A hyperbolic, saturable, competitive dynamic of ligand binding to metabolic enzymes and lipid mediator receptors gives non-linear dose-response interactions that need careful management when planning or interpreting nutrient-based interventions. Relatively indiscriminate metabolism during accumulation of HUFA from n-3 and n-6 nutrients allows the amounts of n-3 and n-6 nutrients to determine the HUFA balance accumulated in tissue phospholipids. However, when HUFA-based eicosanoid actions are more intense with n-6 than n-3 mediators, they cause healthy physiology to shift toward pathophysiology. The proportion of n-6 in tissue HUFA directly relates to the severity of conditions caused by excessive n-6 actions. In the absence of n-3 nutrients, dietary linoleate (18:2n-6) has a very narrow therapeutic window below 1 percent of food energy, and it is widened by n-3 nutrients. The predictable quantitative dynamics of competing n-3 and n-6 nutrients allows design of successful preventive nutrition protocols that confirm and extend the epidemiologically observed benefits of n-3 nutrients.
Keywords: Arachidonic acid; Cardiovascular disease; Eicosanoids; Highly unsaturated fatty acids (HUFA); Linoleic acid.
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