Quote from: ssneha23 on October 03, 2014, 09:24:18 PM
he is not comfortable with my current E dosage level as it affecting my liver
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Have your liver values been checked out and are they above normal values? I'm assuming you are taking bio-identical estradiol and if so, you can ask why your doctor is so concerned about your liver if pregnant women experience levels up to 75,000 pg/ml (up to 640 during menstrual cycle) and yet do not seem do have an increased incidence of liver complications. Liver complications are more typically observed with non bio-identical forms of estrogen. If you really want to remain on the safe side, it's best usually to take estradiol non-orally. Discussion with your doctor about these matters is imperative. You need to be on the same page, otherwise find someone else.
QuoteWhat is difference between AA and GnRH methods for T blocking?
Some AAs only block androgen from binding to receptors, others block AND reduce production of androgen while GnRh only reduce production of androgen from testicles. GnRh also tend to increase production of androgen for the first 2-3 weeks after which production ceases.
QuoteHow does GnRH make E more effective that a third of my original dose would be as effective?
If androgen is more strongly inhibited by GnRh as compared to the AA you were taking and even then, who knows if really 1/3 of E dose would be as effective? Time would reveal the answer.
QuoteWill the new method slow my transition or does YMMV matter here as well?
Time will tell.
p.s. : regarding progesterone, be sure that bio-identical progesterone is prescribed and not any other form, especially medroxyprogesterone acetate (Provera, Depo-Provera) as this tends to be associated with negative side-effects not observed or observed to a much lesser extent with bio-identical progesterone.
Good luck.

I'm not a doctor but you can bring up these issues with your doctor and see what they say.
Quote from: Flan on October 03, 2014, 09:51:22 PM
AA either binds with anrdogen receptors or makes the body believe there is plenty of it.
Pure androgen blockers such as flutamide or bicalutamide actually tend to make the body think not enough androgen is being produced and, as a result, androgen production is INCREASED. Since androgen is blocked though, the excess androgen is converted to estrogen increasing levels of estrogen and feminization. These blockers, by binding to androgen receptors, prevent actual androgen from binding to androgen receptors.

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GnRH tells the gonads (either LH or FSH) basically "nothing to see here, move along" and effectively stops their function.
GnRh overstimulates pituitary gland so that LH and FSH are increased initially but this overstimulation eventually leads to desensitization where LH and FSH production end up being abolished, leading to a marked decreased in testicular production of androgen and sperm.
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GnRH is more effective/safe but a lot more expensive and not all androgen production is blocked (nor conversion of the remaining testosterone to hair killing DHT).
GnRh only reduces testicular production of androgen. Adrenal production of androgen, although weak and quite insignificant persists.