https://pubmed.ncbi.nlm.nih.gov/17018654/u

Quote Originally Posted by BigTex View Post
...So saying I trust him and he knows his business when buying this product and I have CJC 1295, is it better to stick with small doses (50-100mcg) of CJC 1295 2-3 x day or it is better to do with larger doses (250mcg) and go twice a week?
Why dose CJC-1295 3x a day?

Pulsation is paramount for growth because it is the pulses that act as communication signals to the Growth Hormone receptors in tissue. Naturally our hypothalamus releases a concentrated amount of GHRH during a period when somatostatin is not very active. This concentration of GHRH acts to communicate to somatotroph cells in the anterior pituitary to coordinate amongst themselves a network (see in the archive: post #487) which will act together in concert to "squirt" out GH in the blood stream.

This concentrated GH makes its way to receptors in tissue and they (many many GH ligands) bind in mass to growth hormone receptors. An analogy would be if one Alien landed on Earth a few people would notice and run away screaming. BUT if a whole bunch of aliens landed in mass on the Earth the entire population would hear about, panic, run and scream.

What happens if Aliens dribble in from the sky here and there over time in an unconcentrated & uncoordinated fashion?

Some towns might be in an uproar but by and large the invasion effect would be diluted and although many would hear rumors about these things it probably wouldn't motivate them to action.

CJC-1295 enters the bloodstream and binds to albumin in plasma. When you inject it, it is concentrated and acts on the somatotrophs similar to natural GHRH release. BUT that is the ONLY time CJC-1295 amplifies a pulse. If you take it twice a week only because the half-life is long you rarely will amplify a pulse.

Instead CJC-1295 circulates and when the somatrophs are ready to act again some of the CJC-1295 binds to the somatrophs and they secrete growth hormone. However the measured result of CJC-1295 is that although it increases the total amount of GH, it does so only by raising base levels. It doesn't amplify a pulse.

However it doesn't interfere with pulsation. This means that the hypothalamus continues to release GHRH in response to neurological events that communicate concentrated release in a coordinated fashion with somatostatin withdrawal. It is the body's natural biorhythm that maintains natural pulsation.

CJC-1295 just makes the somatotrophs "leak" GH between the natural "squirts" therefore causing a rise in base levels (or troughs (i.e. between the waves/pulses)) ONLY.

Now GHRP-6 (or GHRP-2 or Hexarelin or Ipamorelin) ALWAYS (almost without fail) initiates an amplified GH pulse. These GHRPs cause those natural events that inhibit somatostatin, that promote GHRH release and initiate their own amplifying effects directly on the somatrophs (probably even increasing coordination among somatroph populations) to occur within 5 minutes of injection.

The result of a GHRP (GHRP-6, GHRP-2, Ipamorelin) injection is an amplified GH pulse.

So if there is added GHRH around GHRP (GHRP-6, GHRP-2, Ipamorelin) will synergistically create a much greater wave of GH release. It doesn't matter whether GHRH is in the form of Sermorelin (unmodified GRF(1-29) or modified GRF(1-29) or CJC-1295)... GHRP (GHRP-6, GHRP-2, Ipamorelin) will synergize with it.

Although we don't need to, is there any benefit to coordinating an injection of CJC-1295 w/ GHRP-6?

Yes.

For the simple reason that injecting CJC-1295 creates a concentrated amount of GHRH that is available at the somatroph network in the pituitary AT THE SAME TIME as GHRP (GHRP-6, GHRP-2, Ipamorelin) and in SUFFICIENT AMOUNT/CONCENTRATED FORM such that there is a greater contribution to that single GHRP (GHRP-6, GHRP-2, Ipamorelin) initiated pulse.

How much of an extra contribution?

I don't know. I do know that there is a likely contribution simply from the GH release profile of CJC-1295 as exhibited in the studies. A guesstimate without any real data would be 10% contribution...

Have a read boys this is the only time I will post anything like this so make the most
Preamble (11/6/2014):

The following article was written 6 years ago. It makes no reference to Mod GRF (1-29) only to endogenous GHRH and CJC-1295. For all intents and purposes keep the following in mind:

Nomenclature
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GHRH is the native growth hormone releasing hormone & GRF (1-29) is the SAME hormone w/ the inactive 15 amino acid tail removed. A Pharmaceutical named GRF (1-29) Sermorelin. These exhibit quick breakdown when administered into the blood stream (best to inject directly into the pituitary which is close to how the body does it... we can not do that)

Modified GRF (1-29) takes that native GRF (1-29) and swaps 4 amino acids for more resilient ones. This allows Mod GRF (1-29) to survive long enough when administered into the blood stream.

Attaching the reactive moiety maleimidopropionic acid via an added lysine linker to Modified GRF (1-29) yields a compound that will stick to albumin and survive for days. The original makers of this compound called the reactive moiety maleimidopropionic acid the drug affinity complex which some have shortened to DAC. This same now bankrupt company also used the Modified GRF (1-29) to attach to what they called the drug affinity complex (DAC). They used the letters CJC as an acronym for their company ConjuChem and they arbitrarily chose to label Modified GRF (1-29) as 1295. Everything they did in this space had the DAC attached so there was never any with DAC or without DAC designation. CJC-1295 is what they called Modified GRF (1-29) linked by an extra lysine to reactive moiety maleimidopropionic acid (which they called the drug affinity complex).

Why are we evaluating CJC-1295?

This entire subform will be devoted to this topic. The IGF-1 system is finally revealing itself enough for us to get a handle on it for body building and anti-aging purposes and we are finding that effective growth may come from a blend of systemic and local activity which will involve the isoforms of IGF-1, IGF Binding proteins, IGF receptors but also the interplay with insulin and other hormones.

GH that is elevated can increase many components of the IGF system

GH that is pulsed will have less abnormal impact on the IGF system

TRADEOFF - there is a trade-off in risk between pulsatile GH and elevated GH the latter of which creates higher systemic IGF-1 to all tissues which increases the risk of aiding the growth of errant tissue some of which may be malign. <- BECAUSE of this... because there are tradeoffs and impacts the forum exists. If it were as easy as simply administration and walk away there'd be no need for toggled approaches... there'd be no need for serious thought given to protocols... instead there would be a thousand monkeys with a thousand youtube channels with 100,000 humans glowing their attention span of a gnat.

The members of this forum have evolved brains that make them intelligent and capable and the forum itself will strive to be much more than a monkey typing random sound goods on a youtube channel... for gods sake!

We know now that both the local pool of IGFs and autocrine/paracrine activity is sufficient to maintain muscle. For anti-aging purposes a pulsed GH approach should help and I believe not hinder longevity. It should contribute to proper health, repair and skeletal muscle and bone growth/repair and maintenance.

We know now that skeletal muscle in an abnormal mass gathering phase can be greedy enough to absorb both local and systemic IGF-1. Bodybuilding is about feeding that abnormality in several ways.

Practical Toolset availability [Modified GRF (1-29) + MPA (aka CJC-1295) & IGF-1 LR3]

To the quick... if you combine approaches and compounds you do not need to rely on any single one. Using a GHRP with a CJC-1295 will increase growth hormone without the need to dose high amounts of CJC-1295. IGF-1 LR3 administered in micro-dose fashion [in a way originally envisioned by Grunt years ago] can prove more effective if compbined with a way that creates natural IGFs to go along with this topping approach.

This forum only permits discussion of the compounds used in the science. My regular contact with a chemist who has tested a significant quantity of what is sold on the Internet (which all comes from the Far East) as CJC-1295 finds that none of it is quality. That most of it is not true CJC-1295 and to the extent that any attempt was made to provide a link to the DAC they failed and they are not linked.

The same chemist has tested a significant amount of IGF-1 as well (again sold cheaply on the internet and likely coming form the Far East) and it is not IGF-1. Many times it is unidentifiable. I'm going to refrain from mentioning what a lot of it is because it sounds too negative... I hate to hear this stuff.

This forum's resource will be in a position to make available a practical high quality toolset. The latter compound will need to be built from scratch in a purely synthetic way rather than an engineered bacterial way which is a good thing, but it makes the item a boutique item.

IGF-1 LR3 in the muscle community was never intended to be an item most should have. It was expensive and effective and still is... however what has been sold for the last 10 years is not that... it was only labeled that. I'm starting to think that the problem with Grunt and his simplistic ideas (I still don't like his timing) had little to do with him and a lot to do with the faux compound.

Is this a Sea change? ... is pulsatility a thing of the past?

Absolutely not! It's my preferred approach... in fact I believed that if exogenous IGF-1 LR3 is a boutique item for use in only the higher levels as a top up, that CJC-1295 should only be used by advanced body sculptures capable of understanding when to use and when to pull back.

The following article on CJC-1295 has been on this forum all along but read only by a few... it included an updated preamble written in 2009 which I include below... a significant amount of which is still an area of concern for me.

Partial explanation (Oct 21, 2009)
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"Cell-to-cell communication is also likely to reflect the density and proximity of adjacent cells as GH responsiveness (but not sensitivity) to GHRH is enhanced at higher densities and basal GH release is greatest at low densities."

"Cell-to-cell contact may therefore affect the cellular integrity of somatotrophs because GH synthesis or secretory granule storage may be better maintained in high density cell concentration then in low-density concentrations." - Growth Hormone, Stephen Harvey

What happens is cells in the pituitary communicate. They self organize and create a firing network for coordinated growth hormone release. This communication creates a high density of GH releasing cells. They are in close proximity through their communicatory network. The cells have specific spatial relationships that may be modulated by peripheral endocrines. These include sex steroids, thyroid hormones, glucorticoids and even the pancreatic and gut hormones. Their spatial relationship is also effected by physiological state such as nutrient status, age and pregnancy.

As a quick example, corticotroph, thyrotrophs and folliculostellate cells are in close proximity to somatotrophs and communicate with them through gap junctions (almost like just reaching out and touching signaling). They have the potential to effect and be effected by their neighbors.

What happens when you have GHRH always around is you force these somatotrophs to release GH because they are sensitive to the GHRH binding to them and effecting release. By constantly occupying you are preventing them from coordinating with surrounding cell populations. You force these cells to act as low density subpopulations. Basal GH release is greatest when you can disperse the spatial relationship between somatotrophs and that is what an always on GHRH will do.

CJC-1295 as an always on GHRH will force upon somatotrophs loner behavior with a single constant chore. This reduces GH responsiveness as this only occurs when somatotrophs can communicate, self organize and maintain social relationships with the surrounding community. These types of social somatotrophs are better able to make and store GH then the loner cells.

So CJC-1295 seems to disperse somatotrophs and enslave them getting less from them then if it had just let them congregate in towns and cities. <-11/06/204 Note: Probably over-stated or overly dramatic by me

Aging has an effect on the vitality of city centers as well and as we age these somatotroph population centers become less vigorous. By using a more physiological GHRH such as modified GRF(1-29) together with a modulator GHRP-2 we revitalize that inner city and allow our cells to be more social and thus more productive. If instead we choose to use CJC-1295 we not only fail to remedy the problem associated with age , but we may end up exacerbating it.

I conjecture that it also makes them better neighbors to corticotroph, thyrotrophs and folliculostellate cells as well.

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

Revision 2 [8/31/08]

Restoring Growth Hormone
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"It has been argued that the age-dependent decline in sex steroid, Growth Hormone, and IGF-I production is nature’s way of protecting us from cancer and heart disease, but a far more likely scenario is that once we reach our reproductive capacity, nature begins programming us for death."- Roy G. Smith, Ph.D. Director, Huffington Center on Aging; Professor, Department of Molecular & Cellular Biology; former Vice President for Basic Research at Merck Research Laboratories, Merck & Co

Such programming begins as the second decade of life draws to a close, the negative consequences of which become more noticeable with each passing year.

We begin to experience a steady decline in immune function. (1,2) Our bodies increase production of glucocorticoids (catabolic hormones) and cytokines (inflammatory) which negatively impact metabolism, bone density, strength, exercise tolerance, cognitive function, and mood. (3,4–8)

The hormones of sex, dehydroepiandrosterone (DHEA), Growth Hormone (GH), and Insulin-like Growth Factor (IGF-1) are positively correlated with the health and well-being of the body in general and the specific functioning of metabolism, the cardiovascular system, the musculature skeletal system, cognitive function & the immune system. However these hormonal levels naturally decline as we age and as a consequence those systems necessary to maintain optimal health decline as well. (1-4,9)
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"Hence, if we wish to maintain quality of life during aging we must oppose nature." - Roy G. Smith, Ph.D.

A progressive decline in lean body mass, atrophy of its component organs & reduction in their function and increased deposition of adipose tissue mass characteristic of the aging human body result partially from the body's diminished secretion of growth hormone. (10-13) These negative changes resulting from growth hormone deficiency have been shown to be reversible by replacement doses of growth hormone. (14-21)

Growth Hormone is a vital anabolic hormone whose positive stimulatory effects on protein synthesis (particularly in the liver, muscle, bone, cartlidge, spleen, kidney, skin, thymus, and red blood cells) and on lipolysis (the breakdown of fat stored in fat cells) contributes greatly to growth, repair & well-being. (10)

Growth Hormone (GH) secretion is primarily regulated by the release of two peptides, Growth Hormone-Releasing Hormone (GHRH) and Somatostatin. The hypothalamus region of the brain releases these hormones in response to signals from the central nervous system. GHRH once released makes its way to the receptors on the somatotrope cells of the pituitary gland below the brain where it stimulates Growth Hormone release.

Somatostatin once released makes its way to the receptors on the somatotrope cells of the pituitary gland below the brain where it inhibits Growth Hormone release. (15)

The primary physiological action of somatostatin is to inhibit synthesis and release of GH. (16-19) The primary physiological action of Growth Hormone-Releasing Hormone (GHRH) is to stimulate synthesis and release of GH.

The end product of this cascade, Growth Hormone (GH) once secreted exerts its effect in the body as a whole both directly and indirectly through its initiation of Insulin-like Growth Factor (IGF-1) synthesis in the liver. IGF-1 in turn exerts its effect in the body and its rise in turn begins to inhibit any further GH release.

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Growth Hormone (GH) is released periodically within the body in a controlled pulsating fashion. This periodic pattern plays an important role in transmitting the GH "growth, repair & well-being" message to tissue. A review of several studies involving GH replacement in GH-deficient animals reveals the biological significance of episodic secretion. These studies conclude that GH released in a pulsatile pattern is far more efficient in improving mammalian growth and repair than the method of GH administration by constant infusion.

In males GH pulses occur approximately every three (3) hours, a frequency that appears across most mammals. The secretion bursts are preceded and followed by almost undetectable levels of plasma GH.

In females however GH pulses occur more frequently and the base level of plasma GH remains higher than males who have fewer GH pulses but the amplitude of which are more pronounced.

GH pulse amplitudes are increased during slow wave sleep such that particularly in males, most GH secretion occurs at night. (22)

Growth Hormone secretion is highest during the growing years of youth and early adulthood. In humans the secretion rate starts to noticeably decrease during the third decade of life and strongly decreases during the fourth decade of life. As we age the daytime secretory pulses diminish first, while the sleep associated GH pulse persists and diminishes gradually.

Nudging Nature

Growth Hormone levels may be increased either by exogenically administering Growth Hormone or by administering Growth Hormone-Releasing Hormone which then endogenically stimulates the somatrope cells of the pituitary to secrete additional Growth Hormone. The primary advantage of GHRH is that GH ends up being released in physiological conformance to the body’s natural biorhythm. This biorhythm is pulsatile.

Studies have concluded that endogenous Growth Hormone Releasing Hormone (GHRH) is the principal regulator of pulsatile GH secretion in humans and that continuous GHRH infusion augments pulsatile GH release. Whereas exogenic administration of GH raises overall GH levels but has no effect on amplifying the pulses.

People of all ages naturally continue to possess the ability to secrete GH from stores within the pituitary. Most studies are in agreement on this point. One study in particular examined the effects of administration of GHRH & a Growth Hormone Releasing Peptide on all adult age groups from those in their 20's to those above 75 years of age. They observed substantial increases in GH release as a direct result of administration of GHRH & GHRP-6. This prompted them to conclude, "...that the lack of side-effects & safety of the protocol and the discovered lack of age-related decline in the 'GHRH-GHRP-6-mediated' GH release opens the possibility of using it as a therapeutical tool to revert some deleterious manifestations of aging in man." (23)

Long-lasting GHRH analog CJC-1295

While the studies have demonstrated repeatedly that administration of GHRH does increase GH secretion and amplifies the release pulse there does remain a significant drawback. GHRH has a very short half life, measured in minutes with a fairly short clearance rate measured in hours. (24) While this is a sufficient amount of time to exert a positive effect on GH secretion, particularly if GHRH is administered multiple times a day, the result is less than optimal. (25,26)

It is for this reason that longer-lasting analogs of GHRH were researched and developed. (28) The most effective of which is CJC-1295.

Exposure of native GHRH to blood plasma results in rapid degradation. CJC-1295, a synthetic human GHRH analog avoids rapid degradation by possessing the ability to selectively and covalently bind to endogenous albumin after subcutaneous administration. Albumin possesses a half-life of 19 days in humans and so modified GHRH bound to albumin greatly extends its half-life and duration of action. (27)

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In a recent (2006) study "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. Journal of Clinical Endocrinology & Metabolism 91(3):799-805, CJC-1295 was found to result in "sustained, dose-dependent increases in GH and IGF-I levels in healthy adults and was safe and relatively well tolerated, particularly at doses of 30mcg/kg or 60 mcg/kg."

It has been demonstrated repeatedly in various studies that GHRH is effective at instigating GH release and longer acting analogs do increase the overall effectiveness. So it is no surprise that the results of this CJC-1295 study comport with what has been previously demonstrated.

What was unknown was what effect persistent elevation of GH by a long-lasting GHRH analog would have on the pulsatility of release. This was explored in a follow up study, "Pulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295, a Long- Acting GH-Releasing Hormone Analog", Madalina Ionescu, et al. The Journal of Clinical Endocrinology & Metabolism 91(12):4792-4797.

That study found that pulsatility was not interfered with and was in fact preserved in all subjects both immediately after administration and continuing 7 days post-administration.

This is obviously a very beneficial characteristic to preserve. In fact episodic release appears to be imperative to growth and repair of tissue in mammals.

The study further found that while growth hormone secretion was increased by almost fifty percent there was no increase in pulse amplitude or frequency. All of the increase came from a substantial elevation of trough levels with preserved pulsatility.

One further note of interest is that study participants were all of young age with lower lean body masses which may indicate that GHRH in the form of CJC-1295 is an effective avenue for growth hormone release for those of young age.

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The results of the study charted above show that administration of single doses of CJC-1295 remained in high concentration for 7 days with measurable concentration for 14 subsequent days. (29)

As seen in the chart below this resulted in substantial increases in mean serum GH levels in all dosing groups, which were dose incremental and persisted for up to 7 days.

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As seen in the chart below this chronic elevation in CJC-1295 levels resulted in substantial increases in mean serum IGF-1 levels in all dosing groups, which were dose incremental and persisted for up to 7 days.

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The results from a toxicology study wherein 50mcg/kg of CJC-1295 was administered subcutaneously to monkeys for a period of six months found no ill effects and no indication of presence of neutralizing antibodies. They concluded that the Drug Affinity Complex (DAC) a technology that enables covalent binding (conjugation) of a drug to albumin produced no evidence of immunogenic or immunotoxic effects in monkeys. (30)

In summary, although the added Drug Affinity Complex adds complexity and increases the expense of CJC-1295 peptide synthesis, it does add tremendously to both the dosing convenience and the biological activity of GHRH without any identifiable adverse toxicity.
References:

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3 - Ershler WB, Keller ET 2000 Age-associated increased interleukin-6 gene expression, late-life diseases, and frailty. Annu Rev Med 51:245–270

4 - van Eekelen JA, Rots NY, Sutanto W, de Kloet ER 1992 The effect of aging on stress responsiveness and central corticosteroid receptors in the brown Norway rat. Neurobiol Aging 13:159–170

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6 - Liu J, Mori A 1999 Stress, aging, and brain oxidative damage. Neurochem Res 24:1479–1497

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9 - Murialdo G, Barreca A, Nobili F, Rollero A, Timossi G, Gianelli MV, Copello F, Rodriguez G, Polleri A 2001 Relationships between cortisol, dehydroepiandrosterone sulphate and insulin-like growth factor-I system in dementia. J Endocrinol Invest 24:139–146

10 - Rudman D. Growth hormone, body composition, and aging. J Am Geriatr Soc 1985; 33:800-7.

11 - Meites J. Neuroendocrine biomarkers of aging in the rat. Exp Gerontol 1988; 23:349-58.

12 - Finkelstein JW, Boyar RM, Roffwarg HP, Kream J, Hellman L. Age-related change in the twenty-four-hour spontaneous secretion of growth hormone. J Clin Endocrinol Metab 1972; 35:665-70.

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14 - van Buul-Offers S, Van den Brande JL. The growth of different organs of normal and dwarfed Snell mice, before and during growth hormone therapy. Acta Endocrinol 1981; 96:46-58.

15 - Parra A, Argote RM, Garcia G, Cervantes C, Alatorre S, Perez-Pasten E. Body composition in hypopituitary dwarfs before and during human growth hormone therapy. Metabolism 1979; 28:851-7.

16 - van der Werff ten Bosch JJ, Bot A. Effects of human pituitary growth hormone on body composition. Neth J Med 1987; 30:220-7.

17 - Crist DM, Peake GT, Mackinnon LT, Sibbitt WL Jr, Kraner JC. Exogenous growth hormone treatment alters body composition and increases natural killer cell activity in women with impaired endogenous growth hormone secretion. Metabolism 1987; 36:1115-7.

18 - Jorgensen JOL, Pedersen SA, Thuesen L, et al Beneficial effects of growth hormone treatment in GH-deficient adults. Lancet 1989; 1:1221-5.

19 - Crist DM, Peake GT, Egan PA, Waters DL. Body composition response to exogenous GH during training in highly conditioned adults. J Appl Physiol 1988; 65:579-84.

20 - Salomon F, Cuneo RC, Hesp R, Sonksen PH. The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency. N Engl J Med 1989; 321:1797- 803.

21 - Jones AJS, O’Connor JV. Chemical characterization of methionyl human growth hormone. In: Hormone drugs: proceedings of the FDA–USP Workshop on Drug and Reference Standards for Insulins, Somatropins, and Thyroid- axis Hormones, Bethesda, Maryland, May 19–21, 1982.

22 - Holl RW, Hartman ML, Veldhuis JD, et al. Thirty-second sampling of plasma growth hormone in man: correlation with sleep stages. J Clin Endocrinol Metab 1991;72:854–61.

23 - Micic D, et al. Preserved Growth Hormone (GH) Secretion in Aged and Very Old Subjects after Testing with the Combined Stimulus GH-Releasing Hormone plus GH-Releasing Hexapeptide-6. J Clin Endocrinol Metab. 1998 Jul;83(7):2569-72

24 - Frohman LA, Downs TR, Williams TC, Heimer EP, Pan YCE, and Felix AM. Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive, N-terminally cleaved product. J Clin Invest 78: 906–913, 1986.

25 - Iordanova VK, Wen SY, Moreau IA, Smith SY, Frohman LA, and Castaigne JP. Every other day subcutaneous administration of CJC-1295, a drug affinity complex (DAC)-growth hormone releasing factor (GRF) analogue, increases body weight and bone mineral content in dogs (Abstract). 87th Annual Meeting of The Endocrine Society, 2005, p. P1–78.

26 - Jette L, Leger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, Pham K, and Bridon DP. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology 146: 3052–3058, 2005.

27 - Peters JRT. All About Albumin. Biochemistry, Genetics and Medical Applications. San Diego, CA: Academic, 1996.

28 - Hoffman, Andrew R., et al. Efficacy of a Long-Acting Growth Hormone (GH) Preparation in Patients with Adult GH Deficiency. J Clin Endocrinol Metab 90(12):6431–6440

29 - Teichman SL, Neale A, Lawrence B, Cagnon C, Castaigne JP, and Frohman LA. 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. J Clin Endocrinol Metab 91: 799–805, 2006.

30 – Wen, S. et al. Immunogenicity AND Immunotoxicity Assessments of Two Drug Affinity Complexe Compounds in Cynomogus Monkeys. Toxicologist, Report 170, 2005.

CJC-1295 Decay Rate Chart

A single dose of CJC-1295 "decays" by about 10% a day. So that single dose will follow the "effectiveness" percentages indicated below over the week:
_______Dose (2mg)
Day 0 - 100% (2mg)
Day 1 - 90% (1.8mg remaining)
Day 2 - 81% (1.6mg remaing)
Day 3 - 73% (1.4mg remaining
Day 4 - 65% (1.3mg remaining)
Day 5 - 59% (1.1mg remaining)
Day 6 - 53% (1mg remaining)
Day 7 - 47% (.9mg remaining)
Day 8 - 43% (.8mg remaining)

So a once a week dosing protocol would result in less consistent GH blood levels then the twice a week dosing indicated below (especially so after the initial buildup):

______Dose #1_(1mg)__________Dose #2_(1mg)__________Dose #3_(1mg)
Day 0 - 100% (1mg)
Day 1 - 90% (.9mg remaining)
Day 2 - 81% (.8mg remaing)
Day 3 - 73% (.7mg remaining)
Day 4 - 65% (.6mg remaining) + 100% (1mg) = 1.6mg
Day 5 - 59% (.5mg remaining) + 90% (.9mg remaining) = 1.4mg
Day 6 - 53% (.5mg remaining) + 81% (.8mg remaing) = 1.3mg
Day 7 - 47% (.4mg remaining) + 73% (.7mg remaining) = 1.1mg
Day 8 - 43% (.3mg remaining) + 65% (.6mg remaining) + 100% (1mg) = 1.9mg

who gives a crap about this GH bleed. CJCDAC is the GOD of peptides!! I get blast after blast in waves of GH almost to the point of being high on the stuff. It's something I can actually feel working. And the gains achieved have spoken for themselves.

http://press.endocrine.org/doi/full/10.1210/jc.2006-1702?queryID=%24{resultBean.queryID}

hers the study you wanted bro. this is the one that disproves the "bleed theory"

Interesting read but I cant say I agree... lots of holes and assumptions there.