I think we have an answer, Green Tea Extract- GTE inhibits prostate cancer by reducing the cell growth and blocks the androgen receptor. Green tea extract need to be @ 60-80% in EGCG polyphenols though. The dosage needs to be determined, recommend use is 2-3 capsules per day, I'm thinking it's slightly more (4-5?) from what this study says. Would this elimante the need for other anti-androgens?, possibly. Soooo- I see a good plan as follows: (though, it's up to you, it won't hurt my feelings).
1-pro-estrogen source
1-pro-aromatase
Green tea extract (imo 4-5 caps per day)
1-growth hormone source
Add the standard healthy fats, exercise, massage, pumping, etc.
Quote: Epigallocatechin-3-gallate EGCG, the major polyphenolic constituent present in green tea, imparts antiproliferative effects against both androgen-sensitive and androgen-insensitive human PCA cells, and this effect is mediated by deregulation in cell cycle and induction of apoptosis. GTE is potent inhibitors of type 1 but not type 2 5α-reductase. (−)Epigallocatechin-3-gallate also inhibits accessory sex gland growth in the rat. These results suggest that certain tea gallates can regulate androgen action in target organs.
Quote: EGCG (green tea) acts as an antagonist of androgen function, similar to the pharmacological inhibitor Casodex, which was used as a control.
So what does this mean?,........it means green tea acts like a pro-pharma class of anti-androgens named Casodex, as in brand name
Bicalutamide-aka, a pure antiandrogen used in the treatment of prostate cancer:
Bicalutamide
https://en.m.wikipedia.org/wiki/Casodex
Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer
The present study is one of the first few reports demonstrating the antiandrogenic action of a plant product and the first report showing the effect of EGCG, a naturally occurring polyphenol present in green tea, in inhibiting human prostate carcinoma cell growth. We have shown that EGCG effectively inhibits the transactivation functions and expression of AR by interfering with its stability as a result of decreased interdomain interaction (Fig. 5). We also showed that EGCG is a novel antagonisAR signaling, which can block AR-regulated gene expression and cell growth in human PCa cells. We thus suggest that EGCG could be developed as a chemotherapeutic agent against hormone-refractory PCa.
http://www.fasebj.org/content/25/4/1198.full