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Supported by multiple clinical trials and systematic reviews

Thyroid Disorders (Hypothyroidism, Hyperthyroidism, Autoimmune Thyroid Disease)

Thyroid disorders encompass underactive thyroid (hypothyroidism), overactive thyroid (hyperthyroidism/thyrotoxicosis), structural changes (goiter, nodules), and autoimmune conditions (Hashimoto’s thyroiditis, Graves’ disease). Western medicine defines and monitors thyroid status biochemically—principally using TSH, free T4, and when indicated, total/free T3 and thyroid antibodies (anti-TPO, anti-thyroglobulin, and TSH receptor antibodies [TRAb]). Imaging (ultrasound) and functional tests (radioactive iodine uptake [RAIU]) help characterize nodules and distinguish causes of thyrotoxicosis. Treatment decisions weigh severity, etiology, symptoms, pregnancy status, age, and comorbid risk (cardiovascular, bone). Hypothyroidism is most often autoimmune (Hashimoto’s) in iodine-sufficient regions. The gold standard treatment is levothyroxine (synthetic T4), titrated to normalize TSH and alleviate symptoms, with rechecks 6–8 weeks after dose changes and at steady state. Debate persists about adding liothyronine (T3) for persistent symptoms despite normalized TSH; current guidelines reserve combination therapy for carefully selected, monitored trials after ruling out other causes. Subclinical hypothyroidism (elevated TSH, normal FT4) management is individualized: treatment is favored when TSH ≥10 mIU/L, in pregnancy or infertility, with significant symptoms, goiter, positive TPO antibodies, or in younger patients planning conception; watchful waiting is often reasonable otherwise. Special attention to drug and nutrient interactions (iron, calcium, proton pump inhibitors, soy, high-fiber diets) and conditions that impair absorption (celiac disease, H. pylori, atrophic gastritis) is essential. Hyperthyroidism most commonly arises from Graves’ disease, toxic multinodular goiter, or a toxic adenoma. First-line options include antithyroid drugs (methimazole; propylthiouracil [PTU] in the first trimester of pregnancy or for thyroid storm), radioactive iodine ablation, and thyroid

Endocrine Updated February 19, 2026

This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication regimen.

Western Medicine

Diagnosis

Diagnosis relies on serum TSH (screening and monitoring), free T4 (overt thyroid dysfunction), and selectively free/total T3 (T3-toxicosis or severity assessment). Autoantibodies refine etiology: anti-TPO and anti-thyroglobulin support Hashimoto’s; TRAb confirms Graves’ and predicts relapse/ophthalmopathy risk. RAIU and scan distinguish Graves’ (diffuse uptake) from thyroiditis (low uptake) and nodular autonomy (focal uptake). Ultrasound evaluates goiter/nodules and guides FNA by TI-RADS criteria. Monitoring: • Hypothyroidism—recheck TSH 6–8 weeks after starting/changing levothyroxine; then every 6–12 months once stable. Target TSH generally within reference range; individualized in elderly, pregnancy (trimester-specific ranges), and thyroid cancer. • Hyperthyroidism—track FT4/T3 every 2–6 weeks when initiating titration; TSH often lags. On antithyroid drugs, check counts/liver enzymes if symptomatic; assess TRAb at end of course to gauge relapse risk.

Treatments

  • Hypothyroidism: Levothyroxine monotherapy (first-line). Optimize absorption (empty stomach, consistent timing, separate from iron/calcium/PPIs/soy by ≥4 hours). Consider combination T4/T3 only as a monitored trial in select, persistent-symptom cases.
  • Subclinical hypothyroidism: Treat if TSH ≥10 mIU/L; consider if TSH 4.5–9.9 with symptoms, positive TPOAb, goiter, atherosclerotic risk, pregnancy/infertility; otherwise observe with periodic labs.
  • Hyperthyroidism (Graves’, toxic nodules): Antithyroid drugs (methimazole; PTU in 1st trimester/thyroid storm), radioactive iodine ablation, or thyroidectomy (large goiter, compressive symptoms, suspicion of cancer, severe ophthalmopathy, patient preference).
  • Symptom control: Beta-blockers (e.g., propranolol, atenolol) for adrenergic symptoms in hyperthyroidism; cautious use in asthma or heart block.
  • Thyroiditis: Often self-limited; manage hyperthyroid phase with beta-blockers; avoid antithyroid drugs; use NSAIDs or short glucocorticoids for painful subacute thyroiditis.
  • Graves’ ophthalmopathy: Risk-factor control (smoking cessation), selenium 200 mcg/day in mild active disease; glucocorticoids/biologics or orbital therapies in moderate-severe cases (specialist care).
  • Pregnancy: Trimester-specific TSH targets; use levothyroxine for hypothyroidism; methimazole generally after 1st trimester; PTU preferred in 1st trimester; avoid RAI.
  • Post-treatment hypothyroidism after RAI/surgery: Lifelong levothyroxine with regular monitoring.

Medications

  • Levothyroxine (T4)
  • Liothyronine (T3; adjunct only in select cases)
  • Desiccated thyroid extract (not recommended by guidelines)
  • Methimazole (MMI)
  • Propylthiouracil (PTU)
  • Beta-blockers (propranolol, atenolol)
  • Glucocorticoids (thyroiditis; Graves’ orbitopathy; thyroid storm)
  • Potassium iodide/Lugol’s solution (pre-op; thyroid storm)
  • Cholestyramine (adjunct in severe thyrotoxicosis)

Limitations

A subset of patients remain symptomatic despite normalized TSH on levothyroxine; biomarkers to guide combination T4/T3 therapy are lacking and long-term outcome data are limited. Antithyroid drugs carry risks (agranulocytosis, hepatotoxicity); RAI can worsen ophthalmopathy and usually causes hypothyroidism; surgery entails anesthesia/hypoparathyroidism/recurrent laryngeal nerve risks. Optimal management of subclinical disease is debated, requiring individualized risk–benefit discussions.

Evidence: Strong Evidence

Sources

  • Jonklaas J et al. Guidelines for the treatment of hypothyroidism. Thyroid. 2014;24(12):1670-1751 (ATA).
  • Ross DS et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343-1421.
  • Pearce SH et al. 2013 ETA Guideline: Management of Subclinical Hypothyroidism. Eur Thyroid J. 2013;2:215-228.
  • Bartalena L et al. 2018 European Thyroid Association Guidelines for the Management of Graves’ Hyperthyroidism. Eur Thyroid J. 2018;7:167-186.
  • ATA Statement on Thyroid Hormone Replacement. Thyroid. 2014;24(12):1670–1751.
  • Bahn RS et al. Hyperthyroidism and other causes of thyrotoxicosis. Lancet. 2016;388:906-918.

Eastern & Traditional Medicine

Traditional Chinese Medicine (TCM)

TCM interprets hypothyroidism commonly as kidney yang deficiency and spleen qi deficiency (fatigue, cold intolerance, edema), sometimes with phlegm accumulation (goiter/nodules). Hyperthyroidism/Graves’ often reflect liver qi stagnation transforming to fire and yin deficiency with empty heat (palpitations, anxiety, weight loss). Treatment aims to restore yin–yang balance, move liver qi, transform phlegm, and support kidney–spleen systems while addressing stress and sleep.

Techniques

  • Individualized herbal formulas: e.g., Jin Gui Shen Qi Wan/You Gui Wan (tonify kidney yang) for hypothyroid patterns; Zhi Bai Di Huang Wan (nourish yin, clear deficiency heat) for hyperthyroid patterns; Hai Zao Yu Hu Tang (transform phlegm, soften hard masses) for goiter/nodules—with caution due to iodine-rich seaweeds.
  • Acupuncture: points selected to regulate qi, calm shen, and support endocrine balance (e.g., ST36, SP6, KI3, LR3, CV4/6); adjunctive moxibustion for yang deficiency.
  • Diet/qi regulation: warming, easily digestible foods for yang deficiency; stress reduction, sleep hygiene, and gentle movement (tai chi, qigong).
Licensed acupuncturist (L.Ac.) TCM herbalist Integrative MD/DO/ND with TCM training
Evidence: Traditional Use

Ayurveda

Ayurveda views thyroid dysfunction through doshic imbalance. Hypothyroidism aligns with kapha and vata aggravation (manda agni, fatigue, weight gain, coldness), while hyperthyroidism reflects pitta/vata aggravation (heat, restlessness, catabolism). Management centers on correcting agni/dosha, supporting ojas, and addressing stress via rasayana (rejuvenation) and lifestyle.

Techniques

  • Herbal formulations: Kanchanara Guggulu traditionally for goiter/nodules; Guggulu (Commiphora mukul) to support metabolism; Ashwagandha (Withania somnifera) as an adaptogen with RCT evidence improving TSH/T4/T3 in subclinical hypothyroidism.
  • Diet/lifestyle: light, warming, easily digested foods in hypothyroid; cooling, grounding foods and meditation/pranayama in hyperthyroid; regular sleep and daily routine (dinacharya).
  • Adjunct yoga/pranayama to modulate stress axis (HPA) and autonomic tone.
Ayurvedic practitioner (BAMS) Integrative MD/DO/ND with Ayurvedic training
Evidence: Emerging Research

Nutritional and micronutrient support (integrative)

Supports immune balance, thyroid hormone synthesis, and peripheral conversion while complementing conventional therapy. Particular focus on selenium for Hashimoto’s autoimmunity, iodine sufficiency (not excess), zinc and vitamin D for immune and thyroid enzyme function, and iron/B12 for symptom overlap and levothyroxine efficacy.

Techniques

  • Selenium 100–200 mcg/day (e.g., selenomethionine) for 3–6 months in Hashimoto’s can modestly reduce TPO antibody titers; clinical symptom/TSH benefits are inconsistent; avoid excess (>400 mcg/day).
  • Iodine balance: achieve RDA (150 mcg/day adults; 220–250 mcg/day pregnancy) through diet/prenatal vitamins; avoid high-iodine supplements (e.g., kelp) that may trigger or worsen dysfunction, especially autoimmune disease.
  • Assess and replete vitamin D, zinc, iron, and B12 when low; optimize protein and omega-3 intake.
  • Consider myo-inositol (with selenium) in subclinical Hashimoto’s—early RCTs suggest TSH/antibody improvements, but evidence is still emerging.
Registered dietitian nutritionist (RDN) Integrative MD/DO/ND Endocrinologist with nutrition focus
Evidence: Moderate Evidence

Acupuncture (as adjunct)

Used to moderate sympathetic overactivity, anxiety, and sleep disturbance common in hyperthyroidism/Graves’, and to support fatigue, mood, and well-being in hypothyroidism. Not a replacement for antithyroid drugs or thyroid hormone.

Techniques

  • Body acupuncture and electroacupuncture tailored to symptoms; relaxation-focused protocols; adjunctive eye-focused protocols for Graves’ orbitopathy symptoms (specialty care).
Licensed acupuncturist (L.Ac.) Medical acupuncturist
Evidence: Emerging Research

Sources

  • Chen JK, Chen TT. Chinese Medical Herbology and Pharmacology. Art of Medicine Press, 2004.
  • Fang X et al. Chinese herbal medicine for hyperthyroidism: overview of clinical evidence (low quality). Complement Ther Med. 2013;21:200-208.
  • Wang Y et al. Acupuncture and endocrine function: narrative reviews highlight limited, heterogeneous data. Med Acupunct. 2018;30:52-60.
  • Sharma AK et al. Efficacy and Safety of Ashwagandha Root Extract in Subclinical Hypothyroid Patients: A Randomized, Double-Blind, Placebo-Controlled Trial. J Altern Complement Med. 2018;24(3):243-248.
  • Srivastava A et al. Ayurvedic approach to thyroid disorders: narrative review. J Ayurveda Integr Med. 2011;2:65-72.
  • Winther KH et al. Selenium supplementation for Hashimoto’s thyroiditis: systematic review and meta-analysis. Clin Endocrinol (Oxf). 2017;86:62–73.
  • Leung AM, Braverman LE, Pearce EN. American Thyroid Association Statement on Excess Iodine Ingestion. Thyroid. 2015;25(2):145-146.
  • Nordio M, Basciani S. Myo-inositol and selenium in subclinical hypothyroidism: randomized trial. Int J Endocrinol. 2017:ID 2874292.
  • Zhu J et al. Acupuncture for Graves’ disease and related symptoms: small trials with high risk of bias; insufficient evidence. Altern Ther Health Med. 2018;24:26-34.
  • Wang Y et al. Acupuncture and endocrine function: narrative review. Med Acupunct. 2018;30:52-60.

Integrative Perspective

Safety first: Thyroid hormone replacement and antithyroid therapies are essential, precisely dosed medications that should not be replaced by herbs or supplements. Sudden discontinuation or substitution can be dangerous. Coordinate all complementary therapies with an endocrinologist, especially in pregnancy, cardiac disease, or severe symptoms. Practical integration: • Medication optimization: Take levothyroxine consistently on an empty stomach; separate from calcium/iron/fiber/soy by ≥4 hours. Address malabsorption (celiac disease, H. pylori, atrophic gastritis); consider liquid/soft-gel formulations if absorption issues persist. • Nutrient support: Check and replete vitamin D, ferritin/iron, B12, zinc. Consider selenium 100–200 mcg/day for 3–6 months in Hashimoto’s to modestly lower TPOAb; stop if no clear benefit and avoid excess. Ensure adequate—not excessive—iodine intake; avoid kelp/high-iodine supplements. Omega-3s and adequate protein may support inflammation control and metabolic health. • Autoimmunity and gut: Both Western and Eastern paradigms recognize a gut–immune–thyroid axis. Screen for celiac disease when suggestive symptoms or refractory levothyroxine dosing are present. Emphasize a diverse, fiber-rich diet, fermented foods if tolerated, and stress/sleep hygiene to support immune regulation. • Symptom relief: Mind–body practices (yoga, tai chi, breathwork), acupuncture (limited evidence), and TCM/Ayurvedic approaches may help with anxiety, sleep, and fatigue while biomedical therapy normalizes hormones. • Special populations: Use pregnancy-specific TSH targets and iodine needs (220–250 mcg/day). Selenium use in pregnancy should be individualized due to mixed data; avoid high doses. In older adults and those with heart disease, start thyroid medications low and go slow. • Subclinical conditions: Partner with clinicians to individualize therapy. Combine watchful waiting with lifestyle and nutrient optimization when deferring medication; treat when guideline criteria are met.

Sources

  1. Jonklaas J et al. Guidelines for the treatment of hypothyroidism. Thyroid. 2014;24(12):1670-1751.
  2. Ross DS et al. 2016 ATA Guidelines for Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343-1421.
  3. Pearce SH et al. ETA Guideline: Management of Subclinical Hypothyroidism. Eur Thyroid J. 2013;2:215-228.
  4. Bartalena L et al. 2018 ETA Guidelines for the Management of Graves’ Hyperthyroidism. Eur Thyroid J. 2018;7:167-186.
  5. Sharma AK et al. Ashwagandha in Subclinical Hypothyroidism RCT. J Altern Complement Med. 2018;24(3):243-248.
  6. Winther KH et al. Selenium and Hashimoto’s Meta-analysis. Clin Endocrinol (Oxf). 2017;86:62–73.
  7. Leung AM et al. ATA Statement on Excess Iodine Ingestion. Thyroid. 2015;25:145-146.
  8. Virili C, Centanni M. Gastrointestinal malabsorption of thyroxine and the gut–thyroid axis. Endocrine. 2015;49:51-57.

Health Disclaimer

This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication regimen.