**2.15 Prostate health and androgens**

T and its metabolites have trophic effects on the prostate in addition to other reproductive structures of males from early development. Among older men, decline in androgens, and an increase in estrogens, may underlie risk for prostate proliferation. Indeed, treatments for prostate cancer include those that alter androgen levels (releasing hormone or metabolism inhibitors) [37] and/or actions (androgen receptor antagonists). DHT binds with a higher affinity than does T to ARS [36], and DHT is highly active in prostate, where it may cause proliferation [38]. Because of this, 5α-reductase inhibitors have been used as a treatment for BPH and prostate cancer [39–41]. As prostate cancer progresses, carcinomas can become steroid-insensitive and metastasize, leaving no effective treatments. Moreover, there can be side effects of such androgen manipulations. For instance, men have a slightly decreased sex drive with finasteride, which can be reversed upon treatment cessation [42], among most individuals. There is a clinical situation where there is a prolonged response to such androgen manipulations, even when the therapy has ceased, that is informing present studies (below).
