Clinical Note

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

Types of HRT Formulations

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

Oral Tablets

Hepatic first-pass metabolism

Transdermal Patches

Bypasses hepatic first-pass metabolism

Gels & Sprays

Transdermal delivery with flexible dosing

Subcutaneous Implants

Specialist use with steady-state hormone levels

Vaginal / Local Oestrogen

Minimal systemic absorption

Injectable Oestrogen

Not standard UK menopausal practice

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

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

Key Points

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

Intrauterine Progestogen System (IUS)

Endometrial protection with low systemic exposure

Androgenic Activity of Progestogens

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

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

Androgenicity may arise through:

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

These mechanisms do not always occur together.

Norethisterone (NET)

Norethisterone illustrates this complexity well.

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

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

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

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

Androgenic Activity of Progestogens

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

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

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

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

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

Oral vs Transdermal Oestrogen: the Hair and Scalp Difference

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

ORAL OESTROGEN AND SHBG

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

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

TRANSDERMAL OESTROGEN AND SHBG

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

Which HRT is Best for Androgen-Sensitive Conditions?

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

ACNE

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

ANDROGENETIC HAIR LOSS (AGA)

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

HIRSUTISM

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

SEBORRHOEA (OILY SKIN/SCALP)

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

Summary Reference

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

References

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

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

[3]  Kloosterboer HJ, Vonk-Noordegraaf CA, Turpijn EW. Selectivity in progesterone and androgen receptor binding of progestagens used in oral contraceptives. Contraception. 1988;38(3):325-32. PMID: 2851054

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

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

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

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

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

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

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

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

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

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

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/

What is a Progestogen?

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

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

Generations of progestins and their androgenic character

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

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

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

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

Relative androgen receptor binding affinity of progestins

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

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

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

Why androgenic activity matters clinically

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

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

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

Clinical consequences by condition

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

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

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

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

Drospirenone: a structurally distinct progestin

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

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

Drospirenone and androgen-related skin conditions

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

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

Dienogest: a different route to anti-androgenic activity

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

Safety considerations and prescribing context

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

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

Summary

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

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

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

References

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

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

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

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

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

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

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

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

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

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

Dr Iaisha Ali Consultant Dermatologist

Dr Iaisha Ali, MB ChB MRCP MSc(Oxon)

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

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

iadermatology.com/