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So essentially, we know that administering exogenous growth hormone lowers our endogenous production dose-dependently via increasing circulating IGF-1, which in turn promotes the nucleus arcuatus’ and periventricular hypothalamic neurons to produce more somatostatin that directly affects the somatotropies in the pituitary. This is the reason why many people believe adding GH secretagogue on top of this suppressive state has no effect as they would an unresponsive pituitary. However, ghrelin via GHS-1RA activation locally antagonizes somatostatin in the pituitary. GHS-R1a stimulation somatotrophes to functionally oppose somatostatin despite tone being elevated originally .
In rat studies, post-CH administration was superior, three to four times IGF-1 mRNA, however, in human administration and pathopsychology, even in psychological amounts of continuous growth hormone yield high hepatic and low IGF-1 mRNA. My hypothetical view is that IDA-835 is a species-specific AUC integrator. In rats, time weighted extended STAT5B signaling is the most detrimental than Cmax. And in humans, amplitude per weight, makes the exact opposite signaling pattern optimal for each species.
The mechanistic and PK theory also explain why BBS can profit from GHS on top of obscene growth hormone in the first place. The exact observations are interesting. Bodybuilders report greatly enhanced fat loss as we know that HSL in adipocytes prefer pulsatile growth hormone signaling. It seems as if the benefits of endogenous pulsality and the secretion of 20kDa variant are real. As already implied, the goal is to create a more AUC with FGH with extremely potent self-potentiating local IGF-1 signaling. Reverse growth hormone, human growth hormone, 0.071 milligrams per kilogram a day if allometrically scaled, 80 kilogram individual, approximately 16.8 IU a day, shows statistically significant increases in under a year of administration of Tanner Boys, Rothenbühler, 2015, may be tiltrated to or over 0.1 milligram per kilogram a day, 80 kilogram. So basically, you use 80 kilogram, 25 IU.
See, I'm treating this as a base concept right now. Ignore the dosages since 25IU dosent apply to everyone in the crowd. but anyways, next, gonadotropin releasing hormone choice. Although it has less clinical evidence that tesamorelin, semorelin, or CJC with DAC, mod GRF, also known as CJC no DAC, has a pharmacokinetically superior pulse profile that synergizes optimally with both GRP, GHRP2, and if morelin without elevating basal growth hormone, which could potentially degrade the unique STAT 5 to 3 ratio advantage over time without delivering a sufficient compensatory AUC, as long as it is used at 300 micrograms daily injected alongside the respective growth hormone.
Alright I will see y’all in the next ice age.
In rat studies, post-CH administration was superior, three to four times IGF-1 mRNA, however, in human administration and pathopsychology, even in psychological amounts of continuous growth hormone yield high hepatic and low IGF-1 mRNA. My hypothetical view is that IDA-835 is a species-specific AUC integrator. In rats, time weighted extended STAT5B signaling is the most detrimental than Cmax. And in humans, amplitude per weight, makes the exact opposite signaling pattern optimal for each species.
The mechanistic and PK theory also explain why BBS can profit from GHS on top of obscene growth hormone in the first place. The exact observations are interesting. Bodybuilders report greatly enhanced fat loss as we know that HSL in adipocytes prefer pulsatile growth hormone signaling. It seems as if the benefits of endogenous pulsality and the secretion of 20kDa variant are real. As already implied, the goal is to create a more AUC with FGH with extremely potent self-potentiating local IGF-1 signaling. Reverse growth hormone, human growth hormone, 0.071 milligrams per kilogram a day if allometrically scaled, 80 kilogram individual, approximately 16.8 IU a day, shows statistically significant increases in under a year of administration of Tanner Boys, Rothenbühler, 2015, may be tiltrated to or over 0.1 milligram per kilogram a day, 80 kilogram. So basically, you use 80 kilogram, 25 IU.
See, I'm treating this as a base concept right now. Ignore the dosages since 25IU dosent apply to everyone in the crowd. but anyways, next, gonadotropin releasing hormone choice. Although it has less clinical evidence that tesamorelin, semorelin, or CJC with DAC, mod GRF, also known as CJC no DAC, has a pharmacokinetically superior pulse profile that synergizes optimally with both GRP, GHRP2, and if morelin without elevating basal growth hormone, which could potentially degrade the unique STAT 5 to 3 ratio advantage over time without delivering a sufficient compensatory AUC, as long as it is used at 300 micrograms daily injected alongside the respective growth hormone.
Alright I will see y’all in the next ice age.
