Hair shedding vs. breakage: how to tell them apart and what each means for treatment

Hair loss is not a single phenomenon — "hair falling out" describes two biologically distinct processes that require completely different responses. Misidentifying shedding as breakage (or breakage as shedding) leads to the wrong treatment and often worsens the problem. Here's how to tell them apart and what to do about each.

The fundamental distinction: roots vs. mid-shaft

The single most reliable diagnostic tool is the hair you've lost. Pick it up and look at it.

Shed hair: Has a white bulb at the root end — the telogen bulb, the club-shaped root of a hair that has completed its cycle and released naturally from the follicle. The hair is full length (or near full length for your current hair length). The root end is intact.

Broken hair: Has a tapered or jagged end where it snapped — no white bulb, no root structure. The strand is shorter than your full hair length. Both ends are rough or tapered rather than smoothly shaped.

When you find hair in your brush, on your pillow, or in the shower drain, this distinction is diagnostic. A mix of long shed hairs with white bulbs is shedding. Short fragments without roots is breakage. In many people both processes occur simultaneously.

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Hair shedding: biology and causes

Normal shedding

Hair grows in cycles — each follicle independently cycles through:
Anagen (growth): 2–7 years; active cell division in the matrix; hair elongates
Catagen (transition): 2–3 weeks; growth stops; follicle shrinks; hair detaches from dermal papilla
Telogen (resting): 3 months; hair rests in the follicle as a club hair; eventually shed when the next anagen begins

At any given time, approximately 85–90% of scalp follicles are in anagen and 10–15% in telogen. With ~100,000 follicles on the scalp, normal daily shedding is 50–100 hairs per day — all telogen hairs that have completed their cycle.

Shedding more than this consistently = a condition affecting the hair cycle. The clinical term for excessive shedding (>100–150 hairs/day) is telogen effluvium (TE).

What causes excessive shedding

Systemic triggers that push follicles prematurely into telogen:

| Trigger | Lag time | Duration |
|---|---|---|
| Major physical illness/surgery | 6–12 weeks | 3–6 months |
| High fever | 6–12 weeks | 3–6 months |
| Significant weight loss | 6–12 weeks | 3–6 months |
| Postpartum (after childbirth) | 2–4 months | 3–6 months |
| Nutritional deficiency (iron, protein, zinc) | Variable | Until corrected |
| Thyroid dysfunction | Variable | Until treated |
| Chronic psychological stress | Variable | Until resolved |
| Stopping hormonal contraception | 6–12 weeks | 3–6 months |
| COVID-19 infection | 2–3 months | 3–6 months |

The 3-month lag: The most important concept in shedding evaluation. Because hairs spend ~3 months in telogen before shedding, the trigger occurred approximately 3 months before the hair falls out. Patients presenting with sudden heavy shedding need to be asked: "What happened in your life 3 months ago?" — not "what changed this week?"

Androgenetic alopecia (AGA): Chronic progressive shedding with miniaturization — shed hairs are progressively finer and shorter with each cycle (terminal → vellus). Distinguished from TE by the miniaturization pattern on dermoscopy and the chronic progressive course vs. acute trigger.

The shedding test

Gather a handful of shed hairs (don't wash your hair for 24 hours first, then collect all hairs shed in one day from brush, drain, and pillow combined). Count them. >150/day consistently over several weeks = excessive shedding warranting investigation.

Tug test (less standardized): Grasp 40–60 hairs near the root and apply firm, smooth traction. >6 hairs released = positive for active shedding; useful at the scalp margins where shedding is most active in acute TE.

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Hair breakage: biology and causes

Breakage is mechanical fracture of the hair shaft — not follicular cycling. Broken hairs have no root involvement; the follicle is functioning normally.

The structure that breaks

The hair shaft is composed of:
Cortex: The bulk of the shaft; tightly packed keratinized cortical cells with macro- and microfibrils oriented along the shaft axis; held together by disulfide bonds (strongest) and hydrogen/salt bonds
Cuticle: Overlapping keratin scales protecting the cortex; when damaged, cortical cells are exposed to mechanical and environmental stress
Medulla: Variable innermost core; absent in fine hair

Breaking point: Hair breaks when applied stress exceeds the shaft's tensile strength. Healthy hair can withstand significant mechanical stress. Breakage occurs when the shaft is structurally weakened or repetitively stressed beyond its fatigue limit.

Causes of hair breakage

Chemical damage:
Bleaching: Hydrogen peroxide breaks disulfide bonds → irreversible cortex weakening → significantly reduced tensile strength; high-lift bleaching can reduce breaking strength by 50%+
Relaxers and perms: Reducing agents break disulfide bonds; incomplete re-oxidation leaves permanently weakened zones
Frequent color processing: Cumulative oxidative damage even without full bleaching

Thermal damage:
Direct thermal cleavage of disulfide bonds at >230°C (450°F) — flat iron at maximum setting is typically 230–240°C
Cumulative heat damage degrades the cuticle → exposes cortex → reduced mechanical resistance

Physical/mechanical damage:
Tight hairstyles pulling the shaft repeatedly — repeated micro-bending at the same point causes fatigue fractures
Rough detangling of wet hair (wet hair has ~30% lower tensile strength than dry hair)
Friction against cotton pillowcases and towels
Elastic bands cutting into the shaft

Hygral fatigue:
Repeated wet-dry cycling causes the shaft to swell and contract repeatedly → weakens the cortex over time
Particularly relevant for very frequent washing with incomplete drying

Nutritional factors affecting shaft quality:
Severe protein deficiency → inadequate keratin synthesis → structurally weaker shaft
Iron deficiency affects keratin quality (independent of TE effects on cycling)

Breakage patterns by location

The location of breakage along the shaft is diagnostic:

Near the scalp: Recent damage (from a current practice affecting newly grown hair) — chemical treatment, mechanical stress, tight styling at roots
Mid-shaft: Recurring stress at a specific point — consistent elastic band placement, tight ponytail at the same height daily
Ends only: Old cumulative damage; natural weathering is worst at the oldest (most distal) hair; also from poor end maintenance
Variable/random: General diffuse damage throughout the shaft — overall structural compromise from chemical or cumulative thermal treatment

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How to assess what you have

Evidence collection

Collect shed/lost hair for one full day (brush, shower drain, pillow)
Examine each strand:
Root bulb present (white rounded end) → shed
Tapered/jagged end, no bulb → broken
Mixture → both processes active
Length comparison: Shed hairs ≈ your full hair length; broken hairs 150 hairs/day for >3 months
Visible scalp thinning
No identifiable trigger found after history review
Work-up: CBC, ferritin (target >70 ng/mL), TSH, free T4, fasting glucose, serum zinc, comprehensive metabolic panel

For breakage:
Significant loss of length/volume without corresponding scalp shedding
Severe breakage despite stopping obvious damaging practices

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Treatment approach by type

Addressing shedding

Identify and correct the trigger: The most important step. Nutritional deficiencies, thyroid disorders, and iron deficiency are the most commonly correctable causes.
Iron/ferritin correction: Ferritin ≥70 ng/mL is the threshold for optimal hair cycling — most labs report normal at >12 ng/mL (not sufficient for hair). Oral iron supplementation if deficient; 3–6 months to see response.
Protein intake: ≥0.8 g/kg body weight daily minimum; higher for active individuals. Adequate protein prevents catabolism-driven TE.
Minoxidil (for AGA or prolonged TE): Extends anagen; reduces shedding as an adjunct while the underlying cause resolves. Topical 2–5% or low-dose oral 0.25–1 mg/day.
Time: Acute TE resolves spontaneously once the trigger resolves — typical timeline is 3–6 months for full recovery. Reassurance is appropriate for acute cases with identified triggers.

Addressing breakage

Stop the causative practice: Identify the damage source and eliminate or modify it.
Reduce chemical processing: Extend intervals between bleach sessions; use bond-repairing treatments (bis-aminopropyl diglycol dimaleate — Olaplex No. 1/2) during bleaching.
Reduce heat: Lower temperature settings; heat protectant before any heat styling; regular air-dry days.
Gentle handling: Wide-tooth comb or finger-detangle wet hair; detangle from ends upward; avoid elastic bands on the same shaft location daily.
Protein treatments: Hydrolyzed proteins temporarily fill shaft damage; strengthens structurally weak hair. 1–2× monthly for chemically damaged hair.
Bond repair: Genuine bond-repairing treatments (maleic acid chemistry) form new covalent cross-links in the damaged cortex → measurably increased tensile strength.
Protective styling and protective ends: Styles that tuck ends away reduce exposure to friction and mechanical stress at the most vulnerable (oldest) part of the shaft.

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