OK dat lay it out for us....we want max mass and as little fat accumulation as possible.
Whats the best protocol for cjc 1295/ GHRP-6 for maxx muscle?
Thanks
I'm not sure if hyperplasia can occur with cjc and ghrp use. My guess would be no because it would not cause your body to produce enough gh in order to cause a big enough igf spike. 8+ius is when hyperplasia occurs. Even with the cjc/ghrp combo, your body would only be producing around 5ius of gh from what I've read from dat's posts. I could be wrong.
I'm not sure if hyperplasia can occur with cjc and ghrp use. My guess would be no because it would not cause your body to produce enough gh in order to cause a big enough igf spike. 8+ius is when hyperplasia occurs. Even with the cjc/ghrp combo, your body would only be producing around 5ius of gh from what I've read from dat's posts. I could be wrong.
OK dat lay it out for us....we want max mass and as little fat accumulation as possible.
Whats the best protocol for cjc 1295/ GHRP-6 for maxx muscle?
Thanks
OK dat lay it out for us....we want max mass and as little fat accumulation as possible.
Whats the best protocol for cjc 1295/ GHRP-6 for maxx muscle?
Thanks
Lr3 from my experience does not induce hyperplasia. However, pmgf does because that is the direct byproduct of gh+slin. You would need some hefty doses of mgf to induce hyperplasia.
Lr3 from my experience does not induce hyperplasia. However, pmgf does because that is the direct byproduct of gh+slin. You would need some hefty doses of mgf to induce hyperplasia.
JM there is no MGF receptor. MGF is a variant if IGF-1 and is capable of binding to the IGF-1 receptor if injected and acting like IGF-1.
Injected MGF will not act like MGF.
Native MGF is only expressed within the cell of its birth and mediates its action by translocating from the cytoplasm to the nucleus of the cell.
The reason MGF apparently is effective for people at high dose is simply that it is acting as a better IGF-1 than IGF-1 LR3.
The reason?
It is too early to discuss it BUT I ran some calculations an believe that the acetic acid concentration most use to reconstitute IGF-1 LR3 is almost 6 times stronger then it should be.
This means IGF-1 LR3 is likely quickly degraded.
So those people who have dosed IGF-1 LR3 in very large amounts and claim great results likely are using the vial quickly before IGF-1 LR3 is degraded to zero.
MGF may either really be a better IGF-1 then LR3 or following my thought process here.... be used at higher dose more quickly and thus used up before it degrades to zero.
Again I am waiting for someone to recheck my math and analysis...
JM there is no MGF receptor. MGF is a variant if IGF-1 and is capable of binding to the IGF-1 receptor if injected and acting like IGF-1.
Injected MGF will not act like MGF.
Native MGF is only expressed within the cell of its birth and mediates its action by translocating from the cytoplasm to the nucleus of the cell.
The reason MGF apparently is effective for people at high dose is simply that it is acting as a better IGF-1 than IGF-1 LR3.
The reason?
It is too early to discuss it BUT I ran some calculations an believe that the acetic acid concentration most use to reconstitute IGF-1 LR3 is almost 6 times stronger then it should be.
This means IGF-1 LR3 is likely quickly degraded.
So those people who have dosed IGF-1 LR3 in very large amounts and claim great results likely are using the vial quickly before IGF-1 LR3 is degraded to zero.
MGF may either really be a better IGF-1 then LR3 or following my thought process here.... be used at higher dose more quickly and thus used up before it degrades to zero.
Again I am waiting for someone to recheck my math and analysis...
JM there is no MGF receptor. MGF is a variant if IGF-1 and is capable of binding to the IGF-1 receptor if injected and acting like IGF-1.
Injected MGF will not act like MGF.
Native MGF is only expressed within the cell of its birth and mediates its action by translocating from the cytoplasm to the nucleus of the cell.
The reason MGF apparently is effective for people at high dose is simply that it is acting as a better IGF-1 than IGF-1 LR3.
The reason?
It is too early to discuss it BUT I ran some calculations an believe that the acetic acid concentration most use to reconstitute IGF-1 LR3 is almost 6 times stronger then it should be.
This means IGF-1 LR3 is likely quickly degraded.
So those people who have dosed IGF-1 LR3 in very large amounts and claim great results likely are using the vial quickly before IGF-1 LR3 is degraded to zero.
MGF may either really be a better IGF-1 then LR3 or following my thought process here.... be used at higher dose more quickly and thus used up before it degrades to zero.
Again I am waiting for someone to recheck my math and analysis...
LOL
Now how did I know you would delete that post...LOL
Its ok...
I printed it out and shrunk it down and have it laminated tucked away in my wallet for future reference....
for personal use only of course...J/K
I'm not sure if hyperplasia can occur with cjc and ghrp use. My guess would be no because it would not cause your body to produce enough gh in order to cause a big enough igf spike. 8+ius is when hyperplasia occurs. Even with the cjc/ghrp combo, your body would only be producing around 5ius of gh from what I've read from dat's posts. I could be wrong.
If I recall, with CJC with the DAC and ghrp dosed 3 times a day, its upwards of 20ius, but I could be mistaken, I'd have to go back and check, but pretty sure thats what i wrote in my notes.
Its in dats posts...estimated equivalents that cjc/ghrp cause endo gh as opposed to exo administered gh:"...These results indicate that 22iu is between 3.8 and 3.4 more efficacious then a single administration of GHRH & GHRP which means that a single dose of GHRH & GHRP has the potential to produce better then the equivalent of 5iu of GH in plasma.
A dosing protocol of GHRH + GHRP at saturation dose, administered 3 times per day has the potential to exceed the equivalent of 15iu.
Note though that using this methodology GHRP-6 at a saturation dose by itself may add the equivalent of 1.4 to 1.8 iu per administration... or 4.2 to 5.4 iu per day if administered three times..."So, its my opinion that absolutely, cjc/ghrp CAN induce hyperplasia, if the muscle load is there.
And again JM, this whole "only 8+iu's of exo GH can induce hyperplasia" business....conjecture on your part at the very best...I've posted the studies bro....extreme muscle workloads, absent any gh manipulation whatever, can cause hyperplasia if conditions are optimal....Its your opinion this 8+iu thing....yes, I know, based on all your pro bb'ing friends.....but its still just your opinion...it has no basis in fact.
Its in dats posts...estimated equivalents that cjc/ghrp cause endo gh as opposed to exo administered gh:"...These results indicate that 22iu is between 3.8 and 3.4 more efficacious then a single administration of GHRH & GHRP which means that a single dose of GHRH & GHRP has the potential to produce better then the equivalent of 5iu of GH in plasma.
A dosing protocol of GHRH + GHRP at saturation dose, administered 3 times per day has the potential to exceed the equivalent of 15iu.
Note though that using this methodology GHRP-6 at a saturation dose by itself may add the equivalent of 1.4 to 1.8 iu per administration... or 4.2 to 5.4 iu per day if administered three times..."So, its my opinion that absolutely, cjc/ghrp CAN induce hyperplasia, if the muscle load is there.
And again JM, this whole "only 8+iu's of exo GH can induce hyperplasia" business....conjecture on your part at the very best...I've posted the studies bro....extreme muscle workloads, absent any gh manipulation whatever, can cause hyperplasia if conditions are optimal....Its your opinion this 8+iu thing....yes, I know, based on all your pro bb'ing friends.....but its still just your opinion...it has no basis in fact.
That is not just my opinion. It's the opinions by many advanced bbers on this board and many others as well. Also, 8+ius of gh along with slin produces enough igf for hyperplasia to happen. At lower doses, IMO there is simply not enough igf floating around for hyperplasia to happen. I'm not talking out of my ass here, I've put this entire thing in motion. I'll just say this. Let's agree to disagree.
I agree that we disagree...but lets not overlook ghrh/ghrp combo's for high enough endo hgh for hyperplasia....theoretically. Exo gh is not the only way...and the body's own gh is better IMHO-
I think you are both talking past each other a little bit though...
The truth is nothing is an absolute.
The more GH you have in your system the more potential for growth.
Higher synthetic GH levels will jack systemic IGF-1 levels while an equivalent amount of GHRH/GHRP "may" result in high levels of locally made/used IGFs/MGF, it will not raise systemic levels as much as synthetic GH. [Why? different release profiles]
Also studies are not really reliable to peg a specific amount. For instance I have seen a study with elderly that said 8ius of synthetic GH was the threshold for anabolism in that group.
But the elderly have a different set of obstacles to overcome then the young. For instance delayed protein synthesis as well as a need for prolonged GH to eventually see an increase in MGF post-exercise.
So is 4iu anabolic in the elderly after several months? Probably but these studies have limitations.
A better indicator is IGF-1. Injury repair takes a tiny amount of local IGF-1 while anabolism requires 500 times this amount.
"The doses of IGF-1 in PRP [platelet-rich plasma’] are subtherapeutic in terms of producing systemic anabolic actions by a factor of 500 (300 ng versus 160 mg)." - Growth factor delivery methods in the management of sports injuries: the state of play, L Creaney,Br. J. Sports Med. 2008;42;314-320
Most GH protocols & GHRH/GHRP are eventually anabolic and achieve both a reduction in catabolism & an increase in anabolism. Most of these protocols will raise IGF-1 levels to the bare minimum IGF-1 threshold for anabolism.
jm425 if someone wants to add a few pounds of muscle per year and lose fat lower dose GH can be effective. This has been demonstrated many, many times, especially in the older bodybuilder.
But jm425 is correct that if you really want to grow as much as possible (and I am not saying this is healthy) more is better. ...and in regard to muscle you need either a lot of circulating IGF-1 or a lot of locally produced IGF-1.
BUT is high amounts of circulating IGF-1 needed? No! It is a sledgehammer approach... which means you will grow.
What may be better? Getting GH to do its job, make local IGF-1/MGF and then get the hell out.
How do you achieve this with synthetic GH?
Intravenous administration. This mode delivers GH in mass to receptors and peaks and clears within an hour. So GH is in and out in an hour, while subcutaneous or IM delivery means GH will release into plasma all day.
Think about what you could accomplish with this mode of delivery?
Take a look at this Humatrope chart. Look at the intravenous peak GH level with a lot less synthetic GH then subcutaneous/IM delivery.
Do this several times a day, especially with Insulin and...
Wow bro. Gh intravenously? I've thought about that but that's not something I'd do on my own. Correct me if I'm wrong, but what your saying is that with endogenous gh, gh levels rise rapidly compared to the cjc/ghrp combo which raises gh levels slowly over a longer period of time?