Dat's - CJC-1295 & GHRP-6 (Basic Guides)

DatBtrue · Mar 2, 2009

qwerty said:
Thanks Dat. But what is the timing on the leucine and glucose?

Peptides immediately PWO. 25 or so minutes later the hi-GI carbs/leucine followed by protein 10 minutes later.

Normally you could have carbs/protein together 25 minutes after the peptides but in your case you are using leucine to boost insulin. Leucine just like glutamine needs to be taken by itself w/o any other protein in order for it to act the way you want. If you ingest either of these aminos with protein the special characteristics are either lost or substantially diluted.

As an aside before I forget any one with intestinal problems remember that glutamine is used in nucleotide synthesis by all swiftly dividing cells. The intestinal lining and certain immune cells love glutamine and soak it up when they can. The intestines atrophy without it and are structurally strong when they get sufficient amounts of it.

EasyEJL · Mar 4, 2009

Hey Dat, i've got a question about comparing ghrp-6/cjc-1295 and semorelin. If a longevity clinic doctor recommended 200mcg semorelin/day prebed to help with low IGF levels from a blood test, what sort of dosing scheme would you think would give similar results with ghrp6/cjc-1295?

DatBtrue · Mar 5, 2009

EasyEJL said:
Hey Dat, i've got a question about comparing ghrp-6/cjc-1295 and semorelin. If a longevity clinic doctor recommended 200mcg semorelin/day prebed to help with low IGF levels from a blood test, what sort of dosing scheme would you think would give similar results with ghrp6/cjc-1295?

Seromrelin (+) is GHRH (Growth Hormone Releasing Hormone). It is opposed by the hormone Somatostatin (-)

Because GHRH travels a short distance from the Hypothalamus to the adjacent Pituitary, GHRH endogenous release is effective. The vulnerability is limited and plasma degradation is of no consequence.

But exogenous administration is not extremely effective.

It has been demonstrated that degradation at the site of injection of GHRH after subcutaneous administration is extremely rapid. The estimated amount in the circulation after subcutaneous injection was only 4% of that obtained after intravenous administration. *

It is rapidly metabolized in the plasma, as a result of the Ala-Asp (at the 2nd & 3rd position respectively) peptide bond cleavage by dipeptidylpeptidase IV leading to the inactive Growth Hormone Releasing Fragment of amino acids 3–29. **

As a consequence those clinical studies that show longer term benefit and elevated GH & IGF-1 rely on Sermorelin dosages measured in milligrams not micrograms.

Therefore analogs of GHRH have been created that decrease the vulnerability of GHRH in plasma. In particular an amino-acid substitution is made at the 2nd position to reduce the very quick cleavage that normally would occur.

One such analog is what I call modified GRF(1-29). Because of 5 amino acid substitutions it will not rapidly metabolize in plasma and will make its way to the pituitary where it will effect growth hormone release.

Now Dr. Crisler who posts here and in this thread as Swale found in his clinical practice that when he added GHRP-6 to Sermorelin his patients experienced a 1/3 increase in IGF-1 over a Sermorelin only protocol.

So aside from degradation issues, if you don't use a Growth Hormone Releasing Peptide such as GHRP-6 or GHRP-2 with the GHRH then you will have inconsistent GH pulses.

Growth Hormone Releasing Peptides are modulating peptides (analogs of the hormone Ghrelin). They bind to their own receptor in the hypothalamus & pituitary and they initiate a GH pulse (or wave). They do this in part by minimizing the influence of the inhibiting hormone, Somatostatin (-) and increasing the influence of the positive hormone GHRH (+), in addition to their own distinct action of effecting GH release from cells in the pituitary.

There is synergy (i.e. more than additive) in GH release when both GHRH & a GHRP are administered together. But in addition there is consistency & predictability when a GHRP is added because it will initiate a fresh GH pulse (in large part by inhibiting the "off switch", Somatostatin).

So what happens if you administer GHRH or Sermorelin alone?

Remember that naturally GH release is pulsatile. Sometimes there is a big pulse, sometimes a little pulse and sometimes no pulse.

Exogenously administered GHRH administered during a naturally occurring GH trough results in low amounts of GH release while GHRH administered during a rising natural GH pulse will result in high amounts of GH release. See:

The Interaction Between Clonidine And Growth Hormone Releasing Hormone In The Stimulation Of Growth Hormone Secretion In Man, D. Suri, Clinical Endocrinology (1990), 33, 399-406

* - Rafferty B, Poole S, Clarke R, Shulster D., Growth hormone-releasing factor analogue (hGRF1-29NH2): immunoreactive-GRF plasma levels after intravenous and subcutaneous administration, J. Endocrinol. 1985; 107: R5–R8.

** - Frohman LA, Downs TR, Williams TC, Heimer EP, Pan Y-CE, Felix AM, Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma, J. Clin. Invest. 1986; 78: 906–913.

toby25 · Mar 5, 2009

Dat-Could you mix say 50mcg of Seromelin-GF-29 with 50mcg of CJC-1295, and 100mcg GRP-6-Would that still give an effective response-what do you think about the idea-if only to get more bang for your buck.!

DatBtrue said:
Seromrelin (+) is GHRH (Growth Hormone Releasing Hormone). It is opposed by the hormone Somatostatin (-)

Because GHRH travels a short distance from the Hypothalamus to the adjacent Pituitary, GHRH endogenous release is effective. The vulnerability is limited and plasma degradation is of no consequence.

View attachment 25056

But exogenous administration is not extremely effective.

It has been demonstrated that degradation at the site of injection of GHRH after subcutaneous administration is extremely rapid. The estimated amount in the circulation after subcutaneous injection was only 4% of that obtained after intravenous administration. *

It is rapidly metabolized in the plasma, as a result of the Ala-Asp (at the 2nd & 3rd position respectively) peptide bond cleavage by dipeptidylpeptidase IV leading to the inactive Growth Hormone Releasing Fragment of amino acids 3–29. **

As a consequence those clinical studies that show longer term benefit and elevated GH & IGF-1 rely on Sermorelin dosages measured in milligrams not micrograms.

Therefore analogs of GHRH have been created that decrease the vulnerability of GHRH in plasma. In particular an amino-acid substitution is made at the 2nd position to reduce the very quick cleavage that normally would occur.

One such analog is what I call modified GRF(1-29). Because of 5 amino acid substitutions it will not rapidly metabolize in plasma and will make its way to the pituitary where it will effect growth hormone release.

Now Dr. Crisler who posts here and in this thread as Swale found in his clinical practice that when he added GHRP-6 to Sermorelin his patients experienced a 1/3 increase in IGF-1 over a Sermorelin only protocol.

So aside from degradation issues, if you don't use a Growth Hormone Releasing Peptide such as GHRP-6 or GHRP-2 with the GHRH then you will have inconsistent GH pulses.

Growth Hormone Releasing Peptides are modulating peptides (analogs of the hormone Ghrelin). They bind to their own receptor in the hypothalamus & pituitary and they initiate a GH pulse (or wave). They do this in part by minimizing the influence of the inhibiting hormone, Somatostatin (-) and increasing the influence of the positive hormone GHRH (+), in addition to their own distinct action of effecting GH release from cells in the pituitary.

There is synergy (i.e. more than additive) in GH release when both GHRH & a GHRP are administered together. But in addition there is consistency & predictability when a GHRP is added because it will initiate a fresh GH pulse (in large part by inhibiting the "off switch", Somatostatin).

So what happens if you administer GHRH or Sermorelin alone?

Remember that naturally GH release is pulsatile. Sometimes there is a big pulse, sometimes a little pulse and sometimes no pulse.

Exogenously administered GHRH administered during a naturally occurring GH trough results in low amounts of GH release while GHRH administered during a rising natural GH pulse will result in high amounts of GH release. See:

View attachment 25057

The Interaction Between Clonidine And Growth Hormone Releasing Hormone In The Stimulation Of Growth Hormone Secretion In Man, D. Suri, Clinical Endocrinology (1990), 33, 399-406

* - Rafferty B, Poole S, Clarke R, Shulster D., Growth hormone-releasing factor analogue (hGRF1-29NH2): immunoreactive-GRF plasma levels after intravenous and subcutaneous administration, J. Endocrinol. 1985; 107: R5–R8.

** - Frohman LA, Downs TR, Williams TC, Heimer EP, Pan Y-CE, Felix AM, Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma, J. Clin. Invest. 1986; 78: 906–913.

DatBtrue · Mar 6, 2009

toby25 said:
Dat-Could you mix say 50mcg of Seromelin-GF-29 with 50mcg of CJC-1295, and 100mcg GRP-6-Would that still give an effective response-what do you think about the idea-if only to get more bang for your buck.!

There is nothing negative about what you propose...and I like your thought process.

But Sermorelin just flat out is poor at low dose.

Now I did a quick survey of retail places which have at least someone saying decent things about them and I see modified GRF(1-29) which takes the second amino acid in the peptide chain alanine (symbolized as Ala or A) and substitutes for the "D" form of alanine (D-alanine) (symbolized by D-Ala or a) as well three other amino acid modifications... a glutamine (Gln or Q) at the 8-position, alanine (Ala or A) at the 15-position, and a leucine (Leu or L) at the 27-position...selling for fairly decent prices.

Of course these places continue to erroneously label modified GRF(1-29) as CJC-1295.

So back to your question... if you want to use 50mcgs of modified GRF(1-29) & 50mcgs of genuine CJC-1295 (which is mod GRF(1-29) + the 30th amino acid Lysine linked to a 3-maleimidopropionic acid (MPA) unit (often referred to as the "drug affinity complex (DAC)") and 100mcg of GHRP-6 that would be an effective dose.

Wise Guy · Mar 6, 2009

DatBtrue said:
Of course these places continue to erroneously label modified GRF(1-29) as CJC-1295.

Dat,

Do you know what form of sermorelin Dr John is using for the GHRT for his patients (Or if Dr John wants to chime in that would work as well!).

Meaning is he using the modified GRF(1-29) or the older version of sermorelin.

How much more effective is the newer, modified form?

DatBtrue · Mar 6, 2009

Wise Guy said:
Dat,

Do you know what form of sermorelin Dr John is using for the GHRT for his patients (Or if Dr John wants to chime in that would work as well!).

Meaning is he using the modified GRF(1-29) or the older version of sermorelin.

How much more effective is the newer, modified form?

Sermorelin (GHRH) is available as a prescription drug (thats why it is used by doctors) and is clinically beneficial in larger doses.

Analogs of GHRH are better in both binding affinity & half-life which leads to much higher efficacy.

Modified GRF(1-29) is not necessarily the best amino-acid substituted analog. It is just the version of amino-acid substitutions used in the CJC-1295 experiments. Of course that compound adds an amino acid Lysine plus a linked Drug affinity complex.

Since the added Drug affinity complex is expensive & difficult to produce it was dropped by Chinese chemical houses and they sold the remainder as CJC-1295.

This remainder is effective though primarily because it stops quick cleavage at the 2nd/3rd positions.

What modified GRF(1-29) doesn't do is make the amino-acid substitutions that prevent trypsin induced cleavages that are active in the hypothalamus & pituitary axis.

DatBtrue · Mar 6, 2009

Ghrelin (assumed GHS) increases GH signalling in muscle

I have always maintained that GH signaling activity in muscle or autocrine/paracrine IGFs in muscle are more important then circulating systemic levels.

That GH increases such local activity (in addition to systemic levels) is supported at my post Post #480 - GH leads to creation of IGF-1 in muscle cells & MGF in muscle cells

Well here is support for Ghrelin (assumed the mimetics of GHRPs as well) inducing these important changes.

Ghrelin infusion stimulated endogenous GH secretion, which peaked at t = 60 min ...Western blots performed on skeletal muscle biopsies revealed distinct STAT5 phosphorylation in all six subjects 30 min after the endogenous GH burst
...
This investigation is also the first to document that ghrelin-induced endogenous GH release translates into Janus kinase/STAT signaling in skeletal muscle. - Ghrelin Infusion in Humans Induces Acute Insulin Resistance and Lipolysis Independent of Growth Hormone Signaling, Esben Thyssen, Diabetes, December 1, 2008; 57(12): 3205 - 3210

weltweite · Mar 6, 2009

Copy & Pasted:
Rhodiola's stimulating and adaptogenic effects are attributed to p-tyrosol, one of several antioxidants, along with organic acids and flavonoids, and to compounds such as salidroside (syn: rhodioloside and rhodosin), rhodioniside, rhodiolin, rosin, rosavin, rosarin, and rosiridin. Rhodiola is believed to influence levels of biogenic monoamines such as serotonin, dopamine, and norepinephrine in the cerebral cortex, brain stem, and hypothalamus. It has been reported to prevent both catecholamine release and subsequent cyclic AMP elevation in the myocardium (heart) and the stress-induced depletion of adrenal catecholamines. Rhodiola's adaptogenic activity may also rely on induction of opioid peptide biosynthesis and activation of central and peripheral opioid receptors.

Would this fall under the lines of the synergy between GHRP/GHRH/Benzo since its targeting the opioid receptors? Without the obvious sides from benzo type drugs.

layinwood · Mar 6, 2009

Dat, my rat is currently doing 100mcg of cjc and 150 mcg of ghrp6 3 times per day. He is getting ready to go on cycle, would there be any benefit of adding igf lr3 to this cycle for say 6 weeks?

DatBtrue · Mar 7, 2009

layinwood said:
Dat, my rat is currently doing 100mcg of cjc and 150 mcg of ghrp6 3 times per day. He is getting ready to go on cycle, would there be any benefit of adding igf lr3 to this cycle for say 6 weeks?

In my previous post you will find a link. If you follow that link you will find a post/study that answers your question. But it is important to understand so I'll repost it below. If you have more money to spend then increase the dose of CJC-1295.

REPOST of Post #480

GH leads to creation of IGF-1 in muscle cells & MGF in muscle cells. That autocrine production and use is really the only thing that matters. In other words systemic IGF-1 can do a lot (but not as well) of what autocrine/paracrine IGF does IF a mutation eliminates autocrine/paracrine action. However IF autocrine/paracrine is functional it will function w/ 100% capacity even if there is no systemic IGF-1 present. It appears that autocrine/paracrine action is THE factor within muscle and probably most organs & tissue as well including the brain.

In fact for bodybuilding I conjecture that low systemic (i.e. endocrine) IGF-1 levels would be fine IF we could increase the expression of IGFs in local tissues (i.e. autocrine = within the cell & also paracrine = neighboring cells such as connective tissue).

Here is a post I made in on another forum in September. (keep in mind IGF-IEa is the muscle form of IGF-1 & MGF is an IGF variant that is only expressed in muscle):

Cultured muscle cells as a system for the analysis of IGF-I splicing regulation by factors present in the circulation, Velloso,Cristiana P, The Physiological Society (2004) J Physiol 558P, C5

It has recently been shown that muscle cells grown in 3-D collagen matrixes upregulate IGF-I transcript expression in response to stretching of the matrix (Cheema et al., 2004). In the present work we have studied muscle cells in culture with the aim of determining if either or both of the two splice variants of IGF-I would be upregulated when treated with GH and/or IGF-I, in the absence of mechanical signals C2C12 myoblasts were grown to 50% confluency in medium containing 10% foetal calf serum (FCS). The cells were transferred to medium containing i) 1%FCS only, ii) 100 ng/ml rhGH iii) 100 pg/ml IGF or iv) both. In the untreated cells (i) both isoforms (IGF-IEa and MGF) were present. Treatment with rhGH alone lead to an increase in IGF-IEa and MGF of about 3 fold over control (Table 1). However, treatment with IGF-I abolished expression of both isoforms. When used in combination, the inhibitory effect of IGF-I overode the GH stimulation of IGF-IEa and MGF transcription. We conclude that muscle tissue can upregulate IGF-I isoform expression as a direct result of hormonal stimulation or stretch stimuli. The isoforms of IGF-I seem equally sensitive to GH stimulation in vitro. In vivo, a negative feedback mechanism may modulate the action of GH on IGF-I transcription in muscle tissue in by circulating or local IGF-I expression.

Table 1. IGFIa and MGF transcript levels (x 10-8 ng mRNA / µg RNA) in C2C12 cells following GH and IGF-I treatment.

Data are Means ± S.D. of three separate experiments. * Significant difference (P<0.5) relative to control (unpaired t-test).

DatBtrue · Mar 7, 2009

weltweite said:
Copy & Pasted..

Would this fall under the lines of the synergy between GHRP/GHRH/Benzo since its targeting the opioid receptors? Without the obvious sides from benzo type drugs.

Don't cut & paste just reference the study or article.

The source for your article is not really a top journal & I did not see direct evidence (lack of source notation for the statement).

If you have ever used Rhodiola you will know that its effects are very, very mild at best. If it were to have an effect on GH it would not be significant and it would not be primarily from interaction w/ opoid receptors. It could act as a somatostatin antagonist. But why use it for that?

My experiment of adding to my peptides, 250mcg of Mucuna pruriens (standardized for 40% L-Dopa) EOD pre-bed is working well for me.

A general review of studies on herbs & a quick recitation of DSHEA law in the U.S. can be found at: **broken link removed**

DatBtrue · Mar 7, 2009

Hormonal Set-Points

Here is evidence that there are set-points for hormones which can change based on environmental factors. It is very interesting that these environmental events can shift hormonal parameters that exhibit themselves throughout the post-shift life period.

It is a deep but possible conjecture that we could shift hormonal set-points in general as a therapy for those with low hormonal levels perhaps by triggering a "famine state" or prolonged fast.

Exposure to the Dutch Famine of 1944 -1945 and Shifts in Hormonal Set Points: Parathyroid Hormone, Paulus A. H. van Noord, J. Nutr. 135:3037S-3060S, December 2005

BACKGROUND: Exposure to the 1944–1945 Dutch famine was shown to be associated with increased levels of androgens, estrogens, and insulin-like growth factor later in life, hormones under control of the pituitary luteinizing hormone/follicle stimulating hormone and growth hormone axes. Moreover, exposed women were at increased risk of breast cancer.

A neurodevelopmental set-point-shift hypothesis, proposed to consolidate these findings, predicts a mechanism of shifting in hormonal set points. In the present study, we tested whether famine exposure affects parathyroid hormone (PTH).

STUDY DESIGN: We used data from a study on osteoporosis nested within the DOM breast cancer screening cohorts including 212 women born in 1911 to 1925 whose hormones were measured in 1980. During a subsequent screening round 2 y later, 156 women provided information about exposure to the Dutch Famine of 1944–1945, thus enabling secondary analyses.

RESULTS: A clear univariate increase in postmenopausal PTH levels was found among women who indicated exposure to the Dutch famine. Odds ratio by extreme PTH tertiles was 1.5 (95% CI: 0.6, 3.4) for moderately exposed women and 2.3 (95% CI: 1.1, 5.2) for severely exposed women. In a regression analysis of famine exposure on PTH levels, after controlling for levels of phosphorus, calcium, calcitonin, alkaline phosphatase, and estrone; having been pregnant; parity; age at famine; age at blood donation; smoking; hormone replacement therapy use at time of blood collection; height; weight; and socioeconomic status, the independent significant contribution of PTH remained.

CONCLUSIONS: The results corroborate the hormonal set-point hypothesis and seem to extend effects of famine exposure to hormones such as PTH, which plays a role in early bone growth as well as in osteoporosis later in life. Though PTH is not under hypothalamic or pituitary control, it is partially under ganglion control. Embryologically, the parathyroids and the adenohypophysis share a common origin from pharyngeal endodermal pouches.

EasyEJL · Mar 7, 2009

DatBtrue said:
My experiment of adding to my peptides, 250mcg of Mucuna pruriens (standardized for 40% L-Dopa) EOD pre-bed is working well for me.

related to this part, have you considered any of deprenyl, cabergoline or bromocriptine (or a combination of deprenyl + either of the other 2)?

DatBtrue · Mar 7, 2009

EasyEJL said:
related to this part, have you considered any of deprenyl, cabergoline or bromocriptine (or a combination of deprenyl + either of the other 2)?

Nope.The question to you would be why would I?

The increase in dopamine inhibits somatostatin, perhaps at my age it is an additive benefit to that of GHRP-6's somatostatin inhibition as was demonstrated in studies w/ Arginine.

In my estimation the herb is safe and the other components inhibit peripheral action on tissue such as the heart so it is better then straight L-Dopa & better then the compounds you mention.

EasyEJL · Mar 7, 2009

Makes sense. I had looked at deprenyl for the "resensitization" of dopamine receptors and carbergoline/bromocriptine to decrease the enzymatic processing out of dopamine (or do I have that reversed now? its been a while since I looked at it) but wasn't sure on its real value

DatBtrue · Mar 7, 2009

GHRH binds to GHS-receptor & potentiates GHRP's GH releasing action!

Wow ! ! !

We have spent a lot of time in this thread discussing how GHRPs (such as GHRP-6, GHRP-2, Hexarelin & Ipamorelin) potentiate GHRH's GH releasing effect. We talk of synergy, note GHRPs somatostatin inhibition at the hypothalumus & pituitary and note that GHRPs use a different method then GHRH in changing calcium concentrations within somatotrophs (GH releasing cells in the pituitary) that lead to GH secretion.

But now we learn that GHRH also enhances GHRP's effect on GH release by binding to the GHS-receptor (obviously in addition to binding to their own GHRH receptors) and increasing the binding strength for GHRPs when they in turn bind. In other words GHRH will partially bind to a GHS-receptor and still allow GHRPs to bind as well. In fact this arrangement likely permits a double stack of two GHRP ligands thus modulating (increasing) GHRPs action.

The study uses Ghrelin but the peptides should behave identically. However the non-peptide mimetics may not.

From the CONCLUSION of Growth hormone-releasing hormone as an agonist of the ghrelin receptor GHS-R1a ,Felipe F. Casanuevaa, PNAS December 23, 2008 vol. 105 no. 51

In the present study, we provide the first evidence that GHRH specifically binds to the ghrelin receptor GHS-R1a, increasing the binding capacity of its natural ligand. This binding activates the signaling route of inositol phosphate, leading to an intracellular calcium rise, and finally leads to a GHRH-mediated ghrelin receptor endocytosis. Furthermore, GHRH augments the maximal response to ghrelin in respect to inositol phosphates turnover through Gq-associated signal transduction that increases the potency of ghrelin, at least on intracellular calcium rise.
...
Thus, GHRH is able to bind to the ghrelin receptor and does not compete for binding against ghrelin. Instead, GHRH increases the affinity of ghrelin, displaying positive binding cooperativity. Furthermore, GHRH increased the maximal response to ghrelin with respect to inositol phosphates turnover through Gq-associated signal transduction. This is in accordance with the concept of GHRH being an allosteric modulator (28, 29). This enhancer function is further supported by the fact that GHRH decreased the EC50 for ghrelin, at least as measured in the calcium assay.
...
Finally, and quite remarkably, GHRH activated the endocytosis of the ghrelin receptor. The GHRH/GHSR1a complex progressively disappears from the plasma membrane after 20 minutes exposure to GHRH and accumulates in the perinuclear region after 60 minutes. This observation fits in well with the kinetics of receptor endocytosis described for ghrelin in the present and previous works (27).
...
With regard to molecular mechanisms, it is not possible from the present data to establish a model of GHRH action on the ghrelin receptor. A homodimeric model was recently proposed for the ghrelin receptor, in which, because of negative cooperativity, the binding of ghrelin occurs only in one subunit, preventing another ghrelin molecule from binding to the other subunit (32). On the basis of this model, we suggest that GHRH might be able to bind in a multivalent form. When GHRH is present alone, it might bind to one subunit of the dimeric receptor interacting with the orthosteric site (main ghrelin binding site) that determines the agonist properties. However, when ghrelin is also present, GHRH occupies an ‘‘allosteric site,’’ acting as co-agonist that stabilizes the ghrelin binding. This implies that GHRH allows two ghrelin molecules to bind at the same time in the two subunits, which might explain the increase in ghrelin binding capacity observed in the present study.

Wise Guy · Mar 7, 2009

Thanks for all the information Dat. Love this thread.

It is my understanding that mechanism in which Rhodiola works is mostly due to its energizing effects on mitochondria, all completely outside of any sort of endocrine/hormone actions - Meaning mostly it's benefits are purely objective, can't be measured quantitatively in any accurate way and probably differ greatly from one person to the next.

I've known people who use it primarily as a nootropic agent, or as a substitute for morning coffee.

disgraziato · Mar 8, 2009

Awesome data Dat! So essentially, GHRP's act synergistically w/ GHRH to increase GH production, but the opposite holds true as well, GHRH also "energizes" GHRP's influence on GH production. I suppose, therin lies the true synergy of these compounds.

DatBtrue · Mar 8, 2009

A Couple of quick notes:

Beware taking MTII with CJC-1295/GHRP-6 seems to prolong and intensify nausea. (Sample of two at the moment... one of them being me.)
Beware GHRP-6 (assume all GHRPs) has been shown conclusively to increase gastic motility & "accelerate gastric emptying of solids ...through activation of GHS receptors, possibly located on local cholinergic enteric nerves" (Sample various effects from different people) *
Beware that as part of the gastric response, "GHRP-6 enhances neural contractile responses, partially via interaction with the motilin receptor on noncholinergic nerves with tachykinins as mediator, and partially via another receptor that may be a GHS-R subtype on cholinergic nerves that corelease tachykinins." (Sample at least two reports, occurs from time to time) **
Exogenic GH when administered every 3 hours does not inhibit pulsation. See my post at: Post #662

The reason this is interesting is that it may be possible to dose say 2iu of synthetic GH every 3 hours with mod GRF(1-29)/GHRP-6 taken say 10 minutes prior. This could be done up to six times a day.

Alternatively 2iu of GH could be alternated with mod GRF(1-29)/GHRP-6.

The key has to be strict adherence to a schedule or else synthetic GH will inhibit natural GH.

It is just interesting to think about.

* - Gastric motor effects of peptide and non-peptide ghrelin agonists in mice in vivo and in vitro, T Kitazawa, Gut 2005 54;1078-1084

** - Interaction of the Growth Hormone-Releasing Peptides Ghrelin and Growth Hormone-Releasing Peptide-6 with the Motilin Receptor in the Rabbit Gastric Antrum, Inge Depoortere, The Journal Of Pharmacology And Experimental Therapeutics Vol. 305, No. 2