Subject: Fwd: Does Tesamorelin Have a Monopoly on Visceral Fat? Not So Fast.
From: TJ Bourdeau <[email-masked]>
To: [email-masked]
Date: Tue, 17 Mar 2026 15:31:51 -0400

TJ

Begin forwarded message:

From: Derek from Peptide Price <[email-masked]>
Date: March 17, 2026 at 2:53:26 PM EDT
To: [email-masked]
Subject: Does Tesamorelin Have a Monopoly on Visceral Fat? Not So Fast.
Reply-To: Derek from Peptide Price <reply+35vy39&4iwoe6&&[email-masked]>

There’s a claim that gets repeated constantly in the peptide research space:

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Does Tesamorelin Have a Monopoly on Visceral Fat? Not So Fast.

Derek

Mar 17

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There’s a claim that gets repeated constantly in the peptide research space:

“Tesamorelin is the only peptide proven to burn visceral fat.”

And if you’ve spent any time researching GH secretagogues, you’ve probably accepted this as settled fact and moved on. I did for a while too.

But the more I dug into it, the more I realized we’ve been conflating two very different things: “this compound has been studied for visceral fat” and “this compound burns visceral fat.” Those aren’t the same statement. Not even close.

So let’s actually pull this apart.

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What Is Visceral Fat, and Why Does It Matter?

Before anything else, it helps to understand what we’re actually talking about.

Your body stores fat in two main places. Subcutaneous fat sits just under your skin — it’s the stuff you can grab with your fingers. Visceral fat is different. It sits deep inside your abdominal cavity, packed around your organs — your liver, intestines, kidneys. You can’t see it or pinch it. Someone can look relatively lean on the outside and still be carrying a dangerous amount of visceral fat internally.

Why does it matter? Because visceral fat isn’t just stored energy sitting quietly. It’s metabolically active tissue that releases inflammatory molecules, disrupts insulin signaling, raises cardiovascular risk, and drives a whole cascade of metabolic dysfunction. High visceral fat is strongly associated with type 2 diabetes, heart disease, and all-cause mortality. It’s not a cosmetic issue — it’s a health issue.

And here’s the part that’s directly relevant to this conversation: visceral fat and growth hormone have an inverse relationship. When GH is high, visceral fat tends to be low. When GH is low or blunted — which happens naturally as we age, and more severely in certain medical conditions — visceral fat tends to accumulate. They regulate each other in a feedback loop that, once it tips the wrong way, is genuinely hard to reverse through diet and exercise alone.

So Where Did Tesamorelin Come From?

Tesamorelin is a synthetic version of a molecule your body already makes called Growth Hormone-Releasing Hormone, or GHRH. Your hypothalamus — a small structure deep in your brain — produces GHRH naturally to tell your pituitary gland to release growth hormone. Tesamorelin mimics that signal.

It was developed and studied specifically in HIV/AIDS patients who developed a condition called lipodystrophy. When antiretroviral drugs became widely used in the late 1990s and 2000s, doctors started noticing that patients on these medications were accumulating large amounts of visceral fat around their organs while simultaneously losing fat from their face and limbs. It was disfiguring, uncomfortable, and metabolically dangerous.

Researchers noticed something else too: these patients had blunted GH secretion. The feedback loop had tipped the wrong way. More visceral fat suppressing GH, lower GH allowing even more visceral fat to accumulate. Tesamorelin was used to try to restore that GH signaling and break the cycle.

The pivotal clinical trials — published in the New England Journal of Medicine in 2010 by Falutz and colleagues — showed roughly 15 to 18 percent reduction in visceral fat over 26 weeks. That’s a meaningful, measurable, clinically significant result. The FDA approved it that same year under the trade name Egrifta.

The evidence is real. Nobody is disputing that.

But Here’s What the Story Leaves Out

The reason Tesamorelin got a $10 million clinical trial and most other peptides didn’t has less to do with biology and more to do with pharmaceutical economics.

Running a proper visceral fat trial — 26 weeks, randomized, placebo-controlled, with MRI or CT imaging to accurately measure visceral fat at baseline and endpoint — is enormously expensive. You need to fund it, and you need a reason to fund it. That reason, in the pharmaceutical world, is a patent.

Tesamorelin was a novel, proprietary compound. Theratechnologies, the company that developed it, had patent protection and a clear commercial pathway. Investing in the trial made financial sense.

Sermorelin? No patent protection. CJC-1295? Same story. Ipamorelin? Nobody’s running a $10 million visceral fat trial on a compound they can’t exclusively profit from. That’s just the reality of how drug development works.

So when people say “Tesamorelin is the only peptide with evidence for visceral fat reduction,” what they’re really saying — whether they realize it or not — is “Tesamorelin is the only peptide that a pharmaceutical company had sufficient financial incentive to study for visceral fat reduction.” That’s a funding gap. Not necessarily a biology gap.

How Growth Hormone Actually Burns Visceral Fat

This part matters because it applies to every GH secretagogue, not just Tesamorelin.

When growth hormone rises in your body, it activates an enzyme called hormone-sensitive lipase. That enzyme breaks down stored triglycerides — the form fat is stored in — into free fatty acids that your body can actually use for energy. That process is called lipolysis, and it’s the fundamental mechanism through which GH drives fat loss.

Here’s the key detail: visceral fat has a higher density of GH receptors than subcutaneous fat. When GH goes up, your body preferentially mobilizes visceral fat first. It’s more sensitive to GH-driven lipolysis than the fat under your skin. This isn’t a Tesamorelin-specific phenomenon — it’s just how GH receptor distribution works in adipose tissue.

Growth hormone also stimulates your liver to produce IGF-1 — Insulin-like Growth Factor 1 — which acts downstream to support muscle preservation while fat is being broken down. So the full cascade looks like this: GH rises, visceral fat breaks down preferentially, IGF-1 rises, lean mass is protected. Tesamorelin triggers this cascade. So do the other secretagogues.

The question isn’t whether this mechanism exists. It does, and it’s well documented. The question is how effectively each compound triggers it, and for how long.

The Other Secretagogues: What We Actually Know

Let’s go through them one by one.

Sermorelin

Sermorelin is the oldest GH secretagogue in widespread research use. Like Tesamorelin, it’s a GHRH analogue — it works on the same receptor and through the same mechanism. The difference is half-life. Sermorelin is cleared from your body in about 10 to 12 minutes. It triggers a GH pulse, and then it’s gone.

A 2001 study by Vittone and colleagues looked at sermorelin in healthy older adults — a population with naturally declining GH — over six months. Fat mass decreased. Lean mass increased. Visceral fat wasn’t the specific endpoint, so we don’t have precise imaging data. But the directional result is exactly what you’d expect given the mechanism.

The honest limitation here is that 10 minutes may simply not be long enough to drive consistent, meaningful visceral fat mobilization over time. You’re getting a pulse, not sustained signaling.

CJC-1295

CJC-1295 comes in two versions and they behave very differently, so it’s worth separating them.

CJC-1295 without DAC — sometimes called Mod GRF 1-29 — has a half-life of around 30 minutes, putting it in the same range as Tesamorelin. It produces a pulsatile GH response and is typically dosed multiple times per day.

CJC-1295 with DAC is a different animal. DAC stands for Drug Affinity Complex — it’s a modification that allows the peptide to bind to albumin, a protein that circulates in your blood, dramatically extending how long it stays active. Half-life stretches out to around 8 days. Instead of a pulse, you get sustained, elevated GH over the better part of two weeks from a single injection.

A 2006 pharmacology study by Teichman and colleagues published in the Journal of Clinical Endocrinology and Metabolism showed that CJC-1295 produced dose-dependent, sustained increases in both GH and IGF-1 in healthy adults. Body composition wasn’t the primary focus — researchers were studying how the compound behaved in the body. But the hormonal environment it created is essentially identical to what Tesamorelin creates. The study just wasn’t designed to look at what happened to visceral fat.

Ipamorelin

Ipamorelin is a GHRP — a Growth Hormone Releasing Peptide — which means it works through a completely different receptor than the GHRH analogues. It mimics ghrelin, a hormone that powerfully stimulates GH release through its own separate pathway. When you combine a GHRH analogue with a GHRP, you hit both pathways simultaneously and get significantly more GH than either would produce alone — which is why CJC-1295 plus Ipamorelin became such a common research stack.

Ipamorelin’s half-life is roughly 2 hours, and it’s notable for being the most cortisol-sparing of the GHRPs. That distinction matters for this conversation. Cortisol — your primary stress hormone — is one of the main drivers of visceral fat accumulation. Some GHRPs, particularly GHRP-2 and GHRP-6 at higher doses, raise cortisol meaningfully, which can actively work against visceral fat reduction. Ipamorelin largely avoids this, which theoretically makes it a cleaner option.

Dedicated visceral fat data doesn’t exist for Ipamorelin in humans. But the mechanism is there, the cortisol problem is largely absent, and the GH response is real.

MK-677 (Ibutamoren)

MK-677 is the outlier of the group. It’s taken orally — no injection required — and has a half-life of around 24 hours, meaning it keeps GH and IGF-1 elevated throughout the day rather than producing discrete pulses.

It actually has some of the better human data in this class. A 1998 study by Murphy and colleagues in the Journal of Clinical Endocrinology and Metabolism showed MK-677 restored GH and IGF-1 to youthful levels in elderly adults with improvements in body composition. A 2008 study by Svensson and colleagues showed increased fat-free mass in GH-deficient adults. These aren’t visceral fat specific endpoints, but the direction is consistent.

The complication with MK-677 is that it’s a ghrelin mimetic — and ghrelin is your hunger hormone. Most research subjects report a significant increase in appetite on MK-677, which in practice can offset fat loss outcomes. It’s also worth noting that chronic, around-the-clock GH elevation — as opposed to the pulsatile release your body expects — may over time cause GH receptors to become less sensitive, potentially blunting the response.

Hexarelin and GHRP-2

Most of the data here comes from animal studies. In rodent models, both compounds have been associated with reductions in overall adiposity and improvements in lipid metabolism. Hexarelin has also shown cardioprotective effects in animal models of GH deficiency that are worth noting separately. Human visceral fat data simply doesn’t exist for either compound — again, not because the biology doesn’t support it, but because no one has funded the trial.

Why Tesamorelin Is Still Probably the Best Option for This Specific Goal

To be fair to the conventional wisdom: Tesamorelin isn’t just backed by evidence because of luck or funding. There are legitimate biological reasons it performs well for visceral fat specifically.

The half-life sweet spot matters. At roughly 26 minutes, dosed daily, Tesamorelin produces consistent pulsatile GH release that mirrors your body’s natural rhythm. This appears to be important. Your body expects GH in pulses — it’s how the system evolved. Sustained, flat GH elevation can eventually trigger receptor downregulation, meaning your body becomes less responsive over time. Tesamorelin avoids this by working with your physiology rather than overriding it.

The cortisol issue is real. For the GHRPs, cortisol elevation at higher doses is a genuine concern for anyone specifically targeting visceral fat. Cortisol and visceral fat accumulation are closely linked — elevated cortisol drives fat deposition centrally, right where you’re trying to reduce it. Tesamorelin as a GHRH analogue doesn’t have this problem. Neither does Ipamorelin, which is why it stands out from the other GHRPs.

And the studied population amplified the measurable effect. HIV lipodystrophy patients had severely, abnormally elevated visceral fat. A 15 to 18 percent reduction is a large signal that’s easy to detect statistically. In a metabolically healthier research subject, the starting visceral fat burden is lower, the change will be smaller, and you’d need a larger, longer, more expensive study to detect it reliably. This makes it harder to prove efficacy for other compounds even if the effect is real — it’s a statistical challenge, not a biological one.

The Honest Bottom Line

Tesamorelin has the clinical evidence. That’s not in question.

What is worth questioning is the leap from “Tesamorelin has been studied for this” to “nothing else works for this.” That leap isn’t supported. The mechanism for visceral fat reduction — GH restoration driving preferential lipolysis in visceral depots — is shared across this entire class of compounds. The studies that do exist for the others point in the same direction. The gap is in the research, not the biology.

We don’t know exactly how much visceral fat benefit Sermorelin, CJC-1295, Ipamorelin, or MK-677 provide because no one has designed a proper study to find out. That’s a funding and incentive problem in pharmaceutical research. It doesn’t mean the answer is zero.

The most accurate thing you can say is: Tesamorelin is the best-evidenced option for visceral fat reduction, it has legitimate biological advantages around half-life and cortisol profile, and the other secretagogues almost certainly have meaningful overlap through the same mechanism — we just can’t quantify it yet.

That’s a very different statement than “the others don’t work.”

What I’m Actually Curious About

This is the part I genuinely don’t have a clean answer to, and I think it’s worth sitting with.

If you’ve run a longer protocol with CJC-1295, Ipamorelin, or MK-677 — did you track body composition with any precision? DEXA scans, waist circumference, anything consistent? And if you’ve run Tesamorelin specifically targeting visceral fat — did the fat loss pattern feel different? Did it come off in a different place than other secretagogue cycles you’ve run?

The human trials may not exist yet. But the people actually running these protocols are accumulating observations that matter. Not controlled data — but directional signal worth paying attention to.

If you have experience here, I’d genuinely like to hear it.

As always — research use only.

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