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

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          Abstract

          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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          Most cited references63

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          Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain.

          Despite a growing body of evidence that Vitamin D is involved in mammalian brain functioning, there has been a lack of direct evidence about its role in the human brain. This paper reports, for the first time, the distribution of the 1,25-dihydroxyvitamin D3 receptor (VDR), and 1alpha-hydroxylase (1alpha-OHase), the enzyme responsible for the formation of the active vitamin in the human brain. The receptor and the enzyme were found in both neurons and glial cells in a regional and layer-specific pattern. The VDR was restricted to the nucleus whilst 1alpha-OHase was distributed throughout the cytoplasm. The distribution of the VDR in human brain was strikingly similar to that reported in rodents. Many regions contained equivalent amounts of both the VDR and 1alpha-OHase, however the macrocellular cells within the nucleus basalis of Meynert (NBM) and the Purkinje cells in the cerebellum expressed 1alpha-OHase in the absence of VDR. The strongest immunohistochemical staining for both the receptor and enzyme was in the hypothalamus and in the large (presumably dopaminergic) neurons within the substantia nigra. The observed distribution of the VDR is consistent with the proposal that Vitamin D operates in a similar fashion to the known neurosteroids. The widespread distribution of 1alpha-OHase and the VDR suggests that Vitamin D may have autocrine/paracrine properties in the human brain.
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            Autism risk factors: genes, environment, and gene-environment interactions

            The aim of this review is to summarize the key findings from genetic and epidemiological research, which show that autism is a complex disorder resulting from the combination of genetic and environmental factors. Remarkable advances in the knowledge of genetic causes of autism have resulted from the great efforts made in the field of genetics. The identification of specific alleles contributing to the autism spectrum has supplied important pieces for the autism puzzle. However, many questions remain unanswered, and new questions are raised by recent results. Moreover, given the amount of evidence supporting a significant contribution of environmental factors to autism risk, it is now clear that the search for environmental factors should be reinforced. One aspect of this search that has been neglected so far is the study of interactions between genes and environmental factors.
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              Maternal infection and immune involvement in autism.

              Recent studies have highlighted a connection between infection during pregnancy and the increased risk of autism in the offspring. Parallel studies of cerebral spinal fluid, blood and postmortem brains reveal an ongoing, hyper-responsive inflammatory-like state in many young as well as adult autism subjects. There are also indications of gastrointestinal problems in at least a subset of autistic children. Work on the maternal infection risk factor using animal models indicates that aspects of brain and peripheral immune dysregulation can begin during fetal development and continue through adulthood. The offspring of infected or immune-activated dams also display cardinal behavioral features of autism, as well as neuropathology consistent with that seen in human autism. These rodent models are proving useful for the study of pathogenesis and gene-environment interactions as well as for the exploration of potential therapeutic strategies. Copyright © 2011 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                elisabeth.fernell@gnc.gu.se
                susanne.bejerot@ki.se
                joakim.westerlund.jwd@psychology.su.se
                carmela.miniscalco@gnc.gu.se
                vh.simila@uq.edu.au
                d.eyles@uq.edu.au
                christopher.gillberg@gnc.gu.se
                vmats.humble@oru.se
                Journal
                Mol Autism
                Mol Autism
                Molecular Autism
                BioMed Central (London )
                2040-2392
                14 January 2015
                14 January 2015
                2015
                : 6
                : 3
                Affiliations
                [ ]Gillberg Neuropsychiatry Centre, Sahlgrenska Academy, University of Gothenburg, Kungsgatan 12, 411 19 Gothenburg, SE Sweden
                [ ]Research and Development Centre, Skaraborg’s Hospital, Skövde, Sweden
                [ ]Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
                [ ]Department of Psychiatry, Faculty of Medicine and Health, Örebro University, Örebro, Sweden
                [ ]Department of Psychology, University of Stockholm, Stockholm, Sweden
                [ ]Queensland, Brain Institute, University of Queensland, Brisbane, Australia
                [ ]Queensland Centre for Mental Health Research, University of Queensland, Brisbane, Australia
                Article
                150
                10.1186/2040-2392-6-3
                4396835
                25874075
                a58d4661-4eb0-455a-8c09-d169d1ce7c09
                © 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.

                History
                : 28 September 2014
                : 2 January 2015
                Categories
                Research
                Custom metadata
                © The Author(s) 2015

                Neurosciences
                autism spectrum disorder,vitamin d,25-hydroxyvitamin d,neonatal,dried blood spots
                Neurosciences
                autism spectrum disorder, vitamin d, 25-hydroxyvitamin d, neonatal, dried blood spots

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