Remember the first post of the thread this statement:
Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol E2)
The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).
.02% of E is converted by the enzyme aromatase, this small percentage can be misleading, estradiol is 100 more potent at the receptor sites then T, that means T needs to balance at the same level to have the same affinity.
Although naturally-occurring estrogens circulate in the blood largely bound to sex hormone-binding globulin and albumin, only unbound estrogens enter target tissue cells.
The statement from above is explaining Free E, exactly the same principle as FREE T, and the target tissues are E-receptors.
Below is what I'm talking about if anybody would like some supported info:
Testosterone-derived estradiol production by male endothelium is robust and dependent on p450 aromatase via estrogen receptor alpha.
http://www.springerplus.com/content/2/1/214
Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol E2)
The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).
.02% of E is converted by the enzyme aromatase, this small percentage can be misleading, estradiol is 100 more potent at the receptor sites then T, that means T needs to balance at the same level to have the same affinity.
Although naturally-occurring estrogens circulate in the blood largely bound to sex hormone-binding globulin and albumin, only unbound estrogens enter target tissue cells.
The statement from above is explaining Free E, exactly the same principle as FREE T, and the target tissues are E-receptors.
Below is what I'm talking about if anybody would like some supported info:
Testosterone-derived estradiol production by male endothelium is robust and dependent on p450 aromatase via estrogen receptor alpha.
http://www.springerplus.com/content/2/1/214