Iodine is essential in nutrition, being necessary for synthesis of the thyroid hormones thyroxine and thyridothyronine. Hence, an excess of iodine can cause an enlargement of the thyroid gland, i.e. a goitre.
How much iodine is excessive?
- for adults who are not lactating or pregnant, the US Institute of Medicine, and jointly by the WHO, United Nations Children's Fund (UNICEF) and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), recommend a daily iodine intake of 150 µg and state a tolerable upper level (the approximate threshold below which notable adverse effects are unlikely to occur in the healthy population) of 1,100 µg per day in adults (1,3)
- in the UK the British Dietetic Association (4) though notes that "..As a guide, adult intakes should not exceed 600 mcg/day.." because higher levels may result in thyroid dysfunction
Thyroidal adaptation to excess iodine
- the acute Wolff-Chaikoff effect was described in 1948 by Drs Jan Wolff and Israel Lyon Chaikoff
- Wolff and Chaikoff observed a transient reduction (lasting approximately 24 h) in the synthesis of thyroid hormones in rats exposed to high amounts of iodide administered intraperitoneally
- mechanism not completely understood
- may be at least partially explained by the generation of several inhibitory substances (such as intrathyroidal iodolactones, iodoaldehydes and/or iodolipids) on thyroid peroxidase activity
- reduced intrathyroidal deiodinase activity as a result of the increased iodine load might also contribute to decreased synthesis of thyroid hormones
In most individuals, the decreased production of thyroid hormones is only transient and resumes after adaptation to the acute Wolff-Chaikoff effect
Iodine-induced hypothyroidism
- susceptible patients with specific risk factors might have an increased risk of failing to adapt to the acute Wolff-Chaikoff effect
- susceptible patients include:
- those with autoimmune thyroid disease;
- a previous history of
- surgery, 131I or antithyroid drug therapy for Graves disease;
- subacute thyroiditis;
- postpartum thyroiditis;
- amiodarone-induced thyrotoxicosis (AIT);
- hemithyroidectomy;
- concomitant use of potential goitrogens, such as lithium
- failure to escape from the acute Wolff-Chaikoff effect might also be more likely during fetal development, a period when the hypothalamic-pituitary-thyroid axis is still immature, and during neonatal life
- exposure to high concentrations of iodine might also decrease the release of thyroid hormone
- may lead to mild decreases in serum levels of thyroid hormone and increases in the serum level of TSH to the upper limit of the normal range
- administration of iodine to patients with severe hyperthyroidism or thyroid storm is efficacious, as it results in an acute decrease in the release of thyroid hormones (3)
Iodine-induced hyperthyroidism
- in some susceptible patients, an excess iodine load provides a rich substrate for increased production of thyroid hormones
- iodine-induced hyperthyroidism (the Jod-Basedow phenomenon) - first described in the early 1800s
- thyrotoxicosis was observed to be more common among patients with endemic goitre treated with iodine supplementation than in individuals without goitre
- iodine-induced hyperthyroidism might be transient or permanent
- risk factors include nontoxic or diffuse nodular goiter, latent Graves disease and long standing iodine deficiency
- iodine-induced hyperthyroidism in euthyroid patients with nodular goitre in iodine-sufficient areas has also been reported when iodine supplementation is excessive
Measures of iodine excess
- overall iodine levels cannot be reliably measured in individuals given the considerable day-to-day variation in iodine intake
- median urinary iodine concentrations (UIC) have been widely used as a biomarker of population iodine intake, with levels >300 µg/l considered excessive in children and adults and levels >500 µg/l considered excessive in pregnant women (3)
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