ABSTRACT
There is little doubt that alcoholic liver disease (ALD) is a nutritional disease. It has been argued that ethanol is a direct liver toxin because of the formation of its metabolite, acetaldehyde, which forms adducts with proteins. However, the importance of acetaldehyde adducts in ALD pathogenesis is still at the theoretical level. In fact, increasing the levels of blood acetaldehyde by giving acetaldehyde dehydrogenase inhibitors actually prevented liver injury in rats fed ethanol.1 On the other hand, it has been clearly shown that a number of nutritional factors are involved in ALD pathogenesis, which is the subject of this review. Each of these factors will be discussed as follows: (1) alcohol changes the requirements of proteins, carbohydrates, and lipids by altering liver metabolism, (2) high blood ethanol levels decrease the NAD/NADH ratio and O2 consumption rate, which changes the energy available for the metabolism of nutrients, (3) ethanol alters the enzymes involved in the methyl-donor-dependent pathways such as methyltransferases in the metabolism of S-adenosyl-methionine, in phosphatidyl choline synthesis, and the methylation of DNA, and (4) alcohol increases the requirement of antioxidants to reduce lipid peroxidation, i.e., manganese, copper, and zinc.
