Thoughts on tesa?

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.
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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
  1. 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.
  2. When GH exposure is supraphysiologic and more continuous (rhGH 4 mg), subcutaneous fat loss and insulin resistance are more pronounced.
  3. 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.
  4. 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.
 
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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.
 
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On a side note, is it ideal to do meal and workout timing with HGH admin (such as to prevent insulin resistance)?

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.
 
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.
 
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.


"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.
 
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.
 

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