Peptides S XxX Obliterate E XxX HGH XxX and XxX IGF XxX

[RSNUK]

I'm a considering the possibility that peptides may be much more potent and cost effective than striaght HGH.

Consider these posts:

http://forums.steroid.com/showthread.php?t=313311

http://forums.steroid.com/showthread.php?t=329674

Now humour me for a second, i'll keep this simple.

Kids on GH therapy = minimal improvement.

Kids with excess pituitary activity = Leonid Stednik and Yao Ming

Why?

Simple because excessive natural pulsatile GH release is superior to excessive artificial release.

Why?

Because our bodies trained to eliminate the effects of anything foreign thats entered into our body. If you use a peptide to cause our body to release excessive GH, it will interpret the GH as natural, however i'm sure it may try to fight against the effects of the peptide causing the release.

In the case of CJC 1295, what i want to be a topic of discussion it's such an awesomely designed peptide, i doubt the body will resist much.

I know it;s not really science, but it's a sort of logic.

HGH orginating from our brains in a natural pulsatile fashion is superior to HGH emminates from a random wound created in some random point of our body.

Not really provable beyond this formula i offer:

Kids on GH therapy = minimal improvement.

Kids with excess pituitary activity = Leonid Stednik and Yao Ming

But at the least i believe i have given evidence that CJC provides more (an incredibly great amount more) at equal or cheap costs than HGH and this is just the beginning.

[RSNUK]

I am quoting someone from another forum:

IGF/LR3IGF-1 is NOTHING like what you are saying. NOTHING.

Ive been using Lr3IGF-1 since I was 18 years old. When I first used it I was using the australian company who created it, GroPep's stuff before they caught on that 99% of their sales were to bodybuilders.

Ive also used GenSci's Igtropin (overpriced bullshit), generic chinese LR3IGF-1 (blue top), and LR3IGF-1 from a half dozen various suppliers.

Its alright. But not in anyway shape or form anything like what your saying.

First, LR3IGF-1 nor IGF-1 gives DICKALL for gains. Seriously. Anyone is DAMN LUCKY if they gain just 5lbs in a 4 week cycle of LR3IGF-1. I can gain 30lbs in 4 weeks with Dianabol at 1/5th the cost of LR3IGF-1.

Lr3IGF-1 gives OKAY pumps. NOTHING like what your saying, nothing. Try OXANDROLONE if you want to feel a REAL PUMP, will make Lr3IGF-1 pumps look like a day at the beach...... *reminiscing time - wavey flashback distortions* Years ago a new canadian UG lab released an Oxandrolone product that was supposed to be 25mg/capsule of Oxandrolone. However to stir up good feedback with their first batch, they doubled up the dosage, to 50mg per capsule yet said it was just 25mg. So everyone, including me, was taking 2 capsules thinking we was using 50mg, but in reality using 100mg (a whopping dose of Oxandrolone). Just standing there, not lifting any weights or anything, gave such an INTENSE pump in the lower back it was painful as ****ing hell, this is without any exercise, just simply standing there. If I lifted a cup of coffee my arms would get pumped, if I lifted a weight, theyd get so pumped I was literally afraid the muscle was going to rip off its ligaments from the pump alone.

Even off 50mg of Oxandrolone, I get pretty bad lower back pain from the lower back PUMP, this is without exercise. Alls I do is take 50mg of Oxandrolone, and walk up 15 steps, and by the top my lower back is pumped up so tightly it actually hurts.

Lr3IGF-1 has never come 1/10th as close. I get better pumps from many other AAS, LR3IGF-1 pumps are 6/10 on my pump scale. Oxandrolone is 10/10.


Lr3IGF-1 and HGH do dickall for mass gains, dick-****ing-all. What they do do and why people DO use them is because they allow body composition changes. Meaning you can gain 2lbs in a 4 week Lr3IGF-1 cycle, yet at the same time, you lost 3lbs of fat as well. Not many steroids can make you LOSE fat and gain muscle simultaneously. THATS why we use LR3IGF-1 and HGH, because they allow that. But neither the fat loss nor the muscle gain will be as dramatic as what you can achieve with either steroids or special lipolytic agents. Instead you get a balance between the two happening simultaneously, which is beneficial. This is why people ADD steroids and/or lipolytic agents ontop of the Lr3IGF-1 or HGH, to further expand its effects in either or both directions.



Now that-that totally exaggerated bullshit has been cleared out. Onto the topic at hand.

HGH fragment = complete scam, useless shit, utterly, useless, dont ever waste a penny, horrible failure to deliver ANYTHING

PEG-MGF = totally nutsuckingly shitty, another utter failure to deliver anything, local, systemic, either way, it blows chunks, simply not worth the money, too little result for too much cash, save ur cash, pegylation sucks compared to bioconjugation, and MGF sucks period


CJC-1295 = GOD!! ****ing GOD! Ive been using this almost non-stop since the day I first tried it. This shit is GOD. The single most beautifully developed peptide ever to come across the BBing scene. In-****ing-credible. This is seriously a FLAWLESSLY designed pharmacologic agent. The things ConjuChem did for developing this peptide is phenomenal. Ive never been more proud to be Canadian (ConjuChem is Montreal based company!). Even more incredible, this product provides the perfect foundation for enhancing it to a level greater than anything thats ever existed for the bodybuilding scene before. Something I discovered that ive been experimenting with for the past little while that no one else seems to have realized, and I need to break the silence on it and open up the can of worms.

Im telling you, CJC-1295 is PEPTIDE PERFECTION. There will never, ever, be any greater peptide than this peptide to ever hit the BBing scene, ever, thats a guarantee. It cannot get any better than this, it really cannot its the pinnacle. Lr3IGF-1 is OBSOLETE, HGH is OBSOLETE, SERMORELIN? HEXARELIN? GHRELIN? GHRP-2? GHRP-6? ALL OBSOLETE, LAUGHABLE by comparison. Its PERFECT dude.


First these dudes (ConjuChem) realized that natural pulsatile release patterns are more effective and less likely to promote acr*****lic deformations verse exogenously supplier recombinant HGH. So they chose GHRH to base their masterpiece off of, and thats exactly what it is a fawkin masterpiece.

Next, these sons of bitches analyzed all the proteases in the body that cleave various amino acids from the GHRH peptide and therefore degrade and deactivate it after approximately 7 minutes. They then chose to remove all the exact specific amino acids that undergo proteolytic cleavage in the GHRH peptide string and replace them with amino acids that cannot be cleaved by the bodies proteases. GENIUS. It makes it virtually immortal. They then modify it to undergo bioconjugation and bind to albumin, one of the most abundant compounds in the body, to further enhance its duration and prevent its clearance from the body. Creating a monstrously mutant masterpiece.


GHRH lasts around 7 minutes because of proteolytic cleavage. CJC-1295, a GHRH-derivative, lasts between 8-10 days from a SINGLE injection. Because its a GHS (Growth Hormone Secretagogue), it maintains the natural pulsatile release patterns rather than injecting exogenous recombinant growth hormone. By maintaing the patterns it allows the bodies other systems to work in harmony with it, such as GHBP's (Growth Hormone Binding Proteins), GHBP's control/prevent side effects such as acr*****ly by dictating the actions of GH, like IGFBP's dictate the actions of IGF-1. When you inject exogenous HGH, the body isnt "prepared" for its existence, therefore it does not provide sufficien GHBP's to control its actions, etc, and therefore you get random abnormal growth of organs and such because theres insufficient GHBP's to deliver the HGH to where its NEEDED, and instead it just binds to whatever receptors it comes across at random. This leads to acr*****lic side effects more readily.


CJC-1295 has many more things going for it as well aside from flawless pharmacokinetics. Its LEGAL. When you buy it you KNOW what your getting, not like HGH which is sometimes HCG counterfeits. Your not going to get scammed trying to buy it like what happens countless times buying HGH. Its much cheaper to use than HGH. From the resellers you pay about $****/2mg, from the China supplier (who supplies the resellers too), its just $***/2mg when buying 10mg. Even cheaper if you buy more than 10mg.



So how does CJC-1295 and GHRH work?

They are GHS, Growth Hormone Secretagogues. They work by binding to the GHSR (Growth Hormone Secretagogue Receptor), where they signal the pituitary to release HGH. Once a 'surge' of HGH is released, the negative feedback mechanism kicks in and causes a rise in Somatostatin. Somatostatin is an inhibitor of HGH release. Once somatostatin levels decline, more HGH can be released, but wont be released immediately in the natural endocrine system. However because CJC-1295 lasts 8-10 days straight and thus signals the GHSR 24 hours a day for 8-10 days straight, the moment somatostatin levels decline after a surge, the CJC-1295 will immediately signal another surge. This occurs throughout the entire day and while you sleep.

HGH lasts only like 15-20 or so minutes in the body before its deactivated by proteases and whatnot. Because of CJC-1295's constant GHSR agonist activity, you therefore get MANY surges of HGH per day. Rather than just a couple under normal endocrine activity with GHRH. And rather than just 1 additional surge you get when injecting exogenous recombinant HGH.

This is why HGH takes sooo long to show results. Because everyday you inject it, your only getting 15-20 minutes of supraphysiological HGH exposure. Therefore if HGH lasted lets say 10 minutes, after 7 days of injecting, thats only 70 minutes of total exposure to supraphysiological HGH youve had. The body cant do much growing in just 70 minutes. Hence why it takes months of HGH use to accumulate significant enough time under supraphysiological levels to elicit a noticeable effect. CJC-1295 on the otherhand gives MANY surges per day, therefore its like injecting HGH 10 or 20 times or even more in a single day. The results come FAR faster and are greater.

CJC-1295 gives me the most INSANELY vivid and long lasting dreams. It also gives me numb extremeties and all the other effects of supraphysiological HGH levels. GREAT STUFF.


I will expand into my "UBER-PITUITARY" optimizing method tommorow when I explain why CJC-1295 is the PERFECT foundation for doing something simply INCREDIBLE.


In short: CJC-1295 is the greatest peptide ever made available. It makes ALL other peptides useless. L3IGF-1 is useless. HGH is useless. Its all useless now. CJC-1295 has taken over. Its the only thing worth buying.

[RSNUK]

More from same guy:

In the short term, GH side effects are all that from supraphysiological levels of growth hormone. Meaning, if your NOT experiencing these side effects, it means your NOT using a large enough dosage of HGH (or CJC-1295 or anyother somatotropic-modulator) to bring your GH levels beyond their natural levels thus causing the side effects of supraphysiological levels. So you WANT to exeperience these short-term below side effects;

- Vivid dreams (long, vivid dreams you'll rememebver well)
- Numbing in the extremeties (fingers/hands should go numbish)
- Aching joints (its not a painful ache really, its a very very very dull ache feeling in the joints - like growing pains)
- Mild hypoglycemia if on a low-carb diet (eating carbs is a must when using HGH/IGF-1 otherwise you'll notice mild hypoglycemia as in you'll feel faint, weak, fatigued, lightheaded, dizzy, you wont go comatose but it does take you down a notch)

You WANT to experience the above, that lets you know your using a high enough dosage. If you dont experience those, you must increase your dosage, as it means your only using a large enough dosage to replace your natural levels, which defeats the entire purpose of using GH/GH-mimetics. None of these side effects have any long-term reprecussions.

Long-term side effects are those below. However these take YEARS to develop, you must use HGH and friends for months or years straight, or very frequently, before you will have a chance of developing these to a notiecable level, the average GH user wont ever worry about these to any significant degree unless theyre spending $***+ dollars on HGH;

- Excess organ enlargening
- Excess circumferential skeletal growth (acr*****lic facial distortions such as enlarged forehead and thickened brow-bone creating neanderthal look)
- Increased hand and foot size



Whereas anabolic steroids can have side effects that appear MUCH MUCH faster (weeks or even days for some), and can be pretty nasty and some long-term;

- Acne or BACNE (rocky mountain back which virtually never goes away)
- Extreme body hair growth (I can vouch for this disgusting side effect, I HATE IT, 24/7 battle against the body hair)
- Liver damage
- Cholesterol problems
- Accelerated male pattern baldness
- Increased blood pressure
- Infertility/testicular problems
- Breast development (gyno)



I think GH/IGF-1 have much less side effects than AAS. The short-term sides of GH are indicators of effectiveness and dont ever stay after you discontinue use. The long-term sides take a long long time to develop, ive been using for years and never encountered any noticeable changes in facial bone or anything. Alls ive noticed is mild increase in hand and feet size and tiny increase in wrist circumference. I feel way more comfortable, side effect wise, using HGH than steroids thats for sure. Im sure MOST do.

I mean with AAS you NEED to use lots of ancillary components to prevent the side effects, such as aromatase inhibitors, alpha-reductase inhibitors, blood pressure meds (for some users), liver protectorants, special acne meds, post-cycle therapy protocols, etc.

But you dont need nor does anyone use anything to combat GH/IGF-1 side effects because theyre virtually non-existent in the long-term. And the short-term effects have no relavancy to anything other than to identify the legitimacy of the stuff your using and the effectiveness of your dosage.

[RSNUK]

Another post by same person:

Now onto enhancing CJC-1295 to blow it into the next universe of effects.

CJC-1295 is the perfect foundation for doing this. Because it lasts 24 hours a day for 8-10 days straight. Whereas GHRH, which does the same signalling of the GHSR, only lasts 7 minutes.


First its important to understand how GH surges work. Pay especial attention to Somatostatin.

When a secretagogue of GH, such as GHRH, Ghrelin, Hexarelin, or CJC-1295, signals the GHSR it causes the pituitary to release HGH, IF, Somatostatin levels are low enough to allow it. Once a surge of GH is released, Somatostatin levels will rise up again, thus even if something is binding to the GHSR, it CANNOT signal the release of GH because Somatostatin levels are too high.

Somatostatin is what controls the negative feedback mechanisms of GH release in the pituitary. After a surge of GH is released from a secretagogue wether natural or man-made, Somatostatin levels will rise, preventing further GH release until the GH levels decrease, at which point the ultra-short feedback mechanisms of the hypothalamus-pituitary-axis (HPA) kick in and cause Somatostatin levels to decrease.

The moment somatostatin levels decrease sufficiently, more GH can be released. However under natural conditions, there wont be sufficient GHRH remaining at the GHSR to cause more GH release once Somatostatin levels decrease. Because GHRH is also released in surges, and only lasts 7 minutes upon its circulating release.

However because CJC-1295 lasts 24 hours a day for 8-10 days, its ALWAYS at the GHSR, so the moment somatostatin levels decrease enough, another surge of GH will happen because CJC-1295 is there binding to the GHSR's. Therefore under naturakl endocrine system, you'd get lets say 5 surges of GH a day. Whereas with CJC-1295, youd get lets say 15 surges of GH a day.

So whats the obvious limiters of GH release?? Well first, is the duration of GHRH or whatever GHS is signaling the release. This has been overcome with CJC-1295.

Whats the second limiter? Somatostatin. Somatostatin is an inhibitor of GH release. Not so easy to fix??? WRONG! This is where I come in.


Amazingly, no one that ive seen has realized this. That is, if you could inhibit Somatostatin levels while using CJC-1295, you would allow the CJC-1295 to signal an ENDLESS surge of GH (so long as the body was producing sufficient peptide, which means you need a high protein diet since peptides are made from amino acids in protein). Yes, thats not a typo, an ENDLESS surge of GH. The equivalent of strapping an IV bag of HGH to your back and walking around all-day with a drip of GH into you. The difference between the "surge" system and that would be night and day. Im not saying its the healthiest or safest thing to do, but it is so far beyond the natural endocrine function it will lead to results never before experienced or even imagined with HGH of any kind or any way previously available. I can vouch for this as ive been experimenting with this recently.


There is a class of compounds called Acetylcholineesterase inhibitors, that inihibit acetylcholineesterase, which is responsible for deactivating acetylcholine in the brain. Guess what? Acetylcholine is a very effective inhibitor of Somatostatin. Therefore Acetylcholineesterase inhibitors are indirect somatostatin inihibitors, working by increasing acetylcholine levels which then inhibit somatostatin levels.

Does this really work? YES, its been clinically proven in numerous studies with stunning results. In the studies they used GHRH + Acetylcholineesterase inhibitor Pyrostigmine at a dosage of 120mg. Remember GHRH only lasts 7 minutes, so they only get a single surge of GH from using it. What the study found is that orally administering Pyrostigmine, an acetylcholineesterase inhibitor, and then injecting GHRH vs. the placebo/control group resulted in a dramatically larger amount of GH released in response to the same dosage of GHRH. This is because somatostatin levels were dramatically lowered, and allowed an even larger amount of GH to be released in response to GHRH.

Had the study used CJC-1295 they wouldve had a far greater result. Not only would more GH be released per surge, but they wouldve had an endless or damn near endless surge of GH release, rather than the normal "Pulsatile" release system which is controlled by:

A) The short duration of GHRH and other endogenous secretagogues (overcome with CJC-1295)

B) The GH-inhibitory action of Somatostatin (overcome with acetylcholineesterase inhibitors)



Acetylcholineesterase inhibitors are taken orally, they are legal and readily available for purchase as they are extracted from natural plant sources. They are CHEAP, costing just a dollar or less per day to use in conjunction with CJC-1295. By taking them you can use a lower CJC-1295 dosage and still get much greater results. It totally changes the pituitary system into what I must call the uber-pituitary.

Normally the pituitary functions like this;
1) Endogenous GH secretagogue such as GHRH or Ghrelin, signals pituitary to release HGH, the amount of GH released is controlled by somatostatin and GHRH quantity.
2) Pituitary releases HGH creating a 'surge', immediately after, somatostatin levels rise thus making the pituitary unresponsive to GHRH or other secretagogues, GHRH remaining becomes deactivated due to proteocyltic cleavage.
3) After the HGH released has become deacticated by the body, Somatostatin levels begin to decrease again, and once more endogenous secretagogues arrive, another surge will occur and repeat process.


The pituitary function using CJC-1295 + a somatostatin inhibitor (in this case acetylcholineesterase inhibitors), functions like this:
1) Exogenously supplied GH secretagogue CJC-1295 signals pituitary to release HGH, the amount of GH released is GREATER than without acetylcholineesterase inhibitor due to suppression of somatostatin.
2) Pituitary releases HGH creating a surge, however, somatostatin levels fail to rise after the release, therefore the pituitary remains responsive to secretagogues to signal more release of HGH, and the CJC-1295 fails to degrade due to its design thus lasting 24 hours a day for 8-10 days from an injection.
3) After the HGH is released, ANOTHER surge is immediatley signalled by the still active CJC-1295, and then another surge, and another, and another, and another, and another, and in the time span that 1 natural surge wouldve happened and another would be ready to go, probably 20x as many surges have already occured.



So for just 50 extra cents a day and the consumption of an oral pill of a legal, readily available compound, you can ABSURDLY modify the pituitary response to CJC-1295 by suppressing Somatostatin. YOUVE BEEN WARNED, this is INSANELY potent, beyond the design of humanity. BE CAREFUL!


Theres 3 common acetylcholineesterase inhibitors, they are;

Pyrostigmine (120mg/ed)
Galantamine (8-16mg/ed)
Huperzine A (50-150mcg/ed)


NOTICE, Huperzine A dosage is in the MICROgrams NOT MILLIgrams. If you took 50mg of Huperzine A you would DIE. I use Huperzine A myself for this. But you can use any of the above, perhaps pyrostigmines better because thats what was proven effective in the clinical studies at that specific dosage. But all three of the above are acetylcholineesterase inhibiors and will thuis have the same inhibitory impact on somatostatin.


This is how, for just an extra 50 cents to a dollar a day, you can turn CJC-1295 into the physiological equivalent of strapping an IV bag of HGH to your back and having a 24 hour drip. As you can imagine this is ABSURDLY POWERFUL and needs great respect and caution when you first begin experimenting. Start with a low CJC-1295 dosage and a low acetylcholineesterase inhibitor dosage, and work from there based on your experiences.


EVERYONE should do this. It gives you FAAAAAAAAAAR more bang for your buck from the CJC-1295, and costs just cents per day to do ontop of CJC-1295 use. Its supported fully by clinical studies, just search for the pyrostigmine/GHRH study.

[Jeff1]

Damn Good reads all of them never tried them.

[RSNUK]

I was going to add something else, but first i will summerise.

In this thread: (http://forums.steroid.com/showthread.php?t=329674)

We learned the following:

The IGF LR3 doses we are using ar 100 - 700 times below the level used in IGF replacement therapy.

Some "steroid researchers" have suggested IGFLR3 may be up to 4 times more potent than regular IGF, which is the only thing which made LR3 cost effective against regular IGF, as regular IGF was approximately twice the price at the time of LR3.

LR3 is not somekind of superdrug, but for those who have reaped the placebo effect of believing so, congratulations, it's time to let go and let the next superdrug move in CJC 1295.

In this thread: (http://forums.steroid.com/showthread.php?t=313311)

We learned:

rHGH is dramatically weaker than CJC 1295, a peptide which enduces the pituitary gland to release supraphysiological levels of natural HGH.

Synthetic recombiant human growth hormone has proven itself through the entirety of it's clinical use, to be nowhere near as effective as a pituitary tumour, for enducing growth.

Do kids who get placed on rHGH become giants? Do they become tall even?

No and No.

In this very thread we can tie together these ideas and the ideas of the poster whom i quoted, to create the future of Growth Hormone based physiological enhancement.

More to come...

[RSNUK]

How do we take this even further than CJC 1295 + Acetylcholinesterase Inhibitors (and general cholinergenic system enhancers)?

The key to enhancing the bodies endogenous functioning is synergy.

This is where we find peptides have a unique possibilities, which offer even greater advantages to not using rHGH and bluntly shutting down internal regulatory processes (for little gain anyway, if HGH is so powerful then why has it failed to create tall stature?)

An increase in HGH or GHRH(Growth hormone releasing hormone), would normally result in an increase of Somatostatin (aka GHIH - Growth hormone inhibiting hormone) as part of the bodies natural tendancy to maintain homeostasis (Internal balence).

Recap: We have Somatocrinnin (GHRP) and we have Somatostatin (GHIH), Crinnin (GHRP) releases, statin (GHIH) inhibits release and CJC 1295 is a long acting GHRP class peptide.

When we use CJC, somatostatin levels rise, which inhibits CJC's effects at the pituitary gland.

As we've covered, one way of inhibiting somatostatins release, is to utilise cholinergenic substances, such as Acetylcarnitine + Choline or Acetylcholinesterase Inhibitors.

(You may have read that acetylcarnitine boosts growth hormone levels, this is because when acetylcarnitine is metabolised, it free's up a acetly molecule for the creation of Acetylcholine which then acts to inhibit GHIH (somatostatin) , which then allows for the release of more growth hormone.)

However there are additional ways that we can inhibit somatostatin and jack our pituitary glands endogenous growth hormone production.

There is one other peptide currently in existance that i think would be of value other than CJC, that is GHRP-6.

More to come...

[RSNUK]

I just noticed that there are BIG things happening on other forums with CJC-1295 and GHRP-6.

This is definitely the future.

I am going to summarise this very quickly and simply.

The key to getting high levels of beneficial effects with HGH, without sides, is the pulsatile release, it's all about the pulsatile release and endogenous GH is far superior to exogenous, by a factor of a Midget to Shaq and Yao.

If you take CJC-1295, you can dose with GHRP-6 as frequnetly as every half an hour, even very small doses will result in godly effects.

You can get high doses of these substances at a fraction the cost of growth hormone therapy.

This is the future, i personally will never you exogenous HGH or IGF ever again.

Good luck everyone.

[NotSmall]

I just noticed that there are BIG things happening on other forums with CJC-1295 and GHRP-6.

This is definitely the future.

Dude I remember when there were "big things" happening with LR3 and MGF.

Don't believe the hype...

[Gear]

Dude I remember when there were "big things" happening with LR3 and MGF.

Don't believe the hype...

-Gear

[Pinnacle]

Dude I remember when there were "big things" happening with LR3 and MGF.

Don't believe the hype...

I'd like for someone to explain to me how one shot can over stimulate the pituitary for 7+ days. This peptide isn't attched to a long esters, right?


By over stimulating the pituitary, exactly how many iu's per day are being pulsed out on this peptide?

[Pinnacle]

If you take CJC-1295, you can dose with GHRP-6 as frequnetly as every half an hour, even very small doses will result in godly effects.

.

LMAO...who the f*ck is going to inject every half hour?

[BITTAPART2]

^^ I do
wake up: 2ml test suspension
30 mins later : 1 ml tren ace
30 mins later : 1ml masteron
30 mins later : 2ml test susp
30 mins later : 1ml NPP
30 mins later : 10iu HGH
30 mins later : 10iu slin
30 mins later : 2 ml test susp.
30 mins later : repeat

I run this cycle for about 3 years then cycle off for 25 minuts with clomid and myogen--x got this protocol from A-rob

[goose]

^^ I do
wake up: 2ml test suspension
30 mins later : 1 ml tren ace
30 mins later : 1ml masteron
30 mins later : 2ml test susp
30 mins later : 1ml NPP
30 mins later : 10iu HGH
30 mins later : 10iu slin
30 mins later : 2 ml test susp.
30 mins later : repeat

I run this cycle for about 3 years then cycle off for 25 minuts with clomid and myogen--x got this protocol from A-rob

WOW that looks a good cycle,its from that amazing A-rob.What an amazing PCT too.What were your gains,and did you pay for this from him?

[Pinnacle]

^^ I do
wake up: 2ml test suspension
30 mins later : 1 ml tren ace
30 mins later : 1ml masteron
30 mins later : 2ml test susp
30 mins later : 1ml NPP
30 mins later : 10iu HGH
30 mins later : 10iu slin
30 mins later : 2 ml test susp.
30 mins later : repeat

I run this cycle for about 3 years then cycle off for 25 minuts with clomid and myogen--x got this protocol from A-rob

The term " P*ssies need not apply" certainly holds merit in your case :-)

[goose]

The term " P*ssies need not apply" certainly holds merit in your case :-)

thanks I understand when I need to use it.Wow that MD radio show this week was super,we must get his book,especially his ideas on saturated fats and red meat.

TO the guy who used A-roberts cycle.Your a *****

[MASTER]

^^ I do
wake up: 2ml test suspension
30 mins later : 1 ml tren ace
30 mins later : 1ml masteron
30 mins later : 2ml test susp
30 mins later : 1ml NPP
30 mins later : 10iu HGH
30 mins later : 10iu slin
30 mins later : 2 ml test susp.
30 mins later : repeat

I run this cycle for about 3 years then cycle off for 25 minuts with clomid and myogen--x got this protocol from A-rob

Lol, but you really shouldn't post stuff like this, some fool may actually try it.

[Pinnacle]

I'd like for someone to explain to me how one shot can over stimulate the pituitary for 7+ days. This peptide isn't attached to a long esters, right?


By over stimulating the pituitary, exactly how many iu's per day are being pulsed out on this peptide?

*Yawns*
Another great copy/paste post created, but yet the author avoids questions......typical..

[Pinnacle]

*Yawns*
Another great copy/paste post created, but yet the author avoids questions......typical..

zzzzzzzzzzzzzzz..huh?..zzzzzzzzzzzzzzzzzzzzzzzzz

zzzzzzzzzzzzzzzzzzzzz..no response yet?..zzzzzzz
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
zzzzzzzzzzzzzzz..wake me "if" he shows..zzzzzzzzzz
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz zz

[Pinnacle]

*Yawns*
Another great copy/paste post created, but yet the author avoids questions......typical..

yea, I know

[Dukkit]

hmmm, interesting.

[Pinnacle]

hmmm, interesting.

After 11 days he still hasn't responded back. I DO find that interesting!

[goose]

*Yawns*
Another great copy/paste post created, but yet the author avoids questions......typical..

I know

What a board people who dont reply and half this board gay/bi

[NotSmall]

I know

What a board people who dont reply and half this board gay/bi

[danimality]

i know nothing about peptides or cjc-1295 but i read rsnuk's posts and couldn't help but be more interested. so i did some googling and here is what i found on another board.

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


Restoring Growth Hormone

"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)

"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 of 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 of 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 resulted in a 2 to10-fold increase in mean serum GH levels in all dosing groups, which was dose incremental and persisted for up to 7 days. Similarly, a dose-related increase in mean serum IGF-I levels was observed at all dose levels, ranging from 1.5- to 3-fold and persisting for up to 14 days. (29)

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:

1 - Hadden JW, Malec PH, Coto J, Hadden EM 1992 Thymic involution in aging. Prospects for correction. Ann NY Acad Sci 673: 231–239

2 - Mackall CL, Gress RE 1997 Thymic aging and T-cell regeneration. Immunol Rev 160:91–102

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

5 - Martignoni E, Costa A, Sinforiani E, Liuzzi A, Chiodini P, MauriM, Bono G, Nappi G 1992 The brain as a target for adrenocortical steroids: cognitive implications. Psychoneuroendocrinology 17: 343–354

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

7 - Sapolsky R, Armanini M, Packan D, TombaughG1987 Stress and glucocorticoids in aging. Endocrinol Metab Clin North Am 16:965– 980

8 - Heffelfinger AK, Newcomer JW 2001 Glucocorticoid effects on memory function over the human life span. Dev Psychopathol 13:491–513

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.

13 - Rudman D, Kutner MH, Rogers CM, Lubin MF, Fleming GA, Bain RP. Impaired growth hormone secretion in the adult population: relation to age and adiposity. J Clin Invest 1981; 67:1361-9.

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.

[danimality]

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


Growth Hormone Secretagogues


In the 1980's three classes of compounds where studied to determine their effect on growth hormone release. These three compounds were:

Growth Hormone Releasing Hormone (natural hormone)
Growth Hormone Releasing Peptides (synthetic molecules often termed "GH-Secretagogues")
Opiates (Dermorphin & Benzomorphan)

Individually each class of compound when administered in laboratory rats was found to induce growth hormone release. However when they were all combined growth hormone release dramatically increased.

Growth Hormone Releasing Hormone (GHRH) + Growth Hormone Releasing Peptide (GHRP) was found to induce a large synergistic secretion of growth hormone (GH).

However when the Opiate was combined with GHRH & GHRP the synergy was huge amounting to a release of GH more than double that achieved by the GHRH/GHRP combo alone.

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When all three classes of compounds were examined it was discovered that each compound released GH by a mechanism different and distinct from that of the others. Furthermore it was found that these three modes of action accomplished growth hormone release in ways complementing and not interfering with each other.

Unfortunately opiates have several drawbacks. Not withstanding their illegality chronic use is both toxic and addicting with undesirable alterations in normal physiology.

Fortunately we are left with two tools with which we can maximize a synergistic release of growth hormone. These tools have no toxicity and promote desirable alterations in normal physiology.

Growth Hormone Releasing Hormone (GHRH) in the form of its long-lasting analog (CJC-1295) was discussed in the previous article. It is therefore left to this article to discuss Growth Hormone Releasing Peptides (GHRPs) and the human studies that demonstrate synergy between these two compounds (GHRP + GHRH).

NOTE: The information presented in this section was drawn generally from Refs: 1-11


Growth Hormone Releasing Peptides (GHRPs) - A Quick Look

What are they?

Growth Hormone Releasing Peptides (GHRPs) are synthetic forms of the natural hormone Ghrelin. These simple short-chained amino acid peptide strings possess most of the positive characteristics of Ghrelin (such as effecting GH secretion) and few of the negative properties (such as Ghrelin's lipogenic behavior (i.e. conversion of glucose to fatty acids)).

GHRPs belong to a broader class of compounds all of which share the common trait of being able to bind to the Growth Hormone Secretagogue Receptor (GHS-R) and effect GH release. These compounds include the synthetic peptides (GHRP-6, GHRP-1, GHRP-2, Hexarelin, Ipamorelin) and smaller synthetic non-peptide molecular compounds such as MK-0677 as well as the natural ligand Ghrelin. This broad class which includes all of the above but not Growth Hormone Releasing Hormone (GHRH) is termed Growth Hormone Secretagogues (GHSs).

These Growth Hormone Secretagogues (GHSs) exert their effect on increasing GH output in multiple ways.

First they INDIRECTLY increase growth hormone (GH) secretion by inducing Growth Hormone Releasing Hormone (GHRH) release from the hypothalamus in the brain. GHRH once released makes its way to the Growth Hormone Releasing Hormone Receptors (GHRH-R) in cells within the pituitary (a gland just below the brain) where it binds and exerts its direct influence in signaling GH release.

Second these GHS also make there way to those same pituitary cells where they themselves bind to a Growth Hormone Secretagogue Receptor (GHS-R) and exert a DIRECT influence in signaling GH release. This signaling uses a different mode of action distinct from that of GHRH. As a consequence both bound GHRH & bound GHS can exert their positive influence concurrently resulting in synergistic growth hormone (GH) release.

Third they INDIRECTLY increase GH secretion by reducing release of Somatostatin (the GH inhibiting hormone) from the hypothalamus and DIRECTLY by reducing the magnitude of Somatostatin's inhibiting action once it binds to its receptor on the pituitary cells.

In essence Growth Hormone Secretagogues (GHS) turn up the positive signal to release GHRH, turn down the negative signal to release the inhibiting hormone Somatostatin, speak directly to the growth hormone releasing pituitary cells themselves to encourage them to release GH and speak directly to the growth hormone releasing pituitary cells themselves to encourage them to ignore Somatostatin's message to stop releasing GH.

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Oral GHS

Based on the effectiveness of GHRPs smaller non-peptide molecules were created in an effort to mimic the GH releasing effects of GHRPs with the desire to develop a compound with high oral bioavailability. As a result MK-0677 was eventually created as a non-peptide compound with sustained GH release and higher oral bioavailability. Unfortunately desensitization was found to occur fairly rapidly. In addition the dose for the orally administered MK-0677 is measured in several milligrams while the effective dose for the injectable GHRPs is measured in micrograms making GHRPs more cost effective. Research is ongoing on non-peptide GHSs, particularly with Ipamorelin derivatives so perhaps an oral GHS devoid of desensitization will eventually be developed.

My own thought is that these molecular compounds appear to be small enough to be used in a transdermal formula. Also it would be nice to have these orally/transdermally active compounds available to use on a limited basis perhaps making usage when traveling convenient.

NOTE: The information presented in this section was drawn generally from Ref: 12

Growth Hormone Releasing Peptides - A Longer Look

What are they?

In 1980 the first highly potent GH-Releasing peptide was developed and named GHRP-6. This peptide was found to illicit a strong GH release response and so became the first member of a class of growth hormone releasing peptides more broadly called GH secretagogues. Structurally GHRP-6 is composed of the amino acids L-Histidine, D-Tryptophan, L-Alanine, L-Tryptophan, D-Phenylalanine and L-Lysine. The "L" form of an amino acid is the naturally occurring form and often in the nomenclature the "L" is dropped. The "D" form does not occur in nature and is the isomeric form (i.e. mirror image) of the naturally occurring "L" form.

GHRP-6 is composed of both natural and isomeric forms of those aforementioned six amino acids. Its structure is represented as:

His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Investigators subsequently modified the structure of GHRP-6 and identified more potent peptides. For example, activity was enhanced by replacing D-Trp with D-2-(2-napthyl)alanine and His with D-Alanine to create GHRP-2 whose structure is represented as:

D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2

In 1982, after a long search the natural hormone "Growth Hormone Releasing Hormone" (GHRH) was finally isolated and identified. As a result the interest in Growth Hormone Secretagogues (at that point limited to the three peptides) faded. Eventually researchers discovered that those GH-Releasing Peptides (specifically GHRP-6 & GHRP-2) followed a mode of action which bound them to and was mediated through receptors different from those for GHRH. In addition researches discovered that these GH-Releasing Peptides acted synergistically with the natural hormone Growth Hormone Releasing Hormone (GHRH) in vivo (in both laboratory animals & humans) to produce large releases of Growth Hormone.

Taken together these two discoveries made it clear that GHRPs were not simply surrogates of GHRH. GHRP-6 and its analogues were artificial activators of a separate newly discovered receptor termed the "Growth Hormone Secretagogue Receptor" (GHS-R). Eventually the natural hormone Ghrelin was discovered as the endogenous ligand that binds to the GHS-R. Together the natural hormone Ghrelin, and all the synthetic compounds (both peptides & smaller molecules) such as GHRP-6 were termed "Growth Hormone Secretagogues" (GHSs).

This nomenclature continues in the literature to this day however increasingly new terminology is used. For instance the "Ghrelin Receptor" is synonymous with "GHS-R" and "Ghrelin mimetics" are synonymous with all the synthetic compounds that are capable of binding to the GHS-R. This paper uses the more established nomenclature throughout.

NOTE: The information presented in this section was drawn generally from Refs: All of the Bower's studies

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Pituitary Actions of GHSs

All GHSs act directly on the pituitary. They do so by binding to and activating their specific receptor (GHS-R). Once this occurs GH secretion is commanded to rise. GHRH does the same thing. It acts directly on the pituitary and binds to and activates its specific receptor (GHRH-R). Once this occurs GH secretion is commanded to rise.

However GHSs and GHRH operate through a different "mode of action" or intracellular signaling system within the cell that eventually activates GH secretion. These modes of action are contrasted as follows.

GHRH when it binds to its receptor (GHRH-R) on the cellular membrane of a somatotrope cell activates the cAMP–PKA (cAMP-dependent protein kinase) pathway (in essence a secondary messenger), and by a poorly understood mechanism causes a persistent rise in intracellular Calcium (Ca2+) ions by opening Ca2+ channels (simply ports on the cell membrane that open and close to either permit or deny entry) on the cellular membrane and letting into the cell Ca2+ from the outside. The rise in calcium concentration within the cell signals in conjunction with other signaling processes the instruction to the somatotrope cell to release Growth Hormone.

It should be noted that Somatostatin (the GH inhibiting hormone) once bound to its receptor brings about a decrease in GH in part by inhibiting cAMP formation. As a consequence of limiting this messenger the signaling cascade is weakened resulting in less Calcium (Ca2+) ions entering the cell and thus inhibition of GH release.

GHSs however do not rely on cAMP as a messenger. GHSs once bound to their respective receptor initiate a process that leads to an inhibition of Potassium (K+) ion channels. This action results in a sustained depolarization of the cellular membrane. The result is identical to that affected by GHRH, namely the Calcium ion level rises via voltage-activated channels leading to the signal to secrete GH. But the mode of action relies on the use of depolarization of the cellular membrane and inhibiting Potassium ion channels rather then GHRH's cAMP-mediated opening of Calcium ion channels.

In addition to allowing Ca2+ into the cell, GHSs may also cause a rise in intracellular Ca2+ by redistribution from internal stores of Ca2+ within the cell. This process is mediated by the generation of inositol trisphosphate whose main functions are to mobilize Ca2+ from storage organelles and to regulate cell proliferation.

This brief description is an over simplification. The important point is that GHRH and GHS act through their own receptors and distinct intermediate pathways.

This is not the only difference. Although the image herein depicts one pituitary somatotrope with both types of receptors activated (GHRH-R & GHS-R) this may not give a completely accurate picture. GHRH and GHS appear to act on different somatotrope subpopulations. GHRP has been shown to increase the number of somatotropes releasing GH, without altering the amount of hormone released by each individual cell. On the other hand, GHRH stimulates both the number of cells secreting GH and the amount of GH secreted per cell.

From these limited discoveries we can begin to understand how GHRH and GHSs compliment each other's GH releasing actions rather then duplicate one another.

It should be noted that Somatostatin (the GH inhibiting hormone) has been shown primarily to decrease the number of cells secreting GH without affecting the amount of GH secreted per cell.

To sum up in very general terms GHS increases, while Somatostatin decreases, the number of active GH secreting somatotropes, probably because these two factors act by depolarizing and hyperpolarizing cells, respectively (i.e. GHSs turns the cell into a Calcium ion sponge & Somatostatin turns the cell into a squeegee, squeezing out and repelling Calcium ions).

On the other hand GHRH does both, but acts primarily by stimulating the amount of secreted GH within the active somatotropes.

NOTE: The information presented in this section was drawn generally from Refs: 13-17


Hypothalamic Actions of GHS

In vitro (in a laboratory dish) the amount of GH release from GHRH and GHSs is additive. GHSs cause a rise of 2...GHRH causes a rise of 1...put them together and the GH rise is merely the sum 3.

But something different happens when you put these two compounds into living breathing mammals. In vivo (in body) the GH rise that occurs from the combination of GHRH and GHSs is more then the sum of their individual contributions. There is substantial synergy such that 1 + 2 = 6.

This occurs as a result of GHSs actions within the Hypothalamus (region of the brain) rather then its direct pituitary actions. There are GHS receptors (GHS-R) in the hypothalamus; perhaps even subtype receptors. When GHSs bind to these receptors they behave like a hypothalamic neurohormone and as such exhibit a dual action.

They stimulate endogenous GHRH release and concurrently suppress endogenous Somatostatin release. How they do this is a complex process with much still unknown. Basically they incite electrical activation of arcuate neurons (within the hypothalamus). About seventy-five percent of the cells excited by GHRP-6 project outside the blood brain barrier (hypothalamus) into the median eminence (boundary between hypothalamus & the portal system which connects to the pituitary which lies just below the brain) and are neurosecretory involved in the regulation of pituitary function.

The activation of these neurons by GHRP-6 is extremely long lasting (longer than 1 hour) and reaches the peak rapidly (within 5 to 10 minutes). Non-peptide GHSs respond slower perhaps for the reason that they penetrate the blood brain barrier slower than GHRP-6.

GHRP-6s excitation of neuronal activity beyond those neurons that regulate GHRH & Somatostatin (i.e. the remaining 25%) may account for some of the impact GHRPs have on non-GH releasing activity.

The important point is to recognize that GHSs have an impact on GHRH release and Somatostatin suppression at the hypothalamus which appears to be responsible for the now well-recognized synergistic effect on GH release from concurrent administration of GHRH & GHRPs in vivo.

Furthermore it should now be firmly understood that GH release is regulated by the following trinity - GHRH, Somatostatin and GHSs.

NOTE: The information presented in this section was drawn generally from Refs: 13-5, 9, 18

[danimality]

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

GHS Potency (i.e. efficacy) & Dosing in Humans

When administered at clinical research dosages, all GHSs (both peptides and non-peptides) release significantly larger amounts of GH (i.e. are more efficacious) than GHRH. This is not to be confused with the term potency which takes into account the molecular weight of a compound and thus measures GH output on a "per mol" basis. By this measure GHRH is more potent.

However if the desire is to administer these compounds and effect GH release then the only relevant standard is absolute amount of GH release and in that regard GHSs release more GH than GHRH. The following standards determined through clinical study will specifically clarify this concept.

In humans the maximal i.v. dose for GHRH has been found to be 1 mcg per kg of bodyweight. That is a level that saturates the receptors and beyond which there is no further benefit, until that dosage has dissipated.

In humans the maximal i.v. dose for GHSs such as hexarelin has been found to be 2 to 3 mcg per kg of bodyweight. In normal humans (i.e. those without disease or clinical malady) GH release is increased as the GHS dose increases up to the aforementioned maximal dose. Even very small amounts have been shown to have positive effects.

Unlike GHRH, GHSs are resistant to well-known inhibitors of GH secretion. Studies demonstrate that hexarelin-mediated GH secretion is reduced but not blocked by a rise in circulating free fatty acids or by a glucose load, nor by an infusion of Somatostatin nor drugs that enhance hypothalamic Somatostatin secretion.

GHRH is influenced by metabolic and hormonal factors that consequently make GHRH a very unpredictable GH stimulator, with large variations between individuals and a diversity of peaking times.

In contrast GHSs are not greatly influenced by metabolic and hormonal factors, the absence of which makes GHSs a very predictable GH stimulator. GHSs are potent and efficacious, their actions synchronized and reproducible, with no non-responders.

GHSs have been repeatedly demonstrated in studies to be very strong GH releasers in healthy young males. In addition GHSs have been shown in studies to be very strong GH releasers in females at all stages of the menstrual cycle. This again is important to note because GHSs are not greatly affected by changes in various hormone levels, be they thyroid hormone, estrogen, etc.

There may be an age-related reduction in the GH-releasing capability of GHSs. The studies have not yet been able to come to a consensus. However, the synergistic effect of GHRH and GHS on GH secretion is not reduced as humans age throughout the entire lifespan. This holds true even for the very old (Those in their 90's).

There are no reported side-effects with GHS usage. However both the peptidyl and non-peptidyl compounds have been found to induce slight increases (still within what is deemed the normal range) in prolactin and in adrenocorticotrophin(ACTH)/cortisol, and in a few studies dehydroepiandrosterone (DHEA). Low to moderate dose (1 mcg/kg) administration of GHRP-6 has been found to result in very large GH release with no significant effects on cortisol or prolactin. Of the peptides, Hexarelin appears to induce the highest level of these hormones (prolactin & cortisol). Ipamorelin a newer GHS has no effect on these hormones no matter what the dose.


NOTE: The information presented in this section was drawn generally from Refs: 19-31


Why you need both GHRH analog (CJC-1295) and GHRP

GHS Down Regulation

A single dose of a GHS in vivo brings about an immediate down-regulation of responsiveness to subsequent administration. This desensitization appears to abate and sensitivity fully restored within a few hours.

However continual infusion of large amounts of GHS brings about a substantial initial release of GH, followed, after several hours, by long-term down-regulation of GH secretion.

The only published comparison of the results of differing modes of GHS delivery (twice daily injections vs. continuous infusion) in vivo demonstrated a dramatic dissipation of anabolism following infusions of high-dose GHS. However a pronounced anabolic effect was maintained with the same dose of GHS administered by intermittent injection.

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From the results of this study graphed out above it is evident that with GHSs the optimal dosing pattern is administration by injection with sufficient intervals between dosing so as to maintain sensitivity.

The effectiveness is greatly diminished, perhaps to the point of having no benefit if GHSs duration of action becomes prolonged and sustained. GHSs unlike GHRH are best used to amplify those very import GH pulses while GHRH is effective at raising the total level of GH.

If we understand desensitization than we will easily understand why the oral GHS, MK-0677 in recent studies failed to demonstrate a "maintained acceleration of statural growth in children with GH-deficiency". MK-0677 was developed to be a long lasting orally active analogue of GHRP-6. MK-0677 is to GHRP-6 what CJC-1295 is to GHRH (i.e. long-lasting).

The problem is that while long-lasting analogues of GHRH do not result in desensitization and pronounced down-regulation, long-lasting analogues of GHRP-6 do desensitize and consequently lose effectiveness.

CJC-1295 brings about persistent and chronically elevated levels of GH while GHRP-6 if injected a couple of times a day amplifies the very important GH pulses. The two compounds greatly compliment each other. In the previous article on GHRH & CJC-1295 we discussed the importance of pulsation which has been shown to be necessary for growth. The other important component of anabolism is chronic GH elevation.

Continuously elevated levels of GH increase IGF-I levels more than intermittent increases in GH. The intermittent nature of GH release brought on by GHSs' mode of action does create a rise in IGF-I levels but the anabolic effect may not be pronounced.

It has been repeatedly demonstrated and is now recognized that in children the growth response to injections of IGF-I is far less than the growth response to injections of GH. This is in accordance with most animal studies, which demonstrate that treatment with IGF-I does "not produce the full anabolic and growth-promoting effects of GH treatment".

Protocols that elevate GH while maintaining and amplifying the pulses seem to be effective at producing anabolism. The combination of CJC-1295 and GHRP-6 do just that.

NOTE: The information presented in this section was drawn generally from Refs: 32-37


GHRH (and analogs) + GHSs = a lot of synergistic growth hormone release

There is not a lot of deviation in the published studies on the effect of these peptides and the saturation dose needed to bring about the effect in normal people (who often act as a control group).

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We need only to examine the results of the normal test subjects from three oft-cited studies that established the relevant protocol.

In the first study "Inhibition of growth hormone release after the combined administration of GHRH and GHRP-6 in patients with Cushing's syndrome", Alfonso Leal-Cerro..., Clinical Endocrinology 1994, 41 (5) , 649–654, three different peptide/peptide combinations were used.

GHRH was administered alone at 100mcg. This resulted in area under the curve (AUC) measured for 120 minutes of GH secretion of 1420 ± 330.

GHRP-6 was administered alone at 100mcg. This resulted in area under the curve (AUC) measured for 120 minutes of GH secretion of 2278 ± 290.

GHRH plus GHRP-6 was administered together at 100mcg each. This resulted in area under the curve (AUC) measured for 120 minutes of GH secretion of 7332 ± 592.

As a single dose these results show that GHRP-6 is about twice as effective as GHRH.

The synergy between GHRH & GHRP-6 is clearly evident as co-administration resulted in twice the benefit of the additive values of single doses of the two peptides.

The second study is the one that established the saturation dose for these peptides often used in other studies. "Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone ", CY Bowers..., J. Clin. Endocrinol. Metab., Apr 1990; 70: 975-982.

In that study GHRH at a dose of 1.0 microgram/kg was administered alone and then together with various doses of GHRP-6 (0.1, 0.3, and 1.0 microgram/kg). They found that the submaximal dosages of 0.1 and 0.3 microgram/kg GHRP-6 plus 1 microgram/kg GHRH did have the effect of stimulating GH release synergistically.

However the larger dose of 1 mcg/kg of GHRP-6 was found to be the saturation dose when used in combination w/ 1 mcg/kg of GHRH.

It is also noteworthy that serum prolactin and cortisol levels rose about 2-fold above base levels only at the 1 microgram/kg dose of GHRP-6 and not at the submaximal dosages.

The final study, "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", Micic D..., J Clin Endocrinol Metab. 1998 Jul;83(7):2569-72 is fascinating for several reasons.

By reference to citation it is noted that "GHRH plus GHRP-6 (both at saturating dose) is nowadays considered the most potent stimulus of GH secretion in man being able to restore the GH secretion in states associated with chronic blockade of somatotroph activity (as in obesity)...it elicits a near-normal GH discharge in obesity, in patients with hypothyroidism and in patients with type 2 diabetes mellitus."

This particular study examined the effects of combined administration of GHRH, immediately followed by GHRP-6 in a group of very old subjects (age higher than 75 yr), as compared with both normal adults (less than 40 yr) and aged subjects (age 46–65 yr). The dosing levels used were 90mcg of GHRH followed by 1mcg/kg of GHRP-6.

All the subjects had a positive GH secretory response to the combined administration with no differences observed between men and women. However the group comprising the very old had the highest level of GH release followed by the group comprising the aged subjects with the "less than 40 yr group" experiencing a substantial rise but not as high as the other two groups.

The study concluded 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."

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In CONCLUSION, Growth Hormone (GH) is regulated by a trinity composed of Growth Hormone Releasing Hormone (GHRH), Growth Hormone Secretagogues (GHS) and Somatostatin. GHRH and GHSs individually have a positive impact on GH secretion. These two compounds operate through distinct modes of action which complement each other and when administered together result in synergistic GH secretion.

Growth Hormone Releasing Peptides (GHRPs), a subclass of GHSs are effective across all age groups in amplifying GH pulses. Pulsation is a necessary component of growth generation in mammals. GHRH when co-administered with GHRPs has the effect of further increasing the amplitude and "area under the curve" of a GH pulse. The result is a GH pulse many multiples more effective then that achieved by an unaided GH pulse.

In addition to pulsation, overall growth is better accomplished when total levels of GH are elevated without hindering pulsation. Elevated GH levels appear to be a necessary component of growth generation as well. One of the reasons this is so appears to be that chronically elevated GH levels result in more pronounced sustained levels of IGF-1 then that achieved through intermittent GH elevations.

Persistent levels of GHRH do not result in desensitization. Elevated levels of GHRH result in sustained GH release. A long-lasting version of GHRH, CJC-1295 has demonstrated the ability to sustain elevated GH levels in humans.

GHRP-6 is perhaps the most well studied of all GHSs. In physiological doses there are virtually no side effects. It has been demonstrated to be effective for all age groups.

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Combined administration of CJC-1295 and GHRP-6 is a very effective, well studied method of increasing the total amount of GH secreted within the body. By adjusting the dosing of these compounds and accounting for such factors as age one may choose to achieve a "youthful" restoration, an above normal elevation or a substantially above normal elevation of both GH levels and pulsatile release.

[danimality]

this was someone's response to the posts above.

GHRH actually is found in two forms a 44 and a 40 amino acid chain. The reason the half-life is so short is that the first 3 amino acids are rapidly cleaved off in plasma leaving 4-40 or 4-44 intact.

But it appears that the loss of those 3 aminos is enough to deactivate the GH releasing ability of GHRH.

So analogs were created to keep the full amino acid chain intact for longer periods of time. Some added aminos, some substituted aminos less prone to enzyme deactivation, even pegylation was used. All methods increased the half-life, some by several hours.

The reason that it was important to try to extend the duration of GHRH is that the drug manufacturers would use it to treat people with GH defects. A lot of these defects mean a mutated ability to release active GHRH sufficiently so these types of patients NEEDED to have externally administered GHRH circulating 24 hours a day.

These types of patients could benefit from dosing non-analog GHRH five or more times a day to support 5 or so GH pulses but that is far from optimal for them and inconvenient as well.

So that was the reason that the GHRH analog that binds to endogenous albumin was created.

There are a lot of studies where plain GHRH is administered by itself and in conjunction with a Growth Hormone Secretagogue such as GHRP-6 and there is benefit. You see when you administer GHRP-6 (or its siblings Hex, GHRP-1, GHRP-2, Ipamorelin) you reset pulsation. The GHRPs create a pulse (especially in older people whose + - signaling is diminished) but it needs GHRH to be effective. Normal people have GHRH naturally present BUT if you add GHRH at the moment you add GHRP-6 the eventual GH pulse is a lot larger and lasts longer.

Now older people more than younger people seem to benefit from GHRP-6 alone BECAUSE it amplifies the + signal (GHRH) & decreases the - signal (sst) and returns this signaling to youthful levels. Thats probably why I benefit greatly from GHRP-6 alone and other younger guys don't. That's probably why I snapped at Sol... I was in the process of discovering that I was an "old guy"

CJC-1295 was tested in humans because it will probably eventually become a prescription drug to treat truly GH deficient patients. It flat out works in normal people, in younger people and even older people. From anecdotal evidence it appears that the CJC-1295 can get you into what is termed a pharmacological GH level. So for bodybuilding purposes it should work well. Then there is the added benefit of adding GHRPs to get further into high GH levels.

The dosing is interesting. I see a lot of misinformation on the internet forums. I saw one "guide" posted somewhere that made reference to a 2006 study: "Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse"

This study found greater benefit in dosing CJC-1295 daily rather than E3D so the author of the bodybuilding forum "guide" wrote that daily dosing was better for bodybuilders. The PROBLEM is that the study he referenced tested CJC-1295 in mice whose albumin half-life is 1 day. So obviously if CJC-1295 binds to albumin and it is gone in a day then CJC-1295 must fend for itself there after and it degrades fairly quickly without that stability bond. In humans albumin I believe has a half-life of 19 or so days so you see that study tells us nothing directly about how to dose in humans.

Theoretically CJC-1295 could be stable for 19 days due to albumin's half-life BUT from this study:

"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"

we learn that even when CJC-1295 is bound to albumin it degrades to 90% within 24 hours. That degradation rate reduces the amount of active CJC-1295 to 50% (or half the initial dose) within 7 days. So obviously in humans albumin's long half-life greatly exceeds the life of a single CJC-1295 dose. Three days post dosing reveals that 72% of CJC-1295 remains while 65% remains four days post dosing. Thats why twice a week dosing is more effective then once a week dosing.

But how much needs to be taken at each dose? The CJC-1295 study on humans indicates that the dose needs to be fairly high.

To get a positive effect I suspect it doesn't need to be that high IF GHRP-6 is used concurrently and you aren't going for maximal GH release. The non-analog GHRH studies all used 100mcg of GHRH with 100mcg of GHRP-6 (or sometimes 1mcg/kg) and created substantial above normal GH pulses.

So my one man experiment (or I should say my one "old" man experiment) at the moment is to dose 100mcg of CJC-1295 + 100mcg of GHRP-6 before bed and then 100mcg of GHRP-6 in the morning and 200mcg of GHRP-6 PWO. So far (just a few days) I can report that my sleep is deeper & longer than w/ GHRP-6 alone.

[danimality]

can any cjc-1295 or ghrp-6 users chime in on this topic? is this the route to go?

[goose]

*yawns*

I know.

[Dukkit]

still interesting. lots of info, no first hand users though.

[goose]

still interesting. lots of info, no first hand users though.

For you homie....

http://forum.lef.org/default.aspx?f=36&m=38937


P USSYS NEED NOT APPLY!!!!!

[Dukkit]

For you homie....

http://forum.lef.org/default.aspx?f=36&m=38937


P USSYS NEED NOT APPLY!!!!!

thank you my good man!!

[RuhlFreak55]

good god someone just tell me how much i ****ing need to inject already1!!!!!!!!!!!!!!!!!!!!!!!!!

[Pinnacle]

C*ckfreak55 has practically injected everything in his *ss from spike laden dildo's, to penis's from donkey carcasses. It's a given he'd experiment with this as well :-)

[NotSmall]

C*ckfreak55 has practically injected everything in his *ss from spike laden dildo's, to penis's from donkey carcasses. It's a given he'd experiment with this as well :-)

Very rarely do I ever actually "laugh out loud" when online, that did it though!

[Dukkit]

good god someone just tell me how much i ****ing need to inject already1!!!!!!!!!!!!!!!!!!!!!!!!!

haha. poor ruhl.

[RuhlFreak55]

C*ckfreak55 has practically injected everything in his *ss from spike laden dildo's, to penis's from donkey carcasses. It's a given he'd experiment with this as well :-)

have i mentioned lately i don't like you?

[Pinnacle]

have i mentioned lately i don't like you?

No C*ckfreak55, but I get all warm and bubbly when you do.

So what's your boy friend going to shove up your arse this evening? Please, do tell. You didn't have a problem in the past on other boards.

I really loved the one where you had an enchilada wrapped in pickle sauce shoved up your arse til you couldn't cum anymore, all the while your boy friend had you ball gagged, and was beating you relentlessly with barbed wire.

How long was that thread? 30 pages?

[Dukkit]

hehe