Tesa speeds that up, because its mechanism of action acts like a multiplier of natural GH pulses. So endogenous GH reaches baseline level faster, then exceeds it.
LOL, I’ve read every single published, peer reviewed paper on Tesamorelin, from the pharma development of Egrifta, all phases of the clinical trials, and the alternate use studies. I understand its mechanism of action.
What do you want me to do? Upload the relevant PDFs, since most aren’t public access, highlighting the relevant sections so I can “convince you”? I don’t give enough of a fuck. Not for someone who’s demanding it like I owe you something.