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

To expand on the subtle use of insulin here is a post I had over on AM a while ago that is interesting:

Dat - Adding to our knowledgebase


Insulin & GH act synergistically to produce IGF-1

As of 9/4/08 our knowledgebase possesses the understanding that GHRP-6 (and all GHRPs) increase GH for a 2 hour pulse and this usually (but not always) gives a rise in IGF-1 that is not sustained.

It also appears that the muscle IGF-1 isoforms are not increased.

For growth we need to get a sustained elevation of IGF-1 from somewhere (CJC-1295 or IGF-1/MGF itself) and hopefully this will be sufficient to stimulate localized muscle IGF-1 isoforms.

But when I was just using GHRP-6 several times a day I ran mini-cycles (around 21 days) of test/slin/GHRP-6 and I grew (beyond previous such cycles minus the GHRP-6). At the same time others claimed GHRP-6 did not add to their pursuit of muscle. Why the difference?

The difference might have been insulin.


And while one may argue that this is chickens & in vitro it is noteworthy that the following study treats this insulin/GH synergy almost as a given in humans and in vivo. See: Pharmacokinetics and acute lipolytic actions of growth hormone Impact of age, body composition, binding proteins, and other hormones, Troels Krarup Hansen, Growth Hormone & IGF Research 2002, 12, 342–358

So for the time being this gets added to the known benefits and synergistic actions between GH & insulin discussed in this thread.

Furthermore insulin might possibly be capable of providing the elevated IGF-1 needed with a standalone GHRP-6 protocol OR add to the elevated IGF-1 levels in a CJC-1295/GHRP-6 protocol.

Hmmmm....

Well first off for Vic's question, once you get up above 4iu of synthetic GH a day I think that the negative feeback will inhibit GH induced release at the pituitary by CJC-1295/GHRP-6.

What do we mean by that?

GH in circulation can feedback on the Hypothalamus and the Pituitary. Since we don't need the hypothalamus to give us GHRH (because we supply that with the CJC-1295) we are less concerned with THAT particular inhibition. We can still maintain a concern because GHRP-6 acts in part to also induce further release of GHRH from the hypothalamus but for the most part we have in our syringe THE hypothalamic hormone responsible for GH release so when we inject it, it travels directly to the pituitary and exerts it's effect.

The problem though is GH inhibition at the pituitary. The somatotrophs (i.e. cells in the pituitary that release GH from internal stores) have many types of receptors on the cell membrane. Among those types is the growth hormone receptor (GHR). So GH in circulation can bind to a receptor on the very cells that secrete it in the first place. When this occurs it invokes certain mechanisms that result in the somatotroph ceasing GH release.

There is nothing about our CJC-1295/GHRP-6 protocol that bypasses the negative feedback mechanisms at the pituitary. If a decent amount of synthetic GH is in our system some of it will bind to a receptor on the somatotroph in the pituitary and any subsequent administration of GHRH (in the form of CJC-1295) will be without influence or effect.

So if you are at a bodybuilding dose level in your cycle it is wise to not use both CJC-1295 and GH at least in the same 24 hours.

How about if you run synthetic GH every other day can CJC-1295 be used in those off days?

We can't rely on the studies that spell out inhibition for us because they don't apply to us, because with CJC-1295 we don't need the hypothalamus to get things going...we just need the pituitary to no longer be under the influence of synthetic GH.

I believe (as of today 11/1/08) until I see evidence to the contrary that CJC-1295 will have some effect if used on days when synthetic GH is not used. It may prove to be not as potent as it would be if you waited 2-3 days for the GH "hang over" to clear but IMHO it should still be effective.

finny said:

Dat, to expand on this, what do you think about a single dose of say 20-30IUs once a week for bb purposes or 3x10IUs?

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If you are asking which will be better I can not say.

Many good guys have run these types of experiments and reported their results on UKIRON. Those experiences are very valuable.

What knowledge comes out of those experiments?

- A confirmation of what guys like Massive G discovered long ago that GH gives more results if used EOD or E3D rather then ED.

- A consensus belief that high dose taken once during the day is better then spread out throughout the day.

- A consensus belief that the high dose should be administered PWO.

- A widely-held belief that insulin & GH used together PWO maximized gains

- A statement or two that high dose of GH 15iu+ & insulin administered PWO provided some local benefit at the site of injection.

How much should you dose at one time?

My research indicates that at very high dose 22kDa GH (which is the form of synthetic GH) begans to reduce the amount of active GH by self-antagonizing the receptor. See:


For a more detailed look see Study "22kDa GH vs 20kDa GH antagonism at high concentrations & GHBP affinity"

So is 30iu high enough to envoke self-antagonsim? I don't know but I suspect yes.

Besides that a single administration per week seems a little too low to me. If you have 30iu for the week I would consider splitting it into two post work out adminstrations and use 15iu after one workout and two days later or so 15iu after a second workout.

DatBtrue said:

4ius of GH that has not undergone thermal shape change used over a decent period of time is fine for fat loss.

So you could take it all at once or split it the way you have.

The shape of the GH in plasma curve indictes that a single dose of GH will be active for about 12 hours before it basically flatlines. So your split will elevate GH throughout the entire 24 hour day. That means GH will exert an overall lipolytic effect all day & night.

If you dose the full 4iu at one time you will have have GH elevated in plasma for only half of the day. Now this isn't to bad if you dose in the morning and by the time you go to bed you can hope for at least a partial return of your own natural secretion in the form of the night-time pulse. You could even try to encourage with GHRP-6 and/or a litle gaba and /or attempt to reduce somatostatins negative influence through the use of something like L-Dopa or arginine.

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In the end it is up to you. Not everyone can use 4iu in the morning and get a natural GH release in the evening...some will others might be supressed into the next day or so.

The key though no matter which way you use it is to run it for a long enough period of time to garner some results and that will require a minimum several months.

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THANK YOU SIR!

Much obliged Dat!!

articular cartlidge repair

Dat,

i have a deteriorating shoulder from a torn labrum. i had surgery 2 years ago but it is getting worse. mri's show my articular cartlidge is dissappearing. ive been bodybuilding for 21 years but im only 35.

i am interested is dosing for connective tissue repair and maybe some fat loss but not so much for muscle growth.

what would be the least dose i could take for connective tissue growth for my shoulder?

I know for bodybuilding you state these doses at least.

100 mcg cjc-1295 x 3 per day
100 mcg ghrp-6 x3 per day

but what about for articular cartlidge or joint repair?

thanks

dose

the reason im asking about the lowest dose for connective tissue repair (atricular cartlidge) is for money reasons. If i had the money i would take the recommended dose.

i was just for money sake what would be the minimal dose for connective tissue repair.

I came across this study, http://www.ncbi.nlm.nih.gov/pubmed/9062497 , and I know that it's age group is way off from bbing users, but do you think that the use of steroids w/ GHRPs could actually limit their effectiveness?

I agree Dat, that if one is looking for some sort of bb effect from GH or other peptides, slin should be part of the staple...

vast568 said:

I came across this study, http://www.ncbi.nlm.nih.gov/pubmed/9062497 , and I know that it's age group is way off from bbing users, but do you think that the use of steroids w/ GHRPs could actually limit their effectiveness?

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Why would you ask this? The study reached the opposite conclusion:


augment - To make (something already developed or well under way) greater, as in size, extent, or quantity

You might be interested in the following study:

batman77 said:

the reason im asking about the lowest dose for connective tissue repair (atricular cartlidge) is for money reasons. If i had the money i would take the recommended dose.

i was just for money sake what would be the minimal dose for connective tissue repair.

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GH exerts its effects via locally produced IGF-1. A local stimulation of cartilage proliteration is observed when GH is infused directly into the cartilage plate. GH evokes localized growth response in cartilage in vivo by increasing IGF-1 mRNA, increasing IGF-1 receptor number and the number of chondrocytes containing IGF-1 locally.

In studies resting cartilage was unaffected by exposure in vitro to supraphysiological concentrations of GH. It is GH's effect on local expression of IGF-1 that is paramount.

So the higher the dosing of CJC/GHRP-6 is, the higher both GH in plasma, circulatory IGF-1 and most importantly locally produced IGF-1.

Then on top of that a prolonged elevation is probably more effective then short-term elevations.

So the more you can use and the longer you can run CJC/GHRP the better.

You say you are limited because of funds available to you. The fact that you are 35 years of age and need to lose a little fat kinda precludes you from finding a Sugar Momma and having her fund your endeavour. If the economy was going gang-busters you might be able to offer your stud services at a discount rate to compete with the young bucks ...but in todays economy...not bloody likely.

So run what you can afford for as long as you can.

DatBtrue said:

GH exerts its effects via locally produced IGF-1. A local stimulation of cartilage proliteration is observed when GH is infused directly into the cartilage plate. GH evokes localized growth response in cartilage in vivo by increasing IGF-1 mRNA, increasing IGF-1 receptor number and the number of chondrocytes containing IGF-1 locally.

In studies resting cartilage was unaffected by exposure in vitro to supraphysiological concentrations of GH. It is GH's effect on local expression of IGF-1 that is paramount.

So the higher the dosing of CJC/GHRP-6 is, the higher both GH in plasma, circulatory IGF-1 and most importantly locally produced IGF-1.

Then on top of that a prolonged elevation is probably more effective then short-term elevations.


So the more you can use and the longer you can run CJC/GHRP the better.

You say you are limited because of funds available to you. The fact that you are 35 years of age and need to lose a little fat kinda precludes you from finding a Sugar Momma and having her fund your endeavour. If the economy was going gang-busters you might be able to offer your stud services at a discount rate to compete with the young bucks ...but in todays economy...not bloody likely.

So run what you can afford for as long as you can.

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not that it matters but i actually have quite a build. i have good genetics and have been bodybuilding for 21 years. i have plenty of muscle and am 10% bodyfat with consistant visits to mcdonalds daily So im sure i could get that sugar momma still if i wanted to but thats not my style. but with my shoulder getting worse and worse who knows whats in store for me........

So should i inject these substances into my deltoid locally where the damage is or just subcutaneous anywhere?
thanks

finny said:

I agree Dat, that if one is looking for some sort of bb effect from GH or other peptides, slin should be part of the staple...

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I'm glad you see it this way.

Testosterone is a hormone.
Insulin is a hormone.
Growth Hormone is a hormone.
Growth Hormone Releasing Hormone (CJC-1295) is a hormone.
Ghrelin (mimetics such as GHRP-2, GHRP-6, Hex) is a hormone.
Insulin-like Growth Factor I - is a hormone.

However the final 5 hormones listed are made up of amino acid strings which when bonded together have specific shapes. These amino acids strings are peptides.

Now I don't know why some people say peptides are great but I'll never do steroids because I don't want to play with my hormones.

I don't understand when people like to be dismissive of many of these peptides by derisively referring to them as PEPtides. They are also hormones.

If growth is the end goal then you need to take a holistic approach because THAT is how the body does it. The body uses many signaling pathways inside the cells that then translocate to the nucleus and exert proliferative & metabolic effects. There is synergy and cross-talk between these intracellular pathways which are triggered by a host of hormones from testosterone, insulin, GH, IGF-1, T3, etc.

The body doesn't say for optimal growth "just use test" or just inject me with 22kDa growth hormone or even worse just give me an analog of IGF-1 such as LR3.

NO! It says testosterone is important, a mix of 22kDa, 20kDa & the GH binding proteins are important, native IGF-1 bound to IGFBP & ALS is important, regular insulin is important.

The body doesn't want to be forced to respond in ways you dictate. It knows best how to grow. So Regular insulin and natural GH release are used by the body do such things as effect locally produce/locally used IGF-1, GH & MGF. The body knows how to resensitize signaling pathways far better than we do.

I'll never understand people that want to insist that natural GH, the stuff that CJC/GHRP encourages secretion of is inferior to something made synthetically in a lab. I've said it before... the natural GH in your body grew you from a fetus to a boy and from a boy to a man and yet I still see people say "just use real GH"!

But I guess all it takes is for one to spend good money on something that they think is CJC-1295 only to have mediocre or poor results for them to make such proclamations.

You want to grow? You want to overcome some genetic limitations? Then it is now possible to do so. The reason that some bodybuilders have a genetic advantage is that their bodies resensitize quicker to certain growth triggers which allow more frequent or more pronounced signalling of growth with in the body.

But the coolest thing to me is not all of this bodybuilding stuff that I've spent so much time on. The coolest thing is just how little it really takes to get an anti-aging effect.

A man or woman over say 42 years of age can just take a spot of GHRP-6 or GHRP-2 or Hexarelin or Ipamorelin before bed and they will initiate a nice nightly pulse of GH that looks very youthful when graphed out.

Without a GHRP that pulse when graphed out looks "dribbly".

The GHRPs restore the strength of the hypoathamus signal to release GHRH (the positive hormone) and reduce the signal to reduce somatostatin (the inhibitory hormone). The cool thing is that even if you are 98 years old your pituitary still maintains all the stores of GH you will ever need to surpass youthful levels. You just need to fix the plumbing.

GHRP-6 is just 6 aminos long. It is simple and very effective and should be cheap. An older person could achieve deeper sleep and more youthful levels of GH with just one injection a day and less than $100 spent a year.

What does any of this have to do with your initial question? Not a damn thing ...I'm just on my fourth cup of coffeee this morning.

batman77 said:

not that it matters but i actually have quite a build. i have good genetics and have been bodybuilding for 21 years. i have plenty of muscle and am 10% bodyfat with consistant visits to mcdonalds daily but with my shoulder getting worse and worse who knows whats in store for me........

So should i inject these substances into my deltoid locally where the damage is or just subcutaneous anywhere?
thanks

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The very best anectdotal evidence I've ever seen on how to do injury repair comes from pumpertot over at anabolicminds. He of course used high amounts of a lot of peptides and injected into damaged tissue. He used these things to come back quickly from a pec tear and surgery. He then went on and taught wophood who had a pec tear and he is recovering nicely. He did not inject into injury.

In addition to 300mcg of GHRP-6 injected 3x per day and 100mcg of CJC-1295 injected 3x per day he added IGF-1 LR3 one out of every three days and insulin one out of every three days.

Now specifically to your question CJC/GHRP will have no local effect near the injection site. These two hormones need to travel to the pituitary where they will cause the end hormone GH to be released.

IGF-1, insulin & GH are end product hormones and can have local effects where injected.

DatBtrue said:

The very best anectdotal evidence I've ever seen on how to do injury repair comes from pumpertot over at anabolicminds. He of course used high amounts of a lot of peptides and injected into damaged tissue. He used these things to come back quickly from a pec tear and surgery. He then went on and taught wophood who had a pec tear and he is recovering nicely. He did not inject into injury.

In addition to 300mcg of GHRP-6 injected 3x per day and 100mcg of CJC-1295 injected 3x per day he added IGF-1 LR3 one out of every three days and insulin one out of every three days. His full protocol: **broken link removed**

Now specifically to your question CJC/GHRP will have no local effect near the injection site. These two hormones need to travel to the pituitary where they will cause the end hormone GH to be released.

IGF-1, insulin & GH are end product hormones and can have local effects where injected.

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ok. thanks a bunch. your amount of knowledge in this area is awesome and much appreciated

Sorry I'm a little slow picking this up, so what would be a good weekly protocal with both peptides to equal say 5ius of exogenous gh??? ghrp and cj???

DatBtrue said:

Why would you ask this? The study reached the opposite conclusion:

In conclusion, we have confirmed that Hex is a potent and reproducible stimulus for GH secretion in children. In addition, we have shown that sex steroids markedly augment the GH-releasing effect of Hex. Our data suggest that the sex steroid-induced increase in the GH response to Hex is mediated by estrogens.​

augment - To make (something already developed or well under way) greater, as in size, extent, or quantity

You might be interested in the following study:

Mediation of testosterone action in muscle by growth hormone / IGF-1 signaling,Carl A Morris, Linda Morris, Lan Jiang, Nathan LeBrasseur, Ravi Jasuja, John Flanagan and Shalender Bhasin , The FASEB Journal. 2007;21:769.34

ABSTRACT

Testosterone (T) is considered a potent anabolic agent that increases muscle mass and strength in humans. Similarly, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) have been identified as critical mediators of muscle mass and strength. GH and T exhibit apparent synergism in various populations such as elderly men and prepubertal boys. It is thought that testosterone functions via an androgen receptor-mediated pathway and it’s downstream signaling (e.g. Wnt /ß-catenin). However, T may interact directly with the GH/IGF-I axis to stimulate growth and/or reduce muscle wasting independently of any AR-mediated response. T was found to stimulate GH secretion and production of liver IGF-1, and also to increase IGF-1 mRNA and protein levels in skeletal muscle. Thus it appears that testosterone confers part of its effects via the GH/IGF-I signaling pathway. To test this, we administered either oil or testosterone enanthate (TE) to rats that had been castrated (C), hypophysectomized (H), or both (CH). The body and muscle were weighed and serum and tissue samples stored. In the C, H, and CH groups, the androgen-responsive levator ani muscle exhibited a dose-dependent increase in mass with TE administration. Further, IGF-1Ea and IGF-1Eb (MGF) mRNA expression increased with TE in all three groups (C, H, and CH). These results suggest that the anabolic effects of TE are independent of GH signaling, but are possibly associated with local IGF-1 signaling.​

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LOL sorry I meant increase; I have no idea why I wrote "limit". It was late

Edit: Now I remember why I wrote limit. I was thinking of AIs. Since it's shown that testosterone which doesn't aromatise (Ox) doesn't increase GH but test that does and even EE both increase GH production, would the use of an AI actually limit GH production?

vast568 said:

LOL sorry I meant increase; I have no idea why I wrote "limit". It was late

Edit: Now I remember why I wrote limit. I was thinking of AIs. Since it's shown that testosterone which doesn't aromatise (Ox) doesn't increase GH but test that does and even EE both increase GH production, would the use of an AI actually limit GH production?

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You mean steroids that don't aromatize. Testosterone does but Oxandrolone (Anavar) doesn't. The answer to your question is NO.

Androgens whether they aromatize or not act in complimentary fashion to IGF-1 & act to increase IGF-1 activity within muscle.

An overview of the endocrinology of skeletal muscle , Melinda Sheffield-Moore and Randall J. Urban, TRENDS in Endocrinology and Metabolism Vol.15 No.3 April 2004

...
In young men made hypogonadal by administration of a gonadotropin-releasing hormone (GnRH) agonist, rhGH, increased concentrations of IGF1 mRNA in muscle biopsy samples obtained from the vastus lateralis [43]. In older men, administration of rhGH for one month also increased IGF1 mRNA concentrations in vastus lateralis muscle biopsy samples [44].

IGF1 expression is associated with skeletal muscle hypertrophy, as best demonstrated by animal studies where the IGF1 gene is selectively overexpressed in skeletal muscle [45]. Moreover, one mechanism by which IGF-I causes skeletal muscle hypertrophy might be through the stimulation of satellite cell replication; that is, by accelerating the progression of cell division [46].

There are many different triggers for local IGF1 expression, including androgens [47,13], mechanical load [48] and exercise [49]. Chronic inflammation, as indicated by interleukin-6 synthesis, is thought to cause loss of physical function by inhibiting local IGF1 skeletal muscle expression [50].

Hey DataBtrue, Great stuff, now I know someone who can answer my own research question. Just into all this technical stuff real interesting how it all works. The sesquences for GHRP-6 doesnt have a n-terminus. I thought peptides should have both an n-terminus and a c-terminus in there sequence.

His-(d)Trp-Ala-Trp-(d)Phe-Lys-NH2
His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

When identifiying the isomeric form to the amino acid, does in matter how its wrtten. Do they both mean the same. I have seen them written both ways just want to know the proper way.

I take it that the D-Trp/(d)Trp is the same amono acid but altered? This part I dont understand? I understand its a isomeric form but does it make it a different type of amino acid?

What was that other sequence D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2, I dont fully undersatnd. Is it GHRP-6? Which one are people buying? I dont understand what the D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2 is all about. Can you expalin the 'D-2 Nal' its not an amino acid so can you further explain it. It also doesnt have a n-terminus.

little billy; said:

...The sesquences for GHRP-6 doesnt have a n-terminus. I thought peptides should have both an n-terminus and a c-terminus in there sequence.

His-(d)Trp-Ala-Trp-(d)Phe-Lys-NH2
His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

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Yes it does. It is expressed as NH2 and is present in your example.

little billy; said:

When identifiying the isomeric form to the amino acid, does in matter how its wrtten. Do they both mean the same. I have seen them written both ways just want to know the proper way. I take it that the D-Trp/(d)Trp is the same amono acid but altered? This part I dont understand? I understand its a isomeric form but does it make it a different type of amino acid?

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You have misused the term isomeric. An isomer has the same molecules but different structure.

There are two standard ways to abbreviate an amino acid. Either the three letter form or the single letter form.

For GHRP-6 the first amino acid is Histidine and is abbreviated as either His or H.

Alanine is Ala or A; Tryptophan is Trp or W; Lysine is Lys or K

These are all naturally occuring forms technically written with an L- in front of the name such as L-Alanine. The "L" form called "Levo" of an amino acid is again the naturally occurring form and often in the nomenclature the "L" is dropped. The "D" form called "Dextro" does not occur in nature and is the isomeric form (i.e. mirror image) of the "L" form.

The D form and L form are not interchangeable and their inclusion or exclusion can result in distinct differences in the 3 dimensional structure a peptide undertakes and in how the amino and peptide interacts with its environment & other molecules.

little billy; said:

What was that other sequence D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2, I dont fully undersatnd. Is it GHRP-6? Which one are people buying? I dont understand what the D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2 is all about. Can you expalin the 'D-2 Nal' its not an amino acid so can you further explain it. It also doesnt have a n-terminus.

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You are referring to GHRP-2. You highlight "beta-naphthylalanine". The greek letters for "A", "B", etc. are used to describe which carbon it is attached to. In this case the greek symbol for "B" may be used as above or the word "beta" or the number "2" or "2'". In this instance the attachement is to the second carbon.

You could abbreviate D-Alanine as D{ala} or several variations.

Again the N-terminus (also known as the amino-terminus, NH2-terminus, N-terminal end or amine-terminus is indicated in the formula by the inclusion of NH2. More accurately written as NH with a subscript 2.


NOTE: Using the single letter abbreviations GHRP-6 is written as the following sequence: H-HwAWfK-NH2

I was thinking that the N-teriminus was at the beggining of the sequence and the C-terminus was at the end of the sequence, so if the sequence ends the NH2 what is the C-terminus, should it have one in the start? or Doesnt it require one?