LakeMountD
Doctor Science
- Awards
- 1
Well after reading through a 10+ page study on the entire Growth Hormone Secretion system this is what it boils down to.
"Our working model is that, physiologically, GH self-entrains its pulsatility through the coupling of three biological oscillators: somatostatin, GHRH, and the natural ligand for the GHS-R. However, when a GHS-R ligand is administered exogenously, it acts dominantly to antagonize somatostatin and stimulate GHRH release. This results in synergy between GHRH and the GHS-R ligand to cause increased GH release from somatotrophs. GH then feeds back on the hypothalamus to entrain a new cycle by increasing somatostatin tone on GHRH-containing neurons, thus inhibiting GHRH and GH release. Hence, administration of a GHS-R ligand is capable of resetting the coupled oscillators."
Basically our body produces GH pullses every 3-3.5 hours. This oscillating cycle has been studied very carefully and it is not effected by things such as night/day cycle but instead caused by the negative feedback loop associated with Somatostatin, an inhibitor of somatotropin.
What this article is explaining is that the introduction of a natural ligand GHS-R can actually reset this oscillation process. It will antagonize (basically make it stop working) somatostatin and in turn increase GHRH production, which in turn produces more GH from the somatotrophs.
The best way to view how we can increase our natural GH pulse is to look at what inhibits (prevents) it and what stimulates its release. If you can both antagonize what inhibits it and produce more of what stimulates it, then you can have a profound effect on its release.
--So lets start with inhibition of somatostatin. As said above we know GHS-R antagonizes somatostatin.
--Now lets look at what stimulates the actual GH release, which would be GHRH
--Lastly we know that GHRH works very synergistically with GHRP-6 (more specifically Hexarelin).
The combination of these three things can have a very profound effect on GH release. I am not saying it wouldn't be expensive, because it could be, and I am not saying that it would be worthwhile, because I have not yet come across a study showing how often injections would need to take place. The addition of the GHS-R is sort of nice because it starts the pulsatility over again, unfortunately we don't know when our body is at its peak or its trough of GH production. Not only that but for maximal results, we would have to inject every 3 hours for maximal results and it would have to be during a trough.
All in all these things would work though and it would be interesting to see to what extent. I will continue to look through material and see if I can find human studies that use GHS-R and/or all three of them.
"Our working model is that, physiologically, GH self-entrains its pulsatility through the coupling of three biological oscillators: somatostatin, GHRH, and the natural ligand for the GHS-R. However, when a GHS-R ligand is administered exogenously, it acts dominantly to antagonize somatostatin and stimulate GHRH release. This results in synergy between GHRH and the GHS-R ligand to cause increased GH release from somatotrophs. GH then feeds back on the hypothalamus to entrain a new cycle by increasing somatostatin tone on GHRH-containing neurons, thus inhibiting GHRH and GH release. Hence, administration of a GHS-R ligand is capable of resetting the coupled oscillators."
Basically our body produces GH pullses every 3-3.5 hours. This oscillating cycle has been studied very carefully and it is not effected by things such as night/day cycle but instead caused by the negative feedback loop associated with Somatostatin, an inhibitor of somatotropin.
What this article is explaining is that the introduction of a natural ligand GHS-R can actually reset this oscillation process. It will antagonize (basically make it stop working) somatostatin and in turn increase GHRH production, which in turn produces more GH from the somatotrophs.
The best way to view how we can increase our natural GH pulse is to look at what inhibits (prevents) it and what stimulates its release. If you can both antagonize what inhibits it and produce more of what stimulates it, then you can have a profound effect on its release.
--So lets start with inhibition of somatostatin. As said above we know GHS-R antagonizes somatostatin.
--Now lets look at what stimulates the actual GH release, which would be GHRH
--Lastly we know that GHRH works very synergistically with GHRP-6 (more specifically Hexarelin).
The combination of these three things can have a very profound effect on GH release. I am not saying it wouldn't be expensive, because it could be, and I am not saying that it would be worthwhile, because I have not yet come across a study showing how often injections would need to take place. The addition of the GHS-R is sort of nice because it starts the pulsatility over again, unfortunately we don't know when our body is at its peak or its trough of GH production. Not only that but for maximal results, we would have to inject every 3 hours for maximal results and it would have to be during a trough.
All in all these things would work though and it would be interesting to see to what extent. I will continue to look through material and see if I can find human studies that use GHS-R and/or all three of them.
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