[Lotus]

Biggie because DHT has two to three times greater androgen receptor affinity than testosterone and has 15-30 times greater affinity than adrenal androgens?

Ah yes, exactly. And thank you Eloise, only you'd better not get me going we'll (me) will be here all night lol.

Seriously though you bring up a good point about adrenal androgens.

Other androgens, such as androstenedione, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS), are androgenic by their conversion to testosterone or DHT and, thus, are androgenic prehormones. Androgen production results from glandular secretion and peripheral conversion of these prehormones (mostly androstenedione and DHEA). In normal women, approximately 50% of circulating testosterone is secreted equally by the ovary and the adrenal gland (Longcope, 1986). Androstenedione is also equally secreted by them (Longcope, 1986). In contrast, 50% of DHEA is secreted by the adrenal gland, 20% is secreted by the ovary, and 30% is derived from the peripheral conversion of DHEAS, which is almost completely produced by the adrenal gland (Abraham, 1976). Under normal circumstances, serum DHT is formed entirely from the peripheral conversion of androstenedione (85%) and testosterone (15%) (Ito and Horton, 1971). Thus, androgen production can be increased in abnormal states by the increased glandular secretion of the potent androgen testosterone or by the increased glandular secretion of androgen prehormones such as androstenedione, DHEA, and DHEAS.

receptor or estrogen receptor-beta blockade alters DHEA-, DHT-, and E(2)-induced proliferation and PSA production in human prostate cancer cells.
Arnold JT1, Liu X, Allen JD, Le H, McFann KK, Blackman MR.
Author information

Abstract
Dehydroepiandrosterone (DHEA) is an endogenous steroid that is metabolized to androgens and/or estrogens in the human prostate. DHEA levels decline with age, and use of DHEA supplements to retard the aging process is of unproved effectiveness and safety. LNCaP and LAPC-4 prostate cancer cells were used to determine whether DHEA-modulated proliferation and prostate specific antigen (PSA) production were mediated via the androgen receptor (AR) and/or ERbeta.
METHODS:
Cells were treated with DHEA, DHT, or E(2) and antagonists to AR (Casodex-bicalutamide) or ER (ICI 182,780) or siRNA to the respective receptors. Proliferation was assessed by MTT assay and PSA mRNA and protein secretion were measured by quantitative real-time PCR and ELISA. Associations of AR and ERbeta were analyzed by co-immunoprecipitation studies and fluorescent confocal microscopy.
RESULTS:
DHEA-, T-, and E(2)-induced proliferation of LNCaP cells was blunted by Casodex but not by ICI treatment. In LNCaP cells, Casodex and ICI suppressed hormone-induced PSA production. In LAPC-4 cells, DHT-stimulated PSA mRNA was inhibited by Casodex and ICI, and the minimal stimulation by DHEA was inhibited by ICI. Use of siRNAs confirmed involvement of AR and ERbeta in hormone-induced PSA production while AR-ERbeta co-association was suggested by immunoprecipitation and nuclear co-localization.
CONCLUSIONS:
These findings support involvement of both AR and ERbeta in mediating DHEA-, DHT-, and E(2)-induced PSA expression in prostate cancer cells.