(26-09-2014, 01:56 AM)Lotus Wrote: Yes I would agree, slowing E2 to E1 will (should) be healthier in the long run. Good E moment
Thanks for posting the chart, which I was trying to show its importance. It would indirectly and in a small way slow E2 into E1 conversion, by converting E2 (and E1) into E3 instead.
The point I was trying to make is that Estriol (E3) can be used for NBE, and it is the safest of those 3 estrogens. E1 is the most carginogenic, and E2 can exaggerate cancer. Even though E3 is weaker than E2, it is more bioavailable, perhaps making it more effective for NBE than E2. E3 can also be made from DHEA bypassing testosterone, androstenedione, estradiol, and estrone. If you look at the chart, aromatase and the liver enzyme 16alpha-Ohase together are important for E3 synthesis, no matter which pathway is taken. Progesterone and prolactin lower estradiol, and my theory is perhaps this estradiol is converted into useful E3 by this means. Prolactin, progesterone, and E3 together directly cause NBE on their own, plus the three are compatible with each other.
Estrone (E1)
Estradiol (E2)
Estriol (E3)
Dehydropiandrosterone (DHEA)
Breakdown of hormones and phytohormones into other compounds by the liver is actually usually not a problem, since many metabolites are also effective in NBE.
Metabolites of estradiol are E3, 16alpha-OHE1, 2-OHE2, E1, and two unidentified composition.- Determination of estradiol metabolites in human liver microsome by high performance liquid chromatography-electrochemistry detector.
Some metabolites of E2 are claimed to be carcinogenic, but E3 is a lot safer than estradiol.


