Anastrozole 1mg daily?!?

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Defy Medical TRT clinic doctor
In research on AI monotherapy it's been claimed that there's incomplete suppression of estradiol in men. I've wondered about that, including whether immunoassays were used, which tend to read high. In this case though we might posit that maintenance of normal LH levels allows for a reasonable amount of intratesticular aromatization, which we know is resistant to AI use. HPTA activity is maintained here because of the suppression of estradiol. Estradiol provides a lot of the negative feedback that normally suppresses LH production under TRT; artificially reducing the otherwise excessive estradiol allows LH levels to be maintained.

Addition: now that I think about it, the same thing is happening in AI monotherapy. The estradiol is probably created intratesticularly.
 
So it seems if you take *enough* Anastrozole while on TRT you can keep your hypothalamus producing LH/FSH which keeps estradiol up??
Yes, not that it's necessarily a good idea. There's aromatase in a lot of different tissues, including the brain. Could heavy AI use starve these tissues of estradiol even when serum levels appear ok? I don't know, but I don't think I'd want to be a long-term test subject for this.
 
For what it’s worth, before trt I took aromasin monotherapy for 3 months at 12.5mg eod and did crash my e2.
That's interesting. I wonder if the different action of exemestane lets it better overcome intratesticular aromatization, or if it's simply a question of dose sizes?
 
Anastrazole is relatively weak, and it takes a dose of more like 5-10mg/day to reach maximal suppression (and even at that dose suppression is not complete, more like 97-98%). This probably shut down ~90% of aromatase activity, which is why e2 levels were very low (teens), and why LH/FSH are normal (the HPTA feedback loop is signaled by e2, which is why SERMs produce HPTA stimulation). I would wager that labs around a week in would have shown very low e2 before LH/FSH/aromatase were upregulated in response.
 
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It still could make sense that the de facto destruction of aromatase by exemestane is more effective in the intratesticular environment, where very high testosterone more easily counteracts the competitive inhibition of anastrozole.
 
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