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May 9, 2024

Does Iodine Worsen Thyroid Autoimmunity?

Iodine is an essential trace mineral used to produce thyroid hormones thyroxine (T4) and triiodothyronine (T3). While iodine deficiency can cause hypothyroidism, excess can also cause thyroid dysfunction, including hypothyroidism, hyperthyroidism, and thyroid autoimmunity.

The human requirement for iodine is 150 micrograms (ug) per day, and most needs are met through iodized salt, seafood, and fruit.

However, excess iodine intake can disrupt thyroid homeostasis, increase thyroid hormone production, lead to hyperthyroidism, or cause thyroid inflammation, leading to autoimmune thyroiditis and hypothyroidism.

Excess iodine may be consumed through overconsumption of iodized salt, fortified drinking water, seaweed, or dietary supplements. Measuring urinary iodine excretion is the most accurate method of assessing iodine status (Gong 2023).

Excess iodine (Tox Profile Iodine)

People who have autoimmune thyroid disease may be at increased risk of developing thyroid dysfunction when exposed to excess iodide.

  • Euthyroid patients in a mildly iodine-deficient area who were diagnosed with Hashimoto’s thyroiditis and who were positive for antithyroid (thyroid peroxidase) antibodies:
    • Developed subclinical hypothyroidism after oral doses of 375 µg/day (5.8 µg/kg/day) for six months or
    • Clinical hypothyroidism after exposure to 180 mg I/day (2.6 mg/kg/day) for six weeks, more than 1,000 times the RDA.
  • Iodine excess can accelerate autoimmune thyroiditis in autoimmune-prone individuals, whereas iodine deficiency can attenuate it.
  • As a reference point
    • Chronic dietary intake of iodine in U.S. populations has been estimated to range from approximately 150 to 950 µg/day.
    • Estimates for various populations have ranged from <50 µg/day in iodine-deficient regions to >10 mg/day in populations that regularly ingest seaweeds containing a high iodine content.
    • The National Research Council (NRC) Recommended Dietary Allowance (RDA) for iodine is 150 ug/day (2.1 ug/kg/day for a 70-kg adult), with additional allowances of 25 and 50 ug/day during pregnancy and lactation, respectively.

Tox Profile Iodine 2004

Risk Groups for lodine-induced Hyperthyroidism

Risk Groups for lodine-induced Hypothyroidism

Underlying thyroid disease

Iodine supplementation for endemic iodine-deficiency goiter

Iodine administration to patients with euthyroid Graves disease, especially those in remission after antithyroid drug therapy

Nontoxic nodular goiter

Autonomous nodules

Nontoxic diffuse goiter


Hashimoto’s thyroiditis

Euthyroid patients previously treated for Graves disease with 131I, thyroidectomy, or antithyroid drugs

Subclinical hypothyroidism, especially in the elderly

After transient postpartum thyroiditis

After subacute painful thyroiditis

After hemithyroidectomy for benign nodules

No underlying thyroid disease


Iodine administration to patients with no recognized underlying thyroid disease, especially in areas of mild to moderate iodine



In Japanese subjects with high iodine intake where Hashimoto’s thyroiditis has been excluded


Reported in elderly subjects with and without possible defective organification and autoimmune thyroiditis

Chronic nonthyroidal illness

Cystic fibrosis

Chronic lung disease (including Hashimoto’s thyroiditis)

Chronic dialysis treatment

Thalassemia major

Anorexia nervosa


Euthyroid patients with a previous episode of amiodarone-induced destructive thyrotoxicosis

Euthyroid patients with a previous episode of interferon-alpha-induced thyroid disorders

Patients receiving lithium therapy

Autoimmune thyroid diseases (AITD) (Kravchenko 2023)


  • Autoimmune thyroiditis (AIT)/ Hashimoto’s thyroiditis (HT)
  • Graves’ disease (GD)
  • Graves’ ophthalmopathy (GO)

The development of AITD is influenced by

  • Loss of immune tolerance to thyroid antigens - thyroid peroxidase (TPO), thyroglobulin (Tg) and thyroid-stimulating hormone receptor (TSH-R)
  • Immune-mediated mechanisms - production of autoantibodies to thyroid antigens and lymphocytic thyroid infiltration
  • Insufficiency of regulatory T cells (Treg) and regulatory B cells (Breg)
    Imbalance between Th17-lymphocytes and Treg-lymphocytes
  • Abnormal production of pro-inflammatory cytokines
  • Imbalance between oxidants and antioxidants is disturbed
  • Oxidative stress (OS)
  • Genetic factors
  • Environmental factors
    • Stress
    • Smoking
    • Bacterial and viral infection
    • Chemical pollutants
    • Mineral status

Environmental factors affecting AITD may also include (Franco 2013):

  • Excess iodine
  • Selenium deficiency
  • Use of anovulatory drugs
  • Allergies
  • Radiation exposure (can destroy thyroid tissue or stimulate autoantibodies)
  • Industrial toxins, e.g., BPA in plastics, may bind the TSH receptor and antagonize T3
  • Medications, including IFN-α, IL-2, lithium, amiodarone, and highly active antiretroviral therapy

Iodine Can Induce Autoimmunity (Franco 2013) via:

  • Direct stimulation of immune responses to the thyroid
  • Increased immunogenicity of highly iodinated thyroglobulin
  • Direct toxic effects of iodine on thyrocytes via the generation of reactive oxygen species.

Addressing AITDs (Kravchenko 2023)

  • There is currently no effective pharmacological therapy for AITD.
  • Treatment remains symptomatic and is based on taking, if necessary, synthetic thyroid hormone to correct hypothyroidism or thyrostatics for thyrotoxicosis.
  • Replacement or inhibition therapy may normalize thyroid status but is insufficient for reducing inflammation and oxidative stress, restoring the immune system, and suppressing the autoimmune process in the target organ in AITD.
  • Deficiency or excess consumption of iodine (I) may be a risk factor for thyroid diseases.
    • Careful monitoring of iodine prophylaxis is recommended to avoid the consequences of both deficiency and excess iodine.
  • The addition of selenium (Se) to L-T4 therapy may be appropriate in patients with low Se and mild or early-stage Hashimoto’s.
  • In patients with moderate GO, there is clear evidence of a beneficial effect of Se
  • The main therapeutic mechanisms of AITD are the reduction of oxidative stress, the inflammatory process that damages thyrocytes.
  • For treating GD, GO and HT, an antioxidant approach is possible with mineral supplementation (I, Se, Zn, Fe, Cu and Mg) as an adjunct in patients with associated deficiency.
  • The use of minerals to normalize immune function in AITD may be associated with the following:
    • The normalization of the function of neutrophils as producers of excess ROS and inflammation
    • Reduction of the secretion of pro-inflammatory cytokines Th17 and chemokines, activation of Treg and their cytokines as the main inhibitors of inflammation and autoimmune process.
    • Determining the immunomodulating effect of thyroid hormones, minerals, and researching the possibility of using them as means of immunocorrection

Taking into account the pathogenesis of AITD can contribute to the development of a more effective treatment strategy and approaches to prevention (Kravchenko 2023).

Influence of thyroid hormones and minerals on
innate and adaptive immunity in AITD


Source: Kravchenko, Viktor, and Tamara Zakharchenko. “Thyroid hormones and minerals in immunocorrection of disorders in autoimmune thyroid diseases.” Frontiers in endocrinology vol. 14 1225494. 30 Aug. 2023, doi:10.3389/fendo.2023.1225494 This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

The Bottom Line (Farebroher 2019)

  • The relationship between thyroid disorders and iodine intake follows a U-shaped curve, highlighting the need for maintaining iodine levels within an optimal range to avoid both deficiency and excess.
  • While the body generally tolerates excess iodine well, vulnerable groups like those previously deficient in iodine, pregnant women, and infants might experience adverse physiological changes.
  • Normally, thyroid function normalizes over time or with iodine intake adjustment to recommended levels, but the long-term effects of excessive iodine during pregnancy on children remain uncertain.
  • Iodine intake comes from multiple sources, and effective monitoring should consider total iodine consumption to prevent deficiency while minimizing the risk of excess.
  • In cases where population iodine excess is detected, revising salt iodization policies should be approached with caution due to ambiguous thresholds for defining iodine excess and variable sensitivity across different population groups.
  • Surveillance of iodine levels should include human biomarkers alongside salt iodine concentration assessments, with urinary iodine concentration (UIC) currently being the most sensitive indicator for excessive intake and thyroglobulin (Tg) offering potential as a supplementary measure for broader population assessments.

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Farebrother, Jessica et al. “Excess iodine intake: sources, assessment, and effects on thyroid function.” Annals of the New York Academy of Sciences vol. 1446,1 (2019): 44-65. doi:10.1111/nyas.14041

Franco JS, Amaya-Amaya J, Anaya JM. Thyroid disease and autoimmune diseases. In: Anaya JM, Shoenfeld Y, Rojas-Villarraga A, et al., editors. Autoimmunity: From Bench to Bedside [Internet]. Bogota (Colombia): El Rosario University Press; 2013 Jul 18. Chapter 30. Available from:

Gong, Boshen et al. “Iodine-induced thyroid dysfunction: a scientometric study and visualization analysis.” Frontiers in endocrinology vol. 14 1239038. 20 Sep. 2023, doi:10.3389/fendo.2023.1239038

Kravchenko, Viktor, and Tamara Zakharchenko. “Thyroid hormones and minerals in immunocorrection of disorders in autoimmune thyroid diseases.” Frontiers in endocrinology vol. 14 1225494. 30 Aug. 2023, doi:10.3389/fendo.2023.1225494 This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

Toxicological Profile for Iodine. Atlanta (GA): Agency for Toxic Substances and Disease Registry (US); 2004 Apr. 2, RELEVANCE TO PUBLIC HEALTH. Available from:

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