Types of Hair Loss: How to Tell What You Have

You shed 50–100 hairs a day. That alone is not hair loss⁶ . The question this guide answers is: when shedding isn’t normal, which condition is it, and what does that mean for what you can do about it.

There are at least a dozen distinct disorders that all show up as hair coming out of the scalp. They have different causes, different prognoses, and different treatments. Picking the right intervention starts with knowing which one you have.

The two questions that organise everything else

Is it scarring or non-scarring?

In non-scarring hair loss the follicle is still alive. Hair growth has paused, slowed, or shifted to thinner shafts, but the follicle can be coaxed back. Pattern hair loss, telogen effluvium, and alopecia areata are non-scarring.

In scarring (cicatricial) alopecia the follicle is destroyed and replaced with scar tissue. Once it’s gone, no treatment regrows hair from that follicle. This is why scarring alopecias matter most to identify early: treatment can stop further loss but cannot reverse what’s already scarred.

Is it diffuse, patterned, or patchy?

• Diffuse thinning across the whole scalp suggests telogen effluvium or female pattern hair loss.
• Patterned thinning concentrated in specific zones (temples, crown, mid-scalp) suggests androgenetic alopecia.
• Patchy with sharp borders suggests alopecia areata, traction alopecia, or scarring alopecia.

Those two axes narrow the diagnosis fast¹ .

Androgenetic alopecia (pattern hair loss)

Also called male pattern hair loss, female pattern hair loss, AGA, FPHL, or pattern baldness. The most common form, full stop. Roughly 50% of men show signs by age 50 and around 40% of women by age 60³ .

Mechanism. Hair follicles in genetically susceptible scalp regions are sensitive to dihydrotestosterone (DHT), a metabolite of testosterone. Over years, DHT shrinks (miniaturises) these follicles. They produce progressively shorter, thinner, lighter hairs until cycling stops. The follicle is alive (non-scarring), which is why pharmacological treatment can partially reverse it.

Male pattern. Loss starts at the temples (the “M-shape” recession) and crown, then progresses. The Norwood-Hamilton scale stages this from mild recession (Norwood II) through complete top-of-scalp baldness with a horseshoe rim (Norwood VII).

Female pattern. Diffuse central-scalp thinning with the frontal hairline preserved, the “Christmas tree” widening of the part. The Ludwig and Sinclair scales grade severity. Women rarely progress to complete baldness.

What works. Topical and oral minoxidil and the 5α-reductase inhibitors finasteride and dutasteride have the strongest evidence. Hair transplants move follicles from the DHT-resistant rim to thinning areas. We cover female pattern in detail in our female pattern hair loss guide.

Telogen effluvium

A diffuse shedding disorder. Around 80–95% of scalp hairs are normally in the growth (anagen) phase at any given time, with the rest in transition (catagen) or resting/shedding (telogen). Telogen effluvium happens when a large fraction of follicles get pushed into telogen prematurely and shed together a few months later.

Trigger. Almost always a physiological stressor 2–4 months before shedding starts. Common ones:

• Childbirth (postpartum; see our postpartum hair loss guide)
• Significant illness, COVID-19, surgery, hospitalisation
• Severe psychological stress
• Crash dieting, sudden weight loss, nutritional deficiency
• Starting or stopping certain medications (hormonal contraceptives, retinoids, beta-blockers, anticonvulsants)
• Thyroid dysfunction
• Iron deficiency

Course. Acute telogen effluvium is self-limited. Shedding peaks 2–4 months after the trigger and resolves within 6–9 months once the trigger is gone. Hair density typically returns to baseline.

Chronic telogen effluvium is a less-common variant where shedding persists beyond six months without a clear single trigger. It tends to fluctuate and can run for years, but rarely causes severe loss⁴ .

How it’s distinguished. A “pull test” is positive (more than ~10% of gently pulled hairs come out) and the bulbs of shed hairs are clubbed/white, the telogen morphology. Unlike pattern hair loss, the shed hair shafts are full-thickness, not progressively miniaturised.

Alopecia areata

An autoimmune condition where the immune system attacks hair follicles. Affects roughly 2% of people at some point² . Onset is most common in childhood, adolescence, or early adulthood, but can occur at any age.

Presentation. Sharply-defined round or oval bald patches with smooth skin (no scaling, no scarring) and “exclamation mark” hairs at the borders, which are short broken hairs that taper toward the scalp.

Subtypes:

• Patchy alopecia areata. One or several discrete patches; the most common form.
• Alopecia totalis. Complete loss of scalp hair.
• Alopecia universalis. Complete loss of all body hair, including brows, lashes, body hair.
• Ophiasis. Band-like loss along the back and sides.
• Diffuse alopecia areata. Diffuse thinning rather than patches; rare and easily missed.

Course. Highly variable. Many patches regrow spontaneously within 6–12 months. Others persist or recur. Around 5–10% of cases progress to totalis or universalis² . Predictors of poorer prognosis include early age of onset, extensive involvement, ophiasis pattern, atopic background (eczema/asthma), and nail involvement (pitting).

What works. Intralesional or topical corticosteroids for limited disease. JAK inhibitors (baricitinib, ritlecitinib, deuruxolitinib) are FDA-approved for severe alopecia areata as of recent years and represent a major advance. We cover the full treatment landscape in our alopecia areata guide.

This is autoimmune disease, not a cosmetic problem. The framing matters when you’re choosing a clinician and a treatment.

Traction alopecia

Hair loss from chronic mechanical pulling on hair shafts: tight ponytails, braids, weaves, dreadlocks, hair extensions. Sustained tension over months to years damages the follicles.

Presentation. Thinning along the hairline (especially temples) or wherever the pulling force is concentrated. Early traction alopecia is reversible. Sustained traction over years can convert it into scarring alopecia.

What works. Removing the source of tension is mandatory. Hair often regrows if caught early. Late-stage traction alopecia with scarring is permanent in the affected areas.

Cicatricial (scarring) alopecias

A group of inflammatory conditions that destroy hair follicles permanently. Less common than the categories above, but the most urgent to identify because progression continues until the inflammation is treated⁵ .

The main subtypes:

• Frontal fibrosing alopecia (FFA). Band-like recession of the frontal hairline, often with eyebrow loss; predominantly post-menopausal women but increasingly seen in younger women and some men.
• Lichen planopilaris (LPP). Patchy scarring with redness, scaling, and follicular hyperkeratosis around hair follicles; often itchy or painful.
• Central centrifugal cicatricial alopecia (CCCA). Scarring that begins at the crown and spreads outward; most commonly affects women of African descent.
• Folliculitis decalvans. Inflammatory, sometimes pustular scarring alopecia, often with tufts of multiple hairs from one follicle (“doll’s hair”).
• Dissecting cellulitis of the scalp. Chronic inflammatory condition with painful nodules, sinus tracts, and scarring.

Why this category is the urgent one. Anti-inflammatory treatment (topical/intralesional/oral steroids, hydroxychloroquine, immunomodulators) can halt progression but cannot reverse damage. Anyone with redness, scaling, persistent itch, burning, or visible scarring of the scalp should see a dermatologist promptly, ideally one who specialises in hair disorders. The honest goal here is stabilisation, not regrowth.

Trichotillomania

A psychiatric condition (a body-focused repetitive behaviour) where a person repeatedly pulls out their own hair. Can affect scalp, eyebrows, eyelashes, or body hair.

Presentation. Irregularly-shaped patches with hairs of varying lengths within the affected area (because only longer hairs can be grabbed). May coexist with other body-focused behaviours.

What works. Cognitive behavioural therapy, specifically habit reversal training, has the strongest evidence. Pharmacotherapy (N-acetylcysteine, certain antidepressants) is sometimes used adjunctively.

Anagen effluvium

Sudden loss of growing-phase (anagen) hair. The classic cause is chemotherapy: rapidly-dividing follicle cells get killed by cytotoxic agents. Onset is within 1–4 weeks of treatment, and loss can be near-complete. Hair typically regrows after treatment ends, sometimes with changed texture or colour.

Less common causes: severe protein-calorie malnutrition, certain toxic exposures (thallium, arsenic), and rare genetic disorders.

Quick differential

What you can probably tell at home

Some of these are recognisable without a clinician:

• Slow, decade-scale temple/crown recession in a man → almost certainly androgenetic.
• Sudden diffuse shedding 2–4 months after childbirth, illness, or major stressor → almost certainly telogen effluvium.
• A sharply-bordered round patch on a smooth scalp → almost certainly alopecia areata.
• Thinning along the hairline in someone wearing tight hairstyles → almost certainly traction alopecia.

When to see a dermatologist

• Redness, scaling, itching, burning, or pain on the scalp
• Visible scarring or smooth shiny skin where hair used to be
• Rapid, progressive loss without an obvious trigger
• You’re considering pharmacological treatment (minoxidil, finasteride) and want to confirm the diagnosis first
• You’re a woman with diffuse hair loss plus other symptoms (irregular periods, weight changes, fatigue, acne); see our diagnostic guide and blood tests for hair loss guide

What this article doesn’t cover

This is the overview. We’ve left out hair-shaft disorders (mostly genetic, mostly rare), hair loss from specific medications, and most paediatric hair-loss conditions. Each condition above also has its own dedicated guide on Regrowth Index where we cover treatments, prognosis, and what to expect in much more detail.

Hair loss can be hard, especially when you don’t yet know what’s happening. You’re not making it up, and you’re not alone. If it’s affecting your wellbeing, talk to a GP or dermatologist sooner rather than later. Anything in this article is general education, not personal medical advice.