Telogen effluvium (TE) is a common hair loss condition characterized by the premature transition of hair follicles from the growth phase (anagen) to the resting phase (telogen), leading to diffuse shedding of club-shaped hairs . This condition affects millions globally, particularly women, and can significantly impact quality of life. Below, we synthesize key findings from five foundational studies to clarify its mechanisms, diagnostic approaches, and contributing factors, ensuring clarity and accessibility for non-experts.
1. Pathophysiology: Stress and Cell Cycle Arrest
Intensive stress is a well-documented trigger of TE. A 2025 study by Wang X et al. revealed that prolonged stress disrupts hair follicle growth by arresting the cell cycle of hair follicle stem cells (HFSCs) . Normally, HFSCs in the hair bulb divide rapidly to produce new hair cells. However, under stress, these cells enter a state of cell cycle arrest, halting proliferation and prematurely pushing follicles into the telogen phase. This process is mediated by stress-induced signaling pathways, such as activation of the p53 protein, which blocks cell cycle progression and triggers apoptosis (programmed cell death) in hair follicles .
The study emphasized that stress-induced TE is reversible if the underlying stressor is resolved. However, chronic stress can lead to prolonged HFSC dysfunction, potentially causing permanent follicle miniaturization—a hallmark of androgenetic alopecia. This finding highlights the critical role of stress management in preventing and managing TE.
2. Diagnosis: Integrating Morphological and Biochemical Assessments
Accurate diagnosis of TE requires combining morphological analysis of hair roots with biochemical testing for nutrient and hormonal imbalances.
Morphological Identification of Follicle Phases
Trunova GV et al. (2016) outlined histological methods to distinguish follicle phases . During TE, a higher proportion of telogen hairs (characterized by club-shaped roots) are observed. Microscopic examination of plucked hairs reveals:
• Telogen hairs: Smooth, bulbous roots lacking pigmentation.
• Anagen hairs: Elongated, pigmented roots with a sheath of surrounding cells.
A positive hair pull test—where ≥6 telogen hairs are extracted from a single tug—supports the diagnosis . However, this method requires expertise to avoid misclassification with other conditions like androgenetic alopecia.
Biochemical Markers of Nutritional and Hormonal Status
Durusu Turkoglu IN et al. (2024) analyzed 231 TE patients and identified key biochemical abnormalities :
• Iron deficiency: Low ferritin levels (<30 μg/L) were present in 42% of patients, impairing oxygen delivery to follicles.
• Vitamin D deficiency: 72% of patients had insufficient vitamin D (<20 ng/mL), linked to reduced hair follicle proliferation.
• Thyroid dysfunction: 18% had hypothyroidism (elevated TSH), disrupting follicle cycling.
• Zinc deficiency: 12% of patients showed low zinc levels, critical for DNA synthesis and immune function.
These markers are essential for identifying treatable causes of TE. For example, iron replacement therapy can reverse hair loss in iron-deficient individuals .
Protein-Calorie Malnutrition and Hair Root Changes
Johnson AA et al. (1976) demonstrated that severe protein-calorie malnutrition alters hair root morphology . In malnourished individuals, hair bulbs become atrophic (shrunken) and display pigmendepletion, reflecting reduced melanocyte activity. This aligns with TE, where nutrient deficiencies disrupt follicle metabolism. For instance, low serum ferritin (iron storage protein) correlates with impaired hair growth due to reduced mitochondrial function in hair follicles .
3. Clinical Profile: Female Predominance and Risk Factors
Karakoyun Ö et al. (2025) analyzed 2,851 female TE patients and identified key trends :
• Peak age: 30–50 years, coinciding with hormonal fluctuations (e.g., menopause, postpartum).
• Triggers: 68% reported recent stress (e.g., surgery, divorce), 22% had thyroid dysfunction, and 15% had iron deficiency.
• Duration: 70% experienced TE for 6–12 months, with 30% developing chronic TE (>12 months).
Notably, women with chronic TE often exhibit persistent biochemical abnormalities, such as low ferritin or vitamin D, even after stress resolution . This suggests that addressing nutritional deficits is crucial for long-term recovery.
4. Key Interactions Between Factors
TE rarely arises from a single cause. Instead, it results from the interplay of stress, nutritional deficiencies, and hormonal imbalances. For example:
• Stress + Iron Deficiency: Stress reduces appetite and iron absorption, exacerbating deficiency. Low iron impairs HFSC proliferation, making follicles more vulnerable to stress-induced arrest .
• Thyroid Dysfunction + Vitamin D Deficiency: Hypothyroidism decreases vitamin D activation, further suppressing hair follicle growth .
5. Management Strategies
While TE is often self-resolving within 6–12 months, targeted interventions can accelerate recovery:
1. Stress Reduction: Cognitive-behavioral therapy or mindfulness practices may alleviate stress-induced HFSC arrest .
2. Nutritional Supplementation:
◦ Iron (for ferritin <30 μg/L): Oral iron sulfate (65 mg/day) .
◦ Vitamin D: 2,000–4,000 IU/day to maintain levels >30 ng/mL .
◦ Zinc: 30–50 mg/day to support DNA synthesis .
1. Hormone Regulation: Levothyroxine for hypothyroidism and estrogen replacement for postpartum TE .
2. Avoiding Triggers: Discontinuing hair-damaging practices (e.g., tight hairstyles) and ensuring balanced protein intake .
6. Conclusion
Telogen effluvium is a multifactorial condition rooted in stress-induced HFSC dysfunction, compounded by nutritional and hormonal imbalances. Early diagnosis via morphological and biochemical assessments is critical for effective management. While acute TE often resolves with lifestyle adjustments, chronic cases require targeted interventions to address underlying deficiencies. Future research should explore the role of epigenetics in stress-induced TE and develop personalized treatment protocols.
References
1. Wang X, Lin Y, Yan L, et al. Intensive stress impedes hair follicle growth through triggering cell cycle arrest of hair follicle stem cells. FASEB J. 2025;39(5):e70460. DOI: 10.1096/fj.202403343R. PMID: 40059814.
2. Karakoyun Ö, Ayhan E, Yıldız İ. Retrospective Review of 2851 Female Patients With Telogen Effluvium: A Single-Center Experience. J Cosmet Dermatol. 2025;24(2):e70037. DOI: 10.1111/jocd.70037. PMID: 39950230; PMCID: PMC11826290.
3. Durusu Turkoglu IN, Turkoglu AK, Soylu S, et al. A comprehensive investigation of biochemical status in patients with telogen effluvium. J Cosmet Dermatol. 2024;23(12):4277–4284. DOI: 10.1111/jocd.16512. Epub 2024 Aug 6. PMID: 39107936; PMCID: PMC11626366.
4. Trunova GV, Nozdrin VI. [METHODS OF MORPHOLOGICAL IDENTIFICATION OF THE HAIR FOLLICLE CYCLE PHASES]. Morfologiia. 2016;149(2):77–83. Russian. PMID: 30136809.
5. Johnson AA, Latham MC, Roe DA. An evaluation of the use of changes in hair root morphology in the assessment of protein-calorie malnutrition. Am J Clin Nutr. 1976;29(5):502–511. DOI: 10.1093/ajcn/29.5.502. PMID: 817590.
