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/

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/

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/

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/

What is a Progestogen?

Progestogens are a class of steroid hormones that bind to progesterone receptors. In the context of the combined oral contraceptive pill (COCP), a synthetic progestogen — or progestin — is paired with an oestrogen (typically ethinylestradiol) to suppress ovulation, thicken cervical mucus, and alter the endometrial environment.

All currently used progestins are classified by their structural origin. This matters because some are derived from testosterone and can inadvertently trigger skin pigmentation disorders or worsen existing acne in sensitive patients.

Generations of progestins and their androgenic character

Progestins are commonly grouped by generation, with each successive generation developed partly to reduce androgenic side effects, improve contraceptive reliability, or both.

First-generation progestins — norethisterone and ethynodiol diacetate — were developed in the 1950s and 60s. They are moderately androgenic, with androgen receptor binding affinity of approximately 15% relative to testosterone. At the high doses used in early pills, they contributed to adverse lipid profiles and androgenic side effects including acne and weight changes.

Second-generation progestins, notably levonorgestrel and norgestrel, are more potent and considerably more androgenic. Levonorgestrel has high androgen receptor binding affinity — estimated at 50–100% relative to testosterone depending on the assay system used — and is associated with the highest rates of acne and oily skin among commonly used progestins. Norgestrel is the racemic form; only the levo-isomer is biologically active, giving it approximately half the androgenic potency of equivalent-dose levonorgestrel.

Third-generation progestins — desogestrel, gestodene, norgestimate — were designed to retain progestogenic potency while minimising androgenic activity. Desogestrel and norgestimate have very low AR binding affinity (1–2% vs testosterone) and are considered low androgenic in clinical practice. Gestodene is more complex: intact-cell assays show higher AR binding than simple cytosol assays suggest, though high SHBG affinity is thought to limit free drug at tissue level, explaining lower clinical androgenicity than its receptor binding might predict.

Relative androgen receptor binding affinity of progestins

The table below summarises the androgen receptor relative binding affinity (AR RBA) of progestins used in oral contraceptives, alongside their structural classification, receptor agonism type, and clinical androgenic effect. An important distinction is made between binding affinity and functional activity — a compound can bind the AR with high affinity while acting as an antagonist rather than an agonist, as is the case with cyproterone acetate.

Progestin	Structural origin	AR RBA (approx.)	AR agonism	Functional effect	Relative binding
1ST GENERATION — 19-NORTESTOSTERONE DERIVATIVES
Norethisterone	19-Nortestosterone	~15% vs T	Agonist	Androgenic
Ethynodiol diacetate	19-Nortestosterone	~15% vs T	Agonist	Androgenic
2ND GENERATION — 19-NORTESTOSTERONE DERIVATIVES
Levonorgestrel	19-Nortestosterone	~50–100% vs T  assay-dependent	Agonist	Androgenic (high)
Norgestrel	19-Nortestosterone	~25–50% vs T  racemic; LNG active	Agonist	Androgenic (high)
3RD GENERATION — 19-NORTESTOSTERONE DERIVATIVES
Desogestrel  (active: etonogestrel)	19-Nortestosterone	~2% vs T	Weak agonist	Low androgenic
Gestodene	19-Nortestosterone	~4–30% vs T  SHBG limits free drug	Weak agonist	Low androgenic
Norgestimate  (active: norelgestromin)	19-Nortestosterone	~1% vs T	Weak agonist	Low androgenic
4TH GENERATION — 19-NORTESTOSTERONE DERIVATIVE (ANTI-ANDROGENIC)
Dienogest	19-Nortestosterone	<1% vs T  low binding	Antagonist	Anti-androgenic
4TH GENERATION — SPIRONOLACTONE DERIVATIVE
Drospirenone	Spironolactone	0.6% vs DHT  ~<2% vs T	Antagonist	Anti-androgenic
17Α-HYDROXYPROGESTERONE DERIVATIVE — REFERENCE ANTI-ANDROGEN
Cyproterone acetate  (co-cyprindiol / Dianette)	17α-OH Progesterone	70–100% vs DHT  high affinity	Antagonist	Potent anti-androgenic

AR RBA = Androgen Receptor Relative Binding Affinity. Reference standard varies: “vs T” = vs testosterone (100%); drospirenone and cyproterone acetate values are vs DHT. Binding affinity and agonist/antagonist activity are independent properties — cyproterone acetate binds with high affinity but acts as a competitive antagonist; drospirenone and dienogest have very low binding but produce functional anti-androgenic effects in transactivation assays. Published AR binding values vary substantially according to assay system, reference ligand, receptor preparation and whether the parent compound or active metabolite is tested. The table should therefore be read as a clinical hierarchy rather than a fixed numerical ranking. Sources: Fuhrmann et al. (1996); Kloosterboer et al. (1988); Schindler et al. (2003); Stanczyk et al. (2013); Harada & Taniguchi (2010).

Why androgenic activity matters clinically

Androgens — including testosterone and its metabolite dihydrotestosterone (DHT) — act on multiple cutaneous and follicular targets. In women with underlying androgen sensitivity, the choice of progestin in the COCP can meaningfully worsen or improve four distinct clinical conditions: acne vulgaris, female pattern hair loss, hirsutism, and seborrhoea. Each condition shares the same upstream driver — excessive androgenic stimulation of target tissues — but differs in the receptor distribution and cell type involved.

Conversely, oestrogen raises sex hormone-binding globulin (SHBG), which reduces free androgen levels.

All COCPs provide this benefit to some degree. However, progestins with significant androgen receptor agonist activity can attenuate or override this benefit at the receptor level, negating the favourable oestrogen effect and perpetuating androgenic drive at target tissues.

Clinical consequences by condition

Acne vulgaris. DHT stimulates sebaceous gland hypertrophy and increases sebum production, creating the lipid-rich environment that drives Cutibacterium acnes proliferation and follicular inflammation. Progestins with androgenic activity — particularly levonorgestrel — directly worsen acne by stimulating sebaceous glands via AR agonism. Women prescribed levonorgestrel-containing pills frequently report new-onset or worsened acne, particularly on the lower face, jawline, and back. Conversely, anti-androgenic progestins reduce sebum output and improve acne lesion counts. Women with pre-existing acne who require the COCP should be counselled that progestin choice directly affects their dermatological outcome.

Female pattern hair loss (FPHL). FPHL — characterised by diffuse thinning over the crown and mid-scalp with preservation of the frontal hairline — is androgen-sensitive in a significant proportion of affected women, mediated principally by DHT acting on follicular AR to shorten the anagen (growth) phase and miniaturise follicles over successive cycles. Prescribing a strongly androgenic progestin such as levonorgestrel in a woman with FPHL can accelerate follicular miniaturisation and worsen hair loss. This is an underappreciated consequence of progestin selection: women presenting with FPHL who are on or considering the COCP should be switched to or started on a pill containing a low-androgenic or anti-androgenic progestin. Drospirenone, norgestimate, or cyproterone acetate-containing formulations are preferred. It should be noted that all COCPs can trigger a telogen effluvium on initiation or cessation, which is a separate and usually self-limiting phenomenon distinct from androgenic FPHL.

Hirsutism. Terminal hair growth in androgen-sensitive areas — upper lip, chin, sideburn distribution, chest, abdomen, and inner thighs — is driven by DHT acting on dermal papilla cells in hair follicles, converting vellus hairs to coarser terminal hairs. Androgenic progestins can maintain or worsen hirsutism by sustaining AR activation in these follicles. Anti-androgenic progestins reduce this stimulus, though hair follicle response is slow: meaningful improvement typically requires six to twelve months before a reduction in new terminal hair growth is apparent. Existing terminal hairs do not spontaneously regress and may require concurrent physical treatment. Women with polycystic ovary syndrome (PCOS) are particularly affected, and in this group an anti-androgenic COCP is strongly preferred.

Seborrhoea. Sebaceous gland activity is exquisitely sensitive to androgens; even low-level AR stimulation increases sebum secretion rate measurably. Seborrhoea — characterised by oily skin and scalp — is one of the earliest and most reliable markers of androgen excess in women. Androgenic progestins compound this by adding a direct agonist stimulus on top of any endogenous androgen excess. Anti-androgenic progestins, particularly drospirenone, produce clinically meaningful reductions in skin oiliness through sebaceous AR blockade, and this is often one of the first improvements women notice within the first one to two pill cycles.

Drospirenone: a structurally distinct progestin

Drospirenone is unique because it is derived from spironolactone rather than testosterone. It acts as a functional antagonist, meaning it blocks the androgen receptor. This makes it an excellent choice for patients also undergoing HRT treatment in London who need to balance their hormonal profile.

Its androgen receptor binding affinity is very low (0.6% vs DHT, equivalent to less than 2% vs testosterone), yet in transactivation assays it acts as a functional antagonist — binding does not activate the receptor, and it blocks androgen-stimulated transcriptional activation. This is mechanistically different from cyproterone acetate, which achieves potent anti-androgenic effect through high-affinity competitive binding (70–100% vs DHT), occupying the receptor and preventing DHT from doing so.

Drospirenone and androgen-related skin conditions

Multiple randomised controlled trials have demonstrated that drospirenone-containing COCPs significantly improve acne compared with placebo and with levonorgestrel-containing pills. The mechanism operates at two levels: increased SHBG (reducing circulating free androgens) and direct antagonism at androgen receptors in skin target tissues.

Drospirenone/ethinylestradiol (Yasmin, Yaz) has received FDA approval for treatment of moderate acne in women choosing oral contraception — one of few COCPs to carry this dual indication. In head-to-head comparison with co-cyprindiol (ethinylestradiol/cyproterone acetate 35/2 mg), drospirenone-containing pills produced comparable acne improvement at nine months, with no significant difference between the two formulations.

Dienogest: a different route to anti-androgenic activity

Dienogest, a 19-nortestosterone derivative used primarily in endometriosis treatment (Qlaira, Visanne), achieves anti-androgenic activity by a similar functional mechanism to drospirenone — very low AR binding affinity but antagonism in transactivation assays. Unlike drospirenone, it has no anti-mineralocorticoid activity and lacks the diuretic benefit. It is less commonly used in acne-focused prescribing but is relevant in women requiring treatment for both endometriosis and androgenic skin symptoms.

Safety considerations and prescribing context

Drospirenone-containing pills are generally well tolerated. The anti-mineralocorticoid activity warrants caution in women with renal impairment, adrenal insufficiency, or those taking potassium-sparing diuretics or ACE inhibitors, due to a theoretical risk of hyperkalaemia — though in healthy women at standard doses this is rarely clinically significant.

The venous thromboembolism (VTE) risk profile of drospirenone-containing pills is broadly comparable to other third-generation progestin pills, and modestly higher than levonorgestrel-containing pills — a consideration in women with additional VTE risk factors. The absolute risk remains low in healthy, non-smoking women under 35. Co-cyprindiol carries a higher VTE risk than standard COCPs and is not recommended as a first-line contraceptive; it should be reviewed once acne control is achieved.

Summary

The progestin component of the COCP is not pharmacologically inert with respect to androgen activity. Second-generation progestins, particularly levonorgestrel, carry high androgen receptor binding affinity and agonist activity that can exacerbate acne, female pattern hair loss, hirsutism, and seborrhoea. Third-generation progestins are low androgenic.

Drospirenone stands apart as the only spironolactone-derived contraceptive progestin, with very low AR binding (0.6% vs DHT) but functional anti-androgenic activity, plus unique anti-mineralocorticoid effects — making it the preferred progestin in women with androgen-related dermatological concerns.

An important pharmacological principle underpinning this table is that AR binding affinity and agonist/antagonist activity are independent properties: cyproterone acetate binds with high affinity but blocks the receptor, while drospirenone and dienogest bind very weakly yet still achieve functional antagonism.

References

1.  Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH. Classification and pharmacology of progestins. Maturitas. 2003;46 Suppl 1:S7–S16. doi: 10.1016/j.maturitas.2003.09.014. PMID: 14670641

2.  Stanczyk FZ, Hapgood JP, Winer S, Mishell DR Jr. Progestogens used in postmenopausal hormone therapy: differences in their pharmacological properties, intracellular actions, and clinical effects. Endocr Rev. 2013;34(2):171–208. doi: 10.1210/er.2012-1008. PMID: 23238854

3.  Kloosterboer HJ, Vonk-Noordegraaf CA, Turpijn EW. Selectivity in progesterone and androgen receptor binding of progestagens used in oral contraceptives. Contraception. 1988;38(3):325–332. doi: 10.1016/0010-7824(88)90104-7. PMID: 3139361

4.  Fuhrmann U, Krattenmacher R, Slater EP, Fritzemeier KH. The novel progestin drospirenone and its natural counterpart progesterone: biochemical profile and antiandrogenic potential. Contraception. 1996;54(4):243–251. doi: 10.1016/s0010-7824(96)00195-3. PMID: 8922878

5.  Muhn P, Fuhrmann U, Fritzemeier KH, Krattenmacher R, Schillinger E. Drospirenone: a novel progestogen with antimineralocorticoid and antiandrogenic activity. Ann N Y Acad Sci. 1995;761:311–335. doi: 10.1111/j.1749-6632.1995.tb31386.x. PMID: 7625729

6.  Muhn P, Krattenmacher R, Beier S, Elger W, Schillinger E. Drospirenone: a novel progestogen with antimineralocorticoid and antiandrogenic activity: pharmacological characterization in animal models. Contraception. 1995;51(2):99–110. doi: 10.1016/0010-7824(94)00015-o. PMID: 7750297

7.  Louw-du Toit R, Perkins MS, Hapgood JP, Africander D. Comparing the androgenic and estrogenic properties of progestins used in contraception and hormone therapy. Biochem Biophys Res Commun. 2017;491(1):140–146. doi: 10.1016/j.bbrc.2017.07.063. PMID: 28711501

8.  Harada T, Taniguchi F. Dienogest: a new therapeutic agent for the treatment of endometriosis. Womens Health (Lond). 2010;6(1):27–35. doi: 10.2217/whe.09.72. PMID: 20001868

9.  Oelkers W, Foidart JM, Dombrovicz N, Welter A, Heithecker R. Effects of a new oral contraceptive containing an antimineralocorticoid progestogen, drospirenone, on the renin-aldosterone system, body weight, blood pressure, glucose tolerance, and lipid metabolism. J Clin Endocrinol Metab. 1995;80(6):1816–1821. doi: 10.1210/jcem.80.6.7775629. PMID: 7775629

10.  Fuhrmann U, Slater EP, Fritzemeier KH. Characterization of the novel progestin gestodene by receptor binding studies and transactivation assays. Contraception. 1995;51(1):45–52. doi: 10.1016/0010-7824(94)00003-f. PMID: 7750284

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/

A Landmark Change in Women’s Health

In May 2026, one of the most significant moments in women’s health in decades took place. A landmark paper published in The Lancet — the world’s most respected medical journal — officially renamed Polycystic Ovary Syndrome (PCOS) to Polyendocrine Metabolic Ovarian Syndrome (PMOS). This change was the result of a 14-year global effort led by Professor Helena Teede of Monash University, involving 56 professional societies, thousands of patients, and healthcare professionals from every corner of the world.

If you have been diagnosed with PCOS — or suspect you might have it — this news matters for you. It does not change your diagnosis. It does not change the treatments that work. What it does change is the way medicine understands, names, and ultimately treats this condition. And that, for millions of women who have spent years feeling dismissed or misunderstood, is profound.

Why Was the Name Wrong in the First Place?

The name ‘Polycystic Ovary Syndrome’ told an incomplete — and in some ways misleading — story. It implied the condition was defined by cysts on the ovaries. In reality, those are not true pathological cysts at all. What shows up on an ultrasound are small, immature follicles that failed to develop properly. Calling them ‘cysts’ pointed doctors and patients toward the ovaries as the source of the problem, when the condition is far more complex than that.

The old name caused real harm:

• Women were often told their main issue was fertility or weight — and little else
• Diagnosis was frequently delayed by years, especially in women without obvious ovarian cysts
• Symptoms affecting the skin — acne, excess hair, hair thinning — were treated as cosmetic nuisances rather than clinical signs
• The metabolic risks — including diabetes, cardiovascular disease, and insulin resistance — were routinely overlooked
• Research funding and policy support lagged behind because the condition was framed too narrowly

Over 14,000 patients and professionals contributed to developing the new name, reporting that the old terminology contributed to stigma, delayed care, and a persistent sense of not being taken seriously.

What Does PMOS Actually Mean?

The new name — Polyendocrine Metabolic Ovarian Syndrome — is more than a rebrand. Each word was chosen with care:

How Is PMOS Diagnosed?

The diagnostic criteria have not changed. You receive a PMOS diagnosis if you meet at least two of the following three features:

• Irregular or absent menstrual cycles — a sign that ovulation is not happening regularly
• Clinical or biochemical signs of elevated androgens — including acne, excess facial or body hair, or scalp hair thinning, or raised testosterone on a blood test
• Polycystic ovarian morphology on ultrasound — the appearance of multiple small follicles on the ovaries

Crucially, two of the three diagnostic criteria are visible on the skin. Acne, hirsutism, and hair thinning are not side effects or cosmetic complaints — they are recognised diagnostic features of PMOS.

Your Skin as a Window Into Your Hormones

The connection between PMOS and the skin runs deep, and it begins with one molecule: insulin. In PMOS, cells throughout the body become less sensitive to insulin — a state called insulin resistance. The body responds by producing more insulin to compensate. That excess insulin signals the ovaries (and often the adrenal glands) to produce more androgens — male-type hormones such as testosterone. Those androgens then act on the skin in three important ways.

Hormonal Acne

Androgens stimulate the oil glands in the skin to produce more sebum. This creates the environment in which acne-causing bacteria thrive. PMOS-related acne is typically hormonal in pattern — it tends to appear along the jawline, chin, lower cheeks, neck, chest, and back. It is often deeper and more persistent than teenage acne, can be cystic, and frequently returns despite standard skincare or antibiotic treatments. Left untreated, it can cause scarring and significant emotional distress.

Hirsutism — Unwanted Hair Growth

Androgens stimulate hair follicles in certain areas of the body to grow coarser, darker, terminal-type hair in a typically male distribution — upper lip, chin, sideburns, jawline, chest, abdomen, and inner thighs. This is called hirsutism, and it affects up to 70% of women with PMOS. It is one of the features that most significantly affects quality of life, self-confidence, and mental wellbeing. At our London clinic, we find that Nd:YAG Laser treatment is the gold standard for removing this hair safely and permanently, especially when combined with medical hormone management.

Androgenic Alopecia — Hormonal Hair Loss

The same androgens that drive unwanted hair growth elsewhere can also cause hair to thin on the scalp — particularly at the crown and top of the head, following a pattern similar to female pattern hair loss. This occurs because scalp follicles in susceptible women are sensitive to a potent form of testosterone called DHT. Hair thinning is often a deeply distressing symptom, and one that is frequently attributed to stress or ageing when in fact its root cause is hormonal.

Why Dermatology Is Central to Your PMOS Care

For many women, a dermatology appointment is where the PMOS journey begins. Persistent adult acne, hair loss, or distressing facial hair often bring women to a skin clinic long before anyone connects these symptoms to a hormonal condition. The reclassification of PCOS to PMOS formally acknowledges what dermatologists have long understood: the skin is not just collateral damage in this condition — it is a primary site of disease expression and a vital window into what is happening hormonally and metabolically.

A dermatologist who understands PMOS does not simply treat the surface. They treat the whole picture — addressing skin and hair symptoms with targeted interventions while also considering the metabolic drivers that underlie them. This is the approach we take at our clinic.

How We Support Women with PMOS at Our Clinic

Treating Hormonal Acne

Standard over-the-counter products and short courses of antibiotics rarely resolve PMOS-related acne because they do not address its hormonal cause. Our approach is to treat both the skin and the hormone driving it. We use prescription topical treatments including retinoids and azelaic acid, combined where appropriate with anti-androgen therapies to reduce the hormonal stimulus at source. For suitable patients, oral isotretinoin remains an effective option for severe or scarring acne. We also address post-inflammatory pigmentation, which can be particularly pronounced in women with darker skin tones.

Managing Hormonal Hair Loss

Hair loss associated with PMOS is treatable, and — importantly — early intervention leads to better outcomes. We assess the pattern and cause of your hair thinning carefully and offer treatments that work at the follicular level to reduce androgen sensitivity and support regrowth. Alongside topical and oral treatments, we support patients in understanding how hormonal and metabolic treatment can also help slow hair loss over time.

Hirsutism: Reducing and Removing Unwanted Hair

We offer both medical and physical approaches to hirsutism. Anti-androgen medications can reduce the rate of new hair growth and, with time, reduce the density and coarseness of existing hair. However, they do not remove hair that is already present. For this reason, many patients benefit from combining medical treatment with laser hair removal.

Laser Hair Removal

Laser hair removal offers long-term reduction of unwanted hair by targeting the pigment in the hair follicle and permanently disabling it. For women with PMOS, laser treatment is particularly effective when the hormonal component is also being addressed medically — without this, ongoing androgen stimulation can continue to recruit new terminal hairs. We assess your skin tone, hair type, and hormonal status carefully to recommend the right laser protocol for you, and we provide guidance on the number of sessions typically required to achieve a meaningful and lasting reduction.

Treating the Metabolic Root: Insulin Sensitisers and GLP-1 Medications

One of the most important developments in PMOS care is recognising that treating insulin resistance does not just reduce metabolic risk — it also improves skin and hair symptoms. When the insulin signal is corrected, androgen production falls, and the hormonal drive behind acne, hirsutism, and hair loss is reduced from within.

Insulin sensitisers such as metformin have been used in PMOS care for many years. They work by improving the body’s response to insulin, reducing the compensatory hyperinsulinaemia that drives androgen excess. For many women, this can lead to more regular periods, improvements in acne, and a reduction in excess hair growth — alongside meaningful protection against developing type 2 diabetes.

GLP-1 receptor agonists (such as semaglutide) represent an exciting newer option for women with PMOS who also have significant insulin resistance, weight challenges, or cardiovascular risk factors. Originally developed for type 2 diabetes, these medications have shown remarkable benefits for metabolic health, appetite regulation, and weight. In women with PMOS, improving metabolic health in this way can translate into real improvements in hormonal balance — and therefore in skin and hair. We prescribe and monitor these medications carefully, within a holistic plan that addresses your full picture.

The goal is not simply to treat what you can see in the mirror. It is to understand and address the hormonal and metabolic environment that is producing those changes — so that results are meaningful, durable, and genuinely improve your health.

What This Means for You

If you have been diagnosed with PCOS — or if you recognise yourself in the symptoms described here — the renaming of this condition to PMOS is a moment of validation. Your acne, your hair loss, your excess hair growth: these are not vanity. They are symptoms of a complex hormonal and metabolic condition that deserves — and is now more formally receiving — serious medical attention.

Affecting roughly 1 in 8 women of reproductive age worldwide — around 170 million people — PMOS is one of the most common endocrine conditions in women. Yet up to 70% of cases go undiagnosed. Many of those women are sitting with skin and hair concerns, wondering why nothing seems to work, not yet knowing that the answer lies in their hormones and metabolism.

We are here to help you connect those dots. Our clinic takes an integrated approach to PMOS — treating the skin you see every day while also addressing the hormonal and metabolic conditions that drive it. Whether you are coming to us with acne, unwanted hair, hair loss, or concerns about insulin resistance and weight, you will be seen as a whole person, with a condition that deserves whole-person care.

If you would like to discuss any of the symptoms or treatments mentioned in this article, please book a consultation with our team.

References: Teede HJ et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. The Lancet. Published online 12 May 2026.

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/

Winlevi (clascoterone) is a newer topical treatment that represents a significant shift in how we manage hormonal skin concerns. Unlike traditional creams that focus solely on bacteria or exfoliation, Winlevi works at the root of the problem.

What is Winlevi Cream and How Does it Work?

Winlevi is the first topical androgen receptor inhibitor. It acts locally within the skin to block the effects of androgens—hormones that drive excessive oil production and inflammation. By targeting these receptors directly, it offers a solution for those suffering from PCOS-related skin issues and adult female acne without the systemic side effects of oral medications.

This makes it particularly useful for:

• Adult female acne specifically those experiencing deep, painful cysts.
• Hormonal breakouts (jawline, lower face)
• Patients who cannot tolerate or prefer to avoid oral hormonal treatments

In the right patients, it can be an effective addition to a broader, personalised treatment plan.

As with all acne treatments, careful selection and combination with other therapies is key to achieving consistent, long-term results.

Winlevi UK: Is it Available in London?

While Winlevi has seen massive success in the US, many patients are searching for Winlevi UK availability. At IA Dermatology, we provide expert consultations to determine if this treatment is right for you.

Winlevi Side Effects and Safety

Understanding Winlevi side effects is essential before starting treatment. Because it is a topical cream rather than a pill, it is generally well-tolerated. However, some patients may experience:

• Mild redness or itching at the application site.
• Dryness or peeling.
• Oedema (localised swelling).

Dr Iaisha Ali

iadermatology.com
Consultant-led dermatology | Evidence-based treatment

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/

Why Choose Ferinject UK?

Many patients struggle with the side effects of oral iron tablets, such as constipation or nausea. Your consultant may recommend a Feri inject injection if:

• Your blood tests show significantly low iron levels (iron-deficiency anaemia).
• You are experiencing hair shedding or hair loss that hasn’t responded to topical treatments.
• Oral supplements cause digestive distress or aren’t being absorbed.
• You have an underlying condition like thyroid disease or PCOS which can complicate nutrient absorption and energy levels

The Connection Between Iron Deficiency and Hair Loss

Iron is essential for the production of hair cell proteins. Many patients visiting our clinic for female patterned hair loss or alopecia areata discover that a low ferritin level is a major contributing factor. By opting for an iron drip, you can bypass the gut and deliver iron directly into the bloodstream, which is often a turning point for patients struggling with scalp problems and thinning.

How is the Ferinject Infusion Administered?

• Ferinject is typically given as a slow intravenous (IV) injection.
• The procedure takes about 10–15 minutes, followed by an observation period (usually about 30 minutes) to monitor for any reactions.
• This is usually done in a clinic or hospital by trained medical professionals.

Get Started with Recovery Journey

At IA Dermatology, Dr Iaisha Ali can determine whether you’re experiencing hair shedding or a more serious form of hair loss. Early intervention is key when underlying hair loss is present.

Book An Appointment

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“Dr Iaisha Ali is very friendly and takes time to understand my concerns, tailoring treatments to address expertly. I have been a Client for over 6 years and would have no hesitation in recommending.“

 Verified Patient Review from Doctify
Visited for Hair Loss

Ferinject in Pregnancy

Iron deficiency is common during pregnancy. If you are looking for Ferinject injection in pregnancy or an iron infusion for pregnancy in London, it is vital to consult with a specialist. Ferinject is generally used in the second or third trimester if oral iron is not sufficient, helping to prevent complications and ensuring the mother’s energy levels remain stable.

What to Expect

1. Preparation: Your healthcare provider will explain the process and ensure you are comfortable.
2. Administration: The Feri inject solution will be injected into a vein slowly to minimise side effects.
3. Observation: After the injection, you will be monitored for any adverse reactions.

Benefits

• Rapid restoration of iron levels.
• Improved symptoms, such as reduced fatigue, better hair growth, and healthier skin and nails.
• Often more effective than oral iron for those with absorption issues or intolerance.

Feri inject Side Effects and Precautions

Common side effects include temporary headache or dizziness, nausea or mild stomach discomfort, and skin discolouration or bruising at the injection site (rare). Rare but serious side effects include allergic reactions or flu-like symptoms. Inform your doctor if you have allergies, liver or kidney disease, or other conditions.

Aftercare: You may resume normal activities after your observation period. A follow-up blood test within 4–8 weeks assesses improvement.

Discover how Ferinject UK can boost your vitality at IADermatology, Harley Street, London – contact us for a consultation.

FAQs

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/