QUOTE(Zoldian @ Jul 29 2008, 08:16 PM)
QUOTE(\SHINE/ @ May 30 2008, 12:42 AM)
HGH shuts down endo HGH !
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This just goes to show that H has it's own negative feedback system which all to many refuse to believe. NOw, how long after injectable H use stops the endogenous levels recover is not illustrated here.
Effect of chronic treatment with biosynthetic growth hormone (GH) on the GH response to double GH releasing hormone administration in children with short stature.
Author
Scacchi M; Danesi L; Pincelli AI; Dubini A; Cavagnini F
Address
Cattedra di Endocrinologia II, Universit`a di Milano, Istituto Scientifico Ospedale San Luca, Italy.
Source
J Endocrinol Invest, 20(2):72 6 1997 Feb
Abstract
Growth hormone (GH) exerts a negative feedback on its own secretion through direct and indirect mechanisms. Normal children, unlike adults, display consecutive GH responses after repeated GH releasing hormone (GHRH) administration. In this study, we investigated the effects of long term GH administration on this peculiar secretory pattern. Eight children with severe short stature and impaired GH responses to suprapituitary provocative stimuli associated with normal GH responsiveness to GHRH, underwent, while on chronic treatment with biosynthetic GH and on the 10th day following drug withdrawal, a double bolus GHRH test (two GHRH injections of 1 microg/kg b.w. given as i.v. boluses two hours apart). During GH therapy the GH response to the first GHRH bolus appeared to be reduced, though not significantly so, compared to that observed at diagnosis; after treatment withdrawal, this response returned quite similar to pretreatment. Both during and after treatment, the GH response to the second GHRH bolus was comparable for magnitude to that evoked by the first application. In conclusion, even prolonged treatments with rhGH do not induce persisting alterations of the physiological mechanisms subserving GH regulation.
I am not sure I agree this study is conclusive (especially with 8 patients). They are conluding that GH exerts a negative feedback, yet call the GH resonse to the GHRH dose "reduced, though not significantly so, compared to that observed at diagnosis." Was the difference statistically significant or not? One should really investigate the details of this or any study before forming their own opinion. This abstract uses ambigous language (not significant, quite similar, comparable) and offers no data. Many Dr's in this field would argue that GH does not have feedback inhibition of production. It only lasts in the blood stream a few minutes (about 3-6 minutes) before it's destroyed. During that time, it triggers the production of IGF-1 in the liver. Free IGF-1 has a half-life of about 4.5 minutes. Thus it is active for about 22 minutes. IGF-1 becomes bound to various binding proteins. The primary binding protein is IGF-BP3. These binding proteins prolong the half-life of IGF-1 - just like SHBG prolongs the half-life of Testosterone (Free Testosterone has a half-life of about 10-100 minutes). Depending on the binding protein, the estimates of the half-life of bound IGF-1 varies between 6-20 hours with a common estimate of between 12-15 hours. Assuming the half-life of bound IGF-1 is 15 hours, then IGF-1's activity is prolonged over baseline by the addition of growth hormone approximately 75 hours. I am not positive which side I am on, I do know this study doesn't prove anything.
Maybe the term reduces or supresses rather than the quote "SHUTS DOWN" Is more appropiate,
There's a few studies showing gh to be supressed with the use of endous gh or igf.
I would say your bodies own gh/igf levels are most likely supressed then when using GH/igf.
A Tripeptidyl Ensemble Perspective of
Interactive Control of Growth Hormone
Secretion
Johannes D. Veldhuis
Mayo Medical and Graduate School of Medicine, Mayo Clinic, Rochester, Minn., USA
Infusion of rhIGF-I inhibits pulsatile GH secretion in
the rat and human. A novel strategy has been applied
recently to reveal feedback suppression by systemic IGF-I.
GH release was depressed below baseline levels, suggesting a direct effect of IGF-I on the pituitary. Furthermore We propose that these studies suggest that endogenous hypothalamic IGF-I mediates the influence of GH in the feedback.
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