Androgenetic alopecia guide: DHT miniaturization, staging, and the full treatment ladder

Androgenetic alopecia (AGA) — pattern hair loss — is the most common cause of hair loss in both men and women, affecting approximately 50% of men by age 50 and 40% of women by age 70. It is a chronic, progressive condition with a well-characterized mechanism and a clear evidence-based treatment hierarchy. Here's the complete picture.

The mechanism: DHT and follicular miniaturization

Dihydrotestosterone (DHT) and the androgen receptor

In genetically susceptible hair follicles, DHT — the more potent androgen metabolite of testosterone — binds to androgen receptors in dermal papilla cells and triggers a molecular program that progressively shrinks the follicle:

DHT binds AR in dermal papilla → upregulates DKK-1 (Dickkopf-related protein 1) and TGF-β2 → inhibits Wnt/β-catenin signaling that normally sustains anagen
Anagen progressively shortens with each hair cycle — from years to months to weeks
Follicle miniaturizes: Each cycle produces a thinner, shorter, less pigmented hair (terminal → intermediate → vellus)
Eventually the follicle produces only a fine colorless vellus hair, then ceases production entirely

Key point: The susceptibility is in the androgen receptor sensitivity of the follicle, not in systemic DHT levels. Men with AGA typically have normal serum DHT — their scalp follicles respond more vigorously to DHT than non-susceptible follicles.

5-alpha reductase (5AR): The enzyme that converts testosterone → DHT. Type II 5AR is expressed in scalp follicles — the primary target of finasteride (type II inhibitor) and dutasteride (type I + II inhibitor).

Why specific scalp regions are vulnerable

AGA follows predictable patterns (frontal and vertex scalp in men; crown thinning in women) because androgen receptor expression is highest in follicles in these regions. Occipital and lateral scalp follicles have lower AR density and are largely DHT-resistant — which is why these areas are used as donor sites in hair transplantation.

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Classification: staging the progression

Norwood-Hamilton scale (men)

| Stage | Description |
|---|---|
| I | No significant recession |
| II | Slight recession at temples |
| III | Deeper temporal recession; III vertex = early crown involvement |
| IV | Significant frontal + crown loss; bridge of hair between them |
| V | Bridge narrows; frontal and crown areas nearly merged |
| VI | Frontal and crown fully merged; narrow band of hair remaining |
| VII | Only band of hair at sides and back; severe |

Ludwig scale (women)

Women typically show diffuse thinning across the crown with preservation of the frontal hairline (unlike the frontal recession pattern common in men):

Ludwig I: Mild widening of the central part
Ludwig II: More pronounced central thinning; part noticeably wider
Ludwig III: Extensive central scalp thinning; frontal hairline maintained

Female AGA is frequently confused with telogen effluvium — the key distinction is that AGA shows miniaturized (fine, short) hairs on dermoscopy in the affected area; TE shows normal caliber hairs with increased shedding. Both can co-exist.

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Evidence-based treatments

Minoxidil — the vasodilator that became a hair drug

Minoxidil was originally developed as an oral antihypertensive. Hypertrichosis (excess hair growth) as a side effect led to its development as a topical hair treatment.

Mechanism: KATP channel opener → vasodilation of scalp arterioles → improved follicular blood flow + VEGF upregulation → prolonged anagen duration. Does not address DHT; works through a completely different pathway.

Evidence (topical):
*Olsen et al. (1985, JAAD):* Pivotal RCT establishing 2% minoxidil for female AGA — significant hair count improvement vs. placebo at 32 weeks
DeVillez et al. (1994): 5% vs. 2% minoxidil in men — 5% significantly superior; 5% now standard for men; 2% or 5% for women (5% foam in women to avoid facial hair)

Evidence (low-dose oral):
*Ramos et al. (2020, JAAD):* Systematic review of low-dose oral minoxidil (0.25–5 mg/day) for AGA — significant efficacy across doses; 1–5 mg for men, 0.25–2.5 mg for women; lower side effect burden than topical for some patients (avoids scalp irritation; better consistency)
FDA-approved only in topical form; oral is off-label but widely prescribed

Timeline: Visible response at 3–4 months; maximum effect at 6–12 months. Must continue indefinitely — hair returns to pre-treatment trajectory within 3–6 months of stopping.

Side effects topical: Scalp irritation, contact dermatitis (often to propylene glycol in solution; foam formulation avoids this), initial increased shedding (telogen hairs shed as new anagen begins — lasts 4–8 weeks).

Side effects oral: Fluid retention, hypertrichosis (fine body hair), tachycardia at higher doses (uncommon at 0.5–2.5 mg range used for hair).

Finasteride — the DHT blocker

1 mg finasteride reduces scalp DHT by ~60–70% through selective type II 5AR inhibition.

Evidence:
*Kaufman et al. (1998, JAAD):* 1,553 men, finasteride 1 mg vs. placebo, 2 years — 83% maintained or increased hair count vs. 48% continuing to lose in placebo; +107 hairs/cm² at vertex
5-year extension: Maintained efficacy; discontinuation → return to pre-treatment trajectory within 12 months

For women: Off-label use at 1–2.5 mg/day for postmenopausal women with AGA (requires contraception in premenopausal women — absolutely contraindicated in pregnancy).

Side effects: Sexual dysfunction in ~1–4% (decreased libido, erectile dysfunction, ejaculation disorder); post-finasteride syndrome (persistent effects in subset after stopping — see finasteride guide for full discussion).

Dutasteride — dual 5AR inhibition

Inhibits both type I and type II 5AR → ~90% scalp DHT reduction (vs. ~65% for finasteride).

Evidence:
*Olsen et al. (2006, JAAD):* Head-to-head RCT: dutasteride 0.5 mg vs. finasteride 1 mg vs. placebo — dutasteride superior to finasteride at all time points for hair count
FDA-approved for BPH but not AGA (approved for AGA in South Korea and Japan)

Clinical implication: Modestly superior to finasteride for hair; very long half-life (~5 weeks) means if side effects occur, they take longer to resolve after discontinuation.

Combination: minoxidil + finasteride/dutasteride

The strongest medical protocol for AGA. Complementary mechanisms: finasteride/dutasteride reduces the hormonal driver; minoxidil directly stimulates follicular activity through KATP/VEGF — additive without interaction.

*Khandpur et al. (2020, JAMA Dermatology):* RCT — combination significantly superior to either monotherapy for hair density improvement.

PRP (platelet-rich plasma)

Growth factor injection into the scalp. Modest evidence for AGA — see hair loss treatment guide for full detail. Appropriate as an adjunct to medical therapy, not as a replacement.

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Hair transplantation

Follicular unit extraction (FUE) vs. strip (FUT)

FUT (follicular unit transplant / strip method): Strip of scalp excised from the occipital donor area → dissected into individual follicular units → transplanted. Leaves a linear scar. Higher yield per session; appropriate for patients needing large numbers of grafts.

FUE (follicular unit extraction): Individual follicular units extracted directly from the scalp with a micro-punch tool → transplanted. No linear scar; slower; appropriate for patients wanting the ability to wear very short hair.

Who is a candidate

Norwood III–VII in men with stable (not rapidly progressing) hair loss
Adequate donor density (occipital and temporal area must have sufficient DHT-resistant follicles)
Realistic expectations (transplant redistributes existing hair; doesn't add new hair; donor supply is finite)
On or willing to start medical therapy (finasteride/minoxidil) to preserve non-transplanted hair

Critical point: transplant + medical therapy

Hair transplantation moves DHT-resistant donor follicles to bald areas — those follicles remain DHT-resistant and grow permanently. However, native hairs in the transplanted area and in untreated zones continue to miniaturize unless finasteride/minoxidil is used. Transplant without medical therapy means continuing to lose non-transplanted hairs over time.

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Treatment ladder by severity

| Severity | First-line | Adjunct | Consider |
|---|---|---|---|
| Early (NW II–III / Ludwig I) | Minoxidil + finasteride | Niacinamide, saw palmetto | PRP series |
| Moderate (NW III–V / Ludwig II) | Minoxidil + finasteride | PRP | Dutasteride if inadequate response |
| Severe (NW V–VII / Ludwig III) | Finasteride + minoxidil | Dutasteride | FUE/FUT consultation |
| Stabilized after transplant | Finasteride + minoxidil (lifelong) | — | Touch-up grafts as needed |

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