Iodine Deficiency


Practice Essentials

Severe iodine deficiency results in impaired thyroid hormone synthesis and/or thyroid enlargement (goiter). Population effects of severe iodine deficiency, termed iodine deficiency disorders (IDDs), include endemic goiter, hypothyroidism, cretinism, decreased fertility rate, increased infant mortality, and mental retardation.[1]

Iodine is a chemical element. It is found in trace amounts in the human body, in which its only known function is in the synthesis of thyroid hormones. Iodine is obtained primarily through the diet but is also a component of some medications, such as radiology contrast agents, iodophor cleansers, and amiodarone.

Worldwide, the soil in large geographic areas is deficient in iodine. Twenty-nine percent of the world’s population, living in approximately 130 countries, is estimated to live in areas of deficiency (see image below).[2]  This occurs primarily in mountainous regions such as the Himalayas, the European Alps, and the Andes, where iodine has been washed away by glaciation and flooding. Iodine deficiency also occurs in lowland regions far from the oceans, such as central Africa and Eastern Europe. Persons who consume only locally produced foods in these areas are at risk for IDD. See the distribution of iodine deficiency in the image below.[2, 3, 4]

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Distribution of iodine deficiency in developing countries.

In 2001, the World Health Organization (WHO), United Nations Children's Fund (UNICEF) and International Council for Control of Iodine Deficiency Disorders (ICCIDD) developed a system for classifying iodine deficiency based upon the median urinary iodine concentration in a population (See Table 1. below).[3]

Table 1. Iodine Deficiency Classification

View Table

See Table

Normal dietary iodine intake is 100-150 mcg/day. The US Institute of Medicine’s (IOM’s) recommended dietary allowance (RDA) of iodine is as follows:

WHO’s recommendations are similar for adults and adolescents but vary for infants, children, and pregnant and lactating women as follows[3] :

Sources of dietary iodine

In areas where iodine is not added to the water supply or food products meant for humans or domesticated animals, the primary sources of dietary iodine are saltwater fish, seaweed, and trace amounts in grains. The upper limit of safe daily iodine intake is 1100 mcg/day for adults; it is lower for children.[5, 6, 7, 8]

In the United States, iodine has been voluntarily supplemented in table salt (70 mcg/g). Salt was selected as the medium for iodine supplementation because intake is uniform across all socioeconomic strata and across seasons of the year, supplementation is achieved using simple technology, and the program is inexpensive. The estimated annual cost of iodine supplementation of salt in the United States is $0.04 per person.

Other major sources of dietary iodine in the United States are egg yolks, milk, and milk products because of iodine supplementation in chicken feed, the treatment of milk cows and cattle with supplemental dietary iodine to prevent hoof rot and increase fertility, and the use of iodophor cleaners by the dairy industry.[9]

Changes in US iodine intake

In the early 1900s, the Great Lakes, Appalachian, and northwestern regions of the United States were endemic regions for IDD, but since the iodization of salt and other foods in the 1920s, dietary iodine levels generally have been adequate. However, sustaining these iodization programs has become a concern.

Data collected in the United States by National Health and Nutrition Examination Survey I (NHANES I) for the years 1971-1974 showed that the median urinary iodine level was 320 mcg/L, reflecting adequate dietary iodine intake.[10]  However, by the time of NHANES III (1988-1994), the median urinary iodine value had fallen to 145 mcg/L.

The reduction in US dietary iodine intake since the 1970s has likely been the result of the removal of iodate conditioners in store-bought breads, widely publicized recommendations for reduced salt and egg intake for blood pressure and cholesterol control, the increasing use of noniodized salt in manufactured or premade convenience foods, decreased iodine supplementation of cattle feed, poor education about the medical necessity of using iodized salt, and reduction in the number of meals made at home.[10, 11, 12]

The NHANES surveys of 2001-2002, 2005-2006, and 2007-2008 showed that US dietary iodine intake has stabilized.[11, 12]  Although the most recent NHANES survey reveals adequate iodine intake in the general US population, certain groups have an insufficient intake of iodine, such as pregnant women, who were found to have a median urinary iodine concentration of 125 mcg/L.[13]

Population-based assessment and treatment

In population-based assessments, iodine sufficiency can be determined based on the results of a spot urine test for iodine and creatinine.[11] Supplementation can be achieved by using iodized salt in cooking or a once-daily multiple vitamin containing sodium iodide.[5, 14]

Pediatric considerations

Iodine stores within the thyroid increase with age in pediatric patients. Therefore, infants and young children tend to have higher 131I uptake than adults. Additionally, newborns and young infants are much more severely affected by iodine deficiency than adults and are more likely to become overtly hypothyroid.

Prenatal considerations

Women with severe iodine deficiency are more likely to experience infertility, and pregnancy in this group is more likely to result in miscarriage or congenital anomalies. Thyroid hormones are essential for fetal brain growth and development, and severe maternal iodine deficiency may lead to mental and growth retardation or cretinism in offspring, and even mild maternal iodine deficiency has been associated with lower IQ in children.[15]  Even in areas of borderline iodine intake, as many as 10% of women may develop goiter during pregnancy.


Dietary iodine is taken up readily through the gut in the form of iodide. From the circulation, it is concentrated in the thyroid gland by means of an energy-dependent sodium-iodide symporter. In the follicle cells of the thyroid gland, 4 atoms of iodine are incorporated into each molecule of thyroxine (T4) and 3 atoms into each molecule of triiodothyronine (T3). These hormones are essential for neuronal development, sexual development, and growth and for regulating the metabolic rate, body heat, and energy.

When dietary iodine intake is inadequate for thyroid hormone synthesis, the serum T4 level initially falls and a number of processes ensue to restore adequate thyroid hormone production. The pituitary gland senses low levels of circulating T4 and releases more thyroid-stimulating hormone (TSH). TSH stimulates the growth and metabolic activity of thyroid follicular cells. TSH stimulates each cell to increase iodine uptake and thyroid hormone synthesis and secretion. Increased TSH levels and reduction of iodine stores within the thyroid result in increased T3 production relative to T4 production. T3 is 20-100 times more biologically active than T4 and requires fewer atoms of iodine for biosynthesis. The increased production of T3 results in the maintenance of normal levels of thyroid hormone bioactivity despite the reduction in Tbecause of iodine deficiency.

These processes tend to conserve iodine stores and help maintain normal thyroid function. In addition, thyroid hormones are deiodinated in the liver, and the iodine is released back into the circulation for reuptake and reuse by the thyroid gland. Even under these circumstances, iodine is passively lost in the urine, with additional small (10%) losses from biliary secretion into the gut.

Goiter development and hyperthyroidism

Enlargement of the thyroid gland begins as an adaptive process to low iodine intake. Iodine deficiency is the most common cause of goiter in the world. The goiter initially is diffuse, but it eventually becomes nodular. Some nodules may become autonomous and secrete thyroid hormone regardless of the TSH level. These autonomous nodules have been demonstrated to frequently contain TSH-activating mutations. Initially, thyroid hormone output by the normal thyroid surrounding the autonomous nodules is reduced to maintain euthyroidism. Autonomous nodules may cause hyperthyroidism.

High levels of iodine, such as those found in radiographic contrast dyes or amiodarone, may cause hyperthyroidism in the setting of nodular goiter with “hot” or autonomous nodules or hypothyroidism in the setting of autoimmune thyroid disease. If the total output of thyroid hormone by the autonomous nodules exceeds that of the normal thyroid gland, the patient becomes biochemically hyperthyroid. This condition is known as a toxic multinodular goiter.[16]


When iodine deficiency is more severe, thyroid hormone production falls and the patient may experience a hypothyroid condition. In such cases, adults have the usual signs and symptoms of hypothyroidism. However, congenital hypothyroidism (also known as cretinism) in fetuses and young children prevents central nervous system development and maturation, resulting in permanent mental retardation, neurologic defects, and growth abnormalities.[5, 17]


Occurrence in the United States

Early in the 20th century, the Great Lakes, Appalachian, and northwestern regions of the United States were endemic for iodine deficiency disorders, but since the iodization of salt and other foods in the 1920s, dietary iodine levels generally have been adequate. National survey data suggest that average US dietary iodine intake fell dramatically from 1971-1990 and then stabilized. Urinary iodine values of less than 50 mcg/L, moderate iodine deficiency, are found in 11.1% of the total population, 7.3% of pregnant women, and 16.8% of reproductive-aged women.[10, 11]

International occurrence

Approximately 70% of all households worldwide currently have access to adequately iodized salt.[2] In 2016, the Iodine GlobalNetwork reported that 110 countries had sufficient iodine intake,18 were mildly deficient, and 2 were moderately dificient. No countries were found to be severely iodine-deficient, and 10 countries had excessive iodine intake.[4]  

Race-, sex-, and age-related demographics

No race predilection exists for iodine deficiency disorder; prevalence is affected only by geographic area and diet. However, non-Hispanic black pregnant women from both the NHANES 2005–2010 and the National Children's Study (NCS) consistently had lower uriinary iodine than non-Hispanic whites or Hispanics.[13]

Patients of any age can be affected by iodine deficiency. The most devastating complications of iodine deficiency disorder occur when iodine is deficient during fetal and neonatal growth. After age 10 years, the prevalence of goiter is higher in girls than boys in areas of iodine deficiency. No sex-based difference is observed in the incidence of cretinism.


The supplementation of iodine does not reverse cretinism or reduce the size of large nodular goiters. Small, diffuse goiters of short duration that occur in infants or during pregnancy appear to be managed effectively with iodine supplementation.

Iodine deficiency can recur if iodine supplementation programs lapse.[18] Recurrence of goiter and new cases of cretinism have been noted in some nations where this has occurred. These changes are manifested prominently in school-aged children, who are particularly sensitive to variations in iodine intake. Thyroid volume, prevalence of goiter, and urinary iodine levels may return to pre-iodine supplementation levels 1-2 years following the discontinuation of iodine supplementation.


Mild to moderate IDD can cause thyroid function abnormalities and endemic goiter. Women with severe iodine deficiency are more likely to experience infertility, and pregnancy in this group is more likely to result in miscarriage or congenital anomalies. Thyroid hormones are essential for fetal brain growth and development, and severe maternal iodine deficiency may lead to mental and growth retardation or cretinism in offspring, and even mild maternal iodine deficiency has been associated with lower IQ in children.[15]  One ystematic review of the impact of iodine supplementation in populations with mild-to-moderate iodine deficiency found improvement in some maternal thyroid indices and modest benefits on cognitive function in school-age children, even in marginally iodine-deficient areas.[19]  

Whether iodine deficiency causes an increased risk for thyroid cancer is unclear, but a higher proportion of more aggressive thyroid cancers (ie, follicular thyroid carcinoma) and an increased thyroid cancer mortality rate are found in areas where iodine deficiency is endemic.

Patient Education

The public must understand the importance of using iodized salt, especially in the United States, where iodization of salt is not mandated by law. Several areas of the world, including the United States, Australia, and the Netherlands, where iodine deficiency was eradicated by voluntary methods, have later shown a significant decrease in iodine intake.

For patient education information, see the Thyroid and Metabolism Center and the Pregnancy Center, as well as Thyroid Problems and Miscarriage.

History and Physical Examination

Patients with iodine deficiency tend to come from geographic regions where iodine deficiency disorders (IDDs) are endemic. The first sign of iodine deficiency is diffuse thyroid enlargement, which becomes multinodular over time. In patients with hypothyroidism due to severe iodine deficiency, one might see signs such as dry skin, periorbital edema, and delayed relaxation phase of the deep tendon reflexes.


Patients with IDD most commonly present with goiter. Typical endemic goiters are shown in the image below. Children present with diffuse goiters, while adults present with nodular goiters. If a goiter is large enough, patients may complain of compressive symptoms, such as hoarseness, shortness of breath, cough, or dysphagia.

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Typical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.

Hypothyroidism and cretinism

Individuals with severe iodine deficiency may also have hypothyroidism and may complain of fatigue, weight gain, cold intolerance, dry skin, constipation, or depression.

Cretinism is the most extreme manifestation of IDD. Cretinism can be divided into neurologic and myxedematous subtypes. These subtypes have considerable clinical overlap. Both conditions can be prevented by adequate maternal and childhood iodine intake. Neurologic cretinism is thought to be caused by severe IDD with hypothyroidism in the mother during pregnancy and is characterized by mental retardation, abnormal gait, and deaf-mutism, but not by goiter or hypothyroidism in the child.

Myxedematous cretinism is considered to result from iodine deficiency and hypothyroidism in the fetus during late pregnancy or in the neonatal period, resulting in mental retardation, short stature, goiter, and hypothyroidism.

View Image

A man and 3 females (age range, 17-20 y) with myxedematous cretinism from the Republic of the Congo in Africa, a region with severe iodine deficiency.....

Mental retardation

Worldwide, iodine deficiency is the leading cause of preventable mental retardation. This became a renewed concern as the prevalence of moderate iodine deficiency in the United States among women of childbearing age increased from 4% in the 1970s to 15% by the 1990s. Although children of mothers from iodine-deficient regions may have normal thyroid function test results, they are noted to have lower language and memory performance.

Reduction in IQ has been noted in affected youth from regions of severe and mild iodine deficiency. Mental retardation as a result of iodine deficiency can be exaggerated in the setting of concomitant deficiencies of selenium or vitamin A.[20]

Postnatally, as infants and children are particularly sensitive to fluctuations in iodine intake, this population is at risk for poor mental and psychomotor development (predominantly in language and memory skills). Unlike mental retardation that occurs because of prenatal iodine deficiency, mental retardation from continued postnatal iodine deprivation may be reversible with thyroid hormone replacement.

Approach Considerations

There has been particular interest in monitoring iodine sufficiency in pregnant women and school-aged children. These populations are important, because they are easily accessible and are particularly vulnerable to the adverse effects caused by iodine deficiency.

Surveillance techniques to monitor iodine sufficiency in a population include assessment of thyroid volume, urinary iodine concentration, dried whole-blood spot thyroglobulin (Tg) levels, and dietary questionnaires; the last method is the least reliable. No test can reliably diagnose iodine deficiency in individual patients.

Laboratory Studies

Urinary iodine concentration

The kidneys excrete approximately 90% of ingested iodine. When evaluated at a population level, urinary iodine concentration (UIC) from spot samples has been shown to be a reliable biomarker of recent iodine intake for the population as a whole. Therefore, the best diagnostic test to identify IDD in a population is a median 24-hour iodine urine collection. If a 24-hour urine collection is not practical, a random urinary iodine-to-creatinine ratio can be used instead. In this case, a median of 50-100 mcg of iodine per liter is consistent with mild iodine deficiency, 20-49 mcg of iodine per liter is consistent with moderate deficiency, and less than 20 mcg of iodine per liter is consistent with severe deficiency.

UIC is not a reliable measure for assessing the iodine status of an individual because of very high variation in daily dietary iodine intake. It has been estimated that 10 UIC measurements from spot samples or 24-hour collections are required to establish an individual’s iodine status with 20% accuracy.[21]

Thyroid function testing

Although urinary iodine concentration is a sensitive indicator of recent iodine intake, laboratory tests that detect abnormal thyroid function may be more useful for diagnosing chronic iodine deficiency or excessive iodine intake and for monitoring the effects of iodine supplementation.[22] Thyroid function testing include measurement of serum concentrations of the following:

Results from thyroid function studies are usually within the reference range in the presence of mild iodine insufficiency. However, in patients with euthyroidism and iodine deficiency, serum TSH levels may be normal to increased, T3 levels may be normal or slightly elevated, and T4 levels may be normal or decreased. Only in very extreme iodine deficiency does hypothyroidism develop, accompanied by an elevated serum TSH value and decreased T3 and T4 levels.

Population studies have shown that newborns with iodine deficiency disorder (IDD) have elevated TSH levels at birth that normalize when evaluated again several weeks later. The extent of their transient hypothyroidism correlates with the severity of the iodine deficiency.

Serum Tg concentrations are positively correlated with thyroid volume in iodine-deficient regions, and mean thyroglobulin concentrations are typically elevated in regions of both iodine deficiency and excess. Tg concentrations change more rapidly than goiter rates and thus may be a better tool for gauging responses to increased iodine intake.[21]  

Measurement of a dried whole-blood spot level of Tg can be a useful indicator of the thyroid function in children and may be a more sensitive early measure of iodine repletion than serum TSH or thyroxine (T4).[23]  International reference standards have been established for serum thyroglobulin values in school-aged children.[24]  Current limitations to the use of dried blood spot Tg measurements include assay complexity and the unknown utility of measuring antithyroglobulin antibody levels in children.[25]


Imaging Studies

The 24-hour radioactive iodine uptake value is increased substantially in the presence of iodine deficiency disorder because of increased TSH stimulation and reduction in the nonisotopic iodine pool. Therefore, thyroid uptake values in iodine-sufficient areas, such as the United States, are significantly lower than in areas with iodine deficiency, as in many regions of Europe.

Thyroid size estimated on ultrasonograms has been shown to reflect the iodine sufficiency of a population. When goiter appears in more than 5% of a regional population, iodine deficiency should be considered.[26]

Histologic Findings

In young patients with iodine deficiency, the usual finding is diffuse hyperplasia of the thyroid gland. Histologically, extreme hyperplasia can be seen with little or no colloid, as shown in the image below.

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Histologic sections from a normal thyroid and from an endemic goiter that was removed because of compressive symptoms. The normal thyroid (A) contains....

With aging, the diffuse goiter of iodine deficiency becomes more nodular. Histologically, the nodular goiter develops from areas of hyperplasia separated by areas of degeneration and fibrosis. In older patients, the thyroid gland tends to be extremely heterogeneous, with colloid-containing vesicles, hyperplastic areas, degenerating areas, and fibrosis.

Approach Considerations

Treatment of iodine deficiency

Correction of an individual's iodine deficiency should be instituted at a level recommended by the US Institute of Medicine (IOM) and the World Health Organization (WHO). In a nonpregnant adult, 150 mcg/day is sufficient for normal thyroid function.

Consultation with an endocrinologist should be considered when the etiology of thyroid abnormalities is unclear. Thyroidectomy may be indicated for patients with compressive symptoms of a large goiter.


At a population level, iodine deficiency disorder (IDD) can be prevented by the iodization of food products or the water supply. In practice, this is usually achieved by iodization of salt. An alternative in some developing countries has been the periodic injection of iodized oil supplements.[14, 18]

Iodine treatment-related hyperthyroidism

The primary complication of iodine therapy for IDD is the development of hyperthyroidism. This may occur, especially in patients older than 45 years, because of the hyperfunctioning areas of autonomy that tend to develop in patients with long-standing iodine-deficient goiters.[27]

A Danish study investigating the incidence of hyperthyroidism associated with Denmark's iodine fortification program found that, based on the incident use of antithyroid medication in various parts of the country, the incidence of hyperthyroidism was greater among persons who had suffered from moderate iodine deficiency than it was among those who had had only a mild deficiency.[28] In the moderately deficient population, the incident use of antithyroid medication increased the most in persons younger than 40 years or older than 75 years. Four years after iodine fortification began, the incidence of hyperthyroidism apparently began to decline, returning to prefortification rates in most population groups by the end of 6 years.

Sources of Iodine Replacement

Iodine replacement should be based on the recommendations of IOM and WHO. In an adult, 150 mcg/day is sufficient for normal thyroid function. Replacement of iodine is most easily achieved by requesting that the patient use iodized salt in his or her cooking and at the table or an iodine-containing daily multiple vitamin. Other dietary sources of iodine include milk, egg yolks, and saltwater fish. Not all daily or prenatal multiple vitamins contain iodine, but those that do, typically contain 150 mcg of iodine per tablet.

While a person who follows a vegan diet still might consume iodized salt, only 70% of salt sold from US supermarket shelves currently is iodized. Other major sources of US dietary iodine are saltwater fish, milk and milk products, and eggs. These food items are not included in a true vegan diet.[29]

The Institute of Medicine (IOM) recommended dietary allowance (RDA) is 220 mcg/day of iodine for pregnant women. Not all daily or prenatal multiple vitamins contain iodine, but those that do, typically contain 150 mcg of iodine per tablet. The IOM recommends 290 mcg/day for lactating women and 90-120 mcg/day for children aged 1-11 years. The adequate intake for infants is 110-130 mcg/day.

The American Thyroid Association and the Endocrine Society[30, 31] have recommended that lactating women take vitamins containing 150 mcg of iodide daily to supplement their dietary intake of iodide. This recommendation stems from NHANES reports of low individual maternal urinary iodide concentrations in women of childbearing age and pregnant woment, although it is not clear that lactating women in the United States are at risk for iodine deficiency.[32]  

Infant formula is required by the FDA to contain minimum and maximum calorie-based iodine of 5 and 75 mcg/100 kcal. If an infant formula does not contain at least the minimum amount of each of the nutrients required by the FDA, it is subject to recall.[33]

In developing countries, eradication of iodine deficiency has been accomplished by adding iodine drops to well water or by injecting people with iodized oil.

Using highly concentrated pharmaceutical agents such as a saturated solution of potassium iodide (SSKI), which has a concentration of 35,000-50,000 mcg/drop, is impractical and potentially dangerous.

Treatment of Nontoxic Goiters Caused by Iodine Deficiency

Long-term dietary iodine replacement at levels recommended by IOM and WHO may decrease the size of iodine-deficient goiters in very young children and pregnant women and is indicated for all patients with iodine deficiency.[6] Generally, long-standing goiters associated with iodine deficiency disorder respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism. Patients do not routinely require specific therapy unless the goiter is large enough to cause compressive symptoms (eg, tracheal obstruction, thoracic inlet occlusion, hoarseness).


Exogenous levothyroxine (L-T4) can also be used to decrease goiter size but generally is not effective in adults and older children. Supplemental L-T4, when added to the T3 and T4 secretion by the autonomous nodules in the endemic goiter, may cause thyrotoxicosis. Long-term L-T4 therapy that results in the suppression of the TSH level to below-normal levels may have deleterious effects on cardiac and bone health; therefore, L-T4 therapy is no longer routinely administered to patients with goiter.

Radioactive iodine

Radioactive iodine (iodine-131 [131I]) has been used, primarily in Europe, to decrease thyroid volume in patients with euthyroid goiters (40-60% volume reduction). In the United States, 131I is the most common treatment for toxic multinodular goiters associated with hyperthyroidism. Risks associated with 131I therapy include permanent hypothyroidism.


The standard of care for large goiter associated with obstructive symptoms such as dough, stridor, and dysphagia is thyroidectomy. If the goiter extends into the anterior mediastinum, surgery is the recommended treatment even without obstructive symptoms. After the surgery, the patient will need levothyroxine replacement therapy.

Guidelines Summary

World Health Organization

The World Health Organization (WHO) recommended dietary allowance (RDA) of iodine is as follows[3] :

The WHO notes that although a reduction in the intake of salt to less than 5 g/day, on average, is needed to reduce cardiovascular risk, individuals still consume about 10 g/day, most from household salt used for home cooking and at the table. Therefore, the WHO strongly recommends all food-grade salt should be fortified with iodine as a safe and effective strategy for the population-based prevention and control of iodine deficiency disorders. 

Additional recommendations include the following:

Iodine Deficiency Prevention During Pregnancy

The following organizations have issued guidelines for the managment of thyroid dysfunction during pregnancy, which include recommendations for  management of iodine deficiency:

The Endocrine Society (ES) guidelines offer the following recommendations for iodine nutrition during pregnancy[30] :

The American Thyroid Association (ATA) guidelines concur with the ES guidelines and include the following additional recommendations[31] :

The European Thyroid Association (ETA) recommends daily iodine intake during pregnancy, and lactation should be at least 250 μg and should not exceed 500 µg. Iodine intake should be supplemented with 150 μg of iodine/day, beginning prior to conception and continuing through lactation.[34]  

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Medications used in iodine deficiency include antithyroid agents (potassium iodide) and thyroid products (levothyroxine).

Potassium iodide (SSKI)

Clinical Context:  Potassium iodide is an option in industrialized counties. Absorption from the gastrointestinal tract is rapid and complete. The skin and lungs also can absorb iodine. Iodine equilibrates in extracellular fluids and is specifically concentrated by the thyroid gland.

Class Summary

Iodine deficiency has been treated at a population level by several methods, including voluntary use of iodized salt, iodine supplementation in bread and water, and oral/intramuscular administration of iodized oil. The simplest and least expensive treatment is to have the patient purchase and use iodized salt.

Levothyroxine (Synthroid, Levothroid, Levoxyl)

Clinical Context:  Levothyroxine (L-T4) is generally effective in treating iodine deficiency. It is a considerably more expensive preparation than other forms of iodine (eg, iodized salt), especially when its cost is combined with the added expense of measuring TSH levels to assure that the supplemental L-T4 has not resulted in iatrogenic hyperthyroidism.

Alternatively, thyroid hormone therapy has been used with caution to shrink the goiter of iodine deficiency. An L-T4 dose is chosen that maintains the TSH in the lower part of the reference range. TSH levels should be monitored carefully to avoid thyrotoxicosis due to autonomous nodules in the iodine deficiency goiter.

Class Summary

Thyroid hormone, L-thyroxine, may be used to treat iodine deficiency, because the chemical content of iodine is approximately 60% by weight.


Stephanie L Lee, MD, PhD, Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Disclosure: Nothing to disclose.


Elizabeth N Pearce, MD, MSc, Associate Professor of Medicine, Boston Medical Center, Boston University School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: President-Elect of the American Thyroid Assocaiiton, Member of the Management Council of the Iodine Global Network<br/>Serve(d) as a speaker or a member of a speakers bureau for: received honorarium for one talk from Merck Serono<br/>Received research grant from: SQM.

Sonia Ananthakrishnan, MD, Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center, Boston University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor Emeritus of Medicine, St Louis University School of Medicine

Disclosure: Nothing to disclose.


Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


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Distribution of iodine deficiency in developing countries.

Typical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.

A man and 3 females (age range, 17-20 y) with myxedematous cretinism from the Republic of the Congo in Africa, a region with severe iodine deficiency. Image courtesy of F. DeLange.

Histologic sections from a normal thyroid and from an endemic goiter that was removed because of compressive symptoms. The normal thyroid (A) contains thyroid cells arranged in a monolayered sheet around a storage form of thyroid hormone, colloid, while the endemic goiter (B) shows intense hyperplasia with no colloid. Image courtesy of F. DeLange.

Distribution of iodine deficiency in developing countries.

Typical endemic goiters in 3 women from the Himalayas, an area of severe iodine deficiency. Image courtesy of F. DeLange.

A man and 3 females (age range, 17-20 y) with myxedematous cretinism from the Republic of the Congo in Africa, a region with severe iodine deficiency. Image courtesy of F. DeLange.

Histologic sections from a normal thyroid and from an endemic goiter that was removed because of compressive symptoms. The normal thyroid (A) contains thyroid cells arranged in a monolayered sheet around a storage form of thyroid hormone, colloid, while the endemic goiter (B) shows intense hyperplasia with no colloid. Image courtesy of F. DeLange.

Iodine Deficiency None Mild Moderate Severe
Median urine iodine, mcg/L>10050-9920-49< 20
Goiter prevalence< 5%5-20%20-30%>30%
Neonatal thyroid-stimulating hormone (TSH),

>5 IU/mL whole blood

< 3%3-20%20-40%>40%
Adapted from the World Health Organization (WHO)/United Nations Children's Fund (UNICEF)/International Council for Control of Iodine Deficiency Disorders (ICCIDD).