Goal

Anti-Aging

Name: Peptides for Anti-Aging: What the Research Actually Shows
Creator: Peptide Health Lab

Also known as: Longevity, Healthspan, Healthy aging

A research reference for the compounds mapped to longevity and healthy aging. It sets out what the randomized human trials of oral NAD+ precursors and DHEA actually measured, why the injected forms have no outcomes evidence at all, and where the rest is mice and cell culture.

Last reviewed August 3, 2026

What "anti-aging" actually means in the research

Nothing in the published literature is an anti-aging study. That phrase belongs to a search box, not to a methods section, and the substitutions researchers make in its place are the most useful thing this page can hand you.

Aging biology has a working definition, and it is a list of processes rather than a single thing to slow down. The current framework names twelve hallmarks: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. It also requires that a genuine hallmark be reversible by intervention. That third requirement is a criterion a candidate has to meet, not an achievement any compound on this page has demonstrated.^[1]

So look at what the four studies underneath these compounds actually measured. One measured the concentration of NAD+ metabolites in the muscle of a seventy-year-old man who swallowed a vitamin for three weeks.^[4] One measured bone turnover and skin hydration in French volunteers aged 60 to 79 over a year.^[8] One measured how far a twenty-two-month-old mouse would run.^[11] One measured how much collagen a fibroblast in a dish produced when copper tripeptide was added to the medium.^[13]

Four endpoints, four different questions, and none of them is will I age more slowly. Everything below is arranged around which of those questions a given result actually answers.

What the evidence supports

Raising NAD+ in a human being, with an oral precursor. This is real and it is well done. A two-by-six-week randomized, double-blind, placebo-controlled crossover trial established that chronic nicotinamide riboside is well tolerated and effectively stimulates NAD+ metabolism in healthy middle-aged and older adults; the authors were careful to frame their blood-pressure and arterial-stiffness observations as a reason for future trials rather than as a demonstrated benefit.^[2] A placebo-controlled crossover trial in twelve aged men showed the same target engagement reaches skeletal muscle: the muscle NAD+ metabolome rose and circulating inflammatory cytokines fell, while mitochondrial bioenergetics were unchanged.^[4]

DHEA, where a deficiency has actually been diagnosed. In 24 women with adrenal insufficiency, four months of oral replacement raised initially low concentrations of DHEA, DHEA sulfate, androstenedione, and testosterone into the normal range and significantly improved overall well-being, scores for depression and anxiety, and multiple sexuality measures compared with placebo.^[7] That is a hormone-replacement result in people missing the hormone.

MOTS-c, in mice. The peptide prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity, acting on skeletal muscle by inhibiting the folate cycle and its tethered de novo purine biosynthesis, which activates AMPK.^[10] A later programme enhanced physical performance in young, middle-aged, and old mice and reported that intermittent treatment begun at 23.5 months increased physical capacity and healthspan.^[11] Both results are clean. Both are rodent.

Copper tripeptide, in cell culture. GHK-Cu stimulated collagen synthesis in fibroblast cultures beginning between picomolar and nanomolar concentrations and peaking at a nanomolar dose, independent of any change in cell number.^[13] Thirty-seven years of formulation chemistry has followed from that observation.

Where the evidence is weak

The injected form is precisely the form with no outcomes data. The 2026 PRISMA-guided systematic review looked across 113 intervention studies, 33 of them in humans and 28 of those randomized, and reported that no eligible outcomes trial evaluated intravenous or intramuscular NAD+ itself for anti-aging or wellness indications.^[6] The one human intravenous NAD+ study is a pharmacokinetic pilot: over a six-hour infusion, plasma NAD+ and its metabolites did not change until after two hours, a profile the authors read as the infused molecule being rapidly and completely removed from plasma.^[5] It is a study of where the molecule goes, and it was classified in the review as contextual evidence rather than outcome evidence.

Target engagement kept failing to become benefit. Twelve weeks of nicotinamide riboside in forty obese, insulin-resistant men did not improve insulin sensitivity, endogenous glucose production, glucose disposal, glucose oxidation, resting energy expenditure, lipolysis, lipid oxidation, or body composition. It stayed safe throughout, with normal safety bloods.^[3] The systematic review generalizes that pattern across the field: consistent biochemical engagement, heterogeneous and frequently null functional results.^[6]

The largest anti-aging hormone trial on this page was negative. Two years of placebo-controlled DHEA in 87 elderly men and 57 elderly women raised sulfated DHEA substantially and produced no significant effect on body composition; neither DHEA nor low-dose testosterone altered peak oxygen consumption, muscle strength, or insulin sensitivity, and neither improved quality of life.^[9] The one-year DHEAge study found a narrower set of effects concentrated in women over 70 and its authors said plainly in the abstract that this normalizes some effects of aging without creating "supermen/women".^[8]

No person has been given MOTS-c in a published trial. Every human MOTS-c measurement is of the peptide the body already makes. The observational study is small: plasma concentrations in ten lean and ten obese individuals, similar between groups, correlated with insulin-resistance indices only within the lean group.^[12] The human half of the exercise paper is endogenous expression after exercise, not administration.^[11] There is no dose, no duration, and no adverse-event profile in humans, because there is no human study.

GHK-Cu's clinical file is close to empty. A review asking directly whether topical GHK works as an anti-wrinkle peptide concluded that the cellular studies support the label while noting a surprising absence of clinical studies of GHK-Cu and its palmitoylated derivative, despite their wide use in cosmetic products. The same review reports that the peptide's hydrophilicity and its instability in formulation are unresolved problems.^[14]

Four partial evidence bases do not sum to one. Mapping four compounds to aging can create an impression of convergence that the underlying studies do not support: a vitamin trial, a hormone-replacement trial, a mouse study, and a cell culture do not converge on an outcome. They converge on the observation that several biological processes change with age, which was the starting point.^[1]

How to decide between these

The framework above the citations is the short version. The principle behind it is that the useful comparison is almost never between two of these compounds. It is between a compound and the thing it is quietly being substituted for: a diagnosis, a measurement, or an intervention with outcome data.

Three filters do most of the work here. First, decide which of the three anti-aging questions you are actually asking, because lifespan has no human evidence in this library at all, function has mixed and largely null evidence, and appearance has preclinical evidence with an acknowledged clinical gap.^[14] Second, check whether the human trials studied the same molecule and route you would be given. For NAD+ they did not.^[6] Third, if a hormone is on the table, establish whether there is a diagnosed deficiency, because that is the variable that separated this page's one clearly positive randomized result from its clearly negative one.^[7]

The stack assessment on this site is built to structure that conversation, not to answer it, and its output belongs in a provider visit rather than in a protocol.

Questions to bring to a provider

The productive version of this conversation is not "should I try NAD+." It is "here is what I want to change, here is how I would measure it, and what has actually been shown to move it."

What measurable thing are we trying to change, and over what timescale would a change be detectable?
If the proposal is an infusion rather than an oral precursor, what human outcome evidence exists for that route specifically?^[6]
Is there a diagnosed hormone deficiency here, or an age-typical level? Given that a two-year randomized trial in age-typical older adults found no meaningful benefit, what would change the reasoning? ^[9]
For anything justified by mouse healthspan data, what would have to be true before that transfers to a person?^[11]
What baseline measurements should be taken now so that "it is working" is answerable later with something other than how it feels?
If I compete in a tested sport, what does this year's Prohibited List say about each of these?

Anti-doping status

Two of the four compounds mapped on this page are named on the World Anti-Doping Agency Prohibited List in force for 2026, and both are prohibited at all times, in and out of competition:

MOTS-c: section S4.4.1, metabolic modulators. It is listed by its full name, "mitochondrial open reading frame of the 12S rRNA-c (MOTS-c)", as an example of an activator of AMP-activated protein kinase. Substances in class S4.4 are non-Specified Substances. AMPK activation is the same mechanism the founding mouse work identified for this peptide, so the categorization is not incidental.^[10]
DHEA: section S1.1, anabolic androgenic steroids. It is named as "Prasterone (dehydroepiandrosterone, DHEA, 3ß-hydroxyandrost-5-en-17-one)" in the list of anabolic androgenic steroids prohibited when administered exogenously. Substances in class S1 are non-Specified Substances. Its over-the-counter availability in the United States has no bearing on this.

One further point matters for the other two compounds, and it is a feature of how the list is written rather than an inference. Section S0 covers any pharmacological substance that is not addressed by a later section of the list and that has no current approval by any governmental regulatory health authority for human therapeutic use. Substances do not have to be named to fall inside it; BPC-157 and several others are given only as examples of the class. Whether a particular unapproved preparation of an injectable peptide sits inside S0 is a question for a national anti-doping organization, not for a reference page, and an athlete should ask it before rather than after.

The section assignments above were read from the published Prohibited List itself rather than from the research literature. That distinction is not pedantry. A review article is a source for what the literature shows and never a source for what a regulator has done, and a false statement of prohibited status travels much further than its correction. The list is reissued every year and its sections renumber between editions, so a competing athlete should confirm the current year's list rather than this page.

What the evidence supports for this goal

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Raising NAD+ in humans with an oral precursor

Human RCT evidence human RCT

This is the best-established human result on the page, and it is a biochemical one. A two-by-six-week randomized, double-blind, placebo-controlled crossover trial found chronic nicotinamide riboside well tolerated and effective at stimulating NAD+ metabolism in healthy middle-aged and older adults, with the authors framing blood pressure and arterial stiffness as findings that future trials should assess rather than as established benefits. A separate placebo-controlled crossover trial in twelve aged men found that three weeks of oral nicotinamide riboside elevated the skeletal muscle NAD+ metabolome and depressed circulating inflammatory cytokines. Mitochondrial bioenergetics did not change.

[2] [4]

Functional and metabolic outcomes from NAD+ precursors

Human RCT evidence human RCT · review

Where trials measured what people actually want, the results are mixed and frequently null. A twelve-week randomized placebo-controlled trial in forty obese, insulin-resistant men found that nicotinamide riboside did not improve insulin sensitivity, endogenous glucose production, glucose disposal or oxidation, resting energy expenditure, lipolysis, lipid oxidation, or body composition, while remaining safe. A PRISMA-guided systematic review of 113 preclinical and clinical intervention studies reached the same aggregate conclusion: consistent biochemical target engagement, heterogeneous and often null effects on healthspan-relevant outcomes.

[3] [6]

Injected NAD+ specifically

Anecdotal reports only review · human observational

There is no outcomes evidence for the parenteral form. The 2026 systematic review searched for it and reported that no eligible outcomes trial evaluated intravenous or intramuscular NAD+ itself for anti-aging or wellness indications; the one intravenous pharmacokinetic study it identified was classified as contextual evidence only. That pilot infused NAD+ over six hours in a small cohort and found that plasma NAD+ and its metabolites did not change until after two hours, consistent with the infused molecule being rapidly and completely cleared from plasma. It measured where the molecule went, not what it did.

[6] [5]

DHEA for age-related decline versus for a diagnosed deficiency

Human RCT evidence human RCT

A two-year, placebo-controlled, double-blind trial in 87 elderly men and 57 elderly women with low sulfated DHEA concluded that neither DHEA nor low-dose testosterone replacement had physiologically relevant beneficial effects on body composition, physical performance, insulin sensitivity, or quality of life. A one-year, 280-person, double-blind, placebo-controlled study found selective effects concentrated in women over 70: bone turnover, libido measures, and skin hydration, epidermal thickness, sebum, and pigmentation. Its authors stated in the same breath that this normalizes some effects of aging without creating "supermen/women". Against that, four months of replacement in 24 women with adrenal insufficiency significantly improved well-being, depression and anxiety scores, and sexuality against placebo.

[9] [8] [7]

MOTS-c and mitochondrial aging

Animal studies only animal · human observational

The mouse literature is strong and the human literature contains no administration. MOTS-c treatment prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity in mice, acting through folate-cycle inhibition and AMPK activation in skeletal muscle. A later study enhanced physical performance in young, middle-aged, and old mice and reported that late-life intermittent treatment increased physical capacity and healthspan. The human component of that same paper went no further than showing that exercise induces endogenous MOTS-c expression in muscle and circulation. The only human measurement of the peptide itself is observational: plasma MOTS-c was similar in ten lean and ten obese individuals and correlated with insulin-resistance indices only in the lean group.

[10] [11] [12]

GHK-Cu, collagen, and skin aging

Anecdotal reports only in vitro · review

The founding result is a 1988 fibroblast-culture experiment in which the copper tripeptide stimulated collagen synthesis at picomolar to nanomolar concentrations, independent of any change in cell number. Thirty-seven years later, a review examining whether topical GHK is effective as an anti-wrinkle peptide concluded that cellular studies support the designation while noting a surprising absence of clinical studies of GHK-Cu and its palmitoylated derivative, despite both being widely used in cosmetic products. A wrinkle is also a narrower endpoint than aging.

[13] [14]

Claim area	Evidence & sources	What the research shows
Raising NAD+ in humans with an oral precursor	Human RCT evidence human RCT [2] [4]	This is the best-established human result on the page, and it is a biochemical one. A two-by-six-week randomized, double-blind, placebo-controlled crossover trial found chronic nicotinamide riboside well tolerated and effective at stimulating NAD+ metabolism in healthy middle-aged and older adults, with the authors framing blood pressure and arterial stiffness as findings that future trials should assess rather than as established benefits. A separate placebo-controlled crossover trial in twelve aged men found that three weeks of oral nicotinamide riboside elevated the skeletal muscle NAD+ metabolome and depressed circulating inflammatory cytokines. Mitochondrial bioenergetics did not change.
Functional and metabolic outcomes from NAD+ precursors	Human RCT evidence human RCT · review [3] [6]	Where trials measured what people actually want, the results are mixed and frequently null. A twelve-week randomized placebo-controlled trial in forty obese, insulin-resistant men found that nicotinamide riboside did not improve insulin sensitivity, endogenous glucose production, glucose disposal or oxidation, resting energy expenditure, lipolysis, lipid oxidation, or body composition, while remaining safe. A PRISMA-guided systematic review of 113 preclinical and clinical intervention studies reached the same aggregate conclusion: consistent biochemical target engagement, heterogeneous and often null effects on healthspan-relevant outcomes.
Injected NAD+ specifically	Anecdotal reports only review · human observational [6] [5]	There is no outcomes evidence for the parenteral form. The 2026 systematic review searched for it and reported that no eligible outcomes trial evaluated intravenous or intramuscular NAD+ itself for anti-aging or wellness indications; the one intravenous pharmacokinetic study it identified was classified as contextual evidence only. That pilot infused NAD+ over six hours in a small cohort and found that plasma NAD+ and its metabolites did not change until after two hours, consistent with the infused molecule being rapidly and completely cleared from plasma. It measured where the molecule went, not what it did.
DHEA for age-related decline versus for a diagnosed deficiency	Human RCT evidence human RCT [9] [8] [7]	A two-year, placebo-controlled, double-blind trial in 87 elderly men and 57 elderly women with low sulfated DHEA concluded that neither DHEA nor low-dose testosterone replacement had physiologically relevant beneficial effects on body composition, physical performance, insulin sensitivity, or quality of life. A one-year, 280-person, double-blind, placebo-controlled study found selective effects concentrated in women over 70: bone turnover, libido measures, and skin hydration, epidermal thickness, sebum, and pigmentation. Its authors stated in the same breath that this normalizes some effects of aging without creating "supermen/women". Against that, four months of replacement in 24 women with adrenal insufficiency significantly improved well-being, depression and anxiety scores, and sexuality against placebo.
MOTS-c and mitochondrial aging	Animal studies only animal · human observational [10] [11] [12]	The mouse literature is strong and the human literature contains no administration. MOTS-c treatment prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity in mice, acting through folate-cycle inhibition and AMPK activation in skeletal muscle. A later study enhanced physical performance in young, middle-aged, and old mice and reported that late-life intermittent treatment increased physical capacity and healthspan. The human component of that same paper went no further than showing that exercise induces endogenous MOTS-c expression in muscle and circulation. The only human measurement of the peptide itself is observational: plasma MOTS-c was similar in ten lean and ten obese individuals and correlated with insulin-resistance indices only in the lean group.
GHK-Cu, collagen, and skin aging	Anecdotal reports only in vitro · review [13] [14]	The founding result is a 1988 fibroblast-culture experiment in which the copper tripeptide stimulated collagen synthesis at picomolar to nanomolar concentrations, independent of any change in cell number. Thirty-seven years later, a review examining whether topical GHK is effective as an anti-wrinkle peptide concluded that cellular studies support the designation while noting a surprising absence of clinical studies of GHK-Cu and its palmitoylated derivative, despite both being widely used in cosmetic products. A wrinkle is also a narrower endpoint than aging.

Compounds people map to this goal

Each card carries the compound's FDA status and its overall evidence grade, plus why it shows up on this goal in particular. Follow the card to the full library page for the claim-by-claim evidence review and what published research reported. Dosing and protocol ranges are never on this page.

NAD+

Also known as: Nicotinamide adenine dinucleotide, NAD

Rx via compounding Anecdotal reports only

A research reference for NAD+, a coenzyme whose oral precursors have a real randomized-trial literature, and whose injected form has none.

Why it's on this page

The molecule most readers arrive here for, and the one where the gap between what was studied and what is sold is widest. Every randomized human trial behind the NAD+ story used an oral precursor vitamin, either nicotinamide riboside or nicotinamide mononucleotide, swallowed daily for weeks. A 2026 systematic review of 113 intervention studies found no eligible outcomes trial of intravenous or intramuscular NAD+ itself for any anti-aging indication.

Last reviewed August 2, 2026

DHEA

Also known as: Dehydroepiandrosterone, Prasterone

Rx via compounding Human RCT evidence

A research reference for DHEA, an adrenal steroid precursor sold over the counter as a dietary supplement in the US, dispensed as an approved prescription product only in a local vaginal form and through compounding pharmacies, with randomized evidence that is positive in adrenal insufficiency and largely negative for the anti-aging claims it is best known for.

Why it's on this page

The only compound on this page with a two-year, placebo-controlled aging trial behind it, and the reason it is here is that the trial was negative. Its positive randomized evidence is in adrenal insufficiency, a diagnosed deficiency state, which is a different question from slowing aging in someone whose adrenal glands work. Named on the WADA Prohibited List as prasterone under section S1, prohibited at all times.

Last reviewed August 2, 2026

FOR RESEARCH PURPOSES ONLY

MOTS-c

Also known as: Mitochondrial open reading frame of the 12S rRNA-c, Mitochondrial-derived peptide MOTS-c

Research only Animal studies only

A research reference for MOTS-c, a mitochondria-encoded peptide with a strong mouse metabolic literature, real human biomarker data, and no published trial in which anyone has been given it.

Why it's on this page

A sixteen-residue peptide encoded inside mitochondrial DNA, mapped here because it is the closest thing in this library to a mechanism aimed directly at a hallmark of aging. Its mouse healthspan data are real and striking; the human data are entirely about the peptide the body already makes, because no published trial has administered it to a person. Prohibited at all times under WADA section S4.4.1 as an AMPK activator.

Last reviewed August 2, 2026

FOR RESEARCH PURPOSES ONLY

GHK-Cu

Also known as: Copper tripeptide-1, GHK, Glycyl-L-histidyl-L-lysine, Copper peptide

Research only Animal studies only

A research reference for GHK-Cu, a naturally occurring copper-binding tripeptide with four decades of cell and rodent work on matrix remodeling and almost no controlled human evidence.

Why it's on this page

A copper-binding tripeptide isolated from human plasma in 1973, mapped here for the visible half of what people mean by anti-aging: skin, collagen, wrinkles. Four decades of cell and animal work sit behind it and almost no controlled human work, which is unusual for an ingredient this widely used in cosmetic formulations.

Last reviewed August 2, 2026

How to decide between them

These are the questions that actually change the answer. Work through them with a licensed provider. None of them can be answered by a page that does not know your labs, your history, or your medications.

Are you asking about how long you live, how well you function, or how you look?

These are three different literatures and only one of them has human randomized trials in this library. Aging biology defines its subject as twelve interconnected processes: genomic instability, mitochondrial dysfunction, cellular senescence, chronic inflammation and nine others. It treats reversal by intervention as a criterion a candidate must meet, not a property it is assumed to have. No compound mapped here has been tested against a lifespan or mortality endpoint in humans, so if that is the question, the honest answer is that nothing on this page addresses it. If the question is skin appearance, the evidence is cosmetic and mostly preclinical. If it is metabolic function, it is oral precursor trials, and those are mixed.

Human RCT evidence [1] [6]
Is the human evidence about the molecule you would actually be given, or about an oral precursor of it?

This single question removes most of the NAD+ literature from the column it is usually filed under. Chronic oral nicotinamide riboside raises the NAD+ metabolome in healthy middle-aged adults and in aged skeletal muscle, and those are well-conducted placebo-controlled crossover trials. They are trials of a vitamin taken by mouth. A six-hour intravenous NAD+ infusion has been characterized once, for its plasma and urine pharmacokinetics, in a pilot with no clinical outcome. The 2026 systematic review looking specifically for parenteral outcomes trials found none. Evidence for a precursor is not evidence for an infusion.

Human RCT evidence [2] [5] [6]
Are you correcting a measured deficiency, or adding to a level that is already normal for your age?

DHEA is the clearest natural experiment on this page and the answer differs by which side of that line you are on. In women with adrenal insufficiency, where the deficiency is real and diagnosed, four months of replacement significantly improved well-being, depression and anxiety scores, and sexuality measures against placebo. In healthy elderly people with the ordinary age-related decline, two years of the same hormone produced no physiologically relevant benefit on body composition, physical performance, insulin sensitivity, or quality of life. The diagnosis, not the molecule, is what separated those two results.

Human RCT evidence [7] [9]
Do you compete in a tested sport, at any level?

Then this decision is settled before any evidence question is reached. MOTS-c acts by inhibiting the folate cycle and its tethered purine biosynthesis, which activates AMP-activated protein kinase. AMPK activators are exactly the class the 2026 Prohibited List names under section S4.4.1, with MOTS-c given as an example. DHEA is named as prasterone in the anabolic androgenic steroid list under S1. Both are prohibited at all times, in and out of competition. Read the section below before anything else on this page, and confirm the current year's list rather than this page.

[10]
How would you know afterwards whether anything actually worked?

Aging is the goal where a decision is easiest to make and hardest to evaluate, because the outcome you care about takes decades and the measurement you can get takes weeks. The NAD+ trials are the cautionary case. Blood and muscle NAD+ concentrations rise reliably, which is a real biochemical result and a demonstration that the target was engaged. Effects on function, metabolism, and vascular measures come out heterogeneous and often null. A biomarker that moves is not the same as a person who ages more slowly, and deciding in advance which measurable thing would change your mind is what separates a decision from a subscription.

Human RCT evidence [4] [6]

Questions for your provider

Bring this goal page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here applies to your situation. This goal page cannot. Peptide Health Lab does not prescribe and does not sell peptides.

A goal is not a diagnosis. The most useful version of this conversation usually starts with what is actually driving the symptom, not with which compound to try.

Citations

14 sources · every identifier checked against PubMed

[1] Hallmarks of aging: An expanding universe · Cell, 2023. Review
[2] Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults · Nature Communications, 2018. Human RCT
[3] A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects · The American Journal of Clinical Nutrition, 2018. Human RCT
[4] Nicotinamide Riboside Augments the Aged Human Skeletal Muscle NAD+ Metabolome and Induces Transcriptomic and Anti-inflammatory Signatures · Cell Reports, 2019. Human RCT
[5] A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD · Frontiers in Aging Neuroscience, 2019. Human observational study
[6] NAD+ supplementation for anti-aging and wellness: A PRISMA-guided systematic review of preclinical and clinical evidence · Ageing Research Reviews, 2026. Review
[7] Dehydroepiandrosterone replacement in women with adrenal insufficiency · The New England Journal of Medicine, 1999. Human RCT
[8] Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of the DHEAge Study to a sociobiomedical issue · Proceedings of the National Academy of Sciences, 2000. Human RCT
[9] DHEA in elderly women and DHEA or testosterone in elderly men · The New England Journal of Medicine, 2006. Human RCT
[10] The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance · Cell Metabolism, 2015. Animal study
[11] MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis · Nature Communications, 2021. Animal study
[12] Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals · Journal of Investigative Medicine, 2018. Human observational study
[13] Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ · FEBS Letters, 1988. In vitro study
[14] Topically applied GHK as an anti-wrinkle peptide: Advantages, problems and prospective · BioImpacts, 2025. Review

Before you act on any of this

This page is educational only and is not medical advice. It does not diagnose, treat, or prescribe. Review it with a licensed provider before making any health decision. Peptide Health Lab does not sell peptides.

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