Thoughts on tesa?

[Calm Logic]

Of the GLPs, reta is expected to burn the most visceral fat (and lower cholesterol and triglycerides the most), followed by the dual agonists targeting glucagon (survo, madz), the GIP-targeting tirz, and then sema:

Medication (Brand Names) Mechanism of Action Status (as of July 2025) Average Weight Loss (Clinical Trials) Visceral Fat Reduction Potential (Relative Order) Notes on Visceral Fat Retatrutide ("Reta") Triple GLP-1/GIP/Glucagon Receptor Agonist Phase 3 Clinical Trials ~20-25% of body weight (Phase 2 data) Highest Triple action targets fat metabolism more comprehensively; exceptional overall weight loss strongly indicates superior visceral fat reduction. Strong liver fat reduction also observed. Survodutide Dual GLP-1/Glucagon Receptor Agonist Phase 3 Clinical Trials ~15-19% of body weight (Phase 2 data) Very High Glucagon agonism directly promotes fat breakdown and energy expenditure, which is key for visceral fat. Significant liver fat reduction seen. Mazdutide ("Madz") Dual GLP-1/Glucagon Receptor Agonist Approved in China (Obesity, T2D); Phase 3 in other regions ~12-19% of body weight (Phase 2/3 data from China) Very High Similar to survodutide, its dual GLP-1/glucagon action is highly effective for fat burning and has shown significant reductions in waist circumference and liver fat. Tirzepatide (Zepbound, Mounjaro) Dual GIP/GLP-1 Receptor Agonist Approved (Obesity, T2D) ~15-22% of body weight (Zepbound) High Powerful overall weight loss, with studies specifically showing significant reductions in visceral fat mass and waist circumference. Strong evidence for liver fat reduction. Semaglutide (Wegovy, Ozempic, Rybelsus) GLP-1 Receptor Agonist Approved (Obesity, T2D) ~15% of body weight (Wegovy) High Proven to significantly reduce visceral fat and liver fat, while preserving lean muscle mass more effectively than some other weight loss methods.

 

[hexagonal]

HGH is even worst, like your internal organs growing

Why do you think GH secretagogues don't carry the same risks as exogenous HGH dosed at levels to give you the same amount of GH/IGF-1/etc.?

Because a GH secretagogue increasing your natural production to the same level as you would get from exogenous HGH carries those same risks.

A tesa/ipa stack also massively increased my blood glucose and insulin levels vs. more potent HGH dosages.

I have swapped to HGH and won't look back.

 

[hexagonal]

So the way Im reading it - Tesa Specifically targets VAT vs HGH just reducing overall BF. CJC doesnt seem to be as strong as either in the fat burning dept.

Is there any reason you'd prefer the CJC? or strictly for price.

To the best of my (non-expert) knowledge there is no reason to believe that tesa and HGH actually function any differently in regards to visceral fat. We do not know of any mechanism on which tesa acts on VAT or body fat in general outside of increased GH production.

 

[exploitedworkerbee]

To the best of my (non-expert) knowledge there is no reason to believe that tesa and HGH actually function any differently in regards to visceral fat. We do not know of any mechanism on which tesa acts on VAT or body fat in general outside of increased GH production.

I think the distinction is that tesa only works on visceral fat, it does not have an effect on subcutaneous fat. HGH has an effect on both. I am also non-expert but that’s how i understand it, if you want to know the mechanism I bet chatgpt could tell you.

 

[PackmanJohnny]

To the best of my (non-expert) knowledge there is no reason to believe that tesa and HGH actually function any differently in regards to visceral fat. We do not know of any mechanism on which tesa acts on VAT or body fat in general outside of increased GH production.

As a GHRH I automatically wanted to default to that, but the clinical data on Tesa's effects on visceral fat are aggressive vs GH's, looks like there IS a difference in how they stimulate lipolysis, but we dont have a 'why':

(Per ChatGPT4)

Tesamorelin is a growth hormone–releasing hormone (GHRH) analog . It binds to the GHRH receptor on the anterior pituitary , which:

Triggers pulsatile release of endogenous GH — mimicking how your body naturally secretes GH.

GH then stimulates the liver to produce IGF‑1 , which helps with fat metabolism.

GH and IGF‑1 promote lipolysis — especially in visceral fat depots — via:

Upregulating hormone-sensitive lipase

Downregulating lipoprotein lipase

Inhibiting lipogenesis

GH also reduces lipid uptake and storage in visceral adipocytes.

Why it works better on VAT:

Tesamorelin’s physiologic GH pulses appear to selectively activate VAT lipolysis over subcutaneous fat, likely due to:

More GH receptors in visceral tissue

Tesamorelin’s rhythmic GH mimicking nocturnal secretion (when VAT is more metabolically active)

Whereas GHs mechanics seem to target all fat deposits evenly:

HGH (Somatropin) Mechanism​

Exogenous HGH bypasses your hypothalamic-pituitary axis entirely. It:

Raises blood GH levels non-pulsatile , often sustained

Stimulates IGF‑1 from the liver and tissues

Causes global fat loss (visceral and subcutaneous), muscle growth, and bone turnover

However, chronically elevated GH blunts insulin sensitivity, which can blunt fat loss and increase VAT long-term if not managed

Why it’s less VAT-specific:

HGH affects all fat depots more evenly

High IGF‑1 can stimulate preadipocyte differentiation in some contexts

It lacks the rhythmic, physiologic “fat-burning pulse” seen with Tesamorelin

maybe at a certain dose GH is blunting the fat loss its also responsible for? maybe this is one of Exogenous GH's shortcoming that Endogenous GH stimulated by Tesa is incabale of mimicking? Who knows.

 

[Calm Logic]

For recon for tesa, it seems to benefit from filtering more than other peptides:

https://thinksteroids.com/community/threads/sudden-reaction-to-tesamorelin.134429508/post-3476597

Tesa is already probably the most aggregation prone pharma peptide out there. That's why it (Egrifta) was always only available as a single dose vial that you injected right after reconstitution

 

[kris10karma 6175]

For recon for tesa, it seems to benefit from filtering more than other peptides:

https://thinksteroids.com/community/threads/sudden-reaction-to-tesamorelin.134429508/post-3476597

This is interesting. I wonder if gh aggregates?

 

[PackmanJohnny]

This is interesting. I wonder if gh aggregates?

It absolutely does. Once reconstituted, youve got 30 ish days or less if you refrigerate it. Shaking it around can damage it too.

 

[AndyPanda]

It absolutely does. Once reconstituted, youve got 30 ish days or less if you refrigerate it. Shaking it around can damage it too.

This is correct. HGH is fragile. It’s one of the rare instances where I don’t buy vials in the highest content. Freezing it is also not recommended, so buying in “bulk” can be complicated. If you are going to go down this path these are good things to know.

 

[FlowerFairy]

From what I read, CJC would help more with recovery and sleep, compared to tesa. My Achilles heel is literally my Achilles heel, haha.

Regarding fat burning, a generated table for comparison, including Anavar (the winner) and TRT as well as ipa, CJC, tesa, and HGH:

Comparing recovery, with nothing supposedly beating TB and BPC, and HGH the next best:

Dang. You went all the way through that rabbit hole!

 

[hexagonal]

I think the distinction is that tesa only works on visceral fat, it does not have an effect on subcutaneous fat. HGH has an effect on both. I am also non-expert but that’s how i understand it, if you want to know the mechanism I bet chatgpt could tell you.

We do not have in-vivo mechanistic research on why tesa would work more on VAT than GH and even the proposed reasoning by ChatGPT in the followup post after makes no sense - exogenous HGH would also bind more to VAT if it is a matter of increased receptor density. Plenty of people inject HGH before bed and we know from lots of other research (primarily around IM vs SubQ injections with HGH) that ChatGPT is just flat out wrong in saying that exogenous HGH results in sustained GH levels - it is VERY spikey, even in SubQ, though IM increases this further. And I don't see how tesa couldn't work on subcutaneous fat - even totally natural GH production induces lipolysis in subcutaneous fat cells.

The IGF-1 levels are sustained, unlike GH, but they are with secretagogues as well, and it is the GH itself that induces lipolysis.

[Imported image pending local asset: attachments-1753052193833-webp.7875]

As a GHRH I automatically wanted to default to that, but the clinical data on Tesa's effects on visceral fat are aggressive vs GH's, looks like there IS a difference in how they stimulate lipolysis, but we dont have a 'why':

(Per ChatGPT4)

Whereas GHs mechanics seem to target all fat deposits evenly:

maybe at a certain dose GH is blunting the fat loss its also responsible for? maybe this is one of Exogenous GH's shortcoming that Endogenous GH stimulated by Tesa is incabale of mimicking? Who knows.

See above - a lot of this is just flat out inaccurate or doesn't make much sense when reasoned through.

It is important to remember that LLMs are word association programs and we should not take what they say as gospel.

With that in mind, I asked ChatGPT to focus on this more specifically and try to explain things, and this was it's ultimate answer. Clipped for brevity since it gave me a very long answer from research mode. Take it with a grain of salt.

Putting it all together

Evidence for a qualitative difference (VAT‑selective vs “all‑fat”) is weak. The apparent selectivity of tesamorelin largely stems from dose and pattern used in trials, not from an intrinsic impossibility for rhGH to do the same.

When GH exposure is supraphysiologic and more continuous (rhGH 4 mg), subcutaneous fat loss and insulin resistance are more pronounced.

If you titrate nightly rhGH to yield IGF‑1 in the same range tesamorelin achieves (~+1 SD) and/or split it into true pulses, you would expect similar VAT reduction with fewer metabolic downsides—but this has not been formally tested.

In-vitro studies suggest secretagogues retain normal feedback, mixed isoforms and possible direct adipocyte actions, so the exact equivalence cannot be assumed.

Bottom line for practice

Secretagogues (tesamorelin, ibutamoren, ipamorelin + CJC‑1295, etc.) are a proven way to shrink VAT with a comparatively clean metabolic profile.

rhGH can achieve comparable or larger VAT loss, but only if care is taken with dose, timing and monitoring of IGF‑1 and glucose.

Claims that “HGH works on all‑body fat while secretagogues only target visceral fat” oversimplify the literature—both mobilise fat everywhere; the pattern and magnitude of exposure dictate the depot response.

So far, the question is unresolved mainly because no rigorously designed head‑to‑head study exists . Mechanistic clues suggest mostly quantitative (pulse shape, isoform mix, direct GHRH effects) rather than qualitative differences.

I'll note that the 4mg HGH mentioned in the reference study would be quite a high HGH dose - HGH is 3IU/mg, and most people trying to mimic a similar effect to secretagogues are going to be in the 2-4IU range. You're well into bodybuilder territory at that point.

 

[hexagonal]

This is correct. HGH is fragile. It’s one of the rare instances where I don’t buy vials in the highest content. Freezing it is also not recommended, so buying in “bulk” can be complicated. If you are going to go down this path these are good things to know.

Plenty of people freeze HGH - it's the same concerns as with most other peptides, ice crystals, etc., can cause issue from repeated thaw/freeze cycles. If you have thermal mass insulating things, have one of the vaccine freezers, etc., it's fine.

I've got no concerns about freezing mine and the 7-month old frozen vials are reconstituting and providing as-expected blood results vs. when they were new. I've got about two years worth stocked up currently.

 

[Calm Logic]

On a side note, is it actually helpful to do meal and workout timing with HGH admin (such as to prevent insulin resistance)? Or is it more theory than reality? But I guess continuous glucose monitoring would help, in any case.

The bro science:

https://www.thinksteroids.com/community/threads/a-gh-and-fat-loss-protocol-rhgh-lipolysis-that-is-science-based.134408038/post-2888733

 

[hexagonal]

On a side note, is it ideal to do meal and workout timing with HGH admin (such as to prevent insulin resistance)?

https://www.thinksteroids.com/community/threads/a-gh-and-fat-loss-protocol-rhgh-lipolysis-that-is-science-based.134408038/post-2888733

I don't know that there's good science here to rely on, so it's largely conjecture by bro scientists on the internet.

What we do know is that in the non-chemically assisted population, fasted cardio does not result in greater fat loss than non-fasted cardio, as long as other variables are controlled for, and fasting does increase serum GH levels.

I'm not an expert and I don't have any studies to try and interpret even as a layperson here, so not sure I can provide even random-internet-asshole level insight.

I would keep an eye on blood markers for insulin resistance regardless of which you use and whatever strategy you have for injection. The limited data and my own bloodwork has me not worrying about it - most times, I take it as a single bolus at night because it seems to help me sleep better. If I am going to be out late or otherwise away from home for the night, I'll take it at some point during the day.

 

[Calm Logic]

in the non-chemically assisted population

Haha!

 

[hexagonal]

Haha!

Not actually trying to be funny there - just noting that the study doesn't account for what we might be doing.

And who knows what all that might change!

I find it plausible that under the right conditions, say, strong nutrient partitioning effects from AAS usage, increased lipolysis and availability of FFAs, benefits from GLP-1s, coupled with injections timed around cardio and a body primed for muscle protein synthesis from weight training and increased anabolic signaling from the AAS that you could see some difference in outcomes with the timed injections. You will have more FFAs available in the blood for sure. But your body is already pretty good at liberating FFAs for use when doing all of this even without the timing, so my gut feeling is that any difference, if it does exist, is minimal.

I wouldn't be shocked to find out that there is a significant difference - just don't have enough evidence at current to make me believe that there is one.

 

[PackmanJohnny]

We do not have in-vivo mechanistic research on why tesa would work more on VAT than GH and even the proposed reasoning by ChatGPT in the followup post after makes no sense - exogenous HGH would also bind more to VAT if it is a matter of increased receptor density. Plenty of people inject HGH before bed and we know from lots of other research (primarily around IM vs SubQ injections with HGH) that ChatGPT is just flat out wrong in saying that exogenous HGH results in sustained GH levels - it is VERY spikey, even in SubQ, though IM increases this further. And I don't see how tesa couldn't work on subcutaneous fat - even totally natural GH production induces lipolysis in subcutaneous fat cells.

The IGF-1 levels are sustained, unlike GH, but they are with secretagogues as well, and it is the GH itself that induces lipolysis.

View attachment 7875

See above - a lot of this is just flat out inaccurate or doesn't make much sense when reasoned through.

It is important to remember that LLMs are word association programs and we should not take what they say as gospel.

With that in mind, I asked ChatGPT to focus on this more specifically and try to explain things, and this was it's ultimate answer. Clipped for brevity since it gave me a very long answer from research mode. Take it with a grain of salt.

I'll note that the 4mg HGH mentioned in the reference study would be quite a high HGH dose - HGH is 3IU/mg, and most people trying to mimic a similar effect to secretagogues are going to be in the 2-4IU range. You're well into bodybuilder territory at that point.

Obviously there are a lot of holes and gaps with the two drugs not having head-to-head data among a few other desirable intel points.

From the foggy areas where we're all just guessing, I do think it's just as much of a leap to assume that Exo GH would bind to VAT better than Endo via GHRH(obv dose-dependent). We already know there is a difference to SOME degree in how the body perceives and metabolizes the two from the side effects, both in the immediate(at higher doses) and long term-usage.

Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension - PubMed

Tesamorelin reduces visceral fat by approximately 18% and improves body image distress in HIV-infected patients with central fat accumulation. These changes are achieved without significant side effects or perturbation of glucose.

pubmed.ncbi.nlm.nih.gov

"VAT was reduced by approximately 18% (P < 0.001) in patients continuing tesamorelin for 12 months." (at a 2mg/day dose) - This is a big number, but its also the effect of the drug on individuals who were on meds causing them to stack VAT that they couldn't burn any other way.

https://pubmed.ncbi.nlm.nih.gov/187529778 - in the same vein this GH dosage is much more realistic (1.5~ IU/Day) but being used on a middle aged-older cohort(51-64, mean 58) That could also have positive or negative effects on absorption/efficacy.

The only comparison I'd draw is that Tesa seemed much more effective for women across the board, and these two scenarios both ended up with males down 18% VAT.

I'd love to see more data with less extreme cohorts but I may need to wait. Just the ridiculous, extreme lethargy I experienced on GH makes trying Tesa worth it for me at some point, but I dont want to clap and cheer for the horse in 2nd place lol.

 

[chmuse]

I went with tesa because it's actually prescribed for visceral fat specifically so it just.... Felt safer. So far I like it. I'm not looking to rush things, so maybe I'll switch when I'm out. Or maybe I won't need it anymore. People seem to either love it or hate it.

 

[hexagonal]

I went with tesa because it's actually prescribed for visceral fat specifically so it just.... Felt safer. So far I like it. I'm not looking to rush things, so maybe I'll switch when I'm out. Or maybe I won't need it anymore. People seem to either love it or hate it.

Prescribed for visceral fat in HIV patients on specific medications - they often have significantly impacted IGF-1 levels and egrifta is used to bring it back into the normal range.

Monitoring insulin-like growth factors in HIV infection and AIDS - PubMed

There is a close association between the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis, infection and immunity. Infection with the human immunodeficiency virus (HIV) is often associated with a decrease of the concentrations of IGF-I, IGF-II, IGF-binding protein 3 (IGFBP-3) and an...

pubmed.ncbi.nlm.nih.gov

Personally, I think anyone with normal IGF-1 levels is increasing a variety of risk factors when taking exogenous HGH or a secretagogue. The science seems pretty clear that supraphysiological IGF-1 levels are not without risk.

My personal estimation is that the level of risk is tolerable for me at the level of IGF-1 increase I'm driving with them, but I don't think any of us should believe that the risk profile is similar to that of the GLP-1s.

 

[chmuse]

Prescribed for visceral fat in HIV patients on specific medications - they often have significantly impacted IGF-1 levels and egrifta is used to bring it back into the normal range.

Monitoring insulin-like growth factors in HIV infection and AIDS - PubMed

There is a close association between the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis, infection and immunity. Infection with the human immunodeficiency virus (HIV) is often associated with a decrease of the concentrations of IGF-I, IGF-II, IGF-binding protein 3 (IGFBP-3) and an...

pubmed.ncbi.nlm.nih.gov

Personally, I think anyone with normal IGF-1 levels is increasing a variety of risk factors when taking exogenous HGH or a secretagogue. The science seems pretty clear that supraphysiological IGF-1 levels are not without risk.

My personal estimation is that the level of risk is tolerable for me at the level of IGF-1 increase I'm driving with them, but I don't think any of us should believe that the risk profile is similar to that of the GLP-1s.

I'm hopeful I don't need to use them for long enough for it to be a problem. I do .5-1mg 5 on two off. My 10mg vials tested at 14. Well, the ones that weren't actually mt2. So I figure over the next year or two I do one vial every other month or so, stopping early if I don't feel I need it. We'll see. With the reta added in as well, I might be able to gift the ones that are left.