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

Maternal iodine status in a multi-ethnic UK birth cohort: associations with autism spectrum disorder
Maternal iodine status in a multi-ethnic UK birth cohort: associations with autism spectrum disorder
Background: 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. No study to date has explored the direct link between maternal iodine deficiency and diagnosis of ASD in offspring.

Methods: urinary 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.

Results: median (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).

Conclusions: there 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.
1471-2431
Cromie, Kirsten Jade
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Threapleton, Diane Erin
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Snart, Charles Jonathan Peter
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Taylor, Elizabeth
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Mason, Dan
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Wright, Barry
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Kelly, Brian
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Reid, Stephen
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Azad, Rafaq
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Keeble, Claire
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Waterman, Amanda H.
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Meadows, Sarah
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McKillion, Amanda
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Alwan, Nisreen
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Cade, Janet Elizabeth
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Simpson, Nigel A.B.
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Stewart, Paul M.
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Zimmermann, Michael
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Wright, John
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Waiblinger, Dagmar
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Mon-Williams, Mark
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Hardie, Laura J.
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Greenwood, Darren Charles
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Cromie, Kirsten Jade
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Threapleton, Diane Erin
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Snart, Charles Jonathan Peter
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Taylor, Elizabeth
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Mason, Dan
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Wright, Barry
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Kelly, Brian
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Reid, Stephen
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Azad, Rafaq
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Keeble, Claire
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Waterman, Amanda H.
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Meadows, Sarah
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McKillion, Amanda
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Alwan, Nisreen
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Cade, Janet Elizabeth
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Simpson, Nigel A.B.
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Stewart, Paul M.
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Zimmermann, Michael
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Wright, John
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Waiblinger, Dagmar
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Mon-Williams, Mark
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Hardie, Laura J.
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Greenwood, Darren Charles
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Cromie, Kirsten Jade, Threapleton, Diane Erin, Snart, Charles Jonathan Peter, Taylor, Elizabeth, Mason, Dan, Wright, Barry, Kelly, Brian, Reid, Stephen, Azad, Rafaq, Keeble, Claire, Waterman, Amanda H., Meadows, Sarah, McKillion, Amanda, Alwan, Nisreen, Cade, Janet Elizabeth, Simpson, Nigel A.B., Stewart, Paul M., Zimmermann, Michael, Wright, John, Waiblinger, Dagmar, Mon-Williams, Mark, Hardie, Laura J. and Greenwood, Darren Charles (2020) Maternal iodine status in a multi-ethnic UK birth cohort: associations with autism spectrum disorder. BMC Pediatrics, 20.

Record type: Article

Abstract

Background: 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. No study to date has explored the direct link between maternal iodine deficiency and diagnosis of ASD in offspring.

Methods: urinary 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.

Results: median (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).

Conclusions: there 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.

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More information

Accepted/In Press date: 20 November 2020
e-pub ahead of print date: 5 December 2020

Identifiers

Local EPrints ID: 445513
URI: http://eprints.soton.ac.uk/id/eprint/445513
ISSN: 1471-2431
PURE UUID: 22e0b383-66b8-4b71-a32f-25e3262e9fc4
ORCID for Nisreen Alwan: ORCID iD orcid.org/0000-0002-4134-8463

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Date deposited: 14 Dec 2020 17:30
Last modified: 10 Jan 2022 03:04

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Contributors

Author: Kirsten Jade Cromie
Author: Diane Erin Threapleton
Author: Charles Jonathan Peter Snart
Author: Elizabeth Taylor
Author: Dan Mason
Author: Barry Wright
Author: Brian Kelly
Author: Stephen Reid
Author: Rafaq Azad
Author: Claire Keeble
Author: Amanda H. Waterman
Author: Sarah Meadows
Author: Amanda McKillion
Author: Nisreen Alwan ORCID iD
Author: Janet Elizabeth Cade
Author: Nigel A.B. Simpson
Author: Paul M. Stewart
Author: Michael Zimmermann
Author: John Wright
Author: Dagmar Waiblinger
Author: Mark Mon-Williams
Author: Laura J. Hardie
Author: Darren Charles Greenwood

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