Hexatropin

[john arnold]

any feedback on this yet or any logs?

 

[wojo]

yea i see a lot of ecto..but i wanna hear some hex feedback

 

[mass_builder]

Im going into PCT soon, i will be realy interested to see if it can help me recover.

 

[Syr]

maybe we will pick 10 people for the hexatropin to test as well

*wink wink*

 

[milwood]

I think syr would be an excellent candidate...

 

[Syr]

I think syr would be an excellent candidate...

Thank you bro
And I'm planning to try it anyway.

 

[wojo]

i would love to try it..

 

[SJA]

I'll be trying it and will keep a log. I think that I'll start in a week or so.

 

[mass_builder]

SJA how long are you going to run it?

 

[solarize]

Interested

maybe we will pick 10 people for the hexatropin to test as well

I have PCT coming up for SD/Prostana/Ergomax in two weeks. Would be interested in being a tester for Hexatropin should it become available.

BTW, your Clen is top stuff, thanks.

 

[SJA]

SJA how long are you going to run it?

If it delivers....6 months.

 

[Just A Hack]

Hell Ya!

maybe we will pick 10 people for the hexatropin to test as well

 

[Kristopher]

I start PCT in about 2 weeks.. id love to check this stuff out while coming off M1T and trimax

 

[milwood]

I'd nominate Kristopher as well. Good knowledge, good posts and logs...

 

[Fastflight]

What about this: spiroindoline L-163,191 (MK-0677) little sucker?
Would be a nice addition to your peptide-arsenal?

 

[Enigma76]

What about this: spiroindoline L-163,191 (MK-0677) little sucker?
Would be a nice addition to your peptide-arsenal?

Hehe...I've looked into that badboy for along time now. Also goes by ibutamoren mesylate.

Unfortunately its patented (as far as I can tell). It is a non-peptidyl version of the GHRPs; as in, it is a GH secretagogue that is orally bioavailable, causes sustained 24hr GH release after one oral dose, and is soluble in water.

Alot of GREAT research on mk0677.

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Effects of Study: Raises serum IGF-1/IGFBP-3, able to REVERSE diet induced nitrogen wasting (protein catabolism due to calorie restriction).

Study: Done on healthy volunteers.



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Effects of Study: Sleep patterns were less interrupted, REM and deep sleep was significantly increased.

Study: Done on healthy volunteers of age 18-30. Effect was seen much greater in elderly subjects.



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Effects of Study: 7 day study on GH/IGF-1 effects after once daily administration. Showed similar GH release in all three concentrations (placebo/5mg/25mg) but dose dependant increases in serum IGF-1 in 5mg/25mg. Also showed an increase in GH pulses.

Study: Done on 9 healthy young males.



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This full text shows the full chemical structure of MK0677 as well as how to synthesize it. (It is referred to as L-163,191). Shows oral availability is >60%. Shows can form solution with water greater than 100mg/ml.



N-[1(R)-[(1,2-dihydro-1-methanesulfonylspiro[3H-indole-3,4'-piperidin]-1'-y l)carbonyl]-2-(phenylmethyloxy)ethyl]-2-amino-2-methylpropanamide methanesulfonate is MK-0677



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Patent information regarding ibutamoren mesylate (I believe this is right, though digging through patents is tough ****).

Peruse these articles. Unfortunately I'm pretty sure the patent holder would have a tight hold on this compound, it seems to be a real goldmine for elderly patients/GH deficient young patients.

Might still want to look into it. A pill a day is easier/more cost effective than an oral syringe a day.

 

[Syr]

Might still want to look into it. A pill a day is easier/more cost effective than an oral syringe a day.

great info, bro. In your searches can u quantify the HGH increase respect for istance hexarelin?
It seems less potent but we are speaking of an oral pill.

 

[Enigma76]

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Great abstract basically summing up GH secretagogues.

One thing to note; peptidyl GHS (like ecto/hexa) do have effects on the heart (there are specific GHS receptors for the peptidyl versions on the heart).

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Excellent study. The results, however, are alittle lastluster.

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Done on healthy obese males, showing MK0677 has an anabolic effect (indirectly through increasing GH/IGF1) but not a fat-burning effect.

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Merck's journal article on mk0677.

 

[Enigma76]

Back to hexarelin, just FYI it has been found to significantly increase cortisol production as well as GH secretion.

 

[Syr]

Back to hexarelin, just FYI it has been found to significantly increase cortisol production as well as GH secretion.

thanks, then without AAS a cortisol suppressor would be indicated.

 

[judge-mental]

enigma, Im intersted in GHRH secretagogues, any info on which one of those acts through GHRH?

 

[Enigma76]

enigma, Im intersted in GHRH secretagogues, any info on which one of those acts through GHRH?

I'll try and give you an answer I'm sure of this time :hammer:

I'm fairly certain none of the peptides IBE sells act thru GHRH, as GHRH works via the GH-IGF axis and the secretagogues work independently, with their own receptors.

 

[Mr.50]

So this should be an issue for Hexatropin but not Ectotropin right?

Back to hexarelin, just FYI it has been found to significantly increase cortisol production as well as GH secretion.

 

[Enigma76]

So this should be an issue for Hexatropin but not Ectotropin right?

I dont think the research is out there on that...I could be wrong, as I didnt look for long, but I only found information relating to the agonists.

It seems most (if not all) GHS agonists (GHRPs) exert some type of cortisol increase...one study found a 2fold increase in serum cortisol after GHRP administration. Others claimed "not substantial but still significant", with significant referring to the statistical testing.

The only ones I can find that dont increase cortisol are the non-peptide versions, like mk0677. Also, GHRH administration blunts cortisol.

In addition, GHRP-6/hex are shown to increase prolactin as well.

 

[Mr.50]

This is all a bummer.

I dont think the research is out there on that...I could be wrong, as I didnt look for long, but I only found information relating to the agonists.

It seems most (if not all) GHS agonists (GHRPs) exert some type of cortisol increase...one study found a 2fold increase in serum cortisol after GHRP administration. Others claimed "not substantial but still significant", with significant referring to the statistical testing.

The only ones I can find that dont increase cortisol are the non-peptide versions, like mk0677. Also, GHRH administration blunts cortisol.

In addition, GHRP-6/hex are shown to increase prolactin as well.

 

[judge-mental]

from the first review you linked

GHS release GH via actions at the pituitary and (mainly) the hypothalamic level, probably acting on GH releasing hormone (GHRH) secreting neurons and/or as functional somatostatin antagonists

doesnt sit well with what you just said...

 

[Syr]

In addition, GHRP-6/hex are shown to increase prolactin as well.

wow it seems i have to get more than one box of do$tinex, sigh.

 

[wojo]

um doesnt exercise cause both gh and cortisol to be released? matter of fact worrying about if this causes cortisol release will release cortisol..lol..just making a point in a smartass kinda way

 

[Enigma76]

from the first review you linked


doesnt sit well with what you just said...

I'm confused with what two things I said are contraindicting.

Remember, this is all very new. One study that shows a cortisol release might state that "GHRPs work through an unknown, independant action different than GHRH" while another, newer study will flat out describe the fact that ghrelin was discovered after the GHRPs and because of them, postulating a method of action for them. The GHRPs have been around for a long time, probably 20-30 years, and their method of action is just recently coming to light.

The GHRH comment about blunting cortisol I picked up in another study while reading last night.

Everything I say I try to pull from a study; make sure the ones you look at are the most recent.

The first study I posted was from '99...alot of it, as you can tell, is worded vaguely...such and such might have an effect on this and/or that...

 

[Enigma76]

um doesnt exercise cause both gh and cortisol to be released? matter of fact worrying about if this causes cortisol release will release cortisol..lol..just making a point in a smartass kinda way

I have no idea. I'm not passing judgement, just reading available literature and extracting key points that I feel everyone should know.

Most of the full papers I dont have (and dont plan on getting) access to; I dont know how bad a 2fold increase in cortisol is, or how much is released from exercise. All I know is that its something that should be known.

 

[judge-mental]

it is extermley important for me to elevate GH WITH GHRH. if you can link studies on GHRH secretagogues that would be great...

 

[judge-mental]

so ther you have it, should have researched myself instead of asking questions:
GHRP-6 is called a ghrelin mimicker. it acts synergystcly with and through GHRH to secrete GH. it elevates hunger, prolactine and cortisol and over time will cause fat gain (And anxiety) through cortisol. obviously one must use cortisol suppresors like PS, cissus and cortisol modulators like lean extreme to manage those effects. arginine may also be of help - to block negative feedback of somatostatin. over time it will shut off its effectiveness by lowering GHRH through increasd cortisol which will reduce IL-1 (GHRH is stimulated by IL-1)

its called a ghrelin mimicker but its not, they share many similar actions but some are not shared.

GH-releasing peptide-6 overcomes refractoriness of somatotropes to GHRH after feeding

[font=helvetica,arial][size=+1]CD McMahon, LT Chapin, RP Radcliff, KJ Lookingland, and HA Tucker [/size][/font]



After a meal, somatotropes are temporarily refractory to growth hormone-releasing hormone (GHRH), the principal hormone that stimulates secretion of growth hormone (GH). Refractoriness is particularly evident when free access to feed is restricted to a 2-h period each day. GH-releasing peptide-6 (GHRP-6), a synthetic peptide, also stimulates secretion of GH from somatotropes. Because GHRH and GHRP-6 act via different receptors, we hypothesized that GHRP-6 would increase GHRH-induced secretion of GH after feeding. Initially, we determined that intravenous injection of GHRP-6 at 1, 3 and 10 microg/kg body weight (BW) stimulated secretion of GH in a dose-dependent manner. Next, we determined that GHRP-6- and GHRH-induced secretion of GH was lower 1 h after feeding (22.5 and 20 ng/ml respectively) than 1 h before feeding (53.5 and 64.5 ng/ml respectively; pooleds.e.m.=8.5). However, a combination of GHRP-6 at 3 microg/kg BW and GHRH at 0.2 microg/kg BW synergistically induced an equal and massive release of GH before and after feeding that was fivefold greater than GHRH-induced release of GH after feeding. Furthermore, the combination of GHRP-6 and GHRH synergistically increased release of GH from somatotropes cultured in vitro. However, it was not clear if GHRP-6 acted only on somatotropes or also acted at the hypothalamus. Therefore, we wanted to determine if GHRP-6 stimulated secretion of GHRH or inhibited secretion of somatostatin, or both. GHRP-6 stimulated secretion of GHRH from bovine hypothalamic slices, but did not alter secretion of somatostatin. We conclude that GHRP-6 acts at the hypothalamus to stimulate secretion of GHRH, and at somatotropes to restore and enhance the responsiveness of somatotropes to GHRH.

147: Interactions of growth hormone secretagogues and growth hormone-releasing
hormone/somatostatin.
Tannenbaum GS, Bowers CY. Endocrine 2001 Feb;14(1):21-7

The class of novel synthetic compounds termed growth hormone secretagogues
(GHSs) act in the hypothalamus through, as yet, unknown pathways. We performed
physiologic and histochemical studies to further understand how the GHS system
interacts with the well-established somatostatin (SRIF)/growth hormone-releasing
hormone (GHRH) neuroendocrine system for regulating pulsatile GH secretion.
Comparison of the GH-releasing activities of the hexapeptide growth
hormone-releasing peptide-6 (GHRP-6) and GHRH administered intravenously to
conscious adult male rats showed that the pattern of GH responsiveness to GHRP-6
was markedly time-dependent, similar to that observed with GHRH.
Immunoneutralization of endogenous SRIF reversed the blunted GH response to
GHRP-6 at trough times, suggesting that GHRP-6 neither disrupts nor inhibits the
cyclical release of endogenous hypothalamic SRIF. By striking contrast, passive
immunization with anti-GHRH serum virtually obliterated the GH responses to
GHRP-6, irrespective of the time of administration. These findings suggest that
the GHSs do not act by altering SRIF release but, rather, stimulate GH release
via GHRH-dependent pathways. Our dual chromogenic and autoradiographic in situ
hybridization experiments revealed that a subpopulation of GHRH mRNA-containing
neurons in the arcuate (Arc) nucleus and ventromedial nucleus (VMN) of the
hypothalamus expressed the GHS receptor (GHS-R) gene. These results provide
strong anatomic evidence that GHSs may directly stimulate GHRH release into
hypophyseal portal blood, and thereby influence GH secretion, through
interaction with the GHS-R on GHRH- containing neurons. Altogether, these
findings support the notion that an additional neuroendocrine pathway may exist
to regulate pulsatile GH secretion, possibly through the influence of the newly
discovered GHS natural peptide, ghrelin.

old but relevant - arginine normalizes somatostatin, worth taking

J Endocrinol Invest. 1997 Nov;20(10):597-602.

[size=+1]Reduction of the somatotrope responsiveness to GHRH and Hexarelin but not to arginine plus GHRH in hyperprolactinemic patients.[/size]


Dipartimento di Medicina Interna, Universita di Torino, Italy.

Aim of the present study was to verify the maximal secretory capacity of somatotrope cells in patients with pathological hyperprolactinemia (HPRL) comparing it with that in normal age-matched women (NW). To this goal in 12 HPRL normal weight patients (age 28.6 +/- 2.6 yr, BMI 23.1 +/- 1.1 kg/m2) and 8 NW (27.2 +/- 0.8 yr, 22.8 +/- 0.8 kg/m2) we studied the GH response to GHRH (1 microgram/kg i.v.), GHRH plus arginine (ARG, 0.5 g/kg i.v.), an amino acid probably acting at the hypothalamic level inhibiting somatostatin release, and Hexarelin (HEX, 2 micrograms/kg i.v.), a synthetic hexapeptide belonging to GHRP family, which acts concomitantly at the pituitary and the hypothalamic level. IGF-I levels in HPRL were similar to those in NW (179.2 +/- 16.5 micrograms/l and 218.5 +/- 30.8 micrograms/l). In NW the GH response to GHRH (AUC: 1299.5 +/- 186.9 micrograms 90 min/l) was lower (p < 0.02) than those to GHRH + ARG (5252.7 +/- 846.3 micrograms 90 min/l) and HEX 3216.6 +/- 462.3 micrograms 90 min/l) which, in turn, were similar. In HPRL the GH response to GHRH (894.7 +/- 242.4 micrograms 90 min/l) was lower (p < 0.03) than that to HEX (1586.5 +/- 251.3 micrograms 90 min/l) and both were lower (p < 0.03) than that to GHRH + ARG (4468.8 +/- 941.7 micrograms 90 min/l). In HPRL the GH responses to GHRH and HEX were lower than those that in NW (p < 0.03) while that to GHRH + ARG was similar in both groups. These results demonstrate that the somatotrope responsiveness to GHRH and HEX is clearly reduced in patients with pathological hyperprolactinemia. On the other hand, in this condition the GH response to GHRH + ARG is normal. As arginine likely acts via inhibition of hypothalamic somatostatin release, these findings show that the maximal secretory capacity of somatotrope cells in hyperprolactinemia is preserved and indicate that partial refractoriness of somatotrope cells to GHRH and HEX could be due to somatostatinergic hyperactivity.

PMID: 9438917 [PubMed - indexed for MEDLINE]

not so good the next one ... I would postulate recution GHRH from this...

Psychoneuroendocrinology. 2004 Aug;29(7):851-60.

[size=+1]Hexarelin decreases slow-wave sleep and stimulates the secretion of GH, ACTH, cortisol and prolactin during sleep in healthy volunteers.[/size]


Max Planck Institute of Psychiatry, D-80804 Munich, Germany.

Ghrelin, the endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor and some GHSs exert different effects on sleep electroencephalogram (EEG) and sleep-related hormone secretion in humans. Similar to GH-releasing hormone (GHRH) ghrelin promotes slow-wave sleep in humans, whereas GH-releasing peptide-6 (GHRP-6) enhances stage 2 nonrapid-eye movement sleep (NREMS). As GHRP-6, hexarelin is a synthetic GHS. Hexarelin is superior to GHRH and GHRP-6 in stimulating GH release. The influence of hexarelin on sleep-endocrine activity and the immune system is unknown. We investigated simultaneously the sleep EEG and nocturnal profiles of GH, ACTH, cortisol, prolactin, leptin, tumor necrosis factor (TNF)-alpha, and soluble TNF-alpha receptors in seven young normal volunteers after repetitive administration of 4 x 50 microg hexarelin or placebo at 22.00, 23.00, 24.00 and 01.00 h. Following hexarelin, stage 4 sleep during the first half of the night, and EEG delta power during the total night decreased significantly. Significant increases of the concentrations of GH and prolactin during the total night, and of ACTH and of cortisol during the first half of the night were found. Leptin levels, TNF-alpha and soluble TNF receptors remained unchanged. We hypothesize that sleep is impaired after hexarelin since the GHRH/corticotropin-releasing hormone (CRH) ratio is changed in favour of CRH. There are no hints for an interaction of hexarelin and the immune system.

Publication Types:

• Clinical Trial

PMID: 15177700

: Eur J Endocrinol. 2004 Jun;150(6):905-11.
[size=+1]Glucocorticoid-dependent stimulation of adiposity and appetite by a ghrelin mimetic in the rat.[/size]

Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, Cambridge, UK.

OBJECTIVE: Chronic administration of GH secretagogues (GHSs) induces a state of positive energy balance in rodents by a GH-independent mechanism. Here we sought to determine to what extent the GHS effects to increase food intake and increase fat accumulation are glucocorticoid-dependent. DESIGN: The effects of twice-daily s.c. injections of GH-releasing peptide-6 (GHRP-6) (250 microg/kg) for 2 weeks on body weight, food intake and fat pad weight were determined in both adrenalectomised (ADX) rats (with or without basal corticosterone replacement) and adrenal-intact rats. RESULTS: All GHS-injected rats had a significantly increased body weight at the end of 2 weeks of treatment compared with saline controls. However, increased fat accumulation was only seen in adrenal-intact rats, with a 15% increase in s.c. inguinal (P<0.05 vs saline controls) and 20% increase in visceral mesenteric (P<0.05) fat pad weights following GHS treatment. The increased body weight observed in ADX rats following GHS treatment was not due to increased fat mass or increased weight of other organs measured. Food intake was increased for up to 7 h following a single injection of GHRP-6 in both the adrenal-intact (P<0.01) and corticosterone-replacement groups (P<0.05). This stimulating effect on food intake was not observed at any time point in the ADX rats without corticosterone replacement. CONCLUSION: These data suggest that GHS-induced body weight gain is glucocorticoid-independent. However, basal levels of glucocorticoids are permissive for the GHS-induced increase in food intake whilst activation of the hypothalamo-pituitary-adrenal axis appears to contribute to the GHS-induced accumulation of fat mass.

PMID: 15191362 [PubMed - indexed for MEDLINE]

 

[judge-mental]

this is why ghrelin does not equal GHRP-6.

[D-Lys3]-GHRP-6's antagonist activity in Ghrelin induced growth-hormone secretion in prepubertal rats
[font=Arial, Helvetica, sans-serif]Invalid Link Removed[/font][font=Arial, Helvetica, sans-serif][/font]Ghrelin is a 28-amino-acid peptide, with an essential n-octanoyl modification at Ser3, that elicits growth-hormone (GH) secretion in rats and humans. At present, the mechanisms of ghrelin action and its interactions with other systems controlling GH secretion remain poorly characterized. In this context, the present study was undertaken to obtain information about ontogeny and possible gender differences in the GH-releasing activity of ghrelin, and to delineate its primary site(s) of action at the hypothalamus and/or pituitary. In addition, the interactions between ghrelin and other relevant signals in the control of GH secretion, such as excitatory amino acids (EAAs), nitric oxide (NO) and serotonin, were assessed. Experiments were carried out in infantile-prepubertal animals, when GH pulsatility is not yet established. Systemic administration of ghrelin (25 nmol/rat, i.p.) to 5-, 10- and 23-day-old male and female rats increased plasma GH levels from day 10 onwards. This action was NO dependent, since it disappeared in 23-day-old males after pretreatment with an inhibitor of NO synthase (NAME). Similarly, central infusion of ghrelin (3 nmol/rat, i.c.v.) elicited GH responses in 10- and 23-day-old animals significantly higher than after systemic administration. By contrast, in vitro challenge of pituitary tissue with increasing doses of ghrelin (10(-9)-10(-7) M) failed to enhance GH release into the incubation medium, whereas stimulation with GH-releasing hormone (GHRH; 10(-7) M) or GHRP-6 (10(-7) M) was effective. Finally, effects of ghrelin were blocked by pretreatment with MK-801 and NBQX antagonists of EAA ionotropic receptors and after manipulation of endogenous serotoninergic tone. In addition, the potent releasing activity of EAA agonists NMDA and AMPA was blunted by pretreatment with D-Lys3-GHRP-6, a selective antagonist of the cognate ghrelin receptor, i.e. the GH-secretagogue receptor. In conclusion, our results demonstrate that GH-releasing activity of ghrelin appears early in the infantile period, is NO dependent and involves a primary hypothalamic site of action. The data also demonstrate for the first time the existence of a cross-talk between ghrelin and other neurotransmitter systems, such as EAAs and serotonin, in precise control of GH secretion.
Pinilla L, et al. Neuroendocrinology 2003 Feb;77(2):83-90​

​

BTW unless you are a big morbidly obese fatty why would you wnat to use the ghrelin antagonist [d-lys3]-GHRP6 (ectotropin) never mind potentialy reducing GH/GHRH but it antagonizes the AMPA receptors :sad: also my non-educated guess is that since ghrelin is such a growth factor (apparently... just starting to reveal for instance osteobalstic proliferation and anti-apoptosis effects, as well as antiaging effects on musvle) a ghrelin antagonsits will mess things in a hurry (osteoporosis anyone? unresponsive muscles?) maybe IBE can answer this one.

 

[Enigma76]

After you posed the question before as to why the antagonist would raise GH, I did some more reading and basically came to the same conclusion...why is this good at all? Ghrelin is, everyday, being found to have increasingly more and more important effects for the body.

But from the user results in some of these threads, it seems to indeed elicit some response...I dont know what other factor would cause an increase in body/head hair and fingernails...

 

[lozgod]

It seems alot of studies contradict previous/future ones. My whole take on it is take a look at the results. Plenty of people are using the products. If you don't want to try it without knowing the possible results then wait and read other's experiences. Real world experience is 1000 times more beneficial than 1 billion studies IMO.

 

[judge-mental]

if you would read the artical we posted where it says increase in muscle mass now where do you think this incease in muscle is coming from?

hi - can you link the article in question? thanks

 

[Enigma76]

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[size=+1]Acipimox-mediated plasma free fatty acid depression per se stimulates growth hormone (GH) secretion in normal subjects and potentiates the response to other GH-releasing stimuli.[/size]

Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.

Department of Medicine, School of Medicine, Santiago de Compostela University, Spain.

Increases in plasma free fatty acids (FFA) inhibit the GH response to a variety of stimuli; however, the role of FFA depression in GH control is far from understood. In the present work, FFA reduction was obtained by the administration to normal subjects of acipimox, a lipid-lowering drug devoid of side-effects. Each subject tested underwent two paired tests. In one, acipimox was administered orally at a dose of 250 mg at -270 min and at a dose of 250 mg at -60 min; in the matched test, placebo was given at similar intervals. To induce GH release, four stimuli acting through different mechanisms were used: pyridostigmine (120 mg, orally) at -60 min, GHRH (1 microgram/kg, iv) at 0 min, GH-releasing peptide (GHRP-6; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; 1 microgram/kg, iv) at 0 min, and finally, GHRH plus GHRP-6 at the same doses at 0 min. GH secretion was analyzed as the area under the secretory curve (AUC; mean +/- SE, micrograms per L/120 min). Acipimox pretreatment alone (n = 6) induced a reduction in FFA levels compared with placebo treatment. The FFA reduction led to a sustained GH secretion that increased from 2.4 +/- 1.8 micrograms/L at -120 min to 14.2 +/- 4.0 at 120 min. The GH AUC for placebo was 266 +/- 100, and that for acipimox was 1781 +/- 408 (P < 0.05). In the pyridostigmine-treated group (n = 6), the acipimox-pyridostigmine AUC (2046 +/- 323) was higher (P < 0.05) than the placebo-pyridostigmine AUC (764 +/- 101), but was not different from the AUC of acipimox alone. Previous FFA reduction nearly doubled the GHRH-mediated GH secretion (n = 6; placebo-GHRH AUC, 1817 +/- 365; acipimox-GHRH test, 3228 +/- 876; P < 0.05). A similar enhancement was observed when the stimulus employed was GHRP-6 (n = 6; placebo-GHRP-6 AUC, 2034 +/- 295; acipimox-GHRP-6, 4827 +/- 703; P < 0.05). Furthermore, even the most potent GH stimulus known to date, i.e. GHRH plus GHRP-6, was enhanced by the FFA suppression (placebo-GHRH-GHRP-6 AUC, 2034 +/- 277; acipimox-GHRH-GHRP-6, 5809 +/- 758; P < 0.05). The enhancing effect of lowering FFA levels was additive regardless of the stimulus employed. These results indicate that 1) FFA reduction per se stimulates GH secretion with a delayed time of action; 2) FFA reduction enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH, and GHRP-6; and 3) the observation that FFA reduction enhanced the response to the most potent GH stimulus, GHRH plus GHRP-6, suggests that FFA suppression acts by a separate mechanism. FFA reduction may have value in the clinical setting for assessing GH reserve.


Courtesy of AL. First thing in the morning dosing, I'm assuming this has to do with the "secret delivery system" more than timing right? At what time are FFA the lowest? That would seem to be the best time to dose any of these GHRPs...

 

[lozgod]

I will have to dig up the study, I have no idea where it was, but the D-Lys version (GHRP-6 Antagonist) was very very effective at lowering FFA levels, which would thereby increase GH release according to the above study.

 

[judge-mental]

this is true

IN THE MORBIDLY OBESE.

improvement of leptin sensitivity in those will also help with GH.

well Im not talking about them but about normal training individuals. even if there is a hypothetical minscule rise in GH in the non-obese the actions of ghrelin are to important to antagonize,IMO.

 

[judge-mental]

To gain further insight into the therapeutic potential, we examined whether or not intraperitoneally administered [D-Lys-3]-GHRP-6 produced anorexigenic effects in ob/ob obese mice. [D-Lys-3]-GHRP-6 significantly decreased food intake in ob/ob obese mice as well as in lean mice (fig 3AInvalid Link Removed). Finally, we examined the effects of repeated administration of [D-Lys-3]-GHRP-6 on body weight gain and glycaemic control in ob/ob obese mice. Repeated injections of [D-Lys-3]-GHRP-6 significantly lowered body weight gain and blood glucose concentrations without decreasing muscle weight (fig 3BInvalid Link Removed, table 2Invalid Link Removed). Furthermore, [D-Lys-3]-GHRP-6 treatment significantly reduced FFA levels of ob/ob obese mice by 24% compared with saline treated ob/ob obese mice (fig 3CInvalid Link Removed). Control and [D-Lys-3]-GHRP-6 treated animals exhibited no significant differences in water intake (10.5 (0.43 (200 nmol) v 10.7 (0.43) ml/day (control); n=7).

so where in that article:
there is muscle mass gain?
there are effects beyond reduced food intake in lean non ob/ob mice?
as I said, ob/ob mice are a model for metabolic syndrom, diebetes type II etc.

 

[lozgod]

It is a weight loss supplement. I wouldn't base my entire opinion on studies. I would look at real world experience. The tobacco industry has put out studies saying second hand smoke doesnt cause lung cancer, but that doesn't make it true.

 

[CROWLER]

IBE if you are looking for testers I would be happy to be a tester.

I would also be happy to do a log and if you like include before and after blood tests. Just let me know.


CROWLER

 

[CROWLER]

will do bro pm me your shipping info we will send you 2 kits

I PMed you at IBE forums.

Thanks


CROWLER

 

[judge-mental]

lozgod, I agree this would cause weight loss and in fact would be one of the best weight loss drugs for non-lean people. Im not quite sure what would happen in the lean (below set point)
you are correct there is alot of data missing on this things. time will tell anyway thanks anyone.

 

[Kristopher]

Are you looking for more testers? i would like to try this stuff during my PCT..

 

[Mr.50]

IBE I would love to be a tester for you also for this product and I would keep a stricty log during my PCT. I am about due for bloodwork also if you would like. Please let me know at your convenience. Thank you.


Mr.50

Yes!

 

[ss01]

I'm starting a cycle soon. PCT in 4 weeks. Willing to give this a try if you'll have me in your test group. Will keep log.

 

[CROWLER]

will do bro pm me your shipping info we will send you 2 kits

IBE,

I don't have PMs here because I got guys asking for sources.

What is your board name over at IBE forums please?

I have asked a couple of Mods and they don't know who made the post about the 2 kits.

Thanks


CROWLER

 

[SJA]

I have a log going on IBE's forum right now if anyone is interested.

Invalid Link Removed

 

[CROWLER]

Admin

PM sent

Thanks


CROWLER