[Lotus]

Thanks lotus, keeping in mind i am in the uk and would prefer to source within the uk (makes getting more easier) is there a particular brand of white peony you would recommend? or does this look ok http://www.amazon.co.uk/gp/product/B00A75Y22K/ref=noref?ie=UTF8&psc=1&s=drugstore

Just a reference, this is what I ordered:

http://www.amazon.com/White-Peony-Root-E...B000OAXVK2

It's a 1:1 ratio

I'd try to find out the alcohol content, Iowa select is a whopping 25% though!,

Looks good.

[bobie]

Thanks lotus, i will keep looking for some better stuff then as the one i linked to was 1:3 going on the picture, they wont ship yours here unfortunately

[undecided]

I`m sure Lotus has looked at this one already, but if its ok ill post the link for others to look at. Some interesting reading.

http://en.wikipedia.org/wiki/5-alpha-red..._inhibitor

[Lotus]

I`m sure Lotus has looked at this one already, but if its ok ill post the link for others to look at. Some interesting reading.

http://en.wikipedia.org/wiki/5-alpha-red..._inhibitor

Thanks Janet, (I have) and I don't mind at all, in fact I'd like to see our own NBE list like this, btw the wiki list here needs to be edited. (hint, lovely).

   

[rachel-rache]

Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol)

The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).

Hi Lotus, I'm a little confused. You mention that 4% of T gets converted to DHT, yet also that the prostate converts 95% of T to DHT by 5ar. Did you mean that of the 4% that gets converted, 95% of that is done by the prostate by 5ar? Thanks.

[Lotus]

Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol)

The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).

Hi Lotus, I'm a little confused. You mention that 4% of T gets converted to DHT, yet also that the prostate converts 95% of T to DHT by 5ar. Did you mean that of the 4% that gets converted, 95% of that is done by the prostate by 5ar? Thanks.

Hi RR,

Their two separate events, meaning TT (total testosterone) produced is as I stated (est. 3mg-10mg of T), most of which is produced in the testes (from cholesterol), adrenals make up the remaining difference, (tissues may produce their own androgens though). The prostates job helps controls semen production (spermatozoa), and on the other hand:

estrogen is also able to exert beneficial effects via ERβ in the epithelia, which has been implicated in preventing hyperplasia and hypertrophy, being anti-proliferative and, potentially, anti-carcinogenic.
http://jme.endocrinology-journals.org/co...3.abstract

Of the daily T produced (3mg to 10mg) roughly 4% of that is subject to the conversion of DHT from the enzyme 5 ar (alpha reductase). How? (or the amount) of which drives plasma DHT in the blood stream is roughly 3 to 10x stronger than testosterone. So this small conversion rate is misleading, it makes for a bad day if DHT is given free range to do damage in tissues and prevent feminization, (BPH too). 


The liver and prostate are a highly volatile envoirment for hormones. New advanced anti-cancer prostate research is very promising towards battling androgens, scientists discovered this new pathway:

Δ4-androstenedione by steroid-5α-reductase isoenzyme-1 to 5α-androstanedione, followed by subsequent conversion to DHT.

Which is really saying, that if we catch DHT @ androstenedione (a precursor of testosterone) using a 5 alpha reductase type I inhibitor we deny the formation of DHT entirely. For our applications of NBE/HRT, that's amazing. 

DHT occurs in large part from adrenal 19-carbon precursor steroids, which are dependent on expression of CYP17A1.
http://jim.bmj.com/content/60/2/504

 DHT-enhanced activity of 5 alpha-reductase was inhibited 80% @ 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, (gamma linoliec acid) otherwise known as EPO (evening primrose oil). In my opinion (fwiw)  I'd add EGCG (green tea) which also inhibits DHT.

[rachel-rache]

Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol)

The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).

Hi Lotus, I'm a little confused. You mention that 4% of T gets converted to DHT, yet also that the prostate converts 95% of T to DHT by 5ar. Did you mean that of the 4% that gets converted, 95% of that is done by the prostate by 5ar? Thanks.

Hi RR,

Their two separate events, meaning TT (total testosterone) produced is as I stated (est. 3mg-10mg of T), most of which is produced in the testes (from cholesterol), adrenals make up the remaining difference, (tissues may produce their own androgens though). The prostates job helps controls semen production (spermatozoa), and on the other hand:

estrogen is also able to exert beneficial effects via ERβ in the epithelia, which has been implicated in preventing hyperplasia and hypertrophy, being anti-proliferative and, potentially, anti-carcinogenic.
http://jme.endocrinology-journals.org/co...3.abstract

Of the daily T produced (3mg to 10mg) roughly 4% of that is subject to the conversion of DHT from the enzyme 5 ar (alpha reductase). How? (or the amount) of which drives plasma DHT in the blood stream is roughly 3 to 10x stronger than testosterone. So this small conversion rate is misleading, it makes for a bad day if DHT is given free range to do damage in tissues and prevent feminization, (BPH too). 


The liver and prostate are a highly volatile envoirment for hormones. New advanced anti-cancer prostate research is very promising towards battling androgens, scientists discovered this new pathway:

Δ4-androstenedione by steroid-5α-reductase isoenzyme-1 to 5α-androstanedione, followed by subsequent conversion to DHT.

Which is really saying, that if we catch DHT @ androstenedione (a precursor of testosterone) using a 5 alpha reductase type I inhibitor we deny the formation of DHT entirely. For our applications of NBE/HRT, that's amazing. 

DHT occurs in large part from adrenal 19-carbon precursor steroids, which are dependent on expression of CYP17A1.
http://jim.bmj.com/content/60/2/504

 DHT-enhanced activity of 5 alpha-reductase was inhibited 80% @ 15S-hydroxyeicosatrienoic acid, the 15-lipoxygenase metabolite of GLA, (gamma linoliec acid) otherwise known as EPO (evening primrose oil). In my opinion (fwiw)  I'd add EGCG (green tea) which also inhibits DHT.

Thanks for the response! I drink green tea fairly regularly, so I hope that has some effect. I'm also on 1 mg of finasteride a day, so I hope that takes care of all my DHT inhibiting needs. Anyways, I'm going to start researching a good NBE program. I am a skinny 5'9" bio male, 31 years old. I want to grow breasts as large as possible while not becoming permanently sterile. I think when I'm thinking about looking like a woman and growing breasts almost all the time, I think it's time to take some action. Anyways, as you can see from my post count I've hung around these forums quite a bit, but I need to read and refresh myself on a good program, and go through the FAQ sections. If I have additional questions, I hope you wouldn't mind me asking you or posting about it. Cheers

[spanky (aka Lola)]

For those who take a 5-ARI, here is an interesting article indicating that dutasteride has a higher "risk" of leading to gynocomastia than does finasteride.:  

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312705/