Telogen Effluvium Causes

You’re most likely to develop telogen effluvium when a significant physiologic or psychosocial stressor (high fever, severe infection including COVID‑19, major surgery, childbirth, rapid weight loss, traumatic illness) pushes many anagen hairs into telogen. Abrupt hormonal shifts (postpartum, stopping estrogen pills), thyroid disease, iron or vitamin D deficiency, and drugs (retinoids, anticoagulants, antidepressants, beta‑blockers, chemotherapy) also trigger diffuse shedding 2-3 months later. You’ll see how overlapping triggers and specific scenarios shape this process further.

Telogen Effluvium Causes – An Overview

• Telogen effluvium is usually triggered 2-3 months after major physical or emotional stress: high fevers, severe infections, major surgery, trauma, or rapid weight loss.
• Hormonal shifts such as postpartum estrogen decline, menopause, and stopping estrogen‑containing birth control commonly precipitate diffuse hair shedding.
• Many medications can cause telogen effluvium, including retinoids, excess vitamin A, beta‑blockers, antidepressants, anticoagulants, calcium‑channel blockers, certain anticonvulsants, and chemotherapy.
• Nutritional and endocrine problems such as iron deficiency, low ferritin, vitamin D or B12 deficiency, zinc deficiency, and thyroid disease frequently contribute to telogen effluvium.
• Chronic systemic inflammation and illness (e.g., autoimmune disease, chronic infections) can maintain or worsen telogen effluvium by driving continual follicle stress and telogen shifting.

What Triggers Telogen Effluvium?

Although telogen effluvium can feel sudden, it almost always follows a distinct trigger that disrupts the hair growth cycle and shifts many follicles prematurely into the telogen (resting) phase. You’ll often see shedding 2-3 months after a significant physiological stressor: high fevers, severe infections, major surgery, childbirth, or rapid weight loss.

Sudden endocrine shifts including postpartum estrogen decline, stopping combined oral contraceptives, hypothyroidism, or hyperthyroidism are frequent precipitants.

You should also screen for nutritional deficiencies (iron, zinc, vitamin D, protein), iatrogenic causes such as retinoids, beta‑blockers, antidepressants, calcium‑channel blockers, anticoagulants, chemotherapy, and severe psychological stress. In about one‑third of cases, no clear inciting factor emerges.

Early recognition, systematic history‑taking, targeted labs, and, when indicated, scalp biopsies let you validate the patient’s experience and guide restorative care.

The Role of the Hair Growth Cycle in Shedding

Understanding why those triggers cause shedding requires a look at the hair growth cycle itself. At any time, about 80-90% of your follicles are in anagen (active growth), ~5% in catagen (regression), and 5-15% in telogen (resting). Telogen effluvium occurs when a systemic stressor abruptly shifts a disproportionate number of anagen follicles, sometimes up to 70%, into telogen.

These telogen hairs develop club-shaped, depigmented bulbs with weak anchoring, so you’ll see them on pillows, in drains, and on brushes 1-3 months after the insult. Unlike hair miniaturization or follicle senescence, the follicles themselves remain structurally intact; the disturbance is primarily in cycle kinetics. When the trigger resolves, most follicles re-enter anagen over 3-6 months, restoring a healthier anagen:telogen ratio.

Telogen Effluvium Stress

When you experience significant physical stress such as major surgery, severe infection, high fever, or rapid weight loss can cause your body to trigger a synchronized shift of anagen follicles into telogen, producing diffuse shedding several months later.

Intense mental and emotional stressors, including bereavement, major life changes, or severe anxiety, act through neuroendocrine pathways (e.g., hypothalamic-pituitary-adrenal axis activation and elevated cortisol) to disrupt normal follicular cycling in a similar fashion.

Understanding how both somatic and psychological stressors perturb the hair growth cycle helps you and your clinician target modifiable triggers and implement effective recovery strategies.

Physical Stress

Because hair follicles are exquisitely sensitive to systemic disruption, significant physical stress such as high fever, major surgery, serious infection, traumatic injury, or rapid, marked weight loss can abruptly shift a large proportion of actively growing (anagen) hairs into the resting (telogen) phase, setting the stage for diffuse shedding 2-4 months later.

During an intense fever response or complex trauma recovery, your body prioritizes essential organs over hair, treating follicles as expendable.

You’ll often see shedding after childbirth, severe COVID‑19, or other acute systemic illnesses, when abrupt estrogen or metabolic shifts precipitate telogen effluvium.

Similarly, extreme low‑protein diets, rapid weight loss, and certain medications or hormone withdrawals create physiologic strain that synchronously drives follicles into telogen, yet usually without scarring or permanent loss.

Mental & Emotional Stress

Although telogen effluvium is often linked to obvious physical insults, significant mental and emotional stress such as bereavement, job loss, divorce, or sustained anxiety can act as a potent trigger by dysregulating the hair cycle via neuroendocrine pathways. Intense psychological load elevates cortisol and catecholamines, pushing up to ~70% of anagen hairs prematurely into telogen, with shedding emerging 2-3 months later.

Clinical Aspect	Service-Oriented Response
Acute grief episode	Offer presence, encourage gentle self‑care
Job or financial loss	Support problem-solving, stabilize routines
Chronic anxiety	Normalize help-seeking, suggest mindfulness practices
Past or recent trauma	Advocate for evidence-based trauma therapy
Caregiver burnout	Promote respite, boundary-setting, peer support

You’ll usually see diffuse shedding with a normal-appearing scalp; club hairs on pull test support the diagnosis. Addressing stress, sleep, and nutrition fosters regrowth within 3-6 months.

Hormonal Shifts and Endocrine Disorders

While telogen effluvium is often framed as a response to “stress,” many of the most important triggers are actually abrupt hormonal shifts and underlying endocrine disorders that disrupt follicular cycling.

You’ll frequently see this after childbirth, when the steep postpartum estrogen decline precipitates shedding 2-3 months later. Similar patterns occur with menopause, discontinuing estrogen-containing contraceptives, or poorly titrated hormone replacement.

You should also consider thyroid disease; both hypo- and hyperthyroidism alter anagen duration, so TSH testing is essential when hair loss coexists with fatigue, weight change, or thermoregulatory symptoms.

Beyond thyroid, adrenal dysfunction and other endocrine pathology, such as uncontrolled polycystic ovary syndrome or systemic cortisol derangements, can modify growth-factor and cytokine signaling at the follicular level, driving diffuse telogen shedding.

Telogen Effluvium Nutritional Deficiencies

When you’re evaluating telogen effluvium, you should consider that suboptimal micronutrient status particularly vitamin D deficiency, vitamin B12 deficiency, and zinc deficiency can impair normal hair-cycle kinetics and exacerbate shedding.

Each of these nutrients participates in follicular keratinocyte proliferation, immune modulation, and scalp microenvironment homeostasis, so insufficiency can increase the proportion of hairs entering telogen.

You’ll typically confirm these deficits with targeted serum assays and integrate correction into a broader, etiologically focused management plan.

Vitamin D Deficiency

Linking telogen effluvium to vitamin D status reflects growing evidence that low serum 25‑hydroxyvitamin D is more common in people with diffuse shedding than in the general population, with many patients testing below the typical sufficiency threshold of 30 ng/mL (75 nmol/L). You’ll see this more in individuals with limited sun exposure, darker phototypes, religious covering, seasonal variability, or genetic predisposition affecting vitamin D metabolism.

Because hair follicles express vitamin D receptors that modulate anagen/telogen shifts, deficiency can bias follicles toward premature telogen entry. When you support others with telogen effluvium, you should interpret a single low 25‑OH vitamin D level in context, diet, medications, comorbidities, inflammatory status, ferritin. After confirming deficiency, many clinicians use cholecalciferol 1,000 to 4,000 IU daily (or supervised loading regimens) and recheck levels in 8-12 weeks.

Vitamin B12 Deficiency

Subtle depletion of vitamin B12 can undermine hair follicle cycling by impairing DNA synthesis in rapidly dividing hair matrix keratinocytes, predisposing follicles to premature telogen entry and diffuse shedding.

You’ll often see this several months after the deficit develops, paralleling fatigue, pallor, or neuropathic symptoms.

When you evaluate diffuse hair loss, you serve patients well by ordering serum B12 with confirmatory methylmalonic acid in borderline cases.

Remember that impaired intrinsic factor (as in pernicious anemia), gastric bypass, strict vegan diets, and long‑term metformin or proton pump inhibitor use markedly increase deficiency risk.

Once you replete B12—via oral or intramuscular routes—telogen shedding typically stabilizes first; visible regrowth follows over months as follicles progressively reenter anagen.

Zinc Deficiency

Zinc deficiency quiets hair follicle proliferation and immune regulation in ways that predispose a disproportionate number of follicles to premature telogen entry and diffuse shedding. You’ll often see this in those negotiating restrictive diets, vegetarian or vegan patterns, chronic illness, or malabsorptive states, where zinc deficits cluster with iron and protein insufficiency.

When you evaluate someone with telogen effluvium, integrate serum zinc with ferritin and iron studies, recognizing that inflammation and fasting status can distort values and that interpretation demands clinical correlation. Management centers on short-term zinc supplementation, typically 15-30 mg elemental zinc daily under supervision, alongside dietary optimization and attention to absorption inhibitors such as phytate-rich grains. You’ll also guard against prolonged high-dose zinc, which can precipitate secondary copper deficiency.

Medication Induced Hair Loss

Medications can precipitate telogen effluvium by abruptly shifting a disproportionate number of anagen follicles into the telogen phase, leading to diffuse shedding that typically appears 2-3 months after you start or stop a drug. You support those you serve by recognizing suspicious dose‑response patterns and encouraging pharmacovigilance reporting when shedding coincides with medication changes.

Clinically, you’ll review recent exposure to beta‑blockers, retinoids or excess vitamin A, anticoagulants, select antidepressants, calcium channel blockers, and anticonvulsants such as carbamazepine. You’ll distinguish this reversible telogen shedding from chemotherapy‑related anagen effluvium.

Drug class	Clinical relevance for you to note
Beta‑blockers	May cause delayed diffuse shedding
Retinoids/Vitamin A	Hypervitaminosis A frequently implicated
Anticoagulants	Heparin, warfarin, DOACs occasionally trigger loss
Anticonvulsants/others	Carbamazepine, some antidepressants, calcium blockers

Thoughtful review, labs (iron, thyroid), and collaboration guide safe adjustments and regrowth.

Telogen Effluvium After Surgery

When you undergo surgery, it’s not only the operative trauma and systemic inflammatory response that can precipitate telogen effluvium, but also the anesthetic exposure itself.

General anesthesia alters hemodynamics, oxygen delivery, and neuroendocrine signaling, all of which can transiently disrupt the hair cycle and push anagen follicles into premature telogen.

You’ll often notice the resulting diffuse shedding 2-3 months after anesthesia, temporally correlating the hair loss with your procedure rather than with any ongoing scalp pathology.

Anesthesia

Although people often blame “the anesthesia” itself, it’s the overall physiological stress of major surgery and general anesthesia that commonly precipitates telogen effluvium, with noticeable shedding typically emerging 2-3 months post‑operation. Systemic stressors—hemodynamic instability, intraoperative hypoxia, blood loss, postoperative inflammation, and pain can abruptly shift many follicles from anagen into telogen. You may notice diffuse, non‑scarring shedding, often 150-300 hairs daily, while the hairline remains preserved.

Clinicians should integrate your surgical history, screen for anemia and thyroid dysfunction, and offer reassurance while you heal and continue serving others. In most cases, shedding remits within 3-6 months.

Surgical Factor	Potential Effect on Follicles	Clinical Relevance
Hemodynamic shifts	Telogen shift	Common trigger
Intraoperative hypoxia	Follicular stress	Intensifies shedding risk
Blood loss	Iron depletion	Evaluate ferritin
Anesthesia awareness	Psychological stress	Can compound telogen effluvium
Postoperative infection	Systemic inflammation	May prolong shedding

Postpartum Telogen Effluvium

Because childbirth triggers abrupt endocrinologic and physiologic shifts, postpartum telogen effluvium is a common, self-limited cause of diffuse shedding that typically begins 2-4 months after delivery as pregnancy-related estrogen levels fall. You may notice sudden, generalized thinning with up to ~300 hairs lost daily, yet the scalp remains healthy and non-scarred.

You serve others best when you understand:

1. You experience a synchronized shift of anagen follicles into telogen, then shedding several weeks later.
2. Risk amplifiers include iron deficiency, caloric restriction, high psychosocial stress, breastfeeding impact on nutrient reserves, and genetic predisposition.
3. Shedding usually peaks by 3 months postpartum and remits as regrowth begins around 3-6 months, with typical normalization by 6-12 months.
4. You support recovery through lab-guided correction of deficiencies, gentle hair care, stress modulation, and clinician-directed therapies.

Chronic Diseases and Inflammatory Conditions

Beyond postpartum shifts, chronic diseases and inflammatory conditions frequently act as ongoing triggers for telogen effluvium by sustaining a systemic stress and cytokine burden that disrupts the hair cycle. In rheumatoid arthritis, inflammatory bowel disease, systemic lupus, or psoriasis, chronic inflammation drives excess TNF‑α, IL‑1, and IL‑6, prematurely converting anagen follicles to telogen and producing diffuse shedding.

You should also consider endocrine and infectious contributors: uncontrolled thyroiditis or thyroid dysfunction, chronic hepatitis, HIV, and other persistent infections often maintain telogen effluvium as long as disease activity remains uncontrolled.

Because there’s frequent autoimmune overlap, you need to distinguish telogen effluvium from alopecia areata and other autoimmune alopecias using careful history, scalp examination, targeted serologies, and sometimes biopsy, then coordinate anti‑inflammatory therapy and nutritional support to restore growth.

Environmental, Lifestyle, and Hair-Care Factors

Environmental, lifestyle, and hair‑care factors often converge to tip vulnerable follicles into telogen, even when you don’t have an obvious medical illness. You can serve others more effectively when you recognize and modify these triggers early.

1. Rapid weight loss, low‑protein or highly restrictive diets, and associated micronutrient deficits (iron, zinc, vitamin D) commonly precipitate diffuse shedding 2-3 months later.

2. Medication shifts (starting or stopping oral contraceptives, antidepressants, retinoids, beta‑blockers, anticoagulants) can quietly reset follicular cycling.

3. Chronic psychological stress dysregulates cortisol and sympathetic tone, destabilizing the hair cycle and possibly the scalp microbiome.

4. Repeated chemical processing, tight traction styles, aggressive heat, and even water hardness can damage the cuticle, increase fragility, and clinically amplify telogen effluvium, especially in already stressed scalps.

When Multiple Triggers Occur Together

When telogen effluvium follows more than one trigger at the same time, the cumulative impact on the hair cycle can be substantial, with up to ~70% of anagen follicles shifting into telogen and producing striking diffuse shedding 2-3 months later.

You’ll often see this when cumulative triggers overlap: severe illness plus rapid weight loss, postpartum hormonal shifts plus iron deficiency from blood loss, or major surgery accompanied by intense psychological stress.

Concurrent medication changes (for example, starting or stopping hormonal contraceptives) combined with restrictive dieting further amplify telogen entry through simultaneous hormonal and nutritional disruption.

When you’re serving patients or clients, systematically review the prior 1-6 months—medical, surgical, nutritional, psychosocial—to uncover all triggers.

Addressing each factor shortens the recovery timeline and reduces progression to chronic telogen effluvium.

Telogen Effluvium Post Covid

Although telogen effluvium can follow many systemic stressors, COVID‑19 has emerged as a particularly frequent trigger, with diffuse shedding typically appearing 2-3 months after acute infection.

You may see hundreds of hairs shed daily, often alarming patients already coping with long‑covid fatigue or dysautonomia.

To serve them well, you’ll need to:

1. Clarify mechanism: Explain how cytokine surges, febrile illness, metabolic stress, and possible autoimmune activation abruptly shift anagen follicles into telogen.

2. Risk‑stratify: Recognize higher TE risk after severe COVID, ICU care, or marked weight loss.

3. Exclude alternatives: Screen for iron deficiency, thyroid dysfunction, new medications, and other triggers.

4. Guide recovery: Offer reassurance, correct deficiencies, reduce stress, and consider minoxidil when shedding is prolonged, emphasizing that regrowth usually begins within 3-6 months.

Frequently Asked Questions

Can Telogen Effluvium Be Hereditary or Run in Families?

Telogen Effluvium usually doesn’t run in families, yet you may notice familial clustering suggesting genetic predisposition or inherited susceptibility. You should instead prioritize modifiable triggers, then counsel relatives that shared environments, not fixed family patterns, most strongly influence telogen effluvium.

How Long Until Hair Fully Regrows After Telogen Effluvium Resolves?

Telogen Effluvium sufferers typically see full regrowth 6-12 months after it resolves, as your hair cycle normalizes. Shedding duration usually ends within 3-6 months, then follicles re-enter anagen, progressively restoring density and cosmetic coverage.

Can Telogen Effluvium Turn Into Permanent Hair Loss or Baldness?

No, you usually don’t progress to permanent baldness; imagine a dimmed garden, not scorched earth. Unless coexisting scalp scarring or androgenetic-type follicle miniaturization occurs, telogen effluvium’s follicles remain viable, allowing regrowth and preserving your capacity to serve confidently.

How Is Telogen Effluvium Diagnosed and Distinguished From Other Hair Loss Types?

You’re diagnosed through detailed history, scalp-focused clinical examination, and a gentle hair pull test showing excess telogen hairs. Dermoscopy, trichogram, and targeted labs help distinguish telogen effluvium from androgenetic alopecia, alopecia areata, scarring alopecias, and systemic disorders.

Do Scalp Biopsies or Blood Tests Help Confirm Telogen Effluvium?

Yes, scalp sampling and targeted lab panels can support your diagnosis, yet they don’t always prove telogen effluvium; you’ll integrate histologic telogen counts, systemic workup, medication review, and timeline correlation to serve patients with precision.