hgh pct

[aestheticsfirst]

Would taking ghrp2, ghrp6 and semorelin after taking hgh restore my levels back to normal? I know there is a temporary shut down of natty hgh depending on how long you take it.

[diabeticknowledge]

can you share this study that reveals the gh suppressive effect of exogenic growth hormone ?

[aestheticsfirst]

The physiological and pharmacological functions of the 20-kDa human GH (20K-hGH) isoform are unknown. We conducted a pharmacokinetic study of recombinant 20K-hGH in human subjects (Phase I clinical trial). Placebo or 20K-hGH was administered sc to normal men (20-31 yr of age, n = 6-8 per group) at 2100 h. Serum 20K- and 22K-hGH levels were monitored every 30 min for 24 h by specific enzyme-linked immunosorbent assays. Serum free fatty acid, insulin -like growth factor I, insulin, and glucose levels were measured for 24 h. In the placebo group, the secretion profiles of endogenous 20K- and 22K-hGH were pulsatile and similar to each other. The proportion of 20K- to 22K-hGH was fairly constant. In the 20K-hGH-treated groups, serum 20K-hGH levels increased in a dose-dependent manner over the dose range of 0.01-0.1 mg/kg. Maximum serum 20K-hGH levels were reached at 3-4 h and decreased with half-lives of 2-3 h. Marked suppression of endogenous 22K-hGH secretion was observed in a time-dependent manner. Serum free fatty acid and insulin-like growth factor I levels were significantly elevated (P < 0.01) at 4, 8, and 12 h and at 8, 12, and 24 h after 20K-hGH administration, respectively. Serum insulin and glucose levels did not change significantly within 24 h. These results suggested that: 1) regulation of 20K-hGH secretion is physiologically the same as that of 22K-hGH; 2) the pharmacokinetics after sc injection of 20K-hGH are comparable with those of 22K-hGH; 3) 20K-hGH regulates hGH secretion through "GH-induced negative feedback mechanisms"; and 4) administration of 20K-hGH is expected to exert GH actions (growth-promoting activity and lipolytic activity). Monitoring of serum 20K- and 22K-hGH levels may be useful in evaluating the effects of administered GH isoforms on their own release from the pituitary

[Othello]

The physiological and pharmacological functions of the 20-kDa human GH (20K-hGH) isoform are unknown. We conducted a pharmacokinetic study of recombinant 20K-hGH in human subjects (Phase I clinical trial). Placebo or 20K-hGH was administered sc to normal men (20-31 yr of age, n = 6-8 per group) at 2100 h. Serum 20K- and 22K-hGH levels were monitored every 30 min for 24 h by specific enzyme-linked immunosorbent assays. Serum free fatty acid, insulin-like growth factor I, insulin, and glucose levels were measured for 24 h. In the placebo group, the secretion profiles of endogenous 20K- and 22K-hGH were pulsatile and similar to each other. The proportion of 20K- to 22K-hGH was fairly constant. In the 20K-hGH-treated groups, serum 20K-hGH levels increased in a dose-dependent manner over the dose range of 0.01-0.1 mg/kg. Maximum serum 20K-hGH levels were reached at 3-4 h and decreased with half-lives of 2-3 h. Marked suppression of endogenous 22K-hGH secretion was observed in a time-dependent manner. Serum free fatty acid and insulin-like growth factor I levels were significantly elevated (P < 0.01) at 4, 8, and 12 h and at 8, 12, and 24 h after 20K-hGH administration, respectively. Serum insulin and glucose levels did not change significantly within 24 h. These results suggested that: 1) regulation of 20K-hGH secretion is physiologically the same as that of 22K-hGH; 2) the pharmacokinetics after sc injection of 20K-hGH are comparable with those of 22K-hGH; 3) 20K-hGH regulates hGH secretion through "GH-induced negative feedback mechanisms"; and 4) administration of 20K-hGH is expected to exert GH actions (growth-promoting activity and lipolytic activity). Monitoring of serum 20K- and 22K-hGH levels may be useful in evaluating the effects of administered GH isoforms on their own release from the pituitary

sources? where was this published? when was study done/conducted? how were subjects chosen?

no offense but afaic its just a write up of some sorts ...hope u understand my point OP

now to answer your question, to the best of my knowledge and after a long research I conducted last year both on forums and within medical community, I was not able to find any evidence to prove that such a thing as PCT was necessary for HgH...then again this being a much debated topic, I would be very much interested should there be proof to the contrary.

[marcus300]

Ive posted this before but some might find this interesting..


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.

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

References
↵
Lewis UJ, Bonewald LF, Lewis LJ. 1980 The 20,000 dalton variant of human growth hormone : location of the amino acid deletions. Biochem Biophys Res Commun. 92:511–516.
↵
DeNoto FM, Moore DD, Goodman HM. 1981 Human growth hormone DNA sequence and mRNA structure: possible alternative splicing. Nucleic Acids Res. 9:3719–3730.
↵
Cooke NE, Ray J, Watson MA, Estes PA, Kuo BA, Liebhaber SA. 1988 Human growth hormone gene and the highly homologous growth hormone variant gene display different splicing patterns. J Clin Invest. 82:270–275.
↵
De Vos AM, Ultsch M, Kossiakoff AA. 1992 Human growth hormone and extracellular domain of its receptor: crystal structure of the complex. Science. 255:306–312.
↵
Cunningham BC, Bass S, Fuh G, Wells JA. 1990 Zinc mediation of the binding of human growth hormone to the human prolactin receptor. Science. 250:1709–1712.
↵
Lewis UJ, Dunn JT, Bonewald LF, Seavey BK, VanderLaan WP. 1978 A naturally occurring structural variant of human growth hormone. J Biol Chem. 253:2679–2687.
↵
Baumann G. 1991 Growth hormone heterogeneity: genes, isohormones, variants, and binding proteins. Endocr Rev. 12:424–449.
↵
Lewis UJ, Markoff E, Culler FL, Hayek A, VanderLaan WP. 1987 Biologic properties of the 20K-dalton variant of human growth hormone: a review. Endocrinol Jpn. 34:73–85.
↵
Uchida H, Naito N, Asada N, et al. 1997 Secretion of authentic twenty kilodalton human growth hormone (20K hGH) in Escherichia coli and properties of the purified product. J Biotechnol. 55:101–112.
↵
Wada M, Ikeda M, Takahashi Y, et al. 1997 The full agonistic effect of recombinant 20 kDa human growth hormone (hGH) on CHO cells stably transfected with hGH receptor cDNA. Mol Cell Endocrinol. 133:99–107.
↵
Kostyo JL, Skottner A, Brostedt P, et al. 1987 Biological characterization of purified native 20-kDa human growth hormone. Biochim Biophys Acta. 925:325–331.
↵
Wada M, Uchida H, Ikeda M, et al. 1997 The 20 kDa human growth hormone (hGH) differs from the 22 kDa hGH in the complex formation with cell surface hGH receptor and hGH-binding protein circulating in human plasma. Mol Endocrinol. 12:146–156.
↵
Tsunekawa B, Wada M, Ikeda M, Uchida H, Naito N, Honjo M. 1998 The 20-kilodalton (kDa) human growth hormone (hGH) differs from the 22-kDa hGH in the effect on the human prolactin receptor. Endocrinology. 140:3909–3918.
↵
Hashimoto Y, Ikeda I, Ikeda M, et al. 1998 Construction of a specific and sensitive sandwich enzyme immunoassay for 20 kDa human growth hormone. J Immunol Methods. 221:77–85.
↵
Tsushima T, Katoh Y, Miyachi Y, et al. 1999 Serum concentration of 20K human growth hormone (20K hGH) measured by a specific ELISA. J Clin Endocrinol Metab. 84:317–322.
↵
Ishikawa M, Yokoya S, Tachibana K, et al. 1999 Serum levels of 20-kilodalton human growth hormone are parallel with 22-kilodalton human growth hormone in normal and short children. J Clin Endocrinol Metab. 84:98–104.
↵
Berg GVD, Veldhuis JD, Frölich M, Roelfsema F. 1996 An amplitude-specific divergence in the pulsatile mode of growth hormone (GH) secretion underlies the gender difference in mean GH concentrations in men and premenopausal women. J Clin Endocrinol Metab. 81:2460–2467.
↵
Dieguez C, Page MD, Scanlon MF. 1988 Growth hormone neuroregulation and its alterations in disease state. Crin Endocrinol (Oxf). 28:109–143.
↵
Abrams RL, Grumbach MM, Kaplan SL. 1971 The effect of administration of human growth hormone on the plasma growth hormone, cortisol, glucose, and free fatty acid response to insulin : evidence for growth hormone autoregulation in man. J Clin Invest. 50:940–950.
↵
Mendelson WB, Jacobs LS, JC Gillin. 1983 Negative feedback suppression of sleep-related growth hormone secretion. J Clin Endocrinol Metab. 56:486–488.
↵
Pontiroli AE, Lanzi LD, Monti E, Sandoli E, Pozza G. 1991 Growth hormone (GH) autofeedback on GH response to GH-releasing hormone. Role of free fatty acids and somatostatin. J Clin Endocrinol Metab. 72(2):492–495.
Berelowitz M, Szabo M, Frohman LA, Firestone S, Chu L, Hintz RL. 1981 Somatomedin C mediates growth hormone negative feed-back by effects on both hypothalamus and the pituitary. Science. 212:1279–1281.
↵
Casanueva FF, Villanueva L, Dieguez C, et al. 1987 Free fatty acids block growth hormone (GH) releasing hormone-stimulated GH secretion in man directly at the pituitary. J Clin Endocrinol Metab. 65:634–642.
↵
Dieguez C, Casanueva FF. 1995 Influence of metabolic substrates and obesity on growth hormone secretion. Trends Endocrinol Metab. 6:55–59.
↵
Baumann G, Stolar MW. 1986 Molecular forms of human growth hormone secreted in vivo: nonspecificity of secretory stimuli. J Clin Endocrinol Metab. 62:789–790.
↵
Urae A, Irie S, Amamoto T, Kumamoto M, Urae R, Morise H. 1992 Clinical trial phase I of LY137998 -biological equivarence test of the products manufactured by new method (2 cistron) and conventional method (1 cistron). Clin Report. 26:1063–1084.
↵
Ho KY, Weissberger AJ, Stuart MC, Day RO, Lazarus L. 1989 The pharmacokinetics, safety and endocrine effects of authentic biosynthetic human growth hormone in normal subjects. Clin Endocrinol. 30:335–345.
↵
Baumann G, Stolar MW, Buchanan TA. 1985 Slow metabolic clearance rate of the 20,000-dalton variant of human growth hormone: implications for biological activity. Endocrinology. 117:1309–1313.
↵
Baumann G, Shaw MA. 1990 Plasma transport of the 20,000-daltone variant of human growth hormone (20K): evidence for a 20K-specific binding site. J Clin Endocrinol Metab. 71:1339–1343.
↵
Fairhall KM, Carmignac DF, Robinson ICAF. 1992 Growth hormone (GH) binding protein and GH interactions in vivo in the guinea pig. Endocrinology. 131:1963–1969.
↵
Willoughby JO, Menadue M, Zeegers P, Wise PH, Oliver JR. 1980 Effects of human growth hormone on the secretion of rat growth hormone. J Endocrinol. 86:165–169.
↵
Lanzi R, Tannenbaum GS. 1992 Time course and mechanism of growth hormone’s negative feedback effect on its own spontaneous release. Endocrinology. 130:***–788.
↵
Clark RG, Morthnsen DI, Carlsson LMS, et al. 1996 Recombinant human growth hormone (GH)-binding protein enhances the growth-promoting activity of human GH in the rat. Endocrinology. 137:4308–4315.
↵
Rosenthal SM, Kaplan SL, Grumbach MM. 1989 Short term continuous intravenous infusion of growth hormone (GH) inhibits GH-releasing hormone-induced GH secretion: a time-dependent effect. J Clin Endocrinol Metab. 68:1101–1105.
↵
Imaki T, Shibasaki T, Shizume K, et al. 1985 The effect of free fatty acids on growth hormone-releasing hormone-mediated GH secretion in man. J Clin Endocrinol Metab. 60:290–294.
↵
Briard N, Rico-gomez M, Guillaume V, et al. 1998 Hypothalamic mediated action of free fatty acid on growth hormone secretion in sheep. Endocrinology. 139:4811–4819.
↵
Rosenthal SM, Hulse JA, Kaplan SL, Grumbach MM. 1986 Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men. J Clin Invest. 77:176–180.
↵
Pontiroli AE, Lanzi R, Pozza G. 1989 Inhibition of the growth hormone (GH) response to GH-releasing hormone by constant Met-GH infusions. J Clin Endocrinol Metab. 68:956–959

.

[aestheticsfirst]

So when would you inject hgh? If it raises 12 hours after injection and peaks at 24 hours would it be best to inject at night?

[aestheticsfirst]

The passage is form

J Clin Endocrinol Metab. 2000 Feb;85(2):601-6.

Exogenous 20K growth hormone (GH) suppresses endogenous 22K GH secretion in normal men.

Hashimoto Y1, Kamioka T, Hosaka M, Mabuchi K, Mizuchi A, Shimazaki Y, Tsunoo M, Tanaka T.


I heard eventually levels do get back to normal but that depends on how long you've been taking it. For example, if you have been taking it for 3 months then it will take three months to get back to normal. If you've been taking it for 2 years it will take 2 years to get back to normal. I think there was a study done on kids that supported this.

What I am trying to do is kickstart the production immediately so I wouldn't have to wait so long.