Iodine Deficiency: Symptoms, Causes, and Recovery

Symptom Deep-Dive Pages

Table of Contents

1. Symptom Deep-Dive Pages
2. What Is Iodine Deficiency?
3. Why One Missing Mineral Causes So Many Symptoms
4. Common Causes of Iodine Deficiency
5. Iodine, Selenium, and Iron: How They Work Together
6. How Iodine Deficiency Is Diagnosed
7. How Iodine Deficiency Is Corrected
8. Warning Signs Described in the Research
9. Key Research Papers
10. Connections
11. Featured Videos

What Is Iodine Deficiency?

Iodine is a micronutrient that is essential for the production of thyroid hormones. Its main dietary sources are foods fortified with iodine, including salt, dairy products and bread, and foods naturally abundant in it, such as seafood (Leung and Braverman 2014). Iodine deficiency means the supply is too small for the thyroid to make enough hormone, and the adverse effects that follow are grouped together as the iodine deficiency disorders (Zimmermann 2009).

For adults who are not pregnant or breastfeeding, the U.S. Institute of Medicine, and jointly the WHO, UNICEF and the International Council for the Control of Iodine Deficiency Disorders, recommend 150 micrograms (mcg) of iodine a day, with a Tolerable Upper Intake Level of 1,100 mcg a day for adults (Leung and Braverman 2014). In pregnancy and breastfeeding the Institute of Medicine recommends 220 mcg and 290 mcg a day, and WHO recommends 250 mcg a day for both (Leung 2012). For scale, the USDA, FDA and NIH Office of Dietary Supplements iodine database (Release 4, 2024) lists ¼ teaspoon (1.5 g) of iodized table salt at an average of 78 mcg (26 samples, range 51–134 mcg), and the same amount of non-iodized sea salt at 0 mcg (28 samples). Delange grades deficiency by intake: mild at 50–99 mcg a day, moderate at 20–49 mcg and severe below 20 mcg (Delange 2001).

Iodine status is judged mainly in populations rather than in one person. Leung and Braverman write that overall iodine levels cannot be reliably measured in individuals, given the considerable day-to-day variation in iodine intake (Leung and Braverman 2014); in a 15-month study of 22 Swiss women, about 10 repeat spot or 24-hour urine samples were needed to estimate one woman's iodine status with 20% precision (König 2011). For a population, WHO defines deficiency by the median urinary iodine concentration: mild at 50–99 mcg/L, moderate at 20–49 mcg/L and severe below 20 mcg/L (as reported by Vanderpump 2011). A median of 100–199 mcg/L indicates adequate intake (Zimmermann 2013), and in pregnant women WHO treats 150–249 mcg/L as adequate (Zimmermann 2009, Am J Clin Nutr).

The research describes consequences that scale with the degree of deficiency:

• Mild to moderate deficiency — increased thyroid activity can compensate for the low intake and keep thyroid function normal in most people, but the chronic stimulation raises the prevalence of toxic nodular goiter and hyperthyroidism in the population (Zimmermann and Boelaert 2015). In pregnancy, observational studies have linked mild maternal iodine deficiency with lower child cognition (Pearce 2016). Randomized trials of iodine supplements in mildly to moderately deficient pregnant women have not shown an effect on child neurodevelopment (Gowachirapant 2017; Dineva 2020).
• Severe deficiency — goiter and hypothyroidism, because even with the thyroid working harder to take up and recycle iodine, there is too little to make thyroid hormone (Zimmermann and Boelaert 2015). During development it causes maternal and fetal hypothyroidism, with cretinism and growth retardation among the consequences (Pearce 2016). Delange describes the damage as increasing with the degree of deficiency, with overt endemic cretinism as the severest consequence, and iodine deficiency as the world's greatest single cause of preventable brain damage (Delange 2001).

Salt iodization has changed the global picture. The number of countries with adequate iodine intake nearly doubled from 67 in 2003 to 118 in 2020, while 21 countries remained deficient and 13 had excessive intakes (Zimmermann and Andersson 2021); the Iodine Global Network reports the number of countries with insufficient iodine status falling from 113 in 1993 to 21 in 2021. Deficiency has not disappeared from wealthy countries. A 2013 review lists re-emerging iodine deficiency in parts of the developed world among the emerging issues (Pearce 2013), and Zimmermann's 2009 review reported that about 50% of Europe remained mildly iodine deficient and that iodine intakes in the United States and Australia had fallen (Zimmermann 2009). In the UK, which has no programme of salt iodization, a 2009 survey of 14–15-year-old schoolgirls found a median urinary iodine of 80.1 mcg/L, with values indicating mild deficiency in 51% of participants, moderate in 16% and severe in 1% (Vanderpump 2011).

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Why One Missing Mineral Causes So Many Symptoms

Iodine deficiency is linked to problems as different as a neck swelling, tiredness and, before birth, effects on a child's brain. The reviews trace all of them to one product: the adverse effects of iodine deficiency are due to inadequate production of thyroid hormone (Zimmermann 2009). Thyroid hormone has long been accepted as an important determinant of overall energy expenditure and the basal metabolic rate, and regulating heat production is one of its major tasks in adults (Kim 2008).

The thyroid uses iodine to make thyroxine (T4) and tri-iodothyronine (T3) (Skeaff 2011). Iodide uptake by the sodium–iodide symporter, the pump that carries iodide into thyroid cells, is the first limiting step in thyroid hormone production (Serrano-Nascimento 2022). The research connects a short supply to each group of problems:

• The thyroid gland itself — in iodine deficiency the thyroid increases its activity to maximise iodine uptake and recycling (Zimmermann and Boelaert 2015), and goiter is associated with iodine deficiency and with a rise in thyroid-stimulating hormone (TSH) (Knobel 2016). The enlarged gland is covered on the Goiter page.
• Metabolism and weight — people with hypothyroidism may have nonspecific symptoms due to metabolic slowing, including fatigue (68%–83%) and weight gain (24%–59%) (Chaker and Papaleontiou 2025). See Weight Gain & Cold Sensitivity.
• Energy and thinking — the same review lists cognitive issues such as memory loss and difficulty concentrating (45%–48%) and menstrual irregularities (Chaker and Papaleontiou 2025). In a Danish population study of 140 people with newly diagnosed overt autoimmune hypothyroidism, the most common symptoms were tiredness (81%), dry skin (63%) and shortness of breath (51%), but no single symptom reliably separated patients from controls (Carlé 2014). The fatigue and the broader picture of hypothyroidism page covers this in depth.
• The developing brain — the American Thyroid Association's 2006 statement describes the fetus as totally dependent in early pregnancy on maternal thyroxine for normal brain development, and states that if iodine insufficiency leads to hypothyroidism during pregnancy, irreversible fetal brain damage can result (ATA Public Health Committee 2006). Delange identifies maternal hypothyroxinemia in early pregnancy as a key factor in the neurological damage of cretinism (Delange 2001). This is covered on the Pregnancy & Brain Development page.

The thread through the symptom pages is the same: one mineral feeds one hormone, and a shortage of that hormone shows up wherever it acts.

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Common Causes of Iodine Deficiency

The reviews describe iodine deficiency mainly as a problem of intake. Diets in many countries cannot provide adequate iodine without iodine fortification of salt (Zimmermann and Andersson 2021), and WHO's 2014 salt guideline estimates that about one third of the world's population lives in areas where natural sources of iodine are low. The causes described in the research:

• Iodine-poor soil and water (geography) — the iodine content of plant foods depends on the iodine in soil, irrigation water, crop fertilizers and livestock feed; plants grown in soils of iodine-deficient regions may contain as little as 10 mcg/kg of dry weight, against as much as 1,000 mcg/kg in iodine-rich areas (Leung 2012). Before iodized table salt was introduced in the 1920s, the United States was iodine deficient, particularly in a "goiter belt" covering the Great Lakes, the Appalachians and the northwest (Leung 2012).
• Salt that is not iodized — in the United States, salt iodization is voluntary, the FDA does not require iodine content to be listed on food packaging, and the majority of salt consumed is assumed to come from processed foods, which are made primarily with non-iodized salt (Leung 2012). The USDA, FDA and NIH database lists non-iodized sea salt at 0 mcg per ¼ teaspoon, and iodized sea salt at an average of 70 mcg. In the UK, Bath and Rayman report that iodized table salt is unlikely to contribute to intake because its availability in grocery stores is low (Bath and Rayman 2013). A 2013 review lists the food industry's use of iodized salt, and the possible effect of initiatives to lower population sodium intake on iodine intake, as emerging issues (Pearce 2013); WHO's guideline cites a World Health Assembly resolution confirming that salt-iodization policy is to be compatible with the recommendation to limit salt intake, and describes monitoring salt intake so that iodization levels can be adjusted (WHO 2014).
• Replacing dairy with plant-based drinks — in the UK, milk is the principal dietary iodine source (Bath 2017); in the United States, iodine reaches dairy foods through the iodophor cleansers used on milk cans and teats (Leung 2012). Bath and colleagues measured 47 milk-alternative drinks on sale in the UK in 2015: the median iodine concentration of the 44 unfortified drinks was 7.3 mcg/kg, 1.7% of their value for winter conventional cows' milk (438 mcg/kg), and only three of the 47 were fortified with iodine (Bath 2017). The U.S. database lists 1.1 mcg per 8 fl oz for an almond beverage and 3.2 mcg for a soy beverage, against 82 mcg per cup of whole milk.
• Pregnancy and breastfeeding — not a cause in itself, but a time of higher need: Skeaff reports that a 50% increase in iodine intake is recommended in pregnancy so that the mother can produce enough thyroid hormone for herself and her baby (Skeaff 2011). Increased goiter prevalence during pregnancy has been found only in areas with suboptimal iodine intake, which Knudsen and colleagues interpret as an exacerbation of existing deficiency (Knudsen 2002). After birth, breast milk may be an infant's only source of iodine during the first 6 months (WHO 2014).
• Diets low in seafood and dairy — seafood is naturally abundant in iodine (Leung and Braverman 2014), and the FDA Total Diet Study of 2003–2004 identified dairy and grain products as important sources of dietary iodine in the United States (Leung 2012). Diets that leave out these foods and also use non-iodized salt remove the main sources named in these reviews.
• Goitrogens (food substances that interfere with the thyroid) — Delange's review names vegetables of the Cruciferae family, chronic consumption of poorly detoxified cassava containing large amounts of cyanogenic glucosides, flavonoids, and humic substances from organic residues in soil as clearly involved in endemic goiter (Delange 1988). Knudsen and colleagues describe iodine status as the major environmental factor that determines goiter prevalence, with goitrogens in food and drinking water among the other factors identified (Knudsen 2002).
• Environmental blockers and smoking — perchlorate, nitrate and thiocyanate competitively inhibit iodide uptake through the sodium–iodide symporter. They are found mainly in food, water and cigarette smoke; their impact on people is described as highly controversial, though some studies indicate harmful effects on thyroid function, especially in iodine-deficient areas (Serrano-Nascimento 2022). Wiersinga reports that the slightly greater thyroid size in smokers is seen in iodine-deficient but not iodine-sufficient areas and is caused by competitive inhibition of thyroidal iodide uptake by thiocyanate (Wiersinga 2013).

These causes can occur together. Knobel lists iodine deficiency, a raised TSH, natural goitrogens, smoking, and lack of selenium and iron among the factors associated with goiter, and notes that heredity also has an important role (Knobel 2016).

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Iodine, Selenium, and Iron: How They Work Together

Making and using thyroid hormone involves two other minerals besides iodine, and the research describes both as affecting how the thyroid responds to iodine.

Selenium. The iodothyronine deiodinases, enzymes that convert thyroid hormone between its forms, are selenoproteins, and several other selenoproteins protect thyroid cells from damage by the hydrogen peroxide produced for thyroid hormone synthesis (Köhrle 2005). In endemic cretinism, Delange reports that selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism (Delange 2001). The selenium research is covered on the Selenium overview.

Iron. Thyroid peroxidase, a heme-containing enzyme, catalyses the two initial steps of thyroid hormone synthesis. In rats with iron-deficiency anemia, its activity per thyroid was 33% to 56% lower across three iron-deficient groups than in controls, and the authors concluded that iron deficiency sharply reduces thyroid peroxidase activity (Hess 2002). In goitrous, iodine-deficient children in Côte d'Ivoire given oral iodized oil, goiter prevalence 30 weeks later was 12% in children without anemia and 64% in children with iron-deficiency anemia; after the anemic children were given iron, their thyroid volume fell further (Zimmermann 2000). Zimmermann's review concludes that a high prevalence of iron deficiency among children in areas of endemic goiter may reduce the effectiveness of iodized salt programmes (Zimmermann 2006). See the Iron overview.

Autoimmune thyroid disease. Iodine deficiency is not the only cause of an underactive thyroid. Hypothyroidism can be caused by severe iodine deficiency but is more frequently caused by chronic autoimmune thyroiditis in iodine-replete areas (Chaker 2022); Hashimoto thyroiditis is the cause of primary hypothyroidism in up to 85% of patients living in areas with adequate iodine (Chaker and Papaleontiou 2025). This distinction is covered on the Hashimoto's thyroiditis page, in the diagnosis section below and on the Hypothyroidism & Fatigue page.

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How Iodine Deficiency Is Diagnosed

Because iodine intake varies so much from day to day, overall iodine levels cannot be reliably measured in individuals (Leung and Braverman 2014). The assessment methods described in the major reviews are urinary iodine concentration, goiter, newborn thyroid-stimulating hormone and blood thyroglobulin (Zimmermann 2008). For one person, thyroid blood tests show whether the gland is keeping up.

• Thyroid function blood tests (TSH and free T4) — hypothyroidism is diagnosed by biochemical testing (Chaker and Papaleontiou 2025). Overt primary hypothyroidism is defined as an elevated TSH with free T4 below the reference range, and subclinical hypothyroidism as an elevated TSH with free T4 within the reference range (Chaker 2022). These tests do not measure iodine itself. The Thyroid Panel page explains each value.
• Urinary iodine concentration — the median urinary iodine concentration is a good indicator of iodine status in populations, but there is no established biomarker for an individual's status (König 2011). The WHO population cut-offs are given in the first section of this page.
• Physical examination and ultrasound of the thyroid — Knobel describes measurement of TSH, high-resolution ultrasonography or computed tomography, and fine-needle aspiration biopsy as the methods for evaluating goiter (Knobel 2016). In a survey of 304 schoolchildren in a formerly severely deficient Turkish city, goiter prevalence was 14.6% by ultrasound and 19.4% by palpation (Demirel 2004).
• Thyroglobulin — in 2,512 schoolchildren aged 6–12 in 12 countries, blood thyroglobulin followed a U-shaped curve across iodine intakes, with elevated values more common both in iodine deficiency (median urinary iodine below 100 mcg/L) and in iodine excess (above 300 mcg/L); the authors concluded that thyroglobulin is a sensitive indicator of both low and excess iodine intake in school-aged children (Zimmermann 2013).
• Newborn TSH — TSH in blood collected from newborns 3–4 days after birth may be a sensitive indicator of even mild iodine deficiency in late pregnancy; a frequency below 3% of values above 5 mU/L indicates iodine sufficiency (Zimmermann 2009, Am J Clin Nutr).
• Distinguishing iodine deficiency from autoimmune thyroid disease — in iodine-replete areas, chronic autoimmune thyroiditis is the more frequent cause of hypothyroidism (Chaker 2022; see Hashimoto's thyroiditis). The distinction matters for iodine intake: Leung and Braverman list pre-existing thyroid disease among the factors that raise the risk of iodine-induced thyroid dysfunction (Leung and Braverman 2014), and in a case series two patients with Hashimoto's disease developed severe, symptomatic hypothyroidism after taking a high-dose over-the-counter iodine product (Hoang 2013).

A broader blood panel is described on the Comprehensive Metabolic Panel page; thyroid hormones and TSH are measured by the specific thyroid tests above.

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How Iodine Deficiency Is Corrected

The research describes correction at two levels: population programmes, chiefly salt iodization, and iodine supplements for groups with higher needs, together with evidence on how much is too much.

• Salt iodization as public-health policy. WHO's 2014 guideline recommends that all food-grade salt, used in households and in food processing, be fortified with iodine as a safe and effective strategy for the prevention and control of iodine deficiency disorders, in stable and emergency settings (a strong recommendation); WHO and UNICEF first recommended universal salt iodization in 1993 (WHO 2014). Zimmermann describes carefully monitored universal salt iodization as the best strategy in most countries and one of the most cost-effective ways to contribute to economic and social development (Zimmermann 2009). In 2020, 124 countries had legislation for mandatory salt iodization and 21 had legislation allowing voluntary iodization, and 88% of the global population used iodized salt (Zimmermann and Andersson 2021). In the U.S. database, ¼ teaspoon of iodized table salt averages 78 mcg (range 51–134 mcg); in a U.S. study of 88 freshly opened table-salt samples, 47 contained less iodine than the FDA's recommended range (Dasgupta 2008).
• Iodine in foods. Seafood is naturally abundant in iodine, and dairy products and bread can carry it (Leung and Braverman 2014). Values per serving in the USDA, FDA and NIH database include 146 mcg in 3 oz of baked cod, 82 mcg in a cup of whole milk, 55 mcg in ¾ cup of plain whole-milk yogurt, 31 mcg in a large hard-boiled egg and 11 mcg in 3 oz of baked salmon. Seaweed varies far more: Teas and colleagues measured iodine from 16 mcg per gram in nori to over 8,165 mcg per gram in one sample of processed kelp granules, and noted that some Asian seaweed dishes may exceed the 1,100 mcg upper level (Teas 2004). The individual foods are covered on the cod, sardines, salmon, milk, yogurt and eggs pages.
• Supplements in pregnancy and breastfeeding. The American Thyroid Association recommends that women receive a 150 mcg iodine supplement daily during pregnancy and lactation and that all prenatal vitamin/mineral preparations contain 150 mcg of iodine (ATA Public Health Committee 2006); a CDC analysis describes the recommendation as beginning 3 months before conception (Gupta 2018). Prenatal and other multivitamins sold in the U.S. are not required to contain iodine, and in one survey of 223 U.S. prenatal multivitamins only 51% listed any iodine content (Leung 2012). Where fewer than 90% of households use iodized salt and the median urinary iodine of school-age children is below 100 mcg/L, WHO recommends iodine supplementation in pregnancy and infancy (Zimmermann 2009, Am J Clin Nutr). The trial evidence differs by severity. In a meta-analysis of 37 Chinese studies with 12,291 children, children in severely deficient areas without iodine supplementation scored 12.45 IQ points lower than children in iodine-sufficient areas, and children whose mothers received iodine during pregnancy scored 8.7 points higher than those whose mothers remained deficient (Qian 2005). In mildly deficient pregnant women in India and Thailand, 200 mcg of iodine a day had no effect on child neurodevelopment at 5–6 years (Gowachirapant 2017), and a 2020 systematic review found insufficient good-quality evidence to support current recommendations for iodine supplementation in pregnancy in areas of mild-to-moderate deficiency (Dineva 2020).
• How much is too much. Intakes above the 150 mcg recommendation are generally well tolerated, but people with pre-existing thyroid disease, the elderly, fetuses and newborns are at increased risk of iodine-induced thyroid dysfunction (Leung and Braverman 2014). In a case series of four patients who developed significant thyroid dysfunction after over-the-counter products containing large amounts of iodine, the authors concluded that there is no valid reason for taking high-dose over-the-counter iodine supplements, which they describe as shown to cause harm with no known benefit (Hoang 2013). Introducing iodized salt into regions of chronic deficiency might transiently increase the proportion of thyroid disorders, but the small risks of iodine excess are described as far outweighed by the substantial risks of deficiency (Zimmermann 2008). The Iodine Toxicity hub covers what too much iodine does.
• Treating the thyroid. Levothyroxine is the first-line treatment for hypothyroidism (Chaker and Papaleontiou 2025). Where testing points to Hashimoto's rather than iodine shortage, the underlying condition is a different one, covered on its own page.

Correcting deficiency has been followed by smaller goiters in the studies above. In the Turkish city formerly classed as severely deficient, goiter prevalence fell and the region became mildly endemic three years after salt iodization became mandatory (Demirel 2004); in goitrous Ivorian children without anemia, mean thyroid volume fell by 45.1% within 30 weeks of oral iodized oil (Zimmermann 2000). Zimmermann and Boelaert describe the rise in hyperthyroidism that can follow salt iodization as transient, because iodine sufficiency normalises thyroid activity and in the long term reduces nodular autonomy (Zimmermann and Boelaert 2015). The harm described as irreversible is fetal brain damage (ATA Public Health Committee 2006), and Zimmermann's review states that, to prevent fetal damage in areas of severe deficiency, iodine is to be given before or early in pregnancy (Zimmermann 2009, Am J Clin Nutr). See the Iodine overview and the Iodine Benefits hub for what iodine does when the supply is adequate.

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Warning Signs Described in the Research

Most of the problems on this page develop gradually: the onset of hypothyroidism is insidious in most cases, and symptoms may present relatively late in the disease (Chaker 2022). Because no single symptom reliably identified overt hypothyroidism in the Danish study, its authors concluded that "even minor suspicion should lead to a blood test" (Carlé 2014). The situations the research describes as calling for evaluation include:

• A lump or swelling in the front of the neck — nodular thyroid disease with single or multiple nodules requires evaluation because of the risk of malignancy, toxicity and local compressive symptoms (Knobel 2016). See the Goiter page.
• Pregnancy, breastfeeding, or planning a pregnancy — the period the American Thyroid Association recommendation covers (ATA Public Health Committee 2006; Gupta 2018). In U.S. national survey data for 2011–2014, 72.2% of pregnant women used a dietary supplement but only 17.8% used one containing iodine, and among lactating women the figures were 75.0% and 19.0% (Gupta 2018).
• Severe symptoms of an underactive thyroid — untreated hypothyroidism may progress to myxedema coma, a condition associated with hypothermia, low blood pressure and altered mental status that requires intensive care and has a mortality rate of up to 30% (Chaker and Papaleontiou 2025).
• Symptoms after high-dose iodine products — in the Hoang case series, an acute worsening of thyrotoxicosis and severe, symptomatic hypothyroidism followed over-the-counter high-dose iodine products, and thyroid function recovered in all four patients with appropriate management and discontinuation of the products (Hoang 2013).

The groups the research identifies as most susceptible to iodine deficiency are women of reproductive age, whose babies are at high risk of irreversible mental impairment if iodine deficient in the womb, and breastfeeding women (WHO 2014); for iodine excess, they are people with pre-existing thyroid disease, the elderly, fetuses and newborns (Leung and Braverman 2014). Questions about symptoms, thyroid testing and supplements are for a clinician. For the related conditions, see Hypothyroidism, Thyroid Disorders, and Thyroid Cancer.

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Key Research Papers

1. Zimmermann MB, Jooste PL, Pandav CS (2008). Iodine-deficiency disorders. The Lancet;372(9645):1251-1262. — DOI: 10.1016/S0140-6736(08)61005-3. — doi:10.1016/S0140-6736(08)61005-3
2. Zimmermann MB (2009). Iodine Deficiency. Endocrine Reviews;30(4):376-408. — DOI: 10.1210/er.2009-0011. — doi:10.1210/er.2009-0011
3. Zimmermann MB, Boelaert K (2015). Iodine deficiency and thyroid disorders. The Lancet Diabetes & Endocrinology;3(4):286-295. — DOI: 10.1016/S2213-8587(14)70225-6. — doi:10.1016/S2213-8587(14)70225-6
4. Leung AM, Braverman LE (2014). Consequences of excess iodine. Nature Reviews Endocrinology;10(3):136-142. — DOI: 10.1038/nrendo.2013.251. — doi:10.1038/nrendo.2013.251
5. Bath SC, Steer CD, Golding J, Emmett P, Rayman MP (2013). Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC). The Lancet;382(9889):331-337. — DOI: 10.1016/S0140-6736(13)60436-5. — doi:10.1016/S0140-6736(13)60436-5
6. Pearce EN, Andersson M, Zimmermann MB (2013). Global Iodine Nutrition: Where Do We Stand in 2013? Thyroid;23(5):523-528. — DOI: 10.1089/thy.2013.0128. — doi:10.1089/thy.2013.0128
7. Velasco I, Bath SC, Rayman MP (2018). Iodine as Essential Nutrient during the First 1000 Days of Life. Nutrients;10(3):290. — DOI: 10.3390/nu10030290. — doi:10.3390/nu10030290
8. Pearce EN, Lazarus JH, Moreno-Reyes R, Zimmermann MB (2016). Consequences of iodine deficiency and excess in pregnant women: an overview of current knowns and unknowns. The American Journal of Clinical Nutrition;104(Suppl 3):918S-923S. — DOI: 10.3945/ajcn.115.110429. — doi:10.3945/ajcn.115.110429
9. Bath SC, Rayman MP (2013). Iodine deficiency in the UK: an overlooked cause of impaired neurodevelopment? Proceedings of the Nutrition Society;72(2):226-235. — DOI: 10.1017/S0029665113001006. — doi:10.1017/S0029665113001006
10. Taylor PN, Albrecht D, Scholz A, Gutierrez-Buey G, Lazarus JH, et al. (2018). Global epidemiology of hyperthyroidism and hypothyroidism. Nature Reviews Endocrinology;14(5):301-316. — DOI: 10.1038/nrendo.2018.18. — doi:10.1038/nrendo.2018.18
11. Skeaff SA (2011). Iodine Deficiency in Pregnancy: The Effect on Neurodevelopment in the Child. Nutrients;3(2):265-273. — DOI: 10.3390/nu3020265. — doi:10.3390/nu3020265
12. Qian M, Wang D, Watkins WE, Gebski V, Yan YQ, Li M, et al. (2005). The effects of iodine on intelligence in children: a meta-analysis of studies conducted in China. Asia Pacific Journal of Clinical Nutrition;14(1):32-42. — PubMed PMID: 15734706
13. Zimmermann MB, Andersson M (2021). GLOBAL ENDOCRINOLOGY: Global perspectives in endocrinology: coverage of iodized salt programs and iodine status in 2020. European Journal of Endocrinology;185(1):R13-R21. — PubMed PMID: 33989173
14. Vanderpump MP, Lazarus JH, Smyth PP, Laurberg P, Holder RL, Boelaert K, Franklyn JA; British Thyroid Association UK Iodine Survey Group (2011). Iodine status of UK schoolgirls: a cross-sectional survey. Lancet;377(9782):2007-12. — PubMed PMID: 21640375
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23. Gowachirapant S, Jaiswal N, Melse-Boonstra A, Galetti V, Stinca S, Mackenzie I, et al. (2017). Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. Lancet Diabetes & Endocrinology;5(11):853-863. — PubMed PMID: 29030199
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PubMed Topic Searches

1. PubMed: Iodine deficiency disorders: reviews
2. PubMed: Iodine deficiency in pregnancy and child neurodevelopment
3. PubMed: Iodine deficiency, goiter, and hypothyroidism
4. PubMed: Urinary iodine concentration and population status
5. PubMed: Iodine, selenium, iron, and thyroid function

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