Hynes, KL and Otahal, P and Hay, I and Burgess, JR, Mild Iodine Deficiency During Pregnancy is Associated with Reduced Educational Outcomes in the Offspring: 9-Year Follow-up of the Gestational Iodine Cohort, Prenatal and Childhood Nutrition: Evaluating the Neurocognitive Connections, Apple Academic Press, Inc., C Croft (ed), United States, pp. 193-210. ISBN 978-1-77188-094-7 (2015) [Research Book Chapter]
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Iodine is essential for neurodevelopment in utero and in childhood, with deficiency being a major cause of preventable intellectual impairment (1). The serious neurodevelopmental consequences of severe iodine deficiency (ID) on the fetus are well documented and include cretinism, which manifests as motor, cognitive, and auditory defects (2). ID, however, results in a spectrum of disorders with many speculating that even mild maternal ID has subtle impacts on fetal development. Recent reviews are not conclusive as to whether low maternal dietary iodine intake in areas of mild deficiency leads to measurable effects on cognition and neurodevelopment of the offspring (3, 4).
Clinical trials of iodine supplementation in pregnancy in regions of mild ID have typically focused on positive changes in maternal and fetal thyroid function and volumes but have not examined long-term developmental consequences in the offspring. To our knowledge, there are only three studies reporting neurodevelopmental outcomes in offspring after supplementation of mothers with mild ID. Berbel et al (5) reported significantly delayed neurobehavioral performance in children (aged 18 months) if their mothers did not receive iodine supplementation by 4 to 6 weeks of gestation. Similarly, Velasco et al (6) found that children (aged 3–18 months) had higher psychomotor development scores if their mothers were given supplements from the first trimester. Both interventions provide preliminary evidence that even mild gestational ID may have an adverse impact on fetal neurodevelopment and subsequent infant functioning. In contrast, Murcia et al (7) reported that higher maternal intake of iodine-containing supplements was associated with lower scores on the Psychomotor Development Index of the Bayley Scales of Infant Development in their children (aged 1 year).
In addition to gestational studies, there is increasing evidence from observational population studies that less severe cognitive and motor impairment occurs in apparently normal individuals from areas of ID (8). Children without cretinism from iodine-deficient regions of Iran were found to have growth retardation and neurological, auditory, and psychomotor impairments (9). Boyages et al (10) reported impaired intellectual and neuromotor development in apparently normal Chinese children, with a shift in the distribution of cognitive skills to a lower level. Furthermore, randomized controlled trial data show that postgestational supplementation can lead to significantly improved mental performance of children from areas of mild (11), moderate (12), and severe ID (13).
We compared educational outcomes of children (aged 9 years) born to women assessed as being iodine deficient (urinary iodine concentration [UIC] <150 μg/L) or sufficient (UIC ≥150 μg/L) during pregnancy. Gestation occurred during 1999–2001, a documented period of mild ID (median UIC, 77.5 μg/L) in the Tasmanian population (14), with the children subsequently growing up in an environment considered to be replete (14, 15) (median UIC, 108.0 μg/L) after introduction of voluntary iodine fortification (16). We investigate whether mild gestational ID has long-term effects on educational outcomes.
|Item Type:||Research Book Chapter|
|Keywords:||iodine deficiency, pregnancy, childhood, literacy|
|Research Division:||Medical and Health Sciences|
|Research Group:||Public Health and Health Services|
|Objective Group:||Clinical Health (Organs, Diseases and Abnormal Conditions)|
|Objective Field:||Endocrine Organs and Diseases (excl. Diabetes)|
|Author:||Hynes, KL (Dr Kristen Hynes)|
|Author:||Otahal, P (Mr Petr Otahal)|
|Author:||Hay, I (Professor Ian Hay)|
|Author:||Burgess, JR (Dr John Burgess)|
|Deposited By:||Menzies Institute for Medical Research|
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