[Lotus]

Lotus, 

I think you once said that once you've stomped on DHT long enough estradiol takes a dramatic role over daily hormone production.....in theory. 

I'm *very* curious about this theory. Is there any info already posted here? I'm super curious about this. 

Thank you. 

Hi stevenator,

Let's use how estradiol can suppress prostate cancer as an example, in other words, estradiol lowers androgens and inhibits prostate resistant cancer...as seen in the study below.

Another example would be after SRS when most anti-androgens are dropped in favor of estradiol only supplementation, which estradiol is supremely in control of suppressing androgens (DHT), at the very leas some DHT is leaked from the adrenals, though mostly insignificant (though some DHT rears its wrath even after castration via adrenals, depends on the person though too, meaning individual metabolism vary.


Estradiol suppresses tissue androgens and prostate cancer growth in castration resistant prostate cancer
http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC2889894&blobtype=pdf

Abstract
Background: Estrogens suppress tumor growth in prostate cancer which progresses despite anorchid serum androgen levels, termed castration resistant prostate cancers (CRPC), although the mechanisms are unclear. We hypothesize that estrogen inhibits CRPC in anorchid animals by suppressing tumoral androgens, an effect independent of the estrogen receptor.

Methods: The human CRPC xenograft LuCaP 35V was implanted into orchiectomized male SCID mice and established tumors were treated with placebo, 17β-estradiol or 17β-estradiol and estrogen receptor antagonist ICI 182,780. Effects of 17β-estradiol on tumor growth were evaluated and tissue testosterone (T) and dihydrotestosterone (DHT) evaluated by mass spectrometry.

Results: Treatment of LuCaP 35V with 17β-estradiol slowed tumor growth compared to controls (tumor volume at day 21: 785 ± 81 mm3 vs. 1195 ± 84 mm3, p = 0.002). Survival was also significantly improved in animals treated with 17β- estradiol (p = 0.03). The addition of the estrogen receptor antagonist ICI 182,780 did not significantly change survival or growth. 17β-estradiol in the presence and absence of ICI 182,780 suppressed tumor testosterone (T) and dihydrotestosterone (DHT) as assayed by mass spectrometry. Tissue androgens in placebo treated LuCaP 35V xenografts were; T = 0.71 ± 0.28 pg/mg and DHT = 1.73 ± 0.36 pg/mg. In 17β-estradiol treated LuCaP35V xenografts the tissue androgens were, T = 0.20 ± 0.10 pg/mg and DHT = 0.15 ± 0.15 pg/mg, (p < 0.001 vs. controls). Levels of T and DHT in control liver tissue were < 0.2 pg/mg.

Conclusions: CRPC in anorchid animals maintains tumoral androgen levels despite castration. 17β-estradiol significantly suppressed tumor T and DHT and inhibits growth of CRPC in an estrogen receptor independent manner. The ability to manipulate tumoral androgens will be critical in the development and testing of agents targeting CRPC through tissue steroidogenesis.


In another twist, 17B-estradiol (E2) up-regulates IGF-1 (Insulin-like Growth Factor), so maybe this opens up for further discussion on that we know where and how to increase growth hormones.....meaning it's already in our wheelhouse by using E2.

In summary, our data show that E2 specifically up-regulates IGF- IR in prostate cancer cells and sensitizes cancer cells to the biological effects of IGF-I. The E2 effect can occur through both ERa and ERh and does not involve ER binding to DNA but rather the activation of kinase cascades initiated by the association between ER-Src and PI3K and followed by ER K1/2 phosphorylation.

So....know what this means?, IGF (growth hormones) happens more from a signaling cascade more so than estrogen receptors.....and that pathway is PI3K signaling pathway (or in this example known as a cascade to IGF-1), awesome stuff huh?.

17B-Estradiol Up-regulates the Insulin-like Growth Factor Receptor through a Nongenotropic Pathway in Prostate Cancer Cells
https://www.researchgate.net/profile/Giu...-Cells.pdf