Monitor exposure to iodine; evaluate for iodine deficiency disorders (IDDs), excessive iodine intake, or iodine in the workplace
Iodine is an essential element for thyroid hormone production. It monitors a person’s exposure to iodine and evaluates for iodine deficiency disorders, excessive iodine intake or iodine in the workplace.
Urinary Iodine levels can help determine if a person is getting healthy amounts of iodine from the food they eat. Unusually high or low levels of iodine can lead to a number of disorders such as hyperthyroidism or hypothyroidism.
This test is usually ordered when someone has had irregular results from thyroid tests such as TSH, T3 and T4. Pregnant and nursing women are often tested for iodine because deficiency can have adverse effects on pregnancy and cause developmental difficulties in infants.
What is Iodine?
Iodine is a trace element that is naturally present in some foods, is added to some types of salt, and is available as a dietary supplement. Iodine is an essential component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). Thyroid hormones regulate many important biochemical reactions, including protein synthesis and enzymatic activity, and are critical determinants of metabolic activity. They are also required for proper skeletal and central nervous system development in fetuses and infants.
Iodine and thyroid function:
Thyroid function is primarily regulated by thyroid-stimulating hormone (TSH), also known as thyrotropin. It is secreted by the pituitary gland to control thyroid hormone production and secretion, thereby protecting the body from hypothyroidism and hyperthyroidism. TSH secretion increases thyroidal uptake of iodine and stimulates the synthesis and release of T3 and T4. In the absence of sufficient iodine, TSH levels remain elevated, leading to goiter, an enlargement of the thyroid gland that reflects the body’s attempt to trap more iodine from the circulation and produce thyroid hormones. Iodine may have other physiological functions in the body as well. For example, it appears to play a role in immune response and might have a beneficial effect on mammary dysplasia and fibrocystic breast disease.
Iodine sources and iodine deficiency:
The earth’s soils contain varying amounts of iodine, which in turn affects the iodine content of crops. In some regions of the world, iodine-deficient soils are common, increasing the risk of iodine deficiency among people who consume foods primarily from those areas. Salt iodization programs, which many countries have implemented, have dramatically reduced the prevalence of iodine deficiency worldwide.
Iodine in food and iodized salt is present in several chemical forms including sodium and potassium salts, inorganic iodine, iodate, and iodide, the reduced form of iodine. Iodine rarely occurs as the element, but rather as a salt; for this reason, it is referred to as iodide and not iodine. Iodide is quickly and almost completely absorbed in the stomach and duodenum. Iodate is reduced in the gastrointestinal tract and absorbed as iodide. When iodide enters the circulation, the thyroid gland concentrates it in appropriate amounts for thyroid hormone synthesis and most of the remaining amount is excreted in the urine. The iodine-replete healthy adult has about 15 - 20 mg of iodine, 70%–80% of which is contained in the thyroid.
Median urinary iodine concentrations of 100–199 mcg/L in children and adults, 150–249 mcg/L in pregnant women and >100 mcg/L in lactating women indicate iodine intakes are adequate. Values lower than 100 mcg/L in children and non-pregnant adults indicate insufficient iodine intake, although iodine deficiency is not classified as severe until urinary iodine levels are lower than 20 mcg/L.
Interactions with Medications
Iodine supplements have the potential to interact with several types of medications. A few examples are provided below. Individuals taking these medications on a regular basis should discuss their iodine intakes with their health care providers.
Anti-thyroid medications: Anti-thyroid medications, such as methimazole, are used to treat hyperthyroidism. Taking high doses of iodine with anti-thyroid medications can have an additive effect and could cause hypothyroidism.
Angiotensin-converting enzyme (ACE) inhibitors: ACE inhibitors, such as benazepril, lisinopril, and fosinopril, are used primarily to treat high blood pressure. Taking potassium iodide with ACE inhibitors can increase the risk of hyperkalemia (elevated blood levels of potassium).
Potassium-sparing diuretics: Taking potassium iodide with potassium-sparing diuretics, such as spironolactone and amiloride, can increase the risk of hyperkalemia.
National Research Council, Committee to Assess the Health Implications of Perchlorate Ingestion. Health Implications of Perchlorate Ingestion. Washington, DC: The National Academies Press, 2005.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2001.
World Health Organization. United Nations Children’s Fund & International Council for the Control of Iodine Deficiency Disorders. Assessment of iodine deficiency disorders and monitoring their elimination. 3rd ed. Geneva, Switzerland: WHO, 2007.
Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev. 2008 Jun;13(2):116-127. [PubMed abstract]
Zimmermann MB. Iodine deficiency. Endocr Rev. 2009 Jun;30(4):376-408. [PubMed abstract]
Zimmermann MB, Jooste PL, Pandav CS. Iodine-deficiency disorders. Lancet. 2008 Oct 4;372(9645):1251-1262. [PubMed abstract]
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Hollowell JG, Staehling NW, Hannon WH, Flanders DW, Gunter EW, Maberly GF, Braverman LE, Pino S, Miller DT, Garbe PL, DeLozier DM, Jackson RJ. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994). J Clin Endocrinol Metab. 1998 Oct;83(10):3401-8. doi: 10.1210/jcem.83.10.5168. PMID: 9768638.
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Iodine deficiency has multiple adverse effects on growth and development, and is the most common cause of preventable intellectual disability in the world. Iodine deficiency disorders result from inadequate thyroid hormone production secondary to insufficient iodine. During pregnancy and early infancy, iodine deficiency can cause irreversible effects.
Under normal conditions, the body tightly controls thyroid hormone concentrations via TSH. Typically, TSH secretion increases when iodine intake falls below about 100 mcg/day. TSH increases thyroidal iodine uptake from the blood and the production of thyroid hormone. However, very low iodine intakes can reduce thyroid hormone production even in the presence of elevated TSH levels.
If a person’s iodine intake falls below approximately 10–20 mcg/day, hypothyroidism occurs, a condition that is frequently accompanied by goiter. Goiter is usually the earliest clinical sign of iodine deficiency. In pregnant women, iodine deficiency of this magnitude can cause major neurodevelopmental deficits and growth retardation in the fetus, as well as miscarriage and stillbirth. Chronic, severe iodine deficiency in utero causes cretinism, a condition characterized by intellectual disability, deaf mutism, motor spasticity, stunted growth, delayed sexual maturation, and other physical and neurological abnormalities.
In infants and children, less severe iodine deficiency can also cause neurodevelopmental deficits such as somewhat lower-than-average intelligence as measured by IQ. Mild to moderate maternal iodine deficiency has also been associated with an increased risk of attention deficit hyperactivity disorder in children. In adults, mild-to-moderate iodine deficiency can cause goiter as well as impaired mental function and work productivity secondary to hypothyroidism. Chronic iodine deficiency may be associated with an increased risk of the follicular form of thyroid cancer.
Health Consequences of Iodine Deficiency
Zimmerman MB, "Iodine Deficiency," Endocrine Reviews, The Endocrine Society, 2009, 30:376-408.
Increased susceptibility of thyroid gland to nuclear radiation
Children and adolescents
Impaired mental function
Delayed physical development
Impaired mental function
Reduced work productivity
Toxic nodular goiter; iodine-induced hyperthyroidism
Increased occurrence of hypothyroidism in moderate-to-severe iodine deficiency; decreased occurrence of hypothyroidism in mild-to-moderate iodine deficiency
Other forms of thyroid problems, namely iodine-induced hypothyroidism, autoimmune thyroiditis, and hyperthyroidism associated with excessive iodine intake, have become a greater concern than deficiency disorders.
High intakes of iodine can cause some of the same symptoms as iodine deficiency - including goiter, elevated TSH levels, and hypothyroidism - because excess iodine in susceptible individuals inhibits thyroid hormone synthesis and thereby increases TSH stimulation, which can produce goiter. Iodine-induced hyperthyroidism can also result from high iodine intakes, including when iodine is administered to treat iodine deficiency. Studies have also shown that excessive iodine intakes cause thyroiditis and thyroid papillary cancer. Cases of acute iodine poisoning are rare and are usually caused by doses of many grams. Acute poisoning symptoms include burning of the mouth, throat, and stomach; fever; abdominal pain; nausea; vomiting; diarrhea; weak pulse; and coma.
Responses to excess iodine and the doses required to cause adverse effects vary. Some people, such as those with autoimmune thyroid disease and iodine deficiency, may experience adverse effects with iodine intakes considered safe for the general population.
In most people, iodine intakes from foods and supplements are unlikely to exceed the upper limit (UL). Long-term intakes above the UL increase the risk of adverse health effects. The ULs do not apply to individuals receiving iodine for medical treatment, but such individuals should be under the care of a physician.
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