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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

What 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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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.

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

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

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

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

So, what does the evidence actually show?

Does TRT cause hair loss?

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

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

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

DHT contributes to a process called follicular miniaturisation.

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

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

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

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

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

Why can testosterone increase body hair but reduce scalp hair?

This is one of the interesting paradoxes of testosterone.

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

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

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

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

Does TRT cause acne?

This is where the evidence is considerably stronger.

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

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

TRT can produce a similar effect.

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

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

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

Acne may affect the:

• Face
• Chest
• Shoulders
• Upper back

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

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

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

Does the type of TRT matter?

Possibly.

Different testosterone preparations produce different patterns of testosterone exposure.

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

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

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

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

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

Does testosterone make your skin thicker?

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

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

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

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

However, this area needs some perspective.

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

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

Can you protect your hair while taking TRT?

Potentially.

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

1. Minoxidil

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

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

2. Finasteride

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

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

3. Dutasteride

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

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

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

Should you think about your hair before starting TRT?

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

Look at:

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

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

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

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

So, does TRT mean sacrificing your hair and skin?

No.

But it does mean understanding how testosterone affects them.

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

Individual susceptibility matters enormously.

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

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

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

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

References

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

This guide answers both.

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

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

Key takeaways

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

Can acne linked to high DHEAS be treated?

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

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

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

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

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

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

Can hair loss linked to high DHEAS be treated?

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

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

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

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

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

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

Can unwanted facial or body hair be treated?

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

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

What is DHEAS?

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

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

What does a high DHEAS level mean in a woman?

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

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

What symptoms can high DHEAS cause?

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

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

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

Does high DHEAS mean PCOS?

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

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

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

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

Why does age affect DHEAS results?

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

What causes high DHEAS in women?

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

When should high DHEAS be investigated further?

Further assessment is particularly important when:

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

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

Is high DHEAS dangerous?

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

Is high DHEAS always bad?

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

How treatment is planned at IA Dermatology

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

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

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

Frequently asked questions

The key points

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

Speak to a specialist about treatment

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

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

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

Medical references

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

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

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

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

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

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

Normal ageing and sun-induced ageing are not the same

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

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

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

What happens at the level of methylation?

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

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

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

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

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

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

UV does not only damage DNA

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

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

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

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

Can the skin repair these changes?

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

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

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

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

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

Fibroblasts, senescence and collagen breakdown

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

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

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

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

What stimulates or changes methylation?

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

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

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

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

What do twin studies tell us?

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

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

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

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

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

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

Can food, vitamins or drugs help repair sun damage?

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

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

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

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

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

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

What about vitamin D?

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

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

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

Can we measure sun damage in blood?

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

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

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

Skin cancer: genetics and epigenetics together

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

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

These mechanisms do not replace each other. They interact.

Why prevention still matters most

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

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

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

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

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

Selected references

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

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

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

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

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

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

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

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

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

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

What Our Oxford Research Showed About Menopause Balding

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

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

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

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

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

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

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

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

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

Hair Texture Changes During Menopause

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

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

When Hair Loss Isn’t Just Menopause

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

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

Can Menopause Hair Loss Be Treated?

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

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

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

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

The Emotional Weight

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

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

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

How Does the Thyroid Affect Hair?

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

Both:

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

can cause hair loss.

What Does Thyroid-Related Hair Loss Look Like?

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

Patients may notice:

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

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

Thyroid Disease Is Common in Women

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

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

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

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

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

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

Can Thyroid Disease Cause Sudden Hair Shedding?

Yes.

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

This can lead to:

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

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

What Blood Tests Are Important?

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

Tests may include:

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

Other useful blood tests often include:

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

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

Can Hair Grow Back After Thyroid Treatment?

In many cases, yes.

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

However, recovery may be slower if:

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

When Should You Seek Help?

It is sensible to seek medical assessment if you notice:

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

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

Final Thoughts

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

1. Androgenetic Alopecia and Insulin Resistance

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

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

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

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

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

2. Telogen Effluvium: The Stress-Mediated Pathway

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

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

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

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

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

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

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

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

4. Microvascular Damage and Poor Scalp Circulation

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

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

5. Medication-Related Hair Loss

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

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

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

GLP-1 Receptor Agonists: An Emerging Concern

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

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

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

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

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

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

DPP-4 Inhibitors: A Therapeutic Angle

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

6. The Role of Diabetes-Related Thyroid Disease

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

7. Hair as a Biomarker of Metabolic Risk

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

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

Clinical Implications and Management

The evidence supports several practical clinical considerations:

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

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

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

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

Conclusion

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

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

References

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

What Are GLP-1 Medications?

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

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

Is Hair Loss Really Linked to These Medications?

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

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

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

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

What Type of Hair Loss Occurs?

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

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

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

Why Does It Happen?

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

1. Rapid Weight Loss

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

2. Nutritional Deficiencies

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

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

3. Hormonal Changes

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

When Does It Start, and Will It Stop?

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

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

You should speak to your doctor if:

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

What Can You Do?

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

Don’t Restrict Calories Too Aggressively

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

Check Your Micronutrients

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

Consider a Multivitamin — But Seek Proper Nutritional Guidance

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

Don’t Stop Your Medication Without Talking to Your Doctor

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

Speak to a Dermatologist specialising in hair loss

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

Key Takeaways

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/