One of the most widely used medical treatments is spironolactone, an antiandrogen medication that can reduce the effect of androgens on susceptible hair follicles.

Most spironolactone used for female pattern hair loss is taken orally, and that is where the strongest evidence lies; but topical spironolactone for hair loss is attracting increasing interest, particularly for women who cannot tolerate oral treatment or want to minimise systemic exposure.

So does topical spironolactone actually work?

The short answer is that oral spironolactone still has the stronger evidence base. Topical spironolactone is a reasonable alternative in selected women, but the evidence suggests it works better when combined with topical minoxidil than when used alone.

Here is what the research actually shows.

How does spironolactone work in female pattern hair loss?

Female pattern hair loss is characterised by progressive miniaturisation of susceptible hair follicles. Over time, thick terminal hairs become progressively finer and shorter.

Androgens can contribute to this process in genetically susceptible women, even when blood androgen levels are within the normal range.

Spironolactone has antiandrogen effects. It blocks androgen receptors and reduces androgen signalling within androgen-sensitive tissues.

In hair loss treatment, the aim is therefore different from minoxidil.

Minoxidil primarily stimulates hair growth and prolongs the growth phase of the follicle, whereas spironolactone aims to reduce the androgen signalling that can drive follicular miniaturisation.

This difference in mechanism is one reason the two treatments are often used together.

Does oral spironolactone work for female pattern hair loss?

The evidence for oral spironolactone in female pattern hair loss is substantially stronger than the evidence for topical treatment.

A 2023 meta-analysis pooling four studies involving 192 patients found an overall improvement rate of 56.6% with oral spironolactone.

When spironolactone was combined with other treatments such as minoxidil, the improvement rate increased to 65.8%, compared with 43.2% with spironolactone monotherapy [1].

Individual studies also show a consistent benefit. In the study by Sinclair et al., 80 women were followed for an average of 16 months while taking spironolactone 200 mg daily. Around 80% experienced either improvement or stabilisation of their female pattern hair loss [2].

In another study by Famenini et al., involving women taking an average dose of approximately 110 mg daily, 74.3% reported improvement or stabilisation [3].

A 2022 systematic review by James and colleagues found that 49.3% of patients treated with spironolactone monotherapy achieved improved follicular density. The authors concluded that the strongest clinical results tended to occur with doses of 100 mg daily or above when treatment was continued for more than one year [4].

More recently, a 2026 retrospective comparative study involving 187 women followed for 24 months found that 54.4% of patients receiving spironolactone achieved at least a one-grade improvement on the Sinclair scale. Higher-dose spironolactone, with a median dose of around 130 mg daily, performed better than the maximum dose of the comparator drug bicalutamide in this study [5].

Taken together, these studies support oral spironolactone as an effective treatment option for appropriately selected women with female pattern hair loss.

Does spironolactone have to be given at a high dose?

Not necessarily.

Higher doses may produce a stronger antiandrogen effect, but they can also increase the likelihood of systemic side effects. There is also evidence that lower-dose spironolactone can be effective when combined with minoxidil.

In one prospective study, 100 women were treated with spironolactone 25 mg daily together with low-dose oral minoxidil 0.25 mg daily. Hair shedding and hair density scores improved progressively over 12 months [6].

This is important because it suggests that combination treatment may sometimes allow clinicians to use lower doses of individual drugs rather than relying on high-dose spironolactone alone.

Treatment therefore needs to be individualised according to the pattern and severity of hair loss, other medical conditions and the patient’s tolerance of treatment.

What are the side effects of oral spironolactone?

Oral spironolactone is generally well tolerated, but it is a systemic medication and therefore has potential side effects. Pooled data from 216 patients receiving oral spironolactone found the most commonly reported adverse effects included; menstrual disturbance (7.9%), dizziness or headache (6.5%), scalp itching (3.7%), rash (2.3%). Only around 3.2% of patients discontinued treatment because of side effects [6].

Interestingly, side effects were significantly more frequent at doses of 80–110 mg daily than at 25 mg daily.Other recognised concerns with oral spironolactone include low blood pressure, increased potassium levels and potential effects in pregnancy.

This is where topical spironolactone becomes particularly interesting.

What is topical spironolactone?

Topical spironolactone is spironolactone formulated into a solution, cream or gel that is applied directly to the scalp. The aim is to deliver antiandrogen activity closer to the hair follicle while reducing systemic exposure.

There is currently no FDA-approved topical spironolactone treatment for female pattern hair loss, so formulations used in studies and clinical practice are generally compounded or investigational. Concentrations also vary considerably between studies, commonly ranging from around 1% to 5%. This lack of standardisation is important when interpreting the evidence.

Does topical spironolactone work for female pattern hair loss?

There is evidence that it can work, although the number and quality of studies are still much smaller than for oral spironolactone or topical minoxidil.

A 2021 study published in Dermatologic Therapy compared topical minoxidil 5%, topical spironolactone 1% and a combination of topical minoxidil and spironolactone. Treatment continued for 12 months, with patients also undergoing scalp biopsies before and after treatment. Topical spironolactone alone produced a clinical response in approximately 80% of patients, compared with approximately 90% with topical minoxidil [7].

Importantly, the scalp biopsies also demonstrated biological changes within the follicles. There was an increase in hairs in the active anagen growth phase and reductions in telogen hairs and miniaturised vellus hairs.

Is topical spironolactone as effective as minoxidil?

Probably not when used on its own.

A trial comparing topical finasteride 1%, topical spironolactone 5% and topical minoxidil 5% in women with female pattern hair loss found that topical spironolactone monotherapy was the weakest of the three treatments on clinical and trichoscopic assessment [8]. That is an important finding. Topical spironolactone may have a role, but the current evidence does not support replacing topical minoxidil with spironolactone in most women.

The more interesting question is whether the two should be combined.

Does topical spironolactone work better with minoxidil?

This is where the evidence becomes particularly insightful. Across several studies, topical spironolactone combined with topical minoxidil has performed better than either treatment used alone.

In the 2021 study described above, the combination of minoxidil and spironolactone produced the strongest clinical and histological response of the three treatment groups [7]. Another study assessed a combined spironolactone 5% and minoxidil 5% solution. Compared with minoxidil alone, the combination produced a reduction in miniaturised vellus hairs and an increase in new, upright regrowing hairs over 12 weeks [9].

A 2023 systematic review examining both oral and topical spironolactone in androgenetic alopecia also found a particularly strong efficacy signal when topical spironolactone was combined with minoxidil.

Across the included combination studies, approximately 95% of patients were classified as having an effective response [6]. The exact figure needs to be interpreted cautiously because the studies were relatively small and heterogeneous, but the overall pattern is consistent. Spironolactone appears to work better when paired with minoxidil (oral or topical) than when used alone.

Why might spironolactone and minoxidil work better together?

The combination makes biological sense because the drugs target different aspects of female pattern hair loss.

Minoxidil stimulates follicular growth, it helps prolong the anagen phase and can increase the size and activity of miniaturised follicles.

Spironolactone reduces androgen signalling; it targets one of the mechanisms contributing to progressive follicular miniaturisation.

In simple terms, minoxidil encourages the follicle to grow, while spironolactone may reduce one of the signals causing it to shrink. For some women, targeting both mechanisms may therefore produce a better result than either treatment alone.

Who might benefit from topical spironolactone?

Topical treatment may be particularly useful for women who:

1. cannot tolerate oral spironolactone
2. experience dizziness or low blood pressure with oral treatment
3. have concerns about systemic side effects
4. are unsuitable for systemic antiandrogen treatment
5. have not achieved sufficient improvement with topical minoxidil alone
6. prefer a topical rather than oral treatment approach.

It may also be considered as part of a combination topical treatment containing both spironolactone and minoxidil.

However, topical treatment should not be viewed as automatically safer or suitable for everybody simply because it is applied to the scalp. Systemic absorption may still occur, and pregnancy considerations remain important when using antiandrogen treatments.

Oral spironolactone vs topical spironolactone: which is better?

Based on the evidence currently available, oral spironolactone has the stronger evidence base and is likely to produce a more reliable antiandrogen effect.

Topical spironolactone is promising, but the evidence is still more limited. I therefore tend to think of topical spironolactone not as a direct replacement for oral treatment, but as another option within a personalised treatment plan.

For a woman who can tolerate oral spironolactone and has no contraindications, oral treatment remains the better-established route. For a woman who cannot or does not want to use systemic treatment, topical spironolactone becomes a reasonable alternative.

If topical spironolactone is being used, the evidence currently suggests that combining it with topical minoxidil makes more sense than using it alone.

My practical take

In my experience as a dermatologist treating female pattern hair loss for over two decades, it is rarely managed successfully with a one-size-fits-all approach.

The strongest evidence for spironolactone in female pattern hair loss still lies with oral treatment, particularly when used at an appropriate dose and continued for long enough.

Topical spironolactone is an interesting and evolving option. It may be useful for women who cannot tolerate oral spironolactone, are unsuitable for systemic treatment, or simply prefer a topical approach.

The most convincing signal in the topical literature is not spironolactone used alone. It is topical spironolactone combined with topical minoxidil. That combination targets female pattern hair loss from two different directions: stimulating follicular growth while reducing androgen-driven miniaturisation.

There are, however, important limitations. There is currently no standardised approved topical spironolactone formulation, concentrations vary between studies, and many of the published trials remain small.

We therefore need larger, well-designed randomised trials before topical spironolactone can be placed on the same evidence footing as established treatments such as topical minoxidil.

For now, I see it as a useful additional tool rather than a replacement for the treatments we already know work.

#FemalePatternHairLoss #HairLoss #Spironolactone #Minoxidil #Dermatology #WomensHealth

References

1. Aleissa M. The efficacy and safety of oral spironolactone in the treatment of female pattern hair loss: a systematic review and meta-analysis. Cureus. 2023;15(8). doi:10.7759/cureus.43559
2. Sinclair R, Wewerinke M, Jolley D. Treatment of female pattern hair loss with oral antiandrogens. Br J Dermatol. 2005;152:466-473.
3. Famenini S, Slaught C, Duan L, Goh C. Demographics of women with female pattern hair loss and the effectiveness of spironolactone therapy. J Am Acad Dermatol. 2015;73(4):705-706.
4. James JBF, Jamerson TA, Aguh C. Efficacy and safety profile of oral spironolactone use for androgenic alopecia: a systematic review. J Am Acad Dermatol. 2022;86(2):425-429.
5. Spironolactone versus bicalutamide for female pattern hair loss: a 24-month unicenter retrospective comparative study of effectiveness and safety. Dermatol Ther (Heidelb). PubMed ID 42565959.
6. Wang C, Du Y, Bi L, Lin X, Zhao M, Fan W. The efficacy and safety of oral and topical spironolactone in androgenetic alopecia treatment: a systematic review. Clin Cosmet Investig Dermatol. 2023;16:603-612. doi:10.2147/CCID.S398950 (includes citation to Sinclair R. Female pattern hair loss: a pilot study investigating combination therapy with low-dose oral minoxidil and spironolactone. Int J Dermatol. 2018.)
7. Abdel-Raouf H, Aly UF, Medhat W, Ahmed SS, Abdel-Aziz RTA. A novel topical combination of minoxidil and spironolactone for androgenetic alopecia: clinical, histopathological, and physicochemical study. Dermatol Ther. 2021;34(1). doi:10.1111/dth.14678
8. Clinical and trichoscopic evaluations of topical finasteride 1%, topical spironolactone 5%, and minoxidil 5% in female pattern hair loss treatment. Dermatol Pract Concept.
9. Ammar AM, Elshahid AR, Abdel-Dayem HA, et al. Dermoscopic evaluation of the efficacy of combination of topical spironolactone 5% and minoxidil 5% solutions in the treatment of androgenetic alopecia: a cross-sectional comparative study. J Cosmet Dermatol. 2022;21(11):5790-5799. doi:10.1111/jocd.15328

https://www.linkedin.com/pulse/topical-spironolactone-female-pattern-hair-loss-does-work-iaisha-ali-k5dme

What changed

Alopecia areata has moved from an era of broad immunosuppression to one of targeted oral therapy. The turning point came in 2014, when hair regrowth was reported with two drugs developed for other inflammatory diseases: tofacitinib and ruxolitinib. These clinical observations were supported by laboratory studies in human scalp tissue and mouse models. Researchers identified a self-sustaining inflammatory loop in which cytotoxic T cells attack the hair follicle through cytokines including interferon gamma and interleukin-15. Because these cytokines transmit their signals through the JAK-STAT pathway, blocking JAK activity reduced follicular inflammation and allowed hair growth to resume. This evidence led to formal drug-development programmes. Three oral JAK-pathway inhibitors are now licensed for severe alopecia areata in the United Kingdom: baricitinib, ritlecitinib and, since March 2026, deuruxolitinib. Only ritlecitinib is currently recommended by NICE for routine NHS use; the NICE appraisal of deuruxolitinib is still in progress, while baricitinib was not recommended on cost-effectiveness grounds.

This is an important therapeutic advance, but it is not a cure. Responses are variable, improvement may continue beyond the primary trial endpoint, and relapse is common after treatment withdrawal. Comparisons between drugs must also be cautious: there are no definitive head-to-head trials, and pivotal studies differ in age range, baseline severity, duration, dosing and endpoint timing.

Why blocking JAK signalling can restore hair growth

In alopecia areata, cytotoxic T cells cluster around anagen hair follicles and disrupt their immune privilege. Interferon gamma signalling uses JAK1 and JAK2, while interleukin 2, interleukin 7 and interleukin 15 signal through JAK1 and JAK3. Blocking these pathways can interrupt the inflammatory loop and allow a viable, non-scarring follicle to re-enter anagen. This biological rationale explains why inhibitors with different kinase selectivity can all produce regrowth, although selectivity may affect dose, safety and the balance of clinical activity.

The chronology of clinical discovery

The three licensed treatments

The Severity of Alopecia Tool, or SALT, records the percentage of scalp affected by hair loss on a scale from 0 to 100. A final SALT score of 20 or less means no more than 20 percent scalp hair loss, or at least 80 percent scalp coverage, and became the principal endpoint in the licensing trials. This is different from SALT50, SALT75 or SALT90, which describe a 50, 75 or 90 percent relative improvement from an individual patient’s baseline. These endpoints should not be treated as interchangeable.

How should relative efficacy be interpreted

At first glance, baricitinib 4 mg appears to produce a higher SALT 20 rate than ritlecitinib 50 mg. That comparison is misleading unless time is considered: baricitinib was assessed at 36 weeks, whereas the pivotal ritlecitinib endpoint was 24 weeks. Ritlecitinib responses continued to accumulate through week 48. Deuruxolitinib produced approximately 30 to 33 percent SALT 20 responses at week 24 with the licensed 8 mg twice-daily dose. Its 12 mg twice-daily trial dose produced higher response rates, but this is not the licensed US dose and should not be used to overstate comparative efficacy.

Longer follow-up changes the clinical picture. With ritlecitinib 50 mg daily, approximately 43 percent of participants reached SALT 20 by week 48, compared with 23 percent at week 24. Most week-24 responders maintained their response, while up to one-third of patients who had not yet reached the target at week 24 did so with continued treatment. In the open-label ALLEGRO-LT cohort, responses continued to increase over 24 months. Those open-label results are encouraging but are affected by continued-treatment selection and attrition and cannot be compared directly with placebo-controlled response rates. UK prescribing guidance advises considering discontinuation if there is no therapeutic benefit after 36 weeks.

Indirect and network meta-analyses generally place higher-dose oral regimens above lower-dose regimens and topical preparations, but rankings depend on which endpoint and time point are selected. They cannot establish that one licensed drug is clinically superior for an individual patient. Age, disease duration, alopecia totalis or universalis, eyebrow and eyelash loss, prior treatment, comorbidity, risk factors, dosing preference and access all influence treatment choice.

The emerging group

Upadacitinib

Upadacitinib is a preferential JAK1 inhibitor already licensed for several inflammatory diseases. Early AA evidence came from case reports and small series. The two phase 3 UP-AA trials, published in 2026, moved it into a different evidence category: at week 24, SALT 20 was achieved by 44.6 to 45.2 percent with 15 mg daily and 54.3 to 55.0 percent with 30 mg daily, compared with 1.5 to 3.4 percent with placebo. These are among the strongest short-term phase 3 results reported in AA, but upadacitinib is not yet licensed for this indication. Cross-trial superiority should not be claimed.

Ivarmacitinib and jaktinib

Ivarmacitinib, a selective JAK1 inhibitor, achieved SALT 20 at week 24 in 34.9 percent of participants receiving 4 mg and 40.6 percent receiving 8 mg, versus 9.0 percent with placebo in a phase 3 trial. Jaktinib has also entered randomised and extension studies. These programmes reinforce JAK1 as an effective target, but neither medicine has a UK alopecia areata licence.

Brepocitinib

Brepocitinib inhibits TYK2 and JAK1. In the early phase 2a comparison it produced a larger mean reduction in SALT than ritlecitinib, but the study was small and used investigational regimens. It has not become a licensed AA treatment. It remains scientifically important because it demonstrated that multiple nodes within the cytokine network can be therapeutically relevant.

Tofacitinib ruxolitinib and abrocitinib

Oral tofacitinib and ruxolitinib were the proof-of-concept drugs. Their evidence includes case reports, series and open-label studies, but neither is licensed for AA. Abrocitinib has produced regrowth in case reports and small real-world cohorts, particularly in patients with concomitant atopic dermatitis, but robust AA-specific randomised evidence remains limited. These observations should not be presented as equivalent to phase 3 evidence.

The early quantitative results nevertheless helped establish that the initial dramatic cases were reproducible. In a 2016 open-label study of 66 patients receiving tofacitinib, 32 percent achieved at least a 50 percent improvement in SALT. Patch-type AA and ophiasis responded better than alopecia totalis or universalis; shorter disease duration and persisting peribulbar inflammation were associated with response. Relapse after stopping treatment occurred after a median of approximately 8.5 weeks. In a separate oral ruxolitinib pilot, nine of 12 patients achieved substantial regrowth, accompanied by suppression of interferon and cytotoxic T-cell gene signatures.

Oral and topical JAK inhibition are not equivalent

The strongest evidence is for systemic oral treatment in severe disease. Topical tofacitinib and ruxolitinib have produced occasional local responses, especially in eyebrows or limited patches, but controlled studies have been inconsistent. In a phase 2 vehicle-controlled study, ruxolitinib cream did not significantly improve the main hair-regrowth endpoint. Poor penetration to the deeper follicular bulb and the difficulty of treating extensive scalp disease may help explain the difference. A topical formulation should therefore not be assumed to reproduce the efficacy of its oral counterpart.

Safety and duration of treatment

All systemic JAK inhibitors require careful patient selection and monitoring. Product-specific guidance differs, but considerations include serious and opportunistic infection, herpes zoster, cytopenias, liver enzyme and lipid abnormalities, creatine kinase elevation, thromboembolic and cardiovascular risk, malignancy risk, vaccination status, pregnancy and drug interactions. Regulatory class warnings were shaped substantially by safety data in older rheumatoid arthritis populations with cardiovascular risk factors; the absolute risk in a younger AA population may differ, but it should not be dismissed.

Deuruxolitinib has an additional pharmacokinetic consideration. It is metabolised predominantly by CYP2C9, with a smaller contribution from CYP3A4, and CYP2C9 poor metabolisers may have approximately twice the systemic exposure. Genotype, interacting medicines and the current territory-specific product information therefore require particular attention.

Treatment duration is equally important. Hair regrowth is often gradual, and some patients who have not reached SALT 20 by week 24 respond later. Conversely, withdrawal studies show that many responders lose hair after stopping treatment and may not recapture the same response immediately when treatment restarts. In practice, successful JAK inhibition is better understood as disease control requiring ongoing review rather than a finite curative course.

Baricitinib provides the clearest long-term evidence. Among week-52 responders who continued therapy, approximately 89 percent receiving 4 mg and 84 percent receiving 2 mg maintained SALT 20 through three years. In the randomized BRAVE-AA1 withdrawal substudy, stopping baricitinib led to loss of treatment benefit in almost all responders, while many regained response after retreatment. These findings support maintenance treatment when benefit continues and the risk-benefit balance remains favourable.

Who is more likely to respond

Response is not determined by drug choice alone. Across trials and observational studies, patients with SALT scores approaching 100, alopecia totalis or universalis, and a longer current episode generally respond more slowly and less completely. Evidence of persisting inflammatory activity and shorter disease duration have been associated with better responses in early tofacitinib studies. These are probabilities rather than absolute rules: clinically meaningful regrowth can still occur in longstanding or near-total disease, but expectations, assessment intervals and stopping decisions should reflect the lower average response rate.

Conclusion

The history of JAK inhibition in alopecia areata began with unexpected regrowth from repurposed drugs and has matured into a class of licensed, evidence-based treatments. Tofacitinib and ruxolitinib established the concept; baricitinib delivered the first licence; ritlecitinib extended licensed treatment to adolescents; and deuruxolitinib added a third UK option in 2026. Upadacitinib now has compelling phase 3 results, while ivarmacitinib, jaktinib, brepocitinib and other selective agents broaden the pipeline. The central message is not that all JAK inhibitors are interchangeable, but that pathway selection, dose, exposure, patient characteristics and treatment duration all matter. The next phase will require direct comparative evidence, longer safety follow-up and better predictors of who will respond and maintain regrowth.

Key references

1. Xing et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine. 2014. Link
2. Craiglow and King. Tofacitinib treatment of alopecia universalis. Journal of Investigative Dermatology. 2014. Link
3. Jabbari et al. Treatment of an alopecia areata patient with tofacitinib results in regrowth of hair and changes in biomarkers. Journal of Investigative Dermatology. 2014. Link
4. Jabbari et al. Reversal of alopecia areata following treatment with baricitinib. EBioMedicine. 2015. Link
5. Mackay-Wiggan et al. Oral ruxolitinib induces hair regrowth in moderate-to-severe alopecia areata. JCI Insight. 2016. Link
6. King et al. Phase 2a study of ritlecitinib and brepocitinib. Journal of the American Academy of Dermatology. 2021. Link
7. King et al. Two phase 3 trials of baricitinib for alopecia areata. New England Journal of Medicine. 2022. Link
8. King et al. Ritlecitinib phase 2b and 3 trial. The Lancet. 2023. Link
9. King et al. Deuruxolitinib THRIVE-AA1 phase 3 trial. Journal of the American Academy of Dermatology. 2024. Link
10. THRIVE-AA2 phase 3 trial of deuruxolitinib. Journal of the American Academy of Dermatology. 2025. Link
11. Ivarmacitinib phase 3 trial in severe alopecia areata. Journal of the American Academy of Dermatology. 2025. Link
12. Mostaghimi et al. Upadacitinib for severe alopecia areata in two phase 3 UP-AA trials. JAMA Dermatology. 2026. Link
13. Crispin et al. Safety and efficacy of tofacitinib citrate in patients with alopecia areata. JCI Insight. 2016. Link
14. King et al. Baricitinib withdrawal and retreatment in severe alopecia areata. JAMA Dermatology. 2024. Link
15. Piliang et al. Sustained and late responses to ritlecitinib through week 48. Journal of the American Academy of Dermatology. 2025. Link
16. Tziotzios et al. Long-term safety and efficacy of ritlecitinib in ALLEGRO-LT. Journal of the European Academy of Dermatology and Venereology. 2025. Link
17. US Food and Drug Administration. Leqselvi prescribing information. 2024. Link
18. MHRA approval of ritlecitinib for severe alopecia areata. 2023. Link
19. NICE TA958. Ritlecitinib for treating severe alopecia areata in people aged 12 years and over. 2024. Link
20. MHRA approval of deuruxolitinib for severe alopecia areata in adults. 2026. Link

Is this simply perception, or does human hair actually have a seasonal cycle?

The evidence suggests that seasonal variation in human scalp-hair cycling is real, although it is much more subtle than the dramatic seasonal moulting seen in many other mammals.

Human hair does not grow continuously

Each scalp follicle repeatedly cycles through several phases. Anagen is the active growth phase and typically lasts several years; at any one time, around 85–90% of scalp hairs are in anagen. This is followed by catagen, a short transitional phase lasting around 2–3 weeks, during which the follicle regresses; only about 1% of hairs are normally in catagen. The follicle then enters telogen, a resting phase lasting roughly 2–3 months, with around 10–15% of scalp hairs in telogen at any one time. Finally, during exogen, the old club hair is released and shed, often as a new anagen hair begins to grow beneath it. These proportions vary between individuals and can shift in response to illness, hormones, medications, nutritional factors and, as the seasonal shedding studies suggest, possibly the time of year.

Unlike many mammals, human scalp follicles are largely asynchronous: neighbouring follicles are generally at different stages of their cycle. This is why humans do not normally undergo a dramatic seasonal moult, but asynchronous does not mean completely random.

Several studies conducted over more than three decades suggest that the proportion of follicles moving through these phases changes subtly during the year.

What does the human evidence show?

One of the best-known studies was published by Randall and Ebling in the British Journal of Dermatology in 1991.

They studied 14 healthy men living in Sheffield in the UK, measuring hair-growth parameters every 28 days for 18 months.

The proportion of scalp follicles in active anagen growth exceeded 90% in March, before gradually declining to its lowest point in September.

Measured hair shedding moved in the opposite direction. The largest number of hairs was shed around August and September, when the proportion of follicles in anagen was lowest. At the peak, average shedding was approximately 60 hairs per day; more than twice that measured during the preceding winter. [1]

A particularly valuable study by Courtois and colleagues subsequently followed 10 men for between 8 and 14 years. Using repeated phototrichograms, they again demonstrated annual periodicity, with the highest proportion of telogen hairs occurring towards the end of summer and beginning of autumn.

Importantly, the pattern was not identical in every individual. Some subjects showed a second annual peak, while those with very low telogen proportions showed little or no periodicity at all. [2]

This suggests that seasonal variation in hair cycling exists at a population level, but its expression differs substantially between individuals.

What about women?

The largest frequently cited study was published by Kunz, Seifert and Trüeb in 2009. They retrospectively analysed trichograms from 823 otherwise healthy women presenting with hair-loss complaints over six years, after excluding recognised medical and drug-related causes.

Again, there was a clear annual pattern; the proportion of hairs in telogen was highest during the summer, with a smaller possible second peak during spring. Telogen rates were lowest in late winter. [3]

Because movement through the hair cycle occurs over weeks to months rather than days, a summer shift towards telogen may contribute to increased shedding later in the summer and into autumn.

The pattern is not confined to European populations

In 2014, Liu and colleagues followed 41 healthy Chinese volunteers across a full year using phototrichographic assessment. They demonstrated seasonal variation in scalp-hair cycling, with the highest proportion of telogen hairs occurring around September and the lowest around January. [4]

This provides useful evidence that the phenomenon is not confined to European cohorts, an important distinction.

Seasonal cycling does not necessarily indicate disease. It may simply represent physiological variation within the normal human hair cycle.

Population data point in the same direction

A very different approach was taken by Hsiang and colleagues.

They analysed Google Trends search activity relating to hair loss between 2004 and 2016 and demonstrated a reproducible seasonal pattern in population-level interest in hair loss. [5] This is supportive rather than direct biological evidence.

Search behaviour cannot establish changes in follicular cycling or prove a mechanism. However, the seasonal pattern in public search activity is broadly consistent with the periodicity described in direct studies of human hair growth and shedding.

So how strong is the evidence?

It is useful to separate the different levels of evidence.

The strongest evidence comes from studies that directly examined human hair cycling using hair counts, trichograms or phototrichograms.

Across these studies, the same broad pattern repeatedly emerges; relatively greater anagen activity during late winter or spring, increasing telogen proportions during summer, increased shedding towards late summer and autumn, substantial variation between individuals.

The Google Trends data are interesting because they mirror that pattern at population level, but they should be regarded as corroborative rather than proof of biological seasonality.

So the existence of some degree of seasonal variation in human scalp hair cycling is reasonably well supported.

The next question is much harder; why does it happen?

Why might hair growth vary with the seasons?

This is where the evidence becomes much less certain. We have substantially better evidence that seasonal variation exists than we have explaining why it exists.

Photoperiod may be important

In many mammals, seasonal coat growth is controlled primarily by photoperiod. The changing duration of daylight, rather than simply by temperature.

Changes in day length are detected through the retina and translated into neuroendocrine signals capable of altering follicular activity. Humans retain many of these seasonal biological pathways, making photoperiod an attractive explanation for the subtle seasonal rhythm seen in scalp hair.

There are also clues within the human studies themselves.The long-term Courtois study discussed relationships between hair-cycle periodicity and environmental factors including hours of sunshine, while later studies have considered latitude and daylight duration as possible contributors to variation between populations. [2,4]

Association, however, does not prove causation.

What about melatonin?

Melatonin is one of the major hormones through which mammals translate changes in light exposure into seasonal biological signals. It is secreted predominantly during darkness, so both the timing and duration of melatonin secretion vary with day length.

Experimental studies in animals show that manipulating photoperiod or melatonin signalling can alter seasonal coat growth. Human hair follicles also appear capable of responding to melatonin.

In a small randomised placebo-controlled pilot study, Fischer and colleagues found that topical melatonin increased the proportion of hairs in anagen in women with androgenetic or diffuse alopecia. [6]

This tells us that melatonin can influence the human hair follicle. It does not, however, prove that naturally occurring seasonal changes in melatonin are responsible for seasonal human hair shedding. That distinction is important.

Could other hormones contribute?

Seasonal rhythms have also been described in several human hormones, including testosterone and prolactin. Both are biologically relevant to the hair follicle, and prolactin in particular has recognised effects on follicular and keratinocyte biology.

However, the evidence linking these hormones specifically to seasonal scalp shedding remains largely indirect and correlational. No study has convincingly demonstrated that seasonal fluctuations in testosterone, prolactin or melatonin independently produce the seasonal scalp-hair cycle seen in humans.

The most reasonable interpretation at present is therefore that seasonal shedding may reflect a complex interaction between photoperiod, neuroendocrine signalling and intrinsic follicular biology, rather than a single hormone switching the hair cycle on or off.

Are humans really “moulting”?

Not in the way many mammals do.

Animals with obvious seasonal coats can synchronise very large numbers of follicles, producing dramatic shedding over a short period. Human scalp follicles remain predominantly asynchronous.

What appears to persist is a much weaker biological rhythm: enough to alter the percentage of follicles in anagen and telogen at different times of year, but generally not enough to produce dramatic loss of scalp coverage.

Seasonal shedding may therefore represent a subtle residual expression of a mammalian biological system that is much more prominent in other species.

Seasonal shedding is not the same as telogen effluvium

This is probably the most important clinical distinction.

A modest seasonal increase in shedding can occur as part of normal physiology. Telogen effluvium, however, describes a larger disruption of the follicular cycle and can follow significant illness or fever, surgery, childbirth, rapid weight loss, nutritional deficiency, thyroid disease, major physiological stress, hormonal change and certain medications.

The timing may overlap; someone who develops telogen effluvium in the autumn may understandably assume that the season is responsible when another trigger actually occurred several months earlier.

Seasonal shedding may also reveal underlying pattern hair loss

Another scenario I see clinically is a patient who notices considerably more scalp visibility during a period of increased shedding.

They may already have subtle female or male pattern hair loss. A temporary increase in shedding reduces the amount of remaining hair coverage and makes that underlying reduction in density much more apparent.

The seasonal shed has not necessarily caused androgenetic alopecia -It may simply have unmasked it.

For that reason, persistent widening of the parting, temporal recession, progressive miniaturisation or continuing reduction in hair volume should not automatically be attributed to autumn.

When should seasonal shedding be investigated?

A temporary increase in shedding with preserved overall density can be physiological.

Further assessment is more important when shedding is:

1. Marked or sudden
2. Continuing for several months
3. Accompanied by progressive thinning
4. Associated with widening of the central parting
5. Associated with scalp inflammation, scaling or symptoms
6. Accompanied by eyebrow or body-hair loss
7. Associated with systemic symptoms
8. Preceded by illness, major weight change, dietary restriction or medication change

The fact that hair shedding begins in autumn should not prevent us from looking for another cause.

So, is seasonal hair shedding real?

The available human evidence says yes.

Studies using hair counts, trichograms and phototrichograms — including longitudinal observations lasting more than a decade — demonstrate a reproducible annual rhythm in human scalp-hair cycling.

Broadly, the proportion of telogen hairs tends to rise during summer and early autumn, while anagen activity tends to be greater during late winter and spring. But the size of this effect varies between individuals, and in healthy people it usually appears to represent physiological variation rather than disease.

The mechanism remains considerably less certain. Photoperiod and melatonin provide a biologically plausible explanation, supported by mammalian biology and evidence that human follicles can respond to melatonin, but they have not been proven to be the cause of seasonal human shedding.

So when a patient tells me:

“My hair always sheds more at this time of year,”

I do not automatically dismiss the observation.

There may indeed be a biological explanation.

The more important clinical question is whether we are seeing a normal seasonal fluctuation in hair cycling or whether another cause of increased shedding or progressive hair loss is occurring alongside it.

References

1. Randall VA, Ebling FJ. Seasonal changes in human hair growth. Br J Dermatol. 1991;124(2):146–151. doi:10.1111/j.1365-2133.1991.tb00423.x.
2. Courtois M, Loussouarn G, Hourseau C, Grollier JF. Periodicity in the growth and shedding of hair. Br J Dermatol. 1996;134(1):47–54.
3. Kunz M, Seifert B, Trüeb RM. Seasonality of hair shedding in healthy women complaining of hair loss. Dermatology. 2009;219(2):105–110. doi:10.1159/000216832.
4. Liu C, et al. Changes in Chinese hair growth along a full year. Int J Cosmet Sci. 2014;36(6):531–536.
5. Hsiang EY, Kwatra SG, Pasquali L, Ganta S, Burnett C, Liao Y. Seasonality of hair loss: a time series analysis of Google Trends data 2004 to 2016. Br J Dermatol. 2017;177(3):953–954. doi:10.1111/bjd.16075.
6. Fischer TW, Burmeister G, Schmidt HW, Elsner P. Melatonin increases anagen hair rate in women with androgenetic alopecia or diffuse alopecia: results of a pilot randomized controlled trial. Br J Dermatol. 2004;150(2):341–345.

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.

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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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.

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.

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.

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

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

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

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

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

What Our Oxford Research Showed About Menopause Balding

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

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

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

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

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

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

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

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

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

Hair Texture Changes During Menopause

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

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

When Hair Loss Isn’t Just Menopause

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

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

Can Menopause Hair Loss Be Treated?

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

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

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

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

The Emotional Weight

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

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

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

Abstract

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

1. Introduction

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

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

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

2. Hair Changes Typical of the Menopausal Transition

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

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

• Reduced hair density and volume

• Finer hair texture and decreased shaft diameter

• Increased scalp visibility

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

3. Menopause Does Not Usually Cause Dramatic Shedding

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

Patients with TE typically describe:

• Excessive hair in the shower or brush

• Diffuse reduction in volume

• Onset over weeks to months

• Increased shedding with washing or combing

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

4. Is Hair Thinning Due to Menopause or Ageing?

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

Proposed mechanisms of age-related follicular change include:

• Shortening of the anagen phase

• Reduced follicular proliferative activity and mitotic rate

• Decrease in hair shaft diameter

• Cumulative oxidative and environmental damage to follicular stem cells

• Senescent cell accumulation within the follicular unit

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

5. Thyroid Disease Is More Common Around Menopause

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

• Diffuse scalp shedding

• Brittle, dry hair texture

• Eyebrow thinning (particularly the lateral third)

• Reduced hair quality and shaft diameter

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

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

6. Nutritional Deficiency as a Contributor

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

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

Additional nutritional contributors may include:

• Vitamin D deficiency

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

• Protein deficiency or rapid weight loss

• Restrictive dieting

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

7. Medication-Induced Hair Shedding

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

Drug classes associated with diffuse shedding via TE include:

• Systemic retinoids and psychotropic medications including SSRIs

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

• Antihypertensive agents including beta-blockers

• Statins

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

8. Can HRT Cause Hair Shedding?

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

Some women notice increased shedding:

• After starting HRT

• After changing HRT dose or formulation

• During inconsistent or interrupted use

• During the perimenopausal transition itself

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

9. Why Transdermal HRT May Be Better Tolerated for Hair

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

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

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

10. When Should You Seek Help?

Clinical assessment is warranted when women experience:

• Sudden excessive shedding

• Rapidly visible scalp thinning

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

• Eyebrow thinning

• Major change in hair texture

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

• Persistent shedding lasting more than 6 months

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

11. Conclusions

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Introduction

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

Epidemiology: The UK Burden of Hypothyroidism

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

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

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

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

The Thyroid Gland and the Hair Follicle: Biological Mechanisms

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

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

The Hair Growth Cycle: Disrupted by Hypothyroidism

Normal hair cycling consists of four phases:

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

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

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

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

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

The Menopausal Overlap: A Compounding Factor

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

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

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

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

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

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

Diagnosis: Laboratory Testing for Hypothyroidism

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

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

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

Free Thyroxine (FT4)

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

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

Free Triiodothyronine (FT3)

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

Thyroid Peroxidase Antibodies (TPOAb)

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

Subclinical Hypothyroidism

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

Practical Note on NHS Testing

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

Nutritional Factors Contributing to Thyroid-Related Hair Loss

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

Iron and Ferritin

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

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

Selenium

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

Zinc

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

Iodine

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

Vitamin D

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

Biotin (Vitamin B7)

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

Clinical Implications and Management

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

Alongside pharmacological management, clinicians should:

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

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

Conclusion

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

Key References

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