Health Intelligence
Peptides - When Science Becomes Marketing
Darren Crowder · · 20 min read
Peptides are everywhere. Some of the science is genuinely exciting. But somewhere between the laboratory, the skincare bottle and Instagram, “peptide” has started becoming a promise all by itself.
I’ve been watching something interesting happen with peptides.
They are suddenly everywhere.
Skincare. Supplements. Hair products. Recovery. Muscle building. Weight management. Longevity. Biohacking.
Scroll through social media for long enough and you could be forgiven for thinking we’ve discovered a molecule capable of fixing almost everything.
I recently saw marketing for a well-known skincare product discussing peptides in relation to sagging around the eye area.
And it stopped me.
Not because peptides are nonsense.
They’re absolutely not.
But because we’re beginning to take a legitimate and enormously diverse area of science and compress it into one very convenient marketing word:
PEPTIDES.
And once that happens, something important gets lost.
Context.
What is a peptide anyway?
At its simplest, a peptide is a chain of amino acids.
But saying something “contains peptides” tells you remarkably little about what that product will actually do.
Different peptides have different structures, biological activities, delivery requirements and levels of evidence.
There are peptide-based medicines, including the GLP-1 drugs we’ll come to shortly (Lau and Dunn, 2018).
There are naturally occurring signalling peptides, such as the gut hormone GLP-1 (Holst, 2007).
There are collagen-derived peptides taken orally (Nukaly et al., 2026).
There are synthetic peptides used in cosmetics (van Walraven et al., 2025).
And there are experimental peptides circulating in parts of the biohacking community.
Calling all of those simply “peptides” is a little like calling every vehicle “transport” and then expecting a bicycle and an Airbus to behave the same way.
They don’t.
The evidence is real. But read the small print.
This is where the conversation gets particularly interesting.
A 2026 systematic review and meta-analysis examined 19 randomised controlled trials involving 1,341 participants looking at oral and topical peptides for skin ageing (Nukaly et al., 2026).
The headline sounds encouraging.
The researchers found improvements in hydration and brightness and a modest pooled improvement in wrinkles (Nukaly et al., 2026).
Stop there and you have a fantastic advert for peptide skincare.
But don’t stop there.
Of those 1,341 participants, 1,236, or 92.17%, received oral collagen peptides.
Only 105, or 7.8%, received topical formulations (Nukaly et al., 2026).
And when researchers separated the results, the topical peptide subgroup showed a smaller, non-statistically-significant effect on wrinkles (Nukaly et al., 2026).
Effects on elasticity and skin density were also inconsistent (Nukaly et al., 2026).
That doesn’t mean topical peptides don’t work.
It means the evidence supports a much more careful statement than:
“Peptides fix ageing skin.”
And certainly something much more careful than implying that applying a peptide cosmetic can meaningfully lift structurally sagging tissue around the eye.
A wrinkle isn’t sagging skin
This distinction matters.
Wrinkles, hydration, elasticity, skin density and tissue laxity are related aspects of ageing, but they are not interchangeable outcomes.
Ageing around the eye is particularly complicated.
The appearance of the area can reflect changes across skin, connective tissues, fat compartments, ligaments, muscles and underlying facial structures (Alghoul and Codner, 2013; Hong et al., 2025; Beer et al., 2026).
So evidence that a formulation improves hydration or reduces measured wrinkle depth cannot automatically be extrapolated into:
“This lifts sagging eyelids.”
That’s an entirely different proposition requiring evidence for that particular outcome.
This is one of the biggest problems I see in wellness marketing.
A small piece of legitimate science gets stretched. A biological mechanism becomes a benefit. Then the benefit becomes a claim. Then social media turns the claim into certainty.
The skin has another idea
There is another rather fundamental issue with topical peptides.
Your skin isn’t simply a sponge waiting to absorb whatever expensive serum you put onto it.
It’s a barrier.
And a very good one.
Many peptides have relatively high molecular weights, are hydrophilic and contain ionisable groups, characteristics which can make passage through the stratum corneum difficult (Mortazavi and Moghimi, 2022).
A 2022 scientific review specifically investigating anti-wrinkle peptides concluded that most are not good candidates for passive skin permeation and that many may not reach their intended targets at sufficient concentrations without techniques designed to enhance penetration (Mortazavi and Moghimi, 2022).
That’s enormously important.
Because there are actually several different questions:
- Is the peptide in the bottle?
- Does that peptide demonstrate biological activity in a laboratory?
- Can it penetrate human skin in this particular formulation?
- Can enough of it reach the intended biological target?
- And has the finished product demonstrated the claimed outcome in humans?
Those questions are not interchangeable.
Yet marketing frequently behaves as though answering the first question automatically answers all five.
It doesn’t.
Copper peptides: fascinating biology, surprising evidence gaps
Take GHK-Cu, commonly called a copper peptide.
It is one of the best-known ingredients in peptide skincare (Mortazavi et al., 2024).
There is interesting biological evidence around GHK and its derivatives, including laboratory evidence relevant to extracellular-matrix biology (Mortazavi et al., 2024).
But a scientific review examining topical GHK reported something consumers probably won’t encounter on the front of the bottle:
Published information concerning skin permeability and effectiveness remains insufficient (Mortazavi et al., 2024).
The researchers also described a “surprising absence” of clinical studies using GHK-Cu and Pal-GHK, despite their widespread use in anti-wrinkle products (Mortazavi et al., 2024).
Again, that does not mean copper peptides are useless.
It means:
The confidence of the marketing should not exceed the confidence of the evidence.
What about “Botox-like peptides”?
This might be my favourite example of how far language can travel from science into marketing.
Acetyl hexapeptide-8, sometimes known commercially as Argireline, is frequently described as a “Botox-like” peptide.
There is research suggesting potential improvements in wrinkles, hydration and elasticity (Zdrada-Nowak et al., 2025).
Interesting.
But a 2025 review identified an important problem.
Because of its hydrophilic nature and molecular size, acetyl hexapeptide-8 has limited permeability through the stratum corneum (Zdrada-Nowak et al., 2025).
And whether sufficient peptide reaches neuromuscular junctions to produce the proposed muscle-related mechanism remains uncertain (Zdrada-Nowak et al., 2025).
So when you see:
“Botox-like”
don’t necessarily read:
“Works like Botox.”
Those are very different statements.
102 cosmetic peptides. How much evidence?
A 2025 peer-reviewed review identified 102 commercially available cosmetic peptides (van Walraven et al., 2025).
Their proposed activities were extensive, including collagen and hyaluronic-acid signalling, pigmentation modulation, antioxidant activity, cellular defence, immune modulation, microbiome effects, enzyme inhibition and neurotransmitter inhibition (van Walraven et al., 2025).
That sounds extraordinary.
But the paper was specifically reviewing the in-vitro and ex-vivo evidence behind those commercially available peptides (van Walraven et al., 2025).
In other words, much of what we understand about the biological potential of cosmetic peptides does not automatically constitute evidence that a finished cosmetic produces the same clinically meaningful result in a living person.
And this isn’t a new concern.
A systematic review of clinical studies investigating extracellular-matrix-stimulating peptides found only 15 independent studies (Michalek et al., 2019).
Only 6 used placebo controls.
Only 5 were double-blinded (Michalek et al., 2019).
The researchers concluded that the clinical literature was sparse and contained significant methodological limitations (Michalek et al., 2019).
That’s a rather different picture from the confidence you might get scrolling Instagram.
GLP-1: what strong evidence looks like
Now let’s look at the other end of the scale.
GLP-1 is a peptide too.
It’s a hormone made of 30 amino acids, produced by cells in your gut and released when you eat (Holst, 2007).
It prompts the pancreas to release insulin, holds back glucagon, slows the gut and helps regulate appetite (Holst, 2007).
But your own GLP-1 doesn’t last. An enzyme called DPP-IV breaks it down extremely rapidly, even before the hormone has left the gut (Holst, 2007).
So the medicines aren’t the natural hormone. They’re engineered versions.
Semaglutide, for example, has two amino acid substitutions compared with human GLP-1, plus a fatty acid chain that helps it bind to albumin, a protein in the blood. The aim was a once-weekly medicine, and in mini-pigs its half-life in the blood was 46.1 hours (Lau et al., 2015).
Then came the part most cosmetic peptides are missing: large trials of the finished medicine, in thousands of people.
Weight. In the STEP 1 trial, 1,961 adults with obesity (or overweight with a related health condition) and without diabetes were randomly given semaglutide 2.4 mg once a week or a placebo, alongside lifestyle support, for 68 weeks. On average, the semaglutide group lost 14.9% of their body weight. The placebo group lost 2.4%. And 50.5% of the semaglutide group lost 15% or more, against 4.9% on placebo (Wilding et al., 2021).
Tirzepatide, which acts on GLP-1 and a second gut hormone receptor called GIP, was tested in 2,539 adults for 72 weeks. At the highest dose, average weight loss was 20.9%, against 3.1% on placebo (Jastreboff et al., 2022).
Heart. The SELECT trial followed 17,604 adults aged 45 or over who already had cardiovascular disease and were overweight or had obesity, but did not have diabetes. After an average of 39.8 months, a heart attack, a stroke or death from cardiovascular causes had happened to 6.5% of the semaglutide group and 8.0% of the placebo group. That’s a 20% lower risk (hazard ratio 0.80; 95% confidence interval 0.72 to 0.90) (Lincoff et al., 2023).
Kidneys. The FLOW trial enrolled 3,533 people with type 2 diabetes and chronic kidney disease. Semaglutide cut the risk of a combined outcome (kidney failure, a drop of at least half in estimated kidney function, or death from kidney or heart causes) by 24% (hazard ratio 0.76; 95% confidence interval 0.66 to 0.88). A planned interim analysis recommended stopping the trial early, after a median follow-up of 3.4 years (Perkovic et al., 2024).
Liver. In an ongoing trial of 1,197 people with a fatty liver disease involving inflammation and moderate or advanced scarring (called MASH), a planned interim analysis of the first 800 patients looked at week 72. The liver inflammation had resolved, without the scarring getting worse, in 62.9% of the semaglutide group against 34.3% on placebo. Scarring had reduced, without the inflammation getting worse, in 36.8% against 22.4% (Sanyal et al., 2025). The trial is still running, so these are interim results.
Look at what these trials have in common.
A named peptide.
A stated dose.
The finished medicine tested, not just an ingredient in a dish.
Thousands of people.
Clear outcomes.
That’s what it looks like when a peptide earns its reputation.
One thing worth knowing: every one of those trials was funded by the manufacturer. Novo Nordisk funded the semaglutide trials and Eli Lilly funded the tirzepatide trial (Wilding et al., 2021; Jastreboff et al., 2022; Lincoff et al., 2023; Perkovic et al., 2024; Sanyal et al., 2025). It’s declared in each paper, and you should know.
Even here, read the small print
Strong evidence doesn’t mean no downsides.
In STEP 1, nausea and diarrhoea were the most common side effects, and more people on semaglutide stopped treatment because of stomach and gut problems: 4.5%, against 0.8% on placebo (Wilding et al., 2021). In SELECT, side effects led 16.6% of the semaglutide group to stop permanently, against 8.2% on placebo (Lincoff et al., 2023).
Stopping matters too. In a follow-up of 327 STEP 1 participants, a year after treatment and the lifestyle programme ended, those who had been on semaglutide had regained 11.6 percentage points of body weight, about two thirds of the 17.3% they had lost. Most of the heart and metabolic improvements had moved back towards where they started. The authors say this suggests ongoing treatment is needed to keep the benefits, and this follow-up analysis was exploratory (Wilding et al., 2022).
And in June 2025, the European Medicines Agency’s safety committee concluded that an eye condition called NAION (non-arteritic anterior ischaemic optic neuropathy) is a very rare side effect of semaglutide medicines (EMA, 2025).
None of this is advice on whether anyone should take these medicines. They’re prescription medicines, and that’s a conversation for you and your doctor.
And the brain, and ageing? This is where I slow down.
GLP-1 drugs have now shown benefits in more places than weight loss alone: the heart, the kidneys, the liver. So it’s tempting to assume they’ll work everywhere, including the brain.
The idea isn’t silly. Before the big trials, animal, clinical and real-world studies had suggested a lower risk of dementia and Alzheimer’s disease after GLP-1 drug exposure (Cummings et al., 2026).
So it was tested properly.
The evoke and evoke+ trials gave oral semaglutide, or a placebo, to 3,808 people aged 55 to 85 with confirmed early Alzheimer’s disease, for up to three years. The question was whether it slowed the decline. It didn’t. After two years, scores on the clinical dementia rating scale had worsened by 2.3 points with semaglutide and 2.3 with placebo in evoke, and by 2.2 against 2.1 in evoke+. Both trials were stopped because of the negative result (Cummings et al., 2026).
Notice what that trial tested: treating people who already had Alzheimer’s disease. It didn’t test prevention.
Prevention is a different question, and the evidence is a different kind. Researchers compared 1,320 matched people with mild cognitive impairment and type 2 diabetes who started either a GLP-1 drug or a different diabetes drug. Over up to five years, 101 of the GLP-1 group developed dementia, against 132 in the other group (hazard ratio 0.74; 95% confidence interval 0.57 to 0.95) (Schechter et al., 2026). That’s interesting. But people weren’t randomly assigned, and the authors themselves call it hypothesis-generating.
And ADHD? One study used genetics as a stand-in for the drug’s effect to look at ten mental health conditions, ADHD among them. It found a link with lower schizophrenia risk (odds ratio 0.84; 95% confidence interval 0.71 to 0.98), which the authors suggest may work through body weight. For the other nine, including ADHD, it found insufficient evidence of a link (Xiang and Peng, 2025). That’s not a trial, and it doesn’t show these drugs can’t help. It means the evidence to say they can isn’t there yet.
And “slowing ageing”? You may have seen a headline saying semaglutide slows biological ageing by about 9%. The number is real. But it comes from one measure, in one small trial.
The trial gave semaglutide or a placebo for 32 weeks to adults living with HIV and extra belly fat. Ageing wasn’t what it was designed to test. The researchers went back afterwards and measured “epigenetic clocks”, which estimate biological age from chemical tags on DNA in a blood sample. In 84 people (45 on semaglutide, 39 on placebo), one clock called DunedinPACE ran 0.09 units slower per year on semaglutide (95% confidence interval −0.17 to −0.02; p = 0.010), which the authors describe as about 9% slower (Corley et al., 2026).
Now the small print. The 9% belongs to that one clock, not to all of them. The team looked at more than a dozen clocks, several showed no clear difference, and the authors did not adjust their statistics for testing so many. The analysis was post hoc and exploratory, in people with HIV, over 32 weeks. A “brain ageing” clock did come out lower, but these clocks are estimated from blood, and the authors caution that they aren’t evidence of what is happening inside the tissue itself, or of any change in lifespan (Corley et al., 2026).
A second, smaller study from the same lead author followed 41 people with HIV and fatty liver disease on semaglutide for 24 weeks, with no placebo group. The clocks didn’t fall on average: DunedinPACE changed by a median of +0.018 (Corley et al., 2026, SLIM LIVER). With no comparison group it can’t confirm or rule out anything. But it didn’t show the same slowing.
So here’s where the published evidence stands:
- Weight, heart, kidney and liver: large randomised trials.
- Treating Alzheimer’s disease: a large randomised trial, no benefit.
- Preventing dementia: observational signals, which the authors call hypothesis-generating.
- ADHD: one genetic study, which found insufficient evidence of a link.
- Slowing ageing: one small, exploratory analysis of a randomised trial in people with HIV, using blood-based “clocks”.
That isn’t a failure of the science. That’s the science working.
Some ideas hold up. Some don’t. And some are still waiting for their trial.
Same family of molecules. Completely different levels of evidence.
The word “peptide” didn’t tell us which was which. The trials did.
The problem isn’t peptides
And this is important.
I am not anti-peptide.
Quite the opposite.
Peptide science is fascinating.
There are established peptide therapeutics (Lau and Dunn, 2018), and the GLP-1 trials above show what it looks like when the evidence is really there. There are promising cosmetic applications. There is active research into better delivery technologies (Mortazavi et al., 2024). And there will almost certainly be peptide applications in future medicine that we haven’t yet imagined.
The problem begins when we stop asking which peptide?
Because the word itself isn’t evidence.
It isn’t a dosage.
It isn’t bioavailability.
It isn’t penetration.
It isn’t a clinical endpoint.
And it isn’t proof that the finished product sitting in your bathroom will reproduce an effect observed somewhere else under completely different experimental conditions.
Nine questions I’d ask before believing the claim
When I see PEPTIDES prominently displayed on a product now, these are the questions I want answered:
- 1. Which peptide?
- 2. How much is actually present?
- 3. What formulation is delivering it?
- 4. Can it reach the intended biological target?
- 5. What was demonstrated in humans rather than cells or tissue models?
- 6. Was the finished product actually studied?
- 7. How many people were studied and for how long?
- 8. What endpoint actually improved: hydration, wrinkles, elasticity, pigmentation, laxity, something else?
- 9. Does that evidence genuinely support the words being used in the advert?
That’s not cynicism.
That’s health literacy.
This is why context matters
This takes me straight back to something I’ve written about before at Enbodie.
A product isn’t its hero ingredient.
We learned that recently when looking at a peptide eyelash serum after someone close to me developed a significant reaction around her eye.
The word “peptide” on the front didn’t tell us about the complete formulation, the application area, exposure, individual susceptibility or other ingredients.
And exactly the same principle applies here.
A product doesn’t become effective because an ingredient has an interesting biological mechanism.
The formulation matters.
The concentration matters.
The delivery matters.
The evidence matters.
And the person using it matters.
That’s why we’re building Enbodie around a fundamentally different question.
Not:
“Are peptides good?”
But:
“What does the evidence actually say this product can do, in this formulation, used this way, for this person?”
There is another side to health intelligence too.
Sometimes technology should help us discover something useful.
Sometimes it should warn us about something harmful.
But sometimes its most valuable job might simply be saying:
The evidence doesn’t support that promise yet.
Peptides don’t need the hype.
The real science is interesting enough.
💚🌿🌱
Scientific references
Every claim above is linked to its source where it appears. Here is the full list, with the PubMed record and the full paper for each study, and the regulator’s own page for the one regulator statement.
- Nukaly HY et al. Oral and topical peptides for skin aging: systematic review and meta-analysis of randomized controlled trials. Frontiers in Medicine, 2026. PubMed record | Full paper
- Mortazavi SM, Moghimi HR. Skin permeability, a dismissed necessity for anti-wrinkle peptide performance. International Journal of Cosmetic Science, 2022. PubMed record | Full paper
- Mortazavi SM, Mohammadi Vadoud SA, Moghimi HR. Topically applied GHK as an anti-wrinkle peptide: Advantages, problems and prospective. BioImpacts, 2024. PubMed record | Full paper
- van Walraven N et al. Bioactive peptides in cosmetic formulations: Review of current in vitro and ex vivo evidence. Peptides, 2025. PubMed record | Full paper
- Zdrada-Nowak J, Surgiel-Gemza A, Szatkowska M. Acetyl Hexapeptide-8 in Cosmeceuticals: A Review of Skin Permeability and Efficacy. International Journal of Molecular Sciences, 2025. PubMed record | Full paper
- Michalek IM, Lelen-Kaminska K, Caetano Dos Santos FL. Peptides stimulating synthesis of extracellular matrix used in anti-ageing cosmetics: Are they clinically tested? A systematic review of the literature. Australasian Journal of Dermatology, 2019. PubMed record | Full paper
- Lau JL, Dunn MK. Therapeutic peptides: Historical perspectives, current development trends, and future directions. Bioorganic & Medicinal Chemistry, 2018. PubMed record | Full paper
- Alghoul M, Codner MA. Retaining ligaments of the face: review of anatomy and clinical applications. Aesthetic Surgery Journal, 2013. PubMed record | Full paper
- Hong G-W, Choi W, Yoon S-E, Wan J, Yi K-H. Anatomical-Based Filler Injection Diagnosis to Treatment Techniques: Infraorbital Groove and Hollowness. Life, 2025. PubMed record | Full paper
- Beer J et al. What’s New With Under Eye Treatment: A Multispecialty Systematic Review of Recent Under Eye Treatments. Dermatologic Surgery, 2026. PubMed record | Full paper
- Holst JJ. The physiology of glucagon-like peptide 1. Physiological Reviews, 2007. PubMed record | Full paper
- Lau J et al. Discovery of the Once-Weekly Glucagon-Like Peptide-1 (GLP-1) Analogue Semaglutide. Journal of Medicinal Chemistry, 2015. PubMed record | Full paper
- Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine, 2021. PubMed record | Full paper
- Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine, 2022. PubMed record | Full paper
- Lincoff AM et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. New England Journal of Medicine, 2023. PubMed record | Full paper
- Perkovic V et al. Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes. New England Journal of Medicine, 2024. PubMed record | Full paper
- Sanyal AJ et al. Phase 3 Trial of Semaglutide in Metabolic Dysfunction-Associated Steatohepatitis. New England Journal of Medicine, 2025. PubMed record | Full paper
- Wilding JPH et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Diabetes, Obesity and Metabolism, 2022. PubMed record | Full paper
- European Medicines Agency, Pharmacovigilance Risk Assessment Committee (PRAC). PRAC concludes eye condition NAION is a very rare side effect of semaglutide medicines Ozempic, Rybelsus and Wegovy. 6 June 2025. EMA statement
- Cummings JL et al. Efficacy and safety of oral semaglutide 14 mg (flexible dose) in early-stage symptomatic Alzheimer’s disease (evoke and evoke+): two phase 3, randomised, placebo-controlled trials. The Lancet, 2026. PubMed record | Full paper00459-9)
- Schechter M et al. Dementia progression with GLP-1 receptor agonists in people with mild cognitive impairment and type 2 diabetes: target-trial emulation study. Alzheimer’s & Dementia (N Y), 2026. PubMed record | Full paper
- Xiang L, Peng Y. Impact of Glucagon-like Peptide-1 Receptor Agonists on Mental Illness: Evidence from a Mendelian Randomization Study. International Journal of Molecular Sciences, 2025. PubMed record | Full paper
- Corley MJ et al. Semaglutide slows epigenetic aging in a randomized trial of HIV-associated lipohypertrophy. Nature Communications, 2026. PubMed record | Full paper
- Corley MJ et al. Pilot study of epigenetic aging and treatment response to semaglutide in the SLIM LIVER study. npj Aging, 2026. PubMed record | Full paper