[Dianna1395]

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.
[...]

Lotus,
That makes the mad scientist in me wonder, could we "manage" free T, increase E, and in essence make the best of both worlds?
I somewhat doubt it, but, would be interesting to look into it.
Eventually, though, the E kills the T (Negative feedback on APT loop, I think it is; suppresses Leutenizing hormone, per female cycle.)

But with our cyclic approaches anyway, might be able to accomplish something. :-)

Your thoughts?
-Dianna

[spanky (aka Lola)]

Lotus, Abi and Dianna -

Do you think I am going off on a wrong (or hazardous) direction in combining the dutas and GTE? Advice and input appreciated as always.

spanky

[Lotus]

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.
[...]

Lotus,
That makes the mad scientist in me wonder, could we "manage" free T, increase E, and in essence make the best of both worlds?
I somewhat doubt it, but, would be interesting to look into it.
Eventually, though, the E kills the T (Negative feedback on APT loop, I think it is; suppresses Leutenizing hormone, per female cycle.)

But with our cyclic approaches anyway, might be able to accomplish something. :-)

Your thoughts?
-Dianna

Hey there demonid P, what up B?. (j/k) Lmao

Ok I dig where you're going, and I've spent amount of time thinking about this lol, meaning the idea of boosting free T to benefit biosynthesis of E. Btw, Pharma E2 inhibits DHT (I don't know the exact amount as of yet, (I will though lol).

Negative feedback is a good example, in initial treatment phase some meds increase lutenizing hormone before it (med) stabilizes (30-45 days). To me, this says the science is there to manipulate meds.

Something I'm close to understanding is using our diurnal rhythms to promote growth stages that can boost feminization (similar to some animal based studies). And I think amino acids & peptides in combination with a few other things I'll mention later will trigger this boost.

[Lotus]

Lotus, Abi and Dianna -

Do you think I am going off on a wrong (or hazardous) direction in combining the dutas and GTE? Advice and input appreciated as always.

spanky

Spanky,

Depends on what the motivation (or goal?) is, imo. Dutas has some long term post effects, (did for me), something to keep in mind. Finding a combination that's works for yah sure ain't easy these days huh?. Honeslty?, I think GTE by itself is similar to spiro (polyphenols being the main driver), sooo ......nice discovery.

[Dianna1395]

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.
[...]

Lotus,
That makes the mad scientist in me wonder, could we "manage" free T, increase E, and in essence make the best of both worlds?
I somewhat doubt it, but, would be interesting to look into it.
Eventually, though, the E kills the T (Negative feedback on APT loop, I think it is; suppresses Leutenizing hormone, per female cycle.)

But with our cyclic approaches anyway, might be able to accomplish something. :-)

Your thoughts?
-Dianna

Hey there demonid P, what up B?. (j/k) Lmao

Ok I dig where you're going, and I've spent amount of time thinking about this lol, meaning the idea of boosting free T to benefit biosynthesis of E. Btw, Pharma E2 inhibits DHT (I don't know the exact amount as of yet, (I will though lol).

Negative feedback is a good example, in initial treatment phase some meds increase lutenizing hormone before it (med) stabilizes (30-45 days). To me, this says the science is there to manipulate meds.

Something I'm close to understanding is using our diurnal rhythms to promote growth stages that can boost feminization (similar to some animal based studies). And I think amino acids & peptides in combination with a few other things I'll mention later will trigger this boost.

Hi, Lotus,
I'm probably going in a different direction from you on the Free T line of thought.
I think it would be great to have the Free T for playing with the woman (a woman), and the breasts grow in from aromatization of the Free T. So, control the DHT by kill 5-Alpha-R, which would likely mean Dutas... (But I need to review if that kills T production, or just wipes out the 5Ar). Then using our other goodies, like GTE, Spearmint, Red Clover, PM, WP, induce an environment high in aromatase, high in E, but still forcing E into the system. (How to induce high LH is a question; thinking I'd have to use Clomiphene citrate to rev up the leydig cells... Or, find a way to stimulate ONLY LH, as FSH will cause other, unwanted effects.

It's indicated here though (not a scientific site, though: http://androcycle.com/post-cycle-therapy/ - I don't have much capacity to do research from behind the NWO corporate firewalls, category "illegal drugs" is not allowed. Effing tyrants, both corp and DEA/FedGov.)

Or maybe, from http://www.mayoclinic.org/diseases-condi...n-20033618 - there are a few "shortcuts" to my preferred end goal? Ah, if only... (there were this site in 1990, the internet had spread to Thailand, the gov't wasn't busy coralling us like cattle, and my parents weren't self-righteous abusive pricks...) ;-)

OTOH... Maybe using something else to block FSH, or to eliminate it, would work? And as an add-on, what about finding a means to ensure Prostate stays "normal" and thus allow for a female experience even with the estrogen...? Never thought about that before, but since Prostate is tied to DHT, prob'ly not. But maybe there's something like Clometipene (?) which would not block the creation of the T, but rather interfere with the connectors, so the T cannot be used.... But then that would affect everywhere else, too. So, no erections while on the meds. :-P

Easier to just get an inflatable phallus! :-)

-Dianna

[jannet.duff]

Well .... I'm a little disappointed with my latest blood work.

Total T 10.6 nmol/L ( normal 8.4 to 28.8 )
Free. T 41 pmol/L. ( normal 178 to 475 )

[Dianna1395]

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.
[...]

Lotus,
That makes the mad scientist in me wonder, could we "manage" free T, increase E, and in essence make the best of both worlds?
I somewhat doubt it, but, would be interesting to look into it.
Eventually, though, the E kills the T (Negative feedback on APT loop, I think it is; suppresses Leutenizing hormone, per female cycle.)

But with our cyclic approaches anyway, might be able to accomplish something. :-)

Your thoughts?
-Dianna

Hey there demonid P, what up B?. (j/k) Lmao

Ok I dig where you're going, and I've spent amount of time thinking about this lol, meaning the idea of boosting free T to benefit biosynthesis of E. Btw, Pharma E2 inhibits DHT (I don't know the exact amount as of yet, (I will though lol).

Negative feedback is a good example, in initial treatment phase some meds increase lutenizing hormone before it (med) stabilizes (30-45 days). To me, this says the science is there to manipulate meds.

Something I'm close to understanding is using our diurnal rhythms to promote growth stages that can boost feminization (similar to some animal based studies). And I think amino acids & peptides in combination with a few other things I'll mention later will trigger this boost.

Hi, Lotus,
I'm probably going in a different direction from you on the Free T line of thought.
I think it would be great to have the Free T for playing with the woman (a woman), and the breasts grow in from aromatization of the Free T. So, control the DHT by kill 5-Alpha-R, which would likely mean Dutas... (But I need to review if that kills T production, or just wipes out the 5Ar). Then using our other goodies, like GTE, Spearmint, Red Clover, PM, WP, induce an environment high in aromatase, high in E, but still forcing E into the system. (How to induce high LH is a question; thinking I'd have to use Clomiphene citrate to rev up the leydig cells... Or, find a way to stimulate ONLY LH, as FSH will cause other, unwanted effects.

It's indicated here though (not a scientific site, though: http://androcycle.com/post-cycle-therapy/ - I don't have much capacity to do research from behind the NWO corporate firewalls, category "illegal drugs" is not allowed. Effing tyrants, both corp and DEA/FedGov.)

Or maybe, from http://www.mayoclinic.org/diseases-condi...n-20033618 - there are a few "shortcuts" to my preferred end goal? Ah, if only... (there were this site in 1990, the internet had spread to Thailand, the gov't wasn't busy coralling us like cattle, and my parents weren't self-righteous abusive pricks...) ;-)

OTOH... Maybe using something else to block FSH, or to eliminate it, would work? And as an add-on, what about finding a means to ensure Prostate stays "normal" and thus allow for a female experience even with the estrogen...? Never thought about that before, but since Prostate is tied to DHT, prob'ly not. But maybe there's something like Clometipene (?) which would not block the creation of the T, but rather interfere with the connectors, so the T cannot be used.... But then that would affect everywhere else, too. So, no erections while on the meds. :-P

Easier to just get an inflatable phallus! :-)

-Dianna

So, the answer was already lurking here...
http://www.breastnexus.com/showthread.php?tid=17436&page=329

Lots said "@ Hannah, absolutely, by inhibiting LH it suppresses T, which as I stasted before, this would upreglaues FSH to synthesize (make more) estradiol. Piperine mixed in with_____ fill in the blank lol, red veggies would be my choice."
@ (05-02-2016 08:59 PM) - I can't find the original message!

That tells me the whole idea is just ridiculous, though. :-(

Guess I have to keep dreaming, and now I understand why so many Pros are using implants. Mechanical means to look female, and keep the functionality for the "film" roles (and likely other fun, too.)

-Dianna

[Lotus]

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.
[...]

Lotus,
That makes the mad scientist in me wonder, could we "manage" free T, increase E, and in essence make the best of both worlds?
I somewhat doubt it, but, would be interesting to look into it.
Eventually, though, the E kills the T (Negative feedback on APT loop, I think it is; suppresses Leutenizing hormone, per female cycle.)

But with our cyclic approaches anyway, might be able to accomplish something. :-)

Your thoughts?
-Dianna

Hey there demonid P, what up B?. (j/k) Lmao

Ok I dig where you're going, and I've spent amount of time thinking about this lol, meaning the idea of boosting free T to benefit biosynthesis of E. Btw, Pharma E2 inhibits DHT (I don't know the exact amount as of yet, (I will though lol).

Negative feedback is a good example, in initial treatment phase some meds increase lutenizing hormone before it (med) stabilizes (30-45 days). To me, this says the science is there to manipulate meds.

Something I'm close to understanding is using our diurnal rhythms to promote growth stages that can boost feminization (similar to some animal based studies). And I think amino acids & peptides in combination with a few other things I'll mention later will trigger this boost.

Hi, Lotus,
I'm probably going in a different direction from you on the Free T line of thought.
I think it would be great to have the Free T for playing with the woman (a woman), and the breasts grow in from aromatization of the Free T. So, control the DHT by kill 5-Alpha-R, which would likely mean Dutas... (But I need to review if that kills T production, or just wipes out the 5Ar). Then using our other goodies, like GTE, Spearmint, Red Clover, PM, WP, induce an environment high in aromatase, high in E, but still forcing E into the system. (How to induce high LH is a question; thinking I'd have to use Clomiphene citrate to rev up the leydig cells... Or, find a way to stimulate ONLY LH, as FSH will cause other, unwanted effects.

It's indicated here though (not a scientific site, though: http://androcycle.com/post-cycle-therapy/ - I don't have much capacity to do research from behind the NWO corporate firewalls, category "illegal drugs" is not allowed. Effing tyrants, both corp and DEA/FedGov.)

Or maybe, from http://www.mayoclinic.org/diseases-condi...n-20033618 - there are a few "shortcuts" to my preferred end goal? Ah, if only... (there were this site in 1990, the internet had spread to Thailand, the gov't wasn't busy coralling us like cattle, and my parents weren't self-righteous abusive pricks...) ;-)

OTOH... Maybe using something else to block FSH, or to eliminate it, would work? And as an add-on, what about finding a means to ensure Prostate stays "normal" and thus allow for a female experience even with the estrogen...? Never thought about that before, but since Prostate is tied to DHT, prob'ly not. But maybe there's something like Clometipene (?) which would not block the creation of the T, but rather interfere with the connectors, so the T cannot be used.... But then that would affect everywhere else, too. So, no erections while on the meds. :-P

Easier to just get an inflatable phallus! :-)

-Dianna

So, the answer was already lurking here...
http://www.breastnexus.com/showthread.php?tid=17436&page=329

Lots said "@ Hannah, absolutely, by inhibiting LH it suppresses T, which as I stasted before, this would upreglaues FSH to synthesize (make more) estradiol. Piperine mixed in with_____ fill in the blank lol, red veggies would be my choice."
@ (05-02-2016 08:59 PM) - I can't find the original message!

That tells me the whole idea is just ridiculous, though. :-(

Guess I have to keep dreaming, and now I understand why so many Pros are using implants. Mechanical means to look female, and keep the functionality for the "film" roles (and likely other fun, too.)

-Dianna

FSH (follicle stimulating hormone) aromatizes, the LH (lutenizing hormone) signal can be turned up or down using certain supplements..........fish oil as an example. Dopamine and insulin can also impact this process as an example. If a body builder can use pro-aromatase supps in their cycle what's to say T (or free T) in this theory can't be utilized?.

I suggested this approach about 2 1/2 years ago, we talked about it but I don't think anyone used it. I used periodically when I tank my T..........when depression kicks in.

I see DHEA, PC, vitex, fish oil, Leptin, (simple sugars) as some food/supplements that could be used towards this application. But, I also believe if we can displace more free hormones, fatty acids, etc, trapped in SHBG and total sex steroids we'd see huge gains as similar to the type you'd see in BB world.

[Lotus]

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.

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)





* I think future science will confirm that EFA's contribute to FSH synthesis (just my opinion, lol)

[AcaciaLynn8294]

I found this product on US eBay, 50g, 100g, 125g, 250g and 500g packs. Prices range from $9 - $35. 98% polyphenal, 50% EGCG, 80% Catechins and 1.5% caffeine. Seems like a good deal, has anyone used this product? They have free shipping as well. https://www.ebay.com/ulk/itm/161573245331