What does increasing testosterone actually do to your hair and skin?

Both are highly responsive to androgens. The skin, sebaceous glands and hair follicles contain androgen receptors and can also metabolise testosterone locally.

For some men, the changes are barely noticeable. For others, increased oiliness, acne or accelerated hair thinning can become significant concerns.

The effects are not the same for everyone. Genetics, androgen sensitivity, age, baseline hormone levels, dose and the type of testosterone treatment all play a part.

So, what does the evidence actually show?

Does TRT cause hair loss?

Not necessarily – but it may accelerate male-pattern hair loss in men who are genetically susceptible.

Testosterone acts directly through the androgen receptor, but it can also be converted by the enzyme 5-alpha-reductase into dihydrotestosterone (DHT), a more potent androgen.

In susceptible scalp follicles, particularly around the temples, frontal hairline and crown.

DHT contributes to a process called follicular miniaturisation.

Over successive hair cycles, affected follicles become smaller and produce progressively shorter and finer hairs. Eventually, some may stop producing visible hair altogether.

This is androgenetic alopecia, commonly known as male-pattern hair loss.

TRT therefore doesn’t simply “cause baldness”. A more accurate way of looking at it is that increasing androgen exposure may accelerate androgenetic alopecia in someone whose follicles are already genetically susceptible.

Indeed, major testosterone-treatment guidelines describe familial male-pattern balding as a possible adverse effect of testosterone therapy, although the evidence directly linking therapeutic TRT to balding remains relatively weak.

A strong family history of early male-pattern hair loss is therefore worth considering before starting treatment.

Why can testosterone increase body hair but reduce scalp hair?

This is one of the interesting paradoxes of testosterone.

Higher androgen activity can encourage thicker beard and body hair while having exactly the opposite effect on susceptible scalp follicles.

The reason is that hair follicles in different parts of the body respond differently to androgens.

Androgens stimulate many facial and body hair follicles. In genetically susceptible scalp follicles, however, DHT promotes progressive miniaturisation.

So the same hormonal pathway can effectively encourage one follicle to grow while causing another to shrink.

Does TRT cause acne?

This is where the evidence is considerably stronger.

Acne and increased skin oiliness are recognised adverse effects of testosterone replacement therapy.

Sebaceous glands produce sebum, the lipid-rich substance responsible for the skin’s natural oiliness. Androgens stimulate sebaceous gland activity, which is one reason acne commonly appears during puberty as androgen activity increases.

TRT can produce a similar effect.

A 2026 scoping review specifically examining the dermatological effects of TRT found acne to be the most frequently reported skin complication, affecting approximately 0.6–9.1% of men across the studies included.

Other reported effects included itching, rashes and changes in hair growth.

Importantly, these figures are considerably lower than some of the acne rates quoted online, which may be derived from different populations receiving testosterone rather than men receiving physiological testosterone replacement for hypogonadism.

Acne may affect the:

• Face
• Chest
• Shoulders
• Upper back

For most men it is relatively mild, although inflammatory and occasionally nodulocystic acne can occur.

And developing acne does not automatically mean that TRT needs to be stopped.

Conventional acne treatments — including topical retinoids and, where appropriate, oral treatments — can usually be used while testosterone therapy continues.

Does the type of TRT matter?

Possibly.

Different testosterone preparations produce different patterns of testosterone exposure.

Some injectable preparations can produce greater peaks and troughs in circulating testosterone concentrations, whereas transdermal preparations tend to provide more continuous exposure.

Interestingly, the recent dermatology review found that injectable testosterone preparations generally had higher rates of acne than topical or oral preparations, while oral formulations had the lowest reported rates.

However, the studies were heterogeneous and dermatological side effects were not always systematically assessed. We therefore cannot say that simply changing formulation will prevent acne or hair loss in an individual patient.

The aim of genuine testosterone replacement therapy is generally to restore testosterone to an appropriate physiological range rather than produce supraphysiological concentrations.

If significant skin or hair problems develop, it is reasonable to review the dose, blood levels and formulation with the prescribing clinician rather than treating the skin or hair completely in isolation.

Does testosterone make your skin thicker?

The relationship between testosterone and skin is more complicated than simply causing acne.

Androgen signalling influences several components of skin biology, including sebaceous glands, fibroblasts and the extracellular matrix within the dermis.

Sex hormones also contribute to some of the structural differences between male and female skin, with male skin generally being thicker.

This has led to interest in whether correcting testosterone deficiency might influence dermal structure.

However, this area needs some perspective.

Although there are biological reasons why testosterone could influence dermal thickness and collagen, TRT should not be regarded as a skin rejuvenation or anti-ageing treatment. Evidence that testosterone replacement meaningfully improves wrinkles, elasticity or the cosmetic appearance of ageing skin remains limited.

The much better-established dermatological effects are increased sebaceous activity and the potential for acne.

Can you protect your hair while taking TRT?

Potentially.

If progressive androgenetic alopecia develops while taking testosterone, there are established treatments.

1. Minoxidil

Topical minoxidil can help prolong the hair growth phase and maintain or improve hair density.

Low-dose oral minoxidil is also increasingly used in appropriately selected patients, although its use for hair loss is off-label and requires appropriate medical assessment.

2. Finasteride

Finasteride inhibits 5-alpha-reductase and therefore reduces the conversion of testosterone into DHT.

It is one of the best-established treatments for male-pattern hair loss and can significantly slow progression in many men.

3. Dutasteride

Dutasteride inhibits both type I and type II 5-alpha-reductase and suppresses DHT more strongly than finasteride.

Its regulatory status for androgenetic alopecia differs between countries, and its use needs to be considered individually.

For someone receiving TRT, the decision to use a 5-alpha-reductase inhibitor should ideally be discussed with the clinicians managing both their testosterone treatment and their hair loss.

Should you think about your hair before starting TRT?

If preserving your hair is important to you, it makes sense to establish a baseline before starting treatment.

Look at:

• Your frontal hairline
• Your temples
• Crown density
• Evidence of existing miniaturisation
• Your family history of male-pattern hair loss

Baseline photographs taken under consistent lighting can be surprisingly useful for identifying gradual changes. Dermoscopic or trichoscopic images are a more objective measure of hair follicle appearance and can be undertaken in a specialist clinic.

The same principle applies to the skin. Someone who already has oily or acne-prone skin may notice increased sebaceous activity after starting testosterone.

Early intervention is generally preferable to waiting until significant acne scarring or advanced hair miniaturisation has occurred.

So, does TRT mean sacrificing your hair and skin?

No.

But it does mean understanding how testosterone affects them.

TRT can increase skin oiliness and trigger acne. It can increase facial and body hair while potentially accelerating male-pattern scalp hair loss in genetically susceptible men.

Individual susceptibility matters enormously.

Some men will experience very little change. Others may notice acne or progressive hair thinning relatively quickly.

The important point is that many of these effects are predictable, monitorable and treatable.

If you already have acne or a strong family history of male-pattern hair loss, it is worth thinking about these issues before starting TRT rather than after the changes have become established.

And if skin or hair problems do develop, they can usually be treated without automatically having to abandon medically indicated testosterone replacement therapy.

References

1. Abou Chawareb E, Campos L, Savio L, et al. Dermatological adverse effects of testosterone replacement therapy: a scoping review of the literature. Sexual Medicine Reviews. 2026;14(1).
2. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. 2018;103(5):1715–1744.
3. Lai JJ, Chang P, Lai KP, Chen L, Chang C. The role of androgen and androgen receptor in skin-related disorders. Archives of Dermatological Research. 2012;304:499–510.
4. Zouboulis CC. Acne and sebaceous gland function. Clinics in Dermatology. 2004;22(5):360–366.
5. Zouboulis CC, Degitz K. Androgen action on human skin — from basic research to clinical significance. Experimental Dermatology. 2004;13(Suppl 4):5–10.
6. Kanti V, Messenger A, Dobos G, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men. Journal of the European Academy of Dermatology and Venereology. 2018;32(1):11–22.
7. Kaiser M, Abdin R, Gaumond SI, Issa NT, Jimenez JJ. Treatment of androgenetic alopecia: current guidance and unmet needs. Clinical, Cosmetic and Investigational Dermatology. 2023;16:1387–1406.
8. Piraccini BM, Blume-Peytavi U, Scarci F, et al. Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III randomised controlled clinical trial. Journal of the European Academy of Dermatology and Venereology. 2022;36(2):286–294.

This article is intended for general education and does not replace individual medical advice. Testosterone replacement therapy should be prescribed and monitored by an appropriately qualified clinician.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

This guide answers both.

The most important point first: a raised DHEAS result is not a diagnosis on its own, and the acne and hair changes linked to it can usually be treated effectively. 

At IA Dermatology, our Harley Street clinic in London, assessing hormone-related skin and hair conditions – and tailoring treatment for acne and female hair loss – is a core part of what we do.

Key takeaways

• A high DHEAS level does not automatically mean PCOS or that something serious is wrong.
• DHEAS is one of several androgen hormones that can contribute to acne, facial hair and scalp thinning.
• Hormone-related acne and female-pattern hair loss are usually treatable, often without needing to “normalise” the blood result itself.
• A dermatologist can identify what is actually driving your symptoms and build a treatment plan around them.
• Rapidly progressing symptoms or a markedly raised result should be assessed promptly.

Can acne linked to high DHEAS be treated?

Yes. Hormone-related acne is one of the most common conditions we treat, and it responds well to the right approach.

DHEAS and other androgens can increase activity in the skin’s oil-producing (sebaceous) glands, which contributes to breakouts – particularly persistent adult female acne along the jawline, chin and lower face. But acne is rarely caused by one hormone alone.

Genetics, skin sensitivity, inflammation, skincare products and other hormonal factors all play a part, which is why our acne treatment in London is tailored to the individual rather than to a single blood result.

Depending on your skin, medical history and whether you are planning a pregnancy, hormonal acne treatment may include:

• topical treatments to reduce oil, unclog pores and calm inflammation
• oral medication where acne is more widespread or scarring
• treatments that reduce the effect of androgens on the skin
• a longer-term maintenance plan to keep skin clear and prevent scarring

Where the acne is linked to polycystic ovary syndrome, we treat it as part of our wider PCOS-related skin and hair care. The aim is always to clear the acne effectively while deciding whether the hormone result needs any further investigation. If you are dealing with stubborn or recurring breakouts, a dermatologist assessment is usually the fastest route to a plan that works.

Can hair loss linked to high DHEAS be treated?

In many cases, yes – and earlier assessment generally gives better results.

Higher androgen activity can contribute to female-pattern hair loss in women whose scalp follicles are hormonally sensitive. This typically shows as gradual thinning across the top of the scalp or a widening parting, rather than distinct bald patches.

A high DHEAS result does not prove that hormones are the cause. Female hair loss is frequently driven or worsened by other factors – iron deficiency, thyroid disease, nutritional issues, recent illness, certain medications, menopause and genetic hair loss – and these often need to be assessed and addressed alongside any hormonal contribution. This is exactly why a proper dermatological work-up matters before starting treatment.

Our treatment for female-pattern hair loss is tailored to the pattern, cause and stage of thinning, and may involve:

• correcting any underlying deficiencies or medical contributors
• topical and oral treatments to support regrowth and slow progression
• treatments aimed at reducing androgen activity where appropriate
• in-clinic regenerative options and ongoing monitoring of progress

Because hair responds slowly, the earlier thinning is assessed, the more can usually be preserved. A dermatologist can confirm whether your DHEAS result is clinically relevant to your hair loss and recommend the most suitable options.

Can unwanted facial or body hair be treated?

Yes. Coarse facial or body hair driven by androgens – known medically as hirsutism – is common and manageable. It often affects the upper lip, chin and jawline, chest, lower abdomen, inner thighs and lower back.

The amount of hair growth does not always match the blood-test result, because genetics, ethnicity and follicle sensitivity all matter. Treatment may combine measures that reduce androgen activity with hair-reduction options, and is planned around your symptoms and medical history. Where hirsutism forms part of PCOS, we manage it within our PCOS hormonal skin and hair service.

What is DHEAS?

DHEAS stands for dehydroepiandrosterone sulphate, sometimes written as DHEA-S. It is an androgen hormone produced mainly by the adrenal glands – small glands that sit above the kidneys — and it acts partly as a building block the body uses to make other hormones, including testosterone and oestrogen.

Because DHEAS stays relatively stable in the bloodstream, it can be a useful test when investigating signs of increased androgen activity.

What does a high DHEAS level mean in a woman?

A high DHEAS level means the amount of this adrenal androgen in the blood is above the laboratory’s expected range. On its own it does not provide a diagnosis. A raised result can occur in women with PCOS, but it can also have other explanations, and some women have a mildly elevated level without any significant underlying condition.

The degree of elevation matters. A slightly raised result is interpreted very differently from a level that is markedly above the reference range.

What symptoms can high DHEAS cause?

Higher androgen activity may affect the skin, sebaceous glands and hair follicles. Possible symptoms include:

• acne, particularly persistent or adult female acne
• oily skin
• increased facial or body hair
• female-pattern scalp hair thinning
• irregular or absent periods

Not everyone with a raised DHEAS level develops these symptoms. Some women have significant acne or facial hair despite hormone results within the laboratory range; others have a mildly raised result but few noticeable symptoms. This is because skin and hair follicles vary in how sensitive they are to androgens — and it is why treatment is directed at the symptoms, not just the number.

Does high DHEAS mean PCOS?

No. A high DHEAS result does not automatically mean you have PCOS.

PCOS is diagnosed from a combination of features, which may include:

• irregular or absent periods
• clinical signs of increased androgen activity
• raised androgen levels on blood testing
• polycystic ovarian appearances, where relevant
• exclusion of other possible causes

Total and free testosterone are generally the main blood tests used to assess biochemical androgen excess in suspected PCOS; DHEAS can add information, particularly when testosterone is not elevated. So it is entirely possible to have PCOS with a normal DHEAS level, a raised DHEAS level without PCOS, or androgen-related skin symptoms with blood tests in range. The result needs to be read as part of a wider hormonal assessment — the approach we take in our PCOS-related skin and hair clinic.

Why does age affect DHEAS results?

DHEAS levels rise through childhood and puberty, peak in early adulthood and then gradually decline with age. A result that is expected in a woman in her twenties may be unusually high in a woman in her forties or fifties, so DHEAS should always be assessed against an age-appropriate reference range. A result should never be labelled simply “high” without this context.

What causes high DHEAS in women?

Possible explanations include PCOS, normal individual variation, medications or supplements containing DHEA or androgenic hormones, non-classic congenital adrenal hyperplasia, adrenal hormone disorders and – less commonly – an androgen-producing adrenal or ovarian condition. A mildly elevated result is far more common than a serious androgen-producing disorder, and the pattern and speed of symptoms help determine whether further investigation is needed.

When should high DHEAS be investigated further?

Further assessment is particularly important when:

• the DHEAS level is markedly above the reference range
• symptoms have appeared or progressed rapidly
• facial or body hair has increased suddenly
• acne has become severe over a short period
• scalp hair loss is progressing quickly
• the voice has become deeper
• periods have become significantly irregular or stopped
• there are other signs of pronounced androgen excess

Rapidly progressing symptoms or signs of virilisation warrant prompt medical assessment. Your doctor may repeat the DHEAS test and arrange others – such as testosterone, sex hormone-binding globulin, androstenedione, 17-hydroxyprogesterone or thyroid tests – depending on your history.

Is high DHEAS dangerous?

A mildly raised DHEAS result is not usually dangerous by itself. What matters is how elevated the result is, whether symptoms are present, how quickly they developed, and whether other hormone results are abnormal. A raised result should be assessed rather than ignored – but it is equally important not to assume the worst from a single blood test.

Is high DHEAS always bad?

DHEAS is not simply an “acne hormone.” It has several normal roles in the body, and researchers have studied possible links with bone, muscle, mood and cognitive function. These associations do not prove a high level is beneficial. DHEA supplements have not been shown to give reliable anti-ageing benefits, can cause androgen-related side effects, and should not be started simply because DHEAS naturally falls with age.

How treatment is planned at IA Dermatology

The hormone level and the skin or hair symptoms do not always need to be treated in the same way. Our approach is to treat the visible condition effectively while deciding whether the hormone result needs further work-up. Treatment is tailored to:

• your main symptom and its severity
• your age and medical history
• whether pregnancy is being considered
• your menstrual cycle
• the results of any hormonal investigations
• previous treatments you have tried

Where further hormonal assessment is needed, we work alongside your GP, gynaecologist or endocrinologist, so your skin and hair are treated without delay while any underlying cause is investigated.

Frequently asked questions

The key points

• A high DHEAS result is not a diagnosis by itself.
• DHEAS can be associated with acne, facial hair and scalp hair thinning.
• A raised level does not automatically mean PCOS.
• Results must be read against an age-appropriate reference range.
• Most associated acne and hair concerns can be treated.
• Markedly raised results or rapidly progressing symptoms need prompt assessment.

Speak to a specialist about treatment

If you have acne, unwanted facial hair, scalp thinning or an unexpected DHEAS result, a dermatologist with expertise in hormonal skin and hair conditions can assess whether your symptoms are androgen-related, rule out other causes and recommend a treatment plan built around you. Our clinic is on Harley Street, London (16 Devonshire Street, W1G 7AF).

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“I’m really really pleased with my treatment with Dr Ali. I first came through a word of mouth recommendation from a family friend and it was the best investment into my skin that I could have ever made! I used to struggle with repeated breakouts/ acne on my back and face and a super congested and inflamed dermal layer and 9 months on my skin has been transformed (although I started seeing results really quickly at 2 months!). Really recommend Dr Aisha as a dermatologist she’s fantastic and professional.”

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Visited for Skin Treatment

This article provides general medical information and is not a substitute for an individual consultation or diagnosis.

Medical references

1. International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome, 2023.
2. Endocrine Society Clinical Practice Guideline: Evaluation and Treatment of Hirsutism in Premenopausal Women.
3. Mayo Clinic Laboratories: Dehydroepiandrosterone Sulphate, Serum — clinical interpretation and age-related reference ranges.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

But a more interesting question is now emerging from molecular biology:

Can past sun exposure leave a lasting molecular imprint on the skin?

For many years, dermatology has focused on the visible and genetic consequences of UV exposure: redness, tanning, pigmentation, collagen breakdown, DNA damage and mutation. These remain central to our understanding of photoageing and skin cancer.

However, newer research suggests that UV radiation may also influence the epigenome; the regulatory layer that helps determine how genes are switched on, switched off, or made more or less accessible. Recent reviews have highlighted UV-induced effects on DNA methylation, histone modification and chromatin regulation as potentially important contributors to skin ageing and carcinogenesis (Barnes et al., 2024).

Your DNA is the code. Epigenetics helps decide how that code is read.

This matters because skin ageing is not simply a matter of collagen “wearing out”. The skin is a living, responsive organ. Its cells are constantly interpreting signals from the environment: ultraviolet radiation, pollution, inflammation, hormones, oxidative stress, nutrition, smoking and time itself.

Normal ageing and sun-induced ageing are not the same

There is an important distinction between intrinsic ageing and photoageing.Intrinsic ageing is the natural ageing process of skin. It is influenced by time, genetics, hormones, metabolism and gradual changes in cellular repair. Intrinsically aged skin tends to become thinner, drier, more fragile, less elastic and slower to heal. The wrinkles are often finer, and the skin may appear more delicate or translucent.

Photoageing is different; photoaged skin is skin that has been remodelled by repeated ultraviolet exposure. It tends to show coarser wrinkles, uneven pigmentation, solar lentigines, telangiectasia, rough texture, actinic change and loss of elasticity. Histologically, it is associated with solar elastosis, abnormal dermal matrix remodelling, chronic inflammatory signalling and accumulation of UV-induced DNA damage.

So sun-damaged skin is not simply “older skin”. Chronologically aged skin becomes biologically slower and thinner. UV-aged skin becomes biologically disrupted, inflamed and remodelled.

What happens at the level of methylation?

One of the most studied epigenetic mechanisms is DNA methylation. This involves adding methyl groups to DNA, often in regions that help regulate gene activity. Normal ageing and UV exposure can both alter DNA methylation, but they do not appear to do so in identical ways.

Human skin studies have shown that intrinsic ageing and chronic sun exposure are associated with distinct epigenetic changes in epidermis and dermis (Grönniger et al., 2010). Later whole-genome work also identified widespread genomic regions of altered methylation in older, sun-exposed skin (Vandiver et al., 2015).

With intrinsic ageing, the skin develops gradual epigenetic drift. Some methylation marks are gained, others are lost, and the regulatory system becomes less precise over time. This is one reason methylation patterns can be used to estimate biological age.

With chronic UV exposure, the pattern appears more environmentally driven. UV may contribute to broader disruption of methylation across parts of the genome, while also causing more localised methylation changes in specific regulatory regions.

In normal ageing, the skin’s genetic regulation gradually drifts. In photoageing, UV exposure appears to disturb that regulation more aggressively, loosening control across parts of the genome while also switching off selected protective pathways.

This matters because methylation changes can influence repair pathways, inflammation, matrix regulation and cancer-protective mechanisms. For example, if genes involved in restraining matrix degradation or supporting DNA repair are inappropriately regulated, the skin may become more vulnerable to photoageing and carcinogenesis.

UV does not only damage DNA

UV radiation can damage DNA directly, particularly through UVB-induced photolesions. If these lesions are not repaired before a cell divides, they can become fixed mutations.

UVA penetrates more deeply into the dermis and contributes strongly to oxidative stress, fibroblast dysfunction and matrix degradation.

But beyond these familiar mechanisms, UV can also affect the systems that control cell behaviour. These include DNA methylation, histone modification and chromatin organisation.

This gives us a broader model of sun damage; UV exposure does not only change the DNA code. It may also alter the regulatory machinery that determines how that code is read.

Can the skin repair these changes?

Some environmental effects on DNA and gene regulation can be repaired or reversed.

The skin has DNA repair systems that can remove many forms of UV-induced damage. Some epigenetic changes are also dynamic and may normalise after the environmental stress has passed.

This is important as it would be too simplistic to say that every individual sun exposure permanently changes the skin in the same way.

However, recovery is not limitless; repeated UV exposure can overwhelm repair systems, fix mutations into the DNA sequence, promote cellular senescence, alter immune signalling and leave longer-lasting changes in the regulatory systems that control skin-cell behaviour.

Some of the molecular effects of sun exposure can be repaired. But repeated UV exposure can leave changes that accumulate over time; not only in the DNA code itself, but also in the systems that control how that code is read.

Fibroblasts, senescence and collagen breakdown

The visible signs of photoageing are not simply caused by collagen disappearing.

Fibroblasts are the cells responsible for producing and maintaining collagen, elastin and other components of the extracellular matrix. With repeated UV exposure, fibroblasts may enter altered states, including senescence. Senescent cells no longer behave like healthy young fibroblasts. They may produce inflammatory signals and matrix-degrading enzymes that contribute to wrinkling, thinning and textural change.

This means UV can affect the skin in two linked ways; it can damage the matrix itself, and it can also change the behaviour of the cells responsible for maintaining that matrix.

That is why photoageing is better understood as biological remodelling, not simply “collagen loss”. Recent reviews of skin ageing and senescence increasingly emphasise this shift from structural damage alone to altered cellular state and tissue regulation (Dal Pozzo et al., 2024).

What stimulates or changes methylation?

Methylation is controlled by enzymes called DNA methyltransferases, including DNMT1, DNMT3A and DNMT3B. These enzymes add or maintain methyl marks on DNA.

Methylation also depends on cellular metabolism, including the availability of methyl donors from one-carbon metabolism. Nutrients such as folate, vitamin B12, choline, methionine and related pathways help support methyl-group availability, although this does not mean that taking supplements simply “improves” skin methylation. The methylome is highly regulated. Methylation changes are specific to tissue, cell type, age, disease state and environmental exposure.

In skin, methylation can be influenced by ageing, UV exposure, oxidative stress, inflammation, hormones, smoking, metabolism, cell turnover, DNA damage and DNA repair.

UV does not simply increase or decrease methylation uniformly. It may promote focal methylation changes in selected genes while also destabilising methylation maintenance more broadly through oxidative and DNA-damage stress.

What do twin studies tell us?

Twin studies are particularly helpful because identical twins share essentially the same inherited DNA. When identical twins age differently, this shows the importance of environment.

Genes influence skin type, pigmentation, tanning ability, collagen biology, repair capacity and baseline susceptibility to damage. But environmental factors strongly influence how the skin actually ages.

Sun exposure, smoking, pollution, occupation, weight change, hormones, nutrition and skin-protective behaviour can all produce visible differences between genetically identical individuals. Studies of identical twins have shown that lifestyle and environmental exposures, including smoking and sun exposure, can contribute to visible differences in facial ageing despite shared genetics (Guyuron et al., 2009).

Your genes influence how your skin starts life; your environment influences how your skin travels through life.

This is also relevant to epigenetics. Recent twin methylation work suggests that the skin methylome may be relatively less heritable than the blood methylome, supporting the idea that skin methylation is particularly responsive to environmental and non-genetic influences (Shore et al., 2024).

The skin may be one of the organs where the environment leaves a visible and measurable molecular trace.

Can food, vitamins or drugs help repair sun damage?

There is a crucial distinction between supporting repair and erasing damage.

No food, supplement or skincare product should be described as reversing fixed UV-induced DNA mutations. Once a mutation is established in the DNA sequence, it is generally not simply reversed by nutrition or topical treatment. However, some interventions may support repair pathways, reduce oxidative stress, reduce inflammation or improve the visible consequences of photoageing.

Nicotinamide, a form of vitamin B3, has clinical evidence for reducing actinic keratoses and non-melanoma skin cancers in high-risk individuals while treatment is continued. In the ONTRAC phase 3 trial, oral nicotinamide reduced new non-melanoma skin cancers and actinic keratoses in high-risk patients, but it should be viewed as an adjunct rather than a substitute for sun protection (Chen et al., 2015).

Topical retinoids, especially tretinoin, have some of the best evidence for improving visible photoageing. They can improve fine wrinkling, texture, pigmentation irregularity and collagen regulation over time. They do not remove fixed mutations, but they can improve aspects of the photoaged skin phenotype.

Antioxidant-rich diets may support normal repair biology. Vitamin C, polyphenols, adequate protein and healthy dietary patterns can contribute to resilience, collagen synthesis and oxidative-stress regulation.

Topical antioxidants, including vitamin C, vitamin E, ferulic acid, niacinamide and polyphenol-based formulations, may help reduce oxidative stress when used alongside sunscreen. Again, their role is supportive rather than curative.

What about vitamin D?

Vitamin D is sometimes described as an antioxidant, but in skin it is better understood as a hormone-like regulatory molecule.

Through vitamin D receptor signalling, vitamin D may support DNA repair, modulate oxidative stress, influence inflammation and help maintain normal keratinocyte differentiation and barrier function. Experimental work has suggested that active vitamin D and analogues can reduce some forms of UV-induced DNA damage, but this does not make vitamin D a substitute for photoprotection (Mason et al., 2010).

UVB helps generate vitamin D, but UVB also causes direct DNA damage. Vitamin D can be maintained through diet or supplementation where appropriate, while UV protection remains the primary strategy for preventing photoageing and skin cancer.

Can we measure sun damage in blood?

Oxidative stress and methylation can both be measured in blood, but interpretation is difficult. Reactive oxygen species are short-lived, so tests usually measure downstream oxidative-stress markers such as oxidised DNA products, lipid peroxidation markers, protein oxidation or antioxidant capacity. These can reflect systemic oxidative stress, but they do not specifically measure UV damage in the skin.

DNA methylation can also be measured in blood and is used in biological-age or epigenetic-clock research. However, blood methylation mainly reflects blood and immune-cell biology. It is not the same as the methylation state of sun-exposed facial skin.

Skin-specific methylation studies usually require skin sampling, such as biopsy, tape stripping or other tissue-based methods. There is no routine blood test that can accurately measure a person’s lifetime sun damage or the epigenetic “memory” of UV exposure in their skin.

Skin cancer: genetics and epigenetics together

UV-induced skin cancer is strongly linked to DNA damage and mutation. A tumour-suppressive pathway does not always need to be mutated to become less effective. In some contexts, it may be functionally silenced or dysregulated through epigenetic mechanisms.

This means the biological legacy of UV exposure may include direct DNA damage and mutation, oxidative stress, altered methylation, histone and chromatin changes, cellular senescence, chronic inflammatory signalling, impaired repair responses, and increased risk of photoageing and skin cancer.

These mechanisms do not replace each other. They interact.

Why prevention still matters most

The most important implication of this emerging science is not that everyone needs expensive “epigenetic” skincare. The more important message is simpler and more powerful:

UV protection is not just about avoiding sunburn. It is about reducing the cumulative biological stress that can reshape how skin cells behave over time.

This includes daily broad-spectrum sunscreen, protective clothing, shade, avoiding tanning, and recognising that UVA exposure can occur even when the skin does not burn. It also means understanding that visible ageing and skin cancer risk are influenced by a lifetime of exposures, not only by what happens on a single sunny day.

The skin is not a passive surface. It is a dynamic biological organ that responds, adapts, repairs and sometimes retains traces of what it has experienced.

So the question “Does your skin remember the sun?” is not just poetic. It reflects a serious and evolving area of dermatological science. The answer appears to be –  in several important biological ways, it may.

Selected references

Barnes BM, Shyne A, Gunn DA, Griffiths CEM, Watson REB. Epigenetics and ultraviolet radiation: implications for skin ageing and carcinogenesis. Skin Health and Disease. 2024;4(6):e410.

Grönniger E, Weber B, Heil O, et al. Aging and chronic sun exposure cause distinct epigenetic changes in human skin. PLoS Genetics. 2010;6(5):e1000971.

Vandiver AR, Irizarry RA, Hansen KD, et al. Age and sun exposure-related widespread genomic blocks of hypomethylation in nonmalignant skin. Genome Biology. 2015;16:80.

Dal Pozzo L, Cavallini C, et al. Role of epigenetics in the regulation of skin aging and cellular senescence. Biomedicine & Pharmacotherapy. 2024.

Shore CJ, et al. Genetic effects on the skin methylome in healthy older twins. American Journal of Human Genetics. 2024.

Guyuron B, Rowe DJ, Weinfeld AB, et al. Factors contributing to the facial aging of identical twins. Plastic and Reconstructive Surgery. 2009;123(4):1321–1331.

Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention. New England Journal of Medicine. 2015;373:1618–1626.

Mason RS, Sequeira VB, Dixon KM, et al. Photoprotection by 1α,25-dihydroxyvitamin D and analogs. Journal of Steroid Biochemistry and Molecular Biology. 2010;121(1–2):164–168.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

The current evidence suggests that regular physical activity may improve skin quality and resilience, although there remains limited direct evidence demonstrating reductions in facial wrinkles or increases in dermal collagen content in humans.

Exercise improves skin physiology

The 2024 narrative review by Oizumi et al. provides an overview of the biological mechanisms linking exercise and skin function. The authors describe exercise as producing widespread physiological changes that benefit the skin, including increased cutaneous blood flow, improved thermoregulation, enhanced mitochondrial function and better skin hydration.

Exercise increases blood flow to the skin during activity, improving oxygen and nutrient delivery to epidermal keratinocytes and dermal fibroblasts. Improved microcirculation also facilitates removal of metabolic waste products and supports normal tissue repair. These adaptations may contribute to healthier skin appearance and function over time.

The review also highlights that habitual exercise improves skin barrier function and stratum corneum hydration while reducing chronic low-grade inflammation, an important contributor to intrinsic skin ageing.

The muscle–skin axis

One of the most important concepts emerging from recent research is the “muscle–skin axis.”

During exercise, contracting skeletal muscle releases signalling proteins known as myokines, including IL-15, irisin and other exercise-induced mediators. These circulating factors appear capable of influencing distant tissues, including the skin.

Rather than acting solely through improved circulation, exercise may therefore alter dermal biology through endocrine signalling between skeletal muscle and dermal fibroblasts. This represents a significant shift in understanding how lifestyle interventions may influence skin ageing.

Effects on collagen and the extracellular matrix

The strongest experimental evidence comes from Nishikori and colleagues (2023), who investigated 16 weeks of supervised aerobic or resistance training in sedentary middle-aged women.

Both exercise programmes improved skin elasticity and upper dermal structure. However, resistance training produced an additional increase in dermal thickness.

Mechanistic experiments demonstrated changes in circulating factors that enhanced extracellular matrix-related gene expression in cultured human dermal fibroblasts. The investigators also identified increased expression of biglycan, a proteoglycan involved in collagen fibril organisation and dermal architecture.

Importantly, collagen itself was not directly measured. Consequently, the study supports the concept that exercise enhances extracellular matrix remodelling and creates a more favourable environment for collagen maintenance, rather than proving that exercise directly increases dermal collagen. This distinction is clinically important and avoids overstating the evidence.

Exercise and skin ageing

The 2025 review by Li et al. integrates current evidence and proposes several complementary mechanisms through which regular physical activity may slow aspects of skin ageing.

These include:

• improved dermal blood flow
• enhanced mitochondrial function
• reduced oxidative stress
• improved insulin sensitivity
• reduced chronic inflammation
• enhanced extracellular matrix remodelling
• improved sleep quality and hormonal regulation

Collectively these mechanisms support healthier skin function and may delay age-related deterioration of the dermis.

However, the authors emphasise that evidence directly demonstrating wrinkle reduction remains limited. Most available studies measure physiological markers such as elasticity, hydration, dermal thickness or barrier function rather than validated wrinkle scores.

Exercise and wrinkles

Despite widespread public belief that exercise reduces wrinkles, there are currently no large randomised controlled trials demonstrating clinically significant wrinkle reduction attributable solely to exercise.

Instead, exercise appears to improve the biological environment within which collagen maintenance and tissue repair occur.

Therefore, exercise should be viewed as supporting healthy skin ageing rather than replacing established interventions such as photoprotection, topical retinoids or evidence-based procedural treatments.

The importance of exercise intensity

The literature consistently suggests a dose-dependent relationship.

Moderate, regular exercise appears beneficial.

In contrast, prolonged, intense endurance exercise without adequate recovery may increase oxidative stress, ultraviolet exposure, dehydration and barrier disruption. Outdoor athletes therefore experience competing influences on skin ageing: favourable systemic effects from exercise balanced against accelerated photoageing from cumulative UV exposure.

This distinction is particularly relevant for footballers, runners and cyclists.

Clinical implications

Current evidence suggests that physically active individuals may demonstrate:

• improved skin elasticity
• greater dermal thickness
• healthier extracellular matrix remodelling
• improved barrier function
• increased skin hydration
• improved wound healing
• reduced chronic inflammation

However, these benefits are contingent upon appropriate sun protection, skin hygiene and recovery. Sweat, friction, ultraviolet radiation and environmental exposure remain significant contributors to premature skin ageing in athletes.

Conclusion

The emerging evidence supports regular physical activity as an important component of healthy skin ageing. Exercise appears to improve skin through multiple interconnected mechanisms involving circulation, mitochondrial health, inflammatory regulation and extracellular matrix remodelling.

The strongest evidence currently supports improvements in skin elasticity, dermal thickness and skin physiology rather than direct reductions in facial wrinkles.

Future research should focus on larger randomised trials using validated measures of wrinkle severity, collagen content and long-term clinical outcomes. Until then, exercise should be regarded as a valuable adjunct to—not a replacement for—established dermatological strategies such as sun protection, topical retinoids and evidence-based procedural treatments.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

As a consultant dermatologist specialising in hair treatments, I’ve spent a significant part of my career trying to understand exactly why this happens. During my research at Oxford University, our team investigated hair changes in postmenopausal women across a large population — one of the first studies of its kind — and the findings, later published in the British Journal of Dermatology, helped reframe how we think about this problem.

What they confirmed is something I see in clinic every week: menopausal hair change is extremely common, frequently distressing, and almost always more complex than simply “getting older.”

The Hormone–Hair Connection: Why Does Menopause Cause Hair Loss?

Hair follicles are remarkably hormone-sensitive structures. During menopause, levels of oestrogen and progesterone decline — and both hormones normally play a role in supporting the hair growth cycle, helping to keep follicles in the active growing phase for longer. As those levels fall, hair may spend less time growing and more time resting or shedding. Over time, this leads to reduced density and finer hair overall.

At the same time, the relative influence of androgens — hormones present in all women — can become more noticeable in those who are genetically susceptible. This can drive follicular miniaturisation, a gradual process in which individual hairs become progressively finer, shorter and sparser often diagnosed as female patterned hair loss.

What Our Oxford Research Showed About Menopause Balding

In our Oxford study of 758 postmenopausal women, over 40% reported some degree of hair loss after menopause. The most common pattern — described by around a quarter of participants — was diffuse, all-over thinning. A smaller group developed more noticeable thinning at the front or crown.

Perhaps the most clinically useful finding was that not all menopausal hair change looks the same, or comes from the same cause. We identified two distinct patterns.

The first was a more generalised thinning, associated with increasing age and a reduction in both scalp and body hair. This likely reflects broader, age-related changes in follicular activity rather than hormonal change alone.

The second pattern was rather different: frontal thinning combined with increased facial hair growth. This tended to occur in relatively younger postmenopausal women and is more suggestive of androgen sensitivity playing a prominent role.

This distinction matters enormously in practice, because the two patterns don’t necessarily respond to the same treatments.

Does Your Hair Change During Menopause or Is It Simply Ageing?

This is one of the questions I’m asked most often, and the honest answer is: usually both.

Research by Professor Andrew Messenger and colleagues has shown that female hair thinning increases with age even in women without elevated androgens — which tells us that hormones are not the whole story. The hair growth cycle gradually shortens over time. Follicular activity declines. Hair fibre diameter reduces. Years of environmental exposure take their toll. Genetics plays a background role throughout.

Our Oxford data supported this view: some women appeared to develop thinning driven primarily by these age-related changes, while others showed patterns more clearly linked to hormonal or androgen-related mechanisms. In reality, for most women, all of these factors are operating at once.

Hair Texture Changes During Menopause

Menopause doesn’t only affect scalp hair. In our study, nearly half of women reported increased facial hair — particularly around the chin — while simultaneously noticing less hair on their legs and underarms. This apparent paradox, more hair in some places and less in others, reflects the way different follicles respond differently to the same hormonal shifts.

Many women also notice changes in texture that have nothing to do with density. Hair may become drier, more brittle, less shiny and harder to style. These changes reflect a combination of reduced scalp oil production, alterations in the hair fibre itself, and the cumulative effects of follicular ageing.

When Hair Loss Isn’t Just Menopause

Something I always stress with patients: menopause may be contributing to hair change, but it doesn’t mean it’s the only thing going on. Iron deficiency, thyroid disorders, vitamin D deficiency, chronic stress, inflammatory scalp conditions, autoimmune hair disease and certain medications can all cause or worsen hair thinning — and these are entirely treatable if identified.

This is why a proper assessment matters rather than assuming everything is hormonal. In clinic, that usually means a detailed history, scalp examination, trichoscopy and targeted blood tests where appropriate. Getting the diagnosis right is the foundation for getting the treatment right.

Can Menopause Hair Loss Be Treated?

In many cases, yes — and that’s often reassuring for women who assumed nothing could be done.

Treatment depends entirely on what’s driving the change. Topical minoxidil has a solid evidence base for female hair loss.

Nutritional deficiencies, when identified, are corrected. Scalp inflammation is treated. Some women are good candidates for oral therapies. Procedural options like low-level laser therapy or platelet-rich plasma exist, though the evidence varies and these work best as part of a broader plan rather than standalone solutions.

Hormone replacement therapy isn’t prescribed specifically as a hair treatment, but for some women, stabilising hormonal symptoms more broadly may have a positive indirect effect on hair.

The Emotional Weight

Hair is deeply tied to how women feel about themselves — their confidence, their identity, their sense of being well. When hair changes are dismissed as trivial or inevitable, it can feel isolating.

Our research was motivated partly by the sense that this was an area that deserved to be taken seriously. The changes are common, they’re real, and — with the right approach — many of them can be meaningfully improved.

The first step is understanding what’s actually happening. From there, a targeted, evidence-based plan can make a real difference, not just to the hair itself, but to how a woman feels in her own skin.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

Abstract

Hair changes during the menopausal transition are extremely common. While gradual thinning is the expected hormonal consequence of declining oestrogen levels, dramatic or acute shedding is not a typical feature of menopause itself and more often suggests a concurrent diagnosis such as telogen effluvium, thyroid dysfunction, nutritional deficiency, or medication-related alopecia. This review integrates published evidence to distinguish menopausal thinning from other contributors to menopause hair loss in midlife women, with an emphasis on identifying treatable and reversible causes.

1. Introduction

Many women notice changes in their hair during the menopausal transition. Hair may feel thinner, flatter, drier, or less dense than before. Some women notice widening of the central parting or reduced ponytail volume. These changes are extremely common and can understandably cause anxiety.

However, one important clinical distinction is often overlooked: menopause itself is not usually associated with dramatic or sudden hair shedding. When women describe losing large amounts of hair rapidly — handfuls in the shower, excessive shedding onto clothing or pillows, or sudden diffuse thinning over weeks to months — this pattern more frequently reflects an additional process such as telogen effluvium, nutritional deficiency, thyroid dysfunction, or medication-related shedding.^[1,2]

Understanding these distinctions is clinically important because the underlying causes — and their treatments — are often fundamentally different.

2. Hair Changes Typical of the Menopausal Transition

The most characteristic menopausal hair change is gradual thinning over months to years rather than acute shedding. Women commonly report:

Widening of the central parting (a hallmark of female patterned hair loss)

• Reduced hair density and volume

• Finer hair texture and decreased shaft diameter

• Increased scalp visibility

These features are thought to result from declining oestrogen levels, age-related follicular changes, genetic predisposition, altered androgen sensitivity, and changes in hair cycling dynamics.^[3,4] A cross-sectional study by Chaikittisilpa et al. of 178 postmenopausal women found a 52.2% prevalence of female pattern hair loss (FPHL), predominantly mild diffuse thinning.^[5] The loss of oestrogen signalling at the follicle is thought to be a central mechanism: oestrogen receptors (including ERβ) are expressed in scalp hair follicles, and oestrogen has been shown to prolong the anagen (growth) phase and modulate multiple hair growth factors.^[6,7] Without it, the hair change during menopause becomes more visible.

3. Menopause Does Not Usually Cause Dramatic Shedding

A clinically important distinction must be made between the gradual diffuse thinning associated with menopause, and acute excessive shedding, which is more characteristic of telogen effluvium (TE). TE, first systematically described by Kligman (1961) and subsequently classified by Headington (1993), occurs when a larger-than-normal proportion of hairs prematurely enter the telogen (resting/shedding) phase.^[8,9]

Patients with TE typically describe:

• Excessive hair in the shower or brush

• Diffuse reduction in volume

• Onset over weeks to months

• Increased shedding with washing or combing

Unlike FPHL, TE is primarily a disorder of hair cycling rather than follicular miniaturisation. Histomorphometric data from Anzai et al. confirm that chronic TE and FPHL are distinct entities with separate pathogenic mechanisms.^[10] Identifying which process is active is essential for targeted management.

4. Is Hair Thinning Due to Menopause or Ageing?

A significant question in the dermatology literature is whether postmenopausal hair thinning reflects primarily hormonal changes or intrinsic ageing. Messenger and Sinclair demonstrated that female hair thinning increases progressively with age, even in women without evidence of androgen excess, suggesting that age-related follicular senescence plays a significant independent role.^[11]

Proposed mechanisms of age-related follicular change include:

• Shortening of the anagen phase

• Reduced follicular proliferative activity and mitotic rate

• Decrease in hair shaft diameter

• Cumulative oxidative and environmental damage to follicular stem cells

• Senescent cell accumulation within the follicular unit

A comprehensive review by Davis and colleagues (2025) described how intrinsic cellular senescence — including SASP (senescence-associated secretory phenotype) — may restrict follicular nutrient supply and promote immune privilege collapse, contributing to hair aging independently of hormonal status.^[12] Overall, the evidence suggests that menopausal hair change is multifactorial rather than driven by a single mechanism, with age-related and hormonal pathways often coexisting. For those looking to rejuvenate the scalp at a cellular level, exosome therapy and polynucleotides are emerging as potent options for age-related thinning.

5. Thyroid Disease Is More Common Around Menopause

Thyroid dysfunction is one of the most important reversible causes of excessive hair shedding in midlife women. Both hypothyroidism and hyperthyroidism disrupt the normal hair cycle, leading to diffuse telogen effluvium.^[13] Hair shedding in thyroid disease may present as:

• Diffuse scalp shedding

• Brittle, dry hair texture

• Eyebrow thinning (particularly the lateral third)

• Reduced hair quality and shaft diameter

A systematic review by Hussein et al. (2023) applying PRISMA methodology highlighted that the prevalence and impact of thyroid disorders on hair loss remain substantially underestimated, and that hair shedding may precede other manifestations of thyroid dysfunction by several months.^[13]

A retrospective study of 500 women with TE found that 150 (30%) had hypothyroidism and 102 (20.4%) had hyperthyroidism, underscoring the frequency of thyroid-related TE in clinical practice.^[14] Because fatigue, mood change, and hair loss overlap with menopausal symptoms, thyroid disease may be attributed to menopause and remain untreated. Thyroid function testing — including TSH and free T4 — is therefore indicated in women presenting with significant hair shedding during the menopausal transition.

6. Nutritional Deficiency as a Contributor

Iron deficiency is a well-established contributor to chronic diffuse hair shedding. Low ferritin has been associated with impaired hair regrowth in susceptible individuals, and several studies have investigated the relationship between serum ferritin levels and non-scarring alopecia in women.^[15,16]

Olsen et al. (2010), in a controlled study of 381 women with FPHL or CTE and 76 controls at Duke University, confirmed that iron deficiency — defined at various ferritin thresholds — is highly prevalent in women of all ages but particularly in premenopausal women.^[15] A systematic review and meta-analysis by Saed et al. (2022) further evaluated iron deficiency in non-scarring alopecia and concluded that women with hair loss may benefit from optimising ferritin levels.^[17]

Additional nutritional contributors may include:

• Vitamin D deficiency

• Zinc deficiency — with oral zinc therapy demonstrating benefit in confirmed zinc deficiency-related TE

• Protein deficiency or rapid weight loss

• Restrictive dieting

Midlife women may be particularly vulnerable due to dietary changes, gastrointestinal issues, chronic stress, or medication interactions affecting nutrient absorption.

7. Medication-Induced Hair Shedding

Medication-induced TE is an increasingly recognised cause of diffuse alopecia in women. Piraccini and Tosti (2006) highlighted drug-induced hair disorders as an important but under-recognised cause of alopecia, noting that hair loss is usually completely reversible once the causative agent is identified and discontinued.^[18]

Drug classes associated with diffuse shedding via TE include:

• Systemic retinoids and psychotropic medications including SSRIs

• Anticoagulants (heparin, warfarin) — a common trigger, typically presenting several months after initiation

• Antihypertensive agents including beta-blockers

• Statins

A two-part review by Bhoyrul et al. (2024) systematically catalogued drugs implicated in medication-induced TE, emphasising that the diagnosis is frequently delayed due to the latency of clinically apparent hair loss (typically 2–4 months following drug initiation).^[19,20]Medication review should therefore be a standard component of assessment in any woman presenting with new-onset diffuse hair shedding.

8. Can HRT Cause Hair Shedding?

This is a common clinical question. Oestrogen generally exerts a protective effect on the hair follicle, promoting anagen phase prolongation through oestrogen receptor signalling.^[7]However, fluctuations in hormone levels — particularly during initiation, discontinuation, or dose adjustment of HRT — can trigger temporary TE in susceptible women.

Some women notice increased shedding:

• After starting HRT

• After changing HRT dose or formulation

• During inconsistent or interrupted use

• During the perimenopausal transition itself

This type of shedding reflects disruption of the hair cycle rather than permanent follicular damage, and typically resolves once hormone levels stabilise. A review of the hair follicle as an oestrogen target by Ohnemus et al. (2006) confirmed the complexity of oestrogenic signalling in the follicle and the potential for fluctuations to disrupt cycle timing.^[7]

9. Why Transdermal HRT May Be Better Tolerated for Hair

Transdermal oestrogen delivery (patches, gels, or sprays) provides more stable systemic oestrogen levels compared with oral preparations, which undergo first-pass hepatic metabolism. More stable hormone delivery may theoretically reduce the hormonal fluctuations that can precipitate TE in susceptible individuals.^[21]

L’Hermite et al. (2008) reviewed the evidence for transdermal oestradiol combined with micronised progesterone as a safer HRT option, noting that the transdermal route avoids first-pass metabolism and produces steadier serum oestrogen concentrations.^[21] In terms of progestogen selection, micronised progesterone — which is devoid of androgenic or glucocorticoid activity — is generally considered a more hair-neutral progestogen than synthetic progestins, some of which have androgenic properties that may worsen hair thinning in genetically susceptible women.^[22]

The choice of progestogen is reviewed in detail by Scarborough et al. (2021) who noted that androgenic synthetic progestins may adversely affect hair by increasing free androgen availability (via suppression of SHBG), while micronised progesterone avoids this effect.^[22]Although large, hair-specific comparative trials are lacking, these pharmacological profiles provide a rational basis for preferring transdermal oestradiol plus micronised progesterone in women where hair effects are a clinical concern.

10. When Should You Seek Help?

Clinical assessment is warranted when women experience:

• Sudden excessive shedding

• Rapidly visible scalp thinning

• Patchy hair loss; scalp itching, burning, or scalp problems

• Eyebrow thinning

• Major change in hair texture

• Hair loss associated with weight loss, illness, or medication changes

• Persistent shedding lasting more than 6 months

Assessment typically includes a detailed medical and medication history, scalp examination, and trichoscopy. Blood tests commonly include ferritin, thyroid function (TSH, free T4), vitamin D, B12, and zinc in selected cases.^[1,2] Identifying which processes are active is the most important step in stabilising hair loss and supporting recovery.

11. Conclusions

Hair changes during menopause are common, but dramatic shedding is not a typical feature of menopause alone. When excessive shedding occurs, a systematic assessment should consider telogen effluvium, thyroid dysfunction, nutritional deficiency, medication effects, and hormonal fluctuations as potential contributors. Many of these causes are identifiable and treatable. Accurate diagnosis — rather than attribution to menopause alone — is often the most important step in management.

References

1. Asghar F, Shamim N, Farooque U, et al. Telogen Effluvium: A Review of the Literature. Cureus. 2020;12(5):e8320. PMID: 32572336

2. Pulickal JK, Kaliyadan F. Telogen Effluvium. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024. PMID: 29083801

3. Billero V, Miteva M. Traction alopecia: the root of the problem. Clin Cosmet Investig Dermatol. 2018;11:149–159. [Context: menopausal hair changes overview] PMID: 29692625

4. Marks DH, Penzi LR, Isenhart R, et al. Hormonal changes in menopause: do they contribute to a “midlife hair crisis” in women? Br J Dermatol. 2012;167(Suppl 2):23–28. PMID: 22171679

5. Chaikittisilpa S, Rattanasirisin N, Panchaprateep R, et al. Prevalence of female pattern hair loss in postmenopausal women: a cross-sectional study. Menopause. 2022;29(4):415–420. PMID: 35104837

6. Tran D, Sinclair RD. Menopause and hair loss in women: Exploring the hormonal transition. Maturitas. 2025 [Epub ahead of print]. PMID: 40318238

7. Ohnemus U, Uenalan M, Inzunza J, et al. The hair follicle as an estrogen target and source. Endocr Rev. 2006;27(6):677–706. PMID: 16868246

8. Kligman AM. Pathologic dynamics of human hair loss. I. Telogen effluvium. Arch Dermatol. 1961;83:175–198. PMID: 13729876

9. Headington JT. Telogen effluvium: new concepts and review. Arch Dermatol. 1993;129(3):356–363. PMID: 8447677

10. Anzai A, Pham LH, Bhoyrul B, et al. Chronic telogen effluvium and female pattern hair loss are separate and distinct forms of alopecia: a histomorphometric and immunohistochemical analysis. J Am Acad Dermatol. 2014;71:1051–1058. PMID: 25156792

11. Messenger AG, Sinclair R. Follicular miniaturisation in female pattern hair loss: clinicopathological correlations. Br J Dermatol. 2006;155(5):926–930. PMID: 17034519

12. Davis MG, Pilcher N, Garza LA. Hair Longevity — Evidence for a Multifactorial Holistic Approach to Managing Hair Aging Changes. Int J Mol Sci. 2025. PMID: 40142702

13. Hussein RS, Atia T, Bin Dayel S. Impact of Thyroid Dysfunction on Hair Disorders. Cureus. 2023;15(8):e43266. PMID: 37692605

14. Ragab HM, Farouk HF, Assem EA. Is thyroid dysfunction a common cause of telogen effluvium? A retrospective study. J Cosmet Dermatol. 2024. doi:10.1111/jocd.16151. PMID: 38181279

15. Olsen EA, Reed KB, Cacchio PB, Caudill L. Iron deficiency in female pattern hair loss, chronic telogen effluvium, and control groups. J Am Acad Dermatol. 2010;63(6):991–999. PMID: 20947203

16. Kantor J, Kessler LJ, Brooks DG, Cotsarelis G. Decreased serum ferritin is associated with alopecia in women. J Invest Dermatol. 2003;121(5):985–988. PMID: 14708596

17. Saed S, Ibrahim O, Bergfeld WF. Iron deficiency and nonscarring alopecia in women: systematic review and meta-analysis. J Am Acad Dermatol. 2022;86(5):1062–1074. PMID: 34280480

18. Piraccini BM, Iorizzo M, Rech G, Tosti A. Drug-induced hair disorders. Curr Drug Saf. 2006;1(3):301–305.PMID: 18690941

19. Bhoyrul B, Dinulos JG. Culprits of Medication-Induced Telogen Effluvium, Part 1. Cutis. 2024;113(1):15–20. PMID: 38290075

20. Bhoyrul B, Dinulos JG. Culprits of Medication-Induced Telogen Effluvium, Part 2. Cutis. 2024;113(2):70–75. PMID: 38478950

21. L’Hermite M, Simoncini T, Fuller S, Genazzani AR. Could transdermal estradiol + progesterone be a safer postmenopausal HRT? A review. Maturitas. 2008;60(3–4):185–201. PMID: 23848491

22. Scarborough M, Bhoyrul B, Bhate K, et al. Understanding Hormonal Therapies: Overview for the Dermatologist Focused on Hair. Dermatology. 2021;237(5):786–795. PMID: 34015778

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

Introduction

Hair loss is one of the most distressing and frequently overlooked manifestations of thyroid dysfunction. While fatigue, weight gain, and cold intolerance are the most commonly recognised symptoms of an underactive thyroid (hypothyroidism), a significant number of patients present first — and sometimes exclusively — with diffuse thinning of the scalp. Understanding the bidirectional relationship between thyroid hormones and the hair follicle cycle is essential for clinicians and patients alike, particularly given the rising burden of hypothyroidism in the United Kingdom.

Epidemiology: The UK Burden of Hypothyroidism

Hypothyroidism is among the most common endocrine disorders in the United Kingdom and its prevalence is rising. Data examining NHS and Office of National Statistics records across all 237 health areas found that the prevalence of treated hypothyroidism increased from 2.3% (approximately 1.4 million people) in 2005 to 3.5% (2.2 million) by 2014, with projections estimating a further rise to 4.2% (2.9 million) by 2025 (Leese et al., Thyroid, 2019). This represents one of the steepest increases of any chronic endocrine condition in the UK over the last two decades.

The condition is strongly sex-linked: hypothyroidism is seen ten times more often in women than in men, with a UK female-to-male ratio of approximately 6:1. The incidence of clinical (overt) hypothyroidism has been estimated at 40 per 10,000 women per year compared with just 6 per 10,000 men per year (AAFP, 2015). The overall prevalence of clinically overt hypothyroidism sits at approximately 1–2% of the general UK population, though subclinical hypothyroidism — where TSH is elevated but free T4 remains within range — is found in 8–10% of the population, increasing substantially with age (Thyroid UK).

A UK survey found that approximately 7.5% of women and 2.8% of men have elevated serum TSH levels when screened, suggesting that a large proportion of cases remain undiagnosed or untreated (Hussein et al., PMC, 2019). There is significant geographical variation within the UK: London reports the lowest prevalence of treated hypothyroidism (1.4%), while the Western Isles of Scotland records the highest (6.3%), a pattern partially explained by iodine availability, ethnicity, and environmental factors.

Of particular clinical relevance is the relationship between hypothyroidism and the menopausal transition. The incidence of thyroid disease — including hypothyroidism — is highest in postmenopausal women, and symptoms frequently overlap, leading to diagnostic delays. Hypothyroidism is most commonly diagnosed in women aged 40–50 years, often coinciding with perimenopause. Many women find it difficult to distinguish between hair change during menopause and a pathological thyroid condition.

The Thyroid Gland and the Hair Follicle: Biological Mechanisms

The thyroid gland produces two principal hormones: thyroxine (T4, the prohormone) and triiodothyronine (T3, the biologically active form). These regulate metabolism, cell growth, differentiation, and thermogenesis throughout the body. The hair follicle is a highly metabolically active structure and one of the most sensitive target organs for thyroid hormones.

Thyroid hormone receptors are expressed directly within the hair follicle, particularly in the dermal papilla — the mesenchymal core of the follicle that governs hair cycling. T3 and T4 play a direct role in regulating follicular activity at the root. When hormone levels become insufficient, hair follicles may enter the telogen (resting) phase prematurely, remain there longer than normal, and fail to transition back into the anagen (growth) phase.

The Hair Growth Cycle: Disrupted by Hypothyroidism

Normal hair cycling consists of four phases:

• Anagen – active growth (lasting 2–7 years on the scalp)
• Catagen – regression (2–3 weeks)
• Telogen – resting (approximately 3 months)
• Exogen – shedding

In states of adequate thyroid function, the vast majority of scalp hairs (~85–90%) are in the anagen phase at any given time. In hypothyroidism, this balance is disrupted. Hypothyroidism inhibits cell division in the epidermis and skin appendages, resulting in an increased proportion of hairs in the telogen (resting) phase. The prolonged telogen phase eventually results in excessive shedding — the hallmark of hair shedding or hair loss (telogen effluvium). (Hussein et al., Cureus, 2023).

A retrospective study of 500 female patients with telogen effluvium, examining thyroid function over a decade (2012–2022), found that the hypothyroid group had a significantly higher mean severity of alopecia (SALT) score than both euthyroid and hyperthyroid groups, with a higher proportion of patients experiencing severe hair loss. These findings support the hypothesis that hypothyroidism is a common and frequently underestimated cause of telogen effluvium (published in Medicine, 2024).

Importantly, hypothyroid hair loss typically presents as diffuse thinning across the scalp rather than a localised patch. A classic additional clinical sign is thinning or loss of the outer third of the eyebrows — known as the Sign of Hertoghe — which, while not pathognomonic, is a useful clinical pointer. Hair quality also deteriorates: thyroid hormones regulate sebum production and the structural integrity of the hair cuticle. Without adequate hormonal support, hair becomes dry, brittle, and coarse before visible shedding begins.

It is also important to note that hair loss due to thyroid disease typically becomes apparent several months after the onset of thyroid dysfunction, given the length of the hair growth cycle. This lag frequently confuses both patients and clinicians.

The Menopausal Overlap: A Compounding Factor

The convergence of hypothyroidism with menopause represents a particularly significant clinical challenge. In the first comprehensive population-based study of its kind, the author of this article — Ali and Wojnarowska (2011) — examined subjective hair changes across the scalp, face, and body in postmenopausal women of northern European origin aged 45 years or over, published in the British Journal of Dermatology (164(3):508–513). Crucially, women with a history of thyroid disease were excluded from the study, allowing the authors to characterise hair changes attributable specifically to the menopausal transition rather than thyroid dysfunction.

Their findings revealed two distinct patterns: diffuse generalised scalp hair loss, reported by 26% of women, which was significantly correlated with body hair loss and increasing age; and frontal hair loss, reported by 9% of women, which was associated with higher facial hair scores and relatively younger age. Facial hair gain — particularly at the chin — was reported by 39% of participants. These two patterns likely reflect different underlying pathophysiological mechanisms, with diffuse hair loss representing progressive androgen-related follicular change with ageing, and frontal loss reflecting an earlier androgenic hormonal shift. The study underscores the importance of distinguishing physiological postmenopausal hair change from pathological causes — including hypothyroidism — and provides a critical reference framework for clinicians assessing hair loss in this age group.

The broader hormonal milieu of the menopausal transition — characterised by declining oestrogen and progesterone and a relative increase in androgens — directly impacts the hair follicle, which is an oestrogen-sensitive tissue. These hormonal fluctuations lead to decreased hair density, reduced hair calibre, and changes in hair texture.

The broader literature strongly supports this intersection. A 2025 review in Maturitas (Gupta et al.) notes that female-pattern hair loss, telogen effluvium, and frontal fibrosing alopecia all occur with higher frequency in postmenopausal women. Oestrogen acts as a “hair-friendly hormone,” prolonging the anagen phase and protecting follicles against androgen-mediated miniaturisation. When oestrogen declines, these protective effects are lost — and if hypothyroidism co-exists (as it commonly does in this demographic), the impact on hair is compounded by two independent but synergistic hormonal mechanisms.

A 2023 paper in Biomedicines (Rinaldi et al.) further explored the concept of the hair follicle itself “going through menopause” — proposing that hormonal fluctuations and reduced metabolic efficiency during the menopausal transition directly alter follicular energy metabolism and reduce blood flow to the follicular unit, impairing nutrient delivery. This has important implications for nutritional management (see below).

Given the significant symptomatic overlap between hypothyroidism and menopause — including fatigue, mood changes, weight gain, dry skin, and hair loss — clinicians must maintain a low threshold for thyroid function testing in perimenopausal and postmenopausal women presenting with hair concerns.

Diagnosis: Laboratory Testing for Hypothyroidism

If you suspect a thyroid disease hair issue, comprehensive testing is required:

TSH (Thyroid-stimulating hormone) is the primary and most sensitive first-line test for diagnosing hypothyroidism. Produced by the anterior pituitary, TSH stimulates the thyroid to produce T4 and T3. In primary hypothyroidism, reduced thyroid output results in a compensatory rise in TSH. UK guidelines from the Association of Clinical Biochemistry, the British Thyroid Association, and the British Thyroid Foundation recommend TSH as the frontline investigation, with FT4 automatically reflexed by the laboratory if TSH is abnormal.

A TSH of >10 mU/L combined with a free T4 below the reference range is consistent with overt primary hypothyroidism and warrants treatment.

Free Thyroxine (FT4)

Free T4 measures the amount of unbound (bioavailable) thyroxine circulating in the blood. It is essential when:

• TSH is elevated, to confirm the degree of thyroid failure
• Secondary (central) hypothyroidism is suspected (where TSH may be normal or only mildly raised despite low FT4)
• The patient is on thyroid hormone replacement therapy

Free Triiodothyronine (FT3)

FT3 is rarely requested as a first-line test in the UK context of suspected hypothyroidism, and its utility in diagnosis is limited due to high variability. However, it may be helpful in evaluating suspected secondary hypothyroidism, in patients on combined T3/T4 therapy, and in cases where T3 toxicosis is a differential diagnosis.

Thyroid Peroxidase Antibodies (TPOAb)

Used to identify Hashimoto’s thyroiditis. Research suggests a higher prevalence of these antibodies in patients with alopecia areata. Studies have found a significantly higher prevalence of antithyroid antibodies (25.7%) in patients with alopecia compared to healthy controls (3.3%), highlighting the shared autoimmune pathogenesis of certain hair loss conditions and thyroid disease (Kasumagić-Halilović et al., as cited in MDPI, 2023). Although anti-TPO testing seldom changes the initial treatment (levothyroxine), it identifies patients at higher risk of progression from subclinical to overt hypothyroidism, and those with potential co-existing alopecia areata.

Subclinical Hypothyroidism

In subclinical hypothyroidism, TSH is elevated but FT4 remains within the reference range, and symptoms may be present or absent. This is found in 8–10% of the UK population and is more common in women and older individuals. Hair loss may be a presenting symptom. Current NHS practice is to monitor rather than treat subclinical hypothyroidism in most cases unless the TSH exceeds 10 mU/L, symptoms are significant, or the patient is pregnant.

Practical Note on NHS Testing

In the UK, NHS GPs generally test only TSH as first-line. FT4 is measured reflexively in many, but not all, areas. Testing for FT3 and thyroid antibodies is not routinely undertaken but can be requested when there is clinical reason. Patients undergoing private thyroid screening may access a more comprehensive panel. Clinicians assessing hair loss should ensure thyroid function tests are performed in the appropriate clinical context, alongside other relevant investigations such as ferritin, full blood count, and vitamin D.

Nutritional Factors Contributing to Thyroid-Related Hair Loss

Nutritional deficiencies are both a consequence of hypothyroidism and an independent contributing factor to hair loss. Identifying and addressing these deficiencies alongside thyroid treatment is fundamental to optimising hair recovery.

Iron and Ferritin

Iron is required for the synthesis of thyroid hormones through its role as a cofactor for haem-dependent thyroid peroxidase (TPO), the enzyme responsible for producing T4. When iron stores are depleted, TPO activity is reduced, impairing thyroid hormone production and worsening hypothyroid symptoms. Critically, iron deficiency is independently associated with telogen effluvium even in euthyroid individuals, meaning the two conditions compound one another significantly.

Ferritin (the iron storage protein) is the most sensitive marker of iron status in the context of hair loss. Studies suggest that 25% of women with hypothyroidism experience hair loss partly attributable to low ferritin levels (Avant Medical Group, 2025). Low ferritin is especially prevalent in premenopausal women with heavy menstrual bleeding — a symptom which hypothyroidism itself can exacerbate — and in those following vegetarian or vegan diets. Patients should have both serum ferritin and a full blood count measured; clinicians are advised to request ferritin specifically, as standard iron panels may be normal despite suboptimal stores.

Selenium

Selenium is required for the deiodinase enzymes that convert the inactive T4 into the biologically active T3. Selenium deficiency impairs this conversion, perpetuating a state of functional hypothyroidism even when T4 levels appear adequate. It also plays a role in modulating the autoimmune response in Hashimoto’s thyroiditis: a Cochrane Review (2013) found that selenium supplementation reduced anti-TPO antibody levels by 20–40% in Hashimoto’s patients. Brazil nuts are among the richest dietary sources, with a single nut providing approximately 70–90 mcg.

Zinc

Zinc is required for thyroid hormone synthesis, the function of thyroid hormone receptors, and the production of keratin — the structural protein of the hair shaft. A study published in the Annals of Dermatology (2013) found that zinc deficiency was present in 66.7% of patients presenting with hair loss, underscoring its importance in trichological practice. Dietary sources include pumpkin seeds, oysters, lentils, and chickpeas.

Iodine

Iodine is the essential raw material from which thyroid hormones are constructed: approximately 70–80% of the body’s iodine is concentrated within the thyroid gland. Iodine deficiency can directly cause hypothyroidism and goitre. However, excessive iodine supplementation can paradoxically trigger or worsen thyroid dysfunction, particularly in those with existing autoimmune thyroid disease. Supplementation should only be considered when deficiency is confirmed, and should always be supervised.

Vitamin D

Vitamin D acts as a modulator of immune function and inflammation, and low levels have been associated with increased risk and severity of autoimmune thyroid disorders, including Hashimoto’s thyroiditis. Vitamin D deficiency is highly prevalent in the UK general population — particularly during the autumn and winter months — and is independently associated with hair follicle cycling dysfunction. Public Health England recommends that all adults in the UK consider vitamin D supplementation (10 mcg/day) during autumn and winter.

Biotin (Vitamin B7)

Biotin is widely marketed as a hair growth supplement, and while biotin deficiency can theoretically contribute to hair thinning, clinical deficiency is uncommon. Of greater clinical importance is that biotin supplementation can significantly interfere with thyroid function blood tests, producing falsely abnormal TSH and FT4 results. The MHRA has issued safety guidance on this issue. Patients should be advised to stop biotin supplementation at least 48 hours before thyroid blood tests and should inform their GP and laboratory if they are taking it.

Clinical Implications and Management

The management of hypothyroid-related hair loss centres primarily on adequate thyroid hormone replacement with levothyroxine, targeting a TSH within the normal reference range as per NICE guidance (NG145). Hair regrowth following the commencement of treatment typically begins within several months of achieving euthyroidism, though full restoration may take 6–12 months or longer, depending on the duration of untreated hypothyroidism.

Alongside pharmacological management, clinicians should:

• Assess and correct nutritional deficiencies, particularly ferritin, vitamin D, zinc, and selenium
• Evaluate for co-existing alopecia areata, female-pattern hair loss, or frontal fibrosing alopecia, which may require additional specialist trichological management
• Consider the hormonal context — particularly in perimenopausal and postmenopausal women — and liaise with menopause specialists where appropriate
• Advise patients that thyroid-related hair loss is typically reversible with timely and adequate treatment, provided nutritional status is optimised and concurrent conditions are excluded

As the author’s own landmark population-based study demonstrated (Ali & Wojnarowska, 2011), the subjective experience of hair change following the menopause is highly prevalent and takes distinct clinical forms — and the emotional and psychological burden of hair thinning in women should not be underestimated. Hair loss is deeply connected to identity and wellbeing, and patients benefit significantly from validation, a clear diagnostic framework, and a multidisciplinary approach integrating trichology, endocrinology, and — where relevant — menopause medicine.

Conclusion

Hypothyroidism is a common and rising condition in the UK, disproportionately affecting women — particularly in the perimenopausal and postmenopausal years. Hair loss is a frequently underappreciated manifestation of thyroid dysfunction, mediated through disruption of the hair follicle growth cycle and compounded by nutritional deficiencies that are themselves either caused or exacerbated by hypothyroidism. Diagnosis rests on a stepwise biochemical approach anchored by TSH measurement, with FT4, FT3, and anti-TPO antibodies deployed selectively. Nutritional assessment — particularly of iron/ferritin, selenium, zinc, vitamin D, and iodine — is integral to clinical management. When hypothyroidism coincides with menopause, the effect on hair is compounded, and a holistic, evidence-based approach is essential for effective patient care. If you are experiencing thyroid and hair loss, a multidisciplinary approach at our Harley Street clinic ensures all potential causes — from exercise and skin health to endocrine balance — are considered.

Key References

1. Leese GP et al. (2019). Trends, Determinants, and Associations of Treated Hypothyroidism in the United Kingdom, 2005–2014. Thyroid. doi:10.1089/thy.2018.0251
2. Thyroid UK. Overview of Hypothyroidism. Available at: thyroiduk.org [Accessed May 2026]
3. Hussein RS, Atia T, Bin Dayel S. (2023). Impact of Thyroid Dysfunction on Hair Disorders. Cureus, 15(8):e43266. doi:10.7759/cureus.43266
4. Al-Refu K. (2024). Is Thyroid Dysfunction a Common Cause of Telogen Effluvium? Medicine. doi:10.1097/MD.0000000000036706
5. Gupta AK et al. (2025). Menopause and Hair Loss in Women: Exploring the Hormonal Transition. Maturitas, 198:108378. doi:10.1016/j.maturitas.2025.108378
6. Rinaldi F et al. (2023). The Menopausal Transition: Is the Hair Follicle “Going through Menopause”? Biomedicines, 11(11):3041. doi:10.3390/biomedicines11113041
7. Ali I, Wojnarowska F. (2011). Physiological changes in scalp, facial and body hair after the menopause: a cross-sectional population-based study of subjective changes. British Journal of Dermatology, 164(3):508–513. doi:10.1111/j.1365-2133.2010.10156.x
8. British Thyroid Association / Association of Clinical Biochemistry (2006). UK Guidelines for the Use of Thyroid Function Tests. Available at: baets.org.uk
9. NICE (2019). Thyroid Disease: Assessment and Management. Guideline NG145. Available at: nice.org.uk
10. Bolt Pharmacy (2026). Vitamins for Thyroid Hair Loss: Nutrients, Supplements and NHS Advice. Available at: boltpharmacy.co.uk
11. Study of the Thyroid Profile of Patients with Alopecia. MDPI, 2023. PMC9918246.
12. Vincent M, Yogiraj K. (2013). A Descriptive Study of Alopecia Patterns and their Relation to Thyroid Dysfunction. International Journal of Trichology, 5(1):57–60.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

As a consultant dermatologist specializing in hair disorders, thyroid dysfunction is one of the primary medical causes I investigate when assessing patients with diffuse hair shedding or unexplained thinning.

The reassuring news is that thyroid-related hair loss is often reversible once the underlying hormonal imbalance is identified and treated.

How Does the Thyroid Affect Hair?

The thyroid gland produces hormones that regulate metabolism and energy use. Hair follicles depend on optimal thyroid hormone levels to maintain a healthy growth cycle. When these levels fluctuate, the hair cycle is disrupted, often leading to a condition called Telogen Effluvium, where hair enters the shedding phase prematurely.

Both:

• underactive thyroid disease (hypothyroidism)
  and
• overactive thyroid disease (hyperthyroidism)

can cause hair loss.

What Does Thyroid-Related Hair Loss Look Like?

Many patients ask, “What does thyroid hair loss look like?” Unlike Female Pattern Hair Loss, which usually causes thinning along the part line, thyroid-related shedding is typically diffuse (occurring evenly across the entire scalp).

Patients may notice:

• increased shedding in the shower or hairbrush
• reduced hair volume
• dry or brittle hair
• hair that feels finer or weaker
• slower hair growth
• thinning of the eyebrows, particularly the outer third

Unlike female pattern hair loss, thyroid-related shedding is usually more generalised across the scalp.

Thyroid Disease Is Common in Women

Thyroid dysfunction is much more common in women, particularly during midlife and after menopause.

Importantly, symptoms of thyroid disease often overlap with menopausal symptoms, including:

• fatigue
• low mood
• dry skin
• weight change
• hair thinning

This means thyroid disease may sometimes be missed in women presenting with “menopausal hair loss.”

In our Oxford University study published in the British Journal of Dermatology, we found that diffuse hair thinning becomes increasingly common after menopause and likely reflects a combination of hormonal and ageing-related mechanisms.

However, sudden or dramatic shedding is often a clue that another medical trigger — such as thyroid dysfunction — may also be contributing.

Can Thyroid Disease Cause Sudden Hair Shedding?

Yes.

Thyroid disease commonly triggers a condition called telogen effluvium, where more hairs than usual shift into the shedding phase of the hair cycle.

This can lead to:

• sudden excessive shedding
• hair coming out in large amounts during washing
• noticeable reduction in density over weeks or months

Importantly, hair loss often appears several months after thyroid hormone levels first become abnormal because of the delayed nature of the hair cycle.

What Blood Tests Are Important?

When assessing diffuse hair loss, thyroid testing is often an important part of the investigation.

Tests may include:

• TSH (thyroid stimulating hormone)
• free T4
• thyroid antibodies (in selected cases)

Other useful blood tests often include:

• ferritin (iron stores)
• vitamin D
• B12
• zinc (in selected cases)

Iron deficiency and vitamin deficiencies can coexist with thyroid disease and may worsen shedding.

Can Hair Grow Back After Thyroid Treatment?

In many cases, yes.

Once thyroid hormone levels are stabilised, excessive shedding often improves gradually over several months. Hair regrowth can take time because the hair cycle recovers slowly.

However, recovery may be slower if:

• thyroid disease has been untreated for a long time
• nutritional deficiencies are present
• female pattern hair loss also coexists
• there is underlying inflammatory scalp disease

When Should You Seek Help?

It is sensible to seek medical assessment if you notice:

• sudden excessive hair shedding
• diffuse thinning across the scalp
• eyebrow thinning
• dry, brittle hair
• persistent shedding lasting more than 3–6 months
• hair loss associated with fatigue or weight change

Hair loss is not always simply “stress” or “normal ageing.” Identifying underlying medical causes such as thyroid dysfunction is important because many are treatable.

Final Thoughts

The thyroid gland plays an important role in maintaining healthy hair growth. When thyroid hormone levels become abnormal, diffuse shedding and hair quality changes are common.

Because thyroid disease frequently overlaps with menopause and other causes of hair thinning, careful assessment is important.

The good news is that thyroid-related hair loss is often reversible with appropriate diagnosis, treatment and optimisation of overall hair and scalp health.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

1. Androgenetic Alopecia and Insulin Resistance

The most common form of progressive hair loss is androgenetic alopecia (AGA), characterised by the gradual miniaturisation of hair follicles driven by androgen sensitivity. A growing body of literature links AGA with insulin resistance — a hallmark of type 2 diabetes — suggesting the two conditions may share overlapping pathophysiology.

A landmark population-based case-control study published in The Lancet found a substantially increased risk of hyperinsulinaemia and insulin-resistance-associated disorders — including obesity, hypertension, and dyslipidaemia — in men with early-onset AGA (before age 35), compared with age-matched controls (Matilainen et al., 2000, The Lancet). The authors proposed that early-onset androgenetic alopecia may serve as a clinical marker of insulin resistance, predating the formal diagnosis of type 2 diabetes by years.

The proposed mechanism is biologically plausible. Excess circulating insulin, resulting from peripheral resistance, is hypothesised to stimulate the ovaries and adrenal glands to overproduce androgens, particularly testosterone. This excess testosterone is peripherally converted to dihydrotestosterone (DHT), the more potent androgen responsible for follicular miniaturisation. A study published in ScienceDirect further proposed that elevated insulin also induces microvascular vasoconstriction in the scalp, reducing oxygen and nutrient delivery to follicles and compounding the androgenic effect (Amoretti et al., Journal of the European Academy of Dermatology and Venereology).

A case-control study published in the Indian Journal of Dermatology (Swaroop et al., 2019) examined 50 male patients with early-onset AGA and 50 age-matched controls, finding that metabolic syndrome — of which insulin resistance is a central feature — was present in 82% of those with AGA. While the study found that insulin resistance in isolation did not reach statistical significance (p=0.23) in differentiating the groups, it underscored the broader metabolic context in which AGA often develops.

Research published in the Journal of Clinical and Aesthetic Dermatology further confirmed this relationship, reporting that microvasculature changes associated with insulin resistance represent a distinct mechanistic pathway in AGA pathogenesis — separate from, but synergistic with, the androgen-driven route.

2. Telogen Effluvium: The Stress-Mediated Pathway

Telogen effluvium (TE) is a form of diffuse, non-scarring hair shedding that occurs when a large proportion of follicles prematurely shift from the active growth phase (anagen) into the resting phase (telogen), after which they shed. It is the most commonly reported pattern of hair loss in people with diabetes, and is often reversible once the underlying trigger is addressed.

Poorly controlled diabetes represents a chronic physiological stressor. Sustained hyperglycaemia elevates cortisol levels, and research in Nature (Choi et al., 2021) demonstrated that corticosterone — the rodent equivalent of cortisol — directly inhibits Gas6 signalling in hair follicle stem cells, locking them in a prolonged quiescent state and preventing the onset of hair regeneration. This finding provides a molecular basis for stress-mediated hair loss in diabetic individuals.

The physiological burden of chronic illness, compounded by the psychological impact of managing a complex, lifelong condition, creates the conditions under which TE can become recurrent or persistent rather than a single self-limiting episode. This type of hair loss typically manifests as diffuse thinning across the scalp rather than discrete bald patches, making it harder to attribute clearly to a single cause in clinical settings.

3. Alopecia Areata and Type 1 Diabetes: An Autoimmune Connection

Alopecia areata (AA) is an autoimmune condition in which T-lymphocytes erroneously target hair follicles, resulting in patchy, well-demarcated areas of hair loss on the scalp or body. The condition disproportionately affects individuals with other autoimmune diseases — a pattern well-documented in the literature.

A clinical study published in Skin Appendage Disorders (Thomas and Kadyan, 2008) examining 71 patients with alopecia areata found significant associations with thyroid disorders (observed-to-expected ratio 3.2, p=0.01), atopic dermatitis, and other autoimmune diseases. The co-occurrence of multiple autoimmune conditions in single individuals is consistent with a shared immunological predisposition.

Type 1 diabetes (T1D), itself an autoimmune disease driven by immune-mediated destruction of pancreatic beta cells, shares this vulnerability. A study published in December 2024 found that both prediabetes and diabetes are associated with an increased risk of developing alopecia areata, with chronic systemic inflammation proposed as the mechanistic link connecting metabolic dysregulation to autoimmune follicular attack.

Case reports from the European Congress of Endocrinology further highlighted the interplay between alopecia areata, autoimmune thyroid disease, and the risk of autoimmune diabetes — noting that anti-GAD antibodies (markers of beta cell autoimmunity) were detectable in some patients presenting with alopecia areata in the context of autoimmune polyglandular syndrome, before diabetes had clinically manifested.

4. Microvascular Damage and Poor Scalp Circulation

Chronic hyperglycaemia causes progressive damage to small blood vessels throughout the body — a well-established complication of both type 1 and type 2 diabetes. Hair follicles are metabolically highly active structures with significant demands for oxygen and nutrient delivery. When the microvasculature supplying the scalp is compromised, follicular function deteriorates.

Research suggests this microvascular impairment may operate independently of androgen-mediated mechanisms. Insulin resistance is associated with early vascular dysfunction, even in the absence of overt diabetes, meaning the effects on hair follicle circulation may begin years before a formal diagnosis. Is hair loss a symptom of diabetes on the body as well? Clinical evidence suggests so. Hair loss on legs and diabetes are often linked because of peripheral vascular issues. Diabetes leg hair loss occurs when blood flow to the lower extremities is insufficient to support the hair growth cycle. This hair loss from diabetes on the legs is a key clinical indicator that a patient’s microcirculation may be compromised.

5. Medication-Related Hair Loss

Metformin is the first-line oral medication for type 2 diabetes and is among the most widely prescribed drugs globally. Long-term metformin use is associated with impaired absorption of vitamin B12 in the terminal ileum, a side effect recognised by regulatory bodies including the UK’s Medicines and Healthcare products Regulatory Agency (MHRA), which recommends monitoring B12 levels in patients on prolonged metformin therapy.

A 2013 study documented that chronic metformin use significantly reduced serum levels of both vitamin B12 and folate. Both nutrients are essential for normal cell division and keratinocyte proliferation within hair follicles — their deficiency creates conditions unfavourable to healthy hair growth and can potentiate diffuse shedding. A more recent study, Low-Dose Metformin and Profibrotic Signature in Central Centrifugal Cicatricial Alopecia (Bao et al., 2024), identified an association between metformin and profibrotic signalling in a specific form of scarring alopecia — central centrifugal cicatricial alopecia — adding a new dimension to the medication’s dermatological profile.

Interestingly, research has also explored the potential therapeutic role of metformin in hair loss. A 2025 study in Research (Mai et al.) developed a metformin-based nanosystem that promoted hair growth in androgenetic alopecia models, and a 2023 paper in Medical Hypotheses (Kokhabi et al.) proposed that topical metformin might have therapeutic utility in alopecia areata through its immunomodulatory properties. This apparent paradox — systemic metformin potentially contributing to deficiency-related shedding, while topical metformin may promote regrowth — underscores the importance of route of administration and dosage in pharmacological effects on the hair follicle.

GLP-1 Receptor Agonists: An Emerging Concern

Glucagon-like peptide-1 (GLP-1) receptor agonists — including semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro) — have transformed the management of type 2 diabetes and obesity. However, reports of alopecia as an adverse event have emerged with increasing regularity.

A disproportionality analysis published in the Journal of the European Academy of Dermatology and Venereology(Godfrey et al., 2025) analysed data from the FDA Adverse Event Reporting System (FAERS) between 2022 and 2023, identifying elevated reporting odds ratios for alopecia associated with semaglutide (ROR 2.46; 95% CI 2.14–2.83) and tirzepatide (ROR 1.73; 95% CI 1.42–2.09). These signal-detection figures do not establish causality, but they are statistically meaningful and warrant clinical attention.

A real-world pharmacovigilance study (Nakhla et al., 2024, Cardiovascular Drugs and Therapy) similarly found a significant association between GLP-1 receptor agonists and hair loss in a broad population of diabetic patients. The proposed mechanisms are twofold: first, the rapid and significant weight loss induced by these agents can precipitate telogen effluvium, as the metabolic shock of major caloric restriction pushes follicles into the resting phase; second, GLP-1 receptors have been identified in hair follicle tissue, raising the possibility of a direct pharmacological effect on the hair growth cycle.

A systematic review published in Cureus (Alsuwailem et al., 2025) analysed data from 2,905 adult patients across multiple study designs and found hair loss was a consistent feature across GLP-1 RA user populations, particularly among female patients who were overweight or obese and had experienced hair loss prior to treatment initiation. A 2023 paper by Natarelli et al. (Integrative and Mechanistic Approach to the Hair Growth Cycle and Hair Loss) estimated that Mounjaro was associated with hair loss in approximately 5% of patients, with higher incidence among women experiencing significant weight loss.

A striking counterpoint emerges from a 2024 JAAD case report (Gordon, Musleh, and Bordone), which documented notable improvement in hair loss following tirzepatide treatment in a patient with insulin resistance — suggesting that for some individuals, improved metabolic control may favour hair restoration. This highlights the heterogeneity of individual responses and the need for further investigation into which patient characteristics predispose to hair loss versus improvement with GLP-1 therapy.

A 2024 commentary in the dermatological literature (Desai et al., GLP-1 Agonists and Hair Loss: A Call for Further Investigation) called for formal prospective studies to characterise the incidence, timing, reversibility, and histological features of GLP-1-associated alopecia, noting that the current evidence base is largely retrospective and relies on passive pharmacovigilance data.

DPP-4 Inhibitors: A Therapeutic Angle

In contrast to concerns about GLP-1 agonists, research has explored whether DPP-4 inhibitors — another class of antidiabetic drugs — might actually benefit hair follicle function. A 2023 study in the Journal of Investigative Dermatology (Helm et al.) found that DPP-4 inhibition improved hair follicle activation and regeneration in experimental models, suggesting a potential repurposing of this drug class for hair loss conditions. DPP-4 is an enzyme expressed in dermal papilla cells, and its inhibition appears to support anagen re-entry in hair follicles.

6. The Role of Diabetes-Related Thyroid Disease

Complicating the direct diabetes–hair loss relationship is the high prevalence of thyroid dysfunction in people with diabetes — particularly type 1. Thyroid disorders, especially hypothyroidism, are well-established causes of diffuse hair loss. They can operate independently of glycaemic control, or synergistically with it, making clinical attribution difficult. Clinicians managing diabetic patients with hair loss are advised to screen for thyroid dysfunction as a potential contributing or primary cause.

7. Hair as a Biomarker of Metabolic Risk

An intriguing emerging area of research suggests that changes to hair — including early-onset AGA and even premature greying — may serve as early clinical markers of metabolic dysfunction, potentially preceding the formal diagnosis of type 2 diabetes by years.

A 2017 study in Medical Hypotheses (Miranda et al.) proposed that hair follicle characteristics could serve as early markers of type 2 diabetes. A 2025 lipidomic study published in the International Journal of Molecular Sciences (Wu et al.) identified distinct differences in the lipid composition of hair follicles between women with type 2 diabetes and healthy controls, finding altered lipid profiles that may contribute to accelerated greying in the diabetic population.

Clinical Implications and Management

The evidence supports several practical clinical considerations:

Glycaemic optimisation is the cornerstone of management. Improved blood glucose control reduces the physiological stressors — including microvascular damage and hormonal dysregulation — that underlie most forms of diabetes-associated hair loss. Case reports, including one published in Drugs – Real World Outcomes (Ravi et al., 2021), have documented reversal of alopecia following insulin therapy in patients with previously uncontrolled type 2 diabetes.

Nutritional screening is advisable for patients on long-term metformin, with particular attention to vitamin B12 and folate status. Supplementation where deficiency is confirmed may help reduce medication-related shedding.

Medication review is warranted in patients initiating GLP-1 receptor agonists, particularly those with pre-existing hair loss. Clinicians should counsel patients about the possibility of transient telogen effluvium associated with significant weight loss, and distinguish this from a potential direct drug effect.

Dermatology referral For persistent thinning, we may recommend Advanced PRP Therapy or RF microneedling to stimulate regrowth.

Conclusion

The relationship between diabetes and hair loss is complex, multipath, and still incompletely understood. Published evidence confirms links between insulin resistance and androgenetic alopecia, between chronic stress and telogen effluvium, between type 1 diabetes and alopecia areata, and between antidiabetic medications — particularly metformin and GLP-1 receptor agonists — and hair shedding. At the same time, emerging data suggests that improved metabolic control and novel pharmacological approaches may offer therapeutic promise for hair restoration in some diabetic patients.

If you are experiencing hair thinning and diabetes symptoms, please contact our London clinic for a comprehensive consultation.

References

1. Matilainen, V., et al. (2000). Early androgenetic alopecia as a marker of insulin resistance. The Lancet, 356(9246).
2. Swaroop, M., et al. (2019). The Association of Metabolic Syndrome and Insulin Resistance in Early-Onset Androgenetic Alopecia in Males: A Case-Control Study. Indian Journal of Dermatology.
3. Choi, S., et al. (2021). Corticosterone inhibits GAS6 to govern hair follicle stem-cell quiescence. Nature.
4. Thomas, E.A., & Kadyan, R.S. (2008). Alopecia areata and autoimmunity: a clinical study. Indian Journal of Dermatology, 53(2), 70–74. PMC2763714.
5. Bao, L., et al. (2024). Low-Dose Metformin and Profibrotic Signature in Central Centrifugal Cicatricial Alopecia. Dermatology journal.
6. Godfrey, H., et al. (2025). Alopecia Associated With the Use of Semaglutide and Tirzepatide: A Disproportionality Analysis Using the FDA Adverse Event Reporting System (FAERS) From 2022 to 2023. Journal of the European Academy of Dermatology and Venereology, 39(2), e153–e154.
7. Nakhla, M., et al. (2024). Risk of Suicide, Hair Loss, and Aspiration With GLP1-Receptor Agonists and Other Diabetic Agents: A Real-World Pharmacovigilance Study. Cardiovascular Drugs and Therapy.
8. Gordon, E.R., Musleh, S., & Bordone, L.A. (2024). Treatment of Insulin Resistance With Tirzepatide Leading to Improvement of Hair Loss. JAAD Case Reports, 50, 123–125.
9. Alsuwailem, O.A., et al. (2025). Hair Loss Associated With Glucagon-Like Peptide-1 (GLP-1) Receptor Agonist Use: A Systematic Review. Cureus. DOI: 10.7759/cureus.92454.
10. Helm, M., et al. (2023). Repurposing DPP4 Inhibition to Improve Hair Follicle Activation and Regeneration. Journal of Investigative Dermatology, 143(11), 2132–2144.
11. Kokhabi, P., et al. (2023). Topical Metformin as a Novel Therapy for Alopecia Areata Due to Its Immunologic Effects. Medical Hypotheses, 179, 111155.
12. Mai, Q., et al. (2025). Robust Metformin Nanosystem Promotes Hair Growth in Androgenetic Alopecia. Research, 8, Article 0780.
13. Miranda, J.J., et al. (2017). Hair Follicle Characteristics as Early Marker of Type 2 Diabetes. Medical Hypotheses.
14. Wu, L., et al. (2025). Lipidomics Combined with Network Pharmacology to Explore Differences in the Mechanisms of Grey Hair Development Between Type 2 Diabetes Mellitus and Normal Populations (Female). International Journal of Molecular Sciences, 26(5), 2034.
15. Natarelli, N., et al. (2023). Integrative and Mechanistic Approach to the Hair Growth Cycle and Hair Loss. Dermatology.
16. Desai, et al. (2024). GLP-1 Agonists and Hair Loss: A Call for Further Investigation. Dermatological commentary.
17. Ravi, K., et al. (2021). Reversal of Alopecia by Insulin Therapy in Uncontrolled Type 2 DM: A Case Report. Drugs – Real World Outcomes.

This article is intended for educational purposes and reflects the published scientific literature. It does not constitute medical advice. Patients experiencing hair loss should consult a qualified healthcare professional.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/

What Are GLP-1 Medications?

Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of medicines widely prescribed for type 2 diabetes and obesity. You may know them by brand names such as Ozempic, Wegovy (semaglutide), Mounjaro, or Zepbound (tirzepatide). These medications work by mimicking a natural hormone that regulates blood sugar and appetite, helping people lose significant amounts of weight alongside other health benefits.

As their use has grown, so has awareness of their side effects. While nausea and digestive symptoms are the most commonly discussed, an increasing number of patients — and the research community — are paying closer attention to a less-expected concern: hair loss.

Is Hair Loss Really Linked to These Medications?

The short answer is: yes, there does appear to be a real association, though the picture is still developing.

A large real-world study using data from over 100 million patients found that GLP-1 users had significantly higher rates of non-scarring hair loss compared to matched controls, with the gap widening particularly from 2021 onwards as usage of these medicines surged. At 12 months, GLP-1 users were roughly 1.4 to 1.8 times more likely to experience certain types of hair loss than non-users.

Pharmacovigilance data from the FDA Adverse Event Reporting System has also flagged elevated reporting of hair loss associated with semaglutide and tirzepatide specifically.

It is important to note that not all studies have found the same signal — results vary depending on study design — and researchers are clear that more work is needed. But the evidence is substantial enough that patients and prescribers should be aware.

What Type of Hair Loss Occurs?

The most commonly reported pattern is telogen effluvium (TE) — a form of diffuse, temporary shedding across the whole scalp. This is often confused with other scalp problems, but you might notice:

• More hair than usual in the shower drain or on your pillow
• A brush that fills up faster than before
• Your ponytail feeling thinner, or a wider parting
• General reduction in volume rather than bald patches

Another pattern that has been reported is androgenetic alopecia (AGA). In women, this more often causes a diffuse thinning over the top of the scalp, similar to female patterned hair loss.
Importantly, these are non-scarring types of hair loss. This means the follicles are not permanently damaged, which is why most people see regrowth once the trigger resolves. If the loss is localized, it is vital to rule out alopecia areata or scarring hair loss through a professional consultation.

Why Does It Happen?

The precise mechanisms are still being investigated. Researchers have found GLP-1 receptors in hair follicles in animal studies, raising the possibility that these medications could have some direct influence on the hair growth cycle — though human evidence for this is currently lacking and the question remains open. What is better established is that several indirect mechanisms play a role:

1. Rapid Weight Loss

Hair follicles are surprisingly sensitive to physiological stress. When the body loses weight quickly, it can interpret this as a threat and redirect resources away from “non-essential” processes like hair growth. This pushes a larger-than-normal proportion of follicles into their resting phase (telogen) simultaneously. Two to three months later, all those resting hairs shed at once — which is why the timing of hair loss often lags a few months behind when you started the medication or increased your dose.

2. Nutritional Deficiencies

GLP-1 medications significantly suppress appetite. While this is the mechanism behind their effectiveness, eating substantially less food also means taking in fewer nutrients. The micronutrients with the best-established evidence as triggers for telogen effluvium are ferritin (iron stores), vitamin D, folate, B12, and zinc — and these are among those most likely to fall short when overall food intake drops significantly.

Protein is sometimes cited in this context, but it is worth being clear about what the evidence actually shows. Protein deficiency causing hair loss is documented mainly in people following crash diets, those with eating disorders, or those with severe malnutrition — in other words, people eating very little indeed. The daily amount needed to avoid deficiency is modest: around 50–60 grams for an average adult, roughly equivalent to a single chicken breast (which contains around 55g on its own), or smaller amounts spread across the day from eggs, fish, dairy, beans, or other sources. Most people on a GLP-1 medication who are eating regular, varied — if smaller — meals are unlikely to fall below this threshold. The evidence for protein supplementation specifically improving hair loss in people who are not genuinely deficient is weak. The stronger, more consistent message from clinical studies points to micronutrient deficiencies as the nutritional factors most worth identifying and correcting.

3. Hormonal Changes

Rapid weight loss can cause transient fluctuations in hormone levels. In some cases, these shifts may unmask an underlying PCOS-related hormonal skin or hair issue.

When Does It Start, and Will It Stop?

Most patients who experience hair shedding notice it two to three months after starting the medication or after a dose increase. This delay is simply how the hair cycle works — follicles that were pushed into a resting phase months earlier are only now shedding.

The good news: for most people, hair loss on GLP-1 medications is temporary. Once weight stabilises and nutritional status improves, regrowth usually follows. How long that takes varies between individuals but is typically several months.

You should speak to your doctor if:

• Shedding is severe or distressing
• Hair loss continues well after your weight has stabilised
• You notice patchy loss rather than diffuse thinning
• The hair loss is accompanied by other symptoms such as fatigue, cold intolerance, or skin changes (which could suggest thyroid or other issues)

What Can You Do?

GLP-1 medications significantly suppress appetite, which is central to how they work. But eating substantially less also means taking in fewer nutrients overall. Maintaining a varied, balanced diet — with adequate protein alongside a range of vegetables, whole grains, and healthy fats — supports hair health as part of overall wellbeing during weight loss.

Don’t Restrict Calories Too Aggressively

Eating too little — particularly below 1,200 calories per day — dramatically increases the risk of nutritional deficiencies that affect hair, bone, and muscle health. The goal is healthy, sustainable weight loss, not near-starvation. If your appetite suppression is so strong that you are struggling to eat enough, speak to your prescribing team about adjusting your approach.

Check Your Micronutrients

Ask your doctor to check your levels of ferritin (iron stores), vitamin D, folate, B12, and zinc before starting or early in your treatment. If you are deficient, targeted supplementation can make a meaningful difference. Don’t wait until your hair starts falling out — the first few months are the most important window for prevention.

Consider a Multivitamin — But Seek Proper Nutritional Guidance

A good-quality multivitamin can act as a useful safety net when overall food intake is reduced. However, a multivitamin alone is no substitute for proper nutritional assessment. Working with your doctor or a registered dietitian to review your diet and blood results means any deficiencies can be identified and addressed in a targeted, evidence-based way — far more effective than a generic supplement approach.

Don’t Stop Your Medication Without Talking to Your Doctor

It can be alarming to notice your hair thinning, but stopping a GLP-1 abruptly can cause its own problems — including rapid weight regain and another round of metabolic disruption that could trigger further shedding. Many patients successfully manage hair concerns while continuing their medication through nutritional support and, in some cases, dose adjustment.

Speak to a Dermatologist specialising in hair loss

If hair loss is significant, a dermatologist specialising in hair loss can confirm the diagnosis. We can also assess if other metabolic factors are at play, such as diabetes-related hair loss.

Key Takeaways

• Hair loss has been reported in a meaningful proportion of GLP-1 users, and research increasingly supports a real association.
• The most common type is telogen effluvium — diffuse, temporary shedding caused by the physical stress of rapid weight loss.
• The exact mechanisms are still being studied; indirect causes such as rapid weight loss, nutritional deficiencies, and hormonal changes are well established, and researchers are also investigating whether the medication may have some direct effect on hair follicles.
• The most effective steps you can take are eating a balanced, nutritious diet, avoiding extreme calorie restriction, and getting your micronutrient levels checked — ideally with proper nutritional oversight from your doctor.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

A London-based dermatologist, specialises in acne, hair loss, hormonal skin disorders, and skin cancer treatment.

Dr Ali has been practising dermatology since 2002, with over 25 years of medical experience delivering consultant-led dermatological care. She previously served as Consultant Dermatologist and Clinical Head of Dermatology at Imperial College Healthcare NHS Trust, where she led complex dermatology services and specialist referral clinics.

iadermatology.com/