[Lotus]

What I would want to know is how to limit DHT enough to grow breasts but not enough to lose erections. I know I don't have the answer because so far erections haven't stopped or even slowed for me in the two years since I started. I have had growth and some different fat allocation (hate to say redistribution), but not as much as I think I can achieve. I think I ideally if you can reduce DHT, leave some remain to do what it does, then backdoor convert the rest you may come close to the best of both worlds.

Froger,

Option #1

I think we could walk the line with something like Finasteride and 25mg to 50mg of DHEA, androstenedione and DHEA are pro-aromatase. If estradiol is higher taking DHEA will go to aromatase, and whatever T is left over by Finsateride still on the table could get the lobido going. It's possible this action could be applied by reishi?, or using something like EFA's (essential fatty acids) epo or borage, which is about 85% ant DHT.


Option #2

Spiro- Although I'm less certain about this approach, meaning:

*Spiro displaces estrogen from SHBG, which lowers free estrogens
*Blocks tetosterones synthesis
*Binds to estrogen receptors (don't know which one yet)

option #3

cAMP or cyclic adenosine monophosphate is another possible NBE tool. Imo cAMP ties into fatty acids, or in large part how cAMP delivers FA's to hormones. In other words increasing blood flow to the receptors increase their bioavailability. Forilskin comes to mind, but quite honestly I think fatty acids work quite the same way.

cAMP is a second messenger important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.

Yes it's the same response seen from Forskolin-, but I believe there's other options besides forskolin though, which good luck finding the real thing.......to be continued (searching)

Sup' BN members,

I think we have more options, we'll call them scientific possibilities at point, because the science is there.

25% of estrogens are synthesized in the testes, however....., testosterone production is a 30:1 ratio over estrogen. So.....when that testosterone production is lowered what happens?, that ratio improves. We can further teak (turn up) that estrogen signal (production), here's how:

high concentrations of FSH-follicle stimulating hormone signal and cyclic AMP (known as) cAMP (cyclic adenosine monophosphate) increase estrogen biosynthesis in the testes.

E1-estrone- the weaker estrogen is synthesis in adipose tissue (breast) by aromatase by way of androstenedione (pathway), this weaker production is similar to what PM does, IMO it isn't enough.

Concerning DHT, that fact is no matter what we do or try they'll be DHT production somewhere (adrenal DHT shows up even after castration).

I made this point before, I think if DHT shows up, we force it to ER-beta and deactivate it. In other words, and it seems crazy to even suggest this, but.......if we give DHT a "free pass" to protien synthesis, we force its immediate exvacuatioin to estrogen receptor beta, we might be tipping the scales. At least that's the indication of what happens in the testes, we're just helping it along faster.

a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

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