HORMONES THAT INFLUENCE SEXUAL BEHAVIOR: EVIDENCE FROM HUMAN CLINICAL STUDIES
On the basis of clinical experience, surprisingly little of which has been systematically documented, testosterone has long been the treatment of choice to induce or restore sexual functioning and drive in hypo-gonadal or castrated men. Estrogens and certain progestogens which suppress testicular testosterone production and/ or compete with testosterone at the target-organ level, typically interfere with male libido and sexual functioning. The clinical data on the effects of other androgens on sexual behavior are too scanty to permit any reasonable conclusion. There is an increasing number of clinical studies, that show a beneficial effect of LH-RH administration on libido and potency in impotent, hypogonadal, and normal men. Although the data are suggestive, one has to reserve judgment at this point because the sample sizes are usually small, the methodology sometimes inadequate and the results inconsistent.
High-dose androgen treatment as it is used in estrogen-dependent cancer in women is known to have a strong, positive impact on sexual drive in many such patients. Analogously, female patients with abnormally high androgen levels due to adrenal tumors or other abnormalities, also show an increased sexual drive. A new report on endocrinologically normal women presented sizable correlations between their plasma testosterone levels, averaged over the menstrual cycle, and their “self-gratification scores” (a more appropriate label might be “self-rated sexual arousal”). Testosterone has been used successfully in the treatment of sexually unresponsive women. It has been shown—although without replication – that adrenalectomy, not ovarectomy, will decrease female sexual drive. Therefore, Money has called adrenal androgen the female “libido hormone.” It appears likely, however, that it is not the weak adrenal androgens, but the much more potent testosterone itself (which, in the female, is largely a conversion product of adrenal androstenedione) that is responsible for such effects. The role of female ovarian hormones, estrogens and progesterone, on female sexuality is even less clear, and menstrual-cycle studies of female sexual activity and desire have not produced a consistent body of data (McCauley and Ehrhardt). Estrogens clearly affect female attractivity to males via their effects on the secondary sex characteristics and facilitate female receptivity, at least indirectly, through their effect on the vaginal mucosa. However, Persky and others failed to show any relationship of plasma estradiol level to sexual behavior in young women. Data on the role of progesterone in female sexual behavior are not yet conclusive (McCauley and Ehrhardt), and data on behavioral LH-RH effects are not available.
In conclusion, the evidence described above names testosterone as the major hormone for sexual motivation and behavior in human males and possibly in females, while hardly anything is known in humans about a facilitory or contributing role of adrenal androgens, and there is only inconsistent but suggestive evidence for such a role of LH-RH in males. Estrogens and progestogens inhibit male sexual behavior, at least when used in pharmacologic dosage. Their role in female sexual motivation is not well established; it is probably much less prominent than in the case of lower mammals, but the available studies on women are not sufficient for ruling out facilitory effects of estrogens or inhibiting effects of progestogens as they have been observed in nonhuman primates.
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