22-03-2013, 01:17 AM
So my education about NBE (phyto) versus bio-identicals (pharma) continues. I share the following for those that are considering combined phyto/pharma personal programs.
I found a technical paper on the interaction of estriol (E3, like in PM) and estradiol (E2, like in Progynova or Estradiol Valerate). This technical paper found via four different assay methods that estriol dampens the effects of estradiol and is at a maximum when estriol is 10x of estradiol and reduces estradiol effects by between 50 and 85 percent. This suggests that personal programs that intend to employ estradiol as the primary agent of feminization could possibly reduce the risk of cancer by also programming PM, but at the cost of lowered efficacy of estradiol. This is a very sophisticated choice and should be programmed with utmost care and should NOT be considered a proven method of risk reduction, in my opinion.
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http://mend.endojournals.org/content/11/...8.abstract
Molecular Endocrinology, Nov 1997
Title: Molecular and Kinetic Basis for the Mixed Agonist/Antagonist Activity of Estriol
Abstract:
Estriol acts as a weak estrogen when administered in a single dose into immature or ovariectomized laboratory animals, but produces full estrogenic responses upon chronic administration. However, when estriol is injected together with estradiol it acts as an antiestrogen.
***
We discuss our results in relation to the massive estriol production during pregnancy and to the “Estriol Hypothesis” on the protective role for estriol in opposing carcinogenic effects of estradiol.
I found a technical paper on the interaction of estriol (E3, like in PM) and estradiol (E2, like in Progynova or Estradiol Valerate). This technical paper found via four different assay methods that estriol dampens the effects of estradiol and is at a maximum when estriol is 10x of estradiol and reduces estradiol effects by between 50 and 85 percent. This suggests that personal programs that intend to employ estradiol as the primary agent of feminization could possibly reduce the risk of cancer by also programming PM, but at the cost of lowered efficacy of estradiol. This is a very sophisticated choice and should be programmed with utmost care and should NOT be considered a proven method of risk reduction, in my opinion.
************************************************************
http://mend.endojournals.org/content/11/...8.abstract
Molecular Endocrinology, Nov 1997
Title: Molecular and Kinetic Basis for the Mixed Agonist/Antagonist Activity of Estriol
Abstract:
Estriol acts as a weak estrogen when administered in a single dose into immature or ovariectomized laboratory animals, but produces full estrogenic responses upon chronic administration. However, when estriol is injected together with estradiol it acts as an antiestrogen.
***
We discuss our results in relation to the massive estriol production during pregnancy and to the “Estriol Hypothesis” on the protective role for estriol in opposing carcinogenic effects of estradiol.