Yep, and that’s interesting to me.
This is less interesting to me. They are obese and on TP therapy with questionable TT end result levels. The fact they need a lot of AI to lower e2 is not surprising at all.
Well, I’m obese and i did 0.1 for 6 days in a row and I had TT of 775 and an E2 of 6! and non-existent LH
Don’t you find it interesting that the end-point E2 always ends up in that 15-20 range whether it’s this study’s 1mg per day, AZ monotherapy up to 10mg a day, or McClain’s 1mg EOD?
I think what’s happening is that if suppressed enough, the hypothalamus? senses that and sends out LH to the boys in an ever repeating cyle.
No, because we’re not comparing apples to apples here. It’s rarely ever equal when considering hormone use.
Unless his patients, and you, are also on pellets, I think you’re drawing just a little bit too much out of this single study. It’s interesting, I give it that. And some follow up would be great. But I won’t be jumping to conclusions that don’t apply to this example. That’s all I’m saying
This is the theory behind SERM use while on TRT (injections). Blocking e2 should have the same physiologic outcome as lowering it to nothing. But we don’t see LH/FSH come up when doing that with a SERM. Maybe an AI is different? Or it’s the continual daily dose?
Sure I agree no conclusions can be drawn definitively. However, we know his protocol is 200mg T weekly with 1mg Anastrozole EOD. In his exact words, “that tends to keep patients in the 15-20 range”. Anyway, would be nice if he’d do an LH test for us if anyone know how to get in touch with him.
Not applicable to McClain, but in this study, the TT was pretty low around 590 in the first 60 days. I think it’s known that T itself has a negative feedback for producing LH so maybe it was the dose as well.
what protocol did you eventually land on?