Essential fatty acids (EFAs) are major structural components of the brain and through their effects on membrane properties can influence nerve conduction, transmitter release, and transmitter action. Prostaglandins (PCs) derived from EFAs have profound behavioral effects and are also able to modify conduction and transmitter function. Effects of alcohol on EFAs and PGs are therefore good candidates for explaining at least some of the actions of alcohol on brain function. Ethanol has three main known actions on EFA and PG metabolism: it reduces blood linoteic acid levels and induces or exaggerates EFA deficiency states; it blocks metabolism of linoteic acid to EFA metabolites which are known to be important in brain structure; and it enhances conversion of the linoteic acid metabolite, dihomo‐γ‐linolenic acid, to PGE1. This review demonstrates that some of the short‐term behavioral effects of ethanoi and some of its long‐term adverse effects on brain, liver, and other tissues may be partly explicable in terms of ethanoi actions on EFA and PG metabolism. Modification of such metabolism by dietary and other means has already been shown to influence the effects of alcohol and alcohol withdrawal in both humans and animals. This promises to be a fruitful source of investigation with substantial implications for the understanding and treatment of alcoholism.