Iodine is an essential micronutrient that has a crucial role in metabolism. The micronutrient is oxidized to produce iodine-containing thyroid hormones. Thyroid hormones are necessary for regulating growth, metabolism, and many other body functions, especially during fetal and neonatal brain development. Iodine deficiency has long been a recognized global problem and remains a leading cause of preventable fetal brain damage. Iodine deficiency in pregnancy leads to hypothyroidism and impaired infant neurobehavioral development.
Although the consequences of iodine deficiency have been recognized for years, the prevalence or the consequences of iodine excess have not been highlighted. Iodine is not synthesized in the human body and must be obtained from food, dietary supplements, medications, and iodinated contrast media. The recommended dietary allowance varies: 150 μg/d for adults, 220 to 250 μg/d for pregnant women, and 250 to 290 μg/d for breastfeeding women. Up to 1 mg/d is considered safe for most individuals. The sources of excess iodine can be from overconsumption of iodized salt, foods containing excess iodine, and dietary supplements containing iodine, in many cases being the treatment of overtreated iodine deficiency. Ingestion of over 1.1 mg/d of iodine may be harmful and can lead to acute or chronic toxicity.
Iodine excess can cause subclinical or overt thyroid dysfunction in patients with specific risk factors, including those with preexisting thyroid disease, older patients, fetuses, and neonates. The effect of excess iodine varies among individuals and is closely related to underlying thyroid function. Iodine toxicity may lead to thyroiditis, hypothyroidism, hyperthyroidism, and thyroid papillary cancer. Clinical features of iodine toxicity from oral ingestion can range from mild to severe. Mild symptoms consist of gastrointestinal upset, nausea, vomiting, and diarrhea, which may progress to more severe manifestations such as delirium, confusion, lethargy, and shock. The condition is rarely fatal.
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