Iodine, a non-metallic trace element, is required by humans for the synthesis of thyroid hormones. Iodine deficiency is an important health problem throughout much of the world. Most of the earth's iodine is found in oceans, and iodine content in the soil varies with region. The older an exposed soil surface, the more likely the iodine has been leached away by erosion. Mountainous regions, such as the Himalayas, the Andes, and the Alps, and flooded river valleys, such as the Ganges, are among the most severely iodine-deficient areas in the world (1).
Iodine is an essential component of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), and is therefore essential for normal thyroid function. To meet the body's demand for thyroid hormones, the thyroid gland traps iodine from the blood and incorporates it into thyroid hormones that are stored and released into the circulation when needed. In target tissues, such as the liver and the brain, T3, the physiologically active thyroid hormone, can bind to thyroid receptors in the nuclei of cells and regulate gene expression. In target tissues, T4, the most abundant circulating thyroid hormone, can be converted to T3 by selenium-containing enzymes known as deiodinases. In this manner, thyroid hormones regulate a number of physiologic processes, including growth, development, metabolism, and reproductive function (1, 2).
The regulation of thyroid function is a complex process that involves the brain (hypothalamus) and pituitary gland. In response to thyrotropin-releasing hormone (TRH) secretion by the hypothalamus, the pituitary gland secretes thyroid-stimulating hormone (TSH), which stimulates iodine trapping, thyroid hormone synthesis, and release of T3 and T4 by the thyroid gland. The presence of adequate circulating T4 and T3 feeds back at the level of both the hypothalamus and pituitary, decreasing TRH and TSH production (Figure 1). When circulating T4 levels decrease, the pituitary increases its secretion of TSH, resulting in increased iodine trapping as well as increased production and release of both T3 and T4. Iodine deficiency results in inadequate production of T4. In response to decreased blood levels of T4, the pituitary gland increases its output of TSH. Persistently elevated TSH levels may lead to hypertrophy (enlargement) of the thyroid gland, also known as goiter (see Deficiency) (3).
Iodine deficiency is now accepted as the most common cause of preventable brain damage in the world. The spectrum of iodine deficiency disorders (IDD) includes mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities (1, 4). WHO estimated that over 30% of the world’s population (2 billion people) has insufficient iodine intake as measured by urinary iodine excretion below 100 micrograms (mcg)/liter (5); urinary iodine is an indicator of iodine status. Moreover, an estimated 31.5% of school-age children (6-12 years old) worldwide (266 million total children) has insufficient iodine intake (5). Major international efforts have produced dramatic improvements in the correction of iodine deficiency in the 1990s, mainly through the use of iodized salt in iodine-deficient countries (6). Today, 70% of households in the world use iodized salt (7). For more information on the international effort to eradicate iodine deficiency, visit the websites of the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) or the WHO.
Thyroid enlargement, or goiter, is one of the earliest and most visible signs of iodine deficiency. The thyroid enlarges in response to persistent stimulation by TSH (see Function). In mild iodine deficiency, this adaptive response may be enough to provide the body with sufficient thyroid hormone. However, more severe cases of iodine deficiency result in hypothyroidism. Adequate iodine intake will generally reduce the size of goiters, but the reversibility of the effects of hypothyroidism depends on an individual's stage of development. Iodine deficiency has adverse effects in all stages of development but is most damaging to the developing brain. In addition to regulating many aspects of growth and development, thyroid hormone is important for myelination of the central nervous system, which is most active before and shortly after birth (2, 6).
The effects of iodine deficiency by developmental stage
Fetal iodine deficiency is caused by iodine deficiency in the mother. One of the most devastating effects of maternal iodine deficiency is congenital hypothyroidism. A severe form of congenital hypothyroidism may lead to a condition that is sometimes referred to as cretinism and result in irreversible mental retardation. Cretinism occurs in two forms, although there is considerable overlap between them. The neurologic form is characterized by mental and physical retardation and deafness and is the result of maternal iodine deficiency that affects the fetus before its own thyroid is functional. The myxedematous or hypothyroid form is characterized by short stature and mental retardation. In addition to iodine deficiency, the hypothyroid form has been associated with selenium deficiency (see Nutrient interactions) and with the presence of goitrogens in the diet that interfere with thyroid hormone production (see Goitrogens) (8).
Newborns and infants
Infant mortality is increased in areas of iodine deficiency, and several studies have demonstrated an increase in childhood survival upon correction of the iodine deficiency (9). Infancy is a period of rapid brain growth and development. Sufficient thyroid hormone, which depends on adequate iodine intake, is essential for normal brain development. Even in the absence of congenital hypothyroidism, iodine deficiency during infancy may result in abnormal brain development and, consequently, impaired intellectual development (10).
Children and adolescents
Iodine deficiency in children and adolescents is often associated with goiter. The incidence of goiter peaks in adolescence and is more common in girls. School children in iodine-deficient areas show poorer school performance, lower IQs, and a higher incidence of learning disabilities than matched groups from iodine-sufficient areas. A meta-analysis of 18 studies concluded that iodine deficiency alone lowered mean IQ scores in children by 13.5 points (11, 12).
Inadequate iodine intake may also result in goiter and hypothyroidism in adults. Although the effects of hypothyroidism are more subtle in the brains of adults than children, research suggests that hypothyroidism results in slower response times and impaired mental function (1). Other symptoms of hypothyroidism include fatigue, weight gain, cold intolerance, and constipation.
Pregnancy and lactation
Iodine requirements are increased in pregnant and breast-feeding women (see The RDA) (6). Iodine deficiency during pregnancy has been associated with increased incidence of miscarriage, stillbirth, and birth defects. Moreover, severe iodine deficiency during pregnancy may result in congenital hypothyroidism and neurocognitive deficits in the offspring (see Prenatal development) (6, 8). Iodine-deficient women who are breast-feeding may not be able to provide sufficient iodine to their infants who are particularly vulnerable to the effects of iodine deficiency (see Newborns and infants) (1). A daily prenatal supplement providing 150 mcg of iodine, as recommended by the American Thyroid Association (13), will help to ensure that US pregnant and breast-feeding women consume sufficient iodine during these critical periods.
Because iodine deficiency results in increased iodine trapping by the thyroid, iodine-deficient individuals of all ages are more susceptible to radiation-induced thyroid cancer (see Disease Prevention) as well as to iodine-induced hyperthyroidism (see Safety) (1).
Selenium deficiency can exacerbate the effects of iodine deficiency. Iodine is essential for the synthesis of thyroid hormone, but selenium-dependent enzymes (iodothyronine deiodinases) are also required for the conversion of thyroxine (T4) to the biologically active thyroid hormone, triiodothyronine (T3) (6, 8). Additionally, deficiencies of vitamin A or iron may exacerbate the effects of iodine deficiency (6, 14).
Some foods contain substances that interfere with iodine utilization or thyroid hormone production; these substances are called goitrogens. The occurrence of goiter in the Democratic Republic of Congo has been related to the consumption of casava, which contains a compound that is metabolized to thiocyanate and blocks thyroidal uptake of iodine. Some species of millet and cruciferous vegetables (for example, cabbage, broccoli, cauliflower, and Brussels sprouts) also contain goitrogens. Further, the soybean isoflavones, genistein and daidzein, have been found to inhibit thyroid hormone synthesis (15). Most of these goitrogens are not of clinical importance unless they are consumed in large amounts or there is coexisting iodine deficiency. Recent findings also indicate that tobacco smoking may be associated with an increased risk of goiter in iodine-deficient areas (16).
Individuals at risk of iodine deficiency
While the risk of iodine deficiency for populations living in iodine-deficient areas without adequate iodine fortification programs is well-recognized, concerns have been raised that certain subpopulations may not consume adequate iodine in countries considered iodine-sufficient. Vegetarian and nonvegetarian diets that exclude iodized salt, fish, and seaweed have been found to contain very little iodine (1, 6, 17, 18). Urinary iodine excretion studies suggest that iodine intakes have declined in Switzerland (19), New Zealand (20), and the US (21), possibly due to increased adherence to dietary recommendations to reduce salt intake. However, data from the latest US assessment, the National Health and Nutrition Examination Survey 2003-2004, indicate that iodine intake has stabilized (22), and the US is currently considered to be iodine-sufficient. Also, a recent study found that the iodine status of children and pregnant women in Switzerland improved after a mandated increase in iodine concentration of iodized salt in 1998 (19). Switzerland is now considered to be iodine-sufficient (23).
The Recommended Dietary Allowance (RDA)
The RDA for iodine was reevaluated by the Food and Nutrition Board (FNB) of the Institute of Medicine in 2001 (Table 1). The recommended amounts were calculated using several methods, including the measurement of iodine accumulation in the thyroid glands of individuals with normal thyroid function (6). These recommendations are in agreement with those of the International Council for the Control of Iodine Deficiency Disorders, the World Health Organization, and UNICEF (2).
Table 1. Recommended Dietary Allowance (RDA) for Iodine
|| 130 (AI)
|| 130 (AI)
||19 years and older
Radiation-induced thyroid cancer
Radioactive iodine, especially 131I, may be released into the environment as a result of nuclear reactor accidents. Thyroid accumulation of radioactive iodine increases the risk of developing thyroid cancer, especially in children. The increased iodine trapping activity of the thyroid gland in iodine deficiency results in increased thyroid accumulation of radioactive iodine (131I). Thus, iodine-deficient individuals are at increased risk of developing radiation-induced thyroid cancer because they will accumulate greater amounts of radioactive iodine. Potassium iodide administered in pharmacologic doses (50-100 mg for adults) within 48 hours before or eight hours after radiation exposure from a nuclear reactor accident can significantly reduce thyroid uptake of 131I and decrease the risk of radiation-induced thyroid cancer (24). The prompt and widespread use of potassium iodide prophylaxis in Poland after the 1986 Chernobyl nuclear reactor accident may explain the lack of a significant increase in childhood thyroid cancer in Poland compared to fallout areas where potassium iodide prophylaxis was not widely used (25). In the US, the Nuclear Regulatory Commission (NRC) requires that consideration be given to potassium iodide as a protective measure for the general public in the case of a major release of radioactivity from a nuclear power plant (26).
Fibrocystic breast condition
Fibrocystic breast condition is a benign (non-cancerous) condition of the breasts, characterized by lumpiness and discomfort in one or both breasts. In estrogen-treated rats, iodine deficiency leads to changes similar to those seen in fibrocystic breast condition, while iodine repletion reverses those changes (27). An uncontrolled study of 233 women with fibrocystic breast condition found that treatment with aqueous molecular iodine (I2) at a dose of 0.08 mg of I2/kg of body weight daily over six to 18 months was associated with improvement in pain and other symptoms in over 70% of those treated (28). About 10% of the study participants reported side effects that were described by the investigators as minor. A double-blind, placebo-controlled trial of aqueous molecular iodine (0.07-0.09 mg of I2/kg of body weight daily for six months) in 56 women with fibrocystic breast condition found that 65% of the women taking molecular iodine reported improvement compared to 33% of those taking the placebo (28). More recently, a double-blind, placebo-controlled, clinical trial in 111 women with documented breast pain reported that molecular iodine (3 mg/day or 6 mg/day) for five months improved overall pain (29). In this study, more than half of the women receiving the highest dosage of molecular iodine reported a ≥50% reduction in self-assessed breast pain compared to 8.3% in those receiving placebo. Large-scale, controlled clinical trials are needed to determine the therapeutic value of molecular iodine in fibrocystic breast condition. The doses of iodine used in these studies (3 to 7 mg/day for a 60 kg person) are several times higher than the tolerable upper intake level (UL) recommended by the Food and Nutrition Board (FNB) of the Institute of Medicine and should only be used under medical supervision (see Safety).
The iodine content of most foods depends on the iodine content of the soil. Seafood is rich in iodine because marine animals can concentrate the iodine from seawater. Certain types of seaweed (e.g., wakame) are also very rich in iodine. Processed foods may contain slightly higher levels of iodine due to the addition of iodized salt or food additives, such as calcium iodate and potassium iodate. Dairy products are relatively good sources of iodine because iodine is commonly added to animal feed in the US. In the UK and northern Europe, iodine levels in dairy products tend to be lower in summer when cattle are allowed to graze in pastures with low soil iodine content (6). Table 2 lists the iodine content of some iodine-rich foods in micrograms (mcg). Because the iodine content of foods can vary considerably, these values should be considered approximate (30).
Table 2. Some Food Sources of Iodine
||2 fish sticks
|Tuna, canned in oil
||3 ounces (1/2 can)
||1 cup (8 fluid ounces)
|Navy beans, cooked
|Potato with peel, baked
|Turkey breast, baked
||1/4 ounce, dried
||Variable; may be greater than 4,500 mcg (4.5 mg)
|*A three-ounce serving of meat is about the size of a deck of cards.
Potassium iodide is available as a nutritional supplement, typically in combination products, such as multivitamin/multimineral supplements. Iodine makes up approximately 77% of the total weight of potassium iodide (15). A multivitamin-mineral supplement that contains 100% of the daily value (DV) for iodine provides 150 mcg of iodine. Although most people in the US consume sufficient iodine in their diets from iodized salt and food additives, an additional 150 mcg/day is unlikely to result in excessive iodine intake (see Safety).
Potassium iodide as well as potassium iodate may be used to iodize salt. In the US and Canada, iodized salt contains 77 mcg of iodine per gram of salt. In other countries, salt commonly contains 20-40 mcg of iodine/gram of salt; the iodization level depends on variables such as iodine intake from other sources and daily salt consumption. Annual doses of iodized vegetable oil are also used in some countries as an iodine source (2, 15).
Acute iodine poisoning is rare and usually occurs only with doses of many grams. Symptoms of acute iodine poisoning include burning of the mouth, throat, and stomach; fever; nausea; vomiting; diarrhea; a weak pulse; and coma (6).
It is rare for diets of natural foods to supply more than 2,000 mcg of iodine/day, and most diets supply less than 1,000 mcg of iodine/day. People living in the northern coastal regions of Japan, whose diets contain large amounts of seaweed, have been found to have iodine intakes ranging from 50,000 to 80,000 mcg (50-80 mg) of iodine/day (1).
In iodine deficiency: Iodine supplementation programs in iodine-deficient populations have been associated with an increased incidence of iodine-induced hyperthyroidism (IHH), mainly in older people and those with multinodular goiter. Iodine intakes of 150-200 mcg/day have been found to increase the incidence of IHH in iodine-deficient populations. Iodine deficiency increases the risk of developing autonomous thyroid nodules that are unresponsive to the normal thyroid regulation system (see Function), resulting in hyperthyroidism after iodine supplementation. IHH is considered by some experts to be an iodine deficiency disorder. In general, the large benefit of iodization programs outweighs the small risk of IHH in iodine-deficient populations (1, 31).
In iodine sufficiency: In iodine-sufficient populations (e.g., the US), excess iodine intake is most commonly associated with elevated blood levels of thyroid stimulating hormone (TSH), hypothyroidism, and goiter. Although a slightly elevated TSH level does not necessarily indicate inadequate thyroid hormone production, it is the earliest sign of abnormal thyroid function when iodine intake is excessive. In iodine-sufficient adults, elevated TSH levels have been found at iodine intakes between 1,700 and 1,800 mcg/day. In order to minimize the risk of developing hypothyroidism, the Food and Nutrition Board (FNB) of the Institute of Medicine set a tolerable upper intake level (UL) for iodine at 1,100 mcg/day for adults. Very high (pharmacologic) doses of iodine may also produce thyroid enlargement (goiter) due to increased TSH stimulation of the thyroid gland. Prolonged intakes of more than 18,000 mcg/day (18 mg/day) have been found to increase the incidence of goiter. The UL values for iodine are listed by age group in Table 3. The UL is not meant to apply to individuals who are being treated with iodine under medical supervision (6).
Table 3. Tolerable Upper Intake Level (UL) for Iodine
|Infants 0-12 months
||Not possible to establish*
|Children 1-3 years
|Children 4-8 years
|Children 9-13 years
|Adolescents 14-18 years
|Adults 19 years and older
||1,100 mcg/day (1.1 mg/day)
|*Source of intake should be from food and formula only.
Individuals with increased sensitivity to excess iodine intake
Individuals with iodine deficiency, nodular goiter, or autoimmune thyroid disease may be sensitive to intake levels considered safe for the general population and may not be protected by the UL for iodine intake (6). Children with cystic fibrosis may also be more sensitive to the adverse effects of excess iodine (32).
Excess iodine and thyroid cancer
Observational studies have found increased iodine intake to be associated with an increased incidence of thyroid papillary cancer. The reasons for this association are not clear. In populations that were previously iodine deficient, salt iodization programs have resulted in relative increases in thyroid papillary cancers and relative decreases in thyroid follicular cancers. In general, thyroid papillary cancers are less aggressive and have a better prognosis than thyroid follicular cancers (33).
Amiodarone, a medication used to prevent abnormal heart rhythms, contains high levels of iodine and may affect thyroid function. Medications used to treat hyperthyroidism, such as propylthiouracil (PTU) and methimazole, may increase the risk of hypothyroidism. Additionally, the use of lithium in combination with pharmacologic doses of potassium iodide may result in hypothyroidism. Further, the use of pharmacologic doses of potassium iodide may decrease the anticoagulant effect of warfarin (coumarin) (6, 32).
Linus Pauling Institute Recommendation
The RDA for iodine is sufficient to ensure normal thyroid function. There is presently no evidence that iodine intakes higher than the RDA are beneficial. Most people in the US consume more than sufficient iodine in their diets, making supplementation unnecessary. Given the importance of sufficient iodine during fetal development and infancy, pregnant and breast-feeding women should consider taking a supplement that provides 150 mcg/day of iodine (see Deficiency).
Older adults (>50 years)
Because aging has not been associated with significant changes in the requirement for iodine, our recommendation for iodine intake is not different for older adults.
Authors and Reviewers
Originally written in 2001 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in April 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in July 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in March 2010 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in March 2010 by:
Elizabeth N. Pearce, MD, MSc.
Associate Professor of Medicine
Section of Endocrinology, Diabetes, and Nutrition
Boston University School of Medicine
Copyright 2001-2015 Linus Pauling Institute
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