We Need To Talk About Peptides.

I get asked about peptides more than almost anything else now.

Friends, patients, other doctors.

And the question is always some version of “do peptides work?”

It’s the wrong question. Let me explain why.

First, a number that should give you pause. US customs data, reported by the New York Times, shows imports of peptide and hormone compounds from China hitting $328 million in the first nine months of 2025, roughly double the $164 million imported over the same stretch a year earlier.¹

And that’s one country’s shipments into one market, declared at a border.

The actual volume moving through “research use only” websites and wellness clinics and group chats, I couldn’t tell you.

Nobody could.

So the stuff is everywhere. It’s migrated out of the bodybuilding forums and into longevity culture proper, with podcasters and influencers and, frankly, a fair number of clinicians cheerleading along the way.

“Do peptides work?” assumes peptides are one thing.

They aren’t.

A peptide is a short chain of amino acids, which means insulin is a peptide. So is every GLP-1 drug currently rewriting how we treat obesity.

Asking whether peptides work is like asking whether chemicals work.

The question worth asking needs to be far more precise.

Does this peptide have credible data to support its use in humans?

It’s the exact same question we ask of any medically prescribed compound, and therefore, the standards we hold peptides to should also be the same.

That’s the whole game. A molecule isn’t good or bad.

It’s useful only once it’s been tested for the purpose you are intending to use it for.

And here’s the part the wellness world keeps skating past: a mechanism is not a result. A clean story about receptors and signalling earns a compound a shot at a trial.

It earns nothing else.

Medicine is littered with molecules that were elegant on paper and inert, or dangerous, when tested properly in humans.

Run the popular grey-market peptides through that filter, and they fall apart fast.

If you do not know the difference between a mechanism study and an outcome trial, then the probability of you being duped into believing something you shouldn’t is very high.

BPC-157 is the one I hear about most often.

Sold for tendons, joints, and gut healing.

There is not a single published full paper with complete data that is a peer-reviewed, randomised controlled trial in humans for any indication, and the overwhelming majority of the literature comes from a single research group connected to the patents.² (Notice the lack of the letter ‘i’ in the last word of that sentence.)

Please reread that last paragraph and recognise that this relates to the MOST commonly touted peptide with the BEST evidence in its class.

The unpublished phase 2 data on ulcerative colitis are interesting.

The rat data is genuinely interesting.

Interesting, however, is not a reason to inject it into your shoulder.

Maybe your rat’s shoulder, but not your patient’s shoulder.

And please remember…. a story is not data.

Yep. Even that story you have in your head about the person who got better.

THAT…. is a story.

What you heard on the podcast last week…. a story.

The Instagram reel…. a story.

The TikTok reel… a story.

Your friend, you met for coffee last week, who had spectacular results…. a story.

If it’s so good, where is the data? It should be pretty easy to find.

CJC-1295 and ipamorelin, the growth-hormone peptides, are sold for muscle and fat loss and recovery.

What’s the human evidence?

For CJC-1295, one set of trials showing it raises growth hormone and IGF-1 the hormone going up, measured over weeks.³

Not muscle. Not fat. Not recovery.

Ipamorelin’s one real efficacy trial was for restarting the gut after surgery, and it failed.⁴

Regulators have since flagged safety concerns, including deaths recorded across the human peptide studies they reviewed, with causation unproven.⁵

Melanotan II, the tanning peptide, does have legitimate trials.

For erectile dysfunction, in small numbers of men.⁶

Not tanning.

That line of work eventually produced an actual licensed drug for something else entirely.⁷

Epitalon, sold for longevity, rests on telomerase activity in a petri dish⁸ and a mortality claim that comes from an unblinded cohort study using a different substance, a pineal extract rather than the peptide, run by a single group, never independently replicated.⁹

Then there’s SS-31, and SS-31 is the one I’d sit you down for.

Real mechanism. Now FDA-approved for Barth syndrome, a brutal mitochondrial disease.¹²

And yet its randomised, placebo-controlled trial missed every endpoint primary and secondary.¹⁰

The encouraging numbers everyone quotes came from the open-label phase, where every patient knew they were on the drug.¹⁰

Its large Phase 3 trial in primary mitochondrial myopathy failed flat.¹¹

Think about that. A peptide with credible biology and a pharmaceutical company behind it can barely show benefit once you blind the trial.

So what exactly are the odds for the ones without any of these benchmarks?

Yep. Very low. Until, of course, a properly conducted trial says otherwise.

That’s the shape of it, over and over.

No human trials. Or maybe a trial of a blood marker (Often in rats) instead of an outcome.

Or a trial in the wrong disease.

Or a trial that failed and got quietly repurposed.

Which brings me to the thing I actually want you to take away.

The fact that you can buy something, and that there’s a neat biological rationale for it, tells you precisely nothing about whether it’ll help you.

People assume the standard I’m describing is some unreachable purist’s bar.

It isn’t, and we know it isn’t, because some peptides have cleared it.

The GLP-1s did. Semaglutide, tirzepatide. Peptides, both.

But they went the long, expensive, deeply boring route.

They jumped through every hurdle and came through with flying colours.

These medications stand to be the most successful medications of all time.

Tirzepatide has shown spectacular reductions in body weight among other health benefits.¹⁴

Semaglutide cut major cardiovascular events, heart attacks, strokes, and cardiovascular death by 20% in more than seventeen thousand people, over years of follow-up.¹³ ¹⁵

We have no doubts that these drugs work.

We know they do, and we know how well, and in whom, and at what dose, and at what risk.

So when someone points to the GLP-1s as proof that peptides are powerful, they’ve got it backwards.

The GLP-1s aren’t the reason to trust the rest. They’re the reason not to.

They show the bar exists and can be met.

The grey-market peptides simply haven’t met it, and until they do, they don’t belong in the same sentence.

None of this means these molecules are worthless forever.

A few may turn out to do something real.

But “might work” and “shown to work” are separated by exactly the process most of them have skipped, and skipping it is not a technicality.

If you’re weighing one up, ask what I ask of any drug before it goes near a patient.

Is there proper evidence that it does the intended thing in humans with the specific issue and claim at play?

Do we know it’s safe, and at what dose?

Do the benefits outweigh the risks?

Is there an approved option that already does this?

For nearly every grey-market peptide, you can’t answer most of those questions in the affirmative.

And to every podcast guest talking up their benefits: they are talking about theoretical mechanisms, not outcome data.

You are being duped. And they know it.

The question is whether you know you are being duped.

And to my own profession, because this matters: a mechanism plus a confident anecdote is not grounds for a recommendation.

We’d laugh that evidence out of the room for a blood pressure-lowering medication or an anticoagulant.

We don’t get to lower the bar because the molecule is fashionable and the patient is keen.

We also don’t let patients decide to ‘Weigh up the risks’ of as-yet-unproven phase 1 or phase 2 drug therapies.

Peptides aren’t the enemy. They are among the best tools we have.

But a peptide earns its place the way every medicine does by being tested, properly, for the thing we’re asking it to do.

Everything else is a story you’re paying to believe.

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1. The Week. The regulation issues with grey-market peptides. 2026 (reporting US customs data via the New York Times).

2. Józwiak M, Bauer M, Kamysz W, Kleczkowska P. Multifunctionality and Possible Medical Application of the BPC 157 Peptide — Literature and Patent Review. Pharmaceuticals (Basel). 2025;18(2):185.

3. Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799–805.

4. Beck DE, Sweeney WB, McCarter MD. Prospective, randomized, controlled, proof-of-concept study of the ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients. Int J Colorectal Dis.2014;29(12):1527–34.

5. US Food and Drug Administration. Evaluation of Ipamorelin-Related Bulk Drug Substances (PCAC briefing document), 2024; and reporting in ProPublica, An FDA Reversal on Peptides Could Open the Market to Unsafe Drugs, 2026.

6. Wessells H, Fuciarelli K, Hansen J, Hadley ME, Hruby VJ, Dorr R, Levine N. Synthetic melanotropic peptide initiates erections in men with psychogenic erectile dysfunction: double-blind, placebo-controlled crossover study. J Urol. 1998;160(2):389–93. (See also Dorr RT, et al. Life Sci. 1996;58(20):1777–84.)

7. Bremelanotide (PT-141), the MC4-receptor–selective analogue developed from this line, is FDA-approved (Vyleesi) for hypoactive sexual desire disorder.

8. Khavinson VKh, Bondarev IE, Butyugov AA. Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bull Exp Biol Med. 2003;135(6):692–695 (page range as indexed; see note above).

9. Khavinson VKh, Morozov VG. Peptides of pineal gland and thymus prolong human life. Neuro Endocrinol Lett.2003;24(3–4):233–240. (Non-blinded cohort of 266 elderly persons; bioregulator extracts Epithalamin/Thymalin.)

10. Reid Thompson W, et al. A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome. Genet Med. 2021; and Thompson WR, et al. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024.

11. Karaa A, et al. Efficacy and safety of elamipretide in individuals with primary mitochondrial myopathy: the MMPOWER-3 randomized clinical trial. Neurology. 2023.

12. US Food and Drug Administration. Accelerated approval of FORZINITY (elamipretide), September 19, 2025 (NDA 215244), to improve muscle strength in Barth syndrome.

13. Lincoff AM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes (SELECT). N Engl J Med.2023;389:2221–2232.

14. Jastreboff AM, et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). N Engl J Med.2022;387:205–216.

15. Wilding JPH, et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). N Engl J Med.2021;384:989–1002.