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

Question for ya Dat. How long would you suggest running your suggested BB dose of (100mcg of CJC-1295 w/ 200mcg of GHRP-6 3X a day). Need to know how much gear to pick up...thanks again for your wealth of information bro.:)
 
Question for ya Dat. How long would you suggest running your suggested BB dose of (100mcg of CJC-1295 w/ 200mcg of GHRP-6 3X a day). Need to know how much gear to pick up...thanks again for your wealth of information bro.:)

My view is that higher doses should be reserved for properly constructed cycles and that lower amounts or a switch over to GH is probably prudent to give the pituitary a break.

How long to run 2.1mgs of CJ-1295 w/ the GHRP-6 on an anabolic cycle?

Minimum 6 weeks to maximum 12 weeks.

I'd also recommend that you use a dose of say 700mcg - 1mg for several weeks or even months before your cycle as a prime.

Also run that lower dose during PCT as well.
 
thank you for the info on anti aging . i showed your thread to one of my kids who is a bio- chemist who has done geneic research for some major outfits .he really complimented your research. he said he has had paid staff who have not been this through thanks again

Thanks for the compliment pgh. It was very nice of you to take the time to tell me that. :)
 
Sorry I overlooked your post Irish.

...do you feel that 1mg of cjc a week and 300-500mcgs a every day of ghrp dosed 3 times a day would provide good gains from someone in there 30s around 215 or so or do you feel that it would be best to use 2mgs of cjc a week for the most gains? the reason i ask is at 2mgs a week it would obviously more costly and this person is trying to save money as this is a cheaper possibly as effective or even more effective than the standard hgh cycle..what are your thoughts?

Yes I do ...as long as we understand/keep in mind that GH or CJC-1295/GHRP-6 released GH is a component of a properly constructed anabolic cycle and is not sufficient as a standalone mass builder.

As a standalone it can really help with recomp and loss of the fat pad on a properly constructed diet/plan BUT if mass is the goal then anabolic agents need to be used to get the most out of it.

That means such things as AAS & possibly slin.

also this individual plans to workout in the AM so would it be better for the person to take his first shot of ghrp-6 after his am workout and antoher in the mid afternoon around 3 or so or should they just go with the first shot upon awakening and last around bed

No the first idea works much better then the second idea. You want your three dosings of GHRP-6 to be spaced throughout the day. If you bunch them up there is a possibility (for many people a probability) that they won't respond strongly to the second attempted initiation of a pulse. The reason is that the factors that inhibit a GHRH action may still not have cleared yet. This is variable among different people.

Some people can be given GHRH and soon thereafter another dose and they get two pulses while others fail to repond to the second dose of GHRH and just have the initial pulse.
 
thank you very much for taking the time to answer my questions..i would like to say that the individual who is thinking of using this is planning on running various aas in conjunction with the cjc and ghrp, do you have any rough idea how 1mg a week and 300-500mcgs of ghrp would compare to say a standard hgh run of 4ius a day? would you say its simliar? or that this may exceed a given hgh cycle? how long till one would see some results, like a hgh cycle so the longer one is on the better the gains? again sorry for all the questions i just find this very intrigueing..
 
Ok, interesting, so you recommened not going over 12weeks on cjc/ghrp6. This leads me to think mabye switching up peptides will yeild better results and be safer. I may do 3months cjc/ghrp6 then 3-5months GH then back to cjc/ghrp6 for now on. Maybe even get freaky and do 3months cjc/ghrp6, 1month IGF, 3-5months Gh, 3months cjc/ghrp6, 3months GH frag,etc...lol

My view is that higher doses should be reserved for properly constructed cycles and that lower amounts or a switch over to GH is probably prudent to give the pituitary a break.

How long to run 2.1mgs of CJ-1295 w/ the GHRP-6 on an anabolic cycle?

Minimum 6 weeks to maximum 12 weeks.

I'd also recommend that you use a dose of say 700mcg - 1mg for several weeks or even months before your cycle as a prime.

Also run that lower dose during PCT as well.
 
...you have any rough idea how 1mg a week and 300-500mcgs of ghrp would compare to say a standard hgh run of 4ius a day? would you say its simliar? or that this may exceed a given hgh cycle? how long till one would see some results, like a hgh cycle so the longer one is on the better the gains? again sorry for all the questions i just find this very intrigueing..

I attempted to make that comparison in post #6 of this thread: Growth Hormone Administration vs. CJC-1295/GHRP-6

Based on that & feedback that I am getting (in addition to tests on my own lab rat) I'd say it is higher than a 4iu GH equivalency.

If you want to know what I have discovered on my own cycle of test/slin/CJC/GHRP-6 it is that:

2.1mg of CJC-1296 + 2.1mcg of GHRP-6 (dosed at 100mcg 3x a day each) is outstanding at helping build muscle in that kind of environment. I ran it at that level for 6 weeks and have stepped it down by 2/3rds to make a comparison.

2mgs is equivalent to a high dose of GH
1mgs is equivalent to a moderate dose of GH
700mcgs is still (I think) a moderate dose equivalent of GH.

Synthetic GH is different then the group of GH forms your body produces so the two can not be exactly compared.
 
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HOLY SHIT DAT!!!!

this is the CJC/GhRP6 bible...

so in a nut shell, this peptide will cost a shit load to take

2.1 mgs a week, thats a vial a week, and for 6-12 weeks thats 3-6 vials of just CJC....and a hell of lot more vials of GHRP6

i dont think i can afford it lol...but damn, the science bind all this makes sense..

what is the lowest effective dose someone can get away with both?

im a 24 yr old 5'11 200 lb male...
 
2mgs is equivalent to a high dose of GH
1mgs is equivalent to a moderate dose of GH
700mgs is still (I think) a moderate dose equivalent of GH.

I'm guessing you meant 700mcgs (micrograms)?
 
haha...that would be super expensive...

Dat...how many mgs of each peptide would one need to run your protocal for 6 weeks...12 weeks?

i suck at math lol
 
...I prefer:

100mcg of CJC-1295 + 100 - 200 mcg GHRP-6 three times a day....

Dosing schedules were mentioned several times in different ways in this thread. Just to be clear, since we are talking about a relatively new research chemical, the above translates to three injections daily:

* 100mcg CJC-1295 with 200mcg GHRP-6 upon waking, 25 minutes before eating
* 100mcg CJC-1295 with 200mcg GHRP-6 six hours later, ideally post workout
* 100mcg CJC-1295 with 200mcg GHRP-6 immediately before bed

For a total of 2.1g CJC-1295 and 4.2 GHRP-6 each week.

and

...an anti-aging dose (still high enough for fatloss) is 100mcg of CJC-1295 pre-bed and 100mcg of GHRP-6 twice a day.

Translates into two injections daily:

* 100mcg GHRP-6 upon waking, 25 minutes before eating
* 100mcg CJC-1295 with 100mcg GHRP-6 immediately before bed

For a total of 700mcg (0.7g) CJC-1295 and 1.4g GHRP-6 each week.

Is that right?
 
GHRH & Pituitary Over-stimulation (I of II)

Written by: M.M. a/k/a DatBtrue
Copyright 2008 by M.M. a/k/a DatBtrue
All rights reserved.
No part of this article may be reproduced in any form without the written permission of the copyright owner.

Does GHRH result in Pituitary Over-stimulation?

Has that type of concern ever been raised in regard to long-lasting analogues of Growth Hormone Releasing Hormone?

Yes but not directly in a study itself or by one of its authors.

In a fairly recent editorial in the New England Journal of Medicine in which the results from a clinical trial for Tesamorelin, a long-acting analogue of growth hormone releasing hormone (GHRH) were also reported, several questions were raised by the editor. Among them "Would such a regimen...overstimulate the pituitary gland...with an increased risk of pituitary neoplasms?" - Manipulation of the Growth Hormone Axis in Patients with HIV Infection, Marc R. Blackman, M.D., NEJM Volume 357:2397-2399 December 6, 2007

I should point out that the referenced study, Metabolic Effects of a Growth Hormone–Releasing Factor in Patients with HIV, Julian Falutz, M.D, et al. administered 2 mg per day of tesamorelin by subcutaneous injection for 26 weeks to study participants without any indication whatsoever of pituitary problems or for that matter any other problems.

Yet it is a valid concern and one we should seek to understand.

Before we preceed to see if we can create a better understanding for ourselves...we need to clarify exactly the type of things that most concern us regarding potential pituitary damage since the phrase "overstimulate the pituitary gland" is not used in any other journal article.

Reviewing the actions of GHRH on the pituitary & reviewing the literature leads me to focus on two primary areas of concern: pituitary hyperplasia/somatotroph hyperplasia and tumors/adenomas.

THE NATURAL ORDER OF THINGS

In non-diseased people of all ages there exists very large amounts of growth hormone (in various isoforms) stored in the pituitary. While this store of growth hormone accounts for ten percent (10%) of the pituitary's dry weight only a very small portion (1-2ng/mL) of it is found in the circulation. No other pituitary hormone is stored in such high amounts. In fact the quantity of growth hormone stored in the pituitary is 800 times larger then the stored quantity for any other pituitary hormone. - Lewis UJ. Growth hormone: what is it and what does it do? Trends Endocrinol Metab 1992;3:117–121

From this simple understanding alone we can fairly accurately surmise that asking the pituitary to release some of that store of growth hormone so that we can achieve youthful levels or double the amount of youthful levels shouldn't "overstimulate it" or tax it in such a way as to force it to unduly expand the somatotroph population.

Only a portion of the population of cells within the pituitary are called upon to secrete growth hormone and this is not static. It is controlled by the three hormones that govern this process - Growth Hormone Releasing Hormone (GHRH), Ghrelin (of which GHRPs are mimetics) and Somatostatin.

GHRH and Ghrelin (i.e. GHRPs) appear to act on different somatotrope subpopulations. GHRP has been shown to increase the number of somatotropes releasing GH, without altering the amount of hormone released by each individual cell. On the other hand, GHRH stimulates both the number of cells secreting GH and the amount of GH secreted per cell.

Somatostatin (the GH inhibiting hormone) has been shown primarily to decrease the number of cells secreting GH without affecting the amount of GH secreted per cell.

In very general terms GHRP increases, while Somatostatin decreases, the number of active GH secreting somatotropes.

On the other hand GHRH does both, but acts primarily by stimulating the amount of secreted GH within the active somatotropes.

So fluctuations in somatotrope populations and secretion activity is a natural occurrence.

SOMATOTROPH HYPERPLASIA

But when we see references in journals and in the medical community to somatotroph hyperplasia and the very rare pituitary hyperplasia they are referring to an abnormal increase in the number of cells with consequent enlargement of tissue.

From an article titled "Pituitary Hyperplasia" in the May 1999 issue of the journal Pituitary we see that "Somatotroph hyperplasia is rare; it is limited to cases of GHRH overproduction by extrapituitary endocrine neoplasms and sporadic examples of gigantism."

For the reason that we may be supplying GHRH beyond what is naturally occurring in our body which subsequently binds to receptors on somatotrophs in the pituitary and act on them we need to consider if the amount of GHRH we are supplying is on par with the level of overproduction that can bring about hyperplasia. But first let's examine our other concern.

TUMORS/ADENOMAS

If we were to somehow bring about somatotroph hyperplasia will this result in tumors?

It doesn't appear to be likely. From the 2008 edition of Diagnosis and Management of Pituitary Disorders, Edited by Brooke Swearingen, MD, et al.:

"It is a common clinical observation that ectopic overproduction of releasing hormones, such as GHRH or corticotropin-releasing hormone (CRH), results in proliferation of the target cells. However, the vast majority of sporadic pituitary tumors do not show hyperplasia in the surrounding tissue. Although these data suggest that hormonal stimulation is not a primary etiologic mechanism in pituitary tumorigenesis, it is worth noting that aggressive GH-secreting adenomas frequently express high intrapituitary amounts of GHRH (45)."​

If we follow up that footnote (45) we discover that the overexpression of GHRH referred to comes from the tumor itself. In other words like a lot of tumors the hormone in question is locally produced and locally used by the tumor within. - Thapar K, Kovacs K, Stefaneau L, et al. Overexpression of the growth-hormone-releasing hormone gene in acromegaly associated pituitary tumors. An event associated with neoplastic progression and aggressive behavior, Am J Pathol 1997;151:769–84.

Let's take a look at someone who had a tumor that hyper-secreted GHRH. This type of overproduction is known as ectopic GHRH hypersecretion. From the autopsy:

"In this report we describe the functional and morphological features of the pituitary removed from a patient with a 10-yr history of a disseminated bronchial carcinoid producing GHRH.
...
Although somatotroph proliferation was widely evident, there was no evidence of adenomatous transformation.
...
We conclude that sustained exposure to ectopic GHRH leads to somatotroph hyperplasia, but, at least in this case, was not sufficient for adenomatous transformation." - Somatotroph hyperplasia without pituitary adenoma associated with a long standing growth hormone-releasing hormone-producing bronchial carcinoid , S Ezzat, SL Asa, L Stefaneanu, R Whittom, HS Smyth, E Horvath, K Kovacs, and LA Frohman, J. Clin. Endocrinol. Metab., Mar 1994; 78: 555 - 560

The general conclusion drawn from similar case studies is that GHRH induced hyperplasia does not bring about tumors.

WHAT DOES BRING ABOUT TUMORS?

From another case study:

"...it is still not known whether hypothalamic hormones have a role in tumorigenesis in human pituitary adenomas.
...
Despite extremely high local levels of hypothalamic releasing hormone, adenoma formation did not occur in our patient. This study provides further evidence that although hypothalamic hormone excess may be important in cellular proliferation, the pathogenesis of pituitary adenoma formation may be mediated by other factors including new oncogenes and suppressor genes that are as yet uncharacterized." - A Growth Hormone-Releasing Hormone-Producing Pancreatic Islet Cell Tumor Metastasized to the Pituitary Is Associated with Pituitary Somatotroph Hyperplasia and Acromegaly, N. Sanno, A. Teramoto, R. Y. Osamura, S. Genka, H. Katakami, L. Jin, R. V. Lloyd, and K. Kovacs, J. Clin. Endocrinol. Metab., August 1, 1997; 82(8): 2731 - 2737

Eventually though we get to the one study that was able to bring about tumor formation in mice after a year of bombardment. What they found was that GHRH hyperstimulation was not sufficient without other factors to bring about adenomas. In fact GHRH by itself was not sufficient to bring about hyperplasia. They highlighted a codependence between GHRH and GH/IGF-I on pituitary cell proliferation.

Tumor formation was likely dependent on other factors relevant to GH signaling. What was most interesting was the process:

"Although supraphysiological levels of hGHRH were present in pituitaries and hypothalami of both GHR+,hGHRH and GHR-/-,hGHRH mice, the appearance of pituitary adenomas was not preceded by a progressive increase in pituitary size. In fact, tumor formation was preceded by a static pituitary growth phase in which mean pituitary weight remained constant for a minimum of 4 months, and in 8% of 12-month-old mice expressing the hGHRH transgene, pituitary weights and gross morphology were indistinguishable from those observed at 2 months of age." - The Effect of GHRH on Somatotrope Hyperplasia and Tumor Formation in the Presence and Absence of GH Signaling, R. D. Kineman, L. T. Teixeira, G. V. Amargo, K. T. Coschigano, J. J. Kopchick, and L. A. Frohman, Endocrinology, Sep 2001; 142: 3764.

This leads us into understanding that the pituitary has defense mechanisms that protect it from such dangers. Nothing happens overnight. The speculation on the actual defense mechanism which resisted adenoma formation for 4 months in mice is as follows:

"...adult somatotropes may become desensitized to the proliferative actions of GHRH. Alternatively, the normal somatotrope may be capable of only a finite number of divisions regardless of the time of onset and duration of GHRH hyperstimulation. Finally, GHRH hyperstimulation could result in an increase in somatotrope proliferation independently of age, but the increase in the rate of proliferation is counterbalanced by an increase in the rate of cell death in the adult gland. Although the exact mechanisms involved in the maintenance of pituitary mass in the presence of elevated GHRH remains to be determined, it is clear that sustained supraphysiological levels of GHRH secondary to expression of the hGHRH transgene ultimately led to a loss of these protective mechanisms in select cells (presumably caused by somatic mutations), thereby allowing for clonal expansion and adenoma formation."​

Continued Below
 
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GHRH & Pituitary Over-stimulation (II of II)

Continued from Above
Written by: M.M. a/k/a DatBtrue
Copyright 2008 by M.M. a/k/a DatBtrue
All rights reserved.
No part of this article may be reproduced in any form without the written permission of the copyright owner.

HOW MUCH GHRH IS TOO MUCH?

First it is not clear that too much leads to tumor formation. For the most part it doesn't. We really just have the mouse study. While it is comforting to know that somataotroph hyperplasia is reversible and does not result in tumor formation it is important to understand that huge amounts of unchecked chronic GHRH may possibly in some cases play a secondary role in tumor formation.

The body has mechanisms to protect itself from unchecked somatotroph proliferation. The everyday mechanism of most import is the inhibiting hormone somatostatin.

Somatostatin acts as a sweeper. It comes into the pituitary and declares "enough is enough" and it reduces the number of cells secreting growth hormone. In the traditional model it played a primary role in growth hormone pulsation. In the present model it must share this role with Ghrelin.

If we completely antagonize somatostatin we likely do away with the biologically significant pulsatile nature of growth hormone release. But just as unfortunate we eliminate our continual check on chronic growth hormone release. While it may be fun to speculate about using Acetylcholinesterase inhibitors to eliminate somatostatin's inhibitory effect and let GHRH exert its action unrestrained and on a continual basis, it probably isn't a terribly wise or healthy way to go about effecting higher GH levels.

What is interesting about CJC-1295 is that despite its long-lasting nature the pulsatility of growth hormone release is maintained. In other words sure GHRH is continually available but its actions are not unchecked. Somatostatin is still able to give our pituitary the break it needs so that we don't end up with somatotroph hyperplasia.

We don't want to put our pituitary in any danger of having to rely on those "fourth quarter" defense mechanisms touched on in the mice study. So that brings us back to the question we previously raised "is the amount of GHRH we are supplying on par with the level of overproduction that can bring about hyperplasia?" Again keeping in mind that hyperplasia may not be such a bad thing but it nonetheless is a step in a direction we don't want to take.

Our best available comparison is to look at the quantities of GHRH that tumors that bring about giantism and acromegaly produce and see how the medical practioners in this field define excess. This is not really fair to us to do it this way because they look to the presence of plasma GHRH levels in a particular range in conjunction with such factors as high levels of growth hormone and other hormones in patients with visibly identifiable characteristics of gigantism or acromegaly.

We don't have those factors that would indicate mutations & processes gone awry. Nor are we necessarily sustaining high levels of unchecked GHRH for periods measured in years.

The following from, "Ectopic GRH syndromes" In: Robbins RJ, Melmed S, eds. Acromegaly: a century of scientific and clinical progress, Frohman LA, Downs TR. 1987, New York: Plenum Press; pp 115-125 serves as our benchmark.

"It is suggested that peripheral plasma GHRH-IR levels greater than 300 ng/L are pathognomonic of an ectopic tumoral source of GHRH, even though levels in most patients exceed 1000 ng/L."​

This benchmark was used in other studies as a standard, such as the study, Congenital gigantism due to growth hormone-releasing hormone excess and pituitary hyperplasia with adenomatous transformation, D Zimmerman, et al., J. Clin. Endocrinol. Metab., Jan 1993; 76: 216 - 222.

So it is these types of patients that demonstrate pituitary/somatotroph hyperplasia and their plasma levels usually exceed 1000ng/L. When the GHRH plasma level exceeds 300ng/L the medical community views this as potentially symptomatic of a GHRH secreting tumor.

HOW DOES THIS STANDARD COMPARE TO CJC-1295?

I am going to use the CJC-1295 pulsatility study * for the reason that the study participants were normal non-GH deficient people and they report the plasma concentration numbers in ng/ml whereas the clinical CJC-1295 trial reports the plasma concentration numbers in nmols. I have found conversion factors for somatostatin, IGF-1 and growth hormone but not for GHRH. So I have no way to equate that study to the system used in the studies cited above.

The GHRH analogue CJC-1295 levels circulating in plasma was found to be between 1 and 2 ng/ml or 1000-2000ng/L one week after injection.

The doses injected were either 60 or 90 mcg/kg of CJC-1295. In a 100kg man that is a 6mg or 9mg per week dose that brought about circulating GHRH levels of 1000-2000ng/L.

If we extrapolate to a 2mg per week dose that equates to 330 to 660ng/L of circulating GHRH in plasma.

If we further extrapolate down to 700mcg per week dose (i.e. 100mcg per night) that equates to 110 to 220ng/L of circulating GHRH in plasma.

Keep in mind that ectopic hypersecretion of GHRH averages 1000ng/L from tumors that cause somatotroph hyperplasia and that 300ng/L is a threshold upon which the medical community begins to look for further symptoms.

* - Pulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295, a Long- Acting GH-Releasing Hormone Analog, Madalina Ionescu and Lawrence A. Frohman, The Journal of Clinical Endocrinology & Metabolism 2006 91(12):4792–4797

IN CONCLUSION

This is not the type of analysis that is meant to have a tidy conclusion. It is what it is.

DISCLAIMER

I am not a licensed practitioner of medicine. I am not a trained professional in the area discussed herein. I am not qualified to give medical advice of any kind. Nothing that I write should be construed as anything other than free expression of thought.
 
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Pituitary Over-stimulation?

Here's another way to look at it.

In this study * they injected 4mg of GHRH sc twice daily (8mg) in old men for 3 months. They described this as a high dose.

There were no health issues reported and no mention of possible pituitary problems.

RESULTS:

GH levels rose to 2ng/ml by month two and 4ng/ml by month three.

IGF-1 levels rose to 200ng/ml by month two and about 280ng/ml by month three.

* - Sustained Growth Hormone (GH) and Insulin-Like Growth Factor I Responses to Prolonged High-Dose Twice-Daily GH-Releasing Hormone Stimulation in Middle-Aged and Older Men, Johannes D. Veldhuis, et al., J. Clin. Endocrinol. Metab., December 1, 2004; 89(12): 6325 - 6330

Compare this to the primary CJC-1295 study **.

Doses used were 30mcg/kg 60mcg/kg 125mcg/kg 250mcg/kg

RESULTS:

GH levels rose to 1.8ng/ml in the 30mcg/kg dose (2mg dose in a 100kg man); 2.8ng/ml in the 60mcg/kg dose (4mg dose in a 100 kg man) and up to 9ng/ml in the 250mcg/kg dose (or 25mg dose in a 100kg man)

IGF-1 levels rose to 180 - 280ng/ml depending on the dose.

** - Prolonged Stimulation of Growth Hormone (GH) and Insulin-Like Growth Factor I Secretion by CJC-1295, a Long-Acting Analog of GH-Releasing Hormone, in Healthy Adults, Sam L. Teichman, et al., The Journal of Clinical Endocrinology & Metabolism 2006 91(3):799–805

So you can see that:

  1. In the first study there was no ethical concern about giving these men such a high dose of GHRH.
  2. In the first study there was no mention of potential for pituitary problem nor were any such effects noted.
  3. In the first study the level of GH ended up being twice the 2mg CJC-1295 dose and still almost 50% higher the pumbs "high" 4mg CJC-1295 dose.
  4. In the first study the level of IGF-1 ended up being 50% high then the 2mg & 4mg doses of CJC-1295.

By comparison the doses we call high for CJC-1295 don't look to be as dangerous as the doses used in the first study ...substantially less in fact if our measure turns out to be the combined factors of: the amount of GHRH + the illicited volume of GH & illicited volume of IGF-1
 
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Question that has popped up into my mind recently.

Is that people say that using HGH will actually help your pituitary reserve.

And by using GHRP and GHRH will possibly use up your pituitary reserve.

By preserving your pituitary reserve your actually helping yourself out more in the long run.

But I need to research and off the cuff I would say... Indvidual cycles of each HgH and Ghrp - Ghrh cycled maybe in some type of monthly intervals would alleviate this possible scenario - "Using pituitary reserve"

**Datbtrue
I speaking in terms of years not immediate comparision or something within a reasonable time frame ...5-10 Years out and the effects on the reserve.

Don't want to litter up your thread its pretty nice :) Thanks for addressing it
 
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Question that has popped up into my mind recently.

Is that people say that using HGH will actually help your pituitary reserve.

And by using GHRP and GHRH will possibly use up your pituitary reserve.

By preserving your pituitary reserve your actually helping yourself out more in the long run.

But I need to research and off the cuff I would say... Indvidual cycles of each HgH and Ghrp - Ghrh cycled maybe in some type of monthly intervals would alleviate this possible scenario - "Using pituitary reserve"

No you're on the wrong track. The body is very capable of remaking & quickly replacing any GH (all the forms) it releases. As long as you provide it with the proper nutrition the body should be very capable of replenishing the store within hours.

I don't have exact data for you at the moment but the studies I have in mind are the ones that instigate a huge pituitary GH release and then try to instigate a second pulse shortly thereafter...

In one study they measure higher concentrations of 20kDa in the first GH wave indicating that most of the stores where accessed and secreted. In a subsequent pulse 2 maybe 4 hours later (I forget) they achieved the same amplitude of GH release but the makeup of the GH forms had less 20kDa & more 22kDa.

In other studies they found that in some people GHRH created a second GH pulse within 2 hours of the first but for many a 2nd GH pulse didn't occur so quickly no matter how much GHRH was given.

The reason was not because the store was depleted but because GH hadn't cleared quickly enough in those people to reverse the inhibition.

Pituitary storehouses aren't rate limiting as far as our proposed uses are concerned.

Also to some extent the GH family of various forms act as prohormones to provide the form that specific tissue may need at different times. So post-exercise the body prefers the form that is anabolic but also less diabetogenic ...that is the 20kDa form. So more of that form is released. Some of it may be quickly created by cleaving those amino acids that interact with the prolactin receptor from 22kDa ...thus creating 20kDa. In this way the store of 22kDa served as a prohormone for the released 20kDa.
 
Dat...do you think one can do the protocal that you have researched, but instead of doing it daily..

pin 100mcg of cjc and 200mcg of ghrp 6 x 3 a day but EOD...

ive done the math and it would be very expensive to by 6 vials of each, so i would assume if you can take cjc once a week, that i could get away with EOD, which would make each vial "last longer" over a period of time..

what do u say about this ?
 
Dat...do you think one can do the protocal that you have researched, but instead of doing it daily..

pin 100mcg of cjc and 200mcg of ghrp 6 x 3 a day but EOD...

ive done the math and it would be very expensive to by 6 vials of each, so i would assume if you can take cjc once a week, that i could get away with EOD, which would make each vial "last longer" over a period of time..

what do u say about this ?

That "protocol" of breaking the CJC-1295 into 100mcg doses & administering it with GHRP-6 is designed to "milk" any potential benefit available from a GH pulse.

The truth is IF you have GHRH in your body (which is there thanks to CJC's long-half life) from administrating it a day, three days ago, even a week ago when you add GHRP-6 on top of this base all by itself you will STILL get a 2 hour pulse...a 2 hour synergistic pulse (i.e. GHRH+GHRP-6).

So it doesn't even come close to being required to do it the way I mentioned (i.e. CJC 3x per day + GHRP-6).

BUT the GH release profile does spike a little when you inject CJC-1295 and then settles down. Also the synergy studies show 100mcg of GHRH to be the saturation dose when administered w/ GHRPs of various doses. So applying this bit of science may get a little more GH release in the form of a little bit higher pulse.

I think it does work because I seem to sleep deeper when I administer 100mcg of each pre-bed even though I have built up plenty of CJC in my system, versus when I just administer 100mcg of GHRP-6 (on top of an already built up CJC base).

But the extra benefit may be small.

I've said before that:

- you should dose in a way that is convenient for your life because you will still get the majority of benefit that way;

- 2.1mgs of CJC-1295 IS a substantial dose and solid benefits can be had at lower dosing. *

*On cycle I have stepped down my dosing. It has been several weeks since I was at 2.1mgs. I moved down to half that and although it is still early I don't feel I am missing anything. In fact I am going to 700mcg per week and will try that for a few months on cycle as a comparison.
So to directly answer your question YES. But instead of:

juliuspleaser said:
pin 100mcg of cjc and 200mcg of ghrp 6 x 3 a day but EOD

I would cut the GHRP-6 dose in half and also use it as a standalone on those "off CJC days".

I would also consider reducing the dose of CJC-1295 to 50mcg 3x a day EVERYDAY.

Finally if all of this pinning is too much do the CJC-1295 in larger less frequent doses and do the GHRP-6 at bed and whenever else you feel like you can do it.

None of this is written in stone.

Now for anti-aging or even just plain old dieting you can do just 50mcg of CJC-1295 at night pre-bed wih 100mcg of GHRP-6 and do that forever. Thats not that expensive and over the course of months you'll notice positive differences.
 
Dat...started your suggested BB dose of CJC/GHRP-6 this week, along with a fairly heavy 14 week ASS cycle. Do you have an idea as to when one can expect to start noticing the results of the CJC/GHRP-6 combo?

I have run the same AAS cycle many times before, but this time I'm using the CJC combo. I'm curious as to what to expect, and when to expect it.

I'm trying to add more mass, I know I could better my results using slin...I just don't trust myself enough to use it.

Thanks again bro!!! :cool: :cool:
 
dat brute

what do u think of this protocal:

cjc 2 times a week at 250mcg monday and thurs

ghrp 1000mg a week at 200mcg per ed monday-friday

basically id like each "vial" to last 4 weeks and hopefully acheve good gains while doing so...

please feel free to make any adjustments just as long as you can sort out a way to make each vial last minimum 4 weeks atleast..if thats not possible then i can maybe deal with 2-3 weeks per vial

thanks
 

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