CJC 1295 & D-Lys3 GHRP-6????

mike4266

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New to this forum, and have been reading alot of good info from you guys. Thank you. I am about to start CJC 1295 DAC conjugated & GHRP 6 stack.

CJC 1295 DAC conjugated- 750 mcgs twice per week
GHRP 6- 150 mcgs twice per day

Due to the increase in ghrelin accompained by the GHRP 6 I am a little skeptical. Last week I started clenbeutrol with alot of cardio to shed some bodyfat. I know the GHRP 6 will burn most the extra calories due to the fat burning properties however, i was considering D-Lys3 GHRP-6 because it is a ghrelin antagonist, thus allowing me to eat fewer calories. I am doing the peptide stack not for mass, but to strengethen my tendons, ligaments, and cartlidge and shed some bodyfat.

Do you think GHRP 6, D-Lys3 GHRP 6, GHRP 2, or hexarelin would be best to stack with CJC 1295 for my collagen synthesis, fat burning goals?

Will the absence of ghrelin interfere with the HGH producing properties?

Stats are as follows

247 lbs. probbably 18% bodyfat ( I have been training for powerlifting for the past couple months.)
Currently I am taking

IGF-1 40 mcg, PWO
Clenbeutrol 50 mcg x2 ED
Maintenacne dose of test 250 mg. per week

I will be adding equipoise 400mg in two weeks.

Any help would be appreciated!
 
Rhyno

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D-lys3-ghrp-6 is quite nice for appetite suppression but the effects seem to wear off after 2-3 weeks. I've heard the same is true for ghrp-6's appetite stimulation. You'll still see the benefits of the added GH with time with both: one kills your appetite the other makes you hungry.
 

mike4266

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So you think the D-Lys3 GHRP-6 will have the same GH producing properties without the appetite increase?
 
CEDeoudes59

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mike you'll need hoodia or something like that to crush the appetite methinks...
eq + any sort of GH stimulator + igf... no way that appetite is going down. the body is yelling feed me from that anabolic environment.
 
datBtrue

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So you think the D-Lys3 GHRP-6 will have the same GH producing properties without the appetite increase?
No.

d-Lys-3-GHRP-6 is a GH secretagogue receptor (GHS-R) antagonist (inhibitor). It has been shown to significantly reduce GHRH-mediated growth hormone release.

The following quote is from a study that used d-Lys-3-GHRP-6 as an GHS-R antagonist in conducting their experiments.

"...two of the three independent experiments did not show an increase in GH release in the presence of the GHS-R antagonist, but all showed a consistent reduction in GHRH-induced GH release in the presence of the antagonist." - The Role of Pituitary Ghrelin in Growth Hormone (GH) Secretion: GH-Releasing Hormone-Dependent Regulation of Pituitary Ghrelin Gene Expression and Peptide Content Endocrinology, Jun Kamegai,..., Aug 2004; 145: 3731 - 3738

Its primary "use" in humans would be to reduce hunger induced by ghrelin (the endogenous GHS). Unfortunately it would reduced or eliminate GH release as well.

It is not something you would ever want to use unless you feel you already make too much growth hormone.
 
Rhyno

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Damn...I hate giving out incorrect advice. :pat: I appreciate you clearing things up. Reps.


The only statement, I am not sure about though is this:
No.
Unfortunately it would reduced or eliminate GH release as well.

It is not something you would ever want to use unless you feel you already make too much growth hormone.
From the article in Endocrinology 145.8 (2004) entitled "The Role of Pituitary Ghrelin in Growth Hormone (GH) Secretion: GH-Releasing Hormone-Dependent Regulation of Pituitary Ghrelin Gene Expression and Peptide Content:"

We also conducted functional studies to examine whether the pituitary ghrelin/GHS-R system contributes to GH release after GHRH stimulation, by challenging pituitary cell cultures with GHRH in the presence of a GHS-R-specific inhibitor ([D-Lys-3]-GHRP-6). The GHS-R inhibitor did not affect GH release in the absence of GHRH, but significantly reduced GHRH-mediated GH release. This is the first report demonstrating that endogenous pituitary ghrelin can play a physiological role in GH release, by optimizing somatotroph responsiveness to GHRH.
I also remember reading about the breeding of "ghrelin-null" mice who showed no deficiencies in growth. I'll dredge it up if I have the time.

Of course, experiments done on small mammals do not always have the same results as human trials. But I think they still point us in the right direction.

Any thoughts and/or counter-arguments would be much appreciated. :)
 
datBtrue

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Damn...I hate giving out incorrect advice. :pat: I appreciate you clearing things up. Reps.


The only statement, I am not sure about though is this:


From the article in Endocrinology 145.8 (2004) entitled "The Role of Pituitary Ghrelin in Growth Hormone (GH) Secretion: GH-Releasing Hormone-Dependent Regulation of Pituitary Ghrelin Gene Expression and Peptide Content:"



I also remember reading about the breeding of "ghrelin-null" mice who showed no deficiencies in growth. I'll dredge it up if I have the time.

Of course, experiments done on small mammals do not always have the same results as human trials. But I think they still point us in the right direction.

Any thoughts and/or counter-arguments would be much appreciated. :)
I'm not sure exactly what you are asking my friend. The study you sited identified D-Lys-3 as a GH-secretagogue receptor INHIBITOR.

"a GHS-R-specific inhibitor ([D-Lys-3]-GHRP-6). The GHS-R inhibitor did not affect GH release in the absence of GHRH, but significantly reduced GHRH-mediated GH release."

D-Lys-3 did not "have an influence on" (affect) GH release. But significantly reduced GHRH's activity. GHRH's activity is to bind to a somatotroph and effect GH release. GHRH is THE hormone that causes GH release. Thus if you have an an inhibitor such as D-Lys-3 bind to the GHS-R on the same somatotroph cell and reduce its GH releasing activity...

...you end up with less GH then you would have if you never administered D-Lys-3. Again D-Lys-3 also failed to bring about an increase in GH itself. So it is a big nothing and a significant inhibitor.

The following line is not speaking to D-Lys-3.

"This is the first report demonstrating that endogenous pituitary ghrelin can play a physiological role in GH release, by optimizing somatotroph responsiveness to GHRH."

This line speaks to what Ghrelin and Ghrelin mimetics (i.e. GHRP-6, GHRP-2, Hexarelin, Ipamorelin... and the molecules MK-0677 & the molecules derived from Ipamorelin research) are capable of. What they are capable of is binding to a GHS-Receptor and optimizing (not inhibiting GH release). This occurs in part through their own actions and in part by enhancing (not inhibiting) the actions of GHRH.

It sucks that the place that sells D-Lys-3 is not more clear. But thats just the way it is...
 
Rhyno

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The study you sited identified D-Lys-3 as a GH-secretagogue receptor INHIBITOR.

"a GHS-R-specific inhibitor ([D-Lys-3]-GHRP-6). The GHS-R inhibitor did not affect GH release in the absence of GHRH, but significantly reduced GHRH-mediated GH release."

D-Lys-3 did not "have an influence on" (affect) GH release. But significantly reduced GHRH's activity. GHRH's activity is to bind to a somatotroph and effect GH release. GHRH is THE hormone that causes GH release. Thus if you have an an inhibitor such as D-Lys-3 bind to the GHS-R on the same somatotroph cell and reduce its GH releasing activity...

...you end up with less GH then you would have if you never administered D-Lys-3. Again D-Lys-3 also failed to bring about an increase in GH itself. So it is a big nothing and a significant inhibitor.

The following line is not speaking to D-Lys-3.

"This is the first report demonstrating that endogenous pituitary ghrelin can play a physiological role in GH release, by optimizing somatotroph responsiveness to GHRH."

This line speaks to what Ghrelin and Ghrelin mimetics (i.e. GHRP-6, GHRP-2, Hexarelin, Ipamorelin... and the molecules MK-0677 & the molecules derived from Ipamorelin research) are capable of. What they are capable of is binding to a GHS-Receptor and optimizing (not inhibiting GH release). This occurs in part through their own actions and in part by enhancing (not inhibiting) the actions of GHRH.

It sucks that the place that sells D-Lys-3 is not more clear. But thats just the way it is...
I appreciate the clarification, Dat. :cheers:

I still have a fair amount of d-lys-3-ghrp in my possesion. Given my new knowledge of the substance's actions, I won't be purchasing it again.

Would using the remainder of my supply for 20 days (100mcg, 3 times a day) be ok or is it peptide best reserved for the trash can? I'd rather just cut my losses and throw it out if it is going to have a significant effect on my body-composition, physiology, etc.
 

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