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DOI: http://dx.doi.org/ 313-320 First published online: 1 January 1983


In the chronic male alcoholics several mechanisms are involved in the pathogenesis of the sexual dysfunction that manifests itself clinically as testicular atrophy, gynaecomastia, impotence and sterility. Animal studies have distinctly demonstrated the ability of alcohol to impair testosterone production and spermatogenesis both through its direct toxic effects on the testes and through interference in the function of the hypothalamic-pituitary-gonadal axis. The alcohol-induced enhancement of testosterone catabolism also contributes to the loss of plasma testosterone. Apart from being hypoandrogenized, chronic alcoholic men are also exposed to the excessive oestrogen effect that results from the accumulation of oestrogenic hormones, principally from that of oestrone, and from the changes in oestrogen receptors. The role of hyperprolactinaemia in the alterations of sexual function of chronic male alcoholics is unknown. The significance of liver damage in the pathogenesis of hormonal disturbances is emphasized by the finding that, apart from impairment of spermatogenesis, the hormonal changes seem to be most marked in alcoholic men with liver cirrhosis.

Animal studies have again dearly demonstrated the toxicity of alcohol to female gonads. Consistent with the animal findings, menstrual abnormalities, decreased female sexual characteristics and sterility associated with ovarian atrophy have been reported in chronic alcoholic women. The loss of oestrogens and progesterone provides the hormonal basis for these changes. In spite of marked hypo-oestrogenization, plasma gonadotropin levels have not been elevated in chronic female alcoholics, indicating that disturbed regulation of gonadotropin secretion is an important factor in the genesis of ovarian failure in these patients, even if ovarian function may also be directly impaired. Hyperprolactinaemia is not one of the hormonal hallmarks of sexual dysfunction in chronic alcoholic women.

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