Considerable evidence has accrued over the preceding two decades to establish that ethanol is a gonadal toxin. In the male such toxicity is both direct, being expressed at the level of the hypothalamus and/or pituitary. Moreover, such toxicity is due in part to direct ethanol exposure and also in part to the consequences of ethanol metabolism (e.g., acetaldehyde generation, redox changes and alterations in enzyme levels and activities). Thus as a result of studies performed both in man and in animals, it has been shown conclusively that ethanol abuse per se, and not the associated liver disease that occurs with alcohol abuse, is responsible for the impotence, loss of libido, and testicular atrophy which are seen commonly in chronic alcoholic men. With prolonged alcohol abstinence, recent studies have suggested that spontaneous recovery of normal sexual function is possible in some chronic alcoholic men if testicular atrophy has not yet occurred and if their responses to clomiphene and/or luteinizing hormone releasing factor stimulation are normal. In contrast, abstinent alcoholic men with either overt testicular atrophy or inadequate responses to such pharmacologic challenges fail to recover despite continued alcoholic abstinence. Such men will require either a penile prosthesis or long-term oral androgen therapy to achieve "acceptable" sexual functioning. Considerably less information is available concerning the adverse effects of ethanol and alcohol abuse in women. The available data however, suggests that women, like men, develop gonadal injury as a consequence of alcohol abuse and that such injury occurs both at the level of the ovary and at the level of the hypothalamus and pituitary.