(29-06-2015, 04:09 PM)spanky Wrote: Thanks Lotus. Your sage advice is always appreciated.
I am thinking I will try black cohosh liquid extract, although I am not sure it is standardized, on the theory that liquid extract may carry less risk of causing liver damage than capsules. But then again, there may be no real difference in that regard.
I don't see a down-side for red clover, so will probably resume taking that as well.
Hi spanky,
I agree, I have RC as a slight aromatase/progesterone and ERa promoter, as with all NBE use it in moderation.
As mentioned, FSH follicle stimulating hormone stimulates estradiol synthesis, the science is there, so it's possible. Same with vitamin D3, the science is there too, meaning it upreglates T and E2. And as we know, when we try to eliminate most of DHT, what remains?, exactly, T and E2, other hormones too , but for this purpose we'll limit it to the 2 . But let's say we use an anti-androgen in the presence of an aromatase promoter (pick one, WP, forskolin, inositol triphosphate, FSH, etc) which will upregluate both (T and E2) then synthesize thru aromatase. More research (by BN members) should be done on second messengers, (e.g-cAMP,) which imo is key in aroamtase expression and will result in improved breast growth.
Interactions between FSH, estradiol-17 beta and transforming growth factor-beta regulate growth and differentiation in the rat gonad.
Estradiol-17 beta (E2) is a mitogen in vivo for the proliferation of granulosa cells in the rat ovary.
E2 is synthesized by the preovulatory follicle through a series of gonadotrophin-dependent events: LH stimulates thecal cells to synthesize androgens (androstenedione and testosterone) which are substrates for FSH-induced aromatization to estrogens in granulosa cells. More recently, we have found that transforming growth factor-beta (TGF-beta) stimulates DNA synthesis in rat granulosa cells in vitro and this effect is augmented by FSH. Since E2 is a mitogen in vivo and TGF-beta is the only known growth factor to stimulate proliferation in vitro, the possible link between the actions of E2 and TGF-beta were examined. E2 stimulated the secretion of a TGF-beta-like factor by rat granulosa cells in culture, and with time DNA synthesis was stimulated. The mitogenic action of E2 was enhanced in the presence of FSH, and attenuated by a neutralizing antibody to TGF-beta. The latter observations have identified TGF-beta as the "missing-link" in the mitogenic actions of E2 on rat granulosa cells. In addition to the growth-promoting actions of TGF-beta plus FSH, TGF-beta enhanced FSH-induced aromatase activity. Consequently, FSH plus TGF-beta stimulates both the proliferation and aromatization capacity of rat granulosa cells. We propose that interactions between FSH, E2 and TGF-beta lead to the exponential increase in serum E2 levels that occurs during the follicular phase of the cycle.
Similarly, FSH stimulates the aromatization of exogenous androgens to estrogen by Sertoli cells isolated from immature rat testes, and there is a correlation between FSH-induced aromatization and mitotic activity. We have shown that FSH plus TGF-beta stimulates DNA synthesis in Sertoli cells. Since E2 increases the secretion of TGF-beta by Sertoli cells, interactions between FSH, E2 and TGF-beta may provide the mitogenic stimulus for Sertoli cells during the prepubertal period. In summary, our findings suggest that the estrogen-induced growth of rat granulosa cells is mediated through the production of TGF-beta, which acts as an autocrine regulator of proliferation.
We also propose that the growth-promoting actions of FSH on Sertoli cells may depend upon a cascade series of events involving estrogens and TGF-beta.
From post #2618
Sertoli cells synthesize estradiol 17b from testosterone, and when testosterone is introduced with FSH (Follicle-stimulating hormone) it produced a 12 fold increase in E2 synthesis. And is markedly increase when cAMP (Cyclic adenosine monophosphate) is also added. Estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate). On another note, FSH and cAMP produce a 30 fold increase in aromatase, quite possibly making it the strongest aromatase.
(24-06-2015, 04:51 AM)Lotus Wrote: Inhibit LH (luteinizing hormone) using black cohosh (nbe) Goserelin (pharma)
Stimulate FSH (follicle stimulating hormone) E2 or red clover, *(essential fatty acids)
Inhibit DHT in the liver. (reishi inhibits serum DHT @ 80%) dutas @93%, finasteride @70% and saw palmetto inhibits DHT @ 32% (combo's possible).
Inhibit adrenal DHT (calmodulin -via the calcium/calmodulin/CaMK pathway) (spiro or licorice root)
![[Image: attachment.php?aid=9789]](http://www.breastnexus.com/attachment.php?aid=9789)
* I think future science will confirm that EFA's contribute to FSH synthesis (just my opinion, lol) 
And quite possibly from Phospholipids
https://en.m.wikipedia.org/wiki/Phospholipid
. Without muscle stimulation, hormone delivery is significantly reduced, that's going in the wrong direction. 
thanks. You so funny, ah well......I'll just say they grew another inch since the last update, which was in Feb. How I got there is buried between the lines of the tech stuff posted in this thread, my apologies for being so technical though. I'll talk less shop..........(maybe) 
