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Autism spectrum disorder and low vitamin D at birth: a sibling control study

BACKGROUND: Insufficient vitamin D activity has attracted increasing interest as a possible underlying risk factor in disorders of the central nervous system, including autism. METHODS: In this study, 25-hydroxyvitamin D (25(OH)D) was analysed in 58 Sweden-born sibling pairs, in which one child had...

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Autores principales: Fernell, Elisabeth, Bejerot, Susanne, Westerlund, Joakim, Miniscalco, Carmela, Simila, Henry, Eyles, Darryl, Gillberg, Christopher, Humble, Mats B
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396835/
https://www.ncbi.nlm.nih.gov/pubmed/25874075
http://dx.doi.org/10.1186/2040-2392-6-3
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author Fernell, Elisabeth
Bejerot, Susanne
Westerlund, Joakim
Miniscalco, Carmela
Simila, Henry
Eyles, Darryl
Gillberg, Christopher
Humble, Mats B
author_facet Fernell, Elisabeth
Bejerot, Susanne
Westerlund, Joakim
Miniscalco, Carmela
Simila, Henry
Eyles, Darryl
Gillberg, Christopher
Humble, Mats B
author_sort Fernell, Elisabeth
collection PubMed
description BACKGROUND: Insufficient vitamin D activity has attracted increasing interest as a possible underlying risk factor in disorders of the central nervous system, including autism. METHODS: In this study, 25-hydroxyvitamin D (25(OH)D) was analysed in 58 Sweden-born sibling pairs, in which one child had autism spectrum disorder (ASD) and the other did not. The study group consisted of two representative samples; 47 Gothenburg sibling pairs with mixed ethnicities and 11 Stockholm sibling pairs with Somali background. 25(OH)D levels were analysed in the stored dried blood spots taken in the neonatal period for metabolic screening. RESULTS: The collapsed group of children with ASD had significantly lower vitamin D levels (M = 24.0 nM, SD = 19.6) as compared with their siblings (M = 31.9 nM, SD = 27.7), according to a paired samples t-test (P = 0.013). The difference was - most likely - not only accounted for by a difference in season of birth between ASD and non-ASD siblings since the mean 25(OH)D levels differed with similar effect size between the sibling pairs born during winter and summer, respectively. All children with African/Middle East background, both the children with ASD and their non-ASD siblings, had vitamin D deficiency. CONCLUSIONS: The findings suggest that low prenatal vitamin D may act as a risk factor for ASD, however, there is a need for replication with larger samples. Future research should study whether or not adequate supplementation of vitamin D to pregnant women might lower the risk for ASD in the offspring.
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spelling pubmed-43968352015-04-15 Autism spectrum disorder and low vitamin D at birth: a sibling control study Fernell, Elisabeth Bejerot, Susanne Westerlund, Joakim Miniscalco, Carmela Simila, Henry Eyles, Darryl Gillberg, Christopher Humble, Mats B Mol Autism Research BACKGROUND: Insufficient vitamin D activity has attracted increasing interest as a possible underlying risk factor in disorders of the central nervous system, including autism. METHODS: In this study, 25-hydroxyvitamin D (25(OH)D) was analysed in 58 Sweden-born sibling pairs, in which one child had autism spectrum disorder (ASD) and the other did not. The study group consisted of two representative samples; 47 Gothenburg sibling pairs with mixed ethnicities and 11 Stockholm sibling pairs with Somali background. 25(OH)D levels were analysed in the stored dried blood spots taken in the neonatal period for metabolic screening. RESULTS: The collapsed group of children with ASD had significantly lower vitamin D levels (M = 24.0 nM, SD = 19.6) as compared with their siblings (M = 31.9 nM, SD = 27.7), according to a paired samples t-test (P = 0.013). The difference was - most likely - not only accounted for by a difference in season of birth between ASD and non-ASD siblings since the mean 25(OH)D levels differed with similar effect size between the sibling pairs born during winter and summer, respectively. All children with African/Middle East background, both the children with ASD and their non-ASD siblings, had vitamin D deficiency. CONCLUSIONS: The findings suggest that low prenatal vitamin D may act as a risk factor for ASD, however, there is a need for replication with larger samples. Future research should study whether or not adequate supplementation of vitamin D to pregnant women might lower the risk for ASD in the offspring. BioMed Central 2015-01-14 /pmc/articles/PMC4396835/ /pubmed/25874075 http://dx.doi.org/10.1186/2040-2392-6-3 Text en © Fernell et al.; licensee BioMed Central. 2015 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Fernell, Elisabeth
Bejerot, Susanne
Westerlund, Joakim
Miniscalco, Carmela
Simila, Henry
Eyles, Darryl
Gillberg, Christopher
Humble, Mats B
Autism spectrum disorder and low vitamin D at birth: a sibling control study
title Autism spectrum disorder and low vitamin D at birth: a sibling control study
title_full Autism spectrum disorder and low vitamin D at birth: a sibling control study
title_fullStr Autism spectrum disorder and low vitamin D at birth: a sibling control study
title_full_unstemmed Autism spectrum disorder and low vitamin D at birth: a sibling control study
title_short Autism spectrum disorder and low vitamin D at birth: a sibling control study
title_sort autism spectrum disorder and low vitamin d at birth: a sibling control study
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396835/
https://www.ncbi.nlm.nih.gov/pubmed/25874075
http://dx.doi.org/10.1186/2040-2392-6-3
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