What Are GHRPs (Tesa/Cjc/Serm/Ipa) Actually Trying to Achieve?

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faloppi

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On forums I constantly run into posts about these compounds, and all too often two things stand out: the importance of baseline igf1/zscore testing gets overlooked, and people seem unclear on what the RS is even hoping to get out of them (I was in that same spot once and wanted to try them just for the sake of trying, honestly!).

The attachment I put together is meant to illustrate which measurable changes MAY be within reach (based on online data Claude was able to locate). I'm sure it's far from perfect. Nothing in it was vetted by me, and there are certainly errors, studies I missed, and so on, plus some of the studies that do exist are fairly small. I'm aware that AI chats can sometimes do more harm than good. Still, my aim was to give newer researchers a way to think about what GHRPs can realistically do or help with. Each person should do their own research to decide whether it's worth the time and effort (along with pros/cons/benefits/risks), but hopefully this at least gets some thinking started.

I asked Claude to review the studies/trials/data available for GHRPs and HGH, looking at visceral fat changes, subq fat, ifg-1 levels, and lean mass, and to see what takeaways could be drawn. I did not ask it to weigh any risks/side effects. Naturally, researchers should also spend time looking into that and work it into their analysis/decision making.
 
faloppi said:

On forums I constantly run into posts about these compounds, and all too often two things stand out: the importance of baseline igf1/zscore testing gets overlooked, and people seem unclear on what the RS is even hoping to get out of them (I was in that same spot once and wanted to try them just for the sake of trying, honestly!).

The attachment I put together is meant to illustrate which measurable changes MAY be within reach (based on online data Claude was able to locate). I'm sure it's far from perfect. Nothing in it was vetted by me, and there are certainly errors, studies I missed, and so on, plus some of the studies that do exist are fairly small. I'm aware that AI chats can sometimes do more harm than good. Still, my aim was to give newer researchers a way to think about what GHRPs can realistically do or help with. Each person should do their own research to decide whether it's worth the time and effort (along with pros/cons/benefits/risks), but hopefully this at least gets some thinking started.

I asked Claude to review the studies/trials/data available for GHRPs and HGH, looking at visceral fat changes, subq fat, ifg-1 levels, and lean mass, and to see what takeaways could be drawn. I did not ask it to weigh any risks/side effects. Naturally, researchers should also spend time looking into that and work it into their analysis/decision making.
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The study doesn't provide the igf-1 elevation seen with hgh. Since I've pushed my igf-1 past 330 and my Z-score above 2.0 using only tesamorelin, I'm wondering whether the fat reduction comes straight from the igf-1 rise, or whether HGH contributes to fat loss through mechanisms beyond just lifting igf-1 — and whether moving to hgh would offer me anything extra. It definitely backs up tesa?cjc/ipa, which lines up with what I'd been thinking about trying both.

Great info! appreciate it!
 
dpo08 said:

faloppi said:

On forums I constantly run into posts about these compounds, and all too often two things stand out: the importance of baseline igf1/zscore testing gets overlooked, and people seem unclear on what the RS is even hoping to get out of them (I was in that same spot once and wanted to try them just for the sake of trying, honestly!).

The attachment I put together is meant to illustrate which measurable changes MAY be within reach (based on online data Claude was able to locate). I'm sure it's far from perfect. Nothing in it was vetted by me, and there are certainly errors, studies I missed, and so on, plus some of the studies that do exist are fairly small. I'm aware that AI chats can sometimes do more harm than good. Still, my aim was to give newer researchers a way to think about what GHRPs can realistically do or help with. Each person should do their own research to decide whether it's worth the time and effort (along with pros/cons/benefits/risks), but hopefully this at least gets some thinking started.

I asked Claude to review the studies/trials/data available for GHRPs and HGH, looking at visceral fat changes, subq fat, ifg-1 levels, and lean mass, and to see what takeaways could be drawn. I did not ask it to weigh any risks/side effects. Naturally, researchers should also spend time looking into that and work it into their analysis/decision making.
Click to expand...
The study doesn't provide the igf-1 elevation seen with hgh. Since I've pushed my igf-1 past 330 and my Z-score above 2.0 using only tesamorelin, I'm wondering whether the fat reduction comes straight from the igf-1 rise, or whether HGH contributes to fat loss through mechanisms beyond just lifting igf-1 — and whether moving to hgh would offer me anything extra. It definitely backs up tesa?cjc/ipa, which lines up with what I'd been thinking about trying both.

Great info! appreciate it!
Click to expand...
For most of the HGH studies, the summary does indicate a rise in igf-1, though it lacked precise numbers. One thing absent from the file, which comes from my own research, is this: Tesa produces a gh SPIKE large enough to drive visceral fat reduction, yet it does not sustain the steady GH elevation that HGH provides, which is what's needed for fat loss at the subq level. Fat surrounding organs carries different receptors and responds more strongly to GH spikes, which explains why Tesa works there, while having no meaningful effect on other fat (and based on what we know about tesa, neither does cjc). Compared with Tesa/Cjc/Ipa, HGH also appears to have more data backing increased lean mass. So the question becomes: what are you trying to target/accomplish with your protocol?
 
One more key point about Tesa in particular: a 50-person study arm tracked results after participants stopped, and by 13 weeks most had regained a large share of the visceral fat they had lost, while by 26 weeks they had returned to their pre-treatment baseline. If avoiding giving back the benefits matters to you, most people are more inclined to stay on HGH long-term rather than Tesa.
 
faloppi said:


The summary does show increased igf-1 for most of the HGH studies, but didn't have exact figures. What isn't in the file that I have gathered from my own research, is Tesa creates enough of a gh SPIKE that it triggers visceral fat reduction, but it doesn't create the constant increase of GH that HGH does that is required to promote fat loss at the subq level. The fat around organs has different receptors and is more sensitive to spikes in GH so that's why Tesa is effective there, but has no meaningful impact on other fat (nor does cjc based on what we know about tesa). HGH also seems to have more data supporting increased lean mass versus Tesa/Cjc/Ipa. So the question is, what are you trying to target/accomplish with your protocol?

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The goal is fat loss along with muscle gain. What dose of HGH was used here, and over what length of time?
 
dpo08 said:


Burn fat and build muscle. What was the dosage of HGH for this? and how long was the period?

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Is the target visceral fat, or subcutaneous fat? Based on this data and on what I've come across in other places, HGH should outperform Tesa when it comes to subq fat and to adding lean mass (though naturally each option comes with its own tradeoffs and things to weigh). A number of different HGH studies were cited, and whether they were the ideal ones to lean on is unclear to me (that choice came from Claude), but 2 involved HIV patients over 12 weeks, while 1 ran 9 months in non-HIV subjects and another ran 6 months in non-HIV subjects. In both HIV studies the dose was 4mg/day (which is a lot), whereas the others sat around 1mg/day. That said, judging by what the data pulled actually supports — this is in no way my recommendation — my reading is this: if subq fat reduction is the subject (and even then it's still nowhere close to a GLP in effectiveness), along with encouraging additional muscle growth, then HGH, dosed at the right IU to keep your z score elevated while staying below +2.0 for long-term safety, would be the most likely to move you toward your goals (compared with Tesa or other GHRPs, and assuming you're set on raising your GH/IGF through supplementation rather than through other routes to your goals (glp, training, diet, etc., which I realize you might still be folding into your wider plan)).
 
faloppi said:

One more key point about Tesa in particular: a 50-person study arm tracked results after participants stopped, and by 13 weeks most had regained a large share of the visceral fat they had lost, while by 26 weeks they had returned to their pre-treatment baseline. If avoiding giving back the benefits matters to you, most people are more inclined to stay on HGH long-term rather than Tesa.
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Another thing worth keeping in mind: a large share of the people in the tesa studies did not really drop much weight. The way it appears to work is that visceral fat gets shifted around rather than eliminated.

A lot of folks using GHRP's these days stack them alongside GLP's. The thinking behind that is once your target weight is reached, then simply maintaining with a GLP on its own ought to be sufficient to hold most of that weight off.

You're correct that choosing HGH over any GHRP will produce stronger and quicker outcomes. The reason HGH has a poor reputation comes from the large amounts bodybuilders use, which bring on more side effects. I'm not claiming that low doses in someone who isn't GH deficient would be free of side effects either. It simply hasn't been researched, so there's no way to state with certainty that low-dose HGH is equally safe as tesa when used at small dosages by people who aren't GH deficient.
 
That's a fascinating point. From what I gather, HGH might have an edge when it comes to subcutaneous fat thanks to its longer-lasting GH pulse — does that hold true even when tesa pushes your igf-1 score up to the same number? Since I'm also on glp's, I'm not sure how the risk-reward math works out between hgh and tesa in my case. I'm just 36 and tesa gives me a strong igf-1 response, but I feel like I'm only now grasping why hgh could be the better route.
 
dpo08 said:

That's a fascinating point. From what I gather, HGH might have an edge when it comes to subcutaneous fat thanks to its longer-lasting GH pulse — does that hold true even when tesa pushes your igf-1 score up to the same number? Since I'm also on glp's, I'm not sure how the risk-reward math works out between hgh and tesa in my case. I'm just 36 and tesa gives me a strong igf-1 response, but I feel like I'm only now grasping why hgh could be the better route.
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Yeah, broadly speaking—and this is just from my own completely lay, non-medical perspective—I think that's right. Still, when I say it's better at burning subcutaneous fat, that comparison only applies against Tesa or other GHRPs, not against tirz/reta.
 
A few problems come up right away.

1. When it comes to CJC-1295 no DAC, the “data” is entirely fabricated. Claude itself says outright that it is an estimate built on data that does not exist. Think about that for a second. An “estimate” with nothing behind it. Pure fantasy.

2. The majority of compounds being talked about here are not GHRPs at all. GHRP is a distinct drug class, and ipamorelin is the only one of these that belongs to it. Everything else listed falls under GHRHs (or is simply growth hormone).

3. Almost all of the metabolic trial data we have for these drugs comes from monotherapy studies in people with obesity, diabetes, or HIV lipodystrophy. Employing them as an add-on to GLP-1 therapy is a completely different clinical scenario. A big limitation across most of that trial data is that growth hormone is being given to insulin resistant populations, and their elevated insulin levels blunt the lipolytic action of growth hormone (while growth hormone makes the insulin resistance worse). The picture changes dramatically when the patients are on powerful insulin sensitizers (retatrutide above all). That population tends to be highly insulin sensitive, insulin levels are frequently extremely low, and it stands to reason that growth hormone would produce a far greater lipolytic effect than anything seen in those trials. In most trial populations, the lipolysis that does occur does not amount to much: the freed lipids never get burned and are simply reesterified back into lipids. With GLP-1 patients, though, large caloric deficits are common, which creates an ideal situation for the body to actually use those mobilized lipids instead of reesterifying them. This also lets us kill two birds with one stone, because the more the body can cover the deficit by burning mobilized lipids (and growth hormone raises the amount mobilized, particularly when insulin sensitivity is high), the less catabolic strain gets placed on lean tissue. That said, this is mechanistic speculation. There is no metabolic trial data on insulin sensitive GLP-1 patients using growth hormone axis treatments as an ancillary. Nothing close to it exists. All we have is trial data from insulin resistant populations on regimens that share little with what we actually care about. The mechanistic speculation is valuable precisely because the trial data is so far removed from the question we want answered.
 
dpo08 said:

That's a fascinating point. From what I gather, HGH might have an edge when it comes to subcutaneous fat thanks to its longer-lasting GH pulse — does that hold true even when tesa pushes your igf-1 score up to the same number? Since I'm also on glp's, I'm not sure how the risk-reward math works out between hgh and tesa in my case. I'm just 36 and tesa gives me a strong igf-1 response, but I feel like I'm only now grasping why hgh could be the better route.
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Put simply, a GHRP signals your system to attempt to make additional GH, whereas HGH directly supplies your system with additional GH.

Naturally, additional variables exist, but that's the most straightforward way to grasp it.
 
I lean toward HGH personally. Over a 4–5 month stretch, HGH eliminated hard-to-lose subcutaneous abdominal fat that persisted despite meaningful weight reduction while on Tirzepatide (I was training 3–5 hrs/week the whole time). The scale barely moved (±1–2 lbs), yet body fat fell by roughly 1.5%.

On CJC: I think labeling it 'completely hallucinated' overlooks the core issue. CJC no DAC is essentially a standard Mod-GRF - a substituted GHRH(1-29) fragment that acts through the very same receptor pathway as Tesamorelin (GHRH 1-44). Sure, Claude might have invented particular numerical trial figures, but drawing mechanistic parallels between GHRH analogues isn't baseless.
 
SVT810E said:

A few problems come up right away.

1. When it comes to CJC-1295 no DAC, the “data” is entirely fabricated. Claude itself says outright that it is an estimate built on data that does not exist. Think about that for a second. An “estimate” with nothing behind it. Pure fantasy.

2. The majority of compounds being talked about here are not GHRPs at all. GHRP is a distinct drug class, and ipamorelin is the only one of these that belongs to it. Everything else listed falls under GHRHs (or is simply growth hormone).

3. Almost all of the metabolic trial data we have for these drugs comes from monotherapy studies in people with obesity, diabetes, or HIV lipodystrophy. Employing them as an add-on to GLP-1 therapy is a completely different clinical scenario. A big limitation across most of that trial data is that growth hormone is being given to insulin resistant populations, and their elevated insulin levels blunt the lipolytic action of growth hormone (while growth hormone makes the insulin resistance worse). The picture changes dramatically when the patients are on powerful insulin sensitizers (retatrutide above all). That population tends to be highly insulin sensitive, insulin levels are frequently extremely low, and it stands to reason that growth hormone would produce a far greater lipolytic effect than anything seen in those trials. In most trial populations, the lipolysis that does occur does not amount to much: the freed lipids never get burned and are simply reesterified back into lipids. With GLP-1 patients, though, large caloric deficits are common, which creates an ideal situation for the body to actually use those mobilized lipids instead of reesterifying them. This also lets us kill two birds with one stone, because the more the body can cover the deficit by burning mobilized lipids (and growth hormone raises the amount mobilized, particularly when insulin sensitivity is high), the less catabolic strain gets placed on lean tissue. That said, this is mechanistic speculation. There is no metabolic trial data on insulin sensitive GLP-1 patients using growth hormone axis treatments as an ancillary. Nothing close to it exists. All we have is trial data from insulin resistant populations on regimens that share little with what we actually care about. The mechanistic speculation is valuable precisely because the trial data is so far removed from the question we want answered.
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This all lines up with my thinking. When it comes to anything with usable data behind it, the only real comparison point is Tesa (without the ipa blend that a lot of people add) versus HGH. I ran a request through Claude to get its estimate on CJC, mostly so that anyone who hasn't dug into the literature can see that if Tesa has data supporting it, then CJC — even paired with IPA — is very likely to land even further down the effectiveness scale. You're also correct that the demographics and populations studied look nothing like the "normal" groups now stacking these compounds with GLPs.

Having said that, and like I mentioned before, none of this amounts to a genuine scientific analysis. The point was to get people thinking and to push them toward setting realistic goals for why they're running Tesa/cjc/ipa next to their other pep protocols — and whether it's truly needed, weighed against the possible benefits and risks as each researcher judges for themselves.
 
SVT810E said:

A few problems come up right away.

1. When it comes to CJC-1295 no DAC, the “data” is entirely fabricated. Claude itself says outright that it is an estimate built on data that does not exist. Think about that for a second. An “estimate” with nothing behind it. Pure fantasy.

2. The majority of compounds being talked about here are not GHRPs at all. GHRP is a distinct drug class, and ipamorelin is the only one of these that belongs to it. Everything else listed falls under GHRHs (or is simply growth hormone).

3. Almost all of the metabolic trial data we have for these drugs comes from monotherapy studies in people with obesity, diabetes, or HIV lipodystrophy. Employing them as an add-on to GLP-1 therapy is a completely different clinical scenario. A big limitation across most of that trial data is that growth hormone is being given to insulin resistant populations, and their elevated insulin levels blunt the lipolytic action of growth hormone (while growth hormone makes the insulin resistance worse). The picture changes dramatically when the patients are on powerful insulin sensitizers (retatrutide above all). That population tends to be highly insulin sensitive, insulin levels are frequently extremely low, and it stands to reason that growth hormone would produce a far greater lipolytic effect than anything seen in those trials. In most trial populations, the lipolysis that does occur does not amount to much: the freed lipids never get burned and are simply reesterified back into lipids. With GLP-1 patients, though, large caloric deficits are common, which creates an ideal situation for the body to actually use those mobilized lipids instead of reesterifying them. This also lets us kill two birds with one stone, because the more the body can cover the deficit by burning mobilized lipids (and growth hormone raises the amount mobilized, particularly when insulin sensitivity is high), the less catabolic strain gets placed on lean tissue. That said, this is mechanistic speculation. There is no metabolic trial data on insulin sensitive GLP-1 patients using growth hormone axis treatments as an ancillary. Nothing close to it exists. All we have is trial data from insulin resistant populations on regimens that share little with what we actually care about. The mechanistic speculation is valuable precisely because the trial data is so far removed from the question we want answered.
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Nicely put! It's uncommon for me to come across people who use GHRP/GHRH by themselves. That's exactly why anecdotal reports matter so much. A genuinely ethical trial testing a combination of the "holy trinity" for body recomp is something we'll likely never get to see.
 
di_peppil said:

I lean toward HGH personally. Over a 4–5 month stretch, HGH eliminated hard-to-lose subcutaneous abdominal fat that persisted despite meaningful weight reduction while on Tirzepatide (I was training 3–5 hrs/week the whole time). The scale barely moved (±1–2 lbs), yet body fat fell by roughly 1.5%.

On CJC: I think labeling it 'completely hallucinated' overlooks the core issue. CJC no DAC is essentially a standard Mod-GRF - a substituted GHRH(1-29) fragment that acts through the very same receptor pathway as Tesamorelin (GHRH 1-44). Sure, Claude might have invented particular numerical trial figures, but drawing mechanistic parallels between GHRH analogues isn't baseless.
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Before you started HGH, had you ever given tesa or cjc a try?
 
dpo08 said:

di_peppil said:

I lean toward HGH personally. Over a 4–5 month stretch, HGH eliminated hard-to-lose subcutaneous abdominal fat that persisted despite meaningful weight reduction while on Tirzepatide (I was training 3–5 hrs/week the whole time). The scale barely moved (±1–2 lbs), yet body fat fell by roughly 1.5%.

On CJC: I think labeling it 'completely hallucinated' overlooks the core issue. CJC no DAC is essentially a standard Mod-GRF - a substituted GHRH(1-29) fragment that acts through the very same receptor pathway as Tesamorelin (GHRH 1-44). Sure, Claude might have invented particular numerical trial figures, but drawing mechanistic parallels between GHRH analogues isn't baseless.
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Before you started HGH, had you ever given tesa or cjc a try?
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No. Back then, getting GH seemed simpler to me than obtaining CJC or Tesa. These days, that's likely flipped.
 
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