Abstract
Maternal iodine requirements increase during pregnancy to supply thyroid hormones critical for fetal neurodevelopment. Iodine insufficiency may result in poorer cognitive or child educational outcomes but current evidence is sparse and inconsistent. To quantify the association between maternal iodine status and child educational outcomes. Urinary iodine concentrations (UIC) and iodine/creatinine ratios (I:Cr) were measured in 6971 mothers at 26-28weeks' gestation participating in the Born in Bradford cohort. Maternal iodine status was examined in relation to child school achievement (early years foundation stage (EYFS), phonics, and Key Stage 1 (KS1)), other learning outcomes, social and behavioural difficulties, and sensorimotor control in 5745 children aged 4-7years. Median (interquartile range) UIC was 76µg/L (46, 120), and I:Cr was 83µg/g (59, 121). Overall, there was no strong or consistent evidence to support associations between UIC or I:Cr and neurodevelopmental outcomes. For instance, predicted EYFS and phonics scores (primary outcomes) at the 25th vs 75th I:Cr percentiles (99% confidence intervals) were similar, with no evidence of associations: EYFS scores were 32 (99% CI 31, 33) and 33 (99% CI 32, 34), and phonics scores were 34 (99% CI 33, 35) and 35 (99% CI 34, 36), respectively. In the largest single study of its kind, there was little evidence of detrimental neurodevelopmental outcomes in children born to pregnant women with iodine insufficiency as defined by World Health Organization-outlined thresholds. Alternative functional biomarkers for iodine status in pregnancy and focused assessment of other health outcomes may provide additional insight.
Highlights
Maternal iodine requirements increase during pregnancy to supply thyroid hormones critical for fetal neurodevelopment
Urinary iodine concentrations (UIC) and iodine/creatinine ratios (I:Cr) were measured in 6971 mothers at 26-28 weeks' gestation participating in the Born in Bradford cohort
Maternal iodine status was examined in relation to child school achievement (early years foundation stage (EYFS), phonics, and Key Stage 1 (KS1)), other learning outcomes, social and behavioural difficulties, and sensorimotor control in 5745 children aged 4-7 years
Summary
Maternal iodine requirements increase during pregnancy to supply thyroid hormones critical for fetal neurodevelopment. Conclusions: In the largest single study of its kind, there was little evidence of detrimental neurodevelopmental outcomes in children born to pregnant women with iodine insufficiency as defined by World Health Organization–outlined thresholds. Iodine is an essential mineral required for thyroid hormone production, supporting normal metabolic processes throughout the life course.[1] During pregnancy, iodine demands increase to support normal fetal development and compensate for increased renal iodine clearance.[2] Because thyroid hormones are necessary for normal neuronal migration and myelination during brain development, severe maternal iodine deficiency can potentially hinder child growth and development, including psychomotor and neurological development.[1,3] Irreversible mental retardation and neurological abnormalities can result from hypothyroxinaemia during critical developmental periods.[2]. The World Health Organization defines iodine insufficiency in pregnant populations as median urinary iodine concentration (UIC) < 150 μg/L, with several studies reporting insufficient iodine status in pregnant women at this concentration, but there is little evidence for the functional importance of this threshold.[1,5]
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