[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.