Alopecia Androgenetica vs Telogen Effluvium: how to distinguish pattern hair loss from reactive shedding

Hair loss is not a single condition. In clinical dermatology, alopecia androgenetica and telogen effluvium represent two distinct non-scarring disorders with different biological mechanisms, progression patterns and long-term implications.

Correct classification is essential. Effective support depends on determining whether hair follicles are undergoing progressive miniaturisation or a temporary shift within the hair growth cycle.

This overview reflects clinical classification principles applied in dermatological practice.

Illustratie van alopecia androgenetica bij mannen en vrouwen met kenmerkend verdunningspatroon.

What is Alopecia Androgenetica?

Alopecia androgenetica (AGA) is a genetically influenced, androgen-dependent condition characterised by progressive follicular miniaturisation in response to dihydrotestosterone (DHT).

In genetically predisposed individuals, DHT shortens the growth phase (anagen phase) and progressively miniaturises hair follicles. Over time, thick terminal hairs become thinner, shorter and less pigmented.

For a comprehensive clinical explanation of progression patterns, underlying mechanisms, and long-term interpretation, see our full guide to alopecia androgenetica.

Over time, repeated shortening of the anagen phase leads to a reduction in hair shaft diameter and visible scalp exposure in pattern-specific areas.

Typical clinical features of alopecia androgenetica include:

  • Gradual, progressive thinning over years
  • Pattern-specific distribution (frontal recession or vertex thinning in men; central part widening in women)
  • Variation in hair shaft diameter due to follicular miniaturisation
  • Absence of sudden diffuse shedding

For a deeper explanation of the DHT mechanism, see our overview of DHT and hair loss.

In contrast to this slow, androgen-driven process, telogen effluvium follows a fundamentally different biological pathway.

diffuse haaruitval zonder patroon met behouden haarlijn bij telogeen effluvium

What is Telogen Effluvium?

Telogen effluvium (TE) is a reactive, non-scarring form of diffuse hair shedding. It occurs when a significant number of hair follicles prematurely shift from the growth phase (anagen) into the resting phase (telogen), leading to increased shedding several weeks to months later.

Unlike pattern-based hair loss, telogen effluvium does not involve follicular miniaturisation. The follicle structure remains intact, which means recovery is biologically possible once normal cycle regulation resumes.

Clinical characteristics of telogen effluvium:

  • Diffuse thinning across the entire scalp
  • Preserved frontal hairline
  • Sudden increase in daily shedding
  • Onset typically 2–4 months after a trigger
  • Uniform hair shaft thickness (no miniaturisation)

Common triggers include:

  • Acute physical illness or high fever
  • Surgery or medical procedures
  • Emotional or psychological stress
  • Rapid weight loss or dietary restriction
  • Postpartum hormonal shifts
  • Medication changes

Hair shedding typically increases 2–4 months after the triggering event.

In most cases, regrowth begins once the underlying trigger resolves and the hair cycle rebalances.

For a deeper clinical discussion of triggers, recovery timelines, and diagnostic interpretation, see our complete overview of telogen effluvium.

Alopecia Androgenetica vs Telogen Effluvium: clinical differentiation

This table is designed as a clinically oriented guide: how to distinguish pattern-based miniaturisation (AGA) from reactive diffuse shedding (TE) using course over time, distribution, and assessment findings (incl. trichoscopy). Educational information only; not a medical diagnosis.

Clinical feature Telogen effluvium (TE) Alopecia androgenetica (AGA)
Primary process (follicle level) Temporary shift of many follicles into telogen (resting) phase; follicle structure remains intact Progressive miniaturisation of genetically sensitive follicles; growth phase shortens and shafts become finer
Distribution pattern Diffuse across the scalp (overall density reduction) Pattern-based (e.g., temples/crown in men; central part widening in women)
Onset & timing Often acute/subacute; shedding typically noticeable 6–12 weeks after a trigger Gradual; becomes visible over months to years
Shedding volume Often clearly increased (more hair in shower/brush) Variable; often progressive thinning with limited “sudden” shedding
Hair pull test More often positive (multiple telogen hairs released) Usually negative or mildly positive; not the primary differentiator
Hair shaft diameter variability Typically relatively uniform; loss is mainly in counts rather than diameter diversity Typical: marked diameter diversity (anisotrichosis) due to miniaturisation
Trichoscopy / dermoscopy No pronounced miniaturisation; more “empty” ostia due to simultaneous telogen shedding Characteristic: miniaturisation, diameter diversity, increased vellus hairs; often >20% diameter diversity in affected zones
Course without targeted support Usually temporary; stabilises as the trigger resolves and cycling normalises Typically progressive; stabilisation usually requires a long-term, consistent strategy
Regrowth expectation Recovery often possible (months) because follicles remain intact Limited recovery once advanced miniaturisation is present; focus is often on preservation/stabilisation and follicle condition
Trigger / context Often identifiable stressor: illness/fever, surgery, postpartum, dietary change/deficiency, medication change, emotional stress Inherited sensitivity to hormonal signalling (incl. DHT); family history is common
Overlap (common in practice) TE can “unmask” underlying AGA via temporary volume loss; ongoing triggers can prolong TE AGA can coexist with TE; pattern thinning often remains visible after TE resolves
When further evaluation is advisable Shedding > 6 months, unclear trigger, or persistent pattern thinning Rapid progression, atypical pattern, scalp symptoms (pain/redness/scaling/burning), or diagnostic uncertainty

If you recognise both diffuse shedding and progressive pattern thinning, overlap is common. In those cases, combining pattern, timeline, and trichoscopic findings provides the clearest interpretation.

→ Read the clinical overview of telogen effluvium → Read the clinical overview of alopecia androgenetica

When alopecia androgenetica and telogen effluvium overlap

In clinical practice, telogen effluvium and alopecia androgenetica frequently coexist rather than present as clearly isolated conditions.

A common scenario involves acute diffuse shedding following illness, surgery, hormonal shifts, or psychological stress. As overall hair density temporarily decreases, underlying pattern-based miniaturisation may become more apparent. In such cases, telogen effluvium does not cause alopecia androgenetica, but it may unmask a previously unrecognised predisposition.

Conversely, early-stage alopecia androgenetica may initially be misinterpreted as stress-related shedding when gradual thinning coincides with life events.

Accurate differentiation therefore relies on longitudinal pattern assessment rather than a single moment in time.

Careful evaluation typically considers the following.

Key differentiation factors in overlapping cases:

  • Evolution of distribution pattern over months to years
  • Presence of hair shaft diameter variability (anisotrichosis)
  • Family history of pattern hair loss
  • Duration and intensity of shedding
  • Trichoscopic findings in affected zones

Understanding this overlap is essential for setting realistic expectations and determining whether temporary cycle disruption, progressive miniaturisation, or a combination of both is present.

Common diagnostic pitfalls when differentiating AGA and TE

Despite clear biological differences, alopecia androgenetica and telogen effluvium are frequently misinterpreted, particularly in early stages or during periods of physiological stress.

Several diagnostic pitfalls occur in practice:

1. Assuming all diffuse thinning is temporary

Diffuse density reduction is often attributed to stress-related shedding. However, early alopecia androgenetica in women may initially present as subtle diffuse thinning without obvious recession.

Without assessing diameter variability and distribution over time, progressive miniaturisation may be overlooked.

2. Interpreting seasonal shedding as telogen effluvium

Temporary increases in shedding during seasonal transitions are common and self-limiting. Not all increased shedding reflects a true telogen effluvium episode.

Duration, intensity, and trigger history remain essential.

3. Overestimating shedding in early alopecia androgenetica alopecia

In AGA, patients often perceive increased shedding, while the dominant process is progressive miniaturisation rather than acute telogen shift.

Density reduction can occur even when daily shedding appears “normal.”

4. Missing combined pathology

A common real-world presentation includes underlying alopecia androgenetica with superimposed telogen effluvium.

In these cases:

  • Shedding may stabilise
  • But pattern thinning persists

Failure to recognise this overlap may lead to unrealistic expectations regarding recovery.

Why correct classification matters

Because each condition follows a different biological pathway, effective long-term planning depends on distinguishing:

  • Temporary cycle disruption
  • Progressive follicular miniaturisation
  • Or coexistence of both

Correct classification precedes responsible support.

From differentiation to structured decision-making

Accurate differentiation between alopecia androgenetica and telogen effluvium is not an academic exercise. It directly influences long-term strategy.

When follicular miniaturisation is the dominant process, the focus shifts toward preserving follicle function and slowing progressive diameter reduction.

When diffuse shedding reflects temporary cycle disruption, priority lies in stabilising the hair growth cycle and allowing physiological recovery.

In cases where both processes coexist, planning requires acknowledging two biological pathways simultaneously, addressing cycle regulation while monitoring pattern-based progression.

Structured support therefore begins with classification, not assumption.

A system aligned with clinical logic

The TRIX Basic approach reflects this same diagnostic framework.

Rather than offering a single universal solution, different formulations are aligned with distinct biological profiles identified during assessment.

This structured model mirrors clinical reasoning:

  • Identify the dominant mechanism
  • Evaluate duration and progression
  • Select support aligned with follicular biology
  • Reassess over time

Support is positioned as complementary to medical evaluation and long-term care, not as a substitute for diagnosis.

For a structured medical classification of different hair loss conditions, see our full overview of types of hair loss.

Not sure which pattern applies to you?

Because hair loss presentations can overlap, structured assessment is often the most reliable starting point.

The TRIX Hair Check reflects the same classification logic used in clinical evaluation and helps identify the most likely biological profile before considering next steps.

Take the Hair Check (2 minutes)

Based on 20+ years of dermatological expertise

Frequently asked questions about alopecia androgenetica and telogen effluvium

What is the main difference between alopecia androgenetica and telogen effluvium?

Alopecia androgenetica is pattern-based and driven by progressive follicle miniaturisation. Telogen effluvium is diffuse shedding caused by a temporary shift of many follicles into the resting (telogen) phase.

Can telogen effluvium cause alopecia androgenetica?

No. Telogen effluvium does not cause androgenetic alopecia, but it can make underlying pattern thinning more noticeable because overall density temporarily decreases.

How long after a trigger does telogen effluvium usually start?

Telogen effluvium typically becomes noticeable about 2–4 months after a trigger such as illness, surgery, major stress, or hormonal change.

Does alopecia androgenetica usually involve sudden heavy shedding?

Not typically. AGA usually progresses gradually. Some shedding can occur, but the hallmark is progressive thinning and hair shaft diameter variability over time.

What patterns are typical for alopecia androgenetica in men and women?

In men, thinning often starts at the temples and crown. In women, it more often presents as widening of the central parting with relative preservation of the frontal hairline.

What does “miniaturisation” mean?

Miniaturisation is a progressive process where follicles produce thinner, shorter hairs over successive growth cycles. This reduces visible density even if hair shedding is not dramatic.

Can alopecia androgenetica and telogen effluvium overlap?

Yes. It is common to see diffuse shedding on top of underlying pattern-based miniaturisation. Distinguishing the dominant process helps guide expectations and long-term planning.

When is medical evaluation recommended?

If shedding persists beyond 6 months, thinning progresses, bald patches appear, or scalp symptoms occur (pain, redness, scaling, inflammation), clinical evaluation is recommended.