Iodine for Brain Development

Table of Contents

1. Iodine Deficiency as a Preventable Cause of Brain Damage
2. The Fetal Brain Development Window
3. Cretinism — Myxedematous and Neurological Forms
4. Maternal-Fetal Iodine and Thyroid Hormone Transfer
5. Breast Milk as the Infant Iodine Source
6. Universal Salt Iodization
7. IQ Findings: Severe Deficiency, Mild Deficiency and Supplementation Trials
8. Modern U.S. Pregnancy Iodine Status
9. What Guidelines and Studies Report for Preconception, Pregnancy and Lactation
10. Key Research Papers
11. Connections
12. Featured Videos

Iodine Deficiency as a Preventable Cause of Brain Damage

Delange's 2001 editorial summarizes the case: all degrees of iodine deficiency — mild (50–99 µg/day intake), moderate (20–49 µg/day) and severe (below 20 µg/day) — affect thyroid function in the mother and newborn and the mental development of the child, the damage increases with the degree of deficiency, and overt endemic cretinism is the most severe consequence. He described a global loss of 10–15 IQ points at the population level (Delange 2001). Zimmermann's 2009 review estimated that about 2 billion people worldwide had insufficient iodine intake, with South Asia and sub-Saharan Africa particularly affected and about half of Europe mildly deficient (Zimmermann 2009, Endocrine Reviews).

The same review describes carefully monitored universal salt iodization as one of the most cost-effective ways to contribute to economic and social development (Zimmermann 2009, Endocrine Reviews). In a 1983 Lancet paper, Basil Hetzel proposed the term “iodine deficiency disorders” (IDD) in place of “goitre”, to bring together stillbirths, abortions, congenital anomalies, endemic cretinism and impaired mental function under one heading, and described iodized salt and iodized oil as means of correcting deficiency on a mass scale (Hetzel 1983).

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The Fetal Brain Development Window

Morreale de Escobar and colleagues reviewed the evidence on maternal thyroid hormone and the early fetal brain. Small amounts of maternal T4 and T3 are present in the fetal compartment by 4 weeks after conception, with T4 rising steadily thereafter; the “free” T4 available to fetal tissues is determined by the mother's serum T4; and T3 generated locally from T4 in the fetal cerebral cortex reaches adult concentrations by mid-gestation (Morreale de Escobar 2004, Eur J Endocrinol). Before mid-gestation the mother is the only source of T4 for the developing brain, and maternal transfer remains a major fraction of fetal serum T4 even after the fetal thyroid begins secreting hormone (Morreale de Escobar 2004; de Escobar 2004, Best Pract Res Clin Endocrinol Metab).

In rats, even a moderate, transient period of maternal hypothyroxinemia at the start of neurogenesis disrupts the migration of neurons into the cortical layers — an animal finding the authors set beside human epidemiological evidence that early maternal hypothyroxinemia is potentially damaging for the child (de Escobar 2004). 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 irreversible fetal brain damage can result if iodine insufficiency leads to hypothyroidism in pregnancy (ATA Public Health Committee 2006).

On timing, Zimmermann's 2009 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). A CDC analysis notes that the American Thyroid Association recommends a supplement containing 150 µg of iodine beginning 3 months before conception and continuing through pregnancy and lactation (Gupta 2018).

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Cretinism — Myxedematous and Neurological Forms

Severe maternal iodine deficiency in pregnancy is associated with two described forms of endemic cretinism:

• Neurological cretinism — Hetzel described endemic cretinism as characterized most commonly by mental deficiency, deaf-mutism and spastic diplegia, with lesser degrees of neurological defect related to fetal iodine deficiency (Hetzel 1983). Delange identifies maternal hypothyroxinemia in early pregnancy as a key factor in the neurological damage (Delange 2001).
• Myxedematous cretinism — the hypothyroid form, marked by severe hypothyroidism in the affected child. Delange reports that selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism in cretins (Delange 2001).

Beyond cretinism, Delange's 10–15 IQ-point figure is a population-level estimate of the loss across all degrees of deficiency (Delange 2001). The Qian 2005 meta-analysis of Chinese studies found a 12.45-point difference in children living in severely iodine-deficient areas without supplementation compared with iodine-sufficient areas (Qian 2005).

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Maternal-Fetal Iodine and Thyroid Hormone Transfer

The research describes the uterine-placental unit as a highly efficient “barrier” to the transfer of thyroid hormones, which keeps potentially toxic concentrations of free T4 and T3 from reaching fetal tissues before they are needed (Morreale de Escobar 2004; de Escobar 2004). The main points from these reviews:

• T4 — despite the barrier, maternal T4 reaches the fetal compartment; the free T4 in fetal fluids is set by maternal serum T4 and reaches concentrations of biological significance.
• T3 — T3 and free T3 stay very low in fetal fluids throughout pregnancy. The fetal brain relies on local conversion of T4 to T3 by iodothyronine deiodinases, which regulate T3 availability in different brain structures over time.
• The first-trimester T4 surge — Morreale de Escobar proposes that the first-trimester surge in maternal free T4 supplies the fetal cortex with substrate for local T3 production, and that women unable to raise T4 production early in pregnancy form a population at risk for neurological disabilities in their children. The authors identify mild-to-moderate iodine deficiency as the most widespread cause of maternal hypothyroxinemia in Western societies.

An inappropriate first-trimester free-T4 surge may not raise TSH, so a TSH-based test can miss it (de Escobar 2004). WHO raised its recommended iodine intake in pregnancy from 200 to 250 µg/day (Zimmermann 2009, Am J Clin Nutr), compared with a recommended 150 µg/day for adults who are not pregnant or lactating (Leung and Braverman 2014).

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Breast Milk as the Infant Iodine Source

After birth, an exclusively breastfed infant receives iodine only through breast milk. The American Thyroid Association's 2006 statement recommends that women receive a 150 µg iodine supplement daily during lactation as well as pregnancy (ATA Public Health Committee 2006). A CDC analysis of NHANES 2011–2014 found that 75.0% of lactating women used a dietary supplement but only 19.0% used one containing iodine (Gupta 2018).

Other findings on infants and iodine:

• Leung and Braverman list fetuses and neonates among the groups susceptible to iodine-induced thyroid dysfunction, and note that the source of excess iodine may not be readily apparent (Leung and Braverman 2014).
• Zimmermann's review notes that ensuring adequate iodine during parenteral nutrition has become important, particularly in preterm infants, as the use of povidone-iodine disinfectants (an incidental source of iodine) has declined (Zimmermann 2009, Endocrine Reviews).
• A review of soy isoflavones describes animal and human evidence linking soy consumption with goiter; iodine deficiency greatly increases the antithyroid effect and iodine supplementation is protective. Genistein inactivated thyroid peroxidase in rat studies, although other in-vivo thyroid measures in those rats were normal (Doerge and Sheehan 2002).

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Universal Salt Iodization

Universal salt iodization (USI) — iodizing all salt for human and animal consumption — is described as the first-line strategy for eliminating severe iodine deficiency, with supplementation used for vulnerable groups where salt iodization is not feasible or not sufficient (Pearce 2016). According to Zimmermann and Andersson's 2020 global review:

• 124 countries had legislation for mandatory salt iodization and 21 had legislation allowing voluntary iodization, and 88% of the global population used iodized salt.
• Urinary iodine surveys had been done in 152 of 194 countries in the previous 15 years, 132 of them nationally representative.
• The number of countries with adequate iodine intake nearly doubled, from 67 in 2003 to 118 in 2020; 21 countries remained deficient and 13 had excessive intakes, from groundwater iodine or over-iodized salt.
• The authors describe iodine programs as often durable even during national crises, while the equity of iodized-salt programs within countries remains an issue (Zimmermann and Andersson 2021).

Zimmermann's 2009 review states that in countries or regions where fewer than 90% of households use iodized salt and the median urinary iodine in school-age children is below 100 µg/L, WHO recommends iodine supplementation in pregnancy and infancy (Zimmermann 2009, Am J Clin Nutr). The same review notes that introducing iodized salt into regions of chronic deficiency may transiently increase the incidence of thyroid disorders, but that the relatively small risks of iodine excess are far outweighed by the risks of deficiency (Zimmermann 2009, Endocrine Reviews).

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IQ Findings: Severe Deficiency, Mild Deficiency and Supplementation Trials

The research splits into observational studies of deficiency and randomized trials of supplementation, and they do not point the same way for mild deficiency.

• Severe deficiency — Qian 2005 — a meta-analysis of 37 Chinese studies with 12,291 children, comparing children in naturally iodine-sufficient areas with those in severely iodine-deficient areas. Children in severely deficient areas without supplementation scored 12.45 IQ points lower (0.83 standard deviations); children whose mothers received iodine during pregnancy recovered 8.7 points compared with children whose mothers were persistently deficient (Qian 2005).
• Young children — Bougma 2013 — a systematic review of children 5 years old and under found average effect sizes of 0.46–0.68 across four study designs, which the authors translate to 6.9–10.2 IQ points lower in iodine-deficient children; they flag weak designs, omitted confounders and small samples (Bougma 2013).
• Mild deficiency — ALSPAC (Bath 2013) — in 1,040 first-trimester pregnant women in the UK cohort (median urinary iodine 91.1 µg/L, classed as mild-to-moderate deficiency), children of women with an iodine-to-creatinine ratio below 150 µg/g were more likely to score in the lowest quartile for verbal IQ at age 8 (odds ratio 1.58), reading accuracy (1.69) and reading comprehension (1.54) at age 9, after adjustment for 21 confounders; scores worsened as maternal iodine status fell (Bath 2013).
• Mild deficiency — Tasmania (Hynes 2013) — children whose mothers had urinary iodine below 150 µg/L in pregnancy had lower spelling, grammar and English-literacy scores at age 9 than peers, even though they grew up in an iodine-replete environment; only the spelling difference remained significant after adjustment for socioeconomic factors (Hynes 2013).
• Pooled cohorts — Levie 2019 — an individual-participant meta-analysis of 6,180 mother-child pairs from Generation R (Netherlands), INMA (Spain) and ALSPAC found a curvilinear association of maternal urinary iodine with verbal IQ only, present only up to 14 weeks of gestation; a ratio below 150 µg/g was not significantly associated with lower nonverbal or verbal IQ (Levie 2019).
• Small Italian cohort — Vermiglio 2004 — attention-deficit hyperactivity disorder was diagnosed in 11 of 16 children from a moderately iodine-deficient area and in none of 11 children from a marginally iodine-sufficient area (Vermiglio 2004).

Supplementation trials. In a randomized, double-blind, placebo-controlled trial in Bangalore and Bangkok, 832 mildly iodine-deficient pregnant women (median urinary iodine 131 µg/L) received 200 µg of iodine daily or placebo until delivery; at age 5–6 years, verbal IQ, performance IQ and executive-function scores did not differ between the groups, and the authors concluded that supplementation had no effect on child neurodevelopment (Gowachirapant 2017). A 2020 systematic review of 37 publications found that most studies showed no effect of supplementation on maternal or infant TSH and free T4, while most trials found reduced maternal thyroglobulin; a meta-analysis of two trials showed no effect on child cognitive, language or motor scores, and the authors concluded that there is insufficient good-quality evidence to support current recommendations for iodine supplementation in pregnancy in areas of mild-to-moderate deficiency, calling for trials in moderately deficient women (Dineva 2020). Pearce and colleagues had noted in 2016 that the long-term benefits and safety of such supplementation were uncertain (Pearce 2016).

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Modern U.S. Pregnancy Iodine Status

The U.S. National Health and Nutrition Examination Survey (NHANES) tracks urinary iodine in representative samples of the population:

• Median urinary iodine fell by more than 50% between 1971–1974 and 1988–1994 while still indicating adequate intake for the population as a whole; urinary iodine below 5 µg/dL was found in 6.7% of pregnant women and 14.9% of women of child-bearing age in 1988–1994 (Hollowell 1998).
• The American Thyroid Association's 2006 statement reported a U.S. median of 168 µg/L in 2001–2002, and 173 µg/L in pregnant women (ATA Public Health Committee 2006).
• The NHANES median fell from 164 µg/L in 2007–2008 to 144 µg/L in 2009–2010. The median for all pregnant women in NHANES 2005–2010 was 129 µg/L, below the adequate range; women in the third trimester had adequate levels (172 µg/L), while those in the first and second trimesters did not (Caldwell 2013).
• In NHANES 2011–2014, 72.2% of pregnant women used a dietary supplement but only 17.8% used one containing iodine (Gupta 2018).

The CDC authors describe iodine-containing supplement use among pregnant and lactating women as remaining low in contrast with current recommendations (Gupta 2018). The cohort studies above were done in the UK, Australia, Spain and the Netherlands rather than the United States, and the trial evidence in mild deficiency has not shown a benefit for child neurodevelopment (Dineva 2020).

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What Guidelines and Studies Report for Preconception, Pregnancy and Lactation

The positions below are what the named bodies and studies state; decisions about supplements in pregnancy belong with a clinician.

• American Thyroid Association (2006) — recommends that women receive 150 µg of iodine as a daily supplement during pregnancy and lactation, and that all prenatal vitamin/mineral preparations contain 150 µg of iodine (ATA Public Health Committee 2006). A CDC analysis describes the ATA recommendation as starting 3 months before conception (Gupta 2018). The ATA's 2017 pregnancy guideline also covers iodine nutrition (Alexander 2017).
• WHO — recommends 250 µg/day in pregnancy, and treats a median urinary iodine of 150–249 µg/L as adequate in pregnant women (Zimmermann 2009, Am J Clin Nutr).
• The evidence behind supplementation in mild deficiency — the Dineva 2020 review concluded that good-quality evidence is insufficient to support current supplementation recommendations in areas of mild-to-moderate deficiency, and the largest trial found no effect on child neurodevelopment (Dineva 2020; Gowachirapant 2017).
• Seaweed and kelp — iodine content in 12 seaweed species ranged from 16 µg/g in nori to over 8,165 µg/g in one sample of processed kelp granules, and varied with harvest and storage conditions, making the iodine content of prepared foods difficult to estimate (Teas 2004).
• Excess iodine in pregnancy — in 7,190 women at 4–8 weeks of pregnancy in an iodine-sufficient region of China, urinary iodine of 250 µg/L or more was associated with a higher risk of maternal subclinical hypothyroidism, and 500 µg/L or more with a higher risk of maternal isolated hypothyroxinemia (Shi 2015). Pearce and colleagues note that safe upper limits for iodine intake in pregnancy have not been well defined (Pearce 2016). The Wolff-Chaikoff effect is a fall in thyroid hormone synthesis after a large iodide dose, from which the gland normally escapes in about two days (Eng 1999; Leung and Braverman 2014). The high-dose protocol described by the physician Guy Abraham and David Brownstein (12.5–50 mg/day) lies far above the WHO pregnancy figure of 250 µg/day.
• Selenium — the iodothyronine deiodinases that activate and inactivate thyroid hormone are selenoenzymes (Bianco 2002). In cretinism, combined selenium and iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism (Delange 2001). In a randomized, placebo-controlled trial in pregnant women with thyroid peroxidase antibodies (77 given selenomethionine 200 µg/day during and after pregnancy, 74 given placebo), the selenium group had less postpartum thyroid dysfunction (28.6% vs 48.6%) and less permanent hypothyroidism (11.7% vs 20.3%) than placebo (Negro 2007). The thyroid-cofactor research is covered on the Selenium page.

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Key Research Papers

1. Hetzel BS (1983). Iodine deficiency disorders (IDD) and their eradication. Lancet 2(8359):1126-1129 — PubMed PMID: 6138653
2. Qian M, Wang D, Watkins WE, Gebski V, Yan YQ, Li M, Chen ZP (2005). The effects of iodine on intelligence in children: a meta-analysis of studies conducted in China. Asia Pac J Clin Nutr 14(1):32-42 — PubMed PMID: 15734706
3. 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). Lancet 382(9889):331-337 — PubMed PMID: 23706508
4. Zimmermann MB (2009). Iodine deficiency. Endocrine Reviews 30(4):376-408 — PubMed PMID: 19460960
5. Delange F (2001). Iodine deficiency as a cause of brain damage. Postgrad Med J 77(906):217-220 — PubMed PMID: 11264481
6. Morreale de Escobar G, Obregon MJ, Escobar del Rey F (2004). Role of thyroid hormone during early brain development. Eur J Endocrinol 151 Suppl 3:U25-U37 — PubMed PMID: 15554884
7. Bougma K, Aboud FE, Harding KB, Marquis GS (2013). Iodine and mental development of children 5 years old and under: a systematic review and meta-analysis. Nutrients 5(4):1384-1416 (erratum in Nutrients 2014;6(12):5770-5771) — PubMed PMID: 23609774
8. Caldwell KL, Pan Y, Mortensen ME, Makhmudov A, Merrill L, Moye J (2013). Iodine status in pregnant women in the National Children's Study and in U.S. women (15-44 years), National Health and Nutrition Examination Survey 2005-2010. Thyroid 23(8):927-937 — PubMed PMID: 23488982
9. 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. Am J Clin Nutr 104 Suppl 3:918S-923S — PubMed PMID: 27534632
10. Vermiglio F, Lo Presti VP, Moleti M, Sidoti M, Tortorella G, Scaffidi G, Castagna MG, Mattina F, Violi MA, Crisà A, Artemisia A, Trimarchi F (2004). Attention deficit and hyperactivity disorders in the offspring of mothers exposed to mild-moderate iodine deficiency: a possible novel iodine deficiency disorder in developed countries. J Clin Endocrinol Metab 89(12):6054-6060 — PubMed PMID: 15579758
11. Public Health Committee of the American Thyroid Association; Becker DV, Braverman LE, Delange F, Dunn JT, Franklyn JA, Hollowell JG, Lamm SH, Mitchell ML, Pearce E, Robbins J, Rovet JF (2006). Iodine supplementation for pregnancy and lactation — United States and Canada: recommendations of the American Thyroid Association. Thyroid 16(10):949-951 — PubMed PMID: 17042677
12. Hynes KL, Otahal P, Hay I, Burgess JR (2013). Mild iodine deficiency during pregnancy is associated with reduced educational outcomes in the offspring: 9-year follow-up of the gestational iodine cohort. J Clin Endocrinol Metab 98(5):1954-1962 — PubMed PMID: 23633204
13. de Escobar GM, Obregón MJ, del Rey FE (2004). Maternal thyroid hormones early in pregnancy and fetal brain development. Best Pract Res Clin Endocrinol Metab 18(2):225-248 — PubMed PMID: 15157838
14. Gowachirapant S, Jaiswal N, Melse-Boonstra A, Galetti V, Stinca S, Mackenzie I, Thomas S, Thomas T, Winichagoon P, Srinivasan K, Zimmermann MB (2017). Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. Lancet Diabetes Endocrinol 5(11):853-863 — PubMed PMID: 29030199
15. Dineva M, Fishpool H, Rayman MP, Mendis J, Bath SC (2020). Systematic review and meta-analysis of the effects of iodine supplementation on thyroid function and child neurodevelopment in mildly-to-moderately iodine-deficient pregnant women. Am J Clin Nutr 112(2):389-412 — PubMed PMID: 32320029
16. Levie D, Korevaar TIM, Bath SC, Murcia M, Dineva M, Llop S, Espada M, van Herwaarden AE, de Rijke YB, Ibarluzea JM, Sunyer J, Tiemeier H, Rayman MP, Guxens M, Peeters RP (2019). Association of maternal iodine status with child IQ: a meta-analysis of individual participant data. J Clin Endocrinol Metab 104(12):5957-5967 — PubMed PMID: 30920622
17. Zimmermann MB, Andersson M (2021). Global perspectives in endocrinology: coverage of iodized salt programs and iodine status in 2020. Eur J Endocrinol 185(1):R13-R21 — PubMed PMID: 33989173
18. Zimmermann MB (2009). Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. Am J Clin Nutr 89(2):668S-672S — PubMed PMID: 19088150
19. Hollowell JG, Staehling NW, Hannon WH, Flanders DW, Gunter EW, Maberly GF, Braverman LE, Pino S, Miller DT, Garbe PL, DeLozier DM, Jackson RJ (1998). Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994). J Clin Endocrinol Metab 83(10):3401-3408 — PubMed PMID: 9768638
20. Gupta PM, Gahche JJ, Herrick KA, Ershow AG, Potischman N, Perrine CG (2018). Use of iodine-containing dietary supplements remains low among women of reproductive age in the United States: NHANES 2011-2014. Nutrients 10(4):422 — PubMed PMID: 29596306
21. Alexander EK, Pearce EN, Brent GA, Brown RS, Chen H, Dosiou C, Grobman WA, Laurberg P, Lazarus JH, Mandel SJ, Peeters RP, Sullivan S (2017). 2017 Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid 27(3):315-389 — PubMed PMID: 28056690
22. Shi X, Han C, Li C, Mao J, Wang W, Xie X, Li C, Xu B, Meng T, Du J, Zhang S, Gao Z, Zhang X, Fan C, Shan Z, Teng W (2015). Optimal and safe upper limits of iodine intake for early pregnancy in iodine-sufficient regions: a cross-sectional study of 7190 pregnant women in China. J Clin Endocrinol Metab 100(4):1630-1638 — PubMed PMID: 25629356
23. Teas J, Pino S, Critchley A, Braverman LE (2004). Variability of iodine content in common commercially available edible seaweeds. Thyroid 14(10):836-841 — PubMed PMID: 15588380
24. Doerge DR, Sheehan DM (2002). Goitrogenic and estrogenic activity of soy isoflavones. Environ Health Perspect 110 Suppl 3:349-353 — PubMed PMID: 12060828
25. Negro R, Greco G, Mangieri T, Pezzarossa A, Dazzi D, Hassan H (2007). The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. J Clin Endocrinol Metab 92(4):1263-1268 — PubMed PMID: 17284630
26. Eng PH, Cardona GR, Fang SL, Previti M, Alex S, Carrasco N, Chin WW, Braverman LE (1999). Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein. Endocrinology 140(8):3404-3410 — PubMed PMID: 10433193
27. Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR (2002). Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev 23(1):38-89 — PubMed PMID: 11844744
28. Leung AM, Braverman LE (2014). Consequences of excess iodine. Nat Rev Endocrinol 10(3):136-142 — PubMed PMID: 24342882

PubMed Topic Searches

1. PubMed: Iodine and fetal brain development
2. PubMed: Cretinism forms
3. PubMed: Universal salt iodization
4. PubMed: ALSPAC iodine cohort
5. PubMed: Maternal-fetal thyroid hormone transfer

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Connections

• All Minerals
• Iodine Benefits Hub
• Iodine Overview
• Iodine for Thyroid Function
• Iodine for Breast Health
• Iodine for Metabolism & Energy
• Selenium
• Tyrosine
• Infertility
• Hashimoto's Thyroiditis
• Brain Fog
• Vitamin D3 (pregnancy)
• Omega-3 (DHA for fetal brain)
• Folate (neural tube)
• Fluoride (thyroid suppressor)
• Deficiency
• Toxicity
• History

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