Newborn vitamin D levels in relation to autism spectrum disorders and intellectual disability: A case-control study in california / G. C. WINDHAM in Autism Research, 12-6 (June 2019)  

Public ISBD [article]  inAutism Research > 12-6 (June 2019) . - p.989-998 Titre : Newborn vitamin D levels in relation to autism spectrum disorders and intellectual disability: A case-control study in california Type de document : Texte imprimé et/ou numérique Auteurs : G. C. WINDHAM, Auteur ; M. PEARL, Auteur ; M. C. ANDERSON, Auteur ; V. POON, Auteur ; D. EYLES, Auteur ; K. L. JONES, Auteur ; K. LYALL, Auteur ; M. KHARRAZI, Auteur ; Lisa A. CROEN, Auteur Année de publication : 2019 Article en page(s) : p.989-998 Langues : Anglais (eng) Mots-clés : Asd  autism  hydroxy-vitamin D  intellectual disability  vitamin D Index. décimale : PER Périodiques Résumé : Vitamin D deficiency has been increasing concurrently with prevalence of autism spectrum disorders (ASD), and emerging evidence suggests vitamin D is involved in brain development. Most prior studies of ASD examined vitamin D levels in children already diagnosed, but a few examined levels during perinatal development, the more likely susceptibility period. Therefore, we examined newborn vitamin D levels in a case-control study conducted among births in 2000-2003 in southern California. Children with ASD (N = 563) or intellectual disability (ID) (N = 190) were identified from the Department of Developmental Services and compared to population controls (N = 436) identified from birth certificates. 25-hydroxyvitamin D (25(OH)D) was measured in archived newborn dried blood spots by a sensitive assay and corrected to sera equivalents. We categorized 25(OH) D levels as deficient (<50 nmol/L), insufficient (50-74 nmol/L), and sufficient (>/=75 nmol/L), and also examined continuous levels, using logistic regression. The adjusted odds ratios (AOR) and 95% confidence intervals for ASD were 0.96 (0.64-1.4) for 25(OH)D deficiency (14% of newborns) and 1.2 (0.86-1.6) for insufficiency (26% of newborns). The AORs for continuous 25(OH)D (per 25 nmol/L) were 1.0 (0.91-1.09) for ASD and 1.14 (1.0-1.30) for ID. Thus, in this relatively large study of measured newborn vitamin D levels, our results do not support the hypothesis of lower 25(OH)D being associated with higher risk of ASD (or ID), although we observed suggestion of interactions with sex and race/ethnicity. 25(OH)D levels were relatively high (median 84 nmol/L in controls), so results may differ in populations with higher prevalence of low vitamin D levels. Autism Res 2019, 12: 989-998. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: We studied whether vitamin D levels measured at birth were related to whether a child later developed autism (or low IQ). Our results did not show that children with autism, or low IQ, overall had lower vitamin D levels at birth than children without autism. Vitamin D levels were fairly high, on average, in these children born in Southern California. En ligne : https://dx.doi.org/10.1002/aur.2092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=401 [article] Newborn vitamin D levels in relation to autism spectrum disorders and intellectual disability: A case-control study in california [Texte imprimé et/ou numérique] / G. C. WINDHAM, Auteur ; M. PEARL, Auteur ; M. C. ANDERSON, Auteur ; V. POON, Auteur ; D. EYLES, Auteur ; K. L. JONES, Auteur ; K. LYALL, Auteur ; M. KHARRAZI, Auteur ; Lisa A. CROEN, Auteur . - 2019 . - p.989-998. Langues : Anglais (eng) in Autism Research > 12-6 (June 2019) . - p.989-998 Mots-clés : Asd  autism  hydroxy-vitamin D  intellectual disability  vitamin D Index. décimale : PER Périodiques Résumé : Vitamin D deficiency has been increasing concurrently with prevalence of autism spectrum disorders (ASD), and emerging evidence suggests vitamin D is involved in brain development. Most prior studies of ASD examined vitamin D levels in children already diagnosed, but a few examined levels during perinatal development, the more likely susceptibility period. Therefore, we examined newborn vitamin D levels in a case-control study conducted among births in 2000-2003 in southern California. Children with ASD (N = 563) or intellectual disability (ID) (N = 190) were identified from the Department of Developmental Services and compared to population controls (N = 436) identified from birth certificates. 25-hydroxyvitamin D (25(OH)D) was measured in archived newborn dried blood spots by a sensitive assay and corrected to sera equivalents. We categorized 25(OH) D levels as deficient (<50 nmol/L), insufficient (50-74 nmol/L), and sufficient (>/=75 nmol/L), and also examined continuous levels, using logistic regression. The adjusted odds ratios (AOR) and 95% confidence intervals for ASD were 0.96 (0.64-1.4) for 25(OH)D deficiency (14% of newborns) and 1.2 (0.86-1.6) for insufficiency (26% of newborns). The AORs for continuous 25(OH)D (per 25 nmol/L) were 1.0 (0.91-1.09) for ASD and 1.14 (1.0-1.30) for ID. Thus, in this relatively large study of measured newborn vitamin D levels, our results do not support the hypothesis of lower 25(OH)D being associated with higher risk of ASD (or ID), although we observed suggestion of interactions with sex and race/ethnicity. 25(OH)D levels were relatively high (median 84 nmol/L in controls), so results may differ in populations with higher prevalence of low vitamin D levels. Autism Res 2019, 12: 989-998. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: We studied whether vitamin D levels measured at birth were related to whether a child later developed autism (or low IQ). Our results did not show that children with autism, or low IQ, overall had lower vitamin D levels at birth than children without autism. Vitamin D levels were fairly high, on average, in these children born in Southern California. En ligne : https://dx.doi.org/10.1002/aur.2092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=401

Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation / S. VUILLERMOT in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 9p. Titre : Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation Type de document : Texte imprimé et/ou numérique Auteurs : S. VUILLERMOT, Auteur ; W. LUAN, Auteur ; U. MEYER, Auteur ; D. EYLES, Auteur Article en page(s) : 9p. Langues : Anglais (eng) Mots-clés : Animals  Behavior, Animal/*drug effects  Child Development Disorders, Pervasive/chemically induced/*prevention & control  Cytokines/*blood  Disease Models, Animal  Female  Humans  Mice  Phenotype  Poly I-C  Polynucleotides/*adverse effects  Pregnancy  Prenatal Exposure Delayed Effects/chemically induced/*prevention & control  Social Behavior  Stereotyped Behavior/*drug effects  Vitamin D/*administration & dosage  *Autism  *Cytokines  *Dopamine  *Maternal immune activation  *Neurodevelopmental disorders  *Schizophrenia  *Vitamin D Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to infection is a recognized environmental risk factor for neuropsychiatric disorders of developmental origins such as autism or schizophrenia. Experimental work in animals indicates that this link is mediated by maternal immune activation (MIA) involving interactions between cytokine-associated inflammatory events, oxidative stress, and other pathophysiological processes such as hypoferremia and zinc deficiency. Maternal administration of the viral mimic polyriboinosinic-polyribocytidylic acid (poly(I:C)) in mice produces several behavioral phenotypes in adult offspring of relevance to autism spectrum disorder (ASD) and other neurodevelopmental disorders. METHODS: Here, we investigated whether some of these phenotypes might also present in juveniles. In addition, given the known immunomodulatory and neuroprotective effects of vitamin D, we also investigated whether the co-administration of vitamin D could block MIA-induced ASD-related behaviors. We co-administered the hormonally active form of vitamin D, 1alpha,25 dihydroxy vitamin D3 (1,25OHD), simultaneously with poly(I:C) and examined (i) social interaction, stereotyped behavior, emotional learning and memory, and innate anxiety-like behavior in juveniles and (ii) the levels of the pro-inflammatory cytokines IL-1beta, IL-6 and TNF-alpha in maternal plasma and fetal brains. RESULTS: We show that like adult offspring that were exposed to MIA, juveniles display similar deficits in social approach behavior. Juvenile MIA offspring also show abnormal stereotyped digging and impaired acquisition and expression of tone-cued fear conditioning. Importantly, our study reveals that prenatal administration of 1,25OHD abolishes all these behavioral deficits in poly(I:C)-treated juveniles. However, prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains suggesting the anti-inflammatory actions of vitamin D are not the critical mechanism for its preventive actions in this ASD animal model. CONCLUSIONS: This work raises the possibility that early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy. En ligne : http://dx.doi.org/10.1186/s13229-017-0125-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 [article] Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation [Texte imprimé et/ou numérique] / S. VUILLERMOT, Auteur ; W. LUAN, Auteur ; U. MEYER, Auteur ; D. EYLES, Auteur . - 9p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 9p. Mots-clés : Animals  Behavior, Animal/*drug effects  Child Development Disorders, Pervasive/chemically induced/*prevention & control  Cytokines/*blood  Disease Models, Animal  Female  Humans  Mice  Phenotype  Poly I-C  Polynucleotides/*adverse effects  Pregnancy  Prenatal Exposure Delayed Effects/chemically induced/*prevention & control  Social Behavior  Stereotyped Behavior/*drug effects  Vitamin D/*administration & dosage  *Autism  *Cytokines  *Dopamine  *Maternal immune activation  *Neurodevelopmental disorders  *Schizophrenia  *Vitamin D Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to infection is a recognized environmental risk factor for neuropsychiatric disorders of developmental origins such as autism or schizophrenia. Experimental work in animals indicates that this link is mediated by maternal immune activation (MIA) involving interactions between cytokine-associated inflammatory events, oxidative stress, and other pathophysiological processes such as hypoferremia and zinc deficiency. Maternal administration of the viral mimic polyriboinosinic-polyribocytidylic acid (poly(I:C)) in mice produces several behavioral phenotypes in adult offspring of relevance to autism spectrum disorder (ASD) and other neurodevelopmental disorders. METHODS: Here, we investigated whether some of these phenotypes might also present in juveniles. In addition, given the known immunomodulatory and neuroprotective effects of vitamin D, we also investigated whether the co-administration of vitamin D could block MIA-induced ASD-related behaviors. We co-administered the hormonally active form of vitamin D, 1alpha,25 dihydroxy vitamin D3 (1,25OHD), simultaneously with poly(I:C) and examined (i) social interaction, stereotyped behavior, emotional learning and memory, and innate anxiety-like behavior in juveniles and (ii) the levels of the pro-inflammatory cytokines IL-1beta, IL-6 and TNF-alpha in maternal plasma and fetal brains. RESULTS: We show that like adult offspring that were exposed to MIA, juveniles display similar deficits in social approach behavior. Juvenile MIA offspring also show abnormal stereotyped digging and impaired acquisition and expression of tone-cued fear conditioning. Importantly, our study reveals that prenatal administration of 1,25OHD abolishes all these behavioral deficits in poly(I:C)-treated juveniles. However, prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains suggesting the anti-inflammatory actions of vitamin D are not the critical mechanism for its preventive actions in this ASD animal model. CONCLUSIONS: This work raises the possibility that early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy. En ligne : http://dx.doi.org/10.1186/s13229-017-0125-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331

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