does it stop producing it sorta like how AAS makes you stop producing testosterone?
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does it stop producing it sorta like how AAS makes you stop producing testosterone?
I cannot answering with facts, but under the assumption that your body reacts the same as AAS's, I would come to conclusion that one's body would decrease or even stop the production of natural GH when using synthetic HGH. When most people recommend not using IGF or HGH while in their teens or early twenties is definitely due to the fact your growth plates may not be completely closed and that it could possible distort the natural production of GH.
Bump for FACTS!
-Tose
they prescribe it to adolencents..so im assuming it cant be that bad in the long run for future production of natural gh..
Doctors prescribe synthetic GH to adolescents that lack the natural GH levels by which allows the human body to reach its full potential in bone structure and organ/skin growth as well. ie; dwarfs
-Tose
I am not sure but I thought that the reason for injecting gh in the morning and in the afternoon (as most will reccomend) is because your body will produce it naturally at night.
hmm bump for answers from knowledgeable people
i would bet johnny b or redbaron might know the answer to this one
and i wouldnt think it shuts down the gh/igf system too much... reason being, is because IGF is in many ways similar to insulin, and insulin can be cycled off and on without any post cycle "crash" so to speak
however thats just a hypothesis
this is a good topic of discussion though, keep it going
Natural GH-peaks occure independantly from syntethetic gh or IGF administration during strenous training,so itīs not a totally inhibiting negative-feedback-loop as it may be with test/AAS.Quote:
Originally Posted by jgg1221
Supression of gh occurs during a gh-cycle tge rest of the day(and night),but
a recovery is quick and complete once a cycle is stopped.at leasrt quick enough for ne to realoze it has been suppressed.
Stimulants and/or intense training may help in recovery of gh-puls&peak.
Not a new study, but an interesting read. -RedBaron
Lanzi R, Tannenbaum GS. Journal of Endocrinology
Department of Pediatrics, McGill University, Montreal, Quebec, Canada.
Endogenous pulsatile GH secretion is blunted by the administration of exogenous GH; however, few data are available on the time course of GH negative feedback, and the mechanism by which this occurs still remains unclear.
In the present study, we examined the temporal pattern of the inhibitory effect induced by an acute (single) and chronic (5 days) sc recombinant human (rh) GH injection regimen on spontaneous GH release in the rat and assessed the possible involvement of the hypothalamic GH-inhibitory peptide, somatostatin (SRIF), in this response. Eight-hour (0800-1600 h) GH secretory profiles, obtained from free-moving adult male rats administered a single sc injection of 200 micrograms rhGH at 0800 h, revealed a marked suppression of spontaneous GH pulses (GH peak amplitude: 45.7 +/- 10.9 vs. 207.8 +/- 31.7 ng/ml in H2O-injected control rats; P less than 0.001) lasting for up to 4.1 +/- 0.1 h after the injection (mean 4-h plasma GH level: 13.6 +/- 3.6 vs. 49.4 +/- 7.0 ng/ml in H2O-injected controls; P less than 0.01).
During the subsequent 4- to 8-h period, recovery of spontaneous GH secretory bursts was evident, and neither the GH peak amplitude nor mean 4-h plasma GH level of rhGH-treated rats was significantly different from that of H2O-injected controls. The magnitude, time course, and recovery of the rhGH-induced inhibitory effect on pulsatile GH release after chronic rhGH treatment was similar to that after a single injection.
Passive immunization of rhGH-treated rats with SRIF antiserum reversed the rhGH-induced inhibition of spontaneous GH pulses (peak amplitude: 131.7 +/- 53.7 vs. 7.1 +/- 3.4 ng/ml in rhGH-treated control rats given normal sheep serum; P less than 0.05) and restored both the GH peak amplitude and mean plasma GH level to values similar to those in H2O-injected controls.
Taken together, these results demonstrate that:
1) the inhibitory effect of rhGH on endogenous pulsatile GH release is of short duration (approximately 4 h);
2) the time course of this response does not change after 5-day repeated rhGH administration; and
3) the feedback effect of GH on its own spontaneous release is exerted, at least in part, by increasing hypothalamic SRIF secretion. Such a mechanism of GH feedback may be important in the physiological control of pulsatile GH secretion.