Telogen Effluvium and Androgenetic Alopecia Are Fundamentally Different Conditions
Telogen effluvium (TE) causes diffuse shedding that resolves in 3-6 months. Androgenetic alopecia (AGA) shows progressive miniaturization in a patterned distribution. Despite causing very different types of hair loss, these two conditions are frequently confused, especially in the early stages. Tracking data makes the distinction clear by revealing patterns that are invisible in a single snapshot.
Understanding which condition you have determines everything: your treatment plan, your prognosis, and whether you need to act urgently or simply wait.
What Telogen Effluvium Actually Is
Telogen effluvium occurs when a stressor pushes a large number of hair follicles into the resting (telogen) phase simultaneously. Under normal conditions, only about 10-15% of your hair is in telogen at any given time. During a TE episode, that figure can jump to 30% or more.
Common TE Triggers
- Physical stress: major surgery, high fever, severe illness, crash diets, significant weight loss
- Hormonal shifts: postpartum (affects up to 50% of new mothers), starting or stopping birth control, thyroid dysfunction
- Emotional stress: major life events, prolonged psychological stress
- Nutritional deficiency: iron deficiency, zinc deficiency, protein malnutrition, vitamin D deficiency
- Medications: certain antidepressants, beta-blockers, retinoids, anticoagulants
TE Timeline
The key feature of TE is its lag time. The triggering event occurs 2-4 months before shedding begins. This delay confuses many patients because by the time hair starts falling out, the stressor may have already resolved.
- Months 0-2 after trigger: No visible change (follicles are shifting to telogen)
- Months 2-4: Shedding begins, often dramatically (200-300+ hairs per day versus the normal 50-100)
- Months 4-6: Shedding gradually decreases
- Months 6-12: Regrowth becomes visible, density recovers
Most acute TE episodes resolve completely within 6-12 months without any treatment. Chronic TE (lasting beyond 6 months) can occur if the trigger persists or recurs.
What Androgenetic Alopecia Actually Is
AGA is a genetic, hormonal condition where dihydrotestosterone (DHT) causes susceptible hair follicles to progressively miniaturize. Over time, thick terminal hairs become thin vellus hairs and eventually stop growing altogether.
AGA Characteristics
- Gradual onset: progresses over years, not weeks
- Patterned distribution: follows the Norwood scale in men (temple recession, crown thinning) and the Ludwig scale in women (part line widening)
- Miniaturization: the hallmark sign, where individual hairs become thinner in diameter over successive growth cycles
- No spontaneous recovery: without treatment, AGA progresses indefinitely
- Genetic basis: polygenic inheritance from both parents
AGA Progression by Norwood Stage
| Norwood Stage | Description | Grafts (if transplant needed) |
|---|---|---|
| N1 | No significant loss | 0 |
| N2 | Slight temple recession | 800-1,500 |
| N3 | Deeper temple recession | 1,500-2,200 |
| N3V | Temple + early crown thinning | 2,000-2,800 |
| N4 | Further frontal loss + crown | 2,500-3,500 |
| N5 | Bridge between frontal and crown narrows | 3,000-4,500 |
| N6 | Bridge gone, large bald area | 4,000-6,000 |
| N7 | Extensive loss, only horseshoe remains | 5,500-7,500 |
Side-by-Side Comparison
| Feature | Telogen Effluvium | Androgenetic Alopecia |
|---|---|---|
| Onset | Sudden (2-4 months after trigger) | Gradual (years) |
| Pattern | Diffuse, entire scalp | Patterned (temples, crown, part line) |
| Shedding rate | High (200-300+ hairs/day) | Moderate (normal-ish shedding) |
| Miniaturization | No (hairs shed at full thickness) | Yes (progressive thinning of individual hairs) |
| Hair caliber | Shed hairs are normal thickness | Hairs become progressively finer |
| Pull test | Strongly positive (multiple hairs) | Usually negative or weakly positive |
| Recovery | Spontaneous (3-6 months) | No recovery without treatment |
| Trigger identifiable | Usually yes | No specific trigger |
| Age of onset | Any age | Typically begins in 20s-30s |
| Gender distribution | More commonly diagnosed in women | Men and women (different patterns) |
| Treatment | Address trigger, wait for recovery | Finasteride, minoxidil, transplant |
How Tracking Data Distinguishes TE from AGA
Pattern 1: The TE Signature in Tracking Data
TE produces a distinctive tracking pattern:
- Baseline phase: Stable density across all tracked zones
- Rapid decline phase: Sharp density drop (10-30%) across ALL zones simultaneously, usually over 2-4 weeks
- Stabilization: Shedding rate decreases
- Recovery phase: Gradual, even density increase across all zones
- Return to baseline: Density approaches or reaches pre-trigger levels
The key identifiers are "all zones equally affected" and "recovery follows decline." If your temple, crown, and midscalp all dropped by a similar percentage, and all are recovering together, this pattern strongly suggests TE.
Pattern 2: The AGA Signature in Tracking Data
AGA produces a fundamentally different pattern:
- Slow decline: Gradual density decrease, typically 5-15% per year
- Zone-specific: Temples and/or crown show greater loss than sides and back
- Asymmetric: One side may thin faster than the other
- No spontaneous recovery: The trend continues downward without treatment
- Miniaturization visible: Close-up tracking photos show increasingly fine hairs mixed with thicker ones
The key identifiers are "some zones worse than others" and "no recovery phase." If your temples are declining while your occipital (back) density remains stable, this is the hallmark of AGA.
Pattern 3: The TE-Unmasking-AGA Signature
This is the most confusing pattern and the one that causes the most anxiety:
- Sudden diffuse shed: Looks like TE (rapid, widespread density drop)
- Partial recovery: Most zones bounce back, but certain zones do not fully recover
- Persistent patterned loss: After the TE resolves, temples or crown remain thinner than baseline
What happened: the TE episode shed hairs across the scalp, but the follicles in AGA-affected zones were already partially miniaturized. They did not have enough strength to regrow at full density. The TE essentially revealed underlying AGA that was previously compensated.
This pattern requires both TE management (address the trigger, wait for recovery) and AGA treatment (finasteride, minoxidil) for the zones that do not bounce back.
What Miniaturization Looks Like in Tracking
Miniaturization is the single most reliable way to distinguish AGA from TE without a biopsy. For more detail, see our guide on what miniaturization means in tracking.
In AI-powered tracking:
- TE: Density drops, but the remaining hairs maintain their thickness. When regrowth occurs, new hairs come in at normal caliber.
- AGA: Some hairs in affected zones are visibly thinner than their neighbors. Over time, the ratio of thin to thick hairs increases.
In trichoscopy (at a dermatologist):
- TE: Normal hair shaft diameter variation
- AGA: Greater than 20% variation in hair shaft diameter within affected zones, with the miniaturization ratio increasing over time
Treatment Differences Based on Diagnosis
If Your Tracking Suggests TE
- Identify and address the trigger (nutritional deficiency, medication, stress)
- Blood work to rule out thyroid dysfunction, iron deficiency, and other systemic causes
- Wait 3-6 months for spontaneous recovery
- Continue tracking to confirm recovery is occurring
- No finasteride or minoxidil needed in most cases (though minoxidil may speed recovery in some patients)
If Your Tracking Suggests AGA
- Start treatment early (the more follicles still active, the more you can preserve)
- Finasteride 1mg daily: halts progression in 80-90%, produces regrowth in 65%, 2-4% side effect rate
- Minoxidil 5%: 40-60% regrowth, 4-6 months to visible effect
- Consider combination therapy for stronger response
- Long-term commitment required (stopping treatment reverses gains within 6-12 months)
If Your Tracking Suggests Both
- Address the TE trigger first
- Start AGA treatment simultaneously for the patterned component
- Track recovery in all zones, noting which zones recover (TE-only) and which remain depressed (AGA involvement)
- Adjust expectations: TE-affected zones should recover fully, AGA zones will stabilize with treatment but may not fully recover without additional intervention
When to Involve a Dermatologist
Tracking data can strongly suggest which condition you have, but certain situations require clinical confirmation:
- Unclear pattern: Your data does not cleanly match TE or AGA signatures
- No identifiable trigger: Diffuse shedding without an obvious cause needs blood work
- Rapid progression: Any hair loss that progresses faster than expected for AGA warrants evaluation for other conditions
- Scarring signs: Scalp redness, pain, or scaling may indicate a scarring alopecia (not TE or AGA)
- No recovery after 6 months: If TE-like shedding does not resolve, the diagnosis may need revision
Start Tracking to Identify Your Pattern
The distinction between TE and AGA is visible in longitudinal tracking data before it is visible to the naked eye. The earlier you start tracking, the more data you have to work with when patterns emerge.
Get your baseline analysis at myhairline.ai/analyze and start building the tracking history that tells your story.
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Telogen effluvium and androgenetic alopecia require proper diagnosis by a board-certified dermatologist, especially when both conditions may be present simultaneously. Do not self-diagnose or self-treat based on tracking data alone.