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Familial confounding of the association between maternal smoking in pregnancy and autism spectrum disorder in offspring / Amy E. KALKBRENNER in Autism Research, 13-1 (January 2020)
[article]
Titre : Familial confounding of the association between maternal smoking in pregnancy and autism spectrum disorder in offspring Type de document : Texte imprimé et/ou numérique Auteurs : Amy E. KALKBRENNER, Auteur ; Sandra M. MEIER, Auteur ; Paul MADLEY-DOWD, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret Daniele FALLIN, Auteur ; Erik T. PARNER, Auteur ; Diana SCHENDEL, Auteur Article en page(s) : p.134-144 Langues : Anglais (eng) Mots-clés : attention deficit hyperactivity disorder autism autism spectrum disorder confounding family-based designs intellectual disability maternal smoking neurodevelopment tobacco Index. décimale : PER Périodiques Résumé : Evidence supports no link between maternal smoking in pregnancy and autism spectrum disorder (autism) overall. To address remaining questions about the unexplained heterogeneity between study results and the possibility of risk for specific autism sub-phenotypes, we conducted a whole-population cohort study in Denmark. We followed births 1991-2011 (1,294,906 persons, including 993,301 siblings in 728,271 families), from 1 year of age until an autism diagnosis (13,547), death, emigration, or December 31, 2012. Autism, with and without attention deficit hyperactivity disorder (ADHD) and with and without intellectual disability (ID) were based on ICD-8 and ICD-10 codes from Danish national health registers, including 3,319 autism + ADHD, 10,228 autism - no ADHD, 2,205 autism + ID, and 11,342 autism - no ID. We estimated hazard ratios (HRs) and 95% confidence intervals (95% CIs) between any maternal smoking (from birth records) and autism (or sub-phenotypes) using survival models with robust standard errors, stratifying by birth year and adjusting for child sex, parity, and parental age, education, income, and psychiatric history. To additionally address confounding using family designs, we constructed a maternal cluster model (adjusting for the smoking proportion within the family), and a stratified sibling model. Associations with maternal smoking and autism were elevated in conventional adjusted analyses (HR of 1.17 [1.13-1.22]) but attenuated in the maternal cluster (0.98 [0.88-1.09]) and sibling (0.86 [0.64-1.15]) models. Similarly, risks of autism sub-phenotypes with maternal smoking were attenuated in the family-based models. Together these results support that smoking in pregnancy is not linked with autism or select autism comorbid sub-phenotypes after accounting for familial confounding. Autism Res 2020, 13: 134-144. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Smoking during pregnancy has many harmful impacts, which may include harming the baby's developing brain. However, in a study of thousands of families in Denmark, it does not appear that smoking in pregnancy leads to autism or autism in combination with intellectual problems or attention deficits, once you account for the way smoking patterns and developmental disabilities run in families. En ligne : http://dx.doi.org/10.1002/aur.2196 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=415
in Autism Research > 13-1 (January 2020) . - p.134-144[article] Familial confounding of the association between maternal smoking in pregnancy and autism spectrum disorder in offspring [Texte imprimé et/ou numérique] / Amy E. KALKBRENNER, Auteur ; Sandra M. MEIER, Auteur ; Paul MADLEY-DOWD, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret Daniele FALLIN, Auteur ; Erik T. PARNER, Auteur ; Diana SCHENDEL, Auteur . - p.134-144.
Langues : Anglais (eng)
in Autism Research > 13-1 (January 2020) . - p.134-144
Mots-clés : attention deficit hyperactivity disorder autism autism spectrum disorder confounding family-based designs intellectual disability maternal smoking neurodevelopment tobacco Index. décimale : PER Périodiques Résumé : Evidence supports no link between maternal smoking in pregnancy and autism spectrum disorder (autism) overall. To address remaining questions about the unexplained heterogeneity between study results and the possibility of risk for specific autism sub-phenotypes, we conducted a whole-population cohort study in Denmark. We followed births 1991-2011 (1,294,906 persons, including 993,301 siblings in 728,271 families), from 1 year of age until an autism diagnosis (13,547), death, emigration, or December 31, 2012. Autism, with and without attention deficit hyperactivity disorder (ADHD) and with and without intellectual disability (ID) were based on ICD-8 and ICD-10 codes from Danish national health registers, including 3,319 autism + ADHD, 10,228 autism - no ADHD, 2,205 autism + ID, and 11,342 autism - no ID. We estimated hazard ratios (HRs) and 95% confidence intervals (95% CIs) between any maternal smoking (from birth records) and autism (or sub-phenotypes) using survival models with robust standard errors, stratifying by birth year and adjusting for child sex, parity, and parental age, education, income, and psychiatric history. To additionally address confounding using family designs, we constructed a maternal cluster model (adjusting for the smoking proportion within the family), and a stratified sibling model. Associations with maternal smoking and autism were elevated in conventional adjusted analyses (HR of 1.17 [1.13-1.22]) but attenuated in the maternal cluster (0.98 [0.88-1.09]) and sibling (0.86 [0.64-1.15]) models. Similarly, risks of autism sub-phenotypes with maternal smoking were attenuated in the family-based models. Together these results support that smoking in pregnancy is not linked with autism or select autism comorbid sub-phenotypes after accounting for familial confounding. Autism Res 2020, 13: 134-144. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Smoking during pregnancy has many harmful impacts, which may include harming the baby's developing brain. However, in a study of thousands of families in Denmark, it does not appear that smoking in pregnancy leads to autism or autism in combination with intellectual problems or attention deficits, once you account for the way smoking patterns and developmental disabilities run in families. En ligne : http://dx.doi.org/10.1002/aur.2196 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=415 Commentary: How can family-based quasi-experimental designs and national registers be used to address confounding in risk factor studies of psychopathology? A reflection on Obel et al. (2016) / Henrik LARSSON in Journal of Child Psychology and Psychiatry, 57-4 (April 2016)
[article]
Titre : Commentary: How can family-based quasi-experimental designs and national registers be used to address confounding in risk factor studies of psychopathology? A reflection on Obel et al. (2016) Type de document : Texte imprimé et/ou numérique Auteurs : Henrik LARSSON, Auteur Article en page(s) : p.538-539 Langues : Anglais (eng) Mots-clés : Risk factors familial confounding maternal smoking smoking during pregnancy sibling-comparisons Index. décimale : PER Périodiques Résumé : Standard observational studies have reported a robust correlation between maternal smoking during pregnancy and risk of ADHD in offspring. In the accompanying article, Obel et al. used sibling-comparisons to explore the extent to which unmeasured familial confounding explains this association. This commentary highlights three important implications of the study. At a general level, Obel et al. illustrates how (1) family-based quasi-experimental designs and (2) national registers can be used to address confounding in risk factor studies of psychopathology. At a more specific level, the study suggests that maternal smoking during pregnancy is probably not a causal risk factor for ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12519 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285
in Journal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.538-539[article] Commentary: How can family-based quasi-experimental designs and national registers be used to address confounding in risk factor studies of psychopathology? A reflection on Obel et al. (2016) [Texte imprimé et/ou numérique] / Henrik LARSSON, Auteur . - p.538-539.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.538-539
Mots-clés : Risk factors familial confounding maternal smoking smoking during pregnancy sibling-comparisons Index. décimale : PER Périodiques Résumé : Standard observational studies have reported a robust correlation between maternal smoking during pregnancy and risk of ADHD in offspring. In the accompanying article, Obel et al. used sibling-comparisons to explore the extent to which unmeasured familial confounding explains this association. This commentary highlights three important implications of the study. At a general level, Obel et al. illustrates how (1) family-based quasi-experimental designs and (2) national registers can be used to address confounding in risk factor studies of psychopathology. At a more specific level, the study suggests that maternal smoking during pregnancy is probably not a causal risk factor for ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12519 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285 Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study / Christian KIELING in Journal of Child Psychology and Psychiatry, 54-3 (March 2013)
[article]
Titre : Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study Type de document : Texte imprimé et/ou numérique Auteurs : Christian KIELING, Auteur ; Mara H. HUTZ, Auteur ; Júlia P. GENRO, Auteur ; Guilherme V. POLANCZYK, Auteur ; Luciana ANSELMI, Auteur ; Suzi CAMEY, Auteur ; Pedro C. HALLAL, Auteur ; Fernando C. BARROS, Auteur ; Cesar G. VICTORA, Auteur ; Ana Maria B. MENEZES, Auteur ; Luis Augusto ROHDE, Auteur Article en page(s) : p.298-304 Mots-clés : Gene–environment interaction DAT1 maternal smoking MAOA childhood maltreatment externalizing Index. décimale : PER Périodiques Résumé : Background: The study of gene–environment interactions (G × E) is one of the most promising strategies to uncover the origins of mental disorders. Replication of initial findings, however, is essential because there is a strong possibility of publication bias in the literature. In addition, there is a scarcity of research on the topic originated from low- and middle-income countries (LMIC). The aim of this study was to replicate G × E hypotheses for externalizing problems among adolescents in a middle-income country. Methods: As part of the Pelotas 1993 Birth Cohort Study, 5,249 children were enrolled at birth and followed up to the age of 15 years, with an 85.7% retention rate. We sought an interaction between the homozygosity of the 10-repeat allele at the dopamine transporter (DAT1) gene and prenatal maternal smoking in the development of hyperactivity problems during adolescence assessed by the Strengths and Difficulties Questionnaire. We also tested for an interaction between the uVNTR polymorphism at the monoamine oxidase A (MAOA) and the experience of childhood maltreatment in the occurrence of conduct problems among adolescent boys. Results: Although there was a clear association between prenatal maternal smoking and hyperactivity scores in adolescence (p 0.001), no main genetic or interaction effects for the DAT1 gene were detected. Similarly, childhood maltreatment showed to be associated with conduct problems among boys (p 0.001), with no observable main genetic or interaction effects for the MAOA gene. Conclusions: In the largest mental health G × E study performed in a LMIC to date, we did not replicate previous positive findings from the literature. Despite the presence of main environmental effects, there was no evidence of effect modification by genotype status. Additional replication efforts to measure G × E are needed to better understand the origins of mental health and illness, especially in LMIC. En ligne : http://dx.doi.org/10.1111/jcpp.12022 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.298-304[article] Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study [Texte imprimé et/ou numérique] / Christian KIELING, Auteur ; Mara H. HUTZ, Auteur ; Júlia P. GENRO, Auteur ; Guilherme V. POLANCZYK, Auteur ; Luciana ANSELMI, Auteur ; Suzi CAMEY, Auteur ; Pedro C. HALLAL, Auteur ; Fernando C. BARROS, Auteur ; Cesar G. VICTORA, Auteur ; Ana Maria B. MENEZES, Auteur ; Luis Augusto ROHDE, Auteur . - p.298-304.
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.298-304
Mots-clés : Gene–environment interaction DAT1 maternal smoking MAOA childhood maltreatment externalizing Index. décimale : PER Périodiques Résumé : Background: The study of gene–environment interactions (G × E) is one of the most promising strategies to uncover the origins of mental disorders. Replication of initial findings, however, is essential because there is a strong possibility of publication bias in the literature. In addition, there is a scarcity of research on the topic originated from low- and middle-income countries (LMIC). The aim of this study was to replicate G × E hypotheses for externalizing problems among adolescents in a middle-income country. Methods: As part of the Pelotas 1993 Birth Cohort Study, 5,249 children were enrolled at birth and followed up to the age of 15 years, with an 85.7% retention rate. We sought an interaction between the homozygosity of the 10-repeat allele at the dopamine transporter (DAT1) gene and prenatal maternal smoking in the development of hyperactivity problems during adolescence assessed by the Strengths and Difficulties Questionnaire. We also tested for an interaction between the uVNTR polymorphism at the monoamine oxidase A (MAOA) and the experience of childhood maltreatment in the occurrence of conduct problems among adolescent boys. Results: Although there was a clear association between prenatal maternal smoking and hyperactivity scores in adolescence (p 0.001), no main genetic or interaction effects for the DAT1 gene were detected. Similarly, childhood maltreatment showed to be associated with conduct problems among boys (p 0.001), with no observable main genetic or interaction effects for the MAOA gene. Conclusions: In the largest mental health G × E study performed in a LMIC to date, we did not replicate previous positive findings from the literature. Despite the presence of main environmental effects, there was no evidence of effect modification by genotype status. Additional replication efforts to measure G × E are needed to better understand the origins of mental health and illness, especially in LMIC. En ligne : http://dx.doi.org/10.1111/jcpp.12022 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191