Abnormal Development - Iodine Deficiency

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5B5K.3 Iodine deficiency - Iodine deficiency disorders (IDD), caused mainly by a low dietary supply of iodine, refer to all of the consequences of iodine deficiency in a population that can be prevented by ensuring that the population has an adequate intake of iodine. Iodine deficiency is the most frequent cause of preventable brain damage in childhood.

5A00.04 Congenital hypothyroidism due to iodine deficiency - Hypothyroidism is a condition which arises at birth where the thyroid gland produces too little or no thyroid hormone and it can be induced by iodine-deficiency.


Iodinated Salt
Folic acid and iodine fortification (2016)

Iodine deficiency disorders (IDD) is the single most common cause of preventable mental retardation and brain damage in the world. Iodine (Greek, ioeides = violet) is required for the synthesis of thyroid hormone, a key regulator of neurological development. IDD causes goiters and decreases the production of hormones vital to growth and development.

  • 1.6 billion people are at risk
  • IDD affects 50 million children
  • 100,000 cretins are born every year

Children with IDD can grow up stunted, apathetic, mentally retarded and incapable of normal movement, speech or hearing. IDD in pregnant women cause miscarriage, stillbirth and mentally retarded children. A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly. In areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace, food fortification and supplementation have proven highly successful and sustainable interventions. Iodized salt programs and iodized oil supplements are the most common tools in the fight against IDD.

In Australia, salt (where identified) and most breads (except organic varieties) are fortified with iodine. Before mandatory iodine fortification was introduced large proportions of the Australian and New Zealand population had inadequate iodine intakes based upon national surveys measuring median urinary iodine concentration (MUIC) in schoolchildren, an indicator of overall population status, confirmed mild iodine deficiency in both countries. The concentration was 96 μg per litre in Australia, and 66 μg per litre in New Zealand, less than the 100–200 μg per litre considered optimal.

Australia 2018 - Iodine requirements increase during pregnancy and a supplement of 150 micrograms a day is recommended.[1]

Iodine Links: thyroid | neural | neural abnormalities

Nutrition Links: nutrition | Vitamin A | Vitamin B | Vitamin C | Vitamin D | Vitamin E | Vitamin K | folate | iodine deficiency | neural abnormalities | Axial Skeleton Abnormalities

Environmental Links: Introduction | low folic acid | iodine deficiency | Nutrition | Drugs | Australian Drug Categories | USA Drug Categories | thalidomide | herbal drugs | Illegal Drugs | smoking | Fetal Alcohol Syndrome | TORCH | viral infection | bacterial infection | fungal infection | zoonotic infection | toxoplasmosis | Malaria | maternal diabetes | maternal hypertension | maternal hyperthermia | Maternal Inflammation | Maternal Obesity | hypoxia | biological toxins | chemicals | heavy metals | air pollution | radiation | Prenatal Diagnosis | Neonatal Diagnosis | International Classification of Diseases | Fetal Origins Hypothesis

Some Recent Findings

  • Association of Maternal Iodine Status With Child IQ: A Meta-Analysis of Individual Participant Data[2] Although the consequences of severe iodine deficiency are beyond doubt, the effects of mild to moderate iodine deficiency in pregnancy on child neurodevelopment are less well established. OBJECTIVE: To study the association between maternal iodine status during pregnancy and child IQ and identify vulnerable time windows of exposure to suboptimal iodine availability. DESIGN: Meta-analysis of individual participant data from three prospective population-based birth cohorts: Generation R (Netherlands), INMA (Spain), and ALSPAC (United Kingdom); pregnant women were enrolled between 2002 and 2006, 2003 and 2008, and 1990 and 1992, respectively. SETTING: General community. PARTICIPANTS: 6180 mother-child pairs with measures of urinary iodine and creatinine concentrations in pregnancy and child IQ. Exclusion criteria were multiple pregnancies, fertility treatment, medication affecting the thyroid, and preexisting thyroid disease. CONCLUSIONS: Fetal brain development is vulnerable to mild to moderate iodine deficiency, particularly in the first trimester. Our results show that potential randomized controlled trials investigating the effect of iodine supplementation in women with mild to moderate iodine deficiency on child neurodevelopment should begin supplementation not later than the first trimester."
  • The Association of Maternal Iodine Status in Early Pregnancy with Thyroid Function in the Swedish Environmental Longitudinal, Mother and Child, Asthma and Allergy Study[3] "Severe maternal iodine deficiency can impact fetal brain development through effects on maternal and/or fetal thyroid hormone availability. The effects of mild-to-moderate iodine deficiency on thyroid function are less clear. The aim was to investigate the association of maternal urinary iodine concentration corrected for creatinine (UI/Creat) with thyroid function and autoantibodies in a mild-to-moderate iodine-deficient pregnant population. Methods: This study was embedded within the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy (SELMA) study. Conclusions: We could not identify any meaningful differences in thyroid function reference ranges. Lower iodine availability was associated with a slightly lower TSH and a higher TT4. Women with adequate iodine intake had the lowest risk of TPOAb positivity."
  • Review - Systemic endocrinopathies (thyroid conditions and diabetes): impact on postnatal life of the offspring[4] "Fetal programming may influence childhood and adult life, determining the risk of specific diseases. During earlier stages of pregnancy, the transfer of maternal thyroid hormones to the fetus is vital for adequate neurologic development. The presence of severe maternal thyroid dysfunction, particularly severe iodine deficiency, is devastating, leading to irreversible neurologic sequelae. Moreover, mild maternal thyroid conditions, such as a mild-to-moderate iodine deficiency, may also lead to milder neurologic and behavioral conditions later during the life of the offspring. Maternal dysglycemia due to pregestational or gestational diabetes mellitus is another common situation in which fetal development encounters a hostile environment. Hyperglycemia in utero may trigger metabolic conditions in the offspring, including abnormalities of glucose tolerance and weight excess. Physicians assisting pregnant women have to be aware about these conditions, because they may go unnoticed if not properly screened. Because an early diagnosis and appropriate management may prevent most of the possible negative consequences for the progeny, the prevention, early diagnosis, and proper management of these endocrine conditions should be offered to all women undergoing pregnancy. Here, we comprehensively review the current evidence about the effects of maternal thyroid dysfunction and maternal dysglycemia on the cognitive function and carbohydrate metabolism in the offspring, two prevalent conditions of utmost importance for the child's health and development."
  • Iodine Supplementation in Pregnancy - is it time?[5] "Iodine is essential for the synthesis of thyroid hormone and optimal fetal neurological development. Pregnant women living in borderline or moderate-severe iodine deficient areas are at particularly high risk of being iodine deficient, and this may have important clinical consequences, particularly for the neurocognitive development of the offspring. It is a substantial problem and many countries including the UK are mild-moderately iodine deficient. Although the detrimental effects of severe iodine deficiency are well recognised, the benefits of correcting mild-to-moderate iodine deficiency are unclear due to a lack of randomized controlled trials in this area. However, observational data increasingly indicate that there may be substantial health and economic benefits from correcting iodine deficiency in pregnancy. There is now a growing trend from learned societies that iodine supplementation should be utilized in pregnancy in countries with mild-to-moderate iodine deficiency."
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  • Australia NHMRC - Iodine supplementation for Pregnant and Breastfeeding Women [6] "NHMRC and the New Zealand Ministry of Health recommend that women who are pregnant have 220μg of iodine per day. Women who are breastfeeding should have 270μg per day. The World Health Organization (WHO) recommends women who are pregnant or breastfeeding take a daily oral iodine supplement so that the total daily intake is 250μg. Pregnant and breastfeeding women need to top up their dietary iodine intake because of the increased requirements during pregnancy and breastfeeding and the likelihood that they won’t get enough from their diet and mandatory fortification."
  • Neonatal thyroid status in an area of iodine sufficiency[7] "The aim of present study was to assess urinary iodine excretion (UIE) in the three trimesters of pregnancy and evaluate its association with newborn thyroid function in Tehran, an area of iodine sufficiency. Fifty-two pregnant women (38%) had median UIE<150 microg/L and 86 had (62%) UIE≥150 microg/L. Median UIE in groups I and II in the first, second and third trimesters were 125 and 212 microg/L, 97 and 213 microg/L, 93 and 227microg/L respectively. No significant difference was seen in thyroid function of newborns in the two groups. Mean concentrations of T4, T3, FT4 and TSH of newborn did not show significant difference in median UIE of mothers in various quartiles. This study shows that newborns, irrespective of mothers' UIE, in an area with sustained iodine supplementation program, may not be at risk of alterations in thyroid functions."
  • Food Standards Australia New Zealand (FSANZ) - 22nd Australian Total Diet Study A total diet study of five trace elements: iodine, selenium, chromium, molybdenum, and nickel.
  • Modest Thyroid Hormone Insufficiency during Development Induces a Cellular Malformation in the Corpus Callosum: A Model of Cortical Dysplasia[8] "Whilst the majority of Australians had dietary intakes approaching or above the estimated average requirement (EAR) or AI for selenium, molybdenum and chromium, a substantial proportion of the population had iodine intakes below the EAR. FSANZ has subsequently commissioned further analyses of iodine levels in Australian foods and will be introducing mandatory fortification of iodine in bread, from September 2009."

WHO Statistics

World map iodine status 2007.jpg

World map iodine status (2007)[9]

Iodine and Thyroid Hormone

Thyroxine (T4) molecular structure showing iodine positions (red rings).

Iodine incorporated into thyroid horomone, Thyroxine (T4)


Salt shaker.jpg The World Health Organization has made progress recently since the primary intervention strategy for IDD control, Universal Salt Iodization (USI), was adopted in 1993. Iodization can be carried out using potassium iodide or potassium iodate; or sodium iodide or sodium iodate.

Salt was chosen because it is widely available and consumed in regular amounts throughout the year, and because the costs of iodizing it are extremely low - only about US$0.05 per person per year.

Where salt iodization has been in place for over five years, improvement in iodine status has been overwhelming.Over the last decade, the number of countries with salt iodization programmes doubled, rising from 46 to 93. As a result, today 68% of the 5 billion people living in countries with IDD have access to iodized salt and the global rates of goitre, mental retardation and cretinism are falling fast.

(some text information from WHO page)

Iodine Requirements

The current WHO recommended daily iodine intakes are:

  • 50 micrograms for infants (first 12 months of age)
  • 90 micrograms for children (2-6 years of age)
  • 120 micrograms for school children (7-12 years of age)
  • 150 micrograms for adults (beyond 12 years of age)
  • 200 micrograms for pregnant and lactating women

Links: WHO - Micronutrient deficiencies Eliminating iodine deficiency disorders | WHO - Iodine data by country

Thyroid System and Neural Development

Human thyroid system and neural development.jpg

Links: Neural System Development

I - Iodine

This information is about Iodine the element, dietry intake is in the form of iodine as a salt. The solid halogen was discovered in 1811 by Bernard Courtois (1777-1838) in seaweed. Iodine (Greek, ioeides = violet) was named for the color of its vapour.

  • Atomic number 53
  • Density g/mL 4.92
  • Atomic weight u 126.9045
  • Melting point K 386.7
  • Bonding radius A 1.33
  • Boiling point K 458.4
  • Atomic radius A 1.32
  • Heat of vaporization kJ/mol 20.752
  • Ionization Potential V 10.451
  • Heat of fusion kJ/mol 7.824
  • Electronegativity - 2.66
  • Specific heat J/gK 0.214
  • The oxide is a strong acid.
  • Crystal are orthorhombic.
  • Iodine has been used for its antibacterial qualities.

Congenital Hypothyroidism (CH)

This condition is not caused by iodine defficiency. Defined as thyroid hormone deficiency present at birth and occurs in approximately 1:2,000 to 1:4,000 newborns.[10] The condition is classified into permanent and transient forms that can be divided into primary, secondary, or peripheral etiologies.

  • thyroid dysgenesis accounts for 85% of permanent primary
  • inborn errors of thyroid hormone biosynthesis (dyshormonogeneses) account for 10-15% of cases

Australian Data

Mandatory iodine fortification of bread, through the replacement of salt with iodised salt in the making of bread, was implemented in October 2009 in Australia and in November 2009 in New Zealand.

Food Standards Australia New Zealand

Report June 2016: [http://www.foodstandards.gov.au/publications/Pages/Iodine-in-bread-report-.aspx

Monitoring the Australian population’s intake of dietary iodine before and after mandatory fortification]

IDD Prevalence and Control Program

IDD Prevalence and Control Program Data

(For other countries see also IDD Regional Data Page)

IDD Prevalence and Control Program Data

Last Modified: 6/98


I. IDD Prevalence


No national IDD data. Goiter historically limited to mountains of east and Tasmania. Before prophylaxis was introduced in 1950, IDD was greater than 50%. Presently, IDD not likely.


Not present


Neonatal TSH in screening shows levels compatible with iodine sufficiency, including Tasmania.

Urinary Iodine:

Current values: Tasmania 229-356 mcg/L, Sydney 180 mcg/L.

II. Salt Legislation

  • Legislation:
  • Legislation for Animals: No legislation, but widely used.
  • Level Salt Iodization Required (ppm): 50
  • Compound: KI
  • Year Enacted: NA
  • Latest Revision: NA

III. IDD Coordination

IDD Responsible Parties:

No national surveillance program

IV. Salt Supply

  • Is Iodized Salt Available: Yes
  • Percent Iodized Salt Available: No Data Available
  • Percent of Salt Which is Imported:Australia is salt exporter
  • Salt Imported from: NA
  • Salt Production:

Iodized table salt has been available for over 50 years. However, noniodized salt is preferred and data indicate that less than a third of the consumed salt is iodized.

  • Iodine (ppm): 50
  • Compound: KI
  • Method of Iodization: No Data Available
  • Package Method: No Data Available
  • Estimated daily per capita salt consumption: No Data Available
  • Estimated % of all salt consumed by people which is adequately iodized (household level): No Data Available
  • Cost of Iodized Salt (kg): No Data Available
  • Cost of Uniodized Salt (kg): No Data Available
  • Year: No Data Available
  • Price differential between city and rural areas: No Data Available
  • Estimated difference (urban/rural, %): No Data Available
  • Time between production and consumption of iodized salt in remote areas (weeks): No Data Available

V. Supplementation:

  • Total Number Supplemented:None
  • % administered orally: NA
  • % administered by injection: None
  • Target Population: None.
  • Other Supplementation Activities:

Iodized bread was introduced in 1963 in Canberra and in 1966 in Tasmania. It continues to be a source of iodine.

VI. Monitoring Activities

The following indicators are available to monitor IDD:

  • Goitre:
  • Urinary Iodine:
  • Salt:

VII. Comments

Dietary diversification and use of iodine in farm animals has contributed to iodine sufficiency, and iodine deficiency does not appear a current problem. However, no national surveillance system exists. Recent informal reports raise questions of return of iodine deficiency to Tasmania and assessment is underway (1998).

VIII. Sources

IDD NL 9(1):11, 1993

Links: Australia New Zealand Food Standards Code STANDARD 2.10.2 SALT AND SALT PRODUCTS


  1. Department of Health (2018) Clinical Practice Guidelines: Pregnancy Care. Canberra: Australian Government Department of Health. (5 June 2019)
  2. 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, 5957-5967. PMID: 30920622 DOI.
  3. Levie D, Derakhshan A, Shu H, Broeren MAC, de Poortere RA, Peeters RP, Bornehag CG, Demeneix B & Korevaar TIM. (2019). The Association of Maternal Iodine Status in Early Pregnancy with Thyroid Function in the Swedish Environmental Longitudinal, Mother and Child, Asthma and Allergy Study. Thyroid , , . PMID: 31524090 DOI.
  4. Nattero-Chávez L, Luque-Ramírez M & Escobar-Morreale HF. (2019). Systemic endocrinopathies (thyroid conditions and diabetes): impact on postnatal life of the offspring. Fertil. Steril. , 111, 1076-1091. PMID: 31155115 DOI.
  5. Taylor PN & Vaidya B. (2016). Iodine supplementation in pregnancy - is it time?. Clin. Endocrinol. (Oxf) , 85, 10-4. PMID: 26998765 DOI.
  6. NHMRC Iodine supplementation for Pregnant and Breastfeeding Women (2010) Online | PDF
  7. Azizi F, Hosseini MS, Amouzegar A, Tohidi M & Ainy E. (2011). Neonatal thyroid status in an area of iodine sufficiency. J. Endocrinol. Invest. , 34, 197-200. PMID: 20959719 DOI.
  8. Goodman JH & Gilbert ME. (2007). Modest thyroid hormone insufficiency during development induces a cellular malformation in the corpus callosum: a model of cortical dysplasia. Endocrinology , 148, 2593-7. PMID: 17317780 DOI.
  9. Bruno de Benoist, B Erin McLean, Maria Andersson, and Lisa Rogers Iodine deficiency in 2007: Global progress since 1993. Food and Nutrition Bulletin, vol. 29, no. 3 © 2008, The United Nations University. PDF
  10. Rastogi MV & LaFranchi SH. (2010). Congenital hypothyroidism. Orphanet J Rare Dis , 5, 17. PMID: 20537182 DOI.


Zimmermann MB & Crill CM. (2010). Iodine in enteral and parenteral nutrition. Best Pract. Res. Clin. Endocrinol. Metab. , 24, 143-58. PMID: 20172478 DOI.

Hess SY. (2010). The impact of common micronutrient deficiencies on iodine and thyroid metabolism: the evidence from human studies. Best Pract. Res. Clin. Endocrinol. Metab. , 24, 117-32. PMID: 20172476 DOI.

Bürgi H. (2010). Iodine excess. Best Pract. Res. Clin. Endocrinol. Metab. , 24, 107-15. PMID: 20172475 DOI.


Andersson M, Aeberli I, Wüst N, Piacenza AM, Bucher T, Henschen I, Haldimann M & Zimmermann MB. (2010). The Swiss iodized salt program provides adequate iodine for school children and pregnant women, but weaning infants not receiving iodine-containing complementary foods as well as their mothers are iodine deficient. J. Clin. Endocrinol. Metab. , 95, 5217-24. PMID: 20810570 DOI.

Mackerras D, Powers J, Boorman J, Loxton D & Giles GG. (2011). Estimating the impact of mandatory fortification of bread with iodine on pregnant and post-partum women. J Epidemiol Community Health , 65, 1118-22. PMID: 20709857 DOI.

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  • IDD - Iodine deficiency disorder
  • WHO - World Health Organization

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Cite this page: Hill, M.A. (2024, May 25) Embryology Abnormal Development - Iodine Deficiency. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Iodine_Deficiency

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