Hypothyroidism — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Hypothyroidism is a common endocrine disorder in which the thyroid gland produces insufficient thyroid hormone (thyroxine T4 and triiodothyronine T3), slowing metabolic rate and affecting virtually every organ system. It affects approximately 1–2% of adults, with subclinical hypothyroidism (elevated TSH with normal T4) affecting a further 4–10%. Hypothyroidism is significantly more prevalent in women and increases with age. The most common causes are autoimmune thyroiditis (Hashimoto's thyroiditis) in iodine-sufficient countries and iodine deficiency in developing regions. Levothyroxine is the most prescribed endocrine medication worldwide. Primary hypothyroidism (thyroid gland failure) accounts for 95%+ of all cases; secondary hypothyroidism (TSH deficiency from pituitary disease) and tertiary (TRH deficiency from hypothalamic disease) are rare. Autoimmune thyroid disease — including Hashimoto's thyroiditis and post-partum thyroiditis — represents the most common organ-specific autoimmune condition globally.

Hashimoto's thyroiditis (autoimmune hypothyroidism) is the most common cause in developed countries — autoantibodies (anti-thyroid peroxidase, anti-thyroglobulin) attack thyroid tissue causing progressive destruction. Iodine deficiency remains the leading cause globally, affecting populations in mountainous and landlocked regions with inadequate dietary iodine. Iatrogenic causes include post-thyroidectomy, radioactive iodine treatment for hyperthyroidism, and thyroid-damaging medications (amiodarone, lithium, interferon, immune checkpoint inhibitors). Congenital hypothyroidism detected by neonatal TSH screening requires urgent treatment to prevent irreversible cognitive impairment. Secondary hypothyroidism from pituitary disease is rare. Immune checkpoint inhibitor therapy (anti-PD-1: pembrolizumab, nivolumab; anti-CTLA-4: ipilimumab) — increasingly used cancer immunotherapy agents — cause immune-related thyroiditis and hypothyroidism in 5–30% of patients. Sunitinib (tyrosine kinase inhibitor used in renal cell carcinoma) directly inhibits thyroid cell function. External beam radiotherapy to the head, neck, or mediastinum damages the thyroid gland — requiring annual TSH monitoring in cancer survivors.

Hypothyroidism reflects the slowing of metabolic processes across all body systems. Classic symptoms include fatigue and lethargy, cold intolerance, weight gain despite reduced appetite, constipation, dry skin and hair, hair loss, brittle nails, facial puffiness (periorbital oedema), hoarse voice, muscle aches and stiffness, slow reflexes, bradycardia, depression, memory impairment, and menstrual irregularities (menorrhagia). Severe longstanding untreated hypothyroidism causes myxoedema — non-pitting oedema from glycosaminoglycan accumulation in tissues. Myxoedema coma is a rare life-threatening emergency presenting with hypothermia, altered consciousness, and respiratory failure. Pseudo-myotonia — delayed relaxation of tendon reflexes (particularly the ankle jerk) — is a classic physical sign of hypothyroidism detectable on examination before symptoms appear. Macroglossia (enlarged tongue), hoarse voice from myxoedema of laryngeal tissues, and carpal tunnel syndrome from mucopolysaccharide deposition causing median nerve compression at the wrist are characteristic findings in severe hypothyroidism.

TSH (thyroid-stimulating hormone) is the single most sensitive test for primary thyroid dysfunction — elevated TSH (above 4.0–4.5 mIU/L) indicates hypothyroidism. Free T4 measurement confirms the severity: overt hypothyroidism has low free T4 with high TSH; subclinical hypothyroidism has normal free T4 with mildly elevated TSH (4.0–10 mIU/L). Anti-thyroid peroxidase antibodies (anti-TPO) confirm Hashimoto's thyroiditis. Thyroid ultrasound shows heterogeneous echotexture in autoimmune thyroiditis. In congenital hypothyroidism, neonatal heel-prick TSH screening allows diagnosis within days of birth, enabling treatment before irreversible cognitive effects occur. Subclinical hypothyroidism is defined as TSH 4.0–10 mIU/L with normal free T4 — the decision to treat is individualized: treat if symptomatic, if TSH above 10 mIU/L, if pregnant or planning pregnancy, if strong anti-TPO antibodies (high risk of progression to overt hypothyroidism), or if cardiovascular risk factors are present (even mild TSH elevation may worsen dyslipidaemia). The Thyroid Antibody test (anti-TPO and anti-thyroglobulin) is positive in Hashimoto's in 90–95% of cases and confirms autoimmune aetiology.

Levothyroxine (synthetic T4) is the definitive treatment — once-daily oral tablet taken on an empty stomach 30–60 minutes before breakfast for optimal absorption. Starting dose is typically 1.6 mcg/kg/day in healthy adults; lower doses (12.5–25 mcg/day) in elderly, cardiac disease, or severe hypothyroidism to avoid precipitating angina or arrhythmia. TSH is rechecked 6–8 weeks after each dose change; dose is adjusted to achieve target TSH of 0.5–2.5 mIU/L for most patients (0.1–1.5 mIU/L in pregnancy). Many foods and medications impair levothyroxine absorption — take separately from calcium, iron supplements, antacids, and cholestyramine. Treatment is lifelong for most causes. T4 to T3 conversion in peripheral tissues (by deiodinases DIO1 and DIO2) is impaired in some patients — particularly after thyroidectomy or in those with DIO2 polymorphisms — who may benefit from the addition of liothyronine (synthetic T3, 5–10 mcg twice daily) alongside reduced levothyroxine dose; however, evidence remains controversial and practice varies between specialists.

Myxoedema coma is the most severe complication of hypothyroidism — a life-threatening emergency characterised by severe hypothermia (temperature below 35°C), bradycardia, respiratory failure, altered consciousness, and hypotension. It carries 30–60% mortality and requires emergency ICU admission with intravenous liothyronine (T3), hydrocortisone (to cover potential adrenal insufficiency), and supportive care. Cardiovascular complications include pericardial effusion (present in 30% of severe hypothyroidism), bradycardia, and diastolic dysfunction contributing to heart failure. Hyperlipidaemia (elevated LDL cholesterol and triglycerides) from reduced lipid clearance accelerates atherosclerosis in untreated or inadequately treated hypothyroidism, increasing coronary artery disease risk. Neuropsychiatric complications include cognitive impairment, depression, and peripheral neuropathy. In pregnancy, untreated or undertreated hypothyroidism causes miscarriage, preeclampsia, placental abruption, and impaired fetal neurocognitive development — IQ reductions of 7–10 points have been documented in children born to hypothyroid mothers.

See a GP for: persistent fatigue, unexplained weight gain, constipation, feeling cold, dry skin, hair thinning, or low mood — particularly in women over 40 and those with a family history of thyroid disease or autoimmune conditions. A simple TSH blood test diagnoses hypothyroidism. Seek urgent assessment for: myxoedema coma (a rare but life-threatening complication of severe untreated hypothyroidism — characterised by profound hypothermia, bradycardia, hypotension, reduced consciousness, and hypoventilation — requires emergency IV T3 thyroid hormone replacement, IV hydrocortisone, and ICU admission). Seek prompt GP review for: thyroid swelling or goitre (any new thyroid enlargement should be assessed with ultrasound to exclude nodules), rapid changes in levothyroxine requirements in a treated patient, or hypothyroid symptoms persisting despite apparently adequate levothyroxine therapy (consider under-absorption, medication interactions, or conversion issues requiring combined T3/T4 therapy).

Universal iodized salt programs effectively prevent iodine-deficiency hypothyroidism in at-risk populations. Neonatal TSH screening programs identify and treat congenital hypothyroidism before intellectual disability occurs. Screen women with family history of autoimmune thyroid disease and those planning pregnancy; treat subclinical hypothyroidism in pregnancy (TSH above 2.5 mIU/L in first trimester). Take levothyroxine consistently — same time each day, same brand if possible. Inform all prescribers of levothyroxine therapy as many drugs affect thyroid hormone metabolism. Annual TSH monitoring ensures dose remains appropriate with aging and weight changes.