If you work in trichology, you see telogen effluvium constantly. A client comes in distressed, pulling clumps of hair from the shower drain, and they want an answer. Sometimes you can find an obvious trigger: a surgery three months ago, a crash diet, a new medication. Sometimes you can’t. And sometimes, the shedding just keeps going.
The peer-reviewed literature on TE has expanded significantly in the past two years. The COVID-19 pandemic created the largest involuntary case study in hair shedding history. A global systematic review and modeling study now quantifies that epidemiological shift. A 2025 review in JAAD Reviews maps the stress-mediated inflammatory pathways in detail. A 2024 biochemical investigation challenges the routine lab panel assumptions. And the long-running debate about whether chronic TE is even a real diagnosis got its most thorough systematic review to date.
This is the current state of the evidence. It’s worth knowing because the clients sitting in your chair are living it.
The Mechanism: Why Follicles Drop Into Telogen Early
Telogen effluvium is not a disease. It is a disruption pattern. The hair follicle has a built-in cycle: anagen (active growth, lasting 2–7 years), catagen (regression, lasting about 2 weeks), and telogen (resting, lasting 2–4 months). Under normal conditions, roughly 85–90% of scalp follicles are in anagen at any given time, and about 10–15% are in telogen. When something forces a disproportionate number of anagen follicles into premature telogen simultaneously, the clinical result is diffuse shedding that becomes visible 2–4 months later, the time it takes for a telogen hair to reach the exogen phase and fall.
The triggers are varied: physiological stress from fever, surgery, childbirth, or hemorrhage; psychological stress through chronic HPA axis activation; nutritional deficiency, particularly iron, zinc, and vitamin D; medications including retinoids, anticoagulants, and certain antidepressants; and systemic inflammatory conditions. What they share is a final common pathway: premature anagen termination.
But what actually happens at the molecular level between the trigger and the follicle’s decision to shut down growth? The 2024–2025 literature is filling that picture in.
The Cytokine Cascade: IL-6, TNF-α, and the Collapse of Follicular Immune Privilege
This 2025 review in JAAD Reviews provides the most comprehensive mapping of stress-mediated hair loss pathways published to date. The central mechanism is the hypothalamic-pituitary-adrenal (HPA) axis. Under psychological stress, the hypothalamus releases corticotropin-releasing hormone (CRH), which triggers ACTH release from the pituitary, which drives cortisol secretion from the adrenal cortex. Cortisol is the final systemic effector. But the damage to the follicle is not from cortisol alone.
The hair follicle has its own peripheral HPA axis. It expresses CRH receptors, produces cortisol locally, and responds to stress signals independently of the systemic axis. When cortisol levels remain chronically elevated, the follicle’s immune privilege collapses. Under normal conditions, the anagen hair bulb maintains a zone of relative immune tolerance, preventing inflammatory cells from attacking the matrix. Chronic cortisol exposure, amplified by local CRH signaling, degrades that barrier.
What follows is a cascade of proinflammatory cytokines. Interleukin-6 (IL-6) acts directly on the follicle and induces catagen entry. TNF-α and IL-1β inhibit hair follicle growth at the matrix level. Substance P, a neuropeptide released under stress, triggers mast cell degranulation around the follicle and amplifies local inflammation. The result is premature anagen termination, follicles entering catagen and telogen weeks or months ahead of schedule, not because they ran out of growth capacity, but because the inflammatory environment told them to stop.
The review also documents a bidirectional relationship: the psychological distress caused by visible hair shedding can itself sustain HPA axis activation, creating a self-reinforcing cycle where the TE triggers its own perpetuation. This is clinically important. A client who is anxious about their shedding is, in a measurable biological sense, making it harder for their follicles to re-enter anagen.
Stress management is not a soft recommendation in TE. The evidence now shows that sustained HPA axis activation directly drives the cytokine environment that keeps follicles in telogen. Addressing stress, whether through referral, cognitive behavioral approaches, or simply explaining the mechanism to the client so they understand the biology, is part of treating the condition.
The Pandemic Effect: A Three-Fold Increase in TE Incidence
The COVID-19 pandemic created the conditions for a global TE event: systemic viral infection with high fever, cytokine storms in severe cases, mass psychological stress, nutritional disruption, and social isolation. The result was measurable. This systematic review, searching six databases through March 2024, quantified the global epidemiological shift.
Two findings from the epidemiological data are particularly noteworthy. First, post-COVID TE has a shorter latency than classic TE. Where most TE triggers produce visible shedding at 2–4 months, COVID-19-associated TE often presented at 30–57 days. This accelerated timeline suggests the cytokine storm mechanism, direct inflammatory assault on anagen follicles, rather than the slower metabolic or nutritional triggers that produce the standard delay.
Second, TE incidence was not uniform across populations. Hispanic/Latinx and Asian populations showed significantly higher pandemic-era increases in TE incidence, with the study noting generally higher TE prevalence estimates in Asia and Latin regions even before the pandemic. The reasons are likely multifactorial, involving genetic susceptibility, socioeconomic stress exposure, access to care, and possibly differences in hair cycling dynamics, but the disparity is documented and practitioners should be aware of it.
COVID-19 TE: A 113-Patient Retrospective
This 2025 retrospective study provides granular clinical data on 113 patients with TE following COVID-19 infection. The demographics align with the broader literature: 85.8% were female, with the 18–30 age group most represented. The vast majority, 92%, presented with acute TE with a median hair loss duration of two months. Trichodynia (scalp pain or discomfort) and pruritus were commonly associated complaints, consistent with the neurogenic inflammation pathway involving substance P.
The clinically important finding: nine patients with pre-existing chronic TE experienced relapse triggered by COVID-19 infection. This is meaningful for practitioners. COVID-19 did not just cause new TE; it destabilized patients whose follicular cycling was already fragile. The study reinforces the need for micronutrient assessment in post-COVID TE, documenting an association between COVID-19 infection and nutritional deficiency, particularly iron and zinc, that may compound the direct inflammatory trigger.
The Micronutrient Question: What the Biochemistry Actually Shows
This study is important precisely because its findings challenge a common clinical assumption. The researchers performed a comprehensive biochemical panel on 90 women with chronic TE and 90 matched controls, testing hemoglobin, ferritin, vitamin B12, vitamin D, TSH, free T4, zinc, copper, biotin (serum and urine), and selenium.
The result: hemoglobin, ferritin, vitamin B12, vitamin D, copper, biotin levels, and thyroid function did not differ significantly between the CTE and control groups.
This does not mean micronutrients are irrelevant to TE. The well-established role of iron deficiency in acute TE is supported by substantial prior evidence. What this study does show is that in chronic TE specifically, the reflexive assumption that a nutrient deficiency must be driving the shedding may not hold. Many practitioners run a standard panel, find everything “normal,” and are left without an explanation. This study validates that experience: the biochemistry can be entirely unremarkable in a patient who is genuinely shedding.
Run the labs. Always. Iron, ferritin, vitamin D, thyroid, and zinc remain important to check because when they are deficient, correcting them helps. But do not assume that normal labs mean you missed something. In chronic TE, the mechanism may be entirely independent of nutritional status. The cytokine pathways, HPA axis dysregulation, and follicular cycling dynamics described in the JAAD Reviews paper may be doing the work on their own.
Is Chronic TE Even a Real Diagnosis?
This systematic review, authored by six of the most recognized names in hair research, tackled the question directly. They analyzed 18 studies comprising 1,628 cases of chronic TE and arrived at a conclusion that every trichologist should internalize: the diagnostic category of “chronic TE” is poorly characterized and may not represent a distinct disorder at all.
The problems they identified are fundamental. There is no consensual definition of chronic TE. Different studies use different inclusion criteria. The review found that many cases currently labeled chronic TE likely represent one of three things: early-stage female pattern hair loss that hasn’t been recognized yet, secondary TE from an unidentified underlying cause that further workup would reveal, or normal hair shedding in anxious long-haired individuals whose shedding volume falls within physiological range but feels alarming.
97.5% of all cases were female. The review acknowledged that where genuine triggering factors have been definitively excluded, the persistent shedding may represent an alteration in the hair cycle itself, a real biological phenomenon, but not necessarily one that merits its own diagnostic category separate from the broader TE framework.
Before diagnosing “chronic TE,” make sure you have genuinely ruled out early female pattern hair loss (trichoscopic hair diameter variability is the key differentiator), thyroid dysfunction, iron deficiency even within “normal” lab ranges, and medication-related causes. Many cases of apparent chronic TE resolve into a more specific diagnosis with thorough workup. The label should be a diagnosis of exclusion, not a starting point.
Trichoscopy in TE: What to Look For at the Scope
Trichoscopy cannot definitively diagnose TE in isolation, but it plays a critical role in differential diagnosis, particularly in distinguishing TE from early female pattern hair loss. The 2024–2025 literature reinforces the following trichoscopic markers.
In acute TE, the hallmark findings are empty follicular openings and scattered yellow dots, both reflecting follicles that have shed their telogen hair and have not yet re-entered anagen. Hair shaft diameter remains uniform, a critical distinction from androgenetic alopecia where diameter variability exceeds 20%. There should be no miniaturized hairs. Perifollicular hyperpigmentation may be present but is nonspecific.
In chronic TE, the key finding shifts to short upright regrowing hairs, reflecting follicles that are cycling but with shortened anagen phases. Again, diameter uniformity should be maintained. If you see significant diameter variability, or if miniaturized hairs are appearing in the frontal or vertex regions, consider that the diagnosis may actually be early female pattern hair loss masquerading as chronic shedding.
A 2024 study in the International Journal of Trichology demonstrated that hair root dermoscopy from shed hair, examining the shed hairs themselves under dermoscopy rather than the scalp, can be a useful non-invasive adjunct. Shed hairs in TE show a predominance of depigmented club-shaped bulbs (telogen hairs), whereas active alopecia areata shows dystrophic or tapered roots. This is a practical chairside technique that requires only a dermoscope and the collected shed hairs the client brings in.
What This Means for Your Practice
The trigger timeline matters more than you think. Classic TE presents at 2–4 months after the inciting event. Post-COVID TE can present at 30–57 days. Post-surgical TE follows the standard timeline. Drug-induced TE may not appear until 6–12 weeks after starting the medication. When a client comes in with shedding, counting backward from onset to identify the trigger is the single most useful diagnostic step. If you can identify a trigger and the timing matches, you can give the client a confident answer and a realistic timeline for recovery.
Normal labs do not rule out TE. The Turkoglu et al. study makes this clear for chronic TE. Many practitioners feel stuck when the panel comes back normal and the shedding continues. The cytokine and HPA axis pathways operate independently of nutritional status. This doesn’t mean the labs were useless. It means the mechanism is inflammatory or stress-driven rather than deficiency-driven, and the management approach should reflect that.
Explain the mechanism to the client. The JAAD Reviews paper documents that anxiety about hair loss itself sustains the HPA axis activation that drives continued shedding. This is not a platitude. It is a peer-reviewed biological mechanism. When clients understand that their shedding is temporary, that their follicles are intact and will re-enter anagen, and that the stress of worrying about it is measurably contributing to its duration, that understanding itself becomes part of the treatment. Education reduces cortisol. Cortisol reduction accelerates recovery.
Screen carefully before labeling anything “chronic TE.” The Daunton et al. systematic review found that many cases of chronic TE are actually unrecognized early FPHL or secondary TE from occult causes. Trichoscopy is your primary differentiating tool. If there is hair diameter variability, it is not TE. If the shedding persists beyond 6 months, go deeper: repeat iron studies, check for autoimmune markers, revisit the medication list, and consider scalp biopsy if the trichoscopy is equivocal.
Most acute TE resolves. This is the reassurance your clients need, and it is evidence-based. The 113-patient retrospective found that 92% of post-COVID TE cases were acute and self-limiting. The standard clinical course of acute TE, regardless of trigger, is resolution within 3–6 months once the triggering factor is removed or resolved. Recovery is not always complete, some patients report a subjective sense of reduced density even after shedding stops, but active shedding ceases. The follicle is intact. Anagen will return.
The Bottom Line
Telogen effluvium is a disruption pattern, not a disease, and the 2024–2025 evidence base has sharpened every aspect of how practitioners should understand it. The COVID-19 pandemic tripled TE incidence globally and produced a shorter-latency variant driven by direct cytokine assault on anagen follicles. The JAAD Reviews mapping of HPA axis, IL-6, TNF-α, substance P, and local follicular cortisol pathways provides the mechanistic explanation for why stress-mediated TE persists and self-reinforces. The Turkoglu biochemical study shows that normal labs are common in chronic TE, validating the clinical experience of finding nothing on the panel. And the Daunton systematic review challenges practitioners to be more rigorous before applying the “chronic TE” label, because many of those cases are something else. Run the labs. Use the scope. Count the timeline backward. Explain the biology. And know that in most cases, the follicle is intact and the shedding will stop.