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TABLE 1 Dietary Reference Intakes for Iodine by Life Stage Group DRI values (mg/day) EARa RDAb AIc ULd males females males females Life stage group NDe 0 through 6 mo 110 7 through 12 mo 130 ND 1 through 3 y 65 65 90 90 200 4 through 8 y 65 65 90 90 300 9 through 13 y 73 73 120 120 600 14 through 18 y 95 95 150 150 900 19 through 30 y 95 95 150 150 1,100 31 through 50 y 95 95 150 150 1,100 51 through 70 y 95 95 150 150 1,100 ≥ 70 y 95 95 150 150 1,100 Pregnancy £ 18 y 160 220 900 19 through 50 y 160 220 1,100 Lactation £ 18 y 209 290 900 19 through 50 y 209 290 1,100 a EAR = Estimated Average Requirement. b RDA = Recommended Dietary Allowance. c AI = Adequate Intake. d UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents total intake from food, water, and supplements. e ND = Not determinable. This value is not determinable due to the lack of data of adverse effects in this age group and concern regarding the lack of ability to handle excess amounts. Source of intake should only be from food to prevent high levels of intake.

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PART III: IODINE 321 IODINE I odine is an essential component of thyroid hormones that are involved in the regulation of various enzymes and metabolic processes. These hormones regulate many key biochemical reactions, including protein synthesis and enzymatic activity. Major organs that are affected by these processes include the brain, muscles, heart, pituitary gland, and kidneys. The requirements for iodine are based on thyroid iodine accumulation and turnover. The Tolerable Upper Intake Level (UL) is based on serum thyroptropin concentration in response to varying levels of ingested iodine. DRI values are listed by life stage group in Table 1. The iodine content of most food sources is low and can be affected by soil content, irrigation, and fertilizers. Seafood has high concentrations; processed foods may also have high levels due to the addition of iodized salt or additives that contain iodine. In North America where much of the iodine consumed is from salt iodized with potassium iodide, symptoms of iodine deficiency are rare. However, severe iodine deficiency can result in impaired cognitive devel- opment in children and goiter in adults. For the general population, high io- dine intakes from food, water, and supplements have been associated with thy- roiditis, goiter, hypothyroidism, hyperthyroidism, sensitivity reactions, thyroid papillary cancer, and acute responses in some individuals. However, most indi- viduals are very tolerant of excess iodine intake from foods. IODINE AND THE BODY Function Iodine is an essential component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), comprising 65 and 59 percent of their respective weights. These hormones regulate many key biochemical reactions, including protein synthesis and enzymatic activity. Major organs that are affected by these pro- cesses include the brain, muscles, heart, pituitary gland, and kidneys. Absorption, Metabolism, Storage, and Excretion Iodine is ingested in a variety of chemical forms. Most ingested iodine is reduced in the gut to iodide and absorbed almost completely. Some iodine- containing compounds (e.g., thyroid hormones) are absorbed intact. Iodate,

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 322 widely used in many countries as an additive to salt, is rapidly reduced to io- dide and completely absorbed. Once in the circulation, iodide is principally removed by the thyroid gland and kidneys. The thyroid selectively concen- trates iodide in amounts required for adequate thyroid hormone synthesis; most of the remaining iodine is excreted in the urine. A sodium/iodide transporter in the thyroidal basal membrane transfers io- dide from the circulation into the thyroid gland at a concentration gradient of about 20 to 50 times that of the plasma. This ensures that the thyroid gland obtains adequate amounts of iodine for hormone synthesis. During iodine defi- ciency, the thyroid gland concentrates a majority of the iodine available from the plasma. The thyroid of an average adult from an iodine-sufficient geographical region contains about 15 mg of iodine. Most excretion of iodine occurs through the urine, with the remainder excreted in the feces. DETERMINING DRIS Determining Requirements The requirements for iodine are based on thyroid iodine accumulation and turnover. Special Considerations Individuals susceptible to adverse effects: People with autoimmune thyroid disease (AITD) and iodine deficiency respond adversely to intakes that are con- sidered safe for the general population. AITD is common in the U.S. population and particularly in older women. Individuals with AITD who are treated for iodine deficiency or nodular goiter may have an increased sensitivity to the adverse effects of iodine intake. Criteria for Determining Iodine Requirements, by Life Stage Group Life stage group Criterion 0 through 6 mo Average iodine intake from human milk 7 through 12 mo Extrapolation from 0 to 6 mo AI 1 through 8 y Balance data on children 9 through 18 y Extrapolation from adult EAR 19 through 50 y Thyroid iodine accumulation and turnover 51 through > 70 y Extrapolation of iodine turnover studies from 19 through 50 y

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PART III: IODINE 323 Pregnancy £ 18 y through 50 y Balance data during pregnancy Lactation £ 18 y Adolescent female EAR plus average amount of iodine secreted in human milk 19 through 50 y Adult female EAR plus average amount of iodine secreted in human milk The UL The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse effects for almost all healthy people. Members of the general population should not routinely exceed the UL. The UL for iodine is based on thyroid dysfunction, characterized by el- evated serum thyroptropin (also known as TSH) concentrations in response to increasing levels of ingested iodine; it represents intake from food, water, and supplements. A high urinary iodine excretion distinguishes this hypothyroid- ism from that produced in iodine deficiency. The UL is not meant to apply to individuals who are receiving iodine under medical supervision. Based on the Food and Drug Administration’s Total Diet Study, the highest intake of dietary iodine for any life stage or gender group at the 95th percentile was approximately 1.14 mg/day, which is equivalent to the UL for adults. The iodine intake from the diet and supplements at the 95th percentile was ap- proximately 1.15 mg/day. For most people, iodine intake from usual foods and supplements is unlikely to exceed the UL. Special Considerations Goiter: In certain regions of the world where goiter is present, therapeutic doses may exceed the UL. AITD: The UL for iodine does not apply to individuals with AITD (see “Deter- mining Requirements”). Due to inadequate data, a UL could not be set for these individuals. DIETARY SOURCES Foods The iodine content of most food sources is low and can be affected by soil content, irrigation, and fertilizers. Most foods provide 3–75 mg per serving. Seafood has higher concentrations of iodine because marine animals can con-

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 324 centrate iodine from seawater. Processed foods may also have higher levels due to the addition of iodized salt or additives such as calcium iodate, potassium iodate, potassium iodide, and cuprous iodide. Both the United States and Canada iodize salt with potassium iodide at 100 ppm (76 mg iodine/kg salt). Iodized salt is mandatory in Canada and discretionary in the United States. Iodized salt is optionally used by about 50 percent of the U.S. population. Dietary Supplements According to the Third National Health and Nutrition Examination Survey (NHANES III, 1988–1994), the median intake of iodine from supplements was approximately 140 mg/day for adults. The 1986 National Health Interview Sur- vey (NHIS) reported that approximately 12 percent of men and 15 percent of nonpregnant women took a supplement that contained iodine. Bioavailability Under normal conditions, the absorption of dietary iodine by the body is greater than 90 percent. The bioavailability of orally administered thyroxine is approxi- mately 75 percent. Soya flour has been shown to inhibit iodine absorption, and goiter and hypothyroidism were reported in several infants who consumed infant formula containing soya flour. However, if iodine was added to this formula, no goiter appeared. Some foods contain goitrogens, which interfere with thyroid hormone pro- duction or utilization. These foods, which include cassava, millet, and crucifer- ous vegetables (e.g., cabbage), generally are of no clinical significance unless there is a coexisting iodine deficiency. Water from shallow or polluted streams and wells may also contain goitrogens. Deficiencies of vitamin A, selenium, or iron can each exacerbate the effects of iodine deficiency. Some ingested substances contain large amounts of iodine that can inter- fere with proper thyroid function. They include radiocontrast media, food col- oring, certain medications (e.g., amiodarone), water purification tablets, and skin and dental disinfectants. Dietary Interactions This information was not provided at the time the DRI values for this nutrient were set.

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PART III: IODINE 325 INADEQUATE INTAKE AND DEFICIENCY In North America, where much of the iodine consumed is from salt iodized with potassium iodide, symptoms of iodine deficiency are rare. However, most countries currently have some degree of iodine deficiency, including some in- dustrialized countries in Western Europe. Of historical note, during the early part of the 20th century iodine deficiency was a significant problem in the United States and Canada, particularly in the interior, the Great Lakes region, and the Pacific Northwest. The clinical signs and symptoms of iodine deficiency that result from inad- equate thyroid hormone production due to a lack of sufficient iodine, include the following: • Goiter (thyroid enlargement; usually the earliest clinical feature of deficiency) • Mental retardation • Hypothyroidism (elevated thyroid stimulating hormone [TSH]) • Cretinism (extreme form of neurological damage from fetal hypothy- roidism; can be reversed with iodine treatment, especially when begun early) • Growth and developmental abnormalities The most damaging effect of iodine deficiency involves the developing brain. Thyroid hormone is particularly important for myelination of the central ner- vous system, which is most active in the perinatal period and during fetal and early postnatal development. Numerous population studies have correlated an iodine-deficient diet with an increased incidence of mental retardation. The effects of iodine deficiency on brain development are similar to those of hy- pothyroidism from any other cause. Other consequences of iodine deficiency across populations include im- paired reproductive outcome, increased childhood mortality, decreased learn- ing ability, and economic stagnation. Major international efforts have produced dramatic improvements in the correction of iodine deficiency, mainly through the use of iodized salt in iodine-deficient countries. EXCESS INTAKE Most people are very tolerant of excess iodine intake from food. For the general population, high iodine intakes (in excess of the UL) from food, water, and supplements have been associated with the following adverse effects:

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 326 • Thyroiditis • Goiter • Hypothyroidism (elevated thyroid stimulating hormone [TSH]) • Hyperthyroidism • Sensitivity reactions • Thyroid papillary cancer • Acute effects of iodine poisoning, such as burning of the mouth, throat, and stomach; abdominal pain; fever; nausea; vomiting; diarrhea; weak pulse; cardiac irritability; coma; and cyanosis (These symptoms are quite rare and are usually associated with doses of many grams.) KEY POINTS FOR IODINE Iodine is an essential component of thyroid hormones that are 3 involved in the regulation of various enzymes and metabolic processes. The requirements for iodine are based on thyroid iodine 3 accumulation and turnover. The UL is based on serum thyroptropin concentration in response to varying levels of ingested iodine. Certain subpopulations, such as those with autoimmune 3 thyroid disease (AITD) and iodine deficiency, respond adversely to intakes that are considered safe for the general population. AITD is common in the U.S. population and particularly in older women. For most people, iodine intake from usual foods and 3 supplements is unlikely to exceed the UL. In certain regions of the world where goiter is present, therapeutic doses may exceed the UL. The iodine content of most food sources is low and can be 3 affected by soil content, irrigation, and fertilizers. Most foods provide 3–75 mg per serving. Seafood has higher concentrations of iodine because marine animals can concentrate iodine from seawater. Processed foods may also have higher levels due to the 3 addition of iodized salt or additives that contain iodine. Iodized salt is mandatory in Canada and optionally used by about 50 percent of the U.S. population.

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PART III: IODINE 327 In North America, where much of the iodine consumed is from 3 salt iodized with potassium iodide, symptoms of iodine deficiency are rare. However, most countries currently have some degree of iodine deficiency, including some industrialized countries in Western Europe. The clinical signs and symptoms of iodine deficiency include 3 goiter, mental retardation, hypothyroidism, cretinism, and growth and developmental abnormalities. The use of iodized salt has helped reduce iodine deficiency. 3 Most people are very tolerant of excess iodine intake from food 3 and supplements. The potential adverse effects of iodine intakes in excess of the 3 UL include thyroiditis, goiter, hypothyroidism, hyperthyroidism, sensitivity reactions, thyroid papillary cancer, and acute responses in some individuals.