Androgenetic alopecia

[1] [7]

Meet the patient

A 32-year-old man sits down, hat in hand, and turns to show a deepening bitemporal recession and a thinning vertex his barber flagged six months ago. His maternal grandfather, he tells you, was bald as an egg by thirty-five. He has read the internet and has come in asking for finasteride today.[1][2]

Two questions decide this consultation, and they are the two every AGA stem turns on: is this really androgenetic alopecia and not a mimic? (the dermatoscope answers in ninety seconds), and is he safe for the drug he is asking for? (a quick history, a baseline PSA, and a straight warning about mood). Hold those two questions and the rest of the page slots into place.[1]

What it is — and the one sign that rules it in or out

AGA is a genetically determined, androgen-dependent, progressive miniaturisation of susceptible scalp follicles — and it is non-scarring. That last word is the whole exam. The follicle shrinks but it does not die, and the follicular ostium stays open on trichoscopy. Lose the ostia and you are no longer in AGA — you are in cicatricial (scarring) alopecia, and the management changes completely.[1][7]

The single most useful bedside sign in all of hair-loss medicine is preserved versus lost follicular ostia. Put a dermatoscope on the scalp. If you see hair openings — even empty ones — sitting beside hairs of mixed calibre, you are looking at AGA. If the scalp is smooth, shiny, and porcelain, with the follicular markings gone, the diagnosis is scarring alopecia and you biopsy the edge before reaching for minoxidil.[1]

The terminology rewards precision, and examiners pay for it:[1]

• Male pattern hair loss (MPHL) — Hamilton-Norwood, seven stages with substages.
• Female pattern hair loss (FPHL) — Ludwig (three grades) and the Olsen Christmas-tree variant.
• Pattern hair loss (PHL) — the modern gender-neutral umbrella.
• Diffuse unpatterned alopecia (DUPA) — uncommon, severe, often hyperandrogenic; biopsy to confirm.[2]

Within the non-scarring alopecias, AGA is separated from telogen effluvium by hair diameter diversity over 20 percent — telogen effluvium thins every hair uniformly, while AGA leaves thick and thin hairs standing side by side in the same field.[1][2]

Read the pattern: Hamilton-Norwood or Ludwig?

The pattern is so characteristic that diagnosis is clinical. Men lose the bitemporal hairline and the vertex; women keep the frontal hairline and widen the central part. Name the system, then name the stage.[1][2]

[1]

Hamilton-Norwood, reproduced verbatim: I minimal bitemporal recession; II symmetric triangular bitemporal (up to 2 cm anterior to the coronal suture); III deep bitemporal (III vertex adds early vertex thinning); IV frontal and vertex thinning separated by a band; V the band narrows; VI the band disappears into confluence; VII only the occipital horseshoe rim remains.[2][7]

Ludwig, with the frontal hairline as the discriminator: I a widened midline part with scalp visible through parted hair; II a clearly widened part with thinning visible without parting; III the full crown visible — and the frontal hairline preserved in every grade. The Olsen Christmas-tree variant layers a frontal accentuation along the part on top of the Ludwig grade.[1][7]

The histological signature on horizontal scalp biopsy is a terminal-to-vellus ratio below 4:1 (normal scalp runs 7–9:1) — diagnostic when the clinical picture is genuinely uncertain.[7]

[1]

How common, and who is at risk?

AGA is near-universal in susceptible ageing populations, but prevalence, onset, and severity track sex, ethnicity, and genetics. Men present in their late teens to twenties — about one in four by thirty, half by fifty. Women usually notice thinning in the perimenopausal forties-to-fifties, though PCOS and hyperandrogenism pull the onset into the twenties.[2][8]

[2] [8]

Ethnic variation. Prevalence is highest in Caucasians, intermediate in Asians, and lowest in Africans. Asian men show less bitemporal recession and more diffuse frontal and vertex thinning; the African occipital halo of DHT-resistant follicles is robust. African women carry more traction-related marginal (often cicatricial) alopecia and less FPHL, though androgenic contribution to frontal fibrosing alopecia is increasingly recognised.[2][8]

Genetics — the maternal grandfather is not a myth. The androgen receptor gene sits on Xq12, inherited through the maternal line. The CAG repeat length in exon 1 sets AR activity — shorter repeats, more active receptor, more AGA. SRD5A2 polymorphisms tune DHT output; WNT-pathway genes (WNT10A, LEF1) set follicular fate. Inheritance is polygenic, so the paternal line contributes too — but the bedside tradition of asking about the maternal grandfather has a chromosomal basis.[1][2]

The link the examiner now expects: early AGA and the heart

Early-onset AGA in men (before age 25) is an established cardiovascular risk marker, not a cosmetic footnote. It associates with insulin resistance, metabolic syndrome, dyslipidaemia, hypertension, and type 2 diabetes, independent of BMI — roughly a two- to threefold rise in metabolic-syndrome risk. The link runs both ways: hyperinsulinaemia suppresses sex-hormone-binding globulin, raising free androgen availability and accelerating follicular miniaturisation.[12][13]

This does not change how you treat the hair, but it changes the consultation. A young man with an aggressive Norwood III at twenty-three deserves a fasting glucose, a lipid panel, and a blood pressure — not just a prescription. Recent sex-stratified propensity-matched cohort data confirm the cardiometabolic comorbidity.[12][13]

Why the follicle shrinks — DHT, not testosterone

The lay story that testosterone causes baldness is wrong. Testosterone alone does not miniaturise follicles. Its reduced metabolite, dihydrotestosterone (DHT), does — and only in follicles carrying a permissive androgen-receptor signature. DHT binds the AR with roughly five times the affinity of testosterone; the activated complex enters the nucleus and rewires the dermal papilla.[1][2][7]

Run the cascade the way the examiner wants it:[1][2][7]

1. Testosterone enters the dermal papilla of a susceptible follicle and is reduced to DHT by 5-alpha-reductase.
   • Type I (SRD5A1) — skin, sebaceous glands, liver.
   • Type II (SRD5A2) — prostate, hair follicle, beard, liver. This is the one finasteride hits.
2. DHT binds the AR, the complex dimerises and translocates to the nucleus, and gene expression shifts.
3. The dermal papilla secretes paracrine effectors — TGF-β1 and TGF-β2, DKK-1 (a WNT antagonist that blocks anagen entry), PGD2 (via lipocalin-type PGD synthase, acting on GPR44/DP2), and IL-6 — that tell the overlying matrix cells to shorten anagen and shrink the bulb.
4. Across cycles the follicle produces a thinner, shorter, paler vellus hair; the anagen-to-telogen ratio falls from about 9:1 toward 2:1.
5. The follicle becomes clinically invisible — but it does not die, which is why transplantation works.
6. Occipital and lateral-temporal follicles are DHT-resistant (lower local 5-AR Type II, a different AR co-regulator milieu) — they form the donor horseshoe of Norwood VII.[1]

[1]

Etymology for viva gold: alopecia comes from the Greek alopēx, fox — foxes shed and go bald with mange, and the metaphor stuck for two and a half millennia. Androgenetic fuses andros (man) with genesis (origin): the hair loss is born of androgens. Both roots outlived their literal meanings because the pathology they name is unchanged.[1]

[1]

Why occipital escapes — donor dominance

Occipital and lateral-temporal follicles keep their terminal calibre even in Norwood VII. The molecular reason is lower local 5-AR Type II activity and a different AR co-regulator milieu, with higher WNT agonism. The clinical consequence is the single most useful idea in transplant surgery: donor dominance — an occipital follicle transplanted to a balding vertex keeps behaving as occipital and resists DHT in its new home.[3]

That is why the graft is permanent. But — the counselling trap — the surrounding native hairs keep thinning on schedule. Every transplant patient needs ongoing medical therapy to preserve the cosmetic result, or the permanent grafts end up as islands in a widening bald field.[1][3]

The bedside round — two minutes, five moves

Examination in suspected AGA rarely surprises you; its job is to confirm the pattern and exclude a mimic. Run it the same way every time.[1]

1. General inspection — hair density by quadrant, the pattern of thinning, occipital preservation.
2. Hair pull test — grasp 50–60 hairs at the scalp and pull gently. More than 6 telogen hairs means positive. Best done after 5 days without shampooing. Negative in stable AGA; positive in active AGA, telogen effluvium, and alopecia areata.
3. Part-width comparison — central widening (Ludwig), frontal accentuation (Olsen Christmas-tree).
4. Hair calibre — run the fingers from frontal to vertex; reduced vertex calibre suggests AGA.
5. Follicular ostia — preserved in AGA, telogen effluvium, and alopecia areata; lost in cicatricial alopecia. This is the sign that changes everything.[1]

Trichoscopy is the standard diagnostic adjunct — non-invasive, thirty seconds with a polarised handheld dermatoscope (ideally 20–70×), and it distinguishes AGA from every important alternative.[1][7]

[1] [1]

The mimics you must not miss — the Big Five

Every candidate on the differential must be excluded before you commit a patient to lifelong therapy, because the wrong diagnosis wastes a year and misses a treatable cause. The examiner almost always asks about at least one.[1][2][7]

[1]

The one-line discriminator to carry onto every ward round: diameter diversity over 20 percent with preserved ostia is AGA; uniform thinning with preserved ostia is telogen effluvium; smooth shiny scalp without ostia is scarring — and scarring is never AGA.[1]

The classic trap: treating a cicatricial alopecia with minoxidil and missing the window for immunomodulation. Smooth shiny scalp with lost ostia is a biopsy, not a prescription.[1]

Other mimickers worth naming: drug-induced alopecia (anticoagulants, retinoids, beta-blockers, lithium, valproate, carbamazepine, cytotoxics — diffuse and reversible on withdrawal); iron deficiency without anaemia (low ferritin worsens chronic TE and blunts the FPHL response); endocrine causes (hypo- or hyperthyroidism, hypopituitarism); nutritional deficiency (protein, zinc, vitamin D, essential fatty acids); the moth-eaten alopecia of secondary syphilis (VDRL/RPR positive, responds to penicillin); hypotrichosis simplex (autosomal dominant, from childhood); pressure alopecia (post-op or ICU); and traction alopecia from tight braids or weaves — reversible early, scarring late.[1]

Investigations — keep them targeted

Most AGA is diagnosed clinically and trichoscopically; the laboratory exists to unmask mimics and to prescribe safely, never to confirm the obvious.[1][7][8]

Baseline for everyone: full blood count, ferritin (aim above 40–70 µg/L for hair — some experts say above 70), TSH, and vitamin D and zinc. Correct deficiencies when present; supplementing replete patients does nothing for the hair.[1][4]

Female hyperandrogenism screen — if hirsutism, acne, irregular menses, or central obesity accompany the thinning:[1][7]

• Total testosterone and SHBG (low SHBG raises the free androgen index).
• DHEA-S (adrenal androgen; elevated in adrenal hyperplasia or tumour).
• Androstenedione and 17-OH progesterone (screen for non-classic congenital adrenal hyperplasia).
• LH/FSH ratio (classically above 2:1 in PCOS, though not specific) and prolactin.
• Pelvic ultrasound for polycystic ovarian morphology (Rotterdam: at least 12 follicles per ovary, or ovarian volume over 10 mL).[1]

Before finasteride or dutasteride in men: liver function tests as baseline, and a baseline PSA — because these drugs halve it. Consider documenting baseline sexual function (IIEF-5) for monitoring.[1]

When to biopsy. Reserve the 4-mm punch for genuinely uncertain cases — typically a suspected DUPA or a possible cicatricial mimic. The AGA signature on horizontal section is a terminal-to-vellus ratio below 4:1, a normal-to-slightly-raised telogen count, preserved ostia, and a mild perifollicular lymphocytic infiltrate.[1][7]

Alopecia emergencies — when AGA is not the diagnosis

AGA itself is never an emergency, but its differential contains several that are. The examiner rewards recognition above management.[2]

[1]

Treatment — match the drug to the sex and the stage

AGA therapy is longitudinal and lifelong: response guides every adjustment, and withdrawal reverses the benefit within 3–6 months. The clinician who discusses adherence at the first visit prevents the disappointment that arrives three years later.[1][3][5][6]

[1]

The drug table — doses, sex, and the one hazard each:[1][5]

[1] [5] [6] [10]

Minoxidil — the only drug that works in both sexes

Minoxidil is a potassium-channel opener and vasodilator that prolongs anagen and enlarges the follicle — and it is wholly independent of the androgen pathway, which is exactly why it works in both sexes.[6][10]

Topical 5%: men apply it twice daily to vertex and frontal scalp (1 mL per application); women use 5% once daily (the 2% twice-daily solution is the FDA-approved female option, but 5% once daily is widely used and effective). Switch to PG-free foam when contact dermatitis to propylene glycol is suspected. Warn every patient about initial shedding in weeks 2–6 — the telogen-to-anagen transition pushes vellus hairs out before terminal regrowth, and the patient who is not warned stops at week three, convinced the drug is making things worse.[6]

Oral minoxidil (off-label): 0.625 mg in women up to 5 mg in men, titrated to response. Once-daily dosing, no scalp irritation, uniform delivery, better compliance — a viable first-line option when topical adherence is poor (recent international consensus). Adverse effects: hypertrichosis of face and limbs (roughly 15–50%, usually mild and reversible on dose reduction), fluid retention and peripheral oedema, pericardial effusion (rare at low doses, caution in cardiac disease), tachycardia, hypotension.[10]

Counsel realistically. Visible improvement takes 3–6 months, maximum benefit at 1–2 years, and the commitment is lifelong — stopping reverts any gain within 3–6 months.[1][6]

Finasteride — men only, and never in pregnancy

Finasteride is a selective 5-alpha-reductase Type II inhibitor that cuts serum DHT by about 70% and scalp DHT by 60–70%. The FDA approved 1 mg/day for male AGA in 1997 on the back of the Kaufman pivotal trials.[1][5]

Dose: 1 mg orally once daily, with or without food. Kaufman's pivotal RCTs showed 48% vertex improvement versus 7% placebo at one year on global photographic assessment, hair count up about 11% versus 3%, and a five-year extension in which 90% maintained or improved on baseline. The vertex and mid-frontal scalp respond best; bitemporal recession responds less predictably.[1][5]

Adverse effects — name them and their approximate rates: decreased libido (~1.5%), erectile dysfunction (~1.5%), ejaculatory disorder (~1%), gynaecomastia (~0.5%). Most sexual effects are transient and resolve in 50–60% on continued therapy. Depression and suicidal ideation are rare but real — the FDA updated labelling in 2011 — and at the first sign of severe mood change you stop the drug and refer. Post-finasteride syndrome (persistent sexual, neurological, and psychiatric symptoms after stopping) is reported and litigated; the causal link remains controversial, and the FDA has not withdrawn the drug on that basis.[1]

PSA — the number that must be doubled. Finasteride lowers serum PSA by about 50%. In any man on finasteride or dutasteride, multiply the measured PSA by 2 to interpret prostate-cancer screening correctly; the Rossi formula adds about 10% further correction after two years of use. Forget this and you mask a prostate cancer.[1]

Pregnancy — the absolute rule. Finasteride is Category X. DHT is essential for male fetal external genitalia, and inhibition causes ambiguous or female-appearing genitalia in a 46,XY fetus. Pregnant women must not even handle crushed or broken tablets. Prescribe only to men, or to postmenopausal women — and Lucky 2004 showed no benefit from 1 mg finasteride in postmenopausal FPHL anyway.[1]

Dutasteride — men only, more potent, longer half-life

Dutasteride is a dual 5-AR Type I and II inhibitor that suppresses serum DHT by over 90%. It is approved for BPH at 0.5 mg/day and used off-label for male AGA, where head-to-head trials (Rossi 2011, ARES) showed superior vertex hair count versus finasteride at 12 and 24 weeks.[5]

The half-life is roughly 5 weeks (versus 6–8 hours for finasteride) — relevant for blood-donation deferral and for pregnancy planning, where washout takes about six months. The adverse-effect profile is similar, with slightly higher pooled sexual-dysfunction rates. Reserve it for men who fail or tolerate finasteride poorly, or for aggressive early-onset disease where maximum DHT suppression is wanted. The pregnancy contraindication is identical to finasteride.[1][5]

Spironolactone — women only

Spironolactone is an androgen-receptor antagonist (plus reduced testosterone production at higher doses), used off-label but widely for FPHL.[7]

Dose: 100–200 mg orally once daily (some start at 50 mg and titrate). Combine it with an oral contraceptive carrying an antiandrogenic progestin (drospirenone, dienogest) for contraception and a synergistic antiandrogen effect. Monitor potassium at baseline, 1–2 months, then 6-monthly; watch for menstrual irregularity, breast tenderness, and hypotension. Avoid in renal failure and Addison disease. It is not used in men — the gynaecomastia and sexual dysfunction at effective doses are unacceptable.[1]

Other antiandrogens for women: bicalutamide 25–50 mg/day (pure AR antagonist, limited data, promising); flutamide 250–500 mg/day (hepatotoxic, rarely used); finasteride 2.5–5 mg/day in postmenopausal or PCOS-driven FPHL (lower response than in men); and oral contraceptives with antiandrogenic progestins for FPHL with a concurrent need for contraception.[1][7]

Hair transplantation — permanent grafts, lifelong medicine

Transplantation surgically relocates DHT-resistant occipital and lateral-temporal follicles to balding recipient areas — and donor dominance makes the result permanent.[3]

• FUT (follicular unit transplantation, the strip method): an occipital strip is excised, dissected into 1–4-hair follicular units, and transplanted. Leaves a linear scar; one session can move 2000–4000 grafts.
• FUE (follicular unit extraction): individual units are punched out one at a time with a 0.7–1.0 mm punch. No linear scar; more time-consuming; 2000–5000 grafts per session.[1]

Candidacy. Stable Norwood III–VI men with adequate donor density and realistic expectations. Women with Ludwig II–III are poorer candidates — diffuse thinning reduces donor supply and recipient density. Smokers, poorly controlled diabetics, those with cicatricial or unstable disease, and those with body dysmorphic disorder are poor candidates.[1]

Pitfalls. Shock loss of adjacent native hair (10–20%, usually temporary); donor depletion (irreversible); poor graft survival (smoking, sun, infection); a wider-than-expected FUT scar.[1]

The counselling point that protects the result. Transplanted hairs are permanent, but native recipient-area hairs keep thinning on schedule. Every transplant patient needs ongoing minoxidil, with or without finasteride, or the permanent grafts end up as islands.[1]

Adjuncts — evidence is variable, expectations must be modest

• Low-level laser therapy (LLLT) — laser caps and combs; photobiomodulation and follicular ATP; FDA-cleared for AGA; modest RCT benefit.[3]
• Platelet-rich plasma (PRP) — autologous platelet concentrate injected into the scalp; growth factors (PDGF, TGF-β, VEGF, EGF) may prolong anagen; technique not standardised; useful as an adjunct.[3]
• Microneedling — a 1.5 mm dermaroller every 1–4 weeks; micro-wounds release growth factors and enhance topical minoxidil penetration.[3]
• Ketoconazole 2% shampoo — mild anti-inflammatory and anti-androgenic effect; reduces Malassezia. Useful adjunct.[3]
• Cosmetic camouflage — scalp micropigmentation, hair fibres, wigs, weaves. Psychologically important.
• Micronutrients — correct iron, zinc, and vitamin D when deficient; no benefit from supplementing replete individuals.[4]

[1]

The algorithm by stage and sex

Men, Norwood II–IV: first-line topical minoxidil 5% twice daily or oral minoxidil 1.25–2.5 mg/day; add finasteride 1 mg/day (superior to monotherapy); switch to dutasteride 0.5 mg/day if finasteride fails; add adjuncts; transplant once disease stabilises (typically 1–2 years of medical therapy).[1]

Men, Norwood V–VII: combined finasteride plus minoxidil (consider dutasteride) is essential to preserve native hair; transplant is often necessary — counsel realistically about donor supply.[1]

Women, Ludwig I–II, no hyperandrogenism: topical minoxidil 5% once daily or oral minoxidil 0.625–1.25 mg/day; adjuncts as above; replace iron, vitamin D, and zinc if deficient.[1][7]

Women, Ludwig II–III, with PCOS or hyperandrogenism: minoxidil plus spironolactone 100–200 mg/day (with contraception) or bicalutamide 25–50 mg/day; an OC with antiandrogenic progestin if contraception is needed; endocrinology referral for the metabolic management of PCOS.[1][7]

Transgender and gender-diverse individuals: specialist-led care, integrated into the gender-affirming hormonal pathway (below).[9]

The safety-critical drugs — three rules that must not be broken

Humour is off for the rest of this section. These three errors harm patients.[1]

1. Never prescribe finasteride or dutasteride to a woman of childbearing potential. Both are Category X. DHT is required for normal male fetal external genitalia; inhibition causes ambiguous or female-appearing genitalia in a 46,XY fetus. Prescribing mandates a pregnancy test and highly effective contraception (long-acting reversible, or two forms). Pregnant women must not even handle broken tablets. Washout before conception: about 1 month for finasteride, about 6 months for dutasteride (the long half-life).[1]
2. Always double the PSA in a man on finasteride or dutasteride. The drug halves serum PSA; an uncorrected reading masks prostate cancer.[1]
3. Stop the drug at the first sign of severe mood change. Depression and suicidal ideation are rare but FDA-labelled for finasteride; the post-finasteride syndrome debate is ongoing but the patient-safety concern is real. Stop, document, and refer urgently.[1]

Reassuring data on the cardiovascular question: a large 2026 TriNetX propensity-matched cohort found no increased cardiovascular hazard with oral 5-alpha-reductase inhibitors prescribed for AGA.[11]

Special populations — tailor the pharmacology

Women of childbearing potential carry the absolute rules above. Topical minoxidil in pregnancy is Category C — defer to postpartum — and minoxidil enters breast milk, so avoid it in lactation.[1]

Children. AGA in a child is uncommon and warrants investigation for hyperandrogenism (peripubertal PCOS, late-onset congenital adrenal hyperplasia, an androgen-secreting tumour), endocrine and nutritional causes, and genetic mimics (hypotrichosis simplex, ectodermal dysplasia, alopecia areata). Topical minoxidil is the only widely accepted pharmacotherapy (off-label); finasteride, dutasteride, and spironolactone are not consentable in children, and transplantation is inappropriate before adulthood because the donor area is not yet stable.[1]

Elderly patients. Cardiovascular comorbidity is common; start oral minoxidil lower (0.625 mg) and monitor. Check for polypharmacy — antihypertensives potentiate minoxidil hypotension; anticoagulants worsen PRP bruising. Transplant candidacy depends on donor supply, expectations, and cardiovascular fitness for surgery.[1]

Transgender and gender-diverse individuals. AGA care is integrated into the gender-affirming pathway.[9]

• Trans women and transfeminine individuals — estrogen-based gender-affirming hormone therapy slows or reverses AGA; finasteride may be added as part of androgen blockade.
• Trans men and transmasculine individuals — testosterone-based therapy worsens AGA in those predisposed; counsel before starting and consider prophylactic finasteride plus topical or oral minoxidil.
• Non-binary individuals — tailor therapy to hormonal goals.
• Mental-health input, peer support, and culturally competent care are essential.[1][9]

PCOS and metabolic syndrome. About 40–70% of women with PCOS have AGA. Treat both in parallel: PCOS-specific care (metformin or inositol for insulin resistance, lifestyle, a combined OC with antiandrogenic progestin, letrozole for fertility) plus AGA-specific care (spironolactone or bicalutamide, topical or oral minoxidil). Coordinate endocrinology, gynaecology, and dermatology.[1]

Cardiovascular and prostate disease. Finasteride and dutasteride halve PSA — double it for screening. Symptomatic BPH benefits from the same drugs at different doses. Oral minoxidil is a vasodilator; caution in heart failure, severe aortic stenosis, and recent MI.[1][11]

Prognosis — progressive, lifelong, reversible on stopping

Untreated AGA is progressive over decades. Medical therapy slows or halts loss and may regrow hair, but it does not cure — all medical therapies are lifelong, and the benefit reverses within 3–6 months of stopping.[1][5]

Good response: early treatment (within five years of onset, before extensive dropout), younger age, vertex and mid-frontal disease (better than bitemporal), good adherence, adequate donor supply, and no untreated underlying cause (iron, thyroid, androgen, drug).[1]

Poor response: extensive disease (Norwood VI–VII), long-standing miniaturisation (over 10 years — many follicles may be unrecoverable), coexistent scarring, non-adherence (the commonest cause of failure), untreated hyperandrogenism, and donor depletion in transplant candidates. Spontaneous stabilisation occurs in about 10–20% of men after Norwood IV–V; most eventually continue.[1][5]

Transplanted hairs are permanent, but native hairs keep thinning without medical therapy — the reason every transplant patient needs ongoing minoxidil or finasteride.[1]

The mantra, and the viva honesty line

The mantra: diameter diversity and preserved ostia — then check who must not get finasteride.[1]

[1]

Ward-round test — four stems, thirty seconds each

Stem 1 — the man with the receding hairline and the bald maternal grandfather

A 28-year-old man has progressive bitemporal recession over 18 months; his maternal grandfather was completely bald by thirty. What is the diagnosis, and what do you do at this visit? Model: Androgenetic alopecia, Hamilton-Norwood II–III, with a positive family history reflecting the X-linked AR allele. Diagnosis is clinical and trichoscopic — hair diameter diversity over 20 percent, a peripilar sign, and preserved follicular ostia. Baseline ferritin and TSH; a baseline PSA if he is over 40. First-line is finasteride 1 mg/day plus topical minoxidil 5% — counsel on initial shedding, on sexual adverse effects, and on the absolute rule about handling in pregnancy.[1][2]

Stem 2 — the woman with central thinning, hirsutism, and irregular menses

A 36-year-old woman has a widened midline part, mild hirsutism, irregular menses, and acne. Testosterone is mildly raised, SHBG is low-normal, and pelvic ultrasound shows polycystic ovaries. What is the unifying diagnosis, and how do you manage the hair? Model: PCOS with female pattern hair loss (Ludwig I–II) driven by hyperandrogenism. Multidisciplinary: endocrinology and gynaecology for the PCOS (lifestyle, metformin if insulin-resistant, combined OC with antiandrogenic progestin); dermatology with topical minoxidil 5% once daily plus spironolactone 100–200 mg/day with contraception. Monitor potassium, menstrual pattern, and androgens. Finasteride is avoided until she is past childbearing potential.[7][8]

Stem 3 — why does the transplant work, and why does the patient still need finasteride?

Explain donor dominance, and explain why a transplanted patient still needs medical therapy. Model: Occipital and lateral-temporal follicles carry lower local 5-AR Type II activity and a different AR co-regulator milieu, so they are DHT-resistant even in Norwood VII. Transplanted to a bald vertex, they keep that resistance — donor dominance — so the grafts are permanent. But the surrounding native hairs keep thinning on schedule, so ongoing minoxidil, with or without finasteride, is required to preserve the cosmetic result.[3]

Stem 4 — the PSA that must be doubled

A 45-year-old man on finasteride 1 mg/day has a PSA of 1.0 ng/mL. How do you interpret it? Model: Finasteride lowers serum PSA by about 50%, so the true PSA is about 2.0 ng/mL — clinically significant for prostate-cancer screening. The standard correction is to double the measured PSA (the Rossi formula adds about 10% further after two years of use). Without correction, finasteride masks a prostate cancer and delays diagnosis. Communicate the correction to every clinician managing the patient.[1]

References

1. [1]Devjani S, Ezemma O, Kelley KJ, et al. Androgenetic Alopecia: Therapy Update Drugs, 2023.PMID 37166619
2. [2]Oiwoh SO, Enitan AO, Adegbosin OT, et al. Androgenetic Alopecia: A Review Niger Postgrad Med J, 2024.PMID 38826011
3. [3]Nestor MS, Ablon G, Gade A, et al. Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics J Cosmet Dermatol, 2021.PMID 34741573
4. [4]Wang R, Lin J, Liu Q, et al. Micronutrients and Androgenetic Alopecia: A Systematic Review Mol Nutr Food Res, 2024.PMID 39440586
5. [5]Gupta AK, Talukder M, Williams G. Comparison of oral minoxidil, finasteride, and dutasteride for treating androgenetic alopecia J Dermatolog Treat, 2022.PMID 35920739
6. [6]Gupta AK, Talukder M, Venkataraman M, et al. Minoxidil: a comprehensive review J Dermatolog Treat, 2022.PMID 34159872
7. [7]Kearney CA, Brinks AL, Lawrence CN, et al. Androgenetic Alopecia in Women: A Narrative Review of Pathophysiology, Clinical Evaluation, and Treatments Am J Clin Dermatol, 2026.PMID 41714473
8. [8]Li H, Li W, Zhang J, et al. Risk factors for androgenetic alopecia: a systematic review and meta-analysis BMC Public Health, 2026.PMID 41606541
9. [9]Ramos-Rodriguez D, Sanchez-Baez D, Cabrera-Garcia P, et al. Characterization and Management of Androgenetic Alopecia in Transgender and Gender-Diverse Individuals: A Narrative Review Dermatol Ther (Heidelb), 2026.PMID 41920277
10. [10]Gupta AK, Talukder M, Williams G, et al. Low-dose oral minoxidil (LDOM) and topical minoxidil: consensus recommendations for managing male and female pattern hair loss in hair transplant patients using a modified Delphi process Expert Opin Pharmacother, 2026.PMID 41782304
11. [11]Spindler A, Maas D, Adler R, et al. No increased cardiovascular hazard with oral 5-alpha-reductase inhibitors in treatment of androgenetic alopecia: A TriNetX retrospective cohort study J Am Acad Dermatol, 2026.PMID 42036027
12. [12]Husseinali M, Engineer N, Asempa O, et al. Cardiometabolic comorbidities associated with androgenetic alopecia: Findings from a sex-stratified, propensity-matched national cohort Dermatol Online J, 2026.PMID 42246337
13. [13]He J, He M, Zhang D, et al. Early androgenetic alopecia as a possible indicator of diabetes mellitus and its link to cardiovascular risks: A cross-sectional study J Am Acad Dermatol, 2026.PMID 41785995