Thyroid hair loss guide: how hypothyroidism and hyperthyroidism affect hair, and what to expect with treatment

Thyroid disorders are among the most common causes of diffuse hair loss in women — and one of the most important to identify because the hair loss is potentially fully reversible if the underlying thyroid dysfunction is corrected. Both underactive and overactive thyroid cause hair loss through distinct mechanisms, and each follows a different timeline. Here's the complete guide.

How thyroid hormones affect hair follicles

The role of thyroid hormone in the hair cycle

Thyroid hormones — primarily triiodothyronine (T3) and thyroxine (T4) — regulate the rate of cellular metabolism throughout the body. Hair follicles are directly responsive to thyroid hormone through thyroid hormone receptors expressed in dermal papilla cells and keratinocytes.

Thyroid hormone in normal follicular function:
Regulates the duration of anagen (the growth phase)
Stimulates keratinocyte proliferation in the hair matrix
Regulates the production of hair-specific keratin proteins
Influences the follicular stem cell activity in the bulge region

Both deficiency and excess of thyroid hormone disrupt these regulatory functions — though through different mechanisms and with different clinical presentations.

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Hypothyroidism and hair loss

Mechanism

Hypothyroidism (underactive thyroid; most commonly Hashimoto's thyroiditis, an autoimmune condition) produces insufficient thyroid hormone. In the follicle:
Reduced metabolic activity → slower keratinocyte proliferation → anagen phase shortens
Follicles cycle more rapidly through telogen → more hairs in the resting/shedding phase at any time
The hair shaft itself grows more slowly and can become thinner and coarser in texture
Sebaceous gland activity is reduced → scalp becomes dry; hair loses natural lubrication

Net result: Increased shedding (telogen effluvium pattern) + potentially thinner, coarser individual hair shafts.

Clinical presentation

Distribution: Diffuse — thinning across the entire scalp, not patchy. The lateral third of the eyebrows (the "Hertoghe sign") is classically described as an additional finding in hypothyroidism — outer eyebrow thinning. Not specific, but when present alongside scalp thinning, adds to the diagnostic picture.

Associated symptoms (hypothyroidism):
Fatigue and low energy
Weight gain despite unchanged diet
Cold intolerance
Dry skin and brittle nails
Constipation
Slowed heart rate
Depression and cognitive slowing ("brain fog")
Heavy or irregular menstrual periods
Puffiness, particularly around the eyes (myxedema)

Hair characteristics in hypothyroidism:
Diffuse thinning across the scalp
Hair may feel dry, coarse, and brittle
Hair growth rate slows noticeably
Both scalp hair and body hair can be affected (including eyebrows, eyelashes)

Subclinical hypothyroidism and hair

Subclinical hypothyroidism — defined as elevated TSH with normal free T4 — is a common finding. Its relationship to hair loss is more debated: some women with subclinical hypothyroidism and hair loss improve with levothyroxine treatment; others do not. The decision to treat subclinical hypothyroidism for hair loss specifically should be made with an endocrinologist weighing the full clinical picture.

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Hyperthyroidism and hair loss

Mechanism

Hyperthyroidism (overactive thyroid; most commonly Graves' disease, an autoimmune condition) produces excess thyroid hormone. The mechanism of hair loss differs from hypothyroidism:

Excess thyroid hormone accelerates the entire hair cycle — anagen shortens because follicles cycle through more rapidly
More follicles cycle into telogen prematurely → increased shedding rate
High metabolic rate may also create nutritional stress on rapidly dividing cells
The thyrotoxic state can trigger generalized inflammation that further stresses follicles

Clinical presentation

Distribution: Also diffuse — similar pattern to hypothyroidism (TE-type shedding).

Associated symptoms (hyperthyroidism):
Weight loss despite normal or increased appetite
Heat intolerance and excessive sweating
Rapid or irregular heartbeat (palpitations)
Anxiety, irritability, insomnia
Fine tremor of the hands
Frequent bowel movements
Eye changes in Graves' disease (proptosis, lid retraction — Graves' ophthalmopathy)
Irregular or light menstrual periods

Hair characteristics in hyperthyroidism:
Diffuse thinning
Hair often becomes finer and softer (compared to coarser in hypothyroidism)
Scalp may be somewhat oily (increased sebum production with elevated metabolic rate)

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Postpartum thyroiditis: a specific consideration

Postpartum thyroiditis affects approximately 5–10% of women in the year after delivery. It follows a classic pattern:
Hyperthyroid phase (weeks 2–10 postpartum): Often mild and frequently missed; mild palpitations, anxiety, weight loss
Hypothyroid phase (months 3–8 postpartum): Often the phase that causes hair loss, fatigue, and depression
Recovery (by 12 months in ~75% of cases): Thyroid function returns to normal

In the context of postpartum hair loss — which already peaks at months 3–4 due to estrogen withdrawal — concurrent postpartum thyroiditis can significantly worsen and prolong the shedding. Checking TSH at 3–4 months postpartum is appropriate when shedding is severe or prolonged.

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Laboratory evaluation

Primary tests

| Test | What it measures | Clinical use |
|---|---|---|
| TSH (thyroid-stimulating hormone) | Pituitary signal; most sensitive indicator of thyroid status | First-line screening; elevated in hypothyroidism, suppressed in hyperthyroidism |
| Free T4 | Unbound circulating thyroxine | Confirms hypothyroidism (low T4) or overt disease |
| Free T3 | Unbound triiodothyronine | Sometimes useful in T3-predominant hyperthyroidism |
| Anti-TPO antibodies (anti-thyroid peroxidase) | Autoimmune thyroid disease marker | Positive in Hashimoto's and often in Graves' |
| Anti-TSH receptor antibodies (TRAb) | Graves' disease-specific | Positive in Graves' |

Interpreting TSH

Normal range: Approximately 0.4–4.0 mIU/L (varies by laboratory)

TSH elevated (>4.0) with low or low-normal free T4 → overt hypothyroidism; treatment indicated
TSH elevated with normal free T4 → subclinical hypothyroidism; treatment decision case-by-case
TSH suppressed (&lt;0.4) with elevated free T4/T3 → overt hyperthyroidism; treatment indicated
TSH suppressed with normal free T4/T3 → subclinical hyperthyroidism

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Treatment and hair recovery timeline

Hypothyroidism treatment

Levothyroxine (synthetic T4): The standard treatment. Dose is titrated to normalize TSH, typically targeting TSH in the lower half of the normal range (0.5–2.5 mIU/L) for most patients.

Hair response timeline:
TSH typically normalizes within 6–12 weeks of reaching the correct levothyroxine dose
Paradoxical shedding during initiation: Some patients experience increased shedding in the first 1–3 months after starting levothyroxine — as follicles that were in a "prolonged telogen" due to hypothyroidism re-enter anagen, they first shed the old telogen hairs. This is a positive sign of follicular recovery, not worsening.
Visible reduction in shedding: typically 3–6 months after TSH normalization
Meaningful density improvement: 6–12 months after TSH normalization
Full recovery: up to 18 months in some cases, particularly if hypothyroidism was prolonged before diagnosis

Hyperthyroidism treatment

Options include: antithyroid medications (methimazole, propylthiouracil), radioactive iodine ablation, or thyroidectomy, depending on the cause and severity. Hair recovery follows normalization of thyroid levels.

Hair response timeline (similar pattern to hypothyroidism):
Reduced shedding: 3–6 months after thyroid levels normalize
Density improvement: 6–12 months

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Hair loss persisting after thyroid normalization

A significant subset of patients experience persistent hair loss even after thyroid levels have been normalized on treatment. This is one of the most frustrating situations in thyroid-related hair loss.

Reasons for persistent hair loss after treatment

Insufficient time: The hair cycle lag means normalization of thyroid function does not produce immediate visible improvement. Patients who check at 3 months and see no change are often within the expected recovery window — evaluation at 6–12 months is more informative.

Concurrent androgenetic alopecia: AGA may have been masked by the thyroid condition or may have progressed during the period of thyroid dysfunction. AGA is not reversed by thyroid correction. Dermoscopy showing miniaturized hairs suggests AGA as a co-contributing factor.

Concurrent iron deficiency: Hypothyroidism and iron deficiency frequently co-occur (both are common in premenopausal women; hypothyroidism can reduce gastric acid and impair iron absorption; both cause TE). Correcting the thyroid without addressing concurrent low ferritin may leave the hair loss partially uncorrected. Ferritin should be checked alongside thyroid labs.

The thyroid level is normalized but not optimal: Some patients have TSH that falls within "normal" (0.4–4.0) but feel and function better at a lower TSH. Hair-relevant thyroid optimization may require TSH in the lower portion of the normal range — a clinical discussion with the treating endocrinologist.

Autoimmune cross-reactivity: Hashimoto's thyroiditis and other autoimmune conditions can co-occur with alopecia areata. If shedding becomes patchy rather than diffuse, or does not follow the expected TE pattern, alopecia areata should be considered and evaluated by dermoscopy.

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