega-3 fatty acids is well understood and among the most reproducible phenomena in biology. LA and omega-3 alpha-linolenic acid (ALA) compete for access to FADS2, FADS1, ELOVL5 and ELOVL2, converting these PUFA to more unsaturated and longer highly unsaturated fatty acids (HUFA). Ingestion of seed oils with high LA suppresses the conversion and accumulation of all omega-3. FADS1 genetic polymorphisms control the plateau of circulating ARA at high dietary LA levels. Circulating levels of the key neural omega-3 DHA are modulated in three ways, negatively by LA, and positively by DHA and choline. Importantly, no amount of any omega-3 precursor (ALA, stearidonic acid, eicosapentaenoic acid (EPA), or docosapentaenoic acid (DPA)) increases DHA. Scores of animal studies using high LA/low ALA vegetable oils as the sole source of fat in diets of pregnant animals consistently causes neural deficiencies in the offspring.
Many clinical pathologies respond to dietary DHA or EPA (or both), all by increasing DHA or EPA in target tissues. Such studies inherently demonstrate that LA levels are in excess. Chronic reduction of LA is much less studied but show similar effects, especially in chronic pain. Polymorphisms in the FADS gene cluster control ARA levels; high ARA levels are likely to require greater levels of DHA-EPA for clinically efficacy, and should be considered in all future supplementation studies.
