Many variables, aside from the amount and duration of alcohol consumption, play a role in the development and progression of alcoholic liver disease (ALD). One critical factor that can be modified is diet/nutrition. We have made major recent advances in our understanding of the interactions of nutrition and ALD. In this article, we review advances made in zinc metabolism/therapy for ALD. There is major zinc dyshomeostasis with ALD which is mediated, in part, by poor intake and absorption, increased excretion, and altered zinc transporters, especially ZIP14. Zinc deficiency plays an etiologic role in multiple mechanisms of ALD, ranging from intestinal barrier dysfunction to hepatocyte apoptosis. Zinc supplementation is highly effective at correcting these ALD mechanisms and preventing/treating experimental ALD. There is no Food and Drug Administration (FDA) approved therapy for any stage of ALD. Because animal and human data suggest that zinc deficiency occurs early in the course of ALD, we treat most ALD patients with daily oral zinc supplementation (220 mg zinc sulfate which contains 50 mg elemental zinc).
Keywords: Alcoholic liver disease; Liver injury; Malnutrition; Zinc deficiency; Zinc supplementation.