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

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

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

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

So, what does the evidence actually show?

Does TRT cause hair loss?

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

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

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

DHT contributes to a process called follicular miniaturisation.

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

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

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

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

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

Why can testosterone increase body hair but reduce scalp hair?

This is one of the interesting paradoxes of testosterone.

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

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

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

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

Does TRT cause acne?

This is where the evidence is considerably stronger.

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

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

TRT can produce a similar effect.

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

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

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

Acne may affect the:

• Face
• Chest
• Shoulders
• Upper back

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

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

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

Does the type of TRT matter?

Possibly.

Different testosterone preparations produce different patterns of testosterone exposure.

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

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

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

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

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

Does testosterone make your skin thicker?

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

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

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

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

However, this area needs some perspective.

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

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

Can you protect your hair while taking TRT?

Potentially.

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

1. Minoxidil

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

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

2. Finasteride

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

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

3. Dutasteride

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

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

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

Should you think about your hair before starting TRT?

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

Look at:

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

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

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

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

So, does TRT mean sacrificing your hair and skin?

No.

But it does mean understanding how testosterone affects them.

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

Individual susceptibility matters enormously.

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

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

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

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

References

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

This guide answers both.

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

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

Key takeaways

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

Can acne linked to high DHEAS be treated?

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

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

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

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

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

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

Can hair loss linked to high DHEAS be treated?

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

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

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

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

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

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

Can unwanted facial or body hair be treated?

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

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

What is DHEAS?

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

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

What does a high DHEAS level mean in a woman?

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

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

What symptoms can high DHEAS cause?

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

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

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

Does high DHEAS mean PCOS?

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

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

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

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

Why does age affect DHEAS results?

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

What causes high DHEAS in women?

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

When should high DHEAS be investigated further?

Further assessment is particularly important when:

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

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

Is high DHEAS dangerous?

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

Is high DHEAS always bad?

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

How treatment is planned at IA Dermatology

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

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

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

Frequently asked questions

The key points

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

Speak to a specialist about treatment

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

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

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Visited for Skin Treatment

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

Medical references

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

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

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

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

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

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

Normal ageing and sun-induced ageing are not the same

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

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

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

What happens at the level of methylation?

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

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

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

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

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

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

UV does not only damage DNA

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

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

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

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

Can the skin repair these changes?

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

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

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

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

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

Fibroblasts, senescence and collagen breakdown

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

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

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

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

What stimulates or changes methylation?

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

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

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

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

What do twin studies tell us?

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

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

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

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

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

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

Can food, vitamins or drugs help repair sun damage?

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

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

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

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

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

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

What about vitamin D?

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

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

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

Can we measure sun damage in blood?

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

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

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

Skin cancer: genetics and epigenetics together

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

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

These mechanisms do not replace each other. They interact.

Why prevention still matters most

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

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

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

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

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

Selected references

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

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

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

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

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

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

Exercise improves skin physiology

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

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

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

The muscle–skin axis

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

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

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

Effects on collagen and the extracellular matrix

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

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

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

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

Exercise and skin ageing

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

These include:

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

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

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

Exercise and wrinkles

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

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

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

The importance of exercise intensity

The literature consistently suggests a dose-dependent relationship.

Moderate, regular exercise appears beneficial.

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

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

Clinical implications

Current evidence suggests that physically active individuals may demonstrate:

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

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

Conclusion

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

Clinical Note

Direct comparative outcome studies on skin and hair effects between HRT regimens remain limited, and many recommendations are extrapolated from endocrine and pharmacological data combined with clinical experience. Individual prescribing decisions should be made with a qualified clinician.

Types of HRT Formulations

Hormone replacement therapy is delivered through a variety of formulations and routes. The choice between them affects not just efficacy but also the metabolic and hepatic profiles — and, critically for many patients, the impact on skin and hair.

Oral Tablets

Hepatic first-pass metabolism

Transdermal Patches

Bypasses hepatic first-pass metabolism

Gels & Sprays

Transdermal delivery with flexible dosing

Subcutaneous Implants

Specialist use with steady-state hormone levels

Vaginal / Local Oestrogen

Minimal systemic absorption

Injectable Oestrogen

Not standard UK menopausal practice

Injectable estradiol preparations (for example estradiol valerate and estradiol cypionate) are used infrequently in UK menopausal practice and are encountered more commonly in specialist endocrine and gender medicine settings.

Their inclusion here is for completeness and should not be interpreted as a recommendation for routine menopausal management.

Key Points

• Bypasses first-pass metabolism
• Does not produce the hepatic SHBG-raising effect seen with oral therapy
• Variable absorption and hormone-level fluctuation between doses
• Typically administered monthly or fortnightly

Intrauterine Progestogen System (IUS)

Endometrial protection with low systemic exposure

Androgenic Activity of Progestogens

Progestogens vary in their androgenic potency, which is clinically relevant for patients dealing with PCOS-related hormonal skin issues, hirsutism, and oily scalp problems.

However, the degree of androgenicity is frequently overstated in patient-facing resources and even in some clinical guidance. The reality is considerably more nuanced than a simple ranking system, and dosage is critically important.

Androgenicity may arise through:

• Direct binding to the androgen receptor (AR)
• Peripheral conversion to active androgens
• Suppression of sex hormone-binding globulin (SHBG)

These mechanisms do not always occur together.

Norethisterone (NET)

Norethisterone illustrates this complexity well.

It is structurally derived from nortestosterone and possesses measurable androgenic activity, although substantially weaker than testosterone. At the doses used in standard HRT (0.5–1 mg daily), the most clinically relevant effect is suppression of SHBG, which increases free testosterone levels.

Clinically significant sebaceous stimulation and overt androgenic side effects have mainly been demonstrated at substantially higher doses than those used in HRT.

Norethisterone also partially aromatises to ethinylestradiol, providing a counterbalancing oestrogenic effect. For this reason, describing norethisterone as a highly androgenic progestogen at standard HRT doses is often inaccurate.

Levonorgestrel, by contrast, has substantially higher androgen receptor binding affinity and stronger SHBG suppression, making it one of the more androgenic progestogens used in HRT.

Androgenic Activity of Progestogens

Progestogens vary in their androgenic potency, and this is clinically relevant for patients with acne, hirsutism, hair loss, or seborrhoea. However, the degree of androgenicity is frequently overstated in patient-facing resources and some clinical guides. The picture is more nuanced than a simple ranking suggests, and the dose used matters considerably.

Androgenicity arises through several mechanisms: direct binding to the androgen receptor (AR), conversion to active androgens peripherally, and suppression of sex hormone-binding globulin (SHBG) — a protein that keeps circulating androgens biologically inactive. These mechanisms do not always move in parallel.

Norethisterone (NET) illustrates this complexity well. It is structurally derived from nortestosterone and has measurable androgenic activity, substantially weaker than testosterone, though precise estimates vary depending on the assay system used. Its androgenic effects are strongly dose-dependent: clinically significant sebaceous stimulation has mainly been demonstrated at substantially higher doses than those used in HRT, and frank androgenic side effects such as acne or voice changes have mainly been reported at substantially higher doses (e.g. 10–40 mg/day), an order of magnitude above the 0.5–1 mg/day used in standard HRT. At HRT doses, the primary clinically relevant effect is dose-dependent suppression of SHBG, which raises free testosterone, rather than direct androgenic tissue stimulation.

Norethisterone also partially aromatises to ethinylestradiol, contributing a counterbalancing oestrogenic component, and its metabolism is pharmacologically complex with some metabolites potentially having differing receptor effects. The characterisation of norethisterone as a highly androgenic progestogen derives largely from older pharmacological literature at doses not representative of HRT practice; at standard HRT doses, low to moderate androgenic activity is a more accurate description. Levonorgestrel, by contrast, has substantially higher AR binding affinity and more potent SHBG suppression than NET, and is among the more androgenic progestogens used in HRT.

The table below summarises the relative androgenic activity of commonly used progestogens in HRT.

Oral vs Transdermal Oestrogen: the Hair and Scalp Difference

The route of oestrogen delivery profoundly alters its systemic effects — particularly on SHBG — and this is one of the most clinically underappreciated distinctions in HRT prescribing.

ORAL OESTROGEN AND SHBG

When oestrogen is taken orally, it passes through the liver before entering systemic circulation — the hepatic first-pass effect. The liver responds to this supraphysiological oestrogen exposure by upregulating SHBG production. Higher SHBG means more testosterone is bound and biologically inactive, leaving less free androgen available to act on hair follicles, sebaceous glands, and skin.

Published data suggest oral oestrogen can produce substantial SHBG increases, though the magnitude varies considerably depending on dose, formulation (oral oestradiol vs CEE), age, and baseline androgen status. This effect is not seen with transdermal delivery, which is the basis for the anti-androgenic advantage of the oral route in skin and hair conditions.

TRANSDERMAL OESTROGEN AND SHBG

Transdermal oestrogen — patches, gels, sprays — bypasses the liver and delivers oestradiol directly into systemic circulation without hepatic stimulation. SHBG rises little or not at all. Transdermal oestrogen generally has less impact on SHBG and free androgen levels than oral oestrogen, and may therefore provide less anti-androgenic benefit in androgen-sensitive conditions. This is a comparative observation: transdermal oestrogen does not worsen these conditions, but it does not replicate the SHBG-raising advantage of the oral route.

Which HRT is Best for Androgen-Sensitive Conditions?

The optimal approach typically combines the most favourable oestrogen route with the least androgenic progestogen. Even if norethisterone must be used for endometrial protection, its SHBG-suppressing effect is partially offset when paired with oral oestradiol, which simultaneously raises SHBG.

ACNE

Acne in perimenopause or menopause is frequently driven by the relative rise in free androgens as oestrogen wanes. The sebaceous gland is exquisitely sensitive to androgens, particularly DHT.

ANDROGENETIC HAIR LOSS (AGA)

Female AGA is driven by DHT miniaturising follicles in genetically predisposed women. Menopausal oestrogen loss accelerates this. HRT’s role is to reduce free androgen exposure and support the follicular growth cycle.

HIRSUTISM

Excess facial or body hair growth driven by elevated free androgens, commonly reflecting relative hyperandrogenaemia as oestrogen declines at the menopause.

SEBORRHOEA (OILY SKIN/SCALP)

Sebum production is androgen-driven via sebaceous gland 5α-reductase activity. Perimenopausal seborrhoea often coexists with acne and scalp seborrhoeic dermatitis.

Summary Reference

* Mirena IUS provides lower systemic LNG than oral/patch LNG but is not equivalent to androgenically neutral progestogens; androgenic effects can still occur in susceptible women.

References

[1]  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. PMID: 23238854

[2]  Africander D, Verhoog N, Hapgood JP. Comparing the androgenic and estrogenic properties of progestins used in contraception and hormone therapy. PLoS One. 2017;12(8):e0183591. PMID: 28711501

[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):325-32. PMID: 2851054

[4]  Kuhl H. Clinical significance of the androgenicity of progestins in hormonal therapy in women. Gynecol Endocrinol. 1990;4(3):223-38. PMID: 2268868

[5]  Carlstrom K, Karlsson R, von Schoultz B. Binding of levonorgestrel, norethisterone and desogestrel to human sex hormone binding globulin and influence on free testosterone levels. Gynecol Obstet Invest. 1989;28(3):154-7. PMID: 2525511

[6]  Cullberg G, Samsioe G, Astedt B. Effects of different doses of norethisterone on ovarian function, serum sex hormone binding globulin and high density lipoprotein-cholesterol. Acta Obstet Gynecol Scand Suppl. 1993;152:43-51. PMID: 8334889

[7]  Burton JL, Cartlidge M, Shuster S. Effect of synthetic progesterone on sebum excretion rate. BMJ. 1973;2:370-2. PMID: 4703469

[8]  Punnonen R, Rauramo L. Twenty-two weeks of transdermal estradiol increases sex hormone-binding globulin in surgical menopausal women. Maturitas. 1997;26(3):195-8. PMID: 9228496

[9]  Powers MS, Schenkel L, Darley PE, Good WR, Balestra JC, Place VA. Pharmacokinetics and pharmacodynamics of transdermal dosage forms of 17B-estradiol: comparison with conventional oral estrogens. Am J Obstet Gynecol. 1985;152(8):1099-106. PMID: 2512035

[10]  Scarabin PY, Oger E, Plu-Bureau G. Differential association of oral and transdermal oestrogen-replacement therapy with venous thromboembolism risk. Lancet. 2003;362(9382):428-32. PMID: 12927438

[11]  Mohammed K, Abu Dabrh AM, Benkhadra K, et al. Oral vs transdermal estrogen therapy and vascular events: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2015;100(11):4012-20. PMID: 26544651

[12]  Renoux C, Dell Aniello S, Garbe E, Suissa S. Transdermal and oral hormone replacement therapy and the risk of stroke: a nested case-control study. BMJ. 2010;340:c2519. PMID: 20483889

[13]  Canonico M, Fournier A, Camus E, et al. Progestogens and venous thromboembolism among postmenopausal women taking hormone therapy. Maturitas. 2010;66(3):292-6. PMID: 21489728

[14]  Vinogradova Y, Coupland C, Hippisley-Cox J. Use of hormone replacement therapy and risk of venous thromboembolism: nested case-control studies using the QResearch and CPRD databases. BMJ. 2019;364:k4810. PMID: 30626572

[15]  Gompel A, Plu-Bureau G. Progesterone, progestins and the endometrium in perimenopause and in menopausal hormone therapy. Climacteric. 2018;21(4):321-5. PMID: 29860893

[16]  Palacios S, Mejia A, Neyro JL. Treatment of the genitourinary syndrome of menopause. Climacteric. 2015;18(Suppl 1):23-9. PMID: 26366799

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/

At IA Dermatology in Harley Street, London, our Consultant Dermatologists provide expert medical assessments to diagnose the root cause of your scalp diseases and implement evidence-based treatment plans.

We regularly treat:

• Scalp dermatitis
• Seborrhoeic dermatitis (dandruff-related inflammation)
• Scalp eczema
• Scalp psoriasis
• Dry scalp and barrier dysfunction
• Allergic and contact scalp reactions
• Sun damage affecting the scalp
• Scalp cysts and benign lesions
• Scalp mole assessment and monitoring

Understanding Common Scalp Medical Conditions

The scalp is a unique environment with a high density of hair follicles and sebaceous (oil) glands. This makes it susceptible to specific skin conditions on the scalp that do not appear elsewhere on the body.

1. Scalp Dermatitis and Seborrhoeic Dermatitis:
   Often manifesting as “stubborn dandruff,” seborrhoeic dermatitis is caused by an overgrowth of yeast (Malassezia). This can lead to a red scalp and dandruff, itchy red patches, and in severe cases, yellow scabs on the scalp. While many associate this with infants, cradle cap in adults is a frequent diagnosis in our clinic, requiring prescription-strength anti-inflammatory and antifungal care.
2. Scalp Psoriasis and Eczema:
   These chronic inflammatory conditions often present as white scaly patches on the scalp or dryness patches on the scalp. Unlike standard dandruff, scalp psoriasis can feel thick and “plaque-like,” while scalp eczema often leads to a compromised skin barrier, resulting in a burning scalp and extreme sensitivity. If you are experiencing eczema or psoriasis in London, professional intervention is required to prevent the inflammation from damaging hair follicles.
3. Scalp Folliculitis and Infections:
   If you notice small red bumps on the scalp or itchy scalp red bumps that resemble pimples, you may be suffering from scalp folliculitis. This is an inflammation of the hair follicles caused by bacteria or yeast. Without treatment, these red bumps on the scalp can become painful, lead to scalp sores, and eventually cause localized scarring hair loss (alopecia).

The Link Between Scalp Inflammation and Hair Loss

One of the most frequent questions we hear is: “Does itchy scalp mean balding?” or “Can scalp eczema cause hair loss?”

The answer is complex. While a temporary hair shedding event is common during a flare-up of scalp inflammation, chronic untreated conditions can lead to more permanent issues. Red scalp and hair loss together often indicate that the “soil” (the scalp) is too inflamed to support the “plant” (the hair).

Conditions like female patterned hair loss can be worsened by a poor scalp environment. By addressing scalp problems early, we can often halt the progression of thinning hair and restore the health of the hair cycle.

Every consultation is personalised, medically led, and designed to restore scalp health while supporting long-term hair and skin integrity.

Experts in Hair Loss

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I’ve been seeing Doctor Ali about unexpected hair loss for a couple of years now. She is always very willing to answer any deeper questions I may have in a clear, comprehensive way, which alleviates the mystery of the whole process

 Verified Patient Review from Doctify
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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/

Whether your concern is cosmetic, functional (such as irritation or bleeding), or related to possible skin cancer, every procedure is carefully assessed and performed by senior Consultant Dermatologists using evidence-based surgical techniques. Our priority is accurate diagnosis, safe treatment, optimal cosmetic outcomes, and long-term skin health.

Procedures We Offer

We perform a wide range of in-clinic dermatological procedures, including:

• Skin tag removal
• Mole removal and excision of pigmented lesions
• Cyst removal (including punch extrusion technique)
• Excision of benign skin lesions
• Skin surgery for suspected skin cancer
• Curettage and cautery
• Surgical excision
• Hyfrecation (electrosurgical lesion removal)
• Punch biopsy
• Diagnostic skin biopsy
• CO₂ laser-assisted mole removal
• CO₂ laser skin tag removal

All procedures are carried out using sterile technique, appropriate anaesthesia, and careful aftercare planning to support optimal healing and scarring outcomes.

Get Started with Recovery Journey

Discover personalised care and expert guidance to restore your confidence and hair health with elegance and precision.

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

 Verified Patient Review from Doctify
Visited for Skin 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/