Hair Loss: What Could Be Causing It

Hair loss (alopecia) is a symptom, not a diagnosis. The reader question that matters most is not "what are all the causes of hair loss" but "which pattern am I seeing, and does that pattern point toward a self-limited process, a treatable systemic condition, or something that needs a dermatologist before more follicles are lost." A handful of conditions, androgenetic alopecia, telogen effluvium, alopecia areata, thyroid dysfunction, iron deficiency, and medication-related shedding, account for most presentations seen outside specialty clinics. The distinction that changes management most is whether the follicle has been destroyed (scarring alopecia) or is still intact (non-scarring alopecia), because only the second group has a real chance of regrowth.

This article describes patterns and evidence categories. It does not diagnose an individual reader's hair loss, and it does not replace an in-person exam, a pull test, or bloodwork ordered by a clinician who has actually looked at the scalp.

The core distinction: scarring versus non-scarring

The first branch point in any hair loss evaluation is whether the follicular opening (ostium) is still visible on close inspection or dermoscopy. If the follicular openings are gone, replaced by smooth scarring or fibrosis, the process has likely destroyed the follicle. Scarring alopecias (lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, discoid lupus) are a minority of cases seen in general practice but carry the highest urgency, because damage already done cannot be reversed and delay allows more follicles to scar over. These need dermatology referral and usually a scalp biopsy.

Non-scarring alopecias, where the follicle is structurally intact and regrowth is biologically possible, make up the large majority of presentations. Within non-scarring loss, the next question is pattern: focal patches versus diffuse thinning, and within diffuse thinning, whether there is miniaturization (hairs getting progressively finer, pointing toward androgenetic alopecia) or uniform loss without miniaturization (pointing toward telogen effluvium or a systemic cause).

The single paragraph worth quoting on its own: Hair loss that shows preserved follicular openings, no scarring, and no scalp inflammation is very unlikely to be permanent as a starting assumption, and the diagnosis usually narrows to androgenetic alopecia, telogen effluvium, alopecia areata, thyroid dysfunction, iron deficiency, or a medication effect. Hair loss with visible scarring, pustules, or rapid progression over days rather than months is the exception that warrants prompt dermatology evaluation rather than watchful waiting, because scarring alopecias destroy the follicle permanently if untreated. This branch point, scarring versus non-scarring, matters more to a reader's next step than any single cause on the list below.

Androgenetic alopecia (male and female pattern hair loss)

Androgenetic alopecia (AGA) is the most common cause of hair thinning in both sexes and becomes more prevalent with age, driven by genetically determined follicle sensitivity to dihydrotestosterone (DHT), which gradually converts thick terminal hairs into finer, shorter vellus-like hairs. In men this follows a recognizable pattern of bitemporal recession progressing to vertex thinning (Hamilton-Norwood scale). Women more often keep their frontal hairline but develop diffuse thinning over the crown (Ludwig or Sinclair scale). The diagnosis is usually made clinically, supported by dermoscopy showing hair-diameter variability (miniaturization) rather than by biopsy.

The FDA has approved two medications specifically for androgenetic alopecia: minoxidil applied to the scalp and finasteride taken orally by men. Clinical trials demonstrate that minoxidil produces measurable hair count improvements versus placebo, while long-term studies indicate finasteride slows or partially reverses hair loss in most men who use it, though specific effectiveness figures should be verified in the original research rather than cited as universal values. Women typically start with topical minoxidil as the initial treatment option, though some doctors prescribe spironolactone off-label for female pattern hair loss despite lacking FDA approval for this application. Low-level laser devices have received FDA clearance for hair regrowth, though supporting evidence is less extensive than what exists for the two medications. Visible results from any of these approaches usually require four to six months, and ongoing use is typically necessary to preserve gains since androgenetic alopecia is an ongoing condition that progresses over time rather than resolving permanently.

Telogen effluvium: diffuse shedding after a trigger

Telogen effluvium (TE) is diffuse, non-patterned shedding that typically begins roughly two to four months after a physiologic trigger: high fever or acute illness, major surgery, rapid or significant weight loss, childbirth, severe psychological stress, crash dieting, or a new nutrient deficiency. The mechanism is a synchronized shift of a larger-than-normal share of growing (anagen) hairs into the resting (telogen) phase; those hairs then shed together roughly two to three months later, which is why the shedding often seems to come "out of nowhere" relative to the actual trigger.

Diagnosis rests on a compatible timeline, diffuse loss without a miniaturization pattern on dermoscopy, and a positive pull test (more than about six hairs coming out per gentle pull of roughly 60 strands, tested at several scalp sites). Biopsy is not usually needed for a classic presentation. Acute telogen effluvium is self-limited and most cases improve within roughly six to nine months once the trigger resolves; a chronic form lasting longer than six months exists and can overlap clinically with early female pattern hair loss, which is one reason ongoing diffuse shedding beyond that window deserves a second look rather than continued reassurance. There is no drug specifically approved to speed recovery from telogen effluvium; correcting an underlying deficiency (iron, and less often zinc or vitamin D) is reasonable when one is present, but it treats the trigger, not the shedding itself.

Post-viral shedding, including after COVID-19 infection, has been reported as a recognizable variant of telogen effluvium in the medical literature, with wide variation in reported frequency across different patient populations. A precise incidence figure for any single population should not be treated as generally applicable without checking the specific study behind it.

Alopecia areata: patchy autoimmune hair loss

Alopecia areata is a T-cell-mediated autoimmune condition in which the immune system attacks the hair follicle bulb without destroying the follicle structure itself, which is why regrowth is possible even after complete loss in a patch. The classic finding is one or more smooth, round, well-demarcated bald patches with no scarring or scaling. "Exclamation mark" hairs, short hairs that taper and narrow toward the scalp, are a characteristic sign at the active edge of a patch. Nail pitting is a recognized associated finding in a meaningful minority of patients. Most patients with limited patchy involvement have some spontaneous regrowth over the following year, though the disease is unpredictable and can recur or progress to near-total scalp or body hair loss (alopecia totalis or universalis) in a smaller subset.

Intralesional corticosteroid injection is the established first-line treatment for limited patches. For more extensive disease, two JAK inhibitors have received FDA approval specifically for alopecia areata: baricitinib (approved in 2022) and ritlecitinib (approved in 2023), both based on placebo-controlled phase 3 trial programs showing a meaningfully higher proportion of treated patients regaining substantial scalp coverage compared with placebo over roughly eight to nine months of treatment. These are systemic immunomodulators with their own monitoring requirements (infection risk, lipid and blood count monitoring, and other class warnings for JAK inhibitors) and are prescribed by, or in coordination with, dermatology. Exact trial response percentages are cited widely but should be confirmed against the original trial publications rather than repeated from memory, since numbers vary slightly by endpoint and timepoint.

Thyroid disease as a cause of diffuse thinning

Both hypothyroidism and hyperthyroidism can cause diffuse hair thinning, which is why thyroid function is one of the first tests ordered in unexplained diffuse shedding. Thyroid hormone influences the length of the growth phase of the hair cycle and hair matrix cell turnover; in hypothyroidism, more hairs shift prematurely into the resting phase. Hair may also become dry, coarse, or brittle, and lateral eyebrow thinning is a classically described but not very sensitive sign.

A TSH is a reasonable first screening test; an abnormal result is generally followed by free T4 to characterize the disorder. Correcting thyroid hormone levels typically restores more normal hair cycling over a period of months, and patients should be told that visible regrowth lags behind normalized bloodwork by roughly two to three months because of the resting-phase delay described above. Autoimmune thyroid disease (Hashimoto thyroiditis) occurs more often than expected in people who also have alopecia areata, which is a reason to keep both conditions in mind together rather than treating a thyroid finding as fully explaining a patchy pattern.

Iron deficiency: a treatable, often-missed contributor

Low iron stores are a common and correctable contributor to diffuse hair shedding, particularly in premenopausal women, and can be present even when a standard complete blood count shows no anemia. Ferritin is the storage marker most clinicians use; lower ferritin levels have been associated with increased shedding in published studies, and iron is required as a cofactor for the enzyme that supports DNA synthesis in rapidly dividing hair matrix cells. When the body's iron supply is limited, red blood cell production is prioritized over hair follicle activity, since hair is not an essential tissue for survival.

There is no single, universally agreed ferritin cutoff for "hair-loss-relevant" iron deficiency; a low-normal or frankly low ferritin in the setting of diffuse shedding is a reasonable indication to consider supplementation, and many clinicians who treat hair loss aim for levels comfortably above the low end of the normal range rather than simply above the deficiency cutoff, though this target itself is a matter of clinical judgment rather than a settled guideline number. Oral iron supplementation taken with vitamin C is standard first-line; intravenous iron is reserved for people who cannot tolerate or do not respond to oral therapy. Visible improvement, if it occurs, generally takes several months, in keeping with the normal hair growth cycle.

Medication-related hair loss

A long list of medications is associated with hair shedding, including some anticoagulants, retinoids, antithyroid drugs, cytotoxic chemotherapy agents, lithium, valproic acid, some beta-blockers, some ACE inhibitors, and excess vitamin A supplementation. Two distinct mechanisms explain the timing difference reported clinically: cytotoxic chemotherapy typically causes anagen effluvium, an abrupt interruption of actively growing hairs that shows up within days to a few weeks of starting treatment, while most non-cytotoxic medications work through the same telogen-effluvium mechanism described above, with shedding appearing two to four months after the drug was started, which often makes the connection to the medication far less obvious to the patient.

Establishing causality in an individual case relies mostly on timeline correlation, since formal rechallenge testing is rarely done. When the suspected medication is not medically essential and a reasonable alternative exists, a supervised trial off the drug for several months, done in coordination with the prescribing clinician, can help confirm or rule out the medication as the cause. When the medication is necessary, the more common path is reassurance that drug-related telogen effluvium is usually reversible after discontinuation, sometimes supported by concurrent minoxidil.

GLP-1 receptor agonists (such as semaglutide) have drawn attention for reported hair loss. The FDA's Adverse Event Reporting System (FAERS) is a passive surveillance database, and elevated alopecia reports there do not by themselves establish that the drug causes hair loss independent of the weight loss it produces; rapid weight loss is itself a well-established trigger for telogen effluvium, which makes attribution genuinely difficult with this class of drugs. Anyone using a GLP-1 agonist who develops shedding should raise it with the prescribing clinician rather than assume either explanation on their own. (FDA FAERS Public Dashboard, accessed for general reference to the surveillance system; specific incidence figures require verification against the underlying reports and clinical trial data as of the article's publication date.)

Less common causes worth keeping on the list

A few additional diagnoses matter when the common causes above do not fit:

• Tinea capitis (scalp fungal infection): patchy loss with broken hairs and scale, most common in children, confirmed by KOH prep or fungal culture, and requiring systemic (not topical) antifungal therapy because topical treatment cannot reach the fungus inside the hair shaft.
• Trichotillomania (hair-pulling disorder): irregular patches with hairs broken at different lengths, most often in the fronto-parietal scalp; the diagnosis is clinical, and patients frequently do not disclose the behavior spontaneously.
• Secondary syphilis: a recognized but less common cause of a "moth-eaten" non-scarring pattern; RPR/VDRL testing is reasonable in sexually active patients with unexplained patchy loss.
• Systemic lupus erythematosus: can cause both non-scarring diffuse thinning ("lupus hair") and scarring discoid lesions; ANA and anti-dsDNA are reasonable when other lupus features are present.
• Other nutritional deficiencies: zinc (restrictive diets, inflammatory bowel disease, bariatric surgery) and, rarely, biotin deficiency, generally in the context of a specific dietary or metabolic risk factor rather than in an otherwise well-nourished adult.

A practical decision framework for narrowing the cause

This table is a starting orientation, not a diagnostic tool. Several causes can coexist (iron deficiency and androgenetic alopecia are commonly seen together in the same patient, for example), and a clinician who examines the scalp directly may reach a different conclusion than the pattern-matching above suggests.

Building a basic workup

A reasonable first-pass laboratory panel for diffuse, non-scarring hair loss includes TSH, ferritin, and a complete blood count. In women with signs suggesting excess androgen (acne, irregular periods, new or worsening hirsutism), total and free testosterone and DHEA-S are reasonable additions, and evaluation for polycystic ovary syndrome is warranted given that PCOS is a recognized and common endocrine cause of hair thinning in young women. The physical exam should note whether loss is focal or diffuse, patterned or non-patterned, whether scaling or redness is present, and whether follicular openings are preserved. Dermoscopy, where available, adds meaningful diagnostic information by revealing miniaturization, exclamation-mark hairs, black dots, or perifollicular redness that is not visible to the naked eye. A scalp biopsy with horizontal sectioning remains the most definitive test when the clinical picture stays ambiguous after this workup.

When to see a dermatologist rather than wait

Dermatology referral is reasonable, and in some cases urgent, when any of the following apply: scarring alopecia is suspected; the diagnosis remains unclear after basic labs and exam; alopecia areata involves a large portion of the scalp; standard treatment has failed after roughly six months; loss is progressing rapidly over days rather than months; there are pustules, scaling, or pain on the scalp; or hair loss is occurring in a child before puberty. Hair loss combined with signs of virilization in a woman (deepening voice, new significant hirsutism, clitoromegaly) is a distinct red flag that can point toward an androgen-secreting tumor and warrants prompt hormonal evaluation and imaging rather than a routine hair-loss workup. Loss of body hair along with scalp hair also deserves broader evaluation rather than being treated as ordinary pattern hair loss.

What is established, what is plausible, and what is not settled

Established: the six-category framework above (androgenetic alopecia, telogen effluvium, alopecia areata, thyroid dysfunction, iron deficiency, medication effect) captures most non-scarring presentations seen outside specialty clinics; minoxidil and finasteride are FDA-approved for androgenetic alopecia; baricitinib and ritlecitinib are FDA-approved for alopecia areata; scarring alopecias require biopsy and early dermatology involvement because damage is not reversible.

Plausible but not fully settled: the exact ferritin threshold that should trigger iron supplementation for hair loss specifically (as opposed to for anemia); the true incidence of alopecia attributable directly to GLP-1 agonists independent of weight loss; the precise degree to which correcting a mild nutrient deficiency (zinc, vitamin D) speeds recovery from telogen effluvium in someone without a clear deficiency-driven picture.

Not established from the material available here: any individualized dosing recommendation, any claim that a specific supplement or over-the-counter product reverses androgenetic alopecia at a rate comparable to minoxidil or finasteride, and any precise numeric incidence figure quoted without checking it against the original trial or registry study. Readers should treat specific statistics in hair-loss articles, including this one, as approximate unless they have confirmed them against a named primary source.

A note on sources: the studies and figures referenced in earlier versions of hair-loss articles like this one are frequently cited by identifier without being re-checked against the original paper. Specific numbers in this article (trial response rates, prevalence percentages, ferritin cutoffs) should be verified against the named primary literature or current FDA labeling before being used in patient-facing material, rather than treated as fixed facts. The FDA Adverse Event Reporting System dashboard referenced above is a stable, general-purpose regulatory resource appropriate for background on adverse event surveillance; it does not establish causation for any individual drug-symptom pairing on its own.