The pathogenesis of alcoholic steatosis is a complex process that is manifested through several mechanisms involving some of or all the following body metabolism components: increased fat synthesis, increased mobilization of depot fat, defective export of fat from the liver, and decreased fat breakdown. Some of the novel findings in these mechanisms involve the down-regulation of peroxisome proliferator-activated receptor alpha and up-regulation of lipogenic enzymes through the induction of sterol regulatory element-binding protein. Yet another mechanism that remains viable is the adenosine 5′-monophosphate–activated protein kinase, which, through a complex mechanism, may regulate the relative concentrations of intracellular malonyl coenzyme A and long-chain acyl-coenzyme A, the key metabolites responsible for the balance between fat synthesis versus degradation pathways. Finally, excess dietary intake of omega-6 polyunsaturated fatty acids may exacerbate alcohol-induced onset of hepatic steatosis and alcoholic liver disease. This may explain why supplementation with lecithin containing omega-6 polyunsaturated fatty acids in a recent clinical trial in human beings failed to show any beneficial effects, although it was partially effective in an animal model. In contrast, dietary intake of omega-3 polyunsaturated fatty acids in moderation may have a protective effect against steatosis and alcoholic liver disease.