Nuking local e2 and gh pulsation

[myxa8brah]

Is it true that a low-dose AI + SERM + AAS stack—without a testosterone base and without exogenous GH or GHS/GHRHR—lowers aromatase activity to the point where E2 levels drop significantly (though not to zero, assuming an AI like Arimidex at 0.5mg ED or EOD)? Since the combination of very low aromatase activity and Tamoxifen drastically reduces local estradiol—specifically affecting ER-beta and ER-alpha, which in turn suppress growth hormone pulsatility—does it make sense to run this kind of cycle without GH? Or is the potential reduction in pulsatility negligible?

I’m planning to run an Erda + AI/SERM + AAS stack for about a year—without a testosterone base or GH (since I can't afford it)—for a 12-week period.

 

[fattofat]

Basically going to crash your e2, I wouldn't do this without a test base

 

[myxa8brah]

Basically going to crash your e2, I wouldn't do this without a test base

I don't need a testosterone-only baseline; that’s a bad approach for me since my platelets are on the verge of dropping too low regardless of the dosage. Taking 0.5 mg of Arimidex EOD (along with 20 mg of Tamoxifen ED) would be the mildest AI protocol, but I’m not entirely sure about this, which is why I’m posting. Regardless, will using an AI plus a SERM—and the resulting effect on local E2 levels—have a "potential" impact on GH pulsatility? Basically, is GH a "must-have" if I have minimal aromatization but not zero E2?

 

[fattofat]

have a "potential" impact on GH pulsatility?

It will have an impact but its so insignificant I wouldn't even consider doing it, especially when the side is nuking your e2