Alopecia (Hair Loss)

Alopecia means hair loss. It is not one single disease. It is a group of conditions where hair becomes thin, breaks easily, falls out in patches, or stops growing in some or all hair-bearing areas of the body (scalp, eyebrows, beard, eyelashes, body hair). Alopecia can be temporary or permanent. In some types, hair roots (hair follicles) are still alive and can grow again after the trigger is removed (non-scarring alopecia). In other types, the follicles are destroyed by inflammation and replaced by scar tissue (scarring or “cicatricial” alopecia). Because the causes are different—genes, hormones, immune system, infections, nutrition, medicines, hairstyle practices, and skin diseases—the treatment also differs. Good diagnosis looks at the pattern of loss, hair shaft quality, scalp skin changes, and whole-body health.

Alopecia means hair loss. It happens when hair falls out faster than it grows back, or when hair follicles are damaged and stop making hair. Alopecia can be temporary (hair grows back), recurrent (comes and goes), or permanent (hair follicles are scarred and cannot grow hair again). It can affect the scalp, beard, eyebrows, eyelashes, and any hair-bearing skin. The causes range from genetics and hormones (pattern hair loss), immune attack on hair follicles (alopecia areata), stress or illness (telogen effluvium), tight hairstyles or chemicals (traction/chemical alopecia), fungal infections (tinea capitis), to scarring skin diseases (cicatricial alopecias). Diagnosis is usually clinical, supported by trichoscopy (dermoscopy of hair/scalp), simple office tests, lab tests, and sometimes a scalp biopsy when the cause is unclear. (Typical trichoscopy patterns that help tell types apart are well described in recent reviews.) ScienceDirect

Other names

• Hair loss

• Baldness (common word, especially for male pattern hair loss)

• Pattern hair loss (another name for androgenetic alopecia)

• Patchy hair loss (often used when talking about alopecia areata)

• Hair fall (everyday term many people use)

• Pattern hair loss = Androgenetic alopecia (male pattern baldness; female pattern hair loss)

• Patchy autoimmune hair loss = Alopecia areata (severe forms: totalis = whole scalp; universalis = whole body)

• Sudden shedding = Telogen effluvium

• Tight-hairstyle hair loss = Traction alopecia

• Fungal hair loss = Tinea capitis

• Scarring hair loss group = Cicatricial alopecias (e.g., lichen planopilaris)

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Types of alopecia

Non-scarring (hair follicles survive; regrowth is possible)

1. Androgenetic alopecia (pattern hair loss)
   The most common type. Driven by genes and hormones (DHT). In men it causes a receding hairline and thinning at the crown. In women it causes a wider part and diffuse thinning on the top.

2. Alopecia areata (patchy, totalis, universalis)
   An autoimmune disease where the immune system attacks hair follicles. It causes smooth, round patches (patchy), complete scalp loss (totalis), or complete body hair loss (universalis).

3. Telogen effluvium (acute or chronic)
   Excess hairs shift into the resting (telogen) phase after a body stress (illness, fever, surgery, childbirth, crash diet, severe emotional stress, COVID-19). Shedding starts 2–3 months later and is diffuse.

4. Anagen effluvium
   Sudden loss of growing hairs due to toxic injury to hair matrix cells (e.g., chemotherapy, radiation, severe poisoning). Shedding can be rapid and pronounced.

5. Traction alopecia
   Hair loss from constant pulling (tight braids, ponytails, weaves, rollers, extensions). Early stages are reversible; long-term traction can scar.

6. Trichotillomania
   Hair loss from repeated hair pulling or twisting due to a compulsive behavior. Hairs are broken at different lengths; patches have irregular borders.

7. Tinea capitis
   Fungal infection of the scalp. Often seen in children. Causes scaly patches, black dots (broken hairs), and sometimes swollen, tender areas (kerion).

8. Diffuse alopecia from drugs or toxins
   Many prescription drugs can trigger shedding (e.g., retinoids, some blood thinners, amiodarone, interferons, valproate).

Scarring (cicatricial) alopecias (follicles destroyed; regrowth usually not possible)

9. Lichen planopilaris (LPP)
   Autoimmune inflammation around follicles leads to perifollicular redness and scaling, then scarring.

10. Frontal fibrosing alopecia (FFA)
    A form of LPP, mostly in post-menopausal women; the front hairline recedes in a band-like pattern; eyebrows often thin.

11. Central centrifugal cicatricial alopecia (CCCA)
    Starts at the crown and spreads outward. Seen more often in women of African ancestry. Can be linked to inflammation and sometimes hair care practices.

12. Discoid lupus erythematosus (DLE)
    Autoimmune skin disease causing coin-shaped scaly plaques on the scalp; leaves pale, smooth scars without follicles.

13. Folliculitis decalvans
    Chronic bacterial inflammation around follicles causes pustules and tufted hairs; later scarring occurs.

14. Pseudopelade of Brocq
    Slowly progressive scarring hair loss with small “footprint in snow” patches; cause often unclear.

15. Post-trauma or burn scarring alopecia
    Hair cannot grow through scar tissue after burns, surgery, or deep injuries.

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Causes of alopecia

1. Genetics (family history)
   Pattern hair loss runs in families. Follicles are sensitive to DHT, a hormone that miniaturizes hairs over time.

2. Hormones (DHT, estrogen changes)
   DHT shortens the growth phase; menopause and low estrogen reduce hair density; PCOS in women raises androgens and increases thinning.

3. Autoimmune attack (alopecia areata, LPP, DLE)
   The body’s defense cells mistakenly target hair follicles as if they are foreign, stopping growth or destroying follicles.

4. Physical or emotional stress (telogen effluvium)
   A major stress shifts many hairs into the resting phase at once. Shedding becomes visible a few months later.

5. Pregnancy and postpartum changes
   During pregnancy hair often looks fuller; after delivery many hairs enter rest phase together, causing temporary shedding.

6. Fever or serious illness (including COVID-19)
   High fevers and systemic illness disrupt hair cycling, leading to diffuse shedding weeks later.

7. Nutritional deficiencies (iron, zinc, protein, B12, vitamin D)
   Hair needs building blocks. Low stores (especially low ferritin/iron) and poor protein intake weaken growth.

8. Thyroid disease (hypo- or hyperthyroidism)
   Thyroid hormones control metabolism and hair cycling; imbalance causes diffuse thinning and brittle hair.

9. Medications
   Chemotherapy, retinoids, some beta-blockers, anticoagulants, anticonvulsants, antidepressants, and high-dose vitamin A can cause shedding.

10. Radiation therapy
    Damages rapidly dividing hair cells; loss may be permanent at high doses.

11. Fungal scalp infection (tinea capitis)
    Fungus invades hair shafts and follicles, causing breakage, scale, and sometimes pus.

12. Bacterial folliculitis (folliculitis decalvans)
    Recurrent infection/inflammation around follicles leads to destruction and scarring if not controlled.

13. Hairstyle practices (traction, heat, chemicals)
    Tight styles, frequent heat styling, relaxers, bleaching, and harsh products break hairs and can inflame follicles.

14. Trichotillomania (compulsive hair pulling)
    Repeated pulling breaks hairs and traumatizes follicles; behavior therapy is key to recovery.

15. Autoimmune connective tissue disease (lupus)
    Discoid lupus on the scalp scars follicles; systemic lupus can cause non-scarring shedding too.

16. Seborrheic dermatitis and psoriasis
    These cause scale and inflammation; usually they do not cause permanent loss, but they can worsen breakage and shedding if severe.

17. Syphilis and other systemic infections
    Secondary syphilis can cause “moth-eaten” patchy loss; HIV and other infections can also be associated with diffuse shedding.

18. Endocrine disorders other than thyroid (e.g., high prolactin, PCOS, Cushing’s)
    Hormone imbalances alter hair cycling and increase shedding or miniaturization.

19. Chronic medical illness (kidney, liver disease, major weight loss)
    Long-term illness and malnutrition divert resources away from hair growth.

20. Physical scarring (burns, surgery, radiation scars)
    Scar tissue replaces follicles; hair cannot regrow through mature scars.

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Common symptoms and signs

1. Gradual thinning on the top (widening part in women, receding hairline in men).

2. Bald spots that are smooth and round (alopecia areata) or irregular (fungal infection or pulling).

3. Increased hair on pillow, brush, shower drain (especially in telogen effluvium).

4. Short, broken hairs and uneven lengths (traction, trichotillomania, shaft fragility).

5. Itching or burning of the scalp (inflammatory types).

6. Redness with scale around hair openings (lichen planopilaris, psoriasis, seborrheic dermatitis).

7. Pustules or crusts (folliculitis decalvans, tinea capitis kerion).

8. Smooth, shiny patches without visible openings (a clue to scarring alopecia).

9. Eyebrow, eyelash, or beard loss (alopecia areata, frontal fibrosing alopecia).

10. Widening hair part in women (female pattern hair loss).

11. Receding temples or crown thinning in men (male pattern hair loss).

12. Black dots on scalp (broken hair stubs in tinea capitis).

13. “Exclamation mark” hairs (short hairs tapering at the base in alopecia areata).

14. Nail pitting or ridging (sometimes in alopecia areata).

15. Scalp tenderness or pain (trichodynia) (can occur in inflammatory or stress-related shedding).

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Diagnostic tests

Important note: Doctors choose tests based on your history and scalp findings. Not everyone needs every test. Some tests confirm alopecia type; others search for a trigger or a related disease.

A) Physical examination (clinical observation)

1. Pattern mapping and staging
   The clinician studies where hair is thin and how it changes over time. Common scales are Hamilton-Norwood (men) and Ludwig/Sinclair (women). Pattern and preservation of the frontal hairline vs crown give strong clues.

2. Scalp skin inspection
   Looks for redness, scaling, follicular plugging, pustules, or smooth shiny skin without follicle openings. These features help separate non-scarring from scarring alopecia.

3. Hair shaft inspection
   Checks for broken hairs, “exclamation mark” hairs, black dots, or miniaturized fine hairs. The mix of thick and miniaturized hairs suggests pattern loss.

4. Full-body hair and nail exam
   Loss in eyebrows, lashes, beard, or body hair points toward alopecia areata or endocrine causes. Nail pitting supports alopecia areata.

B) Manual bedside tests (simple office procedures)

5. Hair pull test
   The doctor gently pulls a small bundle of hairs. If many telogen hairs come out, the test is positive and suggests active shedding (telogen effluvium, flare of pattern loss).

6. Hair tug test
   Tests hair shaft strength by pulling on a single hair from both ends. Breakage suggests shaft fragility (over-processing, trichorrhexis).

7. Wash test (60-second or standardized count)
   You avoid washing for a few days, then wash and count shed hairs. High numbers support telogen effluvium.

8. Card test (back-combing against a contrasting card)
   Helps visualize short regrowing hairs vs broken hairs to separate shedding from breakage.

9. Daily comb or shed-count diary
   Tracking daily loss helps show trends and response to treatment over weeks to months.

C) Laboratory and pathological tests

10. Complete blood count (CBC)
    Looks for anemia or signs of systemic illness that can worsen shedding or fragility.

11. Iron studies, especially ferritin
    Low ferritin is linked to increased hair shedding in many people, especially women. Repletion can help if low.

12. Thyroid panel (TSH ± free T4)
    Both low and high thyroid function can cause diffuse hair loss; correcting the imbalance helps hair recovery.

13. Micronutrient tests (vitamin D, B12, zinc; sometimes copper/selenium)
    Deficiencies can contribute to hair problems. Testing is guided by diet and symptoms.

14. Androgen profile in women (total/free testosterone, DHEAS, SHBG)
    If there is acne, irregular periods, or hirsutism, testing helps detect PCOS or other androgen excess.

15. Prolactin (when indicated)
    High prolactin can alter hormones and hair cycling; checked if there are symptoms like breast discharge or cycle changes.

16. Autoimmune screening (ANA, ESR/CRP as guided)
    Considered if there are signs of connective tissue disease, scarring alopecia, or systemic symptoms (rash, joint pain, photosensitivity).

17. Infection tests (RPR/VDRL for syphilis, HIV when indicated)
    Ordered when the pattern suggests infectious causes or there are risk factors.

18. Fungal tests (KOH prep, fungal culture)
    Scalp scale or black dots suggest tinea capitis; KOH can rapidly show fungal elements; culture identifies species.

19. Scalp biopsy (usually 4-mm punch, vertical and horizontal sections)
    The gold standard when the diagnosis is unclear or scarring is suspected. Pathology shows whether follicles are inflamed, miniaturized, or destroyed. Direct immunofluorescence can help in autoimmune scarring diseases.

D) Electrodiagnostic tests (rarely needed; used only in special cases)

20. Quantitative sensory testing or nerve studies of the scalp (selected cases)
    If there is severe scalp pain, burning, or suspected neuropathic itch, doctors may do QST or nerve conduction studies to look for nerve dysfunction. These do not diagnose alopecia itself, but they can explain unusual scalp sensations and guide pain management.

Non-pharmacological treatments (therapies and others)

(Each item: description → purpose → mechanism)

1. Gentle hair care routine
   Use mild shampoo/conditioner; avoid harsh scrubbing/heat.
   Purpose: Reduce day-to-day breakage.
   Mechanism: Lowers mechanical damage to hair shafts and cuticle.

2. Stop tight styles and traction (tight braids, ponytails, extensions)
   Purpose: Prevent traction alopecia and allow recovery.
   Mechanism: Removes constant pulling that weakens follicles.

3. Avoid harsh chemicals (strong relaxers/bleach/frequent dyes)
   Purpose: Protect hair shaft and scalp.
   Mechanism: Limits chemical cuticle damage and scalp irritation.

4. Nutritional optimization (iron, protein, vitamin D, zinc adequate through diet)
   Purpose: Support normal hair cycling.
   Mechanism: Corrects low ferritin/iron and micronutrient gaps linked with shedding. (Ferritin optimization is often advised for telogen effluvium.) PMC+1

5. Stress management (mindfulness, CBT, breathing, yoga)
   Purpose: Reduce stress-triggered shedding flares.
   Mechanism: Dampens neuro-endocrine signals (cortisol) that push hairs into the shedding (telogen) phase.

6. Regular sleep schedule
   Purpose: Normalize hair cycle timing.
   Mechanism: Stabilizes circadian signals that affect follicle cycling.

7. Exercise most days
   Purpose: Improve general health and scalp blood flow.
   Mechanism: Vascular and hormonal benefits may support growth phase (anagen).

8. Smoking cessation
   Purpose: Reduce inflammatory and vascular harm to follicles.
   Mechanism: Improves microcirculation and oxidative stress balance.

9. Sun protection for scalp (hats, SPF sprays)
   Purpose: Prevent sunburn/hyperpigmentation of visible scalp.
   Mechanism: Blocks UV injury to exposed skin and follicles.

10. Camouflage options (fibers, scalp concealers, tinted sprays)
    Purpose: Immediate cosmetic coverage.
    Mechanism: Fills visual gaps to reduce contrast with scalp.

11. Wigs, toppers, and hairpieces
    Purpose: Restore appearance when medical therapy is slow/limited.
    Mechanism: External coverage without affecting follicles.

12. Psychological support / peer groups
    Purpose: Reduce anxiety/depression; improve adherence.
    Mechanism: Coping skills; normalizes expectations.

13. Treat scalp seborrhea/dandruff (gentle medicated shampoos)
    Purpose: Reduce itch/scale that worsens shedding by scratching.
    Mechanism: Lowers yeast load/inflammation at scalp surface.

14. Identify and remove triggers (new meds, crash diets, major illness)
    Purpose: Resolve telogen effluvium source.
    Mechanism: Stops signal that forced synchronized shedding.

15. Low-Level Laser / Light Therapy (LLLT) (comb/helmet at home; several times weekly)
    Purpose: Nonsurgical thickening for pattern loss.
    Mechanism: Photobiomodulation may improve cellular energy and prolong anagen; meta-analyses suggest benefit for pattern hair loss. JCAD+1

16. Microneedling (dermaroller/pen, typically with minoxidil in clinic settings)
    Purpose: Boost regrowth in pattern loss.
    Mechanism: Micro-injury triggers growth factors; improves drug penetration; RCTs show added benefit vs minoxidil alone. (Representative RCTs support this approach.) Europe PMC

17. Platelet-Rich Plasma (PRP) procedures
    Purpose: Thicken hair in pattern loss; sometimes used in alopecia areata.
    Mechanism: Platelet growth factors (PDGF, VEGF) may stimulate follicles; meta-analyses show increased hair density, though protocols vary. Frontiers

18. Topical immunotherapy in clinic (DPCP or SADBE) for severe alopecia areata
    Purpose: Restart hair growth by “retraining” local immunity.
    Mechanism: Creates a controlled allergic reaction that diverts auto-immune attack; pooled analyses show ~65% any regrowth in severe AA, with variable complete responses. JAMA Network

19. Phototherapy for alopecia areata (excimer/UV)
    Purpose: Reduce immune attack on follicles.
    Mechanism: Local immunomodulation with ultraviolet light.

20. Behavior therapy for hair-pulling (if trichotillomania co-exists)
    Purpose: Stop self-pulling hair loss.
    Mechanism: Habit-reversal training; CBT.

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Drug treatments

(Each: what it’s for → class → common adult dose/time → purpose → mechanism → key side effects/safety)
Important: Doses are typical references; your doctor will personalize them. Do not start/stop prescription drugs without medical advice.

1. Minoxidil topical (2%/5% lotion/foam) – pattern loss (men/women)
   Class: Vasodilator hair growth stimulant.
   Dose/time: 1 mL twice daily (solution) or foam as labeled; continuous use needed. FDA-labeled OTC product information confirms use and directions.
   Purpose/Mechanism: Prolongs growth phase (anagen), enlarges miniaturized follicles.
   Key effects: Scalp irritation, initial shed, unwanted facial hair. DailyMed+1

2. Low-dose oral minoxidil (off-label) – pattern loss, some other alopecias
   Class: Systemic vasodilator.
   Dose/time: ~0.25–5 mg once daily; start low and titrate.
   Purpose/Mechanism: Same as topical but systemic. Reviews support efficacy with manageable side effects (hypertrichosis, edema, tachycardia in a minority).
   Safety: Not FDA-approved for alopecia; monitor BP/heart symptoms; avoid in pregnancy. PMC

3. Finasteride 1 mg oral (men) – male pattern hair loss
   Class: 5-alpha-reductase inhibitor (type II).
   Dose/time: 1 mg once daily (long-term).
   Purpose/Mechanism: Lowers scalp DHT that miniaturizes hair follicles.
   Key effects: Sexual side effects, mood changes; pregnancy exposure risk (handle tablets cautiously). FDA labeling confirms indication and dosing. FDA Access Data

4. Dutasteride 0.5 mg oral (off-label for hair loss)
   Class: Dual 5-alpha-reductase inhibitor (type I & II).
   Dose: 0.5 mg daily; may be more potent than finasteride but off-label; similar sexual side effects, teratogenic risk to male fetus.

5. Topical finasteride (compounded sprays/solutions)
   Class: 5-ARI topical (off-label).
   Note: FDA recently warned about adverse effects and lack of approval for compounded topical products; discuss risks and proper counseling. Health

6. Spironolactone oral (women, off-label for FPHL)
   Class: Antiandrogen/aldosterone antagonist.
   Dose: ~50–200 mg/day; monitor potassium and BP.
   Mechanism: Blocks androgen effect at follicle.
   Key effects: Diuresis, menstrual changes, breast tenderness; avoid in pregnancy. (Contemporary reviews support use in women with androgen-driven loss.) PMC

7. Topical corticosteroids (varying potencies) – especially alopecia areata patches
   Class: Anti-inflammatory.
   Dose: Once/twice daily courses with breaks to avoid atrophy.
   Mechanism: Calms immune attack around follicles.
   Key effects: Skin thinning if overused.

8. Intralesional triamcinolone acetonide injections (AA)
   Class: Corticosteroid injected into the dermis.
   Dose/time: Commonly 2.5–5 mg/mL for scalp/face, ~0.1–0.2 mL per cm², every 4–6 weeks; technique guidance widely published.
   Mechanism: Local immune suppression to allow regrowth.
   Key effects: Skin atrophy pits, hypopigmentation if too superficial/high dose. DermNet®+2PMC+2

9. Oral corticosteroid pulses (selected severe AA)
   Class: Systemic anti-inflammatory.
   Dose: Specialist regimens (e.g., short pulses); not for long-term due to systemic risks.
   Mechanism: Strong immune suppression.
   Key effects: Weight gain, mood, glucose, BP, osteoporosis; relapse can occur.

10. Baricitinib oral (AA; adults)
    Class: JAK1/2 inhibitor.
    Dose: 2 mg or 4 mg once daily (per label) for severe AA.
    Mechanism: Blocks JAK-STAT signaling driving autoimmune attack.
    Key effects: Infection risk (e.g., shingles), labs monitoring (lipids, LFTs), VTE warning—follow label. FDA approved June 2022. FDA Access Data

11. Ritlecitinib oral (AA; ≥12 years)
    Class: JAK3/TEC inhibitor.
    Dose: 50 mg once daily (per label).
    Mechanism: Selective JAK pathway blockade to reduce follicle autoimmunity.
    Key effects: Similar immune-related risks; lab monitoring per label. FDA approved June 2023. PMC

12. Deuruxolitinib oral (AA; adults)
    Class: JAK1/2 inhibitor.
    Dose: 8 mg twice daily (per FDA label).
    Mechanism: JAK-STAT blockade; improves SALT scores in severe AA.
    Key effects: Infection, lab abnormalities; boxed warnings similar to JAK class. FDA approved Sept 2024 (Leqselvi). NAAF

13. Anthralin (dithranol) topical (AA)
    Class: Irritant immunotherapy.
    Dose: Short-contact 0.5–1% once daily; start minutes and increase to ~30–60 min as tolerated, then wash off.
    Mechanism: Creates mild dermatitis to modulate local immunity.
    Key effects: Irritation, staining of skin and fabrics. PMC+1

14. Topical immunotherapy (DPCP / SADBE) in clinic
    Class: Contact sensitizers (specialist use).
    Dose: Weekly applications with graded concentrations.
    Mechanism: Induces controlled allergic rash to “distract” autoimmunity; meta-analysis shows ~65% any regrowth in severe AA.
    Key effects: Eczema, lymphadenopathy, pigment change; requires experienced clinician. JAMA Network

15. Calcineurin inhibitors topical (tacrolimus/pimecrolimus)
    Use: Limited benefit on scalp hair; sometimes for eyebrows in AA or for inflammatory scalp disease when steroids are risky.
    Key effects: Local irritation, photosensitivity guidance.

16. Antifungals (oral griseofulvin/terbinafine; topical azoles) – tinea capitis
    Class: Antifungal.
    Dose: Weight-based oral courses (weeks).
    Mechanism: Kills dermatophytes to restore hair growth.
    Key effects: LFT monitoring for some agents.

17. Antibiotics for folliculitis decalvans or secondary infection (scarring forms)
    Class: Anti-staph regimens (e.g., rifampin + clindamycin combinations by specialist).
    Mechanism: Reduces infection-driven inflammation.

18. Immunosuppressants (methotrexate, cyclosporine, azathioprine) for severe AA/scarring alopecias
    Class: Systemic immunomodulators.
    Mechanism: Dampens immune-mediated follicle injury.
    Key effects: Organ toxicity; strict monitoring; specialist-led.

19. Prostaglandin analogs (bimatoprost) for eyelashes/eyebrows
    Class: PGF2α analog.
    Dose: 0.03% nightly to lash line (labeled for eyelashes); brows off-label.
    Mechanism: Prolongs anagen in lash follicles.
    Key effects: Iris/skin darkening, irritation, periorbital fat atrophy. (FDA-approved for lash hypotrichosis.)

20. Anti-dandruff meds (ketoconazole shampoo, etc.)
    Class: Antifungal/anti-inflammatory shampoos.
    Mechanism: Reduces Malassezia-related inflammation that can worsen shedding.

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Dietary molecular supplements

(Only useful if you have a deficiency or a documented need. Food-first is best; supplements can interact with medicines. Talk to your clinician.)

1. Iron (ferrous sulfate or gentle iron forms)
   Dose: As prescribed; often 45–65 mg elemental iron/day when low.
   Function/Mechanism: Repletes ferritin to support anagen; several reviews associate low ferritin with shedding; targets often ≥40–70 ng/mL in practice. IJDVL

2. Vitamin D3
   Dose: Per lab results (commonly 800–2000 IU/day; higher if deficient).
   Mechanism: Modulates immune signaling and follicle cycling.

3. Zinc
   Dose: ~15–30 mg elemental/day if low; avoid excess.
   Mechanism: Cofactor for keratin/immune function.

4. Protein/essential amino acids (including lysine)
   Dose: Meet daily protein needs; consider supplements if intake is low.
   Mechanism: Provides building blocks for keratin.

5. Omega-3 fatty acids
   Dose: ~1–2 g/day EPA+DHA from diet/supplement.
   Mechanism: Anti-inflammatory; may help scalp health.

6. Biotin
   Dose: Only if documented deficiency (rare).
   Mechanism: Cofactor in keratin synthesis; unnecessary excess can skew lab tests (e.g., thyroid/troponin).

7. Folate/B-complex (if low)
   Dose: As per labs.
   Mechanism: Supports cell division in matrix keratinocytes.

8. Selenium (if deficient)
   Dose: 50–100 mcg/day short-term if low.
   Mechanism: Antioxidant enzymes in hair follicles.

9. Pumpkin seed oil
   Dose: ~400 mg/day used in some studies of AGA.
   Mechanism: Mild 5-alpha-reductase inhibition; antioxidant effects.

10. Marine collagen/marine protein complexes
    Dose: Follow product trial dosing.
    Mechanism: Provide peptides that may support hair shaft quality; evidence variable.

(Your best “supplement” is balanced diet + correcting proven deficiencies like iron and vitamin D.)

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Regenerative / stem-cell–type” drugs

These are immunomodulators or regenerative approaches used by specialists. Many are off-label or investigational. Use only under expert care or in clinical trials.

1. JAK inhibitors (baricitinib/ritlecitinib/deuruxolitinib) – Approved for severe alopecia areata (see doses above). They modulate over-active immune pathways at the follicle. FDA Access Data+2PMC+2

2. Methotrexate – Off-label for severe AA; slows immune cell proliferation; weekly dosing with folic acid; requires liver/blood monitoring.

3. Cyclosporine – T-cell suppressor; can regrow hair but carries BP/renal risks; short-term specialist use.

4. PRP (platelet-rich plasma) – Regenerative biologic procedure (not a drug): autologous platelets release growth factors that can thicken hair in pattern loss; evidence supports benefit but protocols vary. Frontiers

5. Cell/exosome therapies (MSC-derived products) – Experimental in hair loss; not FDA-approved for alopecia; potential risks; consider only in formal trials.

6. Photobiomodulation (LLLT devices) – Non-drug regenerative signal therapy with supportive evidence in pattern hair loss; home devices exist with variable quality. JCAD

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Surgical/Procedural options

1. FUE hair transplantation (Follicular Unit Extraction)
   What: Individual follicle units harvested and implanted.
   Why: Permanent redistribution for pattern hair loss when donor hair is adequate.

2. FUT strip surgery (Follicular Unit Transplantation)
   What: A strip of scalp is removed from donor area; follicles dissected and placed.
   Why: Efficient graft numbers; leaves linear scar.

3. Eyebrow transplantation
   What: Transplanting scalp hairs to brows.
   Why: Restore brows lost by trauma, over-plucking, some non-active alopecias.

4. Scalp reduction/tissue expansion (rare today)
   What: Removing bald scalp or stretching hair-bearing scalp to cover it.
   Why: Selected cases with stable pattern baldness; largely replaced by FUE/FUT due to scarring/complications.

5. Scalp micropigmentation (cosmetic tattoo)
   What: Medical tattoo creates “stubble” illusion or reduces contrast.
   Why: Camouflage for extensive thinning or donor scars.

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Preventions

1. Use loose hairstyles; rotate styles; avoid prolonged traction.

2. Limit high-heat styling; use heat protectants.

3. Avoid harsh chemical processes or space them out.

4. Treat scalp issues early (seborrhea, psoriasis).

5. Screen and correct iron/vitamin D if you have risk or symptoms.

6. Manage stress and sleep well.

7. Eat a balanced, protein-rich diet; avoid crash diets.

8. Quit smoking; limit heavy alcohol.

9. Protect scalp from sunburn.

10. Review new medications with your doctor if sudden shedding starts.

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When to see a doctor

• Sudden or patchy bald spots, eyebrow/eyelash loss, or rapid shedding over weeks.

• Scalp pain, burning, scale, redness, pustules, or broken hairs—could mean infection or scarring alopecia (urgent to prevent permanence).

• Diffuse shedding 2–3 months after stress, illness, childbirth, surgery, or new meds.

• Family history of pattern baldness and you want early treatment.

• Children with hair loss (tinea capitis, alopecia areata).

• If you plan to use prescription drugs (e.g., finasteride, spironolactone, JAK inhibitors) or oral minoxidil—you need individualized counseling and labs.

• If you have signs of thyroid or iron deficiency (fatigue, cold intolerance, brittle nails, pica). AAFP+1

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What to eat & what to avoid

What to eat

1. Lean proteins (eggs, fish, legumes) to supply amino acids for keratin.

2. Iron-rich foods (red meat in moderation, liver, lentils, spinach) with vitamin C to enhance absorption.

3. Fatty fish (salmon, sardines) for omega-3s.

4. Nuts/seeds (zinc, selenium, vitamin E).

5. Dairy or fortified alternatives (vitamin D, protein).

What to limit/avoid

1. Crash diets/very low calorie plans → trigger shedding.
2. Excess vitamin A supplements → can cause hair loss.
3. Ultra-processed high-sugar foods → inflammation/insulin spikes.
4. Heavy alcohol & smoking → oxidative stress.
5. Unverified “miracle” pills → cost and risk without benefit; test and correct only proven deficiencies

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Frequently Asked Questions

1. Can lost hair grow back?
   Yes—if follicles aren’t scarred. Pattern hair loss is chronic but controllable; alopecia areata can regrow with or without therapy; scarring forms need early treatment to prevent permanent loss.

2. How long until I see results?
   Most treatments need 3–6 months for visible change; 12 months for full effect. Continuous use is key.

3. Is shedding after starting treatment normal?
   A short “shedding phase” can happen when more hairs switch into growth; it usually settles in weeks.

4. Do I need blood tests?
   Often yes—ferritin/iron and thyroid are common screens when shedding is diffuse. AAFP+1

5. Which is better: finasteride or dutasteride?
   Both lower DHT; dutasteride blocks more enzymes but is off-label for hair loss in many countries; discuss risks (sexual/mood) and pregnancy precautions with your doctor.

6. Is oral minoxidil safe?
   Low-dose oral minoxidil can help but is off-label; doctors start low and monitor for swelling, fast heartbeat, or low BP. PMC

7. Are JAK inhibitors a cure for alopecia areata?
   They are the first FDA-approved systemic options for severe AA and can be life-changing, but require lab monitoring and carry infection/clot warnings. FDA Access Data+2PMC+2

8. Do lasers really work?
   LLLT can thicken hair in pattern loss for some users, especially when combined with standard therapy. Choose reputable, well-studied devices. JCAD

9. Will PRP help me?
   Many studies show density gains in pattern hair loss; results vary by protocol and patient. It’s an adjunct, not a stand-alone “cure.” Frontiers

10. What if I’m pregnant or trying to conceive?
    Avoid finasteride/dutasteride and many systemic drugs; ask your obstetrician/dermatologist for a pregnancy-safe plan.

11. Can diet alone fix hair loss?
    Diet supports hair health; correcting deficiencies matters, but diet alone rarely reverses genetic or autoimmune alopecia.

12. Do I need a biopsy?
    Only when the cause is unclear or a scarring alopecia is suspected.

13. Is topical finasteride safer than pills?
    Not necessarily. The FDA has warned about compounded topical sprays and possible systemic side effects; discuss carefully with your clinician. Health

14. How do doctors track progress?
    Standard photos, phototrichograms, and trichoscopy at regular intervals.

15. What’s the single best first step?
    Get an exact diagnosis (pattern vs AA vs telogen vs scarring) because the right treatment depends on the type.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 13, 2025.

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