Ghrp-6, prolactin, and cortisol

TripDog

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Ghrp-6 is said to raise prolactin and cortisol along with gh. I read that clinical trials were stopped due to this fact. There also seems to be a lot of feedback stating that peptides loose their effectiveness over time. (hex for example is said to work very short term)

Given the fact about prolactin, would a dopamine agonist prevent this from being an issue. (selegline,l-dopa,cabergoline,1-carboxy) I assume so.....as dopamine controls prolactin release.

The issue with cortisol (ACTH) seems like it would not be very helpful in post cycle. On a cycle this obviously wont be much of an issue, but off cycle how is the best method to combat this?

Best time to inject I would think is in the middle of the night when blood sugar is low. (get up , piss, shoot a preloaded syringe, go back to sleep)

I also gather that multiple doses in one day probably will add to resistance of the peptide. Any input on this?

Arginine... helpful or worthless to use with it? I am thinking about injectible argine with each dose in the future.

Lets break down this subject

~TriP
 

Bobaslaw

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Ghrp-6 is said to raise prolactin and cortisol along with gh. I read that clinical trials were stopped due to this fact. There also seems to be a lot of feedback stating that peptides loose their effectiveness over time. (hex for example is said to work very short term)

Given the fact about prolactin, would a dopamine agonist prevent this from being an issue. (selegline,l-dopa,cabergoline,1-carboxy) I assume so.....as dopamine controls prolactin release.

The issue with cortisol (ACTH) seems like it would not be very helpful in post cycle. On a cycle this obviously wont be much of an issue, but off cycle how is the best method to combat this?

Best time to inject I would think is in the middle of the night when blood sugar is low. (get up , piss, shoot a preloaded syringe, go back to sleep)

I also gather that multiple doses in one day probably will add to resistance of the peptide. Any input on this?

Arginine... helpful or worthless to use with it? I am thinking about injectible argine with each dose in the future.

Lets break down this subject

~TriP
Hey Trip,

I have always had may reservations regarding these secretagogues due to the unselective nature of their agonism against a number of different pituitary 'trophs' (corticotrphs, lactotrophs, and ofcourse somatotrophs).
I initially wanted to use GHRP during PCT, but due to this , I decided it was not worth the added cortisol and prolactin as it's already difficult enough to keep these at bay.

As far as Arginine goes, its method of action is targeted at reducing somatostatin tone, thus it is beneficial at increasing GH through this mechanism regardless of protocol. Obviously it will be synergistic with secretagogues and CJC, since somatotrophs will be less antagoinised by somatostatin and open to more agonism by the aforementoned GH agonists.

As far as blunting Cort or prolactin (PRL) by the secretagogues (GHRP/HEX). I am speculating that Cort blockers like Phosphatydilserine (PS) will not do much directly for the ghrp/hex ACTH agonism since its method of action is on the hypothalamus receptors. Secretagogues will not care since they agonise corticotrophs directly bypassing any hypothalums mediated cort control. I do surmise that PS would, however, keep the hypothalamus receptors sensitive and keep its own CRH release at a minimum (as this is the normal method of action by PS). This would lower CRH mediated ACTH release, but probably not make a big impact to offset the secretagoge mediated ACTH increase.
Substrate based cort blockers would be more beneficial IMO, as they would bind and keep the excess of 11Beta-HSD1 reductase busy. This would leave less 11Beta-HSD1 reductase available to activate the ACTH mediated increase of corticosterone into cortisol.

I do beleive that L-Dopa mediated Dopamine increase may help, but this would really be dependant on how much of a Dopamine increase the L-Dopa regimen would allow. B-6, preferably P-5-P can also help increase Dopamine levels. P-5-P is the active form converted from B6 and will not pose the negatives of high B6 use. Unutilized pyridoxine (B6) that is not converted to p-5-p can build up in tissue and cause neropathy.
Cabergoline or even Bromocriptine as a dopamine agonist would work more directly to increase dopamine, but have more side effects (Caber and Heart Valve issues). p-5-p/L-dopa regimen could be a safer alternative.
Dopamine, binding to dopamine receptors, directly inhibits the secratory action of prolactin from lactotrophs by controlling intracellular calcium fluxes. This would definitely blunt the opposed action of GHRP/Hex as the lactotroph would be unable to properly respond. Dopamine also reduces PRL gene expression which would also reduce the amount of PRL stored within the cell waiting for release.

Anyhow, all this is why I have decided that CJC is a MUCH better alternative for GH release stimulator. CJC is basically a modified long lasting version of the body's own GHRH and is selective for somatotrophs only.

On a side note, Hullcrush (a forum member) added an interesting study regarding secretagogues (Hex in this case) that shows a very synergistic action when combined with GHRH. In a concurrent application of GHRH with Hex, PRL was minimally affected and there was NO cort increase as opposed to the Hex regimen on it's own. Doses of Hex in combination with GHRH were .125mcg/kg which equates to 125mcg for a 220lb person. This might be a good stack with CJC considering GHRP/Hex is cheaper than CJC. I am uncertain but speculate that this may hold true for GHRP due to its close similarity to Hex, as both are hexapeptides.

Please see below:

Hexarelin-induced growth hormone, cortisol, and pr...[J Clin Endocrinol Metab. 1996] - PubMed Result

Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study.

Massoud AF, Hindmarsh PC, Brook CG.
London Center for Pediatric Endocrinology and Metabolism, Middlesex Hospital, London, United Kingdom.

Dose-response data for GH-releasing peptides are limited. We studied the effects of varying doses (0-1.0 microgram/kg) of hexarelin, a novel GH-releasing peptide, administered iv to healthy adult males on GH, PRL, and cortisol release. In addition, we studied the effect of administration of a single dose of GHRH-(1-29)-NH2 (1.0 microgram/kg), alone or in combination with a low dose of hexarelin (0.125 microgram/kg). Dose-response curves for the maximum GH response and maximum percent change in serum PRL and cortisol concentrations from baseline were constructed. The GH dose-response curve reached a plateau of 140 mU/L, corresponding to a hexarelin dose of 1.0 microgram/kg, with an ED50 of 0.48 +/- 0.02 microgram/kg (mean +/- SEM). The PRL dose-response curve reached a plateau of 180% for the maximum percent rise from baseline, corresponding to a hexarelin dose of 1.0 microgram/kg, with an ED50 of 0.39 +/- 0.02 microgram/kg. The cortisol dose-response curve showed a step increase to approximately 40% at a hexarelin dose of 0.5 microgram/kg. The coadministration of GHRH-(1-29)-NH2 (1.0 microgram/kg) and low dose hexarelin (0.125 microgram/kg) resulted in massive GH release (115 +/- 32.8 mU/L), a moderate rise in serum PRL (84.9 +/- 27.5%), and no rise in serum cortisol. These data show that iv hexarelin was capable of inducing GH, PRL, and cortisol release in a dose-dependent manner. Low dose hexarelin was synergistic with GHRH and potent for GH release with a minimal effect on other hormones.
 
datBtrue

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Well guys I've chosen not to over-analyze these things. Nothing compares to Tren & Deca as far as causing prolactin problems for me ...so IMHO the prolactin problems from all else are managable.

Here is my simple goal... I want to find compounds that increase my daily production of Growth Hormone by at least 1iu to 2iu.

So far the pGH has worked very well ...I will probably replace that w/ GHRP-6 within a week or so and run that for a couple of months...I'm going to go by feel (mostly mood & energy elevation w/ positive effects on maintaining leaness) as well as look for signs that prolactin is a problem (decreased sexual performance & yes the old nipple squeeze ...hopefully zero discharge).

I am hoping that GHRP-6 will be equally or a little bit more effective than the pGH has been. If that proves to be the case I will mix and match dosing between these compounds so as to keep them effective (maybe 4 days of pGH followed by 4 days of GHRP-6).

Trip my approach has always been to try it out and see how it works in my body. If you start out by taking multiple things in anticipation of problems you never discover if the compound even causes a problem let alone to what degree the compound is effective as a standalone. Just my 2 cents.
 
TripDog

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Well guys I've chosen not to over-analyze these things. Nothing compares to Tren & Deca as far as causing prolactin problems for me ...so IMHO the prolactin problems from all else are managable.

Here is my simple goal... I want to find compounds that increase my daily production of Growth Hormone by at least 1iu to 2iu.

So far the pGH has worked very well ...I will probably replace that w/ GHRP-6 within a week or so and run that for a couple of months...I'm going to go by feel (mostly mood & energy elevation w/ positive effects on maintaining leaness) as well as look for signs that prolactin is a problem (decreased sexual performance & yes the old nipple squeeze ...hopefully zero discharge).

I am hoping that GHRP-6 will be equally or a little bit more effective than the pGH has been. If that proves to be the case I will mix and match dosing between these compounds so as to keep them effective (maybe 4 days of pGH followed by 4 days of GHRP-6).

Trip my approach has always been to try it out and see how it works in my body. If you start out by taking multiple things in anticipation of problems you never discover if the compound even causes a problem let alone to what degree the compound is effective as a standalone. Just my 2 cents.
I used a great amout of ghrp-6 last year(also cjc-1295,hexralin,igf) but i didnt keep close tabs on my results. I'm mixing pGH also(w/ ghrp-6) and I know it works great in conjunction to any peptide. I take around 5 grams oral gaba nightly also.
 
datBtrue

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On a side note, Hullcrush (a forum member) added an interesting study regarding secretagogues (Hex in this case) that shows a very synergistic action when combined with GHRH. In a concurrent application of GHRH with Hex, PRL was minimally affected and there was NO cort increase as opposed to the Hex regimen on it's own. Doses of Hex in combination with GHRH were .125mcg/kg which equates to 125mcg for a 220lb person. This might be a good stack with CJC considering GHRP/Hex is cheaper than CJC. I am uncertain but speculate that this may hold true for GHRP due to its close similarity to Hex, as both are hexapeptides.

Please see below:

Hexarelin-induced growth hormone, cortisol, and pr...[J Clin Endocrinol Metab. 1996] - PubMed Result
Interesting abstract Bob. Here is the full study Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study in pdf form.

Full study: View attachment 4338.pdf
 
datBtrue

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I used a great amout of ghrp-6 last year(also cjc-1295,hexralin,igf) but i didnt keep close tabs on my results. I'm mixing pGH also(w/ ghrp-6) and I know it works great in conjunction to any peptide. I take around 5 grams oral gaba nightly also.
So you don't feel the oral GABA makes pGH less effective over time?

That is cool that you are way ahead of me on this bro. Are you dosing pGH & ghrp-6 together or in different dosings on the same day or what?

Synergy would be great if that is what happens.
 
TripDog

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Interesting abstract Bob. Here is the full study Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study in pdf form.

View attachment 21297
Great article bro!!!! Thats exactly the type of info that helps us out!!!..reps
 
TripDog

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So you don't feel the oral GABA makes pGH less effective over time?

That is cool that you are way ahead of me on this bro. Are you dosing pGH & ghrp-6 together or in different dosings on the same day or what?

Synergy would be great if that is what happens.
I do both at the same time(ghrp-6/pGH), as far as oral gaba...I LOVE it and will always use it prior to sleep. My next experiment is inject arginine with the 2.....(ghrp-6/pgh)
 
datBtrue

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Great article bro!!!! Thats exactly the type of info that helps us out!!!..reps
Yeah I love the conclusion in that full study

"Furthermore, using a combination of GHRH and low dose hexarelin restored and exceeded the massive GH release observed with hexarelin alone. This opens up the possibility of using even smaller doses of GHRP in combination with GHRH. The obvious route of GHRP administration would be oral, given perhaps twice daily, with GHRH given as a depot preparation."

Trip this touches on what you've always said about witnessing/feeling synergy between peptides. You are the ultimate peptide stacker. :)
 
datBtrue

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I do both at the same time(ghrp-6/pGH), as far as oral gaba...I LOVE it and will always use it prior to sleep. My next experiment is inject arginine with the 2.....(ghrp-6/pgh)
Trip you'll find this study very interesting on a lot of levels...not just its findings on Arginine but it also touches on many interesting things (by-the-way it studied both young & old). I like to look at the full studies and not the abstract because the discussion is often very useful in educating my feeble head.

Here is the study in full in pdf format:

Arginine and Growth Hormone-Releasing Hormone Restore the Blunted Growth Hormone-Releasing Activity of Hexarelin in Elderly Subjects*

E. ARVAT, L. GIANOTTI, S. GROTTOLI, B. P. IMBIMBO, V. LENAERTS, R. DEGHENGHI, F. CAMANNI, AND E. GHIGO

Division of Endocrinology, Department of Clinical Pathophysiology, University of Turin (E.A., L.G., S.G.,
F.C., E.G.), Turin, Italy; Medical Department. Mediolanum Farmaceutici (B.P.I.), Milan, Italy; Europeptides (V.L., R.D.), Argenteuil, France

Full study: View attachment 1440.pdf

For those to lazy to download the pdf file here is the "Discussion" section of the study:

This study demonstrates that, like GHRP-6 (28, 29), hexarelin has an age-related GH-releasing activity. However, although the stimulating effect of the maximally effective dose of hexarelin on somatotrope secretion is reduced in human aging, it releases more GH than the supramaximal effective dose of GHRH even in elderly subjects. Our results also indicate that the combined administration of hexarelin and GHRH has a synergistic effect in elderly subjects, as previously reported in young subjects (30).

This study also shows that in human aging, the GH releasable pool is markedly larger than previously thought. This observation is supported by previous animal (6) and human (3, 4) studies. In addition, our results indicate that hexarelin, like other GHRPs, has a different mechanism of action from that of GHRH in stimulating somatotrope secretion. GHRPs and GHRH have different receptor sites on the pituitary (16, 17, 18), and GHRP receptor activation does not increase intracellular CAMP levels, contrary to GHRH (19). The GH-releasing activity of GHRPs and their synergistic effect with GHRH are greater in viva than in vitro (17, 20), thus suggesting that GHRPs also act at the hypothalamic level, where specific receptors have been identified (21). Normal GHRH activity is needed before GHRPs can exert their GH- releasing effect (20, 31). Therefore, the reduced activity of hexarelin, either alone or combined with GHRH in human aging, may be explained by a decrease in the activity of GHRH-secreting neurons or by changes in GHRH receptors, as shown by other studies conducted in animals (7, 11, 32) and man (5, 33).

We found that arginine, an amino acid that probably acts by suppressing endogenous somatostatin release (9, lo), counteracts the age-related decrease in the GH-releasing effect of hexarelin in elderly subjects. Both animal (6, 8) and human (3, 4) studies suggest that there is a pronounced somatostatinergic hyperactivity in human aging. This could explain the age-related decline in both spontaneous and stimulated GH secretion and the effectiveness of arginine in restoring the response to hexarelin in the elderly. Arginine’s failure to increase the GH response to hexarelin in young subjects, however, remains to be clarified. It may be that GHRPs act at the pituitary level by antagonizing the effect of somatostatin. In fact, GHRPs counteract the hyperpolarizing effect of somatostatin on rat somatotrope cell membrane (18). In man, the GH-releasing effect of hexarelin is blunted, but not abolished, by a high dose of exogenous somatostatin (30), which abolishes the somatotrope response to all known GH secretagogues, including GHRH (30, 34). Thus, it could be hypothesized that hexarelin’s antagonism of somatostatin at the pituitary level is partially overridden in aging by a pronounced hypothalamic somatostatinergic activity.

In conclusion, this study shows that the maximally effective dose of hexarelin releases more GH than the maximally effective dose of GHRH in both normal young and elderly subjects. The effect of hexarelin on GH secretion is age dependent, and the GH response to the combined administration of the two drugs was significantly higher in young subjects compared to elderly subjects. Arginine does not potentiate the GH response to hexarelin in young subjects, whereas it significantly enhances it in elderly subjects. These findings suggest that hexarelin acts, at least partially, independently from GHRH and/or somatostatin. These results also support the presence of a somatostatinergic hyperactivity in aging, which is probably related to a concomitant reduction in the activity of GHRH-secreting neurons.
 
datBtrue

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Here's another interesting study Arginine Counteracts the Inhibitory Effect of Recombinant Human Insulin-Like Growth Factor I on the Somatotroph Responsiveness to Growth Hormone-Releasing Hormone in Humans

Cutting to the meat of the study "...In agreement with other studies (6, 14), the GH response to the maximal effective dose of GHRH was significantly inhibited by rhIGF-I. By contrast, no inhibitory effect of rhIGF-I on the somatotroph responsiveness to GHRH was recorded when the neurohormone was administered in combination with ARG, which strikingly potentiated its GH-releasing effect."

In conclusion "...In conclusion, this study shows that ARG overrides the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings indicate that the acute inhibitory effect of acute rhIGF-I administration on somatotroph secretion takes place on the hypothalamus, where concomitant triggering of SS release and inhibition of GHRH-secreting neurons might play a major role."​

Full study: View attachment 3604.pdf
 

Bobaslaw

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Here is some more related great info from a previous thread that touched on some of these areas. This is the origninal thread:

http://anabolicminds.com/forum/igf-1-gh/89995-cjc-1295-peg.html#post1287651

Interesting studies discussed in that thread:

http://jcem.endojournals.org/cgi/rep...152.pdf?ck=nck

an interesting excerpt from the above which shows arginine could possibly be useful before eating carbs, countering glucose induced somatostatin tone:

We used an oral glucose load as an approach to investigate
endogenous somatostatin tone, as it is generally accepted
that the acute inhibitory effect of glucose on plasma GH
levels is a consequence of somatostatin reflex discharge from
the hypothalamus. In normal adult subjects, acute hyperglycemia
blocks GH release stimulated by GHRH (4-6, 16-18),
and treatment with pyridostigmine (5, 6) or arginine (19)
counteracts the inhibitory action of glucose on GH release.
Also, originally found by Solarus showing oral arginine does increase GH output when coadministered with GHRH:

http://www.ncbi.nlm.nih.gov/pubmed/7850007?ordinalpos=29&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Effect of 15-day treatment with growth-hormone-releasing hormone alone or combined with different doses of arginine on the reduced somatotrope responsiveness to the neurohormone in normal aging.

Ghigo E, Ceda GP, Valcavi R, Goffi S, Zini M, Mucci M, Valenti G, Muller EE, Camanni F.
Department of Clinical Pathophysiology, University of Turin, Italy.

It is well known that both spontaneous and growth hormone-releasing hormone (GHRH)-stimulated GH secretion undergo an age-related decrease; in addition, there is supportive evidence that the GH hyposecretory state of aging is of hypothalamic origin. The aims of the study in 35 normal elderly subjects (20 males and 15 females aged 65-89 years) were to verify whether the low somatotrope responsiveness to GHRH (1 microgram/kg) can be primed by a daily GHRH treatment and whether the potentiating effect of both high intravenous (0.5 g/kg) and low oral (8 g) doses of arginine (ARG) on GH response to GHRH is maintained with time. In group A (N = 14) the GH response to GHRH on day 1 (AUC: 373.5 +/- 78.5 micrograms.l-1.h-1) was unchanged after 7 (3720 +/- 38 micrograms.l-1.h-1) and 15 days (377.9 +/- 63.8 micrograms.l-1.h-1) of daily GHRH administration. In group B (N = 6) the GH response to GHRH co-administered with iv ARG on day 1 (1614.2 +/- 146.2 micrograms.l-1.h-1) was higher (p < 0.05) than that of GHRH alone (group A) and persisted unchanged after 7 (1514.7 +/- 366.5 micrograms.l-1.h-1) and 15 days (1631.7 +/- 379.1 micrograms.l-1.h-1) of treatment. In group C (N = 15) the GH response to GHRH co-administered with oral ARG on day 1 (950.6 +/- 219.4 micrograms.l-1.h-1) was higher (p < 0.03) than that of GHRH alone (group A) but lower (p < 0.05) than that to GHRH plus iv ARG (group B).(ABSTRACT TRUNCATED AT 250 WORDS)
 

Bobaslaw

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Well guys I've chosen not to over-analyze these things. Nothing compares to Tren & Deca as far as causing prolactin problems for me ...so IMHO the prolactin problems from all else are managable.
Hey DBT

Actually I am less concerned about Prolactin increases and more put off by the significant Cortisol increases from the secretagogues (Ghrp-6/Hex). An my concern is more focused when considering using them during dieting/cutting and/or PCT, since those are the times when cortisol increase has a more dramatic negative impact.
Other than price, I see no advantage in GHRP/Hex vs CJC. And with the study on the blunting effects of GHRH on secretagogue induced cort and prolactin increases, I am definitely going to stack both. If money is tight, one could actually lower the dose of CJC and focus on increasing Hex or GHRP keeping the doses within range of the study guidelines say around 125mcg, couple of times per day. I know the study used .125mcg/kg, but who knows what the upper limits of a reasonable curve would be here.
 

Bobaslaw

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Here's another interesting study Arginine Counteracts the Inhibitory Effect of Recombinant Human Insulin-Like Growth Factor I on the Somatotroph Responsiveness to Growth Hormone-Releasing Hormone in Humans

Cutting to the meat of the study "...In agreement with other studies (6, 14), the GH response to the maximal effective dose of GHRH was significantly inhibited by rhIGF-I. By contrast, no inhibitory effect of rhIGF-I on the somatotroph responsiveness to GHRH was recorded when the neurohormone was administered in combination with ARG, which strikingly potentiated its GH-releasing effect."

In conclusion "...In conclusion, this study shows that ARG overrides the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings indicate that the acute inhibitory effect of acute rhIGF-I administration on somatotroph secretion takes place on the hypothalamus, where concomitant triggering of SS release and inhibition of GHRH-secreting neurons might play a major role."​

Full study: View attachment 21299
Another interesting find DBT.
It does not surprise me that IGF has this effect as this is most likely part of the GH feedback mechanism. As GH mediated IGF levels rise in the body, the hypo/pituitary adjust accordingly and thus GH release is blunted to some degree by the negative feedback at the hypothalmus, thus increasing SS release.
Obviously Arg will blunt SS tone, thus negating the effect of IGF on SS release to some degree.
 

Bobaslaw

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In conclusion, this study shows that the maximally effective dose of hexarelin releases more GH than the maximally effective dose of GHRH in both normal young and elderly subjects. The effect of hexarelin on GH secretion is age dependent, and the GH response to the combined administration of the two drugs was significantly higher in young subjects compared to elderly subjects. Arginine does not potentiate the GH response to hexarelin in young subjects, whereas it significantly enhances it in elderly subjects. These findings suggest that hexarelin acts, at least partially, independently from GHRH and/or somatostatin. These results also support the presence of a somatostatinergic hyperactivity in aging, which is probably related to a concomitant reduction in the activity of GHRH-secreting neurons.[/COLOR][/INDENT]
Another interesting study that shows Hex most likely has direct action against inhibiting somatostatin tone:

http://www.ncbi.nlm.nih.gov/pubmed/9425393?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&dbfrom=pubmed

Interaction of the growth hormone releasing peptide hexarelin with somatostatin.

Massoud AF, Hindmarsh PC, Brook CG.
London Centre for Paediatric Endocrinology and Metabolism, Middlesex Hospital, UK.

OBJECTIVE: Growth hormone releasing peptides (GHRPs) are potent growth hormone (GH) secretagogues. Their interaction with growth hormone releasing hormone (GHRH) has been studied extensively. Data on their interaction with somatostatin (SS) are limited. The aim of this study was to determine the effect of changing SS tone and the effects of SS withdrawal on the somatotroph response to hexarelin and GHRH, alone or in combination. In addition, we studied the effect of SS on the prolactin (PRL) and cortisol response to hexarelin. DESIGN: Boluses of saline, hexarelin (1 microgram/kg), GHRH-(1-29)-NH2 (1 microgram/kg) or hexarelin plus GHRH-(1-29)-NH2 were administered intravenously 1 hour after the start of a 3-hour constant intravenous infusion of saline, SS(1-14) (20 micrograms/m2/h) (SS20) or SS(1-14) (50 micrograms/m2/h) (SS50). In a second group of studies, the same boluses as above were administered intravenously at the time of withdrawal of a 3-hour constant intravenous infusion of saline or SS20. In a subset of the second group of studies, saline, hexarelin (0.5 microgram/kg) or GHRH-(1-29)-NH2 (0.5 microgram/kg) was administered intravenously two hours before the withdrawal of the SS(1-14) infusion, which was administered at a higher dose of 50 micrograms/m2/h. Studies were performed in a random order. SUBJECTS: Twelve healthy adult males (20.3-34.6 years) were studied. MEASUREMENTS: Serum GH and PRL concentrations were measured by immunoradiometric assays. Serum cortisol concentrations were measured by radioimmunoassay. RESULTS: Infusion of SS20 resulted in a significant reduction in the peak GH response to hexarelin, GHRH-(1-29)-NH2 or hexarelin plus GHRH-(1-29)-NH2 (P < 0.05). The peak serum GH concentrations following the intravenous administration of the two secretagogues, separately or in combination, were reduced further by the higher dose of SS50, but these were not significantly different from their respective peak serum GH concentrations obtained during the infusion of SS20. The peak serum GH concentration following the intravenous administration of hexarelin plus GHRH-(1-29)-NH2 remained large (52.6 +/- 7.2 mU/l; mean +/- SEM) despite the high dose of SS(1-14) (50 micrograms/m2/h). SS(1-14) did not affect the PRL and cortisol response to hexarelin. Withdrawal of SS20 infusion at the time of intravenous bolus administration of hexarelin, but not GHRH-(1-29)-NH2 or hexarelin plus GHRH-(1-29)-NH2, resulted in a significant increase in peak serum GH concentration (P = 0.03). The intravenous administration of hexarelin (0.5 microgram/kg) or GHRH-(1-29)-NH2 (0.5 microgram/kg) during an intravenous infusion of SS50 resulted in a small GH response (peak concentrations 6.8 +/- 3.6 mU/l and 2.4 +/- 0.5 mU/l, respectively) but the later withdrawal of the infusion was not followed by a rise in serum GH concentrations. CONCLUSIONS: This study shows that SS and hexarelin counteract their respective inhibitory and stimulatory action on GH secretion and provides further evidence for their interaction in vivo. The stimulatory effect of hexarelin on the lactotroph and the hypothalamo-pituitary-adrenal axis is unaltered by SS. Hexarelin plus GHRH are synergistic and have potent GH-releasing activity despite a high dose SS infusion. Withdrawal of SS enhances the GH response to hexarelin, which may reflect simultaneous endogenous GHRH release synergizing with hexarelin. A single cycle of pretreatment with hexarelin during SS infusion is insufficient to allow synthesis and storage of sufficient GH to influence its release following SS withdrawal. These findings add further to the data already gathered about GHRPs and their complex interaction with the main regulators of GH secretions.
 
TripDog

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Here's another interesting study Arginine Counteracts the Inhibitory Effect of Recombinant Human Insulin-Like Growth Factor I on the Somatotroph Responsiveness to Growth Hormone-Releasing Hormone in Humans

Cutting to the meat of the study "...In agreement with other studies (6, 14), the GH response to the maximal effective dose of GHRH was significantly inhibited by rhIGF-I. By contrast, no inhibitory effect of rhIGF-I on the somatotroph responsiveness to GHRH was recorded when the neurohormone was administered in combination with ARG, which strikingly potentiated its GH-releasing effect."

In conclusion "...In conclusion, this study shows that ARG overrides the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings indicate that the acute inhibitory effect of acute rhIGF-I administration on somatotroph secretion takes place on the hypothalamus, where concomitant triggering of SS release and inhibition of GHRH-secreting neurons might play a major role."​

Full study: View attachment 21299
First off i'm lovin all the studies, second can this effect be achieved by arginine alpha-ketoglutarate, or is injectable arginine the way to go?
 

Bobaslaw

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First off i'm lovin all the studies, second can this effect be achieved by arginine alpha-ketoglutarate, or is injectable arginine the way to go?

Hey Trip,

Look at the study that I posted. It shows 8g of oral arginine makes a pretty significant additional increase in GH when combined with GHRH.
I would go with AAKG or A Ethyl Ester since straight L-Arginine is not as bioavailable orally. AAKG is has a ratio of 2:1 so you can figure out the actual dose of Arginine there...

Take Care.

PS- I use it before carb meals as well since it has a good blunting effect against glucose on somatostatin tone. (another study I posted earlier in this thread).
 
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TripDog

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Hey Trip,

Look at the study that I posted. It shows 8g of oral arginine makes a pretty significant additional increase in GH when combined with GHRH.
I would go with AAKG or A Ethyl Ester since straight L-Arginine is not as bioavailable orally. AAKG is has a ratio of 3:1 so you can figure out the actual dose of Arginine there...

Take Care.

PS- I use it before carb meals as well since it has a good blunting effect against glucose on somatostatin tone. (another study I posted earlier in this thread).
wait 3:1 meaning what? You are the pro with all the numbers so i'll just ask. What dose of aakg...around 4000mg
 
datBtrue

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I would go with AAKG or A Ethyl Ester since straight L-Arginine is not as bioavailable orally....
Good, better, best ...is it really THAT important? I don't know...

L-arginine-induced vasodilation in healthy humans: pharmacokinetic-pharmacodynamic relationship

Authors: Bode-Böger, Stefanie M.; Böger, Rainer H.; Galland, Andrea; Tsikas, Dimitrios; Frölich, Jürgen C.
Source: British Journal of Clinical Pharmacology, Volume 46, Number 5, November 1998 , pp. 489-497(9)

Abstract:

Aims Administration of l-arginine by intravenous infusion or via oral absorption has been shown to induce peripheral vasodilation in humans, and to improve endothelium-dependent vasodilation. We investigated the pharmacokinetics and pharmacokinetic-pharmacodynamic relationship of l-arginine after a single intravenous infusion of 30 g or 6 g, or after a single oral application of 6 g, as compared with the respective placebo, in eight healthy male human subjects.

Methods l-arginine levels were determined by h.p.l.c. The vasodilator effects of l-arginine were assessed non-invasively by blood pressure monitoring and impedance cardiography. Urinary nitrate and cyclic GMP excretion rates were measured as non-invasive indicators of endogenous NO production.

Results Plasma l-arginine levels increased to (mean±s.e.mean) 6223±407 (range, 5100-7680) and 822±59 (527-955) μmol l−1 after intravenous infusion of 30 g and 6 g l-arginine, respectively, and to 310±152 (118-1219) μmol l−1 after oral ingestion of 6 g l-arginine. Oral bioavailability of l-arginine was 68±9 (51-87)%. Clearance was 544±24 (440-620), 894±164 (470-1190), and 1018±230 (710-2130) ml min−1, and elimination half-life was calculated as 41.6±2.3 (34-55), 59.6±9.1 (24-98), and 79.5±9.3 (50-121) min, respectively, for 30 g i.v., 6 g i.v., and 6 g p.o. of l-arginine. Blood pressure and total peripheral resistance were significantly decreased after intravenous infusion of 30 g l-arginine by 4.4±1.4% and 10.4±3.6%, respectively, but were not significantly changed after oral or intravenous administration of 6 g l-arginine. l-arginine (30 g) also significantly increased urinary nitrate and cyclic GMP excretion rates by 97±28 and 66±20%, respectively. After infusion of 6 g l-arginine, urinary nitrate excretion also significantly increased, (nitrate by 47±12% [P<0.05], cyclic GMP by 67±47% [P=ns]), although to a lesser and more variable extent than after 30 g of l-arginine. The onset and the duration of the vasodilator effect of l-arginine and its effects on endogenous NO production closely corresponded to the plasma concentration half-life of l-arginine, as indicated by an equilibration half-life of 6±2 (3.7-8.4) min between plasma concentration and effect in pharmacokinetic-pharmacodynamic analysis, and the lack of hysteresis in the plasma concentration-versus-effect plot.

Conclusions The vascular effects of l-arginine are closely correlated with its plasma concentrations. These data may provide a basis for the utilization of l-arginine in cardiovascular diseases.
 
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Good, better, best ...is it really THAT important? I don't know...

L-arginine-induced vasodilation in healthy humans: pharmacokinetic-pharmacodynamic relationship

Authors: Bode-Böger, Stefanie M.; Böger, Rainer H.; Galland, Andrea; Tsikas, Dimitrios; Frölich, Jürgen C.
Source: British Journal of Clinical Pharmacology, Volume 46, Number 5, November 1998 , pp. 489-497(9)

Abstract:

Aims Administration of l-arginine by intravenous infusion or via oral absorption has been shown to induce peripheral vasodilation in humans, and to improve endothelium-dependent vasodilation. We investigated the pharmacokinetics and pharmacokinetic-pharmacodynamic relationship of l-arginine after a single intravenous infusion of 30 g or 6 g, or after a single oral application of 6 g, as compared with the respective placebo, in eight healthy male human subjects.

Methods l-arginine levels were determined by h.p.l.c. The vasodilator effects of l-arginine were assessed non-invasively by blood pressure monitoring and impedance cardiography. Urinary nitrate and cyclic GMP excretion rates were measured as non-invasive indicators of endogenous NO production.

Results Plasma l-arginine levels increased to (mean±s.e.mean) 6223±407 (range, 5100-7680) and 822±59 (527-955) μmol l−1 after intravenous infusion of 30 g and 6 g l-arginine, respectively, and to 310±152 (118-1219) μmol l−1 after oral ingestion of 6 g l-arginine. Oral bioavailability of l-arginine was 68±9 (51-87)%. Clearance was 544±24 (440-620), 894±164 (470-1190), and 1018±230 (710-2130) ml min−1, and elimination half-life was calculated as 41.6±2.3 (34-55), 59.6±9.1 (24-98), and 79.5±9.3 (50-121) min, respectively, for 30 g i.v., 6 g i.v., and 6 g p.o. of l-arginine. Blood pressure and total peripheral resistance were significantly decreased after intravenous infusion of 30 g l-arginine by 4.4±1.4% and 10.4±3.6%, respectively, but were not significantly changed after oral or intravenous administration of 6 g l-arginine. l-arginine (30 g) also significantly increased urinary nitrate and cyclic GMP excretion rates by 97±28 and 66±20%, respectively. After infusion of 6 g l-arginine, urinary nitrate excretion also significantly increased, (nitrate by 47±12% [P<0.05], cyclic GMP by 67±47% [P=ns]), although to a lesser and more variable extent than after 30 g of l-arginine. The onset and the duration of the vasodilator effect of l-arginine and its effects on endogenous NO production closely corresponded to the plasma concentration half-life of l-arginine, as indicated by an equilibration half-life of 6±2 (3.7-8.4) min between plasma concentration and effect in pharmacokinetic-pharmacodynamic analysis, and the lack of hysteresis in the plasma concentration-versus-effect plot.

Conclusions The vascular effects of l-arginine are closely correlated with its plasma concentrations. These data may provide a basis for the utilization of l-arginine in cardiovascular diseases.
Great post, and I appreciate it.

~trip
 
datBtrue

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Hey DBT

Actually I am less concerned about Prolactin increases and more put off by the significant Cortisol increases from the secretagogues (Ghrp-6/Hex).

On paper ... on paper ...on paper. You can read all you want but you don't truly understand how things will effect you if you don't try these protocols for yourself in your own body.

I'm not taking anything away from what you've read, or what we've read BUT I doubt people will waste away from cortisol...that is my opinion.

An my concern is more focused when considering using them during dieting/cutting and/or PCT, since those are the times when cortisol increase has a more dramatic negative impact.
Again using the word "dramatic" overstates things (in my opinion, f@ck the studies it is my opinion). Have you ever done a 20 week + cycle of AAS? Have you ever used more than 4 grams of AAS in any given week? I have and YES you had better take cortisol into consideration post-cycle. The use of the term "dramatic" IS applicable in that case.

But based on my experience cortisol is just not a problem in short-cycles and very managable in sane-length cycles (primarily managed in the first week).

I respect you concerns ...I just think you overstate the significance...

Other than price, I see no advantage in GHRP/Hex vs CJC.
I certainly would never argue that CJC is not superior based on your concerns. I will myself get around to using and assessing CJC...

...but I like pulsation & not persistant elevation (so whether you "see no advantage" is of little consequence to me BECAUSE I have a different criteria for assessment bro)

Bob you are deadly accurate in everything you have stated here and on other boards ...you are careful with the facts and damn I appreciate the hell out of your posts....seriously...you know that...

...but I like to experiment a bit within my own body first, take notes, make assessments (sometimes w/ objective data such as blood work) and then in that way I have added to MY subjective base of knowledge. It is against that base of earlier acquired knowledge that I will be able to assess something "superior on paper" such as CJC-1295.

You could try the same approach...or not...
 

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I'm not taking anything away from what you've read, or what we've read BUT I doubt people will waste away from cortisol...that is my opinion.
I agree DBT, under normal circumstances. But my concerns are for a scenario such as PCT when being shutdown and having a great hormonal imbalance tipping the ratios in a greater favor of cortisol and its catabolic effects.
Also in dieting when having a great caloric defecit and doing early morning empty stomach cardio for instance which in itself is already prone to greater cortisol spike. I would like to have a good GH spike before cardio to aid in fat burning, but also rather not use GHRP/Hex for this since ANY more cortisol agoinism is definetly not welcom in this circumstance.
I agree though that one's goals will ultimately justify the type of peptide to use in a given circumstance.


Again using the word "dramatic" overstates things (in my opinion, f@ck the studies it is my opinion). Have you ever done a 20 week + cycle of AAS? Have you ever used more than 4 grams of AAS in any given week? I have and YES you had better take cortisol into consideration post-cycle. The use of the term "dramatic" IS applicable in that case.
Now Now DBT, it almost seems you are calling me a "Drama Peptide Queen", LOL! :D
OK, fine, I am to a degree, BUT I have NEVER done Drag, so lets not go there either.... (BTW its early, I'm still groggy, and my humor may be rather strange at this moment) :fool2:

But based on my experience cortisol is just not a problem in short-cycles and very managable in sane-length cycles (primarily managed in the first week).
Not worried about cort during an AAS cycle as the added androgens will keep catabolic cortisol action to a minimum.

I respect you concerns ...I just think you overstate the significance...
I know. I do that a lot. BUT as opposed to understating things, overstating certainly sparks more debates and VERY good info exchange that leads to a greater enlightenment for all of us (especially myself) :)


I certainly would never argue that CJC is not superior based on your concerns. I will myself get around to using and assessing CJC...

...but I like pulsation & not persistant elevation (so whether you "see no advantage" is of little consequence to me BECAUSE I have a different criteria for assessment bro)
Good point DBT. One of the reasons I see a great advantage to stacking ghrp/hex with CJC. Seems you could avoid the negatives (cort, PRL) to some degree when combined, as per the study I posted earlier. Although this is my opinon as interpreted by the data.

Bob you are deadly accurate in everything you have stated here and on other boards ...you are careful with the facts and damn I appreciate the hell out of your posts....seriously...you know that...
I definitely know that DBT, and I always welcome your great knowledge and input especially when you show a different view of the situation. It makes me understand a bit more about the whole scope of things, that I may not see on my own. I do tend to get tunnel vision syndrome when focused on the topics at hand.

...but I like to experiment a bit within my own body first, take notes, make assessments (sometimes w/ objective data such as blood work) and then in that way I have added to MY subjective base of knowledge. It is against that base of earlier acquired knowledge that I will be able to assess something "superior on paper" such as CJC-1295.

You could try the same approach...or not...
Totally agree DBT! Ultimately our own individual bodies will be the final judges to all the actions debated and written on paper.

Thanks DBT for helping me keep a more open mind to all this stuff!!

Take Care.
 
datBtrue

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Thanks DBT for helping me keep a more open mind to all this stuff!!
Damn you're in a very good mood this morning!

On a more serious note ... Bob I don't know how old you are but I'm telling you just getting a little bump in GH as we get older makes a big difference in how we feel & function. I'm a believer now that I see and feel it in my just-turned 42 year old body. Plus I have a fiancee in her early 20's and want to start a family & stay healthy & active so this stuff is very important to me.

My point is I want to know about & be able to use if I need as many ways as I can to elevate my GH ...simple as that. Some of these ways may be taken away from us or may not be available in the future...

Okay back to your cheery Motha F@cking morning. ...you must of gotten laid last night. :)
 
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Ok, can igf-1 be used at the same time(same pin post workout) as ghrp-6/pGH/ cjc etc... or will that cause inhibition to the gh release? From what I gather taking a few grams of AAKG will override the inhibition from the igf-1.
 

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Ok, can igf-1 be used at the same time(same pin post workout) as ghrp-6/pGH/ cjc etc... or will that cause inhibition to the gh release?
I do not see any significant "real world" negative interaction between them. A note about the rhIGF-1 study:

The dosages of rhIGF-1 in the study that showed the reduction of GH response by GHRH were quite high at 20mcg/kg. That equates to 2mg of IGF for a 220lb person!
So keep that in mind, as I do not beleive that the systemic levels of Lr3 are affected to the degree of the 2mg direct systemic doses in the study.

From what I gather taking a few grams of AAKG will override the inhibition from the igf-1.
Since Arg reduces somatostatin tone, it is always good to reduce the effects of anything that works by increasing somatostatin tone. This is actually one of the reasons I've decided to dose some Arg before large carb meals. As per my previous posted study, Arg greatly reduces the action of increased plasma glucose on somatostatin tone. Arg was shown to keep GH release much higher in the presence of glucose...

Take Care.
 

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Damn you're in a very good mood this morning!
A strong brew of Sumatra blend, baby! :)

On a more serious note ... Bob I don't know how old you are but I'm telling you just getting a little bump in GH as we get older makes a big difference in how we feel & function. I'm a believer now that I see and feel it in my just-turned 42 year old body.
I agree DBT! I'm 36 and looking to get the most out of my own GH production at the moment, however, I will be looking to go on a real Growth cycle. Peptides are about all I have access to right now.

Plus I have a fiancee in her early 20's and want to start a family & stay healthy & active so this stuff is very important to me.
You are a stud, bro!!! Very Nice :D
Now, who's the one who should be in a good mood every morning!! :dance:

My point is I want to know about & be able to use if I need as many ways as I can to elevate my GH ...simple as that. Some of these ways may be taken away from us or may not be available in the future...
Hell ya, the worst thing possible is putting so much time into figuring all this stuff out, all the protocols and such, starting regimens, only to find it's all just taken away from you in the end. Sucks...

Okay back to your cheery Motha F@cking morning. ...you must of gotten laid last night. :)
:D
 
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I just happened to run across the following reference to Arginine as a GH potentiator so I thought I'd dump it here:

The following is from a section of

Neuroendocrine Control of Growth Hormone Secretion, EUGENIO E. MULLER, VITTORIO LOCATELLI, AND DANIELA COCCHI, PHYSIOLOGICAL REVIEWS Vol. 79, No. 2, April 1999

Department of Pharmacology, Chemotherapy, and Toxicology, University of Milan, Milan; and
Department of Biomedical and Biotechnology Sciences, University of Brescia, Brescia, Italy



Amino acids are a potent stimulus for GH secretion, either as selected nutrients or when included in a proteinrich meal (99, 283, 516). Parenteral administration of an amino acid solution raises GH secretion by acting on pulsatility and pulse amplitude, an effect presumably mediated by increased GHRH secretion (791).

Arginine is the most striking stimulant, although lysine, ornithine, tyrosine, glycine, and tryptophan are all effective GH releasers (564). An oral mixture of arginine and lysine evokes a sevenfold increase of plasma GH levels (516), and a similar effect is observed after arginine aspartate (99, 163). Arginine-induced GH secretion in humans is blocked by antagonists of a-adrenergic and cholinergic neurotransmission (153, 178), a carbohydrate-rich diet (710), hyperglycemia (711) and NEFA, anti-E2 (878). Estrogens enhance arginine-induced GH secretion in men or women (711).

The effect of arginine on GH secretion appears to be exerted through suppression of hypothalamic SS release, as suggested by neuropharmacological studies (22, 413, 414). Alternatively, the effect of arginine on GH and other pituitary hormones (56, 366) may depend on its conversion to NO, a gaseous neurotransmitter (734). Arginine is in fact a more effective GH releaser than muscarinic cholinergic agonists (414) which inhibit SS release (629). ...L-arginine is a potent GH secretagogue in humans (711); however, its effect does not appear to be linked to NO production...

REFERENCES:

22. ALBA-ROTH, J., A. O. MULLER, J. SCHOPOL, AND K. VON WERDER.
Arginine: stimulates growth hormone secretion by suppressing
endogenous somatostatin secretion. J. Clin. Endocrinol.
Metab. 67: 1186–1189, 1988.

56. ASSAN, R., G. ROSSELIN, AND J. DOLAIS. Effects sur la glucagonemie
des perfusions et ingestions d’acides amines. J. Ann.
Diabetol. Hotel Dieu. Ed. Medicales 7: 25–41, 1967

99. BESSET, A., A. BONARDET, G. RAUDONIN, B. DESCOMPS, AND
P. PASSNANT. Increase in sleep-related GH and Prl secretion
after chronic arginine aspartate administration in man. Acta Endocrinol.
99: 18–23, 1982.

153. BUCKLER, J. H. M., A. M. BOLD, M. TABERNER, AND D. R.
LONDON. Modification of hormonal responses to arginine by
adrenergic blockade. Br. Med. J. 3: 153–154, 1969.

163. CAMPISTRON, G. Approache Pharmacologique de l’Arginine et
de l’Acide Aspartique. Etude Pharmacocinetique e Pharmacodinamique
(PhD thesis). Toulouse, France: Faculte` des Sciences
Pharmacocinetique, 1980, no. 112.

178. CASANUEVA, F. F., L. VILLANUEVA, J. A. CABRANES, J. CABEZAS-
CERRATO, AND A. FERNANDO-CRUZ. Cholinergic mediation
of growth hormone secretion elicited by arginine, clonidine and
physical exercise in man. J. Clin. Endocrinol. Metab. 59: 526–530,
1984.

283. DAUGHADAY, W. H. Growth hormone: normal synthesis, secretion,
control and mechanisms of action. In: Endocrinology, edited
by L. J. De Groot. Philadelphia, PA: Saunders, 1989, vol. 1, p.
318–329.

366. FLOYD, J. C., JR., S. S. FAJANS, J. W. CONN, R. F. KNOPF, AND
J. A. RULL. Stimulation of insulin secretion by amino acids.
J. Clin. Invest. 45: 1487–1502, 1966.

413. GHIGO, E., S. GOFFI, E. ARVAT, M. NICOLOSI, M. PROCOPIO, J.
BELLONE, E. IMPERIALE, E. MAZZA, G. BARACCHI, AND F.
CAMANNI. Pyridostigmine partially restores the GH responsiveness
to GHRH in normal aging. Acta Endocrinol. 123: 169–174,
1990.

414. GHIGO, E., S. GOFFI, M. NICOLOSI, E. ARVAT, J. BELLONE, M.
PROCOPIO, F. VALENTE, E. MAZZA, M. C. GHIGO, AND F. CAMANNI.
Growth hormone responsiveness to combined administration
of arginine and GH-releasing hormone does not vary with
age in man. J. Clin. Endocrinol. Metab. 71: 1481–1485, 1990

564. KNOPF, R. F., J. W. CONN, S. S. FAJANS, J. A. RULL, E. M.
GUNTSCHE, AND C. A. THIFFAULT. The normal endocrine response
to ingestion of protein and infusion of amino acids. Sequential
secretion of insulin and growth hormone. Trans. Assoc.
Am. Phys. 79: 312–321, 1966.

516. ISIDORI, A., A. LOMONACO, AND M. CAPPA. A study of growth
hormone release in man after oral administration of amino acids.
Curr. Med. Res. Opin. 7: 475–481, 1981.

629. LOCATELLI, V., A. TORSELLO, M. REDAELLI, E. GHIGO, F.
MASSARA, AND E. E. MU¨ LLER. Cholinergic agonist and antagonist
drugs modulate the growth hormone response to growth hormone-
releasing hormone in the rat: evidence for mediation by
somatostatin. J. Endocrinol. 111: 271–278, 1986.

710. MERIMEE, T. J. Growth hormone: secretion and action. In: Endocrinology,
edited by L. De Groot. New York: Grune & Stratton,
1980, p. 123–132.

711. MERIMEE, T. J., D. RABINOWITZ, AND S. E. FINEBERG. Arginine initiated
release of human growth hormone: factors modifying the
response in normal man. N. Engl. J. Med. 280: 1434–1438, 1969.

734. MONCADA, S., R. M. J. PALMER, AND E. A. HIGGS. Nitric oxide:
physiology, pathophysiology and pharmacology. Pharmacol. Rev.
43: 109–142, 1991.

791. OKADA, K., H. SUGIHARA, S. MINAMI, AND I. WAKABAYASHI.
Effect of parenteral administration of selected nutrients and central
injection of g-globulin from antiserum to neuropeptide Y on
growth hormone secretory pattern in food-deprived rats. Neuroendocrinology
57: 678–686, 1993.

878. REFETOFF, S., P. H. FRANK, C. ROUBEBUSH, AND L. J. DE
GROOT. Evaluation of pituitary function. In: Endocrinology, edited
by L. J. De Groot. New York: Grune & Stratton, 1979, p.
175–190.​
 
datBtrue

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I agree DBT! I'm 36 and looking to get the most out of my own GH production at the moment, however, I will be looking to go on a real Growth cycle. Peptides are about all I have access to right now.
Yep I might go the Growth Hormone Replacement route eventually. I want to go to a real doctor and according to my research the best in the U.S. is Dr. Rothenberg. But that would require going on his overall anti-aging protocol & that would likely run about $5k per month...
 
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Low doses of either intravenously or orally administered arginine are able to enhance growth hormone response to growth hormone releasing hormone in elderly subjects.Ghigo E, Ceda GP, Valcavi R, Goffi S, Zini M, Mucci M, Valenti G, Cocchi D, Müller EE, Camanni F.
Dipartimento di Fisiopatologia Clinica, Università di Torino, Italy.

Reportedly, the responsiveness of somatotrope cells to GHRH is reduced in elderly humans but it is totally restored by arginine (ARG) which likely acts by inhibiting hypothalamic release of somatostatin. As this effect was observed after infusion of high doses of the amino acid, in this study, we compared the effect of iv administration of 30, 10 and 5 g ARG(group A, B and C, respectively) as well as oral administration of 8 g ARG(group D) on the GH response to 1 microgram/kg i.v.GHRH in 27 healthy elderly subjects (11 M and 16 F, age 70-86 yr, BMI 21-25 kg/m2). In group A (n = 7) 30 g i.v. ARG strikingly enhanced the GHRH-induced GH rise (peak, mean +/- SE: 41.5 +/- 4.4 vs 11.7 +/- 5.3 micrograms/L, p < 0.05). Similarly, in group B (n = 6) and D (n = 7) 10 g i.v. and 8 g oral ARG enhanced the GH response to GHRH (20.9 +/- 4.7 vs 8.3 +/- 2.8 micrograms/L, p < 0.03 and 31.0 +/- 5.3 vs 11.4 +/- 3.4 micrograms/L, p < 0.03, respectively). In contrast, in group C (n = 7) 5 g i.v. ARG failed to modify the GHRH-induced GH rise (6.0 +/- 1.6 vs 3.5 +/- 0.9 micrograms/L). The GH responses to GHRH alone did not significantly differ amongst groups; the GH responses to GHRH and ARG were not significantly different among groups A, B and D and were greater than the GH response in group C. These results show that the GH response to GHRH in elderly subjects is enhanced even by low iv doses of arginine and by the orally administered amino acid, the lowest effective dose being 8 g. Moreover, they imply that the combined administration of GHRH and arginine may be a useful approach to restore the impaired function of the GH-IGF axis in aging.

PMID: 8006330 [PubMed - indexed for MEDLINE]
 
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...arginine and by the orally administered amino acid, the lowest effective dose being 8 g....
Eight (8) grams per day might end up being the lowest effective dose. From the following published in 1993 by THE ENDOCRINE SOCIETY in ENDOCRINE REVIEWS we see that six (6) grams even w/ Lysine wasn't effective.

Human Growth Hormone and Human Aging

EMILIANO CORPAS, S. MITCHELL HARMAN, AND MARC R. BLACKMAN
Endocrinology Section (E.C., S.M.H., M.R.B.), Laboratory of Clinical Physiology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, and the Departments of Medicine (E.C., S.M.H., M.R.B.) Francis Scott Key Medical Center and Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

...
The acute GH response to an iv arginine infusion has been found to be similar in young and old men (139, 147, 148), while an arginine infusion potentiates GH responsivity to GHRH in old men (148). We have recently found that administration of an oral arginine/lysine preparation (6 g of each amino acid /day) for 2 weeks does not increase either spontaneous GH release (as assessed by overnight frequent sampling), plasma IGF-I levels, or GHRH-stimulated GH secretion in old men (148a).
...
NOTES:

148 - Ghigo C, Camanni F 1990 Growth hormone (GH) responsiveness to combined administration of arginine and GH-releasing hormone does not varv with ace in man. J Clin Endocrinol Metab 71: 1481-1485

148a - Corpas, E, Blackman MR. Roberson R. Scholfield DS, Harman SM, bra1 arginine-lysine does not increase growth hormone and insulin-like growth factor-I in old men. J. Gerontol, in press


Good find Trip... so now we have established a baseline for L-Arginine at 8 grams per day. Now we can take into conideration what Bob was pointing out about bioavailabiltiy in other forms of Arginine being greater than L-Arginine and use smaller amounts of those types if we want.

Trip you are one practical mofo...
 
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Eight (8) grams per day might end up being the lowest effective dose. From the following published in 1993 by THE ENDOCRINE SOCIETY in ENDOCRINE REVIEWS we see that six (6) grams even w/ Lysine wasn't effective.

Human Growth Hormone and Human Aging

EMILIANO CORPAS, S. MITCHELL HARMAN, AND MARC R. BLACKMAN
Endocrinology Section (E.C., S.M.H., M.R.B.), Laboratory of Clinical Physiology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, and the Departments of Medicine (E.C., S.M.H., M.R.B.) Francis Scott Key Medical Center and Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

...
The acute GH response to an iv arginine infusion has been found to be similar in young and old men (139, 147, 148), while an arginine infusion potentiates GH responsivity to GHRH in old men (148). We have recently found that administration of an oral arginine/lysine preparation (6 g of each amino acid /day) for 2 weeks does not increase either spontaneous GH release (as assessed by overnight frequent sampling), plasma IGF-I levels, or GHRH-stimulated GH secretion in old men (148a).
...
NOTES:

148 - Ghigo C, Camanni F 1990 Growth hormone (GH) responsiveness to combined administration of arginine and GH-releasing hormone does not varv with ace in man. J Clin Endocrinol Metab 71: 1481-1485

148a - Corpas, E, Blackman MR. Roberson R. Scholfield DS, Harman SM, bra1 arginine-lysine does not increase growth hormone and insulin-like growth factor-I in old men. J. Gerontol, in press


Good find Trip... so now we have established a baseline for L-Arginine at 8 grams per day. Now we can take into conideration what Bob was pointing out about bioavailabiltiy in other forms of Arginine being greater than L-Arginine and use smaller amounts of those types if we want.

Trip you are one practical mofo...
Haha, yea i'll take that as a complement. The only issue I have with oral arginine is always trying to avoid food intake, and keep blood sugar low when taking it. That in itself is a cluster-fukc, because I like to keep nutirents coming in. I have a blend of na-rala/ala/monohydrate that I take before all peptides and the arg.....and with most shakes, and meals. I added the monohydrate just because it keeps the powder from clumping, and ALA helps deliver it to cells(mr.practical..lol).....anyway back to the point, I'm playing with around 5 grams of argining alpha ketogluerate, and see how that works. I usually take some 1-carboxy powder(l-dopa), and about 5-6 grams of oral gaba in that low bloodsugar window. Then add the ghrp-6/pGH shot about 30-40 mins later.

I feel like a dam scientist with all this stuff...lol, but its fun to enhance things.
 
Royd The Noyd

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The study DB posted above I believe does show GH related positives in the ranges of 10-20g's of arginine/day. I cannot recall if it is that study or another similar one (I just remember lysine being involved).

I've been toying with the idea of using 15-20g's of arginine pre-bed (empty stomach if possible) since it is surprisingly reasonable in terms of cost.
 
nattydisaster

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This thread needs to be bumped. Smart convo here. Did you ever try anything trip?
 
TripDog

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This thread needs to be bumped. Smart convo here. Did you ever try anything trip?
I agree this thread was great. I'm starting another long run of ghrp-6 and will be using the similar AAKG methods talked about here.
 
TripDog

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Updates trip?
I started running it again a few weeks ago, 500mcg split into 2 shots usually at night. Gonna run it for a few months that way. Money is tight so I cant other stuff to the mix right now (pGH, 1-carboxy, etc)
 
nattydisaster

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Sounds good to me because that's the exact situation I am in. If you like the results I'm going to copy your idea :D
 
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Sounds good to me because that's the exact situation I am in. If you like the results I'm going to copy your idea :D
I personally think its worth it, cant go wrong really.
 

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Hey Trip, along the lines of the arginine use. My pre-inj stack,...I have used AAKG, and arginine ethyl ester, and finally got around to using Nutra-planets Agmatine. Which I use less of, and like the best.
 
MentalTwitch

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Hey Trip, along the lines of the arginine use. My pre-inj stack,...I have used AAKG, and arginine ethyl ester, and finally got around to using Nutra-planets Agmatine. Which I use less of, and like the best.
How did you decide this? You use it 3 seperate cycle? change weekely?
 

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Pre- stack

I've been using a prep administration protocol continuously with my research of these peps. I formulated the stack based on the findings and threads of Dat, Papa, and others, to address some of the issues that arose. The major points of course dealing with the "potential" increase in PRL, and secondly reducing somatostatin tone. Third, providing a potential synergy or amplification of reduced doses of peps, since my trials are somewhat long term compared to what I'm reading most are doing. 1.Blood glucose must be 99 or less, pre-administration. 2. stack and administration are at natural points of "pulse" 3. Stack consists of A. 3gms L-dopa B. 3 gms GABA c. 1 gms alpha GPC C. 3 gms Agmatine D. 1 gms Quercetin, laced with vitamin C. To address your inquiry more direct, I experimented with the differing forms of arginine,...AAKG,ethyl ester, and arginine hcl. My comment to Trip was to highlight the effectiveness of Agmatine. Anectodal I know, but my percieved BUZZ, I call it, is greatest, and lasts the longest on Agmatine.
 

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Contd.

To answer your question. Weeks 1-12 were AAKG, weeks 13-24 were ethyl ester. weeks 25 to now agamatine.
 
MentalTwitch

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ok, thats pretty much what i was curious about. Thanks.
 
MentalTwitch

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To answer your question. Weeks 1-12 were AAKG, weeks 13-24 were ethyl ester. weeks 25 to now agamatine.
agmatine is a bit pricey, but im pannig to give it a shot. I want to utilize my peptides as much as possible. I have L-Dopa and GABA to last for at least a year.

EDIT: Dont have the wallet for it right now. $25 for 25g agmatine or $50 for 500g arginine. had to go arginine this time.
 

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I read through all of these posts, but still didnt find what I was looking for. I will keep trying, but what I am looking for is a supplement routine to run with my stack of cjc/ghrp/mgf

I will add in arganine, but I am wondering if I should add in others for cortisol and prolactin regulation? I havent started my cyc yet, so I want to be fully prepared before I do....

P37
 

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This thread starts with supplements you can take to regulate increased prlct and cort.
Basically, we know that grf and ghrp's enjoy synergy, so lower doses of each can give a larger gh spike than each dosed separately at higher doses. We also know that ghrp's spike endo gh while grf's raise the baseline of present circulating gh. So, prolactin becomes an issue with higher doses of ghrp's, not so much with lower doses. We only need lower doses of ghrp's if used in conjuction with grf's, hence prolactin, if an issue at all, can be managed with the supplements mentioned by Tripp and others earlier in the thread
 
datBtrue

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agmatine is a bit pricey, but im pannig to give it a shot. I want to utilize my peptides as much as possible. I have L-Dopa and GABA to last for at least a year.

EDIT: Dont have the wallet for it right now. $25 for 25g agmatine or $50 for 500g arginine. had to go arginine this time.
Hey MT

I've been using the Mucuna pruriens, 40% L-Dopa at 250mgs EOD at night w/ my GHRH/GHRP. I think it works well (subjectively). I like it (added somatostain inhibition)..even deeper sleep. ...less then $15 for 75grams.

Plus Ghrelin (assume the Ghrelin-mimetics) synergizes w/ L-Dopa to increase memory. Subjectively my ability to remember the French language I study has increase over the last 30 days.
 
MentalTwitch

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Hey MT

I've been using the Mucuna pruriens, 40% L-Dopa at 250mgs EOD at night w/ my GHRH/GHRP. I think it works well (subjectively). I like it (added somatostain inhibition)..even deeper sleep. ...less then $15 for 75grams.

Plus Ghrelin (assume the Ghrelin-mimetics) synergizes w/ L-Dopa to increase memory. Subjectively my ability to remember the French language I study has increase over the last 30 days.
very nice addition.

I would also like to add this link Agmatine related that natty gave me on SoM site.

http://www.neurotransmitter.net/neardeath.html
 

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