Hair Loss — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Hair loss (alopecia) is the partial or complete loss of hair from the scalp or body, affecting millions of people worldwide and frequently causing significant psychological distress. Hair normally grows in a cycle: anagen (active growth — 2-7 years, 85-90% of hairs at any time), catagen (transitional — 2-4 weeks), telogen (resting — 3-4 months), and exogen (shedding — 50-100 hairs per day is normal). Alopecia is classified as non-scarring (reversible — most common) or scarring (cicatricial — permanent follicle destruction, much less common). Non-scarring causes: androgenetic alopecia (pattern baldness — the most common cause, accounting for 95% of male and 80% of female hair loss); telogen effluvium (diffuse shedding after physiological stress — childbirth, illness, surgery, rapid weight loss, severe emotional stress); alopecia areata (autoimmune — patchy, sudden, non-scarring); traction alopecia (from tight hairstyles); tinea capitis (fungal scalp infection — mainly in children); and systemic disorders (hypothyroidism, iron deficiency, nutritional deficiencies). Scarring alopecias include: lichen planopilaris, discoid lupus erythematosus, frontal fibrosing alopecia, and folliculitis decalvans. Correct classification determines treatment — a scalp biopsy may be required.

Androgenetic alopecia (AGA): genetically determined sensitivity of hair follicles to dihydrotestosterone (DHT — converted from testosterone by 5-alpha-reductase type 2 in the follicle). DHT miniaturises the follicle through progressive shortening of the anagen phase, eventually replacing terminal hairs with vellus (fine, unpigmented) hairs. Affected in a characteristic pattern: men — frontoparietal recession and vertex thinning (Hamilton-Norwood scale); women — diffuse crown thinning with frontal hairline preservation (Ludwig scale). Strong hereditary component — polygenic. Telogen effluvium: a sudden physiological or psychological shock causes a large proportion of hairs to synchronously enter telogen (resting phase) simultaneously; 2-4 months later, these hairs are shed together. Common triggers: childbirth (postpartum telogen effluvium — extremely common, self-limiting), febrile illness (influenza, COVID-19), major surgery, severe physical trauma, crash dieting or rapid weight loss, iron deficiency, hypothyroidism, and severe emotional stress. Alopecia areata (AA): organ-specific autoimmune T-cell attack on anagen follicles — driven by NKG2D/JAK-STAT inflammatory pathway. Triggers include stress and viral infection. Associated with thyroid disease, vitiligo, atopy, and other autoimmune conditions. Three forms: alopecia areata (patchy — one or more smooth, round bald patches), alopecia totalis (complete scalp hair loss), alopecia universalis (loss of all body hair). Tinea capitis: Trichophyton or Microsporum dermatophyte infection — most common in prepubertal children; may cause kerion (boggy inflammatory mass). Drug-induced hair loss: chemotherapy (anagen effluvium — synchronous anagen follicle arrest, usually reversible 3-6 months after stopping), anticoagulants (warfarin, heparin), retinoids, antithyroid drugs, lithium, and valproate.

Androgenetic alopecia: gradual, progressive miniaturisation of hair beginning at characteristic sites — frontal recession and vertex (men); diffuse crown thinning with frontal hairline maintained (women). Hair becomes finer, shorter, and lighter-coloured. No scalp redness, scaling, or symptoms (non-inflammatory). Onset typically in 20s-30s in men; later in women, often accelerating around menopause. Telogen effluvium: sudden onset diffuse scalp hair shedding — excessive hair on the pillow, in the brush, and in the shower drain; positive hair pull test (more than 2-3 hairs per pull of approximately 25-30 hairs — confirms active shedding). Typically begins 2-4 months after the triggering event; resolves over 6-12 months (unless the cause persists). Alopecia areata: sudden onset of one or more smooth, round or oval areas of complete hair loss — the skin in the affected area is smooth with no scarring or scaling; 'exclamation mark' hairs (short, tapered hairs at the patch margins — pathognomonic); may affect eyebrows, eyelashes, beard, and body hair. Nail pitting (fine pitting of the nail surface) and trachyonychia (rough, longitudinally ridged nails) are associated in some patients. Tinea capitis: scaly, inflamed, boggy scalp patches with broken hairs ('black dot' appearance); hair loss in affected area; cervical and occipital lymphadenopathy. Scalp biopsy features: retained follicular architecture (non-scarring) vs loss of follicles and replacement with fibrous tracts (scarring alopecia).

Clinical assessment: detailed history (pattern of loss, rate of progression, timeline, triggers including recent stress, illness, childbirth, medications, diet, family history); scalp examination (pattern of loss, presence of hair follicle orifices, presence of inflammation or scarring); hair pull test; dermoscopy (trichoscopy — handheld dermoscope, assesses miniaturisation, yellow/black dots, exclamation mark hairs, perifollicular scaling). Trichoscopy (dermoscopy of the scalp): AGA — variable hair shaft diameter (heterogeneity) and peripilar signs; AA — yellow dots (keratin plug in empty follicles), black dots (broken off hairs), and exclamation mark hairs; telogen effluvium — increased proportion of short regrowing hairs. Blood tests to identify correctable causes: serum ferritin (iron store — optimal above 70 mcg/L for hair; below 30 mcg/L causes telogen effluvium); TSH (thyroid function — hypothyroidism causes diffuse hair loss); FBC; SHBG, androgens (testosterone, DHEA-S — raised in women with androgenetic or hyperandrogenic alopecia); ANA (if autoimmune alopecia suspected). Scalp biopsy (4mm punch biopsy): definitive investigation for scarring alopecias and when diagnosis is uncertain — characterises the type of follicular inflammation, degree of fibrosis, and follicle counts. Scalp Wood's lamp (UV light): Microsporum tinea capitis fluoresces green. Scalp culture (tinea capitis): fungal culture of scalp hair and skin scrapings.

Androgenetic alopecia (AGA): Topical minoxidil (2% or 5% solution or 5% foam): the first-line over-the-counter treatment — applied to the scalp twice daily; vasodilates the microvasculature, prolongs anagen, and reverses miniaturisation; halts progression in 80% and promotes regrowth in 60%; requires continuous use (shedding resumes on stopping); new once-daily oral minoxidil (2.5mg for women, 5mg for men — off-label) is increasingly used with good efficacy. Finasteride 1mg daily (oral — men only, not women of childbearing age): 5-alpha-reductase type 2 inhibitor — blocks DHT production in the follicle; stabilises AGA in 90% and promotes regrowth in 65% (PLESS trial); requires 3-6 months to assess response; requires continuous use; side effects — sexual dysfunction (erectile dysfunction, reduced libido — 2-4%, often reversible on stopping); post-finasteride syndrome (controversial — persistent sexual and neurological effects in some men after stopping). Dutasteride 0.5mg daily: more potent than finasteride (inhibits both type 1 and 2 5-alpha-reductase — reduces DHT more completely); increasingly used for AGA in men and off-label in women (contraindicated in pregnancy). Hair transplant surgery: follicular unit extraction (FUE) or follicular unit transplantation (FUT/strip method) — moves DHT-resistant occipital donor follicles to the frontal and vertex areas; achieves permanent cosmetically natural results; suitable for stable AGA. Telogen effluvium: address the underlying cause (treat iron deficiency, correct hypothyroidism, ensure adequate protein intake); the condition typically self-resolves within 6-12 months of trigger removal. Alopecia areata: intralesional triamcinolone acetonide (2.5-5 mg/mL every 4-6 weeks — most effective for patchy AA, less than 50% scalp involvement); topical potent corticosteroids (betamethasone, clobetasol); immunotherapy (diphencyprone DPCP — topical sensitiser causing controlled allergic reaction — effective in moderate-severe AA); JAK inhibitors — baricitinib (4mg daily) and ritlecitinib (50mg daily) are the first FDA/EMA-approved oral targeted treatments for severe AA (above 50% scalp involvement); achieve significant hair regrowth in 30-40% of patients (BRAVE-AA trials). Tinea capitis: oral antifungal (griseofulvin — traditional first-line for children; terbinafine, itraconazole for Trichophyton species; 6-8 weeks treatment); selenium sulfide or ketoconazole shampoo to reduce shedding; treat household contacts and pets (source). Scarring alopecias: require early aggressive treatment to prevent permanent follicle loss — hydroxychloroquine, systemic corticosteroids, and doxycycline for lichen planopilaris; dermatology referral essential.

Hair loss carries significant psychological and, in some cases, physical complications depending on its type and severity. Psychological complications: alopecia has a disproportionately large impact on psychological wellbeing relative to its direct physical consequences — anxiety and depression affect 40-60% of people with significant alopecia; body image disturbance, reduced self-esteem, and social withdrawal are common across all alopecia types. The psychological burden is particularly severe in alopecia areata (AAA) — a chronic, unpredictable condition — and in women with androgenetic alopecia, where social stigma and beauty norms create greater distress. Alopecia totalis and universalis: alopecia areata can progress to complete scalp hair loss (alopecia totalis) in 5-10% of cases or complete body hair loss (alopecia universalis) — including eyebrows, eyelashes, and body hair — which has additional physical consequences including lack of nasal hair (increased respiratory infections), absent eyelashes (corneal exposure), and loss of thermal protection. Scarring alopecia complications: irreversible follicular destruction in conditions like lichen planopilaris, discoid lupus erythematosus, and folliculitis decalvans causes permanent bald patches and may involve scalp tenderness, burning, and progressive spread if untreated. Underlying medical condition identification: diffuse hair loss can be the presenting sign of significant conditions including hypothyroidism, SLE, secondary syphilis, and iron deficiency anaemia — missed diagnosis perpetuates both hair loss and the primary condition.

Androgenetic alopecia cannot be prevented — it is genetically determined. However, progression can be slowed significantly with early treatment initiation: starting minoxidil and finasteride as soon as AGA is noticed in men is far more effective than starting after extensive hair loss has occurred. Nutritional optimisation: ensure adequate dietary iron (haem iron from red meat and legumes — optimal serum ferritin above 70 mcg/L for hair); protein (at least 50g daily — hair is 95% protein/keratin); biotin (rarely deficient but often included in hair supplements); zinc; vitamin D. Crash dieting and rapid weight loss trigger telogen effluvium — aim for gradual weight loss (less than 0.5-1 kg per week) to protect hair. Hairstyle and traction: avoid tight hairstyles (braids, weaves, high ponytails) pulling on the follicles — this causes traction alopecia, which can eventually become scarring; vary the parting direction. Heat damage: limit use of blow dryers, straighteners, and curling tongs — use heat protectant sprays. Chemical treatments: limit frequency of bleaching, perming, and relaxing treatments. Scalp health: wash hair regularly (sebum buildup is not a cause of AGA but contributes to itching and dandruff); use mild shampoo appropriate for hair type. Psychological support: hair loss causes significant psychological distress and reduced quality of life — do not dismiss its impact; psychological support, support groups (Alopecia UK), and clinical psychology referral for severe cases.

See a GP for hair loss that is sudden, diffuse, or accompanied by other symptoms (fatigue, weight changes, cold intolerance — hypothyroidism; irregular periods, acne, hirsutism — PCOS; rash — lupus or fungal infection). Request dermatology referral for: patchy alopecia (to exclude alopecia areata and scarring alopecia), scalp redness, scaling, or boggy plaques (tinea capitis or scarring alopecia), rapidly progressive hair loss not responding to standard treatment, and suspected scarring alopecia (where delay causes permanent follicle destruction — early treatment is critical). Women of reproductive age with diffuse hair thinning should have serum ferritin, TSH, and androgens measured. Men noting early androgenetic alopecia should discuss finasteride and minoxidil — the earlier treatment starts, the better the outcome. Seek urgent dermatology review if scalp skin has areas of persistent redness, ulceration, or atrophy with hair loss — possible lupus erythematosus or cutaneous malignancy.