CJC-1295, PEG-MGF and AI?
- Thread starter agent8
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pumbertot
Active member
not sure exemestane will help with this kind of water retention but dosage of 12-25mg/day might help. Impo if it really bothers you, take 20mg/day of Ferusimide (Lasix) until you have lost sufficient water to be happy. But I would just keep that puffiness for the extra strength it should give you(as water retention usually does).
Bobaslaw
Member
I agree with pumber. Exemestane (Aromasin) will only help with estrogen mediated water retention. It might help if your estrogen levels are high (due to some other reason), but that would be regardless of the CJC and PegMGF. Water retention is a side of HGH, so it would be reasonable to assume that the CJC is possibly causing some WR.
Personally, I usually just go with some Dandelion Extract for diuretic effects.
Take Care...
Personally, I usually just go with some Dandelion Extract for diuretic effects.
Take Care...
Bobaslaw
Member
Not to say something else may not be affecting prolactin, but CJC does not increase it. I have not seen any study/trial that showed prolactin increase. Here is a excerpt from writeup:
SOLARUS
Member
that's a strong statement without documentation....
"writeups" are virtually worthless and almost always full of misrepresentations....not saying that one is (wherever it came from), but we'll need a source for that assertion, preferably one with some M.D.'s behind it...
(i genuinely hope it exists, because i'd like to use the peptide and figure out from where the bloat comes from)
Bobaslaw
Member
Sol, I think you may be confusing CJC with GHRP/Hex, since both those do increase cortisol and prolactin on top of GH in their respective studies.
Read this thread with the clinical trial and lab results of prolactin levels for candidates on CJC. I am including an excerpt related to the question you pose.
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I am, however, curious as to why you made a statement that prolactin is the cause given that there is no evidence in any of the available trials to support your claim? Did you just make this up? I certainly hope not since that would be very strong statement without documentation, as you put it earlier. Please show me anything you have to contradict the clinical CJC trial/study in the link above (The full study is farther down in that thread).
Take Care
pumbertot
Active member
SOLARUS
Member
i never asserted that prolactin was the cause - i suggested that there is reason to believe it plays a role, and this is based on the noted prolactin increases that accompany nearly every other GH-related compound i've seen....i was drawing a parallel (and a very logical one, i might add) and creating a hypothesis, i was not making a claim. perhaps you have me confused with some less scrutable member who asserts opinions instead of offering possibilities.
as for the trial, yes they do mention the lack of (significant) increase of prolactin after ONE shot (statistically significant being altogether different than significant to the layperson), but as the study itself says, the results are cumulative, and the prolactin release could potentially increase over time along with the GH increase - we just dont know...also, they dont say how long after administration they tested for prolactin, or how many times....would have been nice.
i did miss this detail when i scanned these studies earlier, so thanks for pointing it out. it is useful, but i'm not sure how much.
anybody else have any ideas where the water retention comes from?
Bobaslaw
Member
Yes, Sol, I do see your points and they are valid questions regarding the long term usage, however, so far nothing shows that... The major difference between CJC and "other" GH releasing compounds is the fact it is basically GHRH and should behave just like the endogenous GHRH we produce. Our own endogenous GHRH is selective only for somatotroph receptors at the pituitary as far as I am aware.
It would be nice, though, to have longer trial results, but that may be up to the Blood Work we decide to do after running it for a while.
I know Agent8 has been using CJC for a while, so why don't we stick him and see :stick:
BTW, I am sorry about my tone in my last post as you were stating an educated opinion on the matter rather than trying to pass it off as a hard fact. My Bad.
On another note, I have a burning question as to the possibility of CJC causing pituitary enlargement over extended use. It's bugging me so I posed the question and the study that seems support this at least in hypopituitary mice (GHRHKO mice).
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PS- Agent, didn't you mention that you were getting puffy possibly from the slin at some point? Did you drop the slin, or still running it at all?
Take Care
SOLARUS
Member
no sweat bro - hard to see intent and nuance on a forum, as always...i was being a little bit sassy, so my bad too.Yes, Sol, I do see your points and they are valid questions regarding the long term usage, however, so far nothing shows that... The major difference between CJC and "other" GH releasing compounds is the fact it is basically GHRH and should behave just like the endogenous GHRH we produce. Our own endogenous GHRH is selective only for somatotroph receptors at the pituitary as far as I am aware.
It would be nice, though, to have longer trial results, but that may be up to the Blood Work we decide to do after running it for a while.
I know Agent8 has been using CJC for a while, so why don't we stick him and see :stick:
BTW, I am sorry about my tone in my last post as you were stating an educated opinion on the matter rather than trying to pass it off as a hard fact. My Bad.
On another note, I have a burning question as to the possibility of CJC causing pituitary enlargement over extended use. It's bugging me so I posed the question and the study that seems support this at least in hypopituitary mice (GHRHKO mice).
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PS- Agent, didn't you mention that you were getting puffy possibly from the slin at some point? Did you drop the slin, or still running it at all?
Take Care
CJC does appear to act very differently than the other secretagogues. the impact to TROUGH GH is really curious, to me. i need to go back and read every word of that trial, actually....
i wish i even had an educated guess as to your pituitary enlargement question. that's about two tiers over my shadetree endocrinologist head....
my $.02 regarding slin and puffiness - i have never ever retained water from it....i've felt "full" as in way-stocked glycogen stores, but it feels entirely different (somehow) than water retention.
i retained crazy water on GHRP-6, it was rather unpleasant. prolactin-induced? i dunno, maybe. there wasnt much of an impact to libido, which tends to be a hallmark of high PRL...any other markers that we can look for? hmm...
Bobaslaw
Member
Ya, that could be prolactin but I suspect the cortisol increase, or both for that matter... GHRP-6 trials that I have seen showed elevated cortisol levels mediated by its unselective stimulatory action on pituitary corticotrophs (ACTH), as well as mammotrophs (Prolactin) and somatotrophs (GH).
My brain is fried for the night along with CJC induced sleepiness. Bed time
Take Care Sol
SOLARUS
Member
is there reason to believe that CJC has a selective stimulatory action on the undesirable -trophs? besides that damned blurb in the study? is there a structure difference that could cause that? i know that CJC is a GHRH analog instead of a GH secretagogue, but i dont really know what that meansYa, that could be prolactin but I suspect the cortisol increase, or both for that matter... GHRP-6 trials that I have seen showed elevated cortisol levels mediated by its unselective stimulatory action on pituitary corticotrophs (ACTH), as well as mammotrophs (Prolactin) and somatotrophs (GH).
My brain is fried for the night along with CJC induced sleepiness. Bed time
Take Care Sol
Bobaslaw
Member
is there reason to believe that CJC has a selective stimulatory action on the undesirable -trophs? besides that damned blurb in the study? is there a structure difference that could cause that? i know that CJC is a GHRH analog instead of a GH secretagogue, but i dont really know what that means
Actually I feel there is no reason to beleive that CJC will not act exactly as endogenous GH as far as selectivity only for somatotrophs. Just like the study/trial shows.
Basically, CJC-1295 is a tetrasubstituted peptide analogue of GHRH with D-Ala, Gln, Ala, and Leu substitutions at positions 2, 8, 15, and 27.
I guess you could loosely compare it to what was done with IGF-1 versus IGF-1lr3 to get the desired effect.. Its agonistic properties are the same as IGF-1, just has an extended halflife.
Sure the substitutions in both peptides open up "uncertainties" as to its altered properties, but so far the alterations in both these peptides only show an extension of halflife and no other deviations from their natural endogenous counterparts.
Read this excellent post with technical info on CJC:
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Secretagogues are just substances that causes the secretion of another substance...
As far as the the other GH secretagogues go (GHRP/Hex, etc), they just seem to agonize a slew of different receptors on the pituitary's cell types. Main difference is that with GHRH analog you are heading into what the body intended to be the "messanger" for the somatotroph only. I mean, the hypothalmus has other RHs to do other jobs: CRH to agonize corticotrophs (ACTH), GnRH to agonize gonadotrophs (LH/FSH), PRLH to agonize mammotrophs (Prolactin), etc...
The other secretagogues are all just a good attempt to manufacture something that is somewhat functional in releasing GH, just not as selective as nature intended for GHRH. But is this not like any medication or drug that is created in the medical field? The all have side effects which is just another term for being unselective for the main intended purpose.
Take Care.
Bobaslaw
Member
Exactly! Nice find on the actual study!
I posed this same question in a pretty dead thread regarding the combination of an effective somatostatin inhibitor with CJC.
http://anabolicminds.com/forum/igf-1-gh/88761-various-somatostatin-inhibitors.html
Arginine sounded like the best candidate (readily available, no notable sides like other somatostain inhibiting compounds).
The only drawback was that oral arginine was not found to do much as compared to IV (from some very brief research)or so I was led to beleive until your posted study just now. It clearly shows oral arginine produced greater results than GHRH alone. Even though it is not as high as with the IV arginine, it is still higher. Given the fact you can buy it bulk for cheap, I see no reason not to run it alongside.
I think Ill give it a try...
Thanx for the info!!
Take Care.
pumbertot
Active member
Exactly! Nice find on the actual study!
I posed this same question in a pretty dead thread regarding the combination of an effective somatostatin inhibitor with CJC.
http://anabolicminds.com/forum/igf-1-gh/88761-various-somatostatin-inhibitors.html
Arginine sounded like the best candidate (readily available, no notable sides like other somatostain inhibiting compounds).
The only drawback was that oral arginine was not found to do much as compared to IV (from some very brief research)or so I was led to beleive until your posted study just now. It clearly shows oral arginine produced greater results than GHRH alone. Even though it is not as high as with the IV arginine, it is still higher. Given the fact you can buy it bulk for cheap, I see no reason not to run it alongside.
I think Ill give it a try...
Thanx for the info!!
Take Care.
think i might try it too.
SOLARUS
Member
with nearly 3 times the AUC for GHRH+oral arg versus GHRH alone, i'd say it's a must-have for a CJC run.The only drawback was that oral arginine was not found to do much as compared to IV (from some very brief research)or so I was led to beleive until your posted study just now. It clearly shows oral arginine produced greater results than GHRH alone. Even though it is not as high as with the IV arginine, it is still higher. Given the fact you can buy it bulk for cheap, I see no reason not to run it alongside.
I think Ill give it a try...
Thanx for the info!!
Take Care.
clonidine would probably also work well.
still not sure about the prolactin/cortisol dimension on this, though.
SOLARUS
Member
speaking of runs, check out this study on this same phenomenon, but for trained runners....
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shows that Arg's effects on GH production by GHRH were limited for the trained set, whereas the sedentary got the most out of it...
and peep this sentence: "In runners, GHRH induced an increase of GH which was significantly higher (p < 0.001) than that observed in the age-matched controls." is frankly amazing to me....P<.001??? that's no small difference, that's huge. they dont mention if the baseline GH was higher for the trained set, which is odd considering they point to the almost 2x baseline for IGF.
this may point to a stronger GH response to GHRH/CJC/GHS's for trained individuals than "norms", or it may be a age-related thing, i'm not sure.
Bobaslaw
Member
Yes sir, thus the recommendation not to eat high carbs before bed, if we want maximum nocturnal GH release.
BTW, you are a researching madman! lol. Great stuff.
I found this interesting study related to this subject:
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A couple of interesting points in the study below:
pumbertot
Active member
yep and it also holds true that taking some insulin on an empty stomach, if you are brave enough, will increase the GH release too as hypoglycemia induces significant GH release.
SOLARUS
Member
wow, so it looks like you CAN have a carb meal with your GHRH/CJC as long as you have arginine in the mix...
i'm curious to find out the effect of arginine+glucose withOUT any GH secretagogues/mimetics/etc...can we keep our endogenous GH up straight thru a carb meal by using arginine?
and if all this is true, why does arg blunt GH release pre-WO?
ugh, so much information...
SOLARUS
Member
or, as Bob's study shows:
"No inhibitory effect on the GHRH-induced GH response
was observed when oral glucose was administered 60 min
before GHRH in terms of either peak [children, 19.9 + 5.3
pg/L (P = NS VS. placebo/GHRH); adults, 15.0 + 3.8 pg/L
(P = NS ‘us. placebo/GHRH)] or AUC levels..."
so if you get your sugar at least an hour beforehand, no problem. in fact, if you look at the graph on page 1154, you'll see an even greater overall GH increase when sugar is adminstered 2 hours before GHRH (presumably due to the natural rebound of natty GHRH after somatostatin suppression by sugar, but that's a guess)
edit - the study goes on to expand on this in subsequent pages. i guess they agree...
edit2 - Bob, this study is priceless for anyone planning to use or using CJC-1295! thanks!
pumbertot
Active member
my guess is the greater GH release is because of the insulin released by the body(in response to consuming sugar) which then lowers your blood glucose possibly to a level that is lower than before you ingested the sugar.
Bobaslaw
Member
True, but insulin itself decreases somatostain tone and is listed among clonidin, pyr., arginine for that purpose in GH testing...
So if glucose causes a somatostain reflex action from the hypothalmus (blunting GHRH action), then wouldn't the following rise in insulin (triggered by the glucose) start to decrease the somatostatin tone? Then both glucose and insulin would drop to baseline after a "certain time" and GH would rebound... Just a thought.
EDIT: Lol, thats what you said here pumber, I missed that when posting
Bobaslaw
Member
Thx! I do wonder though about the diffenece in GHRH action vs CJC. We really do not have much control on the timing of any protocols that we have been discussing, as CJC is a long lasting systemic GHRH analog. It will agonise at the times it wants to. As far as Arginine, just supplementing throughout the day would be the only thing we could do. Timing glucose, or not taking it at a certain time might be beneficial when off, but while on CJC... I don't think we have much control with respect to any timing...
SOLARUS
Member
i was thinking the same thing regarding the un-pulsatile nature of CJC. while i acts like GHRH and is based on GHRH, it seems to just hang around, agonizing the pituitary, even in the troughs (which i still find surprising and perhaps a little disconcerting)
need to look over the CJC studies again and try to draw appropriate parallels and find differences in action as compared to GHRH.
i wonder how much GH increases on an atkins-style diet? i also wonder what other triggers there are for [release or suppression of] GHRH? sleep is obviously one, as is insulin...stress might be....hunger is (ghrelin)....
what i REALLY am curious about is if you eat after a CJC dose, does that blunt the GH release? and could you mitigate that with the arginine, same as you can before GHRH administration? that'd be nice...we suspect that arginine works via somatostatin inhibition, but does insulin increase/potentiate/stimulate somatostatin? it sure seems like it, given that previous study...makes for some really promising protocol theories for CJC, once we can sort out the lack of pulsatility. and even if we can't, it looks like carbs + arginine is a winner regardless.
i am also trying to think what bearing there is on Hex or GHRP-6 protocols...the hunger induced by those is tremendous, and i can't help thinking that eating afterwards ends up being counterproductive from a GH standpoint...so even though they work by a different mechanism, the amelioration of GH release by glucose could be mitigated by simultaneous arg dosing...
Bobaslaw
Member
I believe there is no difference at all with respect to arginine mediated somatostain inhibition when either either GHRH or CJC are used; other than an "optimum" timing protocol, ofcourse.
Somatostatin's effect is on the somatotroph. Upon agonising a somatotroph receptor, somatostatin causes certain physical processes in the somatotroph to change, in turn causing it not to respond to further GHRH agonism, or CJC agonism as pertains to us.
Actully, it is glucose that mediates the somatostatin reflex action, not insulin itself. Insulin decreases somatostatin tone and is grouped for this usage along with arginine and clonidine, etc. One of the thoughts by pumber and myself was that as glucose may cause the initial stimulation of somatostatin but it is reduced/suppressed as soon as insulin starts to rise (response to plasma glucose rise). Thus the GH rebound discussed in earlier posts.
Here is where I think arginine may help us with CJC with respect to negation the glucose/somatostatin trigger. In the study it was shown that an hour after glucose administration things returned to normal, somatostatin tone decreased and GHRH was effective again at stimulation the somatotrophs to release GH.
Since we do not know at what (random?) times CJC is actually binding to and agonising s-trophs, we cannot be certain that any of the meals (carb/glucose) we injest are coinciding with a possible moment(s)when CJC would be trying to bind/agonise s-troph receptors. Thus arginine before meals could increase the likelihood that CJC is more effective at those exact times.
I would say since somatostatin effects the somatotroph in that it is not responsive to gh release via ghrh (since physical processes change inside the somatotroph), it may also apply to the receptor pathways that GHRP/Hex use (One study you showed alluded that Hex agonises different receptors/subtypes than GHRH.
Here are some studies on what effect somatostatin has on somatotrophs:
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Take Care.
SOLARUS
Member
the "GH rebound" doesnt appear to be much of a factor in adults, see figure 2, upper-right...perhaps if the graph went out to 4 hours you might see something, but...
also, i dont think that plasma glucose and insulin are spiked very far apart after glucose administration. both will be high within minutes, usually. even if the insulin (which should promote a GH increase) lags the plasma glucose by an hour, it still isnt showing correspondingly on the GH chart.
see, i dont see things as being "normal" 60 minutes after glucose. GH is still low, and the GH response to GHRH is still much much lower. in fact, it's the same as for placebo+GHRH...which actually means (to me) that glucose clearing after 120 minutes seems to "prime the pump" and allow a much increased GH response to GHRH...so even though we might not naturally have a GH rebound as long as 3.5 hours after glucose, we still respond much more strongly to GHRH when we have more insulin flowing due to having administered glucose 2 hours prior....
my take-away message: if you want to get the most out of GHRH, make sure you have some, but not much, residual blood glucose and insulin flowing when you administer it....for CJC, it's not so simple. i think the only logical advice would be to preload arginine before your carb meal, to get you through to the insulin increase which should help get GH back up and running a couple hours later.
could anyone post the figures from the main CJC study, here:
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pumbertot
Active member
Bobaslaw
Member
Good points and your inerpretation of the study data is superb! Nonetheless, the usefulness of Arginine with CJC is quite obvious here.
Only question is how high a dose and how many times a day before carb meals and/or at other times...
The previous study showed oral arginine at 8g increased the GH response to GHRH, would 4g have done anything? I don't know. Given this, would I want to dose any less than 8g at a time? How many times a day?
Also, studies on patients with heart issues showed that dosages of 20-24g/day of arginine showed no noticable negative side effects.
I deduce you could do 8g 3 times a day and be at the uper limits of "tested" safety... Need to look into this some more...
EDIT: Also oral l-Arginine is degraded in the intestines and not as bioavailable as Arginine AKG (alpha keto gluterate), or AEE (arginine ethyl ester). What kind of oral arginine was used in the study? Was it plain L-Arginine? If so, 8g definitely did not make it into the bloodstream.
On another note, one thing I do not know with regard to arginine's ability to blunt the somatostatin reflex action from glucose is dosage or method of delivery used for the arginine. I'll have to reread that study and see whether it was IV or what dosages negated this response. I cannot assume the 8g oral dosage from the previous study is the same amount/type of delivery that would produce the glucose inhibiting effect...
hullcrush
New member
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I'm sure this has been posted before, but GHRH in conjuction with hexarelin doesn't stimulate cortisol release and reduces prolactin release. I'd cautiously try CJC-1295, Arginine, GHRP-6/hex, and bromocriptine.
Unfortunately, the prolactin increase will lead to a decrease in testosterone, but also a decrease in estrogen. I would add an AAS in there I suppose, but that sure seems like a lot.
I'm sure this has been posted before, but GHRH in conjuction with hexarelin doesn't stimulate cortisol release and reduces prolactin release. I'd cautiously try CJC-1295, Arginine, GHRP-6/hex, and bromocriptine.
Unfortunately, the prolactin increase will lead to a decrease in testosterone, but also a decrease in estrogen. I would add an AAS in there I suppose, but that sure seems like a lot.
Bobaslaw
Member
Great find Hull! Thanks.