Hair Loss: What Could Be Causing It

The First Diagnostic Branch: Scarring vs. Non-Scarring

The single most important clinical distinction is whether the hair follicle has been destroyed. Scarring (cicatricial) alopecias show loss of follicular ostia on dermoscopy, irreversible follicle destruction, and often erythema or scale at the active border. Non-scarring alopecias preserve the follicular unit, meaning regrowth remains possible with appropriate treatment.

Scarring alopecias represent fewer than 7% of hair loss referrals to dermatology according to a North American Hair Research Society registry analysis [1]. They include lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, and discoid lupus. These demand biopsy and specialist management because delayed treatment results in permanent loss.

Non-scarring causes account for the vast majority of presentations. The diagnostic approach then subdivides by pattern: focal vs. diffuse, and within diffuse loss, whether there is a miniaturization pattern (suggesting androgenetic alopecia) or uniform thinning without miniaturization (suggesting telogen effluvium or systemic disease). A standard 4-mm punch biopsy with horizontal sectioning can distinguish these when clinical exam is inconclusive [2].

Androgenetic Alopecia: The Most Common Cause

Androgenetic alopecia (AGA) affects approximately 50% of men older than 50 and up to 40% of postmenopausal women, making it the single most frequent diagnosis in hair loss clinics [3]. The condition results from genetically determined sensitivity of hair follicles to dihydrotestosterone (DHT), which progressively miniaturizes terminal hairs into vellus-like hairs.

In men, AGA follows the Hamilton-Norwood scale: bitemporal recession progressing to vertex thinning. Women typically retain the frontal hairline but show diffuse thinning over the crown, classified by the Ludwig scale or the Sinclair scale. The diagnosis is clinical in most cases. Dermoscopy reveals hair diameter diversity greater than 20%, peripilar signs, and yellow dots.

Treatment options backed by randomized controlled trials include topical minoxidil 5% (JAMA Dermatology meta-analysis: mean hair count increase of 14.9 hairs/cm² vs. placebo at 24 weeks) [4], oral finasteride 1 mg daily in men (a 5-year RCT showed 65% of men maintained or increased hair count vs. 0% on placebo) [5], and low-level laser therapy. For women, minoxidil 5% foam and spironolactone 100-200 mg daily are first-line agents, though spironolactone lacks FDA approval for this indication [6].

Dr. Wilma Bergfeld, former president of the American Academy of Dermatology, has stated: "The earlier you intervene in androgenetic alopecia, the more follicles you can rescue from permanent miniaturization. Once a follicle has been miniaturized for years, reversal becomes far less likely."

Telogen Effluvium: The Stress-Related Shed

Telogen effluvium (TE) is the second most common cause of hair loss in adults. It presents as diffuse, non-patterned shedding that begins 2 to 4 months after a triggering event. Common triggers include high fever (including post-COVID shedding, reported in up to 33% of hospitalized COVID-19 patients) [7], major surgery, rapid weight loss exceeding 10 kg, postpartum hormonal shifts, severe psychological stress, and nutritional deficiency.

The mechanism is straightforward. A physiologic insult prematurely shifts a large percentage of anagen (growing) hairs into the telogen (resting) phase simultaneously. After the 2-3 month telogen rest period, these hairs shed in bulk. Patients often present alarmed by clumps in the shower drain or on their pillow.

Diagnosis rests on three pillars: compatible timeline (trigger 2-4 months prior), diffuse thinning without miniaturization pattern, and a positive hair pull test (more than 6 telogen hairs per 60-strand pull from multiple scalp areas). A trichogram showing more than 25% telogen hairs confirms the diagnosis. No biopsy is needed in classic presentations.

The prognosis is excellent. Acute TE resolves spontaneously within 6-9 months once the trigger is removed [8]. Chronic TE (lasting longer than 6 months) exists but is less common and may overlap with early AGA in women. No specific pharmacologic treatment accelerates recovery, though correcting any underlying deficiency (iron, zinc, vitamin D) supports normal cycling.

Alopecia Areata: Autoimmune Patchy Loss

Alopecia areata (AA) is a T-cell-mediated autoimmune condition targeting the hair follicle bulb. Lifetime prevalence reaches approximately 2% worldwide, with most cases presenting before age 40 [9]. The clinical hallmark is one or more smooth, round, well-demarcated patches of complete hair loss without scarring or scale.

Pathognomonic findings include "exclamation mark" hairs (short broken hairs that taper toward the scalp) at the active margins and smooth, skin-colored patches without follicular dropout. Nail pitting occurs in 10-20% of patients. The condition can progress to alopecia totalis (complete scalp loss) or alopecia universalis (total body hair loss), though most patients with limited patches experience spontaneous regrowth within 12 months.

The American Academy of Dermatology guidelines recommend intralesional triamcinolone acetonide (2.5-10 mg/mL) as first-line for limited patches [10]. For extensive disease (more than 50% scalp involvement), the JAK inhibitor baricitinib 4 mg daily received FDA approval in June 2022 based on the BRAVE-AA1 and BRAVE-AA2 trials, where 35-39% of patients achieved 80% or greater scalp coverage (SALT score of 20 or less) by week 36 vs. 3-6% on placebo [11]. Ritlecitinib, another JAK inhibitor, gained FDA approval in June 2023.

Dr. Brett King, associate professor of dermatology at Yale School of Medicine, noted in a 2022 NEJM editorial: "JAK inhibitors represent the first mechanism-specific, FDA-approved therapies for alopecia areata, ending decades without a labeled treatment for this disease."

Thyroid Disorders and Hair Loss

Both hypothyroidism and hyperthyroidism cause diffuse hair thinning, and thyroid dysfunction should be excluded in every patient presenting with non-patterned shedding. Hypothyroidism is far more common, affecting approximately 5% of the U.S. population, with subclinical disease present in an additional 5-10% [12].

Thyroid hormones directly regulate the hair cycle. T3 and T4 prolong anagen duration and stimulate hair matrix keratinocyte proliferation. In hypothyroidism, hairs prematurely enter telogen and the anagen-to-telogen ratio shifts. The hair itself may become dry, coarse, and brittle. Lateral eyebrow thinning (the "Queen Anne sign") is a classic but insensitive finding.

Screening requires only TSH. If TSH is elevated, free T4 confirms hypothyroidism. Treatment with levothyroxine typically restores normal hair cycling within 4-6 months of achieving euthyroid status. Patients should be counseled that hair regrowth lags behind biochemical normalization by 2-3 months due to the telogen rest phase.

Autoimmune thyroid disease (Hashimoto thyroiditis) deserves special mention because it co-occurs with alopecia areata at higher than expected rates. A 2019 meta-analysis found that patients with alopecia areata had 2.6 times the odds of concurrent thyroid autoimmunity compared to controls [13].

Iron Deficiency: A Treatable and Underdiagnosed Contributor

Iron deficiency is the most common nutritional cause of hair shedding and frequently coexists with other diagnoses, particularly in premenopausal women. A serum ferritin below 30 ng/mL is associated with increased telogen shedding regardless of whether frank anemia is present [14].

The mechanism involves iron's role as a cofactor for ribonucleotide reductase, an enzyme required for DNA synthesis in rapidly dividing hair matrix cells. When iron stores decline, the body preferentially diverts iron to essential functions (erythropoiesis, oxygen transport), and hair follicles, as non-essential tissue, receive reduced supply.

A 2006 study in the Journal of the American Academy of Dermatology found that 72% of premenopausal women presenting with diffuse hair loss had ferritin levels below 40 ng/mL, compared to 29% of age-matched controls without hair complaints [15]. The optimal ferritin target for hair regrowth remains debated, but most trichologists aim for levels above 50-70 ng/mL.

Iron supplementation with ferrous sulfate 325 mg daily (65 mg elemental iron) taken with vitamin C on an empty stomach is standard. Parenteral iron (ferric carboxymaltose) may be appropriate when oral supplementation fails or gastrointestinal intolerance limits adherence. Response takes 3-6 months to become visible.

Medication-Induced Hair Loss

Over 100 medications list hair loss as a documented adverse effect. The most clinically significant drug classes include anticoagulants (heparin, warfarin), retinoids (isotretinoin, acitretin), antithyroid drugs, chemotherapy agents, lithium, valproic acid, beta-blockers, ACE inhibitors, and excess vitamin A supplementation [16].

Drug-induced hair loss occurs through two mechanisms. Anagen effluvium (acute interruption of actively growing hairs) is seen primarily with cytotoxic chemotherapy and presents within days to weeks of drug initiation. Telogen effluvium (premature shift of hairs to resting phase) is the far more common pattern with non-cytotoxic medications and presents 2-4 months after drug initiation, making the temporal association less obvious to patients.

The approach is straightforward: timeline correlation between drug start and hair loss onset. Rechallenge data are rarely available, so clinical judgment guides decisions. When the suspected medication is non-essential or has equivalent alternatives, a 3-6 month drug holiday with monitoring confirms causality. When the medication is medically necessary, patients may require concurrent minoxidil or reassurance that the shedding is self-limited.

GLP-1 receptor agonists deserve mention given their rapid adoption. Post-marketing pharmacovigilance data from the FDA Adverse Event Reporting System (FAERS) show elevated alopecia reports for semaglutide relative to background rates, though the confound of rapid weight loss (itself a telogen effluvium trigger) makes attribution difficult [17]. The STEP trials did not list alopecia as a primary adverse event, but post-hoc analyses and real-world registries suggest 3-5% incidence.

Less Common but Important Causes

Several additional diagnoses should remain on the differential when first-line workup is unrevealing.

Tinea capitis presents as patchy loss with broken hairs and scale, most common in children. KOH prep and fungal culture confirm diagnosis. Systemic antifungal therapy (griseofulvin or terbinafine for 6-8 weeks) is required because topical agents cannot penetrate the hair shaft [18].

Trichotillomania (hair-pulling disorder) affects 1-2% of the population, predominantly females. Patches are irregular, hairs are broken at varying lengths, and the fronto-parietal region is most commonly affected. The diagnosis is clinical but patients frequently deny the behavior.

Secondary syphilis causes a "moth-eaten" pattern of non-scarring alopecia in 4-11% of secondary syphilis cases. RPR/VDRL testing should be considered in sexually active patients with unexplained patchy loss.

Systemic lupus erythematosus produces both a non-scarring diffuse "lupus hair" (fine, fragile frontal hairs) and scarring discoid lesions. ANA and anti-dsDNA should be ordered when other lupus features coexist.

Nutritional deficiencies beyond iron include zinc (seen in restrictive diets, Crohn disease, bariatric surgery), biotin (rare except in carboxylase deficiency or raw egg white consumption), and protein-calorie malnutrition.

The Diagnostic Workup: A Practical Algorithm

For the primary care clinician evaluating hair loss, an efficient laboratory panel includes TSH, ferritin, CBC with differential, and a comprehensive metabolic panel. In women with signs of hyperandrogenism (acne, hirsutism, irregular menses), add total and free testosterone, DHEA-S, and 17-hydroxyprogesterone [19].

The physical exam should document distribution (focal vs. diffuse, patterned vs. non-patterned), presence of scaling or erythema, follicular ostia preservation, and the pull test result. Dermoscopy, when available, adds significant diagnostic power by revealing miniaturization, exclamation mark hairs, black dots, or perifollicular erythema.

Referral to dermatology is appropriate when: the diagnosis remains uncertain after initial workup, scarring alopecia is suspected, alopecia areata involves more than 50% of the scalp, or standard treatments fail after 6-12 months. A scalp biopsy with horizontal sectioning by a dermatopathologist remains the gold standard for ambiguous cases.

According to the American Academy of Dermatology 2022 practice guidelines: "Early, accurate classification of hair loss type is the single most important determinant of treatment success. Misclassification, particularly the failure to distinguish androgenetic alopecia from chronic telogen effluvium in women, leads to inappropriate therapy and delayed improvement" [20].

When to Worry: Red Flags Requiring Urgent Evaluation

Most hair loss is cosmetically distressing but medically benign. However, certain presentations warrant expedited workup. Rapid progression over days to weeks (rather than months), associated systemic symptoms (weight changes, fatigue, fever), scarring or pustules on the scalp, and hair loss in a prepubertal child all require prompt evaluation.

Hair loss accompanied by virilization in women (deepening voice, clitoromegaly, rapid-onset hirsutism) may signal an androgen-secreting tumor and requires urgent hormonal evaluation and imaging. Loss of body hair along with scalp hair raises concern for alopecia universalis, systemic disease, or hypopituitarism.

The 2023 Endocrine Society Clinical Practice Guideline recommends that premenopausal women with hair loss plus menstrual irregularity undergo evaluation for polycystic ovary syndrome, which affects 6-12% of reproductive-age women and represents the most common endocrine cause of female pattern hair loss in young women [21].

Patients losing more than 300 hairs daily (a rough threshold estimated by the modified wash test), experiencing rapid scalp visibility changes over less than 3 months, or developing new patches weekly should receive dermatology referral within 2-4 weeks rather than a watch-and-wait approach.