Juice Freak; said:
Which would be better suited for my goals to gain as much lean mass as possible while still staying very lean.
100mcg of cjc1285 with 100mcg of ghrp6 x 3 daily or 15iu of gh/slin post workout.
First of all Big A has a new rule that prohibits "suggestion of use" for compounds that may be illegal in some jurisdictions. See:
http://www.professionalmuscle.com/forums/showthread.php?t=41851
What I can do and will do is discuss the science and make comparisons and express opinions.
From the CJC studies and my comparison article between CJC & synthetic GH and from anecdotal feedback I would say that 2mgs each of CJC & GHRP-6 per week (dosed 3x times a day) will not result in the comparative equivalent of 15iu of synthetic GH in terms of GH in plasma & systemic IGF-1 levels.
3mgs of each (i.e 30mcg/kg) per week dosed 3x per day may get you to that 15iu synthetic GH equivalency.
What I have noticed is that natural GH probably does more with less. The pulsation probably gives you more intracellular growth promoting events per unit of time and may (this is still conjecture on my part) be better at promoting IGF-1 & MGF creation in local tissue such as muscle on a unit to unit basis.
Synthetic GH does promote muscle IGFs. Systemic IGF-1 may inhibit GH's creation of muscle IGFs. Testosterone overcomes systemic circulating IGF-1s inhibition and works with GH to promote muscle IGFs.
Long-term consistent usage vs short-term
There are many ways to do it. But more and more I am beginning to believe that it is the consistent use of either GH or GH releasing peptides that over time accumulate the ability to make substantial body changes.
In other words studies that often use a short time horizon with either synthetic GH or GHRH+GHRPs are inconsistent in what they find. They look to systemic IGF-1 as a marker. They look to muscle created IGF-1 and MGF as a marker. Sometimes these markers are elevated sometimes not.
BUT there is consistency in longer term studies (i.e. 3+ months). When they do these longer term studies they often find rising levels. For instance the systemic level of IGF-1 may be higher after one month. By the second month it may be even higher. By the third month it may level off at an even higher level.
Of course the marker I am most interested in is the autocrine/paracrine markers. By that I mean that growth factors are not just synthesized in the liver. True the majority of IGF-1 is synthesized there and circulates. This IGF-1 circulates throughout the body and is referred to as systemic because it is capable of binding to receptors anywhere the body has a need. It is also called endocrine.
If for some reason the IGF-1 does not bind to a receptor quickly and fails to bind to a binding protein its half-life is only 10 minutes. But if it does bind to a binding protein its half-life becomes 16 hours. In order for systemic IGF-1 to become anabolic it needs to be in an amount equivalent to around 160
ug.
But for therapeutic or contribution to wound healing the body needs very little. It only needs 300
ng concentrated in the wounded area, if it is found in blood platelets aggregated around the wound which also contain:
platelet-derived growth factor (PDGF)
vascular endothelial growth factor (VEGF)
transforming growth factor beta-1 (TGF-b1)
epidermal growth factor (EGF)
basifibroblast growth factor (bFGF)
hepatocyte growth factor (HGF)
Now all sorts of local tissue is capable and does make its own factors such as IGF-1. It is made within cells in that tissue and used in those cells to mediate events. These are called autocrine actions. The brain, immune system components, muscle tissue, etc. all are capable of making there own IGF-1 and as you can imagine a little goes a long way. Amounts measured in
ngs can have growth effects.
ug amounts are not required.
Paracrine actions also come into play as a neighboring cell or cells which doesn't make its own IGF-1 has some of it "drip over" from its neighbor. This is one way that IGF-1 creation in muscle can positively effect neighboring bone.
What is interesting is that the studies mostly demonstrate that these autocrine/paracrine factors or (muscle IGF-1 creations/uses) are more important then circulating liver made IGF-1. If they shut-off all liver made IGF-1 they still get 100% growth in muscle tissue because of the IGF-1 & MGF made there. Conversely if they shut off the autocrine/paracrine actions so the muscles must await liver-made IGFs... they find that muscles don't grow as much. The systemic IGF-1 benefits for sure but not to the extent as that of locally made/ locally used IGFs.
So over time, with prolonged consistent usage of synthetic GH &/or the growth hormone releasers these important autocrine/paracrine markers increase.
So this might account for at least in part what bodybuilders have already discovered. That is that after 6 months of use things appear to become easier or the effects become more noticeable.
This would also mean that cycles that employee steroids, insulin and GH (using all sorts of cycle protocols) will probably be more beneficial then if someone were to just start using GH on a new cycle (without prior long-term use).
Synthetic GH administration
So if one were to use synthetic GH what would be a beneficial dosing scheme?
There is no definitive answer.
The only aspect we can be sure of is that the intracellular pathways that are triggered when GH binds with a receptor need time off to resensitize.
We know that 15iu of synthetic GH will elevate GH in plasma for close to 24 hours.
We know that 7.5iu of synthetic GH will elevate GH in plasma for close to 12 hours.
We can extrapolate down to 2iu of synthetic GH elevating GH in plasma for about 3.2 hours.
For the most part those intracellular pathways can reset within about a three hour time span. They just need the absence of GH for that length of time.
So this understanding and those dosings levels determine to some extent what we can do. With a 15iu GH dose you need to take time off which occurs during the following day.
With a 7.5iu dose you only need to take time off later that day. So with the proper timing you could use GH every day as long as you have the proper time off each day.
With a 2iu dose you can have multiple doses easily throughout the day spaced by time off. This means you could run it everyday.
Thats all we know for sure.
In my thread I discussed the 2iu dosing scheme multiple times a day for fatloss. But I am conjecturing that this will work well in the long term for growth as well. The reason is simply that we are now beginning to mimic pulsation with this dose scheme & we will be getting more quality growth events per day. But it is conjecture... soundly reasoned...but not firmly established...
Final note
People focus to much on amount of GH. 5iu versus 10iu, etc.
There are several components to the chain of events that lead to growth w/ GH and the amount of GH is just one.
There are the GH binding proteins & prolactin binding proteins. The amount of free growth hormone could be as little as 10% or as high as 90% at various times.
There are the GH-receptors. Both the creation and expression of those receptors waiting for GH to bind to them.
There is the life of the GH-receptor-GH ligand complex. It can be short or a little longer.
There are the intracellular pathways (primarily Stat5b & ERK) which are activated by GH binding to the receptor which may respond with various degrees of "strength" or "timing" ...they may translocate to the nucleus to initiate protein transcription or they may move to the cytoplasm where the events they mediate have a different effect.
The Stat5b pathway when it moves to the nucleus leads to creation of IGF-1.
But the ERK pathway is the most interesting because it can behave in ways that result in proliferation, differentiation, apoptosis all depending on how the GH wave activates its receptor. Is the GH wave a wave with high amplitude or small amplitude? Is the GH wave of long duration or short duration? etc.
The choices that ERK makes on what it wants to do depends on the characteristics of the GH wave. This behavior is different depending on which cell populations we are looking at. A GH wave of particular characteristic may promote cellular differentiation in muscle but that same wave is promoting cell suicide in other non-muscle tissue, while that same GH wave is promoting cellular proliferation on other tissue or organs.
So the point is a lot of things happen beyond absolute amount of GH.
Okay I apologize for rambling on...it is very early morning here & I am well rested & caffeinated up.
.gif "IP Gear")
