What Is the Response of the Thyroid Gland to an Iodine Deficiency?

Contents

• Summary
• Function
• Deficiency
  • Biomarkers of iodine condition
  • Iodine deficiency disorders
  • Individuals and populations
    at risk
  • Nutrient interactions
  • Goitrogens
• The RDA
• Illness Prevention
  • Radiation-induced thyroid cancer
• Disease Treatment
  • Fibrocystic breast changes
• Sources
  • Food
  • Supplements
• Safety
  • Acute toxicity
  • Excessive iodine intakes
  • Drug interactions
  • Contaminants
• LPI Recommendation
• Authors and Reviewers
• References

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Summary

• Iodine is a key component of thyroid hormones, which are required throughout life for normal growth, neurological development, and metabolism. (More information)
• Insufficient iodine intake impairs the product of thyroid hormones, leading to a condition called hypothyroidism. Iodine deficiency results in a range of agin health disorders with varying degrees of severity, from thyroid gland enlargement (goiter) to severe physical and mental retardation known as cretinism. (More information)
• Iodine deficiency-induced hypothyroidism has adverse effects in all stages of development simply is well-nigh damaging to the developing brain. Maternal iodine deficiency during pregnancy can event in maternal and fetal hypothyroidism, equally well as miscarriage, preterm birth, and neurological impairments in offspring. (More data)
• Even in areas with voluntary/mandatory iodization programs and in iodine-replete countries, meaning women, lactating mothers, and young infants are amid the well-nigh vulnerable to iodine deficiency due to their special requirements during these life stages. (More information)
• The recommended dietary assart (RDA) for iodine intake is 150 micrograms (μg)/solar day in adults, 220 μg/day in pregnant women, and 290 μg/day in breast-feeding women. During pregnancy and lactation, the fetus and infant are entirely reliant on maternal iodine intake for thyroid hormone synthesis. (More information)
• Thyroid aggregating of radioactive iodine (¹³¹I) increases the take chances of developing thyroid cancer, especially in children. In example of radiation emergencies, current preventive measures include the distribution of pharmacologic doses of potassium iodide that would reduce the risk of significant uptake of ¹³¹I by the thyroid gland. (More data)
• Seafood is an excellent source of dietary iodine. Dairy products, grains, eggs, and poultry contribute substantially to dietary iodine intakes in the United states. (More information)
• More than 120 countries worldwide have introduced programs of salt fortification with iodine in order to correct iodine deficiency in populations. (More than information)
• In iodine-deficient populations, a rapid increment in iodine intake may precipitate iodine-induced hyperthyroidism. The risk of iodine-induced hyperthyroidism is peculiarly high in older people with multi-nodular goiter. (More information)
• In iodine-sufficient adults, long-term iodine intake above the tolerable upper intake level (UL) of 1,100 μg/day may increase the risk of thyroid disorders, including iodine-induced goiter and hypothyroidism. (More than information)

Iodine (I), a non-metallic trace element, is required by humans for the synthesis of thyroid hormones. Iodine deficiency is an important wellness trouble throughout much of the earth. Nigh of the Earth's iodine, in the form of the iodide ion (I^-), is institute 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, Atlas, Andes, and Alps; flooded river valleys, such as the Ganges River plain in India; and many inland regions, such as central Asia and Africa, central and eastern Europe, and the Midwestern region of North America are among the most severely iodine-deficient areas in the world (i).

Role

Iodine is an essential component of the thyroid hormones, triiodothyronine (T₃) and thyroxine (T_iv), and is therefore essential for normal thyroid function. To come across the body's demand for thyroid hormones, the thyroid gland traps iodine from the blood and incorporates it into the large (660 kDa) glycoprotein thyroglobulin. The hydrolysis of thyroglobulin past lysosomal enzymes gives rise to thyroid hormones that are stored and released into the apportionment when needed. In target tissues, such every bit the liver and the brain, T₄ (the most abundant circulating thyroid hormone) can exist converted to T₃ by selenium-containing enzymes known as iodothyronine deiodinases (DIOs) (Figure 1; see as well Nutrient interactions). T₃ is the physiologically active thyroid hormone that can demark to thyroid receptors in the nuclei of cells and regulate factor expression. In this manner, thyroid hormones regulate a number of physiologic processes, including growth, development, metabolism, and reproductive function (two).

[Effigy 1 - Click to Enlarge]

The regulation of thyroid function is a circuitous process that involves the hypothalamus and the pituitary gland. In response to thyrotropin-releasing hormone (TRH) secretion past the hypothalamus, the pituitary gland secretes thyroid-stimulating hormone (TSH), which stimulates iodine trapping, thyroid hormone synthesis, and release of T₄ and T_three by the thyroid gland. The presence of adequate circulating T₄ and T₃ feeds dorsum at the level of both the hypothalamus and pituitary, decreasing TRH and TSH production (Figure 2). When circulating T₄ levels decrease, the pituitary gland increases its secretion of TSH, resulting in increased iodine trapping, as well as increased production and release of both T_three and T_iv. Iodine deficiency results in inadequate product of T₄. In response to decreased claret T₄ concentrations, the pituitary gland increases its output of TSH. Persistently elevated TSH levels may lead to hypertrophy (enlargement) of the thyroid gland, likewise known every bit goiter (run across Deficiency) (iii).

[Figure 2 - Click to Enlarge]

Deficiency

The thyroid gland of a healthy adult concentrates lxx-80% of a full body iodine content of 15-20 mg and utilizes nearly 80 μg of iodine daily to synthesize thyroid hormones. In contrast, chronic iodine deficiency can result in a dramatic reduction of the iodine content in the thyroid well beneath 1 mg (1). Iodine deficiency is recognized as the most common crusade of preventable brain impairment in the earth. The spectrum of iodine deficiency disorders (IDD) includes mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities (iv). The World Wellness Organisation (WHO) estimated that over 30% of the earth'due south population (2 billion people) have bereft iodine intake as measured by median urinary iodine concentrations below 100 μg/L (v). Moreover, almost one-third of school-age children (6-12 years one-time) worldwide (241 one thousand thousand children in 2011) have insufficient iodine intake (vi, 7). 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 (4). Although about 70% of households in the globe at present have access to iodized salt (eight), mild-to-moderate iodine deficiency remains a public health concern in at to the lowest degree thirty countries; there are no iodine excretion data available for 42 other countries, including Israel, Syria, and Sierra Leone (vii). For more data on the international effort to eradicate iodine deficiency, visit the websites of the Iodine Global Network (formerly the International Quango for the Control of Iodine Deficiency Disorders) and the WHO.

Biomarkers of iodine condition

More than ninety% of ingested iodine is excreted in the urine within 24-48 hours such that daily iodine intakes in a population tin exist extrapolated from measures of median spot urinary iodine concentrations (9, 10). Co-ordinate to WHO criteria, population iodine deficiency is defined by median urinary iodine concentrations lower than 150 micrograms (μg)/L for pregnant women and 100 μg/L for all other groups (Tabular array one). Adequate intakes correspond to median urinary iodine concentrations of 100-199 μg/L in school-age children and 150-249 μg/L in pregnant women (Table 1). While median urinary iodine concentration is a population indicator of recent dietary iodine intake, multiple collections of 24-hour urinary iodine are preferable to gauge intake in individuals (nine-11).

Tabular array one. WHO Criteria for Assessment of Iodine Nutrition through Population-based Median Urinary Iodine Concentrations (iv)

Population Group	Median/Range of Urinary Iodine Concentrations (μg/L)	Iodine Intake
Children (<2 years)	<100	Bereft
	≥100	Adequate
Children (≥6 years), adolescents, and adults*	<100	Insufficient
	100-199	Adequate
	200-299	More than adequate
	>300	Excessive
Pregnant women	<150	Insufficient
	150-249	Adequate
	250-499	More than adequate
	≥500	Excessive
Chest-feeding women#	<100	Bereft
	≥100	Adequate
*Excludes meaning or lactating women. #Given that iodine requirements are increased in chest-feeding women (see The RDA), the numbers for median urinary excretion concentrations are lower than i would expect because iodine is also excreted in breast milk.

In many countries, serum TSH concentration is used in the screening for congenital hypothyroidism in newborns. Newborn TSH can be used as an indicator of population iodine status. Yet, in older children and adults, serum TSH is not a sensitive indicator of iodine condition as concentrations are usually maintained inside a normal range despite frank iodine deficiency (12). Serum thyroglobulin concentration in school-age children is a sensitive marking of iodine status in populations (13). In areas of owned goiter, changes in thyroid size reverberate long-term iodine diet (months to years). Cess of the goiter rate in a population is used to define the severity of iodine deficiency, likewise as to monitor the long-term impact of sustained salt iodization programs (iv, 10). Finally, serum thyroid hormone concentrations exercise non adequately reverberate iodine nutrition in populations (ane).

Iodine deficiency disorders

All the adverse effects of iodine deficiency in animals and humans are collectively termed iodine deficiency disorders (reviewed in 1). Thyroid enlargement, or goiter, is i of the earliest and most visible signs of iodine deficiency. It is a physiologic adaptation of the thyroid gland in response to persistent stimulation by TSH (see Part). In balmy iodine deficiency, thyroid enlargement may be enough to maximize the uptake of available iodine and provide the body with sufficient thyroid hormones. Nevertheless, large goiters can obstruct the trachea and esophagus and damage the recurrent laryngeal nerves.

More astringent cases of iodine deficiency result in dumb thyroid hormone synthesis known as hypothyroidism. Adequate iodine intake will generally reduce the size of goiters, only the reversibility of the effects of hypothyroidism depends on an individual's life phase. Iodine deficiency-induced hypothyroidism has adverse effects in all stages of development but is most dissentious to the developing brain. In improver to regulating many aspects of growth and development, thyroid hormones are important for the migration, proliferation, and differentiation of specific neuronal populations, the overall architecture of the encephalon'due south cortex, the formation of axonal connections, and the myelination of the fundamental nervous system, which occurs both earlier and shortly after nativity (reviewed in 14).

The furnishings of iodine deficiency at different life stages are discussed below.

Pregnancy and lactation

Daily iodine requirements are significantly increased in pregnant and breast-feeding women because of (1) the increased thyroid hormone production and transfer to the fetus in early pregnancy before the fetal thyroid gland becomes functional, (2) iodine transfer to the fetus during late gestation, (iii) increased urinary iodine excretion, and (iv) iodine transfer to the infant via chest milk (run into as well The RDA) (12, 15).

During pregnancy, the size of the thyroid gland is increased by 10% in women residing in iodine-sufficient regions and increased by 20%-40% in those living in iodine-scarce regions (sixteen). Iodine deficiency during pregnancy can effect in hypothyroidism in women. Maternal hypothyroidism has been associated with increased risk for preeclampsia, miscarriage, stillbirth, preterm birth, and low-birth-weight infants (reviewed in 16). In addition, astringent iodine deficiency during pregnancy may issue in congenital hypothyroidism and neurocognitive deficits in the offspring (see Prenatal evolution) (12).

Iodine-deficient women who are breast-feeding may not be able to provide sufficient iodine to their infants who are particularly vulnerable to the furnishings of iodine deficiency (see Newborns and infants) (17). A daily prenatal supplement of 150 μg of iodine, every bit recommended past the American Thyroid Association (ATA) (sixteen), will help to ensure that US meaning and breast-feeding women consume sufficient iodine during these disquisitional periods. In iodine-deficient areas where iodized table salt is not available, the Iodine Global Network (IGN; formerly the International Quango for the Command of Iodine Deficiency Disorders), the World Health Organisation (WHO), and UNICEF recommend that lactating women receive a unmarried annual dose of 400 mg of iodine (or 250 μg/twenty-four hour period) and exclusively chest-feed for at least six months. When breast-feeding is not possible, direct supplementation of the infant (<ii years one-time) with a single annual dose of 200 mg of iodine (or 90 μg/day) is brash (iv). A randomized and placebo-controlled trial recently demonstrated that maternal supplementation (with a single 400-mg dose of iodine) improved the iodine status of chest-fed infants more than efficiently than direct infant supplementation (with a single 100 mg-dose of iodine) for a menstruum of at to the lowest degree six months (18). Even so, supplementation of lactating women failed to increase maternal urinary iodine concentrations above 100 μg/L, suggesting that supplemented mothers remained deficient in iodine (18).

Prenatal evolution

Fetal iodine deficiency is caused past iodine deficiency in the mother (see Pregnancy and lactation). During pregnancy, before the fetal thyroid gland becomes functional at 16-xx weeks' gestation, maternal thyroxine (T₄) crosses the placenta to promote normal embryonic and fetal evolution. Hence, maternal iodine deficiency and hypothyroidism can result in agin pregnancy complications, including fetal loss, placental abruption, preeclampsia, preterm delivery, and congenital hypothyroidism in the offspring (16). The effects of maternal hypothyroidism on the offspring depend on the timing and severity of in utero iodine deficiency. A severe form of built hypothyroidism may lead to cretinism, a status associated with irreversible mental retardation. The clinical pic of neurological cretinism in the offspring includes severe mental and physical retardation, deafness, mutism, and motor spasticity.

A myxedematous grade of cretinism has been associated with coexisting iodine and selenium deficiency in primal Africa (see Nutrient interactions) and is characterized by a less astringent degree of mental retardation than in neurological cretinism. Withal, afflicted individuals showroom all the features of astringent hypothyroidism, including severe growth retardation and delayed sexual maturation (12). Ii longitudinal cohort studies (one in the UK and 1 in Australia) recently observed that even balmy-to-moderate iodine deficiency during pregnancy was associated with reduced scores of IQ and various measures of literacy performance in children 8 to 9 years of age (19, 20).

Newborns and infants (up to one year of age)

Infant mortality is higher in areas of severe iodine deficiency than in iodine-replete regions, and several studies take demonstrated an increase in childhood survival upon correction of the iodine deficiency (8, 21, 22). Infancy is a menses of rapid encephalon growth and evolution. Sufficient thyroid hormone, which depends on adequate iodine intake, is essential for normal encephalon evolution. Fifty-fifty in the absenteeism of congenital hypothyroidism, iodine deficiency during infancy may result in aberrant brain development and, consequently, impaired intellectual development (23, 24).

Children and adolescents

Iodine deficiency in children and adolescents is frequently associated with goiter. The incidence of goiter peaks in adolescence and is more common in girls than boys. Schoolhouse-age children in iodine-scarce areas bear witness poorer schoolhouse functioning, lower IQs, and a higher incidence of learning disabilities than matched groups from iodine-sufficient areas. Iii meta-analyses of mainly cross-sectional studies concluded that chronic iodine deficiency was associated with reduced mean IQ scores past 7-13.v points in participants (primarily children) (25-27). Even so, these observational studies did not distinguish betwixt iodine deficiency during pregnancy and during childhood, and such observational studies may be confounded by social, economic, and educational factors that influence child development.

Adults

Inadequate iodine intake may also result in goiter and hypothyroidism in adults. Although the furnishings of hypothyroidism are more subtle in the brains of adults than children, research suggests that hypothyroidism results in poor social and economic achievements due to low educability, aloofness, and reduced work productivity (28). Other symptoms of hypothyroidism in adults include fatigue, weight proceeds, common cold intolerance, and constipation.

Finally, considering iodine deficiency induces an increase in the iodine trapping capacity of the thyroid, iodine-deficient individuals of all ages are more susceptible to radiations-induced thyroid cancer (see Disease Prevention), too as to iodine-induced hyperthyroidism after an increase in iodine intakes (see Safety) (2).

Individuals and populations at run a 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 in countries considered iodine-sufficient may not consume adequate iodine (7, 29). The greater use of methods assessing iodine condition (see Biomarkers of iodine status) has shown that iodine deficiency also occurs in areas where the prevalence of goiter is low, in littoral areas, in highly adult countries, and in regions where iodine deficiency was previously eliminated (iv).

The U.s. is currently considered to exist iodine-sufficient. Yet, in recent years, dietary intakes of iodine in the US population have decreased. Data from the latest The states National Health and Diet Examination Survey (NHANES 2009-2010) indicated that the median urinary iodine concentration for the general population was 144 μg/L compared to 164 μg/L reported in previous assessments (NHANES 2005-2006 and 2007-2008) (xxx, 31). In addition to regional differences across the United states, ethnic variations have been institute. In all age groups, median urinary iodine concentrations were shown to be lower in African Americans than in Hispanics and Caucasians.

In improver, median urinary iodine concentrations in nonpregnant women of childbearing age and pregnant women indicate that balmy iodine deficiency has re-emerged in the U.s. in recent years (31).

Nonpregnant women

Data from The states NHANES 2007-2010 indicated that 37.three% of nonpregnant women (ages 15-44 years) had urinary iodine concentrations lower than 100 μg/L, reflecting potentially insufficient iodine intakes (see Biomarkers of iodine status) (31). Just one-fifth of nonpregnant women reported using iodine-containing supplements in an earlier NHANES (2001-2006) (32). Yet, acceptable intakes of iodine in women of childbearing historic period (150 μg/day; see The RDA) are essential for optimum stores of iodine, especially if they are considering pregnancy. Some experts suggested a daily consumption of 250 μg of iodine earlier conception to ensure acceptable thyroid hormone production and iodine supply to the embryo and fetus during pregnancy (encounter Pregnancy and lactation) (12).

Significant women

There are no statistics on the global burden of iodine deficiency in meaning women, merely national and regional data propose that this group is especially vulnerable. Given the increased iodine requirements during pregnancy, the median urinary iodine concentration should be at least of 150 μg/50 (encounter Biomarkers of iodine status). Pooled information from NHANES 2005-2010 reported that US meaning women had a median urinary iodine concentration of 129 μg/Fifty, and the lowest median concentration (109 μg/L) was observed during the first trimester of gestation, when the embryo/fetus relies exclusively on maternal thyroid hormones (31).

Breast-feeding women

While data regarding the iodine condition of breast-feeding women in the United states are limited, dietary intakes that were inadequate during pregnancy are likely to be bereft in a significant fraction of breast-feeding women (33, 34). A systematic review of the literature recently reported suboptimal dietary iodine intakes in breast-feeding women in some countries with a mandatory fortification program, including Kingdom of denmark, Australia, and India (35). The American Thyroid Association (ATA) recommends that all Northward American women who are pregnant or breast-feeding supplement their dietary iodine intake with 150 μg/day of iodine (36).

Breast-fed and weaning infants

The body of a healthy newborn contains only near 300 μg of iodine, which makes newborns extremely vulnerable to iodine deficiency (28), and chest-fed infants are entirely reliant on maternal iodine intakes for thyroid hormone synthesis. Even in areas covered by a salt iodization program, weaning infants are at loftier risk of iodine deficiency, especially if they are not receiving iodine-containing infant formula (17).

Individuals consuming special diets

Diets that exclude iodized table salt, fish, and seaweed have been found to comprise very little iodine (ix). Individuals consuming branded weight-loss foods may also be at risk of inadequate intakes (37). A small Us cross-exclusive study in 78 vegetarians and 63 vegans reported median urinary iodine concentrations of 147 μg/L and 78.five μg/L, respectively, suggesting inadequate iodine intakes among vegans (38). Two cases of goiter and/or hypothyroidism have also been recently reported in children post-obit restrictive diets to command esophageal inflammation (eosinophilic esophagitis) (39) or allergies (40).

Patients requiring parenteral diet

Although iodine is usually not added to parenteral nutrition (PN) solutions, topical iodine-containing disinfectants and other adventitious sources provide substantial amounts of iodine to some PN patients such that the occurrence of iodine deficiency is unlikely. Nevertheless, deficiency might occur, especially in preterm infants with limited trunk stores, if chlorhexidine-based antiseptics replace iodinated antiseptics (28, 41).

Nutrient interactions

Concurrent deficiencies in selenium, iron, or vitamin A may exacerbate the effects of iodine deficiency (reviewed in 42).

Selenium

While iodine is an essential component of thyroid hormones, the selenium-containing iodothyronine deiodinases (DIOs) are enzymes (or selenoenzymes) required for the conversion of T₄ to the biologically active thyroid hormone, T₃ (come across the article on Selenium). DIO1 activity may likewise exist involved in regulating iodine homeostasis (43). In add-on, glutathione peroxidases are selenoenzymes that protect the thyroid gland from hydrogen peroxide-induced damage during thyroid hormone synthesis (44). A randomized, placebo-controlled study in 151 pregnant women at risk of developing autoimmune thyroid illness found that selenium supplementation (200 μg/day in the form of selenomethionine) at 12 weeks of gestation until 12 months' postpartum reduced the hazard of thyroid dysfunction and permanent hypothyroidism (45). Nevertheless, another trial (the Selenium in Pregnancy Intervention Trial) plant no benefit of selenium supplementation (sixty μg/day from 12-14 weeks of gestation to delivery) over placebo on circulating autoantibody concentrations in meaning women mildly deficient in iodine (46).

The epidemiology of coexisting iodine and selenium deficiencies in central Africa has been linked to the prevalence of myxedematous cretinism, a severe class of congenital hypothyroidism accompanied by mental and physical retardation. Selenium deficiency may be only 1 of several undetermined factors that might exacerbate the detrimental effects of iodine deficiency (42). Besides, results from randomized controlled intervention trials take shown that correcting only the selenium deficiency may have a deleterious effect on thyroid hormone metabolism in schoolhouse-historic period children with co-existing selenium and iodine deficiency (47, 48). Finally, selenium deficiency in rodents was found to accept little touch on DIO activities as it appears that selenium is existence supplied in priority for adequate synthesis of DIOs at the expense of other selenoenzymes (44).

Iron

Severe iron-deficiency anemia can impair thyroid metabolism in the following ways: (ane) by altering the TSH response of the pituitary gland; (two) by reducing the activity of thyroid peroxidase that catalyzes the iodination of thyroglobulin for the production of thyroid hormones; and (3) in the liver by limiting the conversion of T₄ to T₃, increasing T₃ turnover, and decreasing T₃ binding to nuclear receptors (49). It is estimated that goiter and iron-deficiency anemia coexist in upward to 25% of school-age children in west and north Africa (42). A randomized controlled study in atomic number 26-deficient children with goiter showed a greater reduction in thyroid size following the consumption of iodized salt together with 60 mg/solar day of iron four times per week compared to placebo (50). Additional interventions take confirmed that correcting iron-deficiency anemia improved the efficacy of iodine supplementation to mitigate thyroid disorders (reviewed in 42, 49).

Vitamin A

In north and west Africa, vitamin A deficiency and iodine deficiency-induced goiter may coexist in upwardly to 50% of children. Vitamin A condition, like other nutritional factors, appears to influence the response to iodine prophylaxis in iodine-scarce populations (51). Vitamin A deficiency in beast models was found to interfere with the pituitary-thyroid axis by (i) increasing the synthesis and secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, (2) increasing the size of the thyroid gland, (iii) reducing iodine uptake by the thyroid gland and impairing the synthesis and iodination of thyroglobulin, and (4) increasing circulating concentrations of thyroid hormones (reviewed in 52). A cantankerous-sectional study of 138 children with concurrent vitamin A and iodine deficiencies found that the severity of vitamin A deficiency was associated with higher risk of goiter and higher concentrations of circulating TSH and thyroid hormones (51). These children received iodine-enriched salt together with vitamin A (200,000 IU at baseline and at five months) or a placebo in a randomized, double-blind, ten-month trial. Vitamin A supplementation significantly decreased TSH concentration and thyroid volume compared to placebo (51). In some other trial, vitamin A supplementation solitary (without iodine) to iodine-deficient children reduced the volume of the thyroid gland, besides equally TSH and thyroglobulin concentrations (53). Yet, supplemental vitamin A had no additional effect on thyroid office/hormone metabolism when children were too given iodized oil.

Goitrogens

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 cassava, which contains linamarin, a compound that is metabolized to thiocyanate and blocks thyroidal uptake of iodine (1). In iodine-deficient populations, tobacco smoking has been associated with an increased risk for goiter (54, 55). Cyanide in tobacco smoke is converted to thiocyanate in the liver, placing smokers with depression iodine intake at risk of developing a goiter. Moreover, thiocyanate affects iodine transport into the lactating mammary gland, leading to low iodine concentrations in breast milk and impaired iodine supply to the neonates/infants of smoking mothers (ii). Some species of millet, sweet potatoes, beans, and cruciferous vegetables (e.g., cabbage, broccoli, cauliflower, and Brussels sprouts) also contain goitrogens (one). Further, the soybean isoflavones, genistein and daidzein, have been found to inhibit thyroid hormone synthesis (56). Most of these goitrogens are non of clinical importance unless they are consumed in large amounts or in that location is coexisting iodine deficiency. Industrial pollutants, such equally perchlorate (see Safety), resorcinol, and phthalic acid, may likewise be goitrogenic (1, 57).

The Recommended Dietary Allowance (RDA)

The RDA for iodine was reevaluated by the Food and Nutrition Lath (FNB) of the Institute of Medicine (IOM) in 2001 (Tabular array ii). The recommended amounts were calculated using several methods, including the measurement of iodine uptake in the thyroid glands of individuals with normal thyroid function (nine). Like recommendations take been made by several organizations, including the American Thyroid Association (ATA) (sixteen, 58), the Globe Health Organization (WHO), the Iodine Global Network (IGN; formerly the International Council for the Command of Iodine Deficiency Disorders), and the Un Children's Fund (UNICEF) (four). Of note, the WHO, IGN, and UNICEF recommend daily intakes of 250 μg of iodine for both meaning and breast-feeding women (iv).

Table 2. Recommended Dietary Allowance (RDA) for Iodine

Life Phase	Age	Males (μg/24-hour interval)	Females (μg/twenty-four hours)
Infants	0-6 months	110 (AI)	110 (AI)
Infants	seven-12 months	130 (AI)	130 (AI)
Children	1-3 years	90	90
Children	iv-8 years	ninety	90
Children	9-13 years	120	120
Adolescents	14-eighteen years	150	150
Adults	19 years and older	150	150
Pregnancy	all ages	-	220
Breast-feeding	all ages	-	290

Disease Prevention

Radiation-induced thyroid cancer

Radioactive iodine, especially iodine 131 (¹³¹I), may be released into the environment as a consequence of nuclear reactor accidents, such as the 1986 Chernobyl nuclear accident in Ukraine and the 2011 Fukushima Daiichi nuclear accident in Japan. Thyroid accumulation of radioactive iodine increases the risk of developing thyroid cancer, especially in children (59). The increased iodine trapping action of the thyroid gland in iodine deficiency results in increased thyroid accumulation of radioactive iodine (¹³¹I). Thus, iodine-scarce individuals are at increased risk of developing radiations-induced thyroid cancer because they will accumulate greater amounts of radioactive iodine. Potassium iodide administered in pharmacologic doses (up to 130 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 gamble of radiations-induced thyroid cancer (60). 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 compared to fallout areas where potassium iodide prophylaxis was not widely used (61). 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 constitute (62). Come across also the US FDA's Potassium Iodide Data.

Affliction Handling

Fibrocystic breast changes

Fibrocystic breast changes constitute a benign (non-cancerous) condition of the breasts, characterized past lumpiness and discomfort in ane or both breasts. Cyst germination and fibrous changes in the advent of chest tissue occur in at to the lowest degree 50% of premenopausal women and are non commonly associated with an increased risk of chest cancer (63). The cause of fibrocystic changes is not known, just variations in hormonal stimulation during menstrual cycles may trigger changes in breast tissue (63).

A few observational studies also suggested an clan between beneficial chest diseases (including but not limited to fibrocystic changes) and thyroid disorders. Recently, a small case-command study (166 cases vs. 72 controls) showed that the frequency of benign breast diseases was greater in women with nodular goiter (54.9%) or Hashimoto thyroiditis (47.4%) than in euthyroid controls (29.2%) (64). Conversely, the prevalence of anti-thyroid autoimmunity and hypothyroidism was found to be significantly higher in women with benign breast diseases compared to controls (65, 66). Interestingly, correcting hypothyroidism with supplemental T₄ was found to improve some of the benign breast illness symptoms, including breast pain (mastalgia) and nipple discharge (65).

In estrogen-treated rats, iodine deficiency leads to changes like to those seen in fibrocystic breasts, while iodine repletion reverses those changes (67). An uncontrolled written report of 233 women with fibrocystic changes found that treatment with aqueous molecular iodine (I_two) at a dose of 0.08 mg of I₂/kg of body weight daily over 6 to 18 months was associated with improvement in pain and other symptoms in over 70% of participants (68). About 10% of the study participants reported side furnishings that were described by the investigators as minor. A double-bullheaded, placebo-controlled trial of aqueous molecular iodine (0.07-0.09 mg of I₂/kg of body weight daily for 6 months) in 56 women with fibrocystic changes found that 65% of the women taking molecular iodine reported improvement compared to 33% of those taking the placebo (68). A double-blind, placebo-controlled trial in 87 women with documented breast pain reported that molecular iodine (one.v, three, or vi mg/day) for half dozen months improved overall pain (69). In this study, 38.5% of the women receiving 1.5 mg/twenty-four hour period, 37.9% of those receiving 3 mg/solar day, and 51.7% of those receiving 6 mg/day reported at to the lowest degree a 50% reduction in self-assessed breast pain compared to 8.iii% in the placebo group.

Big-scale, controlled clinical trials are needed to determine the therapeutic value of molecular iodine in fibrocystic breasts. Besides, the doses of iodine used in these studies (ane.five to half-dozen mg/day for a 60 kg person) are higher than the tolerable upper intake level (UL) recommended by the Food and Nutrition Board of the Establish of Medicine and should just be used under medical supervision (run into Condom).

Sources

Food sources

Data from the ongoing US Full Diet Study, which monitors the levels of some contaminants and nutrients in food products, indicates that dietary iodine intakes in adults range between 138 and 268 micrograms (μg)/24-hour interval. Considerably higher average intakes (304-353 μg/24-hour interval of iodine) were reported for boys 14 to xvi years of age (seventy).

Seafood is rich in iodine because marine animals tin can concentrate the iodine from seawater. Certain types of edible seaweed (e.grand., wakame) are also very rich in iodine (71). The iodine content of nutrient that is grown or raised on a detail soil depends on the iodine content of this soil. In the US, dairy products contribute up to 90% of full estimated iodine intakes in infants, at least 70% in children (ages, 2-x years), 53%-63% in adolescents (ages, 14-16 years), and near l% in adults (70). In the UK and northern Europe, iodine levels in dairy products tend to exist lower in summer when cattle are immune to graze in pastures with low soil iodine content (ix).

Other good sources of dietary iodine include eggs, fruit, grain products, and poultry (70). Candy foods tin can contribute to iodine intake if iodized table salt or food additives, such as calcium iodate and potassium iodate, are added during production. Even so, in the United states of america, virtually no iodized salt is used in the manufacturing of processed food and fast food products, and the food industry is not required to list the iodine content on food packaging (72). Table 3 lists the iodine content of some iodine-rich foods in micrograms (μg). Because the iodine content of foods can vary considerably, these values should be considered approximate (73).

Table 3. Some Food Sources of Iodine

Food	Serving	Iodine (μg)
Salt (iodized)	1 gram	77
Cod	3 ounces*	99
Shrimp	3 ounces	35
Fish sticks	2 fish sticks	35
Tuna, canned in oil	three ounces (½ can)	17
Milk (cow'southward)	1 cup (8 fluid ounces)	99
Egg, boiled	1 large	12
Navy beans, cooked	½ cup	32
Tater with peel, baked	1 medium	60
Turkey breast, baked	3 ounces	34
Seaweed	¼ ounce, stale	Variable; may exist greater than 4,500 μg (4.5 mg)
*A three-ounce serving of meat is most the size of a deck of cards.

Supplements

Over-the-counter iodine supplements

Potassium iodide is available equally a nutritional supplement, typically in combination products, such as multivitamin/mineral supplements. Iodine makes up approximately 77% of the total weight of potassium iodide (56). A multivitamin/mineral supplement that contains 100% of the daily value (DV) for iodine provides 150 μg of iodine. Although nigh people in the Usa consume sufficient iodine in their diets (run across Sources), an additional 150 μg/twenty-four hour period is unlikely to effect in excessive iodine intake. The American Thyroid Association (ATA) recommends prenatal supplementation with 150 μg/24-hour interval of iodine and advises confronting the ingestion of ≥500 μg/day of iodine from iodine, potassium iodine, and kelp supplements for children and adults, and during pregnancy and lactation (see as well Safety) (36, 74).

Iodine fortification programs

The fortification of salt with iodine is a viable and cheap method to eliminate iodine deficiency, and salt iodization programs have been implemented in nearly all countries. In Due north America, table salt fortification with iodine is mandated in Canada and some parts of Mexico, simply simply voluntary in the US such that merely 52% of Usa tabular array salt is iodized and only 1-5th of the total common salt consumed in the U.s. is iodized (72, 75). Potassium iodide (KI), cuprous iodide (CuI), and potassium iodate (KIO_iii) are used to iodize salt. The United states of america Nutrient and Drug Administration (FDA) recommends between 46 and 76 μg of iodine per gram of salt in iodized common salt. However, the contempo analysis of 88 The states iodized food-grade common salt samples revealed that the iodine content was below the recommended range in 52% of the samples and above the range in seven% of the samples (76).

In other countries, salt commonly contains xx-fifty μg of iodine per gram of salt, depending on local regulations (76). In countries similar Denmark (77), Australia (78, 79), and New Zealand (80), the use of iodized table salt in the bread-making process is mandated. Additional approaches have been explored, including sugar fortification (81), egg fortification (82), utilise of iodized salt in the preparation of fermented fish and fish sauce (83), and utilise of iodine-rich crop fertilizers (84). In add-on, fortification of livestock feeds with iodine and the apply of iodophors for sanitation during milking contribute to increasing iodine content in dairy products (85). Finally, annual doses of iodized vegetable oil are administered orally or intramuscularly to individuals in iodine-deficient populations who do not accept access to iodized salt (iv, 56).

Safety

Acute toxicity

Acute iodine poisoning is rare and usually occurs merely with doses of many grams. Symptoms of acute iodine poisoning include burning of the mouth, pharynx, and stomach, fever, nausea, airsickness, diarrhea, a weak pulse, cyanosis, and coma (1).

Excessive iodine intakes

Risk of iodine-induced hyperthyroidism in iodine-deficient individuals

Iodine supplementation programs in iodine-deficient populations accept been associated with an increased incidence of iodine-induced hyperthyroidism (IIH), especially in older people with multi-nodular goiter (86). Iodine intakes of 150-200 μg/day have been plant to increase the incidence of IIH in iodine-deficient populations. Iodine deficiency increases the run a risk of developing autonomous thyroid nodules that are unresponsive to TSH control (see Function). These democratic nodules may then overproduce thyroid hormones in response to sudden iodine supply. IIH symptoms include weight loss, tachycardia (high pulse rate), muscle weakness, and skin warmth. IIH tin can exist dangerous in individuals with underlying heart disease. Yet, because the chief cause of nodular goiter and IIH is chronic iodine deficiency, the benefit of iodization programs largely outweighs the adventure of IIH in iodine-deficient populations (1).

Risk of hypothyroidism in iodine-sufficient individuals

In iodine-sufficient individuals, backlog iodine intake is most normally associated with elevated claret concentrations of thyroid stimulating hormone (TSH) that inhibit thyroid hormone production, leading to hypothyroidism and goiter. A slightly elevated serum TSH concentration without a decrease in serum T_iv or T_three is the earliest sign of abnormal thyroid function when iodine intake is excessive. In iodine-sufficient adults, elevated serum TSH has been constitute at chronic iodine intakes of ≥750 μg/twenty-four hours in children and ≥1,700 μg/day in adults. Because various edible seaweed species essentially contribute to traditional Asian meals, average Japanese dietary intakes are estimated to range betwixt one,000 and 3,000 μg of iodine/day (71). Iodine-induced goiter and hypothyroidism are not uncommon in Japan and tin be reversed past restricting seaweed intake (71). Prolonged intakes of more than 18,000 μg/day (18 mg/day) increment the incidence of goiter in adults. In newborns, iodine-induced goiter and hypothyroidism tin can be due to either high maternal intakes or loftier exposure to iodized antiseptics (87). In order to minimize the take chances of adverse health effects, the Food and Nutrition Board of the US Institute of Medicine fix a tolerable upper intake level (UL) for iodine that is likely to be safe in almost all individuals. The UL values for iodine are listed in Table iv past age group; the UL does non apply to individuals who are being treated with iodine under medical supervision (74).

Tabular array four. Tolerable Upper Intake Level (UL) for Iodine

Age Grouping	UL (μg/twenty-four hour period)
Infants 0-12 months	Not possible to constitute*
Children 1-3 years	200
Children 4-8 years	300
Children 9-13 years	600
Adolescents 14-eighteen years	900
Adults 19 years and older	ane,100
*Source of intake should be from nutrient and formula only.

Individuals with increased sensitivity to excess iodine intake

Individuals with iodine deficiency and those with preexisting thyroid affliction, including nodular goiter, autoimmune Hashimoto thyroiditis, Graves disease, and a history of partial thyroidectomy, may be sensitive to iodine intake levels considered safety for the general population and may not be protected past the UL for iodine (9). Infants, the elderly, and pregnant and lactating women may likewise be more susceptible to backlog iodine (come across Supplements) (74).

Do elevated and/or bereft iodine intakes increase the run a risk of thyroid cancer?

Over the past decades, the incidence of thyroid cancer has increased worldwide. In the US, the incidence of thyroid cancer — representing 4% of all newly diagnosed cancers — has increased from four.9 cases per persons in 1983 to 14.7 cases per 100,000 persons in 2011, but bloodshed rate from thyroid cancer has remained low (near 0.5 per 100,000 persons) (88). Bookkeeping for over 80% of all thyroid cancers, thyroid papillary cancer is less aggressive and has a better prognosis than thyroid follicular cancer or anaplastic thyroid cancer. The increasing incidence of thyroid cancer worldwide is likely due at least in role to the improved screening and diagnosis activities. However, considering it has coincided with the introduction of iodine fortification programs, a possible contribution of increased iodine intakes has been hypothesized. Yet, in the The states, the increasing incidence of thyroid cancers (primarily papillary cancer) over the last few decades was paralleled with a reduction in average iodine intake (89).

Ecologic studies also suggested that iodine prophylaxis in populations that were previously iodine deficient was associated with an increased incidence of the papillary rather than the follicular cancer subtype, and with a reduced incidence of the more aggressive anaplastic thyroid cancer (89). While changes in iodine intakes appear to bear upon the histological type of thyroid cancer, it is non yet clear whether iodine deficiency and/or iodine backlog increment the risk of thyroid cancer (88).

Drug interactions

Amiodarone, a medication used to prevent abnormal center rhythms, contains high levels of iodine and may affect thyroid function (ninety, 91). Antithyroid drugs used to treat hyperthyroidism, such as propylthiouracil (PTU), methimazole, and carbimazole, may increase the gamble of hypothyroidism. Additionally, the long-term use of lithium to care for mood disorders may increment the risk of hypothyroidism (92). Further, the apply of pharmacologic doses of potassium iodide may decrease the anticoagulant consequence of warfarin (coumarin) (56).

Contaminants

Perchlorate is an oxidizing agent found in rocket propellants, airbags, fireworks, herbicides, and fertilizer. Mainly as a issue of human being activity, perchlorate has been found to contaminate drinking h2o and many foods (57). Chronic exposure to perchlorate concentrations at levels greater than twenty μg per kg trunk weight (bw) per day interferes with iodine uptake by the thyroid gland and may lead to hypothyroidism (93). The United states Environment Protection Bureau (EPA) recommends that daily oral exposure to perchlorate should not exceed 0.seven μg/kg bw to protect the most sensitive population, i.e., the fetuses of pregnant women who might be deficient in iodine and/or hypothyroid (94). Among all historic period groups, children aged ii years have the highest estimated perchlorate intakes per day with 0.35-0.39 μg/kg bw/day. Average estimated intakes of perchlorate in The states adults range betwixt 0.08 and 0.11 μg/kg bw/twenty-four hour period (70).

Linus Pauling Institute Recommendation

The RDA for iodine is sufficient to ensure normal thyroid office. At that place is presently no evidence that iodine intakes higher than the RDA are beneficial. Most people in the United states of america consume sufficient iodine in their diets, making supplementation unnecessary.

Pregnant and breast-feeding women

Given the importance of sufficient iodine during prenatal evolution and infancy, pregnant and breast-feeding women should accept a supplement that provides 150 μg of iodine per day (see Deficiency).

Older adults (>50 years)

Because aging has not been associated with significant changes in the requirement for iodine, the LPI recommendation for iodine intake is non different for older adults.

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Authors and Reviewers

Originally written in 2001 past:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in Apr 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon Country University

Updated in July 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon Country Academy

Updated in March 2010 past:
Victoria J. Drake, Ph.D.
Linus Pauling Establish
Oregon Country University

Updated in Baronial 2015 by:
Barbara Delage, Ph.D.
Linus Pauling Establish
Oregon State University

Reviewed in August 2015 by:
Elizabeth N. Pearce, Thousand.D., M.Sc.
Associate Professor of Medicine
Boston University Schoolhouse of Medicine

Copyright 2001-2022  Linus Pauling Establish

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Source: https://lpi.oregonstate.edu/book/export/html/228

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