Eden Openly

Skin Effects of Oestrogen in Transfeminine People

Evidence Review · ER-006

Identifier: ER-006 · Version: 1.1 · Status: Current · Published: July 2026 · DOI (all versions): 10.5281/zenodo.21211028 · DOI (this version): 10.5281/zenodo.21223431

This is the full review — the complete evidence and every limitation behind it. A short companion Evidence Note (5-minute read) distils it — see the Evidence Note →. For the cellular mechanism of how oestrogen acts on skin, see the clinical explainer How Oestrogen Changes Your Skin at the Cellular Level; this review grades how strong the evidence is for each change.

Purpose

To review, and grade the strength of, the evidence for how oestrogen affects the skin of transfeminine people on feminising hormone therapy. This is not a prescribing guide, nor a skincare-routine guide, and none of it is a reason to start, stop, or change the route or dose of hormone therapy; feminising hormone therapy should follow local prescribing and monitoring standards under clinical supervision.

Three caveats apply to almost every claim here and are stated once so they can be assumed throughout. First, much of the strongest evidence comes from cisgender menopausal or hormone-replacement studies, not from trans women. Second, oestrogen in feminising therapy is almost never given alone — it is combined with testosterone suppression, so effects attributed to “oestrogen” are usually the combined result of raising oestrogen and lowering androgens; the title is a conventional shorthand for that whole exposure. Third, “oestrogen” is not one thing: oral, transdermal and injectable oestradiol, older conjugated equine oestrogens, and topical preparations differ in pharmacology, and much of the cisgender skin evidence uses formulations and routes that are not those of modern feminising therapy.

Executive summary

What this covers. Seven skin outcomes commonly attributed to oestrogen: sebum (oiliness), acne, dryness, skin thickness and collagen, hydration and barrier, wound healing, and pigmentation (melasma).

The overall state of the evidence. Weak and mostly indirect. As one review of transfeminine dermatology puts it plainly, little data exist on the skin effects of hormone therapy in transfeminine people, and the effects of oestrogen on the skin’s oil glands and hair follicles “remain mostly unknown.”[1,3] The largest prospective trans dermatology cohort (484 participants) measured mainly acne, alopecia and hair-growth/hirsutism outcomes, and its clearest findings were in trans men, not trans women.[1] Most of what is said confidently about “oestrogen and skin” comes from cisgender menopause and hormone-replacement research.

What is reasonably clear. Feminising therapy reduces sebum production — probably the best-supported trans-specific skin change — chiefly by lowering androgens; improvement in acne is biologically plausible and reported, though objective transfeminine acne data remain limited.[1,2,3] In cisgender menopausal women, oestrogen therapy is associated with increased dermal collagen and skin thickness, improved hydration measures, and — for topical oestrogen on experimental wounds in the elderly — faster wound healing, an effect shown in men as well as women.[7,8,10,11]

Where oestrogen may not help — or may hurt. Lower sebum can tip some people’s skin towards dryness (xerosis).[4] And oestrogen can promote pigmentation: it is implicated in melasma, so feminising therapy can, in susceptible people and especially with sun exposure, provoke or worsen facial hyperpigmentation rather than improve it.[13,14,15]

The honest bottom line. The direction of most of these changes is plausible and mechanistically coherent; the trans-specific, measured evidence is thin, and confident numbers are borrowed from cisgender women. This review grades accordingly.

Key take-home messages

  1. Reduced sebum is probably the best-supported skin effect of feminising therapy, driven mainly by androgen suppression; improvement in acne is plausible and reported but not well quantified in trans women, and rests on small studies and self-report.[1,2,3]
  2. Skin thickness, collagen, hydration and wound-healing effects are seen in cisgender hormone-replacement research but have barely been measured in trans women, and often used formulations unlike modern therapy.[7,8,10,11] [Largely cisgender-derived.]
  3. In trans women, androgen loss and oestrogen gain happen together; skin thickness in particular is pulled in two directions (androgens thicken skin; the net effect is unstudied).
  4. Oestrogen can worsen pigmentation: melasma is a recognised, if under-quantified, risk of feminising therapy, especially with sun exposure and in darker skin; whether dose or added progestogen changes that risk in trans women is not established.[13,14,15]
  5. Because oestrogen rarely acts alone here, “oestrogen’s effect on skin” and “feminising therapy’s effect on skin” are not the same thing — this review is about the latter.

1. Introduction and scope

Skin change is a common and often valued effect of feminising hormone therapy, and one of the least rigorously studied. Some changes — particularly reduced oiliness or acne — may be noticed relatively early, but timing and how welcome any given change is vary from person to person. This review takes seven skin outcomes people commonly ask about and asks, for each, a single question: how good is the evidence? It is a companion to the clinical explainer on the cellular mechanism of oestrogen in skin, which describes how oestrogen acts; here the focus is how well established each effect is, and how much of the evidence actually comes from trans women rather than from cisgender research applied by analogy.

The interpretive cautions from the Purpose apply throughout: the evidence is largely cisgender; oestrogen is given with androgen suppression, so most effects are really those of combined feminising therapy; and “oestrogen” spans several formulations. Cells of the pilosebaceous unit express androgen and oestrogen signalling machinery, although expression and functional effects vary by cell type and site, and oestrogen’s actions on them are far less well characterised than androgens’ — a recent trans dermatology study describes oestrogen’s effects on the pilosebaceous unit as “mostly unknown.”[1]

2. How oestrogen reaches the skin (in brief)

Skin is a hormone-responsive organ. Keratinocytes, fibroblasts, sebocytes (oil-gland cells) and melanocytes can express one or more oestrogen receptors — the classical nuclear receptors ERα and ERβ, and the membrane-bound G-protein-coupled oestrogen receptor (GPER) — through which oestradiol can alter gene expression and cell behaviour.[1,13] This is the machinery behind the effects below. The cellular detail is covered in the companion clinical explainer and is not repeated here; what matters for grading the evidence is that plausible receptors and pathways exist for every effect claimed — which makes the direction of these effects biologically reasonable, even where the human, trans-specific data are thin.

Applicability to modern therapy — read this first

One caution underlies almost every grade below: most of the cisgender evidence used exposures unlike modern feminising therapy. The thickness and hydration data come largely from conjugated equine oestrogens or oral menopausal HRT and from topical oestradiol; the wound-healing data use topical oestrogen on experimental wounds in the elderly. Modern feminising therapy typically uses transdermal, oral or injectable oestradiol in younger adults, alongside androgen suppression. Effects seen with one oestrogen, one route, one dose and one population cannot be assumed to transfer cleanly to another — which is a large part of why the trans-specific grades stay low.

3. Sebum and oiliness

What is claimed. Feminising therapy reduces sebum production (and, with it, oiliness).

Evidence. This is probably the best-supported skin effect, and it is chiefly attributable to androgen suppression: sebum production is androgen-driven, and lowering testosterone lowers it — although oestrogens can influence sebaceous activity in some settings, and the specific anti-androgen used may matter; the independent contribution of oestradiol within modern feminising therapy is uncertain. In a frequently cited early study, Giltay and Gooren measured the pilosebaceous unit in 21 transfeminine people on cross-sex hormones and found that sebum production (by Sebutape) declined after combined oestrogen and anti-androgen therapy lowered testosterone to very low concentrations (reportedly below roughly 1 nmol/L); this describes an association in a small physiological study, not a validated dermatological testosterone target.[16] Reviews of transfeminine dermatology consistently report reduced sebum on feminising therapy, and cosmetic-dermatology sources describe the same.[2,3,4]

Limits. The trans-specific studies are small and older, some measures are self-reported, and the effect cannot be cleanly separated from androgen suppression. How much oestrogen itself contributes, and whether the anti-androgen type matters, is not established.

Confidence: 🟡 Low–Moderate. Direction consistent and mechanistically clear; measured trans-specific data limited.

4. Acne

What is claimed. Acne may improve on feminising therapy.

Evidence. Acne may improve, particularly where androgen-driven sebum falls, but transfeminine-specific outcome data are limited, and the evidence is considerably stronger for the acne flare that testosterone causes in trans men than for acne improvement in trans women.[1,2,3] The link to sebum is real but partial: acne is multifactorial, depending also on follicular hyperkeratinisation, inflammation, the skin microbiome (Cutibacterium acnes), genetics, cosmetics and occlusion, and medications — so reduced sebum removes one major driver rather than the whole cause.

Limits. Acne course is variable, can worsen transiently, and interacts with concurrent medications (for example isotretinoin or topical retinoids improve it independently). Acne has its own dedicated clinical review, which covers management; this entry grades the hormonal effect only.

Confidence: 🟡 Low–Moderate. Plausible and reported; limited objective trans-specific measurement, and weaker evidence than for testosterone-related acne. [See companion: Acne (Clinical Review).]

5. Dryness (xerosis)

What is claimed. Some people find their skin becomes dry on feminising therapy.

Evidence. This is the flip side of reduced sebum: with less surface oil, skin can feel drier, and transfeminine dermatology sources — including a systematic review that lists xerosis among the skin effects of gender-affirming treatment — note that feminising hormones, while reducing sebum, may lead to xerosis.[2,4] It sits in genuine tension with oestrogen’s hydrating effect on the deeper skin (Section 7): oestrogen tends to improve water-holding in the dermis and stratum corneum, while reduced sebum lowers surface lipidiness and can contribute to a subjective feeling of dryness. (Sebum is only one part of the skin’s surface lipids; the epidermal permeability barrier itself depends mainly on stratum-corneum lipids, corneocytes and natural moisturising factor, so “less oil” is not the same as “impaired barrier.”) The net experience — oilier, the same, or drier — therefore varies between people.

Limits. Xerosis on feminising therapy is reported clinically rather than quantified in trials, and the supporting sources are cosmetic-dermatology reviews rather than primary measurement; predictors of who becomes dry are not established.

Confidence: 🟡 Low–Moderate. Mechanistically expected and clinically reported; not quantified.

6. Skin thickness and collagen

What is claimed. In oestrogen-deficient cisgender women, oestrogen can increase skin thickness and collagen.

Evidence. In oestrogen-deficient postmenopausal cisgender women this is reasonably supported, though not uniformly. Reviews commonly cite roughly 2% collagen loss per postmenopausal year and about 1% annual decline in skin thickness (estimates vary by site and method), and oestrogen therapy has been associated with increased dermal collagen and skin thickness at studied sites: a randomised controlled trial in 60 postmenopausal women using conjugated oestrogens reported a significant increase in skin and dermal thickness after 12 months, measured by ultrasonography and biopsy at covered (sun-protected) body sites; secondary reviews put the dermal gain at roughly 30%, though the figure varies between accounts and the trial’s own abstract states no single number. Other controlled and topical-oestradiol studies report similar increases in thickness and collagen — although not all studies agree, and at least one found no effect of systemic oestrogen on skin collagen.[7,8,9,17] [Population flag: cisgender postmenopausal women; formulations and routes often unlike modern feminising therapy.]

The trans-specific complication. This is the domain where borrowing from cisgender data is most hazardous. Androgens also thicken skin — skin is, on average, thicker in adult males than females at many measured sites (though the magnitude varies by site, age and method) — so a trans woman on feminising therapy is doing two opposing things to skin thickness at once: adding oestrogen (which builds collagen) while removing androgens (which had been thickening the skin). The net effect on trans women’s skin thickness has not been directly measured, and cannot be assumed to match the collagen gain seen when oestrogen is added to a post-menopausal, already-low-androgen body.

Confidence: 🟡 Moderate (cisgender oestrogen → collagen) / 🔴 Low (net effect in trans women).

7. Hydration and barrier function

What is claimed. Oestrogen improves skin hydration.

Evidence. In menopausal cisgender studies, oestrogen therapy has been associated with improved hydration measures, plausibly through effects on stratum-corneum water handling and on dermal glycosaminoglycans such as hyaluronic acid; barrier and moisture retention decline in the oestrogen-deficient (post-menopausal) state.[7,9] Hydration may change earlier than the slower structural collagen and thickness outcomes, although comparative timing data are limited. [Population flag: cisgender postmenopausal women; older and heterogeneous sources.]

Limits. As with thickness, this is cisgender-derived and complicated in trans women by the simultaneous fall in sebum, which works in the opposite direction at the skin surface (Section 5). Trans-specific hydration measurements are essentially absent.

Confidence: 🟡 Low–Moderate (cisgender) / 🔴 Low (net effect in trans women). Consistent in cisgender data; unmeasured in trans women. [Largely cisgender-derived.]

8. Wound healing

What is claimed. Oestrogen helps skin wounds heal.

Evidence. There is real human experimental support for this — but in a specific setting. In healthy elderly people, topical oestrogen applied to experimental wounds accelerated healing in both men and women: compared with placebo it reduced wound size at day 7, increased collagen deposition, and increased later (day 80) wound strength, via a dampened inflammatory (neutrophil/elastase) response.[10] A later gene-expression study estimated that oestrogen status accounted for a large share of the age-associated differences in wound-healing gene expression in elderly skin — around 80% in that single molecular analysis. That is a gene-expression figure, not a measure of clinical healing, which remains multifactorial (age, immune function, vascular disease, diabetes, nutrition, smoking and medications all matter).[11] The original observation that oestrogen accelerates healing (linked to raised TGF-β1) dates to the late 1990s.[12]

Relevance and limits. Because the effect is demonstrable in men as well as women, the underlying biology is not sex-specific — but this evidence concerns topical oestrogen on experimental wounds in the elderly, an oestrogen-deficient group, not systemic feminising therapy in younger adults, and there are no wound-healing studies in trans women. It should not be read as evidence that feminising therapy improves healing after surgery, laser, electrolysis or other procedures; that inference is not supported.

Confidence: 🟡 Moderate (mechanism and elderly experimental data) / 🔴 Low (trans-specific and procedural). [Population flag: elderly cisgender men and women; topical, experimental wounds.]

9. Pigmentation and melasma

What is claimed. Oestrogen can cause or worsen facial pigmentation (melasma).

Evidence. This is the one domain where oestrogen’s skin effect is a drawback. Melasma — symmetrical facial hyperpigmentation, commonest in women and in darker skin — is classically triggered by pregnancy and combined oral contraceptives. Oestrogen can promote melanogenic signalling in susceptible contexts: acting through ERα, ERβ and the membrane receptor GPER on melanocytes and keratinocytes, it can upregulate the pigment-making machinery (tyrosinase and the master regulator MITF), and melasma-affected skin shows increased oestrogen-receptor expression.[13,14,15] A cross-sectional study of 159 transgender participants — including only 25 trans women — concluded that feminising hormone therapy was associated with melasma (and female-pattern hair loss) in trans women, though a cross-sectional design and small sample cannot establish incidence or causation.[5]

Nuance. In laboratory (in-vitro) models, oestrogen alone does not reliably drive pigmentation and appears to interact with ultraviolet light;[13] clinically, visible light is also relevant to melasma, particularly in darker phototypes, which is why melasma concentrates on sun-exposed skin and why tinted (iron-oxide) sunscreens are often recommended alongside broad-spectrum UV protection.[18] The well-supported risk factors are a darker phototype and light exposure; whether oestrogen dose, route, serum oestradiol level or an added progestogen independently changes melasma risk in trans women is not quantified and should be treated as theoretical — and pregnancy and combined-oral-contraceptive data should not be assumed dose-equivalent to feminising oestradiol therapy. New facial pigmentation also has other causes (post-inflammatory hyperpigmentation, drug-induced pigmentation and others), so it is worth a clinician’s assessment rather than being assumed to be hormonal.

Confidence: 🟡 Low–Moderate. Hormonal-mechanism and pregnancy/contraceptive evidence reasonable; trans-specific incidence and dose relationships under-quantified — there are no reliable incidence estimates for melasma on feminising therapy in trans women, and the single cross-sectional study is hypothesis-generating only. [Population flag: pregnancy/contraceptive and in-vitro data.]

10. Total versus free oestradiol: one reason outcomes may vary

What this proposes. A mechanistic hypothesis — grounded in physiology but untested in transfeminine skin — for some of the person-to-person variation the sections above attribute simply to “unmeasured.”

Every skin effect in this review is receptor-mediated, and hormone signalling is generally most closely related to the unbound, readily available fraction of a hormone rather than the total serum concentration laboratories usually report — although albumin-bound hormone, tissue uptake and local metabolism complicate this simple free-hormone model. That free fraction is influenced strongly by sex-hormone-binding globulin (SHBG), alongside albumin binding and the total hormone concentration: broadly, the more SHBG, the smaller the free fraction for a given total level. Two features of SHBG make this relevant to skin. First, it binds testosterone more avidly than oestradiol, so a rise in SHBG lowers free testosterone proportionally more than it lowers free oestradiol. Second, it is not fixed — oral oestradiol raises SHBG through hepatic first-pass, whereas transdermal oestradiol raises it far less.

Together these predict a specific, testable pattern. All else equal, take two people with the same total serum oestradiol but very different SHBG. The high-SHBG person would be expected to show:

If it holds, two people with identical total oestradiol could still differ in their skin outcomes — and the informative measurement would be free (or calculated free) oestradiol and free testosterone, rather than the total levels usually reported. It also gives the route questions raised elsewhere in this review a candidate mechanism: an oral regimen, because it tends to raise SHBG more than transdermal therapy (a well-documented hepatic first-pass effect in the menopausal-HRT literature), might be predicted to shift skin outcomes towards the androgen-withdrawal end and away from the oestrogen-driven end, relative to a transdermal regimen at the same total oestradiol. (SHBG has its own clinical explainer for the underlying biology.)

Confidence: 🔴 Hypothesis. This predicts a pattern; it does not describe a measured one. No study has stratified transfeminine skin outcomes by free oestradiol, and it is offered as a direction for measurement — a reason to record free fractions and SHBG in future work — not as an explanation to be assumed. [Mechanistic hypothesis; untested in transfeminine skin.]

11. Evidence quality

Ratings use the same traffic-light scheme as the rest of this series — 🟢 reasonably robust, 🟡 moderate, 🔴 limited — judging the type of evidence, its consistency, how directly it applies to trans women, and the size of the effect against its uncertainty. These are editorial judgements, not formal GRADE ratings. For how we weigh evidence in this field — why trials are scarce and how we treat figures borrowed from cisgender populations — see Reading the Evidence.

Skin outcome Confidence Why
Reduced sebum / oiliness 🟡 Low–Moderate Best-supported; small/older trans studies + clear androgen-withdrawal mechanism.[2,3]
Improved acne 🟡 Low–Moderate Plausible and reported; multifactorial; weaker than trans-men acne evidence.[1,2,3]
Dryness (xerosis) 🟡 Low–Moderate Expected from sebum loss; clinically reported, not quantified.[4]
Skin thickness / collagen (cisgender oestrogen) 🟡 Moderate RCT and controlled data in postmenopausal women; often non-modern formulations.[7,8,9]
Skin thickness (net effect in trans women) 🔴 Low Opposing androgen loss + oestrogen gain; not directly measured.
Hydration / barrier (cisgender oestrogen) 🟡 Low–Moderate Consistent in cisgender menopausal data.[7,9]
Hydration / barrier (net effect in trans women) 🔴 Low Unmeasured; opposed at the skin surface by falling sebum.
Wound healing 🟡 Moderate (elderly, topical) / 🔴 Low (trans, procedural) Human elderly experimental data in both sexes; no trans, systemic or procedural data.[10,11,12]
Pigmentation / melasma 🟡 Low–Moderate Hormonal mechanism + pregnancy/OCP; UV and phototype supported; trans dose/incidence not.[13,14,15]
Overall trans-specific skin evidence base 🔴 Low “Little data exists”; largest cohort measured mainly acne, alopecia and hair-growth/hirsutism.[1,3]
Free oestradiol / SHBG effect (net, in trans women) 🔴 Hypothesis Mechanistically grounded but untested in transfeminine skin; predicts outcomes track free, not total, oestradiol (Section 10).

A note on measurement. Almost none of the trans-specific evidence uses objective skin endpoints — sebumetry, corneometry, trans-epidermal water loss, cutometry, or ultrasound/biopsy thickness — relying instead on self-report and clinical observation. Better trans-specific data would start there.

12. Frequently asked questions

Will oestrogen make my skin less oily? Often, yes — feminising therapy reduces sebum, mostly through lowering testosterone, and skin commonly becomes less oily over the first months. Some people find it goes the other way and becomes dry.[2,4]

Will it clear my acne? It may improve, because sebum falls, but this is less certain than the acne flare testosterone causes in trans men, acne has several other causes, and it can flare transiently.[2,3] Management is covered in the dedicated acne review.

How quickly do skin changes happen? Oiliness and acne may shift within the first months; any collagen, thickness or firmness effects (to the extent they occur) are slower and not clinically predictable.

Will oestrogen make my skin thicker or more youthful? In post-menopausal cisgender women, oestrogen increases skin collagen and thickness.[7,8] In trans women this is less certain, because feminising therapy also removes the androgens that had thickened the skin — the net effect has not been measured. [Cisgender-derived.]

Can feminising therapy give me dark facial patches? It can. Oestrogen is one of the hormonal contributors to melasma. The most useful preventive step is sun protection — broad-spectrum (UVA/UVB) sunscreen, and, because visible light also drives melasma in darker skin, a tinted (iron-oxide) sunscreen is often preferred.[18] Any new facial pigmentation is worth discussing with a clinician, as it has other possible causes.[13,14]

Does the route of oestrogen (patch, gel, tablet, injection) change skin effects? This has not been studied for skin outcomes in trans women; route is chosen mainly for systemic safety reasons (see the Feminising Hormone Therapy review), not for skin, and different formulations are not interchangeable in their pharmacology.

Could my other medications be affecting my skin? Yes — anti-androgens (spironolactone, cyproterone acetate, GnRH analogues), 5α-reductase inhibitors (finasteride, dutasteride), isotretinoin, topical retinoids and progestogens all have skin effects of their own and can confound what is attributed to oestrogen.

13. Clinical bottom line

  1. The best-supported skin effect of feminising therapy is less oily skin, driven mainly by lowering testosterone; acne may improve as a result, though this is less well quantified in trans women than testosterone-related acne is in trans men.[2,3]
  2. Effects on skin thickness, collagen, hydration and wound healing come from cisgender hormone-replacement research, are largely unmeasured in trans women, and — for thickness — are complicated by the simultaneous loss of skin-thickening androgens.[7,10]
  3. Dryness is a realistic alternative outcome to oiliness, because surface sebum falls.[4]
  4. Melasma is the notable downside: oestrogen can provoke or worsen facial pigmentation, most clearly with sun exposure and in darker skin — making photoprotection (including tinted sunscreen) worthwhile.[13,14,15]
  5. None of this is a reason to alter hormone therapy; the trans-specific evidence is thin, and the honest position is that the direction of these changes is plausible while the precise, measured effects in trans women mostly await study.[1,3]

Sidebar — Oestrogen and skin, at a glance

Effect Direction Mainly driven by Evidence
Oiliness / sebum ↓ (less oily) Androgen withdrawal 🟡
Acne ↓ (may improve) Androgen withdrawal (partly) 🟡
Dryness ↑ in some Sebum loss 🟡
Collagen / thickness ↑ (cis) / uncertain (trans) Oestrogen (vs androgen loss) 🟡/🔴
Hydration ↑ (deeper skin) Oestrogen 🟡
Wound healing ↑ (elderly, topical) Oestrogen 🟡/🔴
Pigmentation / melasma ↑ (can worsen) Oestrogen (+ UV, phototype) 🟡

Sidebar — Common myths

Myth Evidence Strength
“Oestrogen alone makes skin less oily.” The oiliness change is mostly androgen withdrawal; oestrogen’s independent contribution is unclear.[2] 🟡
“Oestrogen will thicken and rejuvenate my skin like HRT does for menopausal women.” Cisgender-derived; trans women also lose skin-thickening androgens, so the net effect is unmeasured.[7] 🔴
“Feminising therapy always improves skin.” It can cause dryness and can provoke melasma.[4,13] 🟡
“Hormones will help me heal better after surgery or laser.” Wound-healing evidence is from topical oestrogen on experimental wounds in the elderly; it does not support better procedural healing in trans women.[10] 🔴
“Melasma from hormones is just a sun problem.” Hormones and light act together; both matter.[13] 🟡

What we know / What we don’t know

What we know

What we don’t know

Evidence appendix — the key studies at a glance

Design and applicability for the main sources behind this review, so the reader can weigh each claim directly.

Study Design Population (n) Exposure Outcome measured Objective endpoint? Applies to trans women? Key limitation
Giltay & Gooren 2000[16] Prospective physiological 21 trans women (+17 trans men) Oestrogen + anti-androgen Sebum (Sebutape), hair Yes (sebumetry) Directly Small; old; combined exposure
Cocchetti / ENIGI 2023[1] Prospective cohort 484 (193 trans women) Feminising / masculinising therapy Acne, hair, alopecia (scored) Partly (clinical scales) Directly (skin findings mainly in trans men) Sebum/skin not the trans-women focus
Rutnin 2023[5] Cross-sectional 159 (25 trans women) Feminising therapy Acne, melasma, hair loss Partly (clinical scales) Directly, hypothesis-generating No incidence/causation; tiny trans-women subgroup
Maheux 1994[17] RCT 60 postmenopausal cis women Conjugated oestrogens Skin/dermal thickness (ultrasound, biopsy) Yes By analogy only Non-modern formulation; low-androgen population
Ashcroft 1999[10] Experimental (wounds) Elderly cis men + women Topical oestrogen Wound size, collagen, strength Yes By analogy only Topical, experimental wounds, elderly
Hardman & Ashcroft 2008[11] Gene-expression Elderly cis Oestrogen status Wound-gene expression Yes (molecular) By analogy only Mechanistic; clinical healing multifactorial
Melasma mechanism[13,14,15] In-vitro / review Cells/tissue; cis women Oestrogen (± UV) Melanogenesis, receptor expression Yes (laboratory) Mechanistic; pregnancy/OCP by analogy No trans incidence data

What would settle these questions: a prospective trans cohort measuring skin objectively before and during feminising therapy — sebumetry, corneometry, trans-epidermal water loss, cutometry and ultrasound/biopsy thickness, validated acne scores, and melasma incidence — ideally comparing oestrogen routes and doses.

Related Eden Openly reviews

A note on support

This article is health information, not personal medical advice, and it is not a substitute for assessment by a qualified clinician. It should not be used to start, stop, dose-adjust, change the route of, or combine medications without clinical supervision, and feminising hormone therapy should follow local prescribing and monitoring standards. New or changing skin symptoms — including facial pigmentation — are worth discussing with your own clinician.

Revision history

Version 1.0 — July 2026. First published.

Version 1.1 — July 2026. Added a mechanistic hypothesis on free oestradiol and SHBG (Section 10). Tightened the in-body phrasing of two secondary-sourced figures — the Maheux dermal-thickness estimate (Section 6) and the Hardman & Ashcroft wound-gene estimate (Section 8) — to match the certainty their references already carry.

References

Population flags mark sources whose primary evidence is from cisgender (or in-vitro) populations and is extrapolated to trans women.

  1. Cocchetti C, Castellini G, Maggi M, Romani A, Vignozzi L, Greenman Y, den Heijer M, T’Sjoen G, Fisher AD. Effects of hormonal treatment on dermatological outcome in transgender people: a multicentric prospective study (ENIGI). Journal of Endocrinological Investigation. 2023;46(4):779–786. doi:10.1007/s40618-022-01944-x. (Prospective; 484 participants; acne (GAGS), hair (Ferriman–Gallwey) and alopecia (Norwood–Hamilton) scored at baseline, 6 and 12 months; oestrogen’s effects on the pilosebaceous unit described as “mostly unknown.”)
  2. Arcelus J, Kamaruddin K, Bouman WP. Dermatological aspects of gender affirming medical treatment in transgender and gender diverse people: a systematic review. International Journal of Transgender Health. 2024. doi:10.1080/26895269.2024.2374890. (Systematic review of 22 studies; feminising treatment reported to reduce sebum and improve acne, and to be associated with xerosis, pruritus and melasma among other skin effects; summarises the Giltay & Gooren study cited at [16].)
  3. Huang C, Gold S, Radi R, Amos S, Yeung H. Managing Dermatologic Effects of Gender-Affirming Therapy in Transgender Adolescents. Adolescent Health, Medicine and Therapeutics. 2022;13:93–106. doi:10.2147/AHMT.S344078. (States little data exist on skin effects of hormone therapy in transfeminine people; oestrogen and spironolactone reduce sebum and decrease acne.)
  4. Viscomi B, Goldie K, Kerscher M. Injectable Aesthetic Treatments for Improving Facial Skin Quality in Transgender Patients With or Without Gender-Affirming Hormone Therapy. Journal of Cosmetic Dermatology. 2025;24(Suppl 4):e70318. doi:10.1111/jocd.70318. (Cosmetic-dermatology treatment paper; the note that feminising hormones typically reduce sebum but may lead to xerosis appears as background rather than as primary measurement — the xerosis claim rests on this.)
  5. Rutnin S, Suchonwanit P, Kositkuljorn C, Pomsoong C, Korpaisarn S, Arunakul J, Rattananukrom T. Characterizing Dermatological Conditions in the Transgender Population: A Cross-Sectional Study. Transgender Health. 2023;8(1):89–99. doi:10.1089/trgh.2021.0105. (159 participants, including 25 trans women; feminising therapy associated with melasma and female-pattern hair loss in trans women; cross-sectional design and small sample limit incidence and causal conclusions.)
  6. Sabra JJ, Fang CX, Kundu RV. A Knowledge-Based Assessment of Dermatological Care for Transgender Women. Transgender Health. 2018. doi:10.1089/trgh.2018.0001.
  7. Stevenson S, Thornton J. Effect of estrogens on skin aging and the potential role of SERMs. Clinical Interventions in Aging. 2007;2(3):283–297. (Reviews the cisgender evidence, including the Maheux 1994 RCT — ~30% increase in dermal thickness after 12 months; biopsy-site details vary between secondary reports, so see the primary at [17] — and hydration via stratum-corneum water-holding and dermal hyaluronic acid.) [Population flag: cisgender postmenopausal women; non-modern formulations.]
  8. Patriarca MT, Goldman KZ, Dos Santos JM, Petri V, Simões RS, Soares JM Jr, Simões MJ, Baracat EC. Effects of topical estradiol on the facial skin collagen of postmenopausal women under oral hormone therapy: a pilot study. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2007;130(2):202–205. doi:10.1016/j.ejogrb.2006.05.024. (15 postmenopausal women on systemic oestrogen; increased epithelial and dermal thickness and collagen after 16 weeks of topical estradiol, preauricular biopsy.) [Population flag: cisgender postmenopausal women.]
  9. Brincat M, Pollacco J. Menopause and the effects of hormone replacement therapy on skin aging: a short review. GREM – Gynecological and Reproductive Endocrinology & Metabolism. 2024;5(1):34–37. doi:10.53260/grem.2450106. (Collagen loss ~2%/postmenopausal year; ~1%/year skin-thickness decline; controlled data on dermal thickness gains with oestrogen.) [Population flag: cisgender postmenopausal women.]
  10. Ashcroft GS, Greenwell-Wild T, Horan MA, Wahl SM, Ferguson MW. Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response. American Journal of Pathology. 1999;155(4):1137–1146. (Experimental wounds in elderly men and women; reduced wound size at day 7, increased collagen, increased day-80 wound strength.) [Population flag: elderly cisgender men and women; topical, experimental wounds.]
  11. Hardman MJ, Ashcroft GS. Estrogen, not intrinsic aging, is the major regulator of delayed human wound healing in the elderly. Genome Biology. 2008;9(5):R80. (~80% of age-related wound-gene expression differences were oestrogen-regulated; clinical healing remains multifactorial.) [Population flag: elderly cisgender.]
  12. Ashcroft GS, Dodsworth J, van Boxtel E, et al. Estrogen accelerates cutaneous wound healing associated with an increase in TGF-β1 levels. Nature Medicine. 1997;3(11):1209–1215. [Population flag: experimental/animal and human.]
  13. Cario M. How hormones may modulate human skin pigmentation in melasma: an in-vitro perspective. Experimental Dermatology. 2019;28(6):709–718. doi:10.1111/exd.13915. (Oestrogen stimulates melanocyte and keratinocyte pro-pigmentary factors; acts together with UV.) [Population flag: in-vitro.]
  14. Zhang J, Wang T, Li Z, Qin C, Dai J, Zhao Y, Wu S, Jia Z. Hormonal Crosstalk in Melasma: Unraveling the Dual Roles of Estrogen and Progesterone in Melanogenesis. International Journal of Molecular Sciences. 2025;26(22):10856. doi:10.3390/ijms262210856. (Oestrogen and progesterone regulate melanogenesis via ERα, ERβ and GPER, raising tyrosinase and MITF; progesterone findings across models are mixed.) [Population flag: mechanistic/cisgender.]
  15. Liu W, Chen Q, Xia Y. New Mechanistic Insights of Melasma. Clinical, Cosmetic and Investigational Dermatology. 2023;16:429–442. doi:10.2147/CCID.S396272. (Increased oestrogen-receptor expression in melasma-affected skin; oestrogen upregulates PDZK1, enhancing tyrosinase and melanosome transfer; pregnancy and oral contraceptives as classic triggers.) [Population flag: pregnancy/contraceptive; cisgender women.]
  16. Giltay EJ, Gooren LJ. Effects of Sex Steroid Deprivation/Administration on Hair Growth and Skin Sebum Production in Transsexual Males and Females. Journal of Clinical Endocrinology & Metabolism. 2000;85(8):2913–2921. doi:10.1210/jcem.85.8.6710. (21 transfeminine and 17 transmasculine people on cross-sex hormones; sebum measured by Sebutape, hair by Ferriman–Gallwey and image analysis, at baseline and 4, 8 and 12 months.)
  17. Maheux R, Naud F, Rioux M, Grenier R, Lemay A, Guy J, Langevin M. A randomized, double-blind, placebo-controlled study on the effect of conjugated estrogens on skin thickness. American Journal of Obstetrics and Gynecology. 1994;170(2):642–649. (60 postmenopausal women, conjugated oestrogens vs placebo, 12 months; skin thickness by ultrasonography, reported over the right greater trochanter, and dermal thickness by biopsy, with the biopsy site not separately specified in the abstract.) [Population flag: cisgender postmenopausal women; conjugated oestrogens.]
  18. Lyons AB, Trullas C, Kohli I, Hamzavi IH, Lim HW. Photoprotection beyond ultraviolet radiation: a review of tinted sunscreens. Journal of the American Academy of Dermatology. 2021;84(5):1393–1397. doi:10.1016/j.jaad.2020.04.079. (Visible light contributes to hyperpigmentation, particularly in darker phototypes; tinted sunscreens containing iron oxides protect against visible-light-induced pigmentation and benefit melasma and post-inflammatory hyperpigmentation.) [Population flag: general dermatology; not trans-specific.]