When doing HGH does your body shut down natural production?

[GGot FFina?]

Hey,

Just wondering if HGH is similar to Test. Does your body shut down natural HGH production while your taking 4 iu's.

Thanks...

[38jumper38]

If you shot every day, could be possible, hgh is being produce over night that's why everyone shots in the morning hours, to avoid shutting down.

[GGot FFina?]

If you shot every day, could be possible, hgh is being produce over night that's why everyone shots in the morning hours, to avoid shutting down.

Do we have any idea if this is absolutely true? Does it always start back up after being on HGH for so long? 1-2 years for some of us?

[38jumper38]

I use pharma grade, my doc let me use only 15uis per month. he say to use 3 days on and 2 days off. I say anything more than that will shut down my natural production, in case some using chinese, and no one can assure whats inside, is way more difficult to prevent shut down. Pharma grade is so expensive that I can imagine some using for 1 or 2 years in a row.

[ScotchGuard02]

That's why HGH is for those over 30 and is used long term. There is much higher chance of a shutdown with younger people teens and 20's.

[Times Roman]

I've never heard of an HGH feedback mechanism?

....someone please enlighten me?

[marcus300]

Like many hormones which are triggered by the HPTA have a negative feedback
loop, which simply means when levels are to high it will blunt the release
of any further hgh. HGH isnt just produced at night while in REM it pulses
throughout the day but the main the release is at night so taking HGH can
blunt some of the normal pulses throughout the day or night depending when
you take it. Ive read an article by Red Baron stating using exogenous HGH
will create this negative feedback on your HPTA for about 4 hours

[sublyminal]

The answer is no. Exogenous gh will have ZERO effect on endogenous GH secretion shut down concerns. It's not the same as test, but unfortunately it's easy to try and use the same concepts and principals with regards to both. The truth is that test and HGH come from two entirely different sources in the body, and saying exo gh will shut you down like exo test will, is like saying if you're allergic to apples then you must be allergic to buffalo meat. I have never heard of someone taking gh long term stop, get their levels tested, and come up shorter than typical. If you use gh for 10 years, stop for six months and test your levels, your levels will be the same as what you would have been had you never used it in the 1st place. You can't apply standards of apples and oranges to each other, and comparing test and gh is doing just that.

[marcus300]

The answer is no. Exogenous gh will have ZERO effect on endogenous GH secretion shut down concerns. It's not the same as test, but unfortunately it's easy to try and use the same concepts and principals with regards to both. The truth is that test and HGH come from two entirely different sources in the body, and saying exo gh will shut you down like exo test will, is like saying if you're allergic to apples then you must be allergic to buffalo meat. I have never heard of someone taking gh long term stop, get their levels tested, and come up shorter than typical. If you use gh for 10 years, stop for six months and test your levels, your levels will be the same as what you would have been had you never used it in the 1st place. You can't apply standards of apples and oranges to each other, and comparing test and gh is doing just that.

Your wrong and if you do more research especially on the HPTA what regulates the production of gh things will become more clear.

[Isma]

Is there any long-term clinical study? I've found two studies about the use of HGH in sane patients (to improve the athletic performance), between 13-45 years of age, but only with a duration of 6 weeks...

In this studies, the possible shut down of endogenous HGH (because of the use of exogenous) is not considered.

And, one of the conclusions of both studies, it's: "Although the limited available evidence suggests that growth hormone increases lean body mass, it may not improve strength; in addition, it may worsen exercise capacity and increase adverse events. More research is needed to conclusively determine the effects of growth hormone on athletic performance. "

My question is: Do we have this "more research" to say if rHGH have effect on endogenous HGH, or doesn't?

[marcus300]

Is there any long-term clinical study? I've found two studies about the use of HGH in sane patients (to improve the athletic performance), between 13-45 years of age, but only with a duration of 6 weeks...

In this studies, the possible shut down of endogenous HGH (because of the use of exogenous) is not considered.

And, one of the conclusions of both studies, it's: "Although the limited available evidence suggests that growth hormone increases lean body mass, it may not improve strength; in addition, it may worsen exercise capacity and increase adverse events. More research is needed to conclusively determine the effects of growth hormone on athletic performance. "

My question is: Do we have this "more research" to say if rHGH have effect on endogenous HGH, or doesn't?

Yes there are many studies from my research ive done and more so recently ive found some interesting concerns to timing of injections.

This study shows endogenous HGH being blunted by the administration of exogenous hgh, even though this study was based on 2 applications one injection of rHGH and 5 injections of rHGH it shows inhibition in such a short time so you can make your own assumptions up with long term rHGH effects. With that being said the recovery starts to take place as soon as rHGH is stop so timing is the key if you want to still use some of your natural pulse's of hgh seeing that the half life is so short.

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.

In this study which was done on 32 healthy males ages between 20-31 shows exogenous hgh administration will not suppress endogenous hgh production before 4 hours after administration and inhibition occurs after this time lag , which puts a whole new concept of timing IMHO, and IGF level will raise in 12 hours after injection then raise rapidly then peak about 24hrs after injection, so in this case it will have a huge impact on your natural gh for much longer periods of time than we first thought, again timing is the key IMHO

In this study, single sc administration of recombinant 20K-hGH in normal men induced significant elevations in spontaneous serum FFA and IGF-I levels associated with a marked reduction in the serum 22K-hGH level in a different time-dependent manner. hGH secretion is mainly controlled by hypothalamic hormones, GHRH, and somatostatin (18), and also controlled negatively by hGH itself (19, 20, 21) or hGH-dependent substances: IGF-I (21), FFA (23, 24), glucose (18), and so on. The increases in the main hGH-dependent substances (FFA and IGF-I) after 20K-hGH administration suggested that 20K-hGH has direct GH actions on adipose tissue or the liver through hGH receptors similarly to 22K-hGH. Therefore, 20K-hGH is expected to exert GH actions (growth-promoting activity and lipolytic activity) in humans. Furthermore, the suppression of endogenous 22K-hGH secretion could be a result of so-called “GH-induced negative feedback mechanisms.”

We found that the 24-h profile of 20K-hGH secretion in the placebo group was similar to that of 22K-hGH and that the proportion of 20K- to 22K-hGH was fairly constant. These observations suggested that regulation of 20K-hGH secretion is physiologically the same as that of 22K-hGH. Baumann and Stolar (25) suggested that 20K- and 22K-hGH may be stored together in secretory granules in the somatotroph and, hence, released together in response to various stimuli. Our observations support this hypothesis. Furthermore, these results suggested that the endogenous kinetics of 20K-hGH may be comparable with those of 22K-hGH. Interestingly, the pharmaco-kinetics after sc injection of recombinant 20K-hGH were nearly comparable with those of recombinant 22K-hGH (26, 27). In 20K-hGH-treated groups, the serum 20K-hGH levels contained both exogenously administered and endogenously secreted 20K-hGH, but the endogenous 20K-hGH levels were ignored in this study because the mean secreted 20K-hGH levels in the placebo group were fairly low (0.13 ± 0.12 ng/mL). It has been reported that 20K-hGH is cleared more slowly than 22K-hGH in rats (28, 29), but this observation has not been confirmed in guinea pigs (30). These discrepancies may be related to the differences in the species studied (rat, guinea pig, human) and/or assay methods used.

We have demonstrated the time course of the suppressive effect induced by exogenous 20K-hGH on endogenous 22K-hGH secretion in humans. The reduction of serum 22K-hGH level after 20K-hGH administration required a period of ca. 4 h, and the level tended to recover by 24 h. However, the delay in suppression of endogenous 22K-hGH by exogenous 20K-hGH is difficult to define precisely because of the intermittent nature of hGH secretion. Additional studies are required to clarify the time lag between 20K-hGH exposure and suppression of endogenous 22K-hGH. In previous studies (31, 32), single intramuscularly or sc administration of hGH (with monitoring of the resulting plasma profiles) showed a delayed and prolonged suppressive effect on rat GH secretion. The time course of endogenous GH suppression in rats was similar to but faster than that in humans reported here. The fast time course in rats was probably due to the rapid absorption of hGH in this species (14, 33). Willoughby et al. (31) suggested that suppression is achieved through metabolic or other intermediary processes, rather than acutely by a direct membrane effect of the hGH molecule.

The marked suppression of endogenous 22K-hGH secretion occurred in parallel with the FFA elevation; serum FFA levels increased with maximum levels at 4–8 h and recovered by 24 h after 20K-hGH administration. In contrast, serum IGF-I levels increased after 8 h and were prolonged up to 24 h or more, and no increase in circulating glucose levels was observed for 24 h. Our data are consistent with those of Rosenthal et al. (34), who found that 6-h methionyl 22K-hGH infusion raised plasma FFA levels but not IGF-I or glucose levels and blunted GHRH-induced GH secretion in normal men. Of the main hGH-dependent substances, elevation of FFA rather than IGF-I levels may play a leading role at least in the marked 22K-hGH suppression at AUC6–12 h after a single sc administration of 20K-hGH. Administration of FFA markedly reduced the basal GH secretion and blocked GH secretion induced by pharmacological and physiological stimuli in humans (23, 35). Recently, Briard et al. (36) reported that FFA acts both at the hypothalamic level, through increased somatostatin secretion, and at the pituitary level in sheep.

The suppression of 22K-hGH secretion was observed even at the lowest dose of 20K-hGH administered (0.01 mg/kg), with a Cmax of 8.1 ± 4.1 ng/mL. Rosenthal et al. (34) reported that the GHRH-induced GH response in humans was significantly inhibited during 6-h methionyl 22K-hGH infusion, whereas the plasma GH level remained constant (9–13 ng/mL). Therefore, the effect of 20K-hGH on negative feedback may be as potent as that of 22K-hGH.

There are experimental limitations to differentiating between exogenous and endogenous hGH in humans. The time course of GH-induced negative feedback in humans can only be studied indirectly by using the peripheral GH response to GH provocation (21, 34, 37, 38) or the amplitude of sleep-related GH secretion (20) as an indicator of suppression of GH secretion. Our observations extended these studies and indicated that an exogenously administered GH isoform could suppress the other endogenously secreted GH isoform in a time-dependent manner. The proportion of 20K- to 22K-hGH is fairly constant under physiological conditions. Therefore, by measuring the serum 20K- and 22K-hGH levels and using the other hGH isoform as an indicator of the endogenous hGH, it may be possible to monitor the internal behavior of exogenously administered hGH in clinical application of 20K-hGH and, especially, 22K-hGH. Measurement of serum 20K- and 22K-hGH may be useful in evaluating the effects of circulating GH isoforms on their own release from the pituitary.

Previous SectionNext Section
Acknowledgments
We thank Drs. Kohei Yazawa, Fumiaki Ikeda, and Masaru Honjo for advice and encouragement during these studies. We also thank Ms. Noriko Takayama, Ms. Keiko Kawano, and Ms. Hiromi Takeda for technical assistance.

Received August 3, 1999.
Revision received October 12, 1999.
Accepted October 20, 1999.
Previous Section

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.

[Isma]

Thankyou marcus300.

These are the studies I told.

*The Effects of Growth Hormone on Body Composition and Physical Performance in Recreational Athletes --> Annals of Internal Medicine

*Systematic Review: The Effects of Growth Hormone on Athletic Performance --> Annals of Internal Medicine

*Growth Hormone and Sex Steroid Administration in Healthy Aged Women and Men --> The Journal of the American Medical Association

I'm going to read yours now. Thanks again.

[Isma]

Sorry, but what means IMHO?

[SlimmerMe]

^^^ in my humble/honest opinion...........something like that

[Isma]

Thankyou.

Abbreviations are killing me...

[SlimmerMe]

^^^ abbreviations which are related to the forum

http://forums.steroid.com/showthread...-abbreviations..

[Isma]

Great SlimmerMe, I ned it.

[oswaldosalcedo]

.


Exogenous 20K Growth Hormone (GH) Suppresses Endogenous 22K GH Secretion in Normal Men.


https://academic.oup.com/jcem/article-lookup/doi/10.1210/jcem.85.2.6377


.

[Quester]

What's 20k?

[DocToxin8]

Exogenous HGH or exogenous IGF1 will both blunt natural HGH production/secretion.

If it didn't we'd all have acromegaly.

Studies done on children of short stature suggests that EOD dosing is HGH might be less supressive adter HGH is stopped than ED dosing, but have nearly identical outcome on height. (The weekly dose was the same)