Fourteen adult males with alcoholic cirrhosis were studied. Gonadotrophin responses to luteinizing hormone-releasing hormone (LRH) and testosterone (T) responses to human chorionic gonadotrophin (HCG) were determined and basal 17 beta oestradiol (E2) levels were measured in each case. The mean basal luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, and the mean LH and FSH responses to LRH were not significantly different from a group of age-matched male controls. However, the five men with testicular atrophy all had an elevated basal FSH level and an exaggerated FSH response to LRH. The mean serum T of the cirrhotic men was significantly lower than that of the controls (P less than 0.05), while the mean E2 level was not significantly different. However, the mean E2 level in the eight patients with gynaecomastia was significantly higher than in those without gynaecomastic (P less than 0.05). All patients had a T response to HCG, including those 5 with low basal T levels. A significant negative correlation was found between the maximum rise in T after HCG (delta T) and the maximum LH response to LRH (delta LH), suggesting a mediating effect of T reserve on the LH response to LRH. These findings tend to exclude a suppressive effect of alcohol on the pituitary gland as a cause for the hypogonadism found in men with alcoholic cirrhosis. Furthermore, the evidence of some testicular T reserve despite low basal T levels, and the presence of normal basal LH levels, suggests that the low T production is not primarily due to leydig cell dysfunction.