Maternal iodine status in a multi-ethnic UK birth cohort: associations with autism spectrum disorder

Kirsten J Cromie ,Barry Wright,Charles J.p Snart ,Paul M Stewart,Amanda H Waterman,Janet Cade ,Nigel Simpson ,Brian Kelly,Diane Threapleton ,Sean D Reid ,Amanda Mckillion,Nisreen A Alwan ,Elizabeth R Taylor ,Michael Zimmermann,Claire Keeble,John Wright,Sarah Meadows,Rafaq Azad,Mark Mon-Williams,Dagmar Waiblinger,Dan Mason,Laura J Hardie,Darren C Greenwood

doi:10.1186/s12887-020-02440-y

Abstract

BackgroundMaternal iodine requirements increase during pregnancy to supply thyroid hormones essential for fetal brain development. Maternal iodine deficiency can lead to hypothyroxinemia, a reduced fetal supply of thyroid hormones which, in the first trimester, has been linked to an increased risk of autism spectrum disorder (ASD) in the child. No study to date has explored the direct link between maternal iodine deficiency and diagnosis of ASD in offspring.MethodsUrinary iodine concentrations (UIC) and iodine/creatinine ratios (I:Cr) were measured in 6955 mothers at 26–28 weeks gestation participating in the Born in Bradford (BiB) cohort. Maternal iodine status was examined in relation to the probability of a Read (CTV3) code for autism being present in a child’s primary care records through a series of logistic regression models with restricted cubic splines.ResultsMedian (inter-quartile range) UIC was 76 μg/L (46, 120) and I:Cr was 83 μg/g (59, 121) indicating a deficient population according to WHO guidelines. Ninety two children (1·3%) in our cohort had received a diagnosis of ASD by the census date. Overall, there was no evidence to support an association between I:Cr or UIC and ASD risk in children aged 8–12 years (p = 0·3).ConclusionsThere was no evidence of an increased clinical ASD risk in children born to mothers with mild-to-moderate iodine deficiency at 26 weeks gestation. Alternative functional biomarkers of exposure and a wider range of conditions may provide further insight.

Highlights

Maternal iodine requirements increase during pregnancy to supply thyroid hormones essential for fetal brain development
Median (IQR) I:Cr was 83 μg/g (59 to 121) and when the cohort was divided into five groups according to I:Cr, women with lower I: Cr were more likely to be grouped in the lower socioeconomic and education categories (Table 1)
The present study found no evidence to support a link between insufficient iodine status in the second-third trimester and an increased risk of autism spectrum disorder (ASD) in the child, in a large multi-ethnic cohort with mild-to-moderate iodine deficiency, in a setting where there was no routine dietary fortification or supplementation

Summary

Introduction

Maternal iodine requirements increase during pregnancy to supply thyroid hormones essential for fetal brain development. Maternal iodine deficiency can lead to hypothyroxinemia, a reduced fetal supply of thyroid hormones which, in the first trimester, has been linked to an increased risk of autism spectrum disorder (ASD) in the child. The maximal vulnerability to an imbalance of TH exists before the onset of thyroid function in the fetus, which occurs around 16–20 weeks of gestation [4] During this time, the highly orchestrated chain of neurodevelopmental events which characterize the early fetal period are exclusively dependent on maternal TH supply. Severe maternal iodine deficiency can lead to a reduced fetal TH supply [5] (hypothyroxinemia) which, during critical developmental periods, is thought to impair neuronal migration and has been linked to long-term suboptimal child development [1]

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