Peptide Health Lab

Goal

Hair

Also known as: Hair loss, Hair growth

A research reference for the compounds people map to hair loss and hair growth, including the finding that the copper-peptide hair study everyone cites tested a different peptide, and that nothing in this library has a published human efficacy result for hair.

Last reviewed August 3, 2026

What "hair" actually means in the research

This page is thin, and it is thin on purpose. The honest finding is easier to state than to hear: this library holds no compound with a published human efficacy result for hair growth or hair loss. Everything below explains how the adjacent evidence got mistaken for that.

Start with what the studies underneath these compounds actually examined. One tested a copper tripeptide on human hair follicles held in culture and on isolated dermal papilla cells.[3] One examined hair cycling in mice genetically stripped of both main thyroid hormone receptor isoforms.[6] One measured hypothyroid symptom and tiredness scores in adults over 65 whose thyrotropin was mildly elevated.[7] One counted acne lesions and scored hair patterns in trans men on long-term testosterone.[5]

Four experiments, four questions, and none of them is "will this make hair grow back on this head." The gap between those questions and the reader's is where the whole hair-peptide category lives. Reviews of hair loss keep returning to the same three presentations: telogen effluvium, alopecia areata, and androgenetic alopecia. Each has a different mechanism, which is why a single compound framed as a general hair treatment is already a category error.[8]

What the evidence supports

A copper tripeptide lengthened follicles in a dish. Not this one. This is the single most important sentence on the page. The 2007 study reported that AHK-Cu, at picomolar to nanomolar concentrations, stimulated elongation of explanted human hair follicles and proliferation of cultured dermal papilla cells, with a shift in the Bcl-2/Bax ratio and reduced cleaved caspase-3 and PARP. The authors also reported that the reduction in apoptotic dermal papilla cells did not reach statistical significance.[3] AHK-Cu is alanyl-histidyl-lysine-copper. GHK-Cu is glycyl-histidyl-lysine-copper. They differ at the first residue, and no published study has compared them on a hair outcome. The result is real; it is simply not a result about GHK-Cu.

Thyroid hormone matters to the hair cycle, in mice and in clinical description. Mice lacking both TRα1 and TRβ show impaired hair cycling with reduced follicular cell proliferation, and develop alopecia after serial depilation; deleting either receptor alone does not.[6] On the human side, the association between thyroid dysfunction and widespread shedding is described consistently enough that thyroid function is a standard thing to measure in someone losing hair diffusely.[8] That is a diagnostic finding, not a treatment finding.

Androgens change scalp hair. The direction is down. Scalp hair grows constitutively in the absence of androgens, while body hair growth depends on them, and dihydrotestosterone is implicated as the key androgen in the progressive miniaturization that produces pattern hair loss.[1] The clearest human demonstration on this page is a study of trans men on testosterone: after long-term therapy, 32.7% had mild frontotemporal hair loss and 31% had moderate to severe androgenetic alopecia.[5]

What has actually cleared a randomized trial belongs to drugs that are not here. 416 men were randomized to dutasteride at four doses, finasteride, or placebo for 24 weeks, with target-area hair count as the endpoint; hair count rose over placebo in a dose-dependent fashion, confirmed by blinded photographic panel review.[2] That is what a positive hair trial looks like, and it is the comparison every compound on this page is competing against.

Where the evidence is weak

For GHK-Cu and hair, "weak" is the wrong word: there is nothing. A 2025 review set out to answer whether topically applied GHK is sufficiently effective on wrinkles and reported a surprising absence of clinical studies using GHK-Cu and its palmitoylated derivative, despite both being widely used in cosmetic products; permeability and formulation instability remain open questions.[9] If the clinical literature is absent for the indication the ingredient is actually marketed for, the hair literature is not somewhere ahead of it.

A citation can be real and still not be about the compound you are reading about. The AHK-Cu result is the clearest example on this property of a genuine paper attached to the wrong molecule by repetition. It passes any check that asks whether the study exists.[3]

Correcting a deficiency is not the same intervention as adding hormone. In 737 adults aged 65 and over with persisting subclinical hypothyroidism, levothyroxine lowered thyrotropin and produced no difference from placebo in hypothyroid symptoms or tiredness at one year, with no benefit on secondary outcomes.[7] Desiccated thyroid extract has been compared head to head with levothyroxine in a randomized double-blind crossover trial in 70 hypothyroid patients and produced no difference in symptoms or neurocognitive measures.[4] Neither trial had a hair endpoint at all, which is worth stating plainly rather than reading across.

Uncontrolled human data stays uncontrolled. The trans men study had no control group, and the dermatological outcomes were not demonstrably related to individual serum testosterone or dihydrotestosterone levels.[5]

Three thin evidence bases do not sum to one good one. Mapping three compounds to a goal can create an impression of convergence. Here they do not even converge on a mechanism: one is a laboratory result about a different peptide, one is a reason to order a blood test, and one runs in the opposite direction from what the reader wants.[1]

How to decide between these

The decision framework above the citations is the short version. The principle behind it is that on this goal the right comparison is almost never between two compounds on this page. The comparison that matters is between anything on this page and an option with a measured hair count behind it.[2]

Three filters do the work. First, describe the pattern: patterned recession and diffuse shedding lead to different literatures and different clinicians.[8] Second, measure before treating. Thyroid status is testable, and an untested assumption about it is the most common way this goal turns into a compound decision that should have been a laboratory one.[7] Third, decide what counts as evidence, because applying "published human efficacy trial" as a filter removes every compound mapped here.[9]

The stack assessment on this site is built to structure that conversation rather than to answer it, and its output is a starting point for a provider visit.

Questions to bring to a provider

The productive version of this conversation is not "will copper peptides work." It is "here is the pattern of loss, here is when it started, and here is what has actually been measured."

  • Which is the working diagnosis: patterned miniaturization, diffuse shedding, or an inflammatory scalp condition? And what does the evidence offer for that one specifically?[8]
  • Has thyroid function been tested, and if it is abnormal, is the treatment target the laboratory value, the symptoms, or the hair?[7]
  • Given that the copper-peptide hair result was generated with a different tripeptide in cell culture, what would have to exist before GHK-Cu were worth considering at all?[3]
  • If testosterone therapy is already under discussion for another reason, how should the documented rate of androgenetic alopecia on long-term therapy be factored in?[5]
  • Which objective measure would show whether anything changed: standardized photography, a target-area hair count, or trichoscopy?[2]

Anti-doping status

One compound mapped on this page is named in the World Anti-Doping Agency Prohibited List in force for 2026:

  • Testosterone: section S1.1, anabolic androgenic steroids. It is listed by name in S1.1, and S1 is prohibited at all times, both in and out of competition. Substances in this class are non-Specified Substances, which carries different sanctioning consequences from a Specified Substance and is a distinction worth raising with a national anti-doping organization rather than settling from a web page.

Neither GHK-Cu nor thyroid hormone is named in the 2026 List. That is not the same as being cleared: section S0 is written to cover any pharmacological substance not addressed elsewhere on the List and with no current approval by any governmental regulatory health authority for human therapeutic use, so it is defined by regulatory status rather than by name, and an unapproved injectable preparation is exactly the shape it describes. An athlete should confirm the position with a national anti-doping organization rather than infer it from an absence.

Two cautions apply to this section specifically. First, the status above is read from the published Prohibited List itself rather than from any research paper, because a citation can be real, correctly quoted, and still carry a false statement of regulatory fact. Reviews are a source for what the literature shows and never for what a regulator has done. What the literature is good for is the clinical claim sitting beside it: dihydrotestosterone rather than testosterone itself is implicated as the key androgen in pattern hair loss, which is why the anti-doping answer and the hair answer on this page come from different documents.[1] Second, the List is reissued every year and sections renumber, so a competing athlete should confirm the current year's edition 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.

Copper-peptide effects on hair follicles in the laboratory
Anecdotal reports only in vitro

AHK-Cu at picomolar to nanomolar concentrations stimulated elongation of human hair follicles ex vivo and proliferation of cultured dermal papilla cells, with a shift in Bcl-2/Bax ratio and reduced cleaved caspase-3; the accompanying reduction in apoptotic cells was reported by the authors as not statistically significant. The molecule tested was alanyl-histidyl-lysine-copper. That is the whole of the direct follicle evidence, and it is in a dish.

[3]

Hair growth in humans with GHK-Cu
Anecdotal reports only review · in vitro

No controlled human trial of GHK-Cu for hair loss or hair growth is published. A 2025 review examining whether topically applied GHK is effective at all concluded that cellular studies support the ingredient while noting a surprising absence of clinical studies using GHK-Cu and its palmitoylated derivative, and treated skin permeability and formulation instability as still-open questions. The honest position for this goal is that the direct evidence does not exist rather than that it is weak.

[9] [3]

Thyroid hormone and the hair cycle
Animal studies only animal · review

Mice lacking both of the main thyroid hormone receptor isoforms show impaired hair cycling with reduced follicular cell proliferation, and develop alopecia after serial depilation; hypothyroid mice show the same impairment. The human side of this claim is clinical description in review articles rather than trial data with a hair endpoint: telogen effluvium, alopecia areata and androgenetic alopecia all appear in association with thyroid dysfunction.

[6] [8]

Thyroid hormone given to people who are not clearly deficient
Human RCT evidence human RCT

In 737 adults aged 65 and over with persisting subclinical hypothyroidism, levothyroxine lowered thyrotropin but produced no difference from placebo in hypothyroid symptoms or tiredness at one year, and no benefit on secondary outcomes. Separately, a randomized double-blind crossover trial in 70 hypothyroid patients found no difference between desiccated thyroid extract and levothyroxine in symptoms or neurocognitive measures, with a modest weight difference and a preference split. Neither trial measured hair.

[7] [4]

Androgen exposure and scalp hair loss
Anecdotal reports only human observational · review

In a prospective study of 20 hormone-naive trans men plus a cross-sectional study of 50 trans men averaging ten years of testosterone therapy, one participant developed mild frontotemporal loss in the first year, while after long-term therapy 32.7% had mild frontotemporal loss and 31% had moderate to severe androgenetic alopecia. There was no control group and the dermatological outcome was not demonstrably related to individual serum testosterone or dihydrotestosterone levels.

[5] [1]

What has actually cleared a randomized trial for pattern hair loss
Human RCT evidence human RCT · review

416 men aged 21 to 45 with male pattern hair loss were randomized to one of four dutasteride arms, finasteride, or placebo for 24 weeks. Target-area hair count rose over placebo in a dose-dependent fashion, expert panel photographic review and investigator assessment agreed, and scalp and serum dihydrotestosterone fell as testosterone rose. The trial ran 24 weeks. Neither drug is a compound in this library, which is the point of including it here.

[2] [1]

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.

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

The compound almost everyone arrives on this page looking for, and the reason this page reads the way it does. The single most-cited "copper peptide grows hair" result tested AHK-Cu, a different tripeptide, on explanted follicles in a laboratory. No controlled human trial of GHK-Cu for hair loss has been published, so there is nothing here to weigh against a standard-of-care option.

Last reviewed August 2, 2026

NP Thyroid

Also known as: Desiccated thyroid extract, Natural desiccated thyroid, Porcine thyroid extract

Rx via compounding Human RCT evidence

A research reference for NP Thyroid, a porcine desiccated thyroid extract that the FDA classifies as an unapproved biological product marketed without the required license, and that showed no advantage over levothyroxine on symptoms or cognition in two randomized crossover trials.

Why it's on this page

Mapped here because diffuse shedding is one of the ways thyroid dysfunction presents, which makes thyroid function something to measure before anything else is considered. It is not something to treat on the basis of hair. Desiccated thyroid extract is not FDA approved and has never been compared with levothyroxine on a hair endpoint.

Last reviewed August 2, 2026

Testosterone

Also known as: Testosterone replacement therapy, TRT

FDA approved Human RCT evidence

A research reference for testosterone therapy, the one compound in this library with a large randomized trial literature, and a prescription hormone that requires a diagnosis, a prescriber, and ongoing lab monitoring.

Why it's on this page

On this page as the mechanism running in the opposite direction. Androgen exposure is what drives patterned scalp miniaturization, and androgenetic alopecia is a documented long-term outcome of testosterone therapy rather than a target of it. Prohibited in tested sport at all times under WADA section S1.1.

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.

  1. Is the loss patterned at the temples and crown, or diffuse across the whole scalp?

    These are two different literatures and they lead to two different conversations. Patterned loss is androgen-driven miniaturization of scalp follicles, and the controlled human evidence in that space belongs to 5-alpha-reductase inhibition rather than to any peptide. Diffuse shedding is the pattern thyroid dysfunction produces, and the next step there is a blood test and a diagnosis. Neither route arrives at a compound mapped on this page.

    Human RCT evidence [1] [8]

  2. Are you here because you read that copper peptides regrow hair?

    Then the most useful thing this page can do is name the substitution underneath that claim. The study it traces back to tested alanyl-histidyl-lysine-copper, or AHK-Cu, on explanted human follicles and cultured dermal papilla cells. GHK-Cu is glycyl-histidyl-lysine-copper: a different tripeptide with a different first residue. A 2025 review of topically applied GHK found a surprising absence of clinical studies of GHK-Cu and its derivatives despite their wide cosmetic use. For GHK-Cu the claim has never been tested at all.

    Animal studies only [3] [9]

  3. Has anyone actually measured thyroid function?

    If not, that is a laboratory test rather than a compound decision, and it is the one step on this page with a real diagnostic payoff. If it has been measured and it is normal, thyroid hormone is not the lever: a randomized, placebo-controlled trial in 737 adults aged 65 and over with persisting subclinical hypothyroidism found no difference in hypothyroid symptoms or tiredness at one year, and no benefit on any secondary outcome. Correcting a deficiency and giving hormone to someone who does not have one are different interventions with different evidence behind them.

    Human RCT evidence [7] [8]

  4. Would raising testosterone help?

    It points the wrong way. In a cohort of trans men studied after an average of ten years on testosterone, 32.7% had mild frontotemporal hair loss and 31% had moderate to severe androgenetic alopecia, while facial and body hair increased steadily. Scalp hair loss is a consequence of androgen exposure, not a treatment for it, and the same androgen biology is why the controlled trials tested blocking dihydrotestosterone rather than adding testosterone.

    Anecdotal reports only [5] [1]

  5. What would you accept as evidence?

    Applying "a randomized, placebo-controlled human trial with a measured hair-count endpoint" as a filter empties this page completely and leaves only compounds that are not on it. Drugs this library does not cover have met that standard: 416 men randomized across five active arms and placebo, with target-area hair counts and blinded photographic review as endpoints. Nothing mapped here has been through anything comparable.

    Human RCT evidence [2]

  6. Do you compete in a tested sport, at any level?

    Then testosterone is settled before the evidence question is reached: it is named in S1.1 of the WADA Prohibited List in force for 2026 as an anabolic androgenic steroid, prohibited at all times, in and out of competition. That is read from the published list itself rather than from the research literature. It is also the compound on this page whose documented effect on scalp hair is loss rather than growth, so the anti-doping question and the evidence question point the same way here.

    [5]

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

9 sources · every identifier checked against PubMed

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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