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Iodine deficiency disorders
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Iodine deficiency disorders
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Literature review current through: Nov 2016. | This topic last updated: May 04, 2016.

INTRODUCTION — Both insufficient and excessive iodine intake can result in thyroid disease. The term “iodine deficiency disorders” refers to all of the consequences of iodine deficiency, which depend on its severity and the age of the affected subject [1]. When severe iodine deficiency occurs during pregnancy, it is associated with fetal hypothyroidism, mental impairment, and increased neonatal and infant mortality. In adults, iodine-induced hypothyroidism is rare, while the most common manifestation is goiter that progresses to nodular goiter and eventually to thyroid autonomy and hyperthyroidism.

Iodine is an essential component of thyroxine (T4) and triiodothyronine (T3), and it must be provided in the diet. Inadequate iodine intake leads to inadequate thyroid hormone production, and all the consequences of iodine deficiency stem from the associated hypothyroidism.

In developing countries, iodine deficiency has been identified as one of the modifiable factors that have an adverse effect on child development [2]. It is a global public health problem and, in combating it, emphasis should be placed on diagnosis and correction at the level of the community rather than the individual. The Iodine Global Network maintains a website (Iodine Global Network) with databases of information about iodine nutrition in different countries and an information reference desk.

This topic will review the consequences of iodine deficiency, its geographical distribution, diagnostic measures, prophylaxis, and treatment. Other aspects of iodine and the thyroid, including the adverse consequences of iodine excess, are discussed separately. (See "Iodine-induced thyroid dysfunction" and "Thyroid hormone synthesis and physiology".)

IODINE REQUIREMENTS — Iodide is essential for thyroid hormone synthesis. In order for the thyroid gland to synthesize adequate amounts of thyroxine (T4), approximately 52 mcg of iodide must be taken up daily by the thyroid gland. Severe iodine deficiency develops when iodide intake is chronically <20 mcg/day. (See "Thyroid hormone synthesis and physiology", section on 'Thyroid hormone biosynthesis'.)

Iodine can be obtained by consumption of foods that naturally contain it (fish, seafood, kelp, some drinking water, and vegetables grown in iodine-sufficient soil) or to which it is added (table salt). Cow’s milk is a source of iodine owing to iodine in cattle feed and the use of iodophor udder cleansers in the dairy industry. Sea salt naturally contains only a small amount of iodine. Dietary iodine is absorbed as iodide and rapidly distributed in the extracellular fluid, which also contains iodide released from the thyroid and by extrathyroidal deiodination of the iodothyronines. Iodide leaves this pool by transport into the thyroid and excretion into the urine.

The World Health Organization (WHO) recommends [3]:

90 mcg of iodine daily for infants and children up to five years

120 mcg for children 6 to 12 years

150 mcg daily for children ≥12 years and adults

250 mcg daily during pregnancy and lactation

The United States Institute of Medicine (IOM) recommended minimum daily intake of iodine is similar [4]:

90 mcg daily for children one to eight years old

120 mcg for children 9 to 13 years

150 mcg daily for older adolescents and nonpregnant adults

220 mcg for pregnant women

290 mcg for lactating women

The iodine requirements are higher in pregnant women due to an increase in maternal T4 production required to maintain maternal euthyroidism. Severe maternal iodine deficiency during pregnancy results in a reduction in maternal T4 production, inadequate placental transfer of maternal T4, and impairment of fetal neurologic development. (See 'Consequences of iodine deficiency' below.)

CLASSIFICATION OF IODINE STATUS — A system for classifying iodine deficiency and sufficiency has been developed based upon the median urinary iodine concentration in a population (table 1) [5]. The most usual survey group is school-age children, but their nutrition must reflect that of the community in order for the data to be meaningful [3,6,7].

Iodine sufficiency is defined as a median urinary iodine concentration of:

100 to 299 mcg/L for children and nonpregnant adults

150 to 249 mcg/L for pregnant women

Iodine deficiency is defined by the following median urinary iodine concentrations:

Mild iodine deficiency – 50 to 99 mcg/L

Moderate deficiency – 20 to 49 mcg/L

Severe deficiency – <20 mcg/L

A median average daily iodine intake of 150 mcg corresponds to a median urinary iodine concentration of 100 mcg/L [1].

Pregnant women require special attention because their renal threshold for iodine is lower, dietary salt (including iodized salt) is often restricted, and the needs of the fetus and the consequences of iodine deficiency to the fetus are greater [8,9]. (See 'During pregnancy and lactation' below.)

Additional factors that can exacerbate the effects of iodine deficiency include coexistent deficiencies of iron, selenium, and vitamin A [10], and the ingestion of foods such as cassava or millet that contain goitrogenic substances.

GEOGRAPHIC DISTRIBUTION — There has been substantial progress in reducing the frequency of iodine deficiency (figure 1) [7,11]. Between 2003 and 2014, the total number of countries with adequate iodine intake increased from 67 to 116 [12,13].

Although there has been steady progress in many regions (Europe, Asia, Western Pacific), there has been minimal recent progress in Africa [7].

European countries lacking specific iodine prophylaxis programs are also mildly iodine deficient [14]. The prevalence of iodine deficiency in Europe was reduced by 30 percent from 2003 to 2010, but 44 percent of school-age children still have insufficient iodine intake [15]. In a 2009 survey of schoolgirls aged 14 to 15 years living in the United Kingdom, which has long been considered iodine sufficient, median urinary iodine excretion was 80.1 mcg/L, consistent with mild iodine deficiency [16]. In Italy, urinary iodine excretion was randomly measured in 26,913 individuals, as part of a project to eradicate iodine deficiency disorders [17]. Urinary iodine was lower than 100 and 50 mcg/L in 64.3 and 34.9 percent of samples, respectively. Median urinary iodine in non-urban areas was significantly lower than in urban areas (69 versus 79 mcg/L). There were no differences in urinary iodine excretion among children residing in lowland, coastal mountainous hilly, and mountainous hilly areas.

Only a few countries appear to have sustainable iodine sufficiency at the present time: the United States, Canada, Norway, Sweden, Finland, Switzerland, Austria, Bhutan, Peru, Panama, Macedonia, and Japan.

Iodine intake in the United States has decreased slightly since 2007, with a median urinary iodine excretion of 144 mcg/L (1.1 µmol/L) [18]. Among women of reproductive age, the median urinary iodine excretion was 129 mcg/L, with 37 percent of women having levels <100 mcg/L (consistent with mild iodine deficiency). Iodine nutrition in the United States is mainly achieved by silent iodine prophylaxis, a natural increase in iodine intake because of higher consumption of iodine-rich products (eg, industrially prepared dairy products) associated with socioeconomic development [7]. The decline in iodine intake over the last decade may be related to a reduction in the iodine content of dairy products, removal of iodate dough conditioners in commercially produced bread, and increasing use of noniodized salt by the food industry [7].

CONSEQUENCES OF IODINE DEFICIENCY

Diffuse and nodular goiter — Goiter is the most obvious manifestation of iodine deficiency. Low iodine intake leads to reduced thyroxine (T4) and triiodothyronine (T3) production, which results in increased thyroid-stimulating hormone (TSH) secretion in an attempt to restore T4 and T3 production to normal. TSH also stimulates thyroid growth; thus, goiter occurs as part of the compensatory response to iodine deficiency.

The goiter is initially diffuse but eventually becomes nodular because the cells in some thyroid follicles proliferate more than others. Therefore, in regions of iodine deficiency, children and adolescents generally have diffuse goiters, while adults who lived in conditions of longstanding iodine deficiency have nodular goiter. Iodine deficiency favoring thyroid follicular cell replication also increases the chance of mutations in the TSH receptor gene that may lead to constitutive activation of the receptor and TSH-independent growth and function [19,20]. (See 'Hyperthyroidism' below.)

Goiter has traditionally been assessed by palpation, particularly in field studies. In the last decade, ultrasonography, which allows precise estimation of thyroid volume, has become the preferred method of assessment. In regions of iodine deficiency, the median thyroid volume at any age is considerably larger than that in regions of iodine sufficiency. For people living in iodine-sufficient regions, thyroid volume measurements standardized for age, sex, and body size are now available [21]. The volume in subjects living in the United States is smaller than that in Europe, many regions of which have a lower iodine intake than in the United States.

For many individuals, iodine-deficiency goiter is only a cosmetic problem. In some, however, particularly older adults, the goiter may be large enough to cause compression of the trachea or esophagus or delay recognition of coexisting thyroid cancer. (See "Clinical presentation and evaluation of goiter in adults", section on 'Obstructive symptoms'.)

Hyperthyroidism — Iodine deficiency increases the incidence of diffuse and nodular goiter. Over time, autonomous growth and function may ensue, resulting in toxic goiter and hyperthyroidism if iodine deficiency is not extremely severe. In regions of mild to moderate iodine deficiency, toxic multinodular goiter is a common cause of hyperthyroidism in older adults [22,23]. Hyperthyroidism is more likely to develop if iodine intake is supplemented, just as it can occur in patients with nontoxic nodular goiters living in iodine-replete regions who are given large doses of iodine. (See 'Adverse effects' below and "Iodine-induced thyroid dysfunction", section on 'Iodine-induced hyperthyroidism'.)

Hypothyroidism — Hypothyroidism due to very low iodine intake is now extremely rare. Adults have the typical clinical manifestations of hypothyroidism and usually a goiter. (See "Clinical manifestations of hypothyroidism".)

Severe iodine deficiency during pregnancy — Optimal iodine nutrition in the pregnant woman is required for full development of the fetus [8]. For the developing fetus or infant, untreated maternal hypothyroidism due to severe iodine deficiency is a catastrophe because thyroid hormone is essential for normal maturation of the central nervous system, particularly its myelination. For the first 12 weeks of gestation, the fetus is completely dependent upon maternal T4. During the 10th to 12th week of gestation, fetal TSH appears and the fetal thyroid is capable of concentrating iodine and synthesizing iodothyronines. However, little hormone synthesis occurs until the 18th to 20th week. Thereafter, fetal thyroid secretion increases gradually. (See "Overview of thyroid disease in pregnancy", section on 'Thyroid function in the fetus'.)

Hypothyroidism during these critical periods of development leads to permanent intellectual disability which, in its most severe form, is known as cretinism. (See "Clinical features and detection of congenital hypothyroidism".)

Cretinism — In addition to intellectual disability, cretinism is accompanied by other neurologic and somatic defects. This has led to cretinism being subdivided into neurologic and myxedematous types:

Neurologic cretinism is characterized by intellectual disability, deaf mutism, gait disturbances, and spasticity, but not hypothyroidism. It is thought to result from hypothyroidism in the mother during early pregnancy but a euthyroid state postnatally.

Myxedematous cretinism is characterized by intellectual disability, short stature, and hypothyroidism. It is thought to result from iodine deficiency and thyroid injury predominantly late in pregnancy and continuing after birth.

These two syndromes overlap considerably [24], and attributing them to specific developmental periods is undoubtedly overly simplistic. Both can be prevented by adequate maternal and infant iodine intake.

Neonatal and infant mortality — Severe iodine deficiency increases neonatal and infant mortality, an effect that can be reduced by up to 50 percent with correction of severe iodine deficiency [25]. The mechanism of this benefit is not known, but multiple factors are probably involved. Hypothyroid or intellectually disabled infants may suffer more birth trauma and be more prone to infectious diseases and nutritional deficiencies typical of the poor rural communities in which iodine deficiency is so prominent.

Mild to moderate iodine deficiency during pregnancy — The potential adverse effects of mild to moderate iodine deficiency during pregnancy are uncertain. Developmental studies in iodine-deficient regions have many limitations, including an inability to distinguish between the persistent effects of fetal iodine deficiency and the ongoing effects of iodine deficiency in childhood and adolescence.

Subclinical neurologic defects — Minor neuropsychological defects have been described in children born to mothers exposed to mild to moderate iodine deficiency during pregnancy [26-31]. These defects may be detected by appropriate neuropsychological tests.

As examples:

In a study from the United Kingdom, children born to mothers with urinary iodine to creatinine concentrations during pregnancy of less than 150 mcg/g compared with ≥150 mcg/g had lower scores for verbal intelligence quotient (IQ), reading accuracy, and reading comprehension at age eight years [28].

In Australia, children born to mothers with urinary iodine concentrations during pregnancy of <150 mcg/L compared with ≥150 mcg/L had reductions in spelling, grammar, and English-literacy standardized test scores at age nine years [29]. The children grew up in a region considered to be iodine replete (median urinary iodine concentration 108 mcg/L), and therefore the results reflect the effects of fetal rather than childhood iodine insufficiency.

An increased auditory threshold may be another clinical manifestation of iodine deficiency [32]. As an example, in a study of 150 school-age children in Spain, 38 percent had a goiter [33]. In children with goiter and mild to moderate iodine deficiency, there was an inverse relationship between auditory threshold and urinary iodine excretion (ie, the more iodine deficient, the higher the auditory threshold). (See "Hearing impairment in children: Evaluation".)

IMPACT OF IODINE SUPPLEMENTATION

During pregnancy

Severe iodine deficiency – In a randomized trial and several population-based studies of women living in severely iodine-deficient regions, iodine supplementation to women prior to conception or during early pregnancy was associated with substantially better neurologic and developmental outcomes in children [25,34-36].

Mild to moderate iodine deficiency – The results of randomized trials of iodine supplementation in pregnant women with mild to moderate iodine deficiency have reported mixed results [37]. In some [38-40] but not all [41,42] trials, iodine supplementation resulted in smaller thyroid volumes and lower thyroglobulin concentrations in mothers and/or newborns compared with controls. However, there was no effect on maternal or neonatal thyroxine (T4) concentrations in the majority of the trials. In addition, there are no randomized trial data on child development or other long-term outcomes.

In observational studies of women with mild to moderate iodine deficiency and mild hypothyroxinemia, neurodevelopmental outcomes were better in children whose mothers received iodine supplementation (200 to 300 mcg potassium iodide daily) early in pregnancy (prior to the 10th week of gestation) compared with children whose mothers did not [43,44]. The better outcomes noted in the observational studies may be related to improvement in maternal hypothyroxinemia.

However, in a subsequent study, neuro-intellectual outcomes appeared to be more related to maternal nutritional iodine status than to T4 levels throughout pregnancy [31]. In this study, children born to mothers using iodized salt or iodized salt plus T4 (levothyroxine) performed similarly on neuro-intellectual testing at 6 to 12 years of age and better than children born to women not using iodized salt (with our without T4).

During early childhood — Once present, intellectual disability resulting from the effects of iodine deficiency on the central nervous system during fetal development is not reversible. In contrast, the additional impairment caused by continuing postnatal hypothyroidism and/or iodine deficiency may improve with appropriate thyroid hormone replacement and/or iodine supplementation [45]. In a trial of iodine supplementation or placebo in 310 children in Albania, iodine supplementation significantly improved thyroid function (prevalence of hypothyroxinemia was reduced from approximately 30 to <1 percent) and performance on cognitive testing [46].

ASSESSMENT OF IODINE NUTRITION — Iodine nutrition at the community level is best assessed by measurements of:

Urinary iodine

Thyroid size

Neonatal serum thyroid-stimulating hormone (TSH)

Serum thyroglobulin

In practice, urinary iodine is most often used to determine iodine nutrition at the population level. The urinary iodine concentration indicates current iodine nutrition, while thyroid size and the serum thyroglobulin concentration reflect iodine nutrition over a period of months or years.

Urinary iodine excretion — Approximately 90 percent or more of ingested iodine eventually appears in the urine. For assessing the iodine nutritional status of a population, measurements of urinary iodine concentration in randomly collected urine samples have proven to be as useful as measurements of urinary creatinine and iodine and calculation of the iodine:creatinine ratio [47,48]. The results from random samples also correlate well with 24-hour urine collections. As a result, iodine nutrition is often defined by the urinary iodine concentration in randomly collected urine samples. Mild iodine deficiency is defined as a median urinary iodine concentration of 50 to 99 mcg/L, moderate deficiency as 20 to 49 mcg/L, and severe deficiency as <20 mcg/L (table 1) [6].

Thyroid size — Thyroid size is a sensitive marker for iodine deficiency because goiter, although not the most severe consequence of iodine deficiency, is the most clinically evident. Assessment by palpation is too crude to be anything more than qualitative except in severe deficiency, but ultrasonography is precise, quantifiable, and easily performed.

Neonatal serum TSH screening for hypothyroidism — In regions of iodine deficiency, the frequency of supranormal TSH concentrations (>5 mU/L) in blood spots collected as part of neonatal screening programs is higher than in iodine-sufficient areas and roughly correlates with the severity of iodine deficiency [49]. Transient neonatal hypothyroidism is also more frequent. For this reason, the World Health Organization (WHO) has established that the results of neonatal blood TSH screening can be used as convenient indicators for iodine intake. (See "Clinical features and detection of congenital hypothyroidism", section on 'Newborn screening' and "Clinical features and detection of congenital hypothyroidism", section on 'Further evaluation and diagnosis'.)

Serum thyroglobulin concentration — The serum thyroglobulin concentration is a sensitive measure of thyroid activity and hyperplasia. In iodine-deficient infants and children, serum thyroglobulin concentrations are high more often than are serum TSH concentrations. Although a nonspecific test, since any type of thyroid stimulation or injury raises the serum thyroglobulin concentration, the values correlate well with the severity of iodine deficiency. Thyroglobulin has also been shown to be a sensitive measure of excess iodine intake in school-age children [50]. In one study, the serum thyroglobulin level was better than thyroid volume measurement by ultrasound as an indicator of iodine nutrition [51] However, measurement of thyroglobulin requires blood sampling, which is not easily performed in routine surveys.

Other tests — Thyroid radioiodine uptake is increased in iodine deficiency because of both thyroid stimulation and the low iodine pool size, but it is not a practical field test. Serum thyroxine (T4), triiodothyronine (T3), and TSH concentrations are within their respective normal ranges in most children and adults with iodine deficiency; thus, these tests are not sufficiently sensitive for diagnosis of the disorder.

PROPHYLAXIS AND TREATMENT

Community — Iodine deficiency is a global public health problem and, in combating it, emphasis should be placed on diagnosis and correction at the level of the community rather than the individual. Achieving sufficient iodine nutrition in the population would eliminate the need for specific supplementation during pregnancy and lactation. (See 'During pregnancy and lactation' below.)

Iodization of salt — Iodization of salt is the preferred method of increasing iodine intake in a community. Salt iodination is legally mandated in many countries. Salt is a dietary necessity and often the only one that communities cannot provide for themselves. Adding iodine during the packaging or processing of salt is an efficient means for distributing iodine on a mass basis. It is technically easy (and can even be done manually) and the cost is low, although the accompanying changes in salt processing may increase the price to the consumer. The usual “dose” is between 10 and 50 mg of iodine/kg salt (sodium chloride) as potassium iodide or iodate.

The optimal amount to be added for a particular country or region can be calculated from the daily per capita salt consumption, the amount of iodine consumed from other sources, and any losses of iodine between production and consumption. Potassium iodide is added in the United States, Canada, and many countries in Western Europe. However, in hot tropical climates or suboptimal conditions of purity or storage, potassium iodate is preferred over potassium iodide because it is more stable. In Finland, iodization of animal feed resulted in a five- to sevenfold increase in the average individual's iodine intake [52].

The success of salt iodization programs relates to sources of salt within a country. Some countries, such as Congo, Nigeria, and Zimbabwe, import all their salt, making control of iodization fairly simple. In other countries with numerous scattered salt deposits and a complex distribution system, implementation of salt iodization has been more difficult. A determined international effort towards eliminating iodine deficiency by the year 2005 has resulted in major progress, with about 70 percent of households worldwide using adequately iodized salt. In Denmark, the use of iodized salt resulted in a 6 and 14 percent reduction in thyroid gland volume in patients from areas of mild or moderate iodine deficiency, respectively [53].

Other options — Alternatives are needed when salt iodization is impractical or delayed. Effective options are iodized oil (Lipiodol), iodized water, and iodine tablets or drops. Water is an occasional iodization vehicle because it is a daily necessity like salt. The technology can be as simple as adding a few drops of iodine to standing drinking water. Addition of molecular iodine (but not iodide or iodate) carries the additional benefit of sterilizing the water.

In addition, alternative methods of food iodine enrichment are currently under study. Hydroponic experiments were carried out to investigate the possibility of enriching the iodine uptake by spinach [54] or other vegetables such as tomatoes and potatoes. In one study, biofortification of vegetables with iodine increased urinary iodine concentration and, together with the habitual use of iodized salt, improved the iodine nutritional status of the study participants [55].

Individual — Correction of iodine deficiency at the level of the community rather than the individual is preferred. Methods of iodide administration for the individual include oral administration of potassium iodide solution every two to four weeks and daily administration of tablets containing from 100 to 300 mcg potassium iodide. The latter is particularly recommended to meet the increased needs for iodine during pregnancy and lactation, and it can be routinely incorporated into prenatal vitamin/mineral preparations. (See 'During pregnancy and lactation' below.)

Lipiodol, developed as a radiographic contrast agent, contains 480 mg iodine/mL. A single oral dose of 0.5 to 1.0 mL provides an adequate amount of iodine for six months to one year; intramuscular administration of the same dose provides an adequate amount for two to three years [56]. Iodized oil is more expensive than salt iodization and requires direct administration to each person. If given intramuscularly, it requires skilled administration and has a risk of infection if improper technique is used. Its main advantage is that it can be implemented promptly. It has been especially valuable for women of childbearing age and children in regions of severe iodine deficiency, such as Africa.

Nonpregnant — For the general nonpregnant, nonlactating population in the United States and other iodine-sufficient countries (figure 1), iodine supplementation above what is obtained from iodine fortified foods (eg, iodized salt) is not necessary.

During pregnancy and lactation — Consuming an adequate amount of iodine during pregnancy is important for fetal development. In the United States and other iodine-sufficient countries, women who do not consume dairy products or iodized salt may have lower urinary iodine concentrations and require iodine supplementation [57,58].

The World Health Organization (WHO) recommends iodine supplementation in pregnancy and lactation in regions where <90 percent of households use iodized salt (Iodine Global Network) and the median urinary iodine concentration in children is <100 mcg/L [3,59]. In pregnant women, urinary iodine concentrations of 150 to 249 mcg/L indicate adequate iodine intake.

Iodine dosing guidelines are as follows:

WHO [3]:

250 mcg daily during pregnancy and lactation

United States Institute of Medicine (IOM) [4]:

220 mcg daily for pregnant women

290 mcg daily for lactating women

American Thyroid Association (ATA) [9]:

150 mcg potassium iodide daily for pregnant and lactating women in the United States and Canada. This is the dose included in the majority of prenatal vitamins marketed in the United States.

Smoking reduces iodine in breast milk [60,61]. In Denmark, mothers who smoke have reduced iodine in their breast milk (26 versus 54 mcg/L in nonsmokers despite identical urine iodine concentrations), and their infants have reduced urinary iodine concentrations (33 versus 40 mcg/L in nonsmokers) [60]. Smoking cessation efforts are important in this population.

Sustaining iodine sufficiency — Regular monitoring of iodine nutrition is essential for sustaining iodine sufficiency [62]. Iodine deficiency has recurred in some countries with initially successful programs after a regular follow-up program was abandoned. Potential contributing factors include a decrease in salt intake, a reduction in the use of iodine salts in the baking industry, and undoubtedly other unidentified commercial and environmental factors. In some countries that have mandatory programs of salt iodization, inadequate quality control has caused major fluctuations in dietary iodine intake.

Adverse effects — Iodine repletion in the doses used for iodization of salt and in prenatal supplements has few adverse effects. Iodine administration may result in hyperthyroidism in patients with endemic goiter or in patients with nodular goiters containing autonomously functioning tissue. In contrast, iodine administration may induce or exacerbate hypothyroidism in patients with underlying autoimmune thyroiditis [63]. In regions of iodine deficiency, both hyperthyroidism and hypothyroidism have been reported after the introduction of iodine [64,65]. However, the benefits of correcting iodine deficiency outweigh the risks of iodization of salt. Iodine-induced thyroid dysfunction is reviewed in more separately. (See "Iodine-induced thyroid dysfunction", section on 'Iodine-induced hyperthyroidism' and "Iodine-induced thyroid dysfunction", section on 'Iodide-induced hypothyroidism'.)

Excessive iodine ingestion during pregnancy may also have adverse effects on fetal thyroid function. Sudden exposure to excess serum iodide inhibits organification of iodide, thereby diminishing hormone biosynthesis; this phenomenon is called the Wolff-Chaikoff effect. The fetal thyroid gland is particularly susceptible to the inhibitory effects of excess iodine during the third trimester, which can result in a prolonged inhibition of thyroid hormone synthesis, an increase in thyroid-stimulating hormone (TSH), and fetal goiter.

The tolerable upper intake amount for iodine, as established by European and United States expert committees, ranges from 600 to 1100 mcg daily for adults and pregnant women >19 years age [4,66]. For adolescents 15 to 17 years, it ranges from 500 to 900 mcg daily and for younger children, 200 to 450 mcg/day.

SUMMARY AND RECOMMENDATIONS

Iodide is essential for thyroid hormone synthesis. Iodine can be obtained by consumption of foods that naturally contain it (fish, seafood, kelp, dairy products, some drinking water, and vegetables grown in iodine-sufficient soil) or to which it is added (table salt). (See 'Iodine requirements' above.)

The World Health Organization (WHO) recommends 90 mcg of iodine daily for infants and children up to five years, 120 mcg for children 6 to 12 years, 150 mcg daily for children ≥12 years and adults, and 250 mcg daily during pregnancy and lactation. (See 'Iodine requirements' above.)

A system for classifying iodine deficiency and sufficiency has been developed based upon the median urinary iodine concentration in a population (table 1). Pregnant women need special attention because their renal threshold for iodine is lower, the needs of the fetus are greater, and dietary salt (including iodized salt) is often restricted. In pregnant women, urinary iodine concentrations of 150 to 249 mcg/L are considered adequate. (See 'Classification of iodine status' above.)

Iodine deficiency is associated with diffuse and nodular goiter. Hyperthyroidism may occur due to autonomy (toxic multinodular goiter). Hypothyroidism due to very low iodine intake is rare. (See 'Consequences of iodine deficiency' above.)

Severe iodine deficiency during pregnancy may be associated with cretinism and increased neonatal and infant mortality. (See 'Severe iodine deficiency during pregnancy' above.)

Iodine supplementation to severely iodine-deficient women prior to conception or during early pregnancy is associated with substantially better neurologic and developmental outcomes in children. There are few data evaluating the effects of iodine supplementation on child development or other long-term outcomes in pregnant women with mild to moderate iodine deficiency. (See 'Impact of iodine supplementation' above.)

Iodine nutrition at the community level can be assessed by measurements of urinary iodine, thyroid size, thyroglobulin, and neonatal serum thyroid-stimulating hormone (TSH). In practice, urinary iodine is most often used to determine iodine nutrition. The urinary iodine concentration indicates current iodine nutrition, while thyroid size and the serum thyroglobulin concentration reflect iodine nutrition over a period of months or years. (See 'Assessment of iodine nutrition' above.)

Iodine deficiency is a global public health problem and, in combating it, emphasis should be placed on diagnosis and correction at the level of the community rather than the individual. Iodization of salt is the preferred method of increasing iodine intake in a community. The usual amount is between 10 and 50 mg of iodine/kg salt (sodium chloride) as potassium iodide or iodate. Alternatives for when salt iodization is impractical or delayed include iodized oil (Lipiodol), iodized water, and iodine tablets or drops. (See 'Prophylaxis and treatment' above.)

Consuming an adequate amount of iodine during pregnancy is important for fetal development. The WHO and the Iodine Global Network recommend 250 mcg of iodine daily during pregnancy and lactation, whereas the Institute of Medicine (IOM) recommends 220 mcg during pregnancy and 290 mcg during lactation. The American Thyroid Association (ATA) recommends 150 mcg of iodine (in the form of potassium iodide) daily during pregnancy and lactation. This is the dose included in the majority of prenatal vitamins marketed in the United States. (See 'During pregnancy and lactation' above.)

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