Based upon studies in man and animals it is proposed that: 1. Alcohol-induced hypogonadism is primarily due to a direct testicular toxicity of ethanol manifested by alcohol-induced reduced testosterone levels. 2. In addition, an alcohol-induced central defect also may contribute to the observed hypogonadism. 3. In contrast to the ease with which hypogonadism can be ascribed to androgen deficiency per se, the observed feminization can not be ascribed to altered estrogen levels alone. Rather, we would propose, that feminization of such men is due to the combined effects of estrogen excess and androgen deficiency upon the patter of estrogen-binding proteins in hepatic cytosol.