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.

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.

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

Hey Lotus,
I was wondering if you know anything about progestogen. I am thinking that coming off of progestogen may be aiding my breast growth and was wondering if you know of any research to support this theory.
Could the progestogen have simulated progesterone dominance while the implant was working, and then when it ran out, my hormones would have been balanced again causing a growth spurt?
It's just a theory I have.

Hey Lotus,
I was wondering if you know anything about progestogen. I am thinking that coming off of progestogen may be aiding my breast growth and was wondering if you know of any research to support this theory.
Could the progestogen have simulated progesterone dominance while the implant was working, and then when it ran out, my hormones would have been balanced again causing a growth spurt?
It's just a theory I have.

Hi there Kit Kat

That's a god question, based on the research I've read (and posted) is that when progesterone is in combination with estrogen (present with other) they act synergistically with each other, meaning breast growth, (amongst a few other things).

Without some previous (history) labs its difficult to say for sure. But generally, progesterone improves receptor sensitivity. Balancing hormones for optimum growth is no easy task, after a while of doing this (NBE) you get the feel what certain herbs can or can't do, call it the NBE learning curve lol.

But, me thinks you could've have had a spike in E, (from progesterone being lowered). Let me just say I admire the dedication you've put in to solve your IGT. Here's my opinion bout that, fwiw, when we say incomplete growth tissue, it tells me a few things (genes being one of them of course), but more specifically, dormant ER-a receptors (Estrogen Receptor Alpha) . The simple solution is to stimulate that receptor, I posted some research about it, if interested I'll dig it up.

• Prolactin and progesterone may enhance ductal outgrowth by inducing ERα expression.
  

• Activation of ER-α causes elongation or horizontal growth of mammary duct cells. Progesterone receptor activation causes side-branching of mammary gland cells. Density, areolar gland development, and gland lactation development are caused by prolactin receptor activation.
  

Check pages 5 thru 9
Hormone Action in the Mammary Gland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982168/


The Progesterone Thread
http://www.breastnexus.com/showthread.php?tid=21243&highlight=Progesterone

After reading through the first page of that thread, I think I must have had very low progesterone up until my implant ran out as the progestogen would have lowered my blood levels of progesterone.
So I think my body is responding to a rise in progesterone now the progestogen is gone. Could this account for the rapid growth I've seen in the last two months? Or am I misunderstanding things? (I never know whether I've made the correct conclusions)

Hey Lotus,
I was wondering if you know anything about progestogen. I am thinking that coming off of progestogen may be aiding my breast growth and was wondering if you know of any research to support this theory.

[quote='Katana' pid='178498' dateline='1461363478']
Could the progestogen have simulated progesterone dominance while the implant was working, and then when it ran out, my hormones would have been balanced again causing a growth spurt?
It's just a theory I have.

Hi there Kit Kat

That's a god question, based on the research I've read (and posted) is that when progesterone is in combination with estrogen (present with other) they act synergistically with each other, meaning breast growth, (amongst a few other things).

Without some previous (history) labs its difficult to say for sure. But generally, progesterone improves receptor sensitivity. Balancing hormones for optimum growth is no easy task, after a while of doing this (NBE) you get the feel what certain herbs can or can't do, call it the NBE learning curve lol.

But, me thinks you could've have had a spike in E, (from progesterone being lowered). Let me just say I admire the dedication you've put in to solve your IGT. Here's my opinion bout that, fwiw, when we say incomplete growth tissue, it tells me a few things (genes being one of them of course), but more specifically, dormant ER-a receptors (Estrogen Receptor Alpha) . The simple solution is to stimulate that receptor, I posted some research about it, if interested I'll dig it up.

• Prolactin and progesterone may enhance ductal outgrowth by inducing ERα expression.
  

• Activation of ER-α causes elongation or horizontal growth of mammary duct cells. Progesterone receptor activation causes side-branching of mammary gland cells. Density, areolar gland development, and gland lactation development are caused by prolactin receptor activation.
  

Check pages 5 thru 9
Hormone Action in the Mammary Gland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982168/


The Progesterone Thread
http://www.breastnexus.com/showthread.php?tid=21243&highlight=Progesterone

After reading through the first page of that thread, I think I must have had very low progesterone up until my implant ran out as the progestogen would have lowered my blood levels of progesterone.
So I think my body is responding to a rise in progesterone now the progestogen is gone. Could this account for the rapid growth I've seen in the last two months? Or am I misunderstanding things? (I never know whether I've made the correct conclusions)

Could the progestogen have simulated progesterone dominance

Progestogens are not accepted by progesterone receptors. It could be a result of sodium from progestin (from the pill). $$ see the highlights. (A possible alternative).

There are many differences between progesterone and the various progestogens, but unfortunately, there are still some doctors who do not realize this. Progesterone lowers the blood pressure, while progestogens raise it; and while progesterone raises the SHBG level, progestogens lower it (see pages 22, 24). Progestogens are not accepted by progesterone receptors. Progesterone can relieve water and sodium retention, whereas some progestogens used in the Pill, such as norethisterone, cause retention of water and sodium.
Progesterone is converted by the adrenals into all the various corticosteroids, which is not possible with progestogens. One function of progesterone is to maintain a pregnancy, but the progestogens cannot be used for this purpose. Some progestogens have an estrogenic effect as well, which is useful in the contraceptive field. The disposal of progestogens from the body differs from that of natural progesterone, which is excreted in the urine and feces as pregnanediol.

Progestogens also lower the blood level of progesterone (see Figure 19), and this explains why women with PMS so often have difficulty in tolerating the Pill (see pages 152-154), whether the estrogen-progestogen pill or the progestogen-only pill, and also other estrogen/progestogen

Thanks for the info Lotus
I think I'm too tired to comprehend everything i've read today, it's gone midnight here lol. Am I correct in saying we can't know for sure whether stopping progestogen based BC has led to the rapid growth I've experienced, but it probably has contributed to a hormonal change which may have helped?
You've been really helpful and I hope I haven't hijacked your thread too much
[/quote]

It may have been blocking some estrogen receptors. I am just now learning about this!
http://www.breastnexus.com/showthread.php?tid=24497&pid=178543#pid178543

It may have been blocking some estrogen receptors. I am just now learning about this!
http://www.breastnexus.com/showthread.php?tid=24497&pid=178543#pid178543

You can desensitize receptors by a few actions, hormones (proper nutrition) need to be stabilized to re-sensitize.

Squeezed a few drops out (the substance is pure white though)
[attachment=11985]

It may have been blocking some estrogen receptors. I am just now learning about this!
http://www.breastnexus.com/showthread.php?tid=24497&pid=178543#pid178543

You can desensitize receptors by a few actions, hormones (proper nutrition) need to be stabilized to re-sensitize.

Squeezed a few drops out (the substance is pure white though)

It may have been blocking some estrogen receptors. I am just now learning about this!
http://www.breastnexus.com/showthread.php?tid=24497&pid=178543#pid178543

You can desensitize receptors by a few actions, hormones (proper nutrition) need to be stabilized to re-sensitize.

Squeezed a few drops out (the substance is pure white though)

pre milk