This is what is used to market Tesamorelin and if you don’t know that Tesamorelin does NOT reduce visceral fat, you might buy into the hype.
But… but… the clinical trials using Tesa showed a reduction in visceral fat in HIV patients. True but what is the mechanism of how that fat is reduced?
Tesa is a peptide that stimulates the pituitary gland to produce hGH, hGH is what reduces visceral fat, NOT Tesa.
It does not matter how you increase your hGH, Ipamorelin and many other peptides do increase hGH as well as using HRT with Somatropin to replace the hGH.
I’ve puzzled over the Ipa vs Tesa thing for a while now and have come to a couple conclusions.
half-life matters
dose matters
timing matters
The half life of Tesa and Ipa are pretty much the same 1 to 2hrs with Ipa seeming to be closer to 2hrs
Tesa is clinically dosed at 1.0 to 2.0mg
Ipa - internet dose is consider to be 250mcg to 400mcg (the dose i"ve been using for 2.5 years)
Timing, both just before bed time
The dose of Ipa seems way too low as I’ve been comparing what is known about both these peptides so I’ve increased my dose to 1.0mg of Ipa + 250mcg of CJC 1295 noDAC
I’ve asked Perplexity about monotherapy, Tesa alone compared to Ipa alone compared to Ipa in combination with CJC 1295 noDAC, and it looks like combination therapy will provide a bigger hGH boost.
The more one searches and reads what is available in reputable journals, the more you learn.
While there is not the same level of clinical evidence for Ipa re: visceral fat, it has been clinically proven to increase hGH, but not a lot of info on the doses used.
And that is what has spurred me to increase my dose of Ipa to Tesa level dosing.
The study by González-Sales et al. (2015) successfully created a mathematical model that predicts GH and IGF-1 levels in both HIV and healthy populations. The model confirms that the drug’s effect is consistent across health states and changes dynamically over 14 days of treatment.
• Population Consistency: The study statistically proves that HIV infection does not alter the fundamental pharmacodynamic parameters of the drug. The pituitary and liver respond to Tesamorelin with the same capacity and sensitivity in HIV-infected patients as in healthy volunteers.
• Sequential Non-Linearity: The study establishes a sequential link (Tesamorelin \to GH \to IGF-1) that is best described by a power model (exponent 0.35). This confirms that IGF-1 response is not directly proportional to GH changes, but follows a non-linear curve. (Note: The study makes no claims regarding this mechanism’s role in safety).
• Signal Amplification (Day 14 Effect): The most significant finding is the dynamic change in pituitary response over time. On Day 14, the pituitary released GH at a rate (S_{max}) more than double that of Day 1, and required lower concentrations (EC_{50}) to do so. The authors conclude that daily dosing “amplifies the intensity” of the signal transduction cascade.
• Feedback Activation: The study observed that the duration of the GH pulse (T_{GH}) shortened significantly by Day 14 (0.8h \to 0.28h). The authors hypothesize this is due to the amplified signal triggering a faster and stronger negative feedback loop to maintain homeostasis.
You are partially correct, when used as monotherapy, ipamorelin dosage has to be in the mg range, not mcg.
But when used with a ghrh like tesamorelin, you can get away with mcg doses for ipamorelin. This is because studies have shown that the synergy of a ghrh and ghrp enable you to release more growth hormone than using either one separately. Use your favorite Ai to find links to studies in the synergy of ghrh and ghrp, for example, here is one here : https://academic.oup.com/jcem/article-abstract/89/5/2290/2844515?redirectedFrom=fulltext
In summary, in healthy elderly women and men: 1) acute synergy of GHRP-2 and GHRH is greater in the female; 2) 24-h combined GHRP-2 and GHRH drive is more effective than either agonist alone; and 3) 30-d stimulation with GHRP-2 sustains a physiologically activated somatotropic axis.
I was not reading carefully enough, so I’ll modify my Ipa + CJC combo to relect this and drop the IPA back to 400mcg and increase the CJC from what I started with, 250mcg, up to 500mcg to see how that goes.
One of the studies referenced has some interesting information
Conclusion
The development of GHRH agonists focused on enhancing GH release, improving metabolic functions, and promoting tissue repair. MR-409 demonstrated therapeutic potential across various conditions, from cardioprotection to neuroprotection. The development of GHRH antagonists, particularly those in the MIA and AVR series, has provided new opportunities for cancer therapy and the treatment of other diseases. These antagonists have shown efficacy in antitumor and anti-inflammatory activities with minimal adverse effects, positioning them as favorable alternatives to conventional chemotherapeutic agents. MIA-602 and AVR-352 offer promising clinical applications for human cancers, inflammation-related diseases, and neurodegenerative disorders. The ongoing research and development of GHRH agonists and antagonists continue to highlight their potential as versatile therapeutic agents across a wide range of medical conditions.
Here is all my “research” that got started with the visceral fat thing. What hGH does is very interesting