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6
Trichology for GP · Chapter Six
Female Pattern Hair Loss
Multi-factorial crown thinning — hormonal, nutritional, and androgenetic contributions
Overview
Pathophysiology
Classification
Clinical Features
Diagnosis
Treatment
Quick Recall
Anki Cards
References
GP-Level Analogy

"Female pattern hair loss is like a garden where the central lawn is slowly thinning while the border plants stay healthy — but unlike a man's lawn, which responds primarily to one weedkiller (DHT), a woman's lawn can be damaged by five different chemicals simultaneously: androgens, low oestrogen, thyroid imbalance, iron deficiency, and genetics. The treatment approach must address all five possible culprits."

Female pattern hair loss (FPHL) is the most common cause of hair loss in women, affecting approximately 40% of women by age 70. It is frequently under-recognised and under-treated in primary care, partly because its presentation is more diffuse than male AGA, and partly because it is often dismissed as normal ageing.

FPHL is distinct from MAGA in several key ways: it is multi-factorial (not purely androgenetic), it rarely causes complete baldness, it is more emotionally burdensome relative to its visible severity, and it requires a broader investigation panel to identify contributing causes.

Why FPHL is different from MAGA

Aetiology
Multi-factorial
Androgens play a role in approximately 50% of cases, but oestrogen deficiency, iron deficiency, thyroid disease, and genetic factors all contribute independently.
Pattern
Diffuse central thinning
Thinning of the crown with widening of the central part — not the M-shaped bitemporal recession of MAGA. Hairline is typically preserved.
Prognosis
Rarely complete baldness
Even severe FPHL does not usually cause the horseshoe pattern of MAGA. Women retain a fringe and some vertex coverage.
Key GP Insight

Never tell a woman with FPHL it is "just hormones" or "normal ageing." This dismissal delays treatment of contributing factors (iron deficiency, thyroid disease) and withholds effective therapies. Every woman with diffuse thinning deserves a structured history, examination, and targeted blood panel.

Pathophysiology — the DOTGP contributors

FPHL is best understood through the DOTGP framework — five contributing pathways that can act independently or in combination to drive follicular miniaturisation in women.

D
DHT / Androgens
5-alpha reductase overactivity or elevated androgens (PCOS, CAH). ~50% of FPHL cases.
O
Oestrogen deficiency
Menopause, post-OCP, perimenopause. Oestrogen prolongs anagen — its loss accelerates miniaturisation.
T
Thyroid disease
Both hypo- and hyperthyroidism impair the hair cycle. Often co-existing and treatable.
G
Genetics
Polygenic. Maternal and paternal family history of hair loss. Accounts for underlying susceptibility.
P
PCOS / Iron
PCOS drives androgen excess. Iron deficiency (ferritin <70) perpetuates miniaturisation independently.
Fig 6.1 — FPHL: five contributing pathways to follicular miniaturisation
Follicular Miniaturisation D — DHT / Androgens PCOS, CAH, elevated DHEAS 5-alpha reductase overactivity O — Oestrogen drop Menopause, perimenopause, OCP T — Thyroid disease Hypo/hyperthyroid → TE + FPHL G — Genetics AR sensitivity, polygenic loci Family Hx both parents P — PCOS / Iron deficiency Ferritin <70; elevated FAI Irregular cycles, acne, hirsutism Multiple contributors can act simultaneously — all must be assessed
Fig 6.1: The five contributing pathways to FPHL (DOTGP). Unlike MAGA where DHT is the dominant driver, FPHL may result from any combination of these five pathways. Identifying and treating each contributing factor is essential for optimal outcomes.

The role of oestrogen

Oestrogen has a direct anti-androgenic effect on the hair follicle — it increases SHBG (reducing free androgens), stimulates aromatase (converting androgens to oestrogens at the follicle), and directly prolongs the anagen phase. The dramatic decline in oestrogen at menopause explains why FPHL commonly worsens or first appears in the perimenopausal period.

GP Analogy — Oestrogen and Hair

"Oestrogen is the hair follicle's bodyguard. While it's around in sufficient quantities, it neutralises the effects of circulating androgens on the follicle. When it leaves at menopause, the follicle is left unprotected — and androgens that were previously blocked can now cause miniaturisation."

Iron deficiency — a common and reversible contributor

Ferritin is a cofactor for ribonucleotide reductase — the rate-limiting enzyme in DNA synthesis in proliferating matrix cells. Ferritin <30 mcg/L is associated with diffuse hair loss even without anaemia. The target for hair is ferritin >70 mcg/L. Iron deficiency is extremely common in premenopausal women and is the most frequently missed and most easily treated contributing factor.

Classification scales for FPHL

Two scales are in clinical use: the Ludwig scale (most widely used) and the Sinclair scale. Both describe progression of crown-centred diffuse thinning.

Fig 6.2 — Ludwig scale and Sinclair scale: schematic top-view diagrams
Ludwig Scale Ludwig I Mild central widening Ludwig II Moderate thinning scalp visible Ludwig III Severe — near- complete loss Sinclair Scale Grade 1: No part widening Grade 2: Part line widening Grade 3: Crown shows through Grade 4: Near-complete frontal loss Grade 5: Only fringe remains 5-grade linear scale Ludwig vs Sinclair: key differences Ludwig: 3 grades — widely used in research, simple for clinical communication with patients Sinclair: 5 grades — more granular, better for monitoring treatment response over time Both describe crown-centred diffuse thinning with preserved hairline — in contrast to MAGA GP note: A preserved frontal hairline in a woman with diffuse thinning = FPHL, not FFA FFA shows frontotemporal hairline recession with perifollicular scale — always examine the hairline
Fig 6.2: Ludwig and Sinclair classification scales for FPHL. Ludwig grades I–III describe increasing crown thinning. The critical GP finding: hairline is preserved in FPHL. If the hairline is receding with scale, consider FFA (urgent referral).

Clinical features

FPHL presents as gradual diffuse thinning of the crown and upper scalp, most visible as a widened central part. The frontal hairline is typically preserved — a key distinguishing feature from FFA.

Fig 6.3 — Clinical examination findings in FPHL
Preserved frontal hairline KEY difference from FFA Widened central part Earliest sign of FPHL Crown thinning (diffuse) Calibre diversity — no scarring Temporal fringe preserved Full density at temples Occipital fringe preserved Complete baldness rare in women
Fig 6.3: Clinical examination findings in FPHL (top view). The widened central part and diffuse crown thinning with preserved frontal and temporal hairline are pathognomonic. The preserved hairline distinguishes FPHL from FFA — always examine the hairline directly.

Features of androgenisation to look for

FeatureSignificanceAssociated condition
Hirsutism (face, chest, abdomen)Excess androgen productionPCOS, late-onset CAH, androgen-secreting tumour
Acne (adult, treatment-resistant)Sebaceous gland androgen excessPCOS, hyperandrogenism
Irregular menstrual cyclesAnovulation from androgen excessPCOS (most common)
Acanthosis nigricansInsulin resistance markerPCOS, metabolic syndrome
Clitoromegaly, deepening voiceSevere virilisationAndrogen-secreting tumour — urgent workup
None of the aboveNon-hyperandrogenic FPHLGenetic/oestrogen-deficiency mediated (~50%)
Red flags requiring urgent investigation

Rapid hair loss (>50% over 3–6 months) + virilisation features = possible androgen-secreting tumour. Urgent testosterone, DHEAS, and pelvic/adrenal imaging. Do not start hormonal treatments until excluded.

Diagnosis and investigations

FPHL diagnosis is primarily clinical but requires a broader investigation panel than MAGA because of its multi-factorial nature.

Blood tests — the FTVDZ panel

All women with FPHL or diffuse hair loss should have the FTVDZ panel:

TestTarget / thresholdSignificance
Ferritin>70 mcg/L for hair; <30 = deficientMost common treatable contributor in premenopausal women
TSH + free T4TSH 0.4–4.5 mIU/LBoth hypo and hyperthyroid cause diffuse HL
Vitamin D (25-OH)>50 nmol/LDeficiency associated with diffuse hair loss
DHEA-S + free androgen indexFAI <5 in womenIf hirsutism, acne, PCOS features present
Zinc + B12Zinc >10 µmol/L; B12 >200 ng/LVegetarians/vegans; restrict diets; check if symptomatic
FBC + LFTHb, MCV — rule out anaemiaScreen for anaemia; LFTs before systemic treatment
ANA (if features)Titre >1:80If photosensitivity, rash, arthralgia — screen for lupus

Trichoscopy in FPHL

FindingSignificance
Hair calibre diversity (thick + thin shafts)Miniaturisation — diagnostic of AGA/FPHL
Miniaturisation ratio >20% (vertex zone)Confirms FPHL in right context
Peripilar brown haloPerifollicular inflammation — active FPHL
Single-hair follicular units (from loss of companion hairs)Reflects advanced miniaturisation
Yellow dots (advanced)Severely miniaturised follicles producing vellus only
Normal calibre throughout + positive pull testCo-existing telogen effluvium — not FPHL alone
Distinguishing FPHL from CTE (chronic telogen effluvium)

Both are common, both cause diffuse thinning, and both frequently co-exist. Key difference: FPHL shows calibre diversity on trichoscopy (miniaturised + terminal hairs). CTE shows uniform calibre — all hairs the same thickness. Positive pull test across all zones favours CTE. Many women have both simultaneously — treat both.

Treatment of FPHL

Treatment follows the SMART approach: treat the underlying contributors first, then add disease-modifying therapy.

Fig 6.4 — SMART treatment framework for FPHL
S Screen & Supplement Iron to >70 Thyroid Rx Vit D >50 Zinc, B12 M Minoxidil Topical 2% BD or 5% OD Oral 0.625– 1.25 mg/day Level I evidence Lifelong A Anti-androgen Spironolactone 25–200 mg/day If features of hyperandrogen. Contraception required if fertile R Review & Refer Photo at baseline Review 6–12 mo Refer if: Refractory Scarring features Rapid virilisation T Tell her Lifelong Rx 6–12 mo to respond Stop = lose gains
Fig 6.4: SMART treatment framework. Screen and supplement first (address ferritin, thyroid, Vit D), then Minoxidil (first-line), then Anti-androgens (spironolactone if indicated), then Review and Refer, and throughout Tell her realistic expectations.

Spironolactone — prescribing guide

AspectDetail
DoseStart 25–50 mg/day; increase to 100–200 mg/day as tolerated over 2–3 months
MechanismAldosterone antagonist and androgen receptor blocker; reduces adrenal androgen production
Indication in FPHLFeatures of hyperandrogenism (PCOS, hirsutism, acne) OR androgenetic FPHL without contraindications
ContraceptionMandatory in fertile women — teratogenic (feminisation of male fetus). Use reliable contraception throughout
MonitoringPotassium and renal function at baseline and 4–6 weeks (hyperkalaemia risk)
Side effectsBreast tenderness, menstrual irregularity, postural hypotension, polyuria, fatigue
Response6–12 months. 40–50% stabilisation; some regrowth. Lifelong treatment required

OCP considerations in FPHL

Combined oral contraceptive pills with anti-androgenic progestins (drospirenone, cyproterone acetate, dienogest) can be beneficial in women with FPHL and hyperandrogenism. Avoid OCPs with androgenic progestins (levonorgestrel, norgestrel) — these can worsen FPHL. When advising on OCP choice for FPHL patients, always check the progestin component.

Treatment counselling points

1. Treatment is lifelong — stopping any effective treatment loses gains within months. 2. Response takes 6–12 months minimum — photographs at baseline are essential for objective comparison. 3. Treating iron deficiency and thyroid disease alone can produce significant improvement before adding minoxidil. 4. Combining supplement treatment with minoxidil is more effective than either alone. 5. Managing expectations is as important as prescribing.

Quick Recall

Contributors: DOTGP

D·O·T·G·P
  • DHT / androgens (PCOS, CAH)
  • Oestrogen deficiency (menopause, OCP)
  • Thyroid disease (hypo or hyper)
  • Genetics (polygenic, both parents)
  • PCOS / iron deficiency (ferritin <70)

Investigation: FTVDZ

F·T·V·D·Z
  • Ferritin — target >70 mcg/L
  • TSH + T4 — thyroid screen
  • Vitamin D — target >50 nmol/L
  • DHEAS + free androgen index
  • Zinc + B12 (second line)

Treatment: SMART

S·M·A·R·T
  • Screen + Supplement (iron, thyroid, Vit D)
  • Minoxidil — 2%/5% topical or oral
  • Anti-androgen (spironolactone)
  • Review at 6–12 months; Refer if refractory
  • Tell expectations (lifelong, 6–12 mo onset)

FPHL vs FFA: key distinction

PRESERVED HAIRLINE?
  • FPHL: hairline PRESERVED, crown thins
  • FFA: hairline RECEDES, band of loss
  • FFA: perifollicular scale + erythema
  • FFA: urgent referral — scarring!
  • Examine hairline in EVERY woman

GP Quick-Reference Action Card

PresentationKey testsFirst-line treatmentAdd ifRefer if
Crown thinning, preserved hairline, premenopausal FFTVDZ panelCorrect deficiencies + minoxidil 2%Spiro if PCOS/hirsutismNo response 12 months
Crown thinning, post-menopausalFTVDZ + FAIMinoxidil 5% or oral + supplementHRT discussionRefractory or rapid
Thinning + hirsutism + irregular cyclesFAI, DHEAS, SHBG, glucoseEndocrine workup firstAnti-androgenic OCP or spiroIf DHEAS very high
Rapid loss + virilisation featuresUrgent testosterone + imagingDo NOT start hormonal Rx—URGENT — androgen tumour
Thinning + frontotemporal recession + scaleDermoscopy + biopsyDo NOT start minoxidil alone—URGENT — possible FFA

Anki Flashcard Deck — Chapter 6

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References

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← Ch. 5: Male Pattern Hair Loss Chapter Index Ch. 7: Telogen Effluvium →