Intrapartum exposure to synthetic oxytocin, maternal BMI, and neurodevelopmental outcomes in children within the ECHO consortium / Lisa KURTH in Journal of Neurodevelopmental Disorders, 16 (2024)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 16 (2024) Titre : Intrapartum exposure to synthetic oxytocin, maternal BMI, and neurodevelopmental outcomes in children within the ECHO consortium Type de document : texte imprimé Auteurs : Lisa KURTH, Auteur ; T. Michael O'SHEA, Auteur ; Irina BURD, Auteur ; Anne L. DUNLOP, Auteur ; Lisa CROEN, Auteur ; Greta WILKENING, Auteur ; Ting-Ju HSU, Auteur ; Stephan EHRHARDT, Auteur ; Arvind PALANISAMY, Auteur ; Monica MCGRATH, Auteur ; Marie L. CHURCHILL, Auteur ; Daniel WEINBERGER, Auteur ; Marco GRADOS, Auteur ; Dana DABELEA, Auteur Langues : Anglais (eng) Mots-clés : Humans  Female  Pregnancy  Oxytocin  Male  Attention Deficit Disorder with Hyperactivity/epidemiology/etiology  Child  Body Mass Index  Autism Spectrum Disorder/epidemiology/etiology  Prenatal Exposure Delayed Effects  Adult  Pregnancy in Obesity/epidemiology  Child, Preschool  Cohort Studies  Obesity/epidemiology  Adhd  Asd  Autism  Bmi  Neurodevelopment  Obesity  Synthetic oxytocin Index. décimale : PER Périodiques Résumé : BACKGROUND: Synthetic oxytocin (sOT) is frequently administered during parturition. Studies have raised concerns that fetal exposure to sOT may be associated with altered brain development and risk of neurodevelopmental disorders. In a large and diverse sample of children with data about intrapartum sOT exposure and subsequent diagnoses of two prevalent neurodevelopmental disorders, i.e., attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), we tested the following hypotheses: (1) Intrapartum sOT exposure is associated with increased odds of child ADHD or ASD; (2) associations differ across sex; (3) associations between intrapartum sOT exposure and ADHD or ASD are accentuated in offspring of mothers with pre-pregnancy obesity. METHODS: The study sample comprised 12,503 participants from 44 cohort sites included in the Environmental Influences on Child Health Outcomes (ECHO) consortium. Mixed-effects logistic regression analyses were used to estimate the association between intrapartum sOT exposure and offspring ADHD or ASD (in separate models). Maternal obesity (pre-pregnancy BMI ≥ 30 kg/m(2)) and child sex were evaluated for effect modification. RESULTS: Intrapartum sOT exposure was present in 48% of participants. sOT exposure was not associated with increased odds of ASD (adjusted odds ratio [aOR] 0.86; 95% confidence interval [CI], 0.71-1.03) or ADHD (aOR 0.89; 95% CI, 0.76-1.04). Associations did not differ by child sex. Among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of offspring ADHD (aOR 0.72; 95% CI, 0.55-0.96). No association was found among mothers without obesity (aOR 0.97; 95% CI, 0.80-1.18). CONCLUSIONS: In a large, diverse sample, we found no evidence of an association between intrapartum exposure to sOT and odds of ADHD or ASD in either male or female offspring. Contrary to our hypothesis, among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of child ADHD diagnosis. En ligne : https://dx.doi.org/10.1186/s11689-024-09540-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575 [article] Intrapartum exposure to synthetic oxytocin, maternal BMI, and neurodevelopmental outcomes in children within the ECHO consortium [texte imprimé] / Lisa KURTH, Auteur ; T. Michael O'SHEA, Auteur ; Irina BURD, Auteur ; Anne L. DUNLOP, Auteur ; Lisa CROEN, Auteur ; Greta WILKENING, Auteur ; Ting-Ju HSU, Auteur ; Stephan EHRHARDT, Auteur ; Arvind PALANISAMY, Auteur ; Monica MCGRATH, Auteur ; Marie L. CHURCHILL, Auteur ; Daniel WEINBERGER, Auteur ; Marco GRADOS, Auteur ; Dana DABELEA, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 16 (2024) Mots-clés : Humans  Female  Pregnancy  Oxytocin  Male  Attention Deficit Disorder with Hyperactivity/epidemiology/etiology  Child  Body Mass Index  Autism Spectrum Disorder/epidemiology/etiology  Prenatal Exposure Delayed Effects  Adult  Pregnancy in Obesity/epidemiology  Child, Preschool  Cohort Studies  Obesity/epidemiology  Adhd  Asd  Autism  Bmi  Neurodevelopment  Obesity  Synthetic oxytocin Index. décimale : PER Périodiques Résumé : BACKGROUND: Synthetic oxytocin (sOT) is frequently administered during parturition. Studies have raised concerns that fetal exposure to sOT may be associated with altered brain development and risk of neurodevelopmental disorders. In a large and diverse sample of children with data about intrapartum sOT exposure and subsequent diagnoses of two prevalent neurodevelopmental disorders, i.e., attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), we tested the following hypotheses: (1) Intrapartum sOT exposure is associated with increased odds of child ADHD or ASD; (2) associations differ across sex; (3) associations between intrapartum sOT exposure and ADHD or ASD are accentuated in offspring of mothers with pre-pregnancy obesity. METHODS: The study sample comprised 12,503 participants from 44 cohort sites included in the Environmental Influences on Child Health Outcomes (ECHO) consortium. Mixed-effects logistic regression analyses were used to estimate the association between intrapartum sOT exposure and offspring ADHD or ASD (in separate models). Maternal obesity (pre-pregnancy BMI ≥ 30 kg/m(2)) and child sex were evaluated for effect modification. RESULTS: Intrapartum sOT exposure was present in 48% of participants. sOT exposure was not associated with increased odds of ASD (adjusted odds ratio [aOR] 0.86; 95% confidence interval [CI], 0.71-1.03) or ADHD (aOR 0.89; 95% CI, 0.76-1.04). Associations did not differ by child sex. Among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of offspring ADHD (aOR 0.72; 95% CI, 0.55-0.96). No association was found among mothers without obesity (aOR 0.97; 95% CI, 0.80-1.18). CONCLUSIONS: In a large, diverse sample, we found no evidence of an association between intrapartum exposure to sOT and odds of ADHD or ASD in either male or female offspring. Contrary to our hypothesis, among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of child ADHD diagnosis. En ligne : https://dx.doi.org/10.1186/s11689-024-09540-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575

Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts / Irva HERTZ-PICCIOTTO in Autism Research, 15-3 (March 2022)  

Public ISBD [article]  inAutism Research > 15-3 (March 2022) . - p.551-569 Titre : Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts Type de document : texte imprimé Auteurs : Irva HERTZ-PICCIOTTO, Auteur ; Susan A. KORRICK, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret R. KARAGAS, Auteur ; Kristen LYALL, Auteur ; Rebecca J. SCHMIDT, Auteur ; Anne L. DUNLOP, Auteur ; Lisa A. CROEN, Auteur ; Dana DABELEA, Auteur ; Julie L. DANIELS, Auteur ; Cristiane S. DUARTE, Auteur ; M. Daniele FALLIN, Auteur ; Catherine J. KARR, Auteur ; Barry M. LESTER, Auteur ; Leslie D. LEVE, Auteur ; Yijun LI, Auteur ; Monica MCGRATH, Auteur ; Xuejuan NING, Auteur ; Emily OKEN, Auteur ; Sharon K. SAGIV, Auteur ; Sheela SATHYANARAYA, Auteur ; Frances TYLAVSKY, Auteur ; Heather E. VOLK, Auteur ; Lauren S. WAKSCHLAG, Auteur ; Mingyu ZHANG, Auteur ; T. Michael O'SHEA, Auteur ; Rashelle J. MUSCI, Auteur ; program collaborators for Environmental influences on Child Health OUTCOMES, Auteur Article en page(s) : p.551-569 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Given inconsistent evidence on preconception or prenatal tobacco use and offspring autism spectrum disorder (ASD), this study assessed associations of maternal smoking with ASD and ASD-related traits. Among 72 cohorts in the Environmental Influences on Child Health Outcomes consortium, 11 had ASD diagnosis and prenatal tobaccosmoking (n = 8648). and 7 had Social Responsiveness Scale (SRS) scores of ASD traits (n = 2399). Cohorts had diagnoses alone (6), traits alone (2), or both (5). Diagnoses drew from parent/caregiver report, review of records, or standardized instruments. Regression models estimated smoking-related odds ratios (ORs) for diagnoses and standardized mean differences for SRS scores. Cohort-specific ORs were meta-analyzed. Overall, maternal smoking was unassociated with child ASD (adjusted OR, 1.08; 95% confidence interval [CI], 0.72 1.61). However, heterogeneity across studies was strong: preterm cohorts showed reduced ASD risk for exposed children. After excluding preterm cohorts (biased by restrictions on causal intermediate and exposure opportunity) and small cohorts (very few ASD cases in either smoking category), the adjusted OR for ASD from maternal smoking was 1.44 (95% CI, 1.02 2.03). Children of smoking (versus non-smoking) mothers had more ASD traits (SRS T-score+2.37 points, 95% CI, 0.73 4.01 points), with results homogeneous across cohorts. Maternal preconception/prenatal smoking was consistently associated with quantitative ASD traits and modestly associated with ASD diagnosis among sufficiently powered United States cohorts of non-preterm children. Limitations resulting from self-reported smoking and unmeasured confounders preclude definitive conclusions. Nevertheless, counseling on potential and known risks to the child from maternal smoking is warranted for pregnant women and pregnancy planners. Lay Summary Evidence on the association between maternal prenatal smoking and the child's risk for autism spectrum disorder has been conflicting, with some studies reporting harmful effects, and others finding reduced risks. Our analysis of children in the ECHO consortium found that maternal prenatal tobacco smoking is consistently associated with an increase in autism-related symptoms in the general population and modestly associated with elevated risk for a diagnosis of autism spectrum disorder when looking at a combined analysis from multiple studies that each included both pre- and full-term births. However, this study is not proof of a causal connection. Future studies to clarify the role of smoking in autism-like behaviors or autism diagnoses should collect more reliable data on smoking and measure other exposures or lifestyle factors that might have confounded our results. En ligne : https://doi.org/10.1002/aur.2665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Maternal tobacco smoking and offspring autism spectrum disorder or traits in ECHO cohorts [texte imprimé] / Irva HERTZ-PICCIOTTO, Auteur ; Susan A. KORRICK, Auteur ; Christine LADD-ACOSTA, Auteur ; Margaret R. KARAGAS, Auteur ; Kristen LYALL, Auteur ; Rebecca J. SCHMIDT, Auteur ; Anne L. DUNLOP, Auteur ; Lisa A. CROEN, Auteur ; Dana DABELEA, Auteur ; Julie L. DANIELS, Auteur ; Cristiane S. DUARTE, Auteur ; M. Daniele FALLIN, Auteur ; Catherine J. KARR, Auteur ; Barry M. LESTER, Auteur ; Leslie D. LEVE, Auteur ; Yijun LI, Auteur ; Monica MCGRATH, Auteur ; Xuejuan NING, Auteur ; Emily OKEN, Auteur ; Sharon K. SAGIV, Auteur ; Sheela SATHYANARAYA, Auteur ; Frances TYLAVSKY, Auteur ; Heather E. VOLK, Auteur ; Lauren S. WAKSCHLAG, Auteur ; Mingyu ZHANG, Auteur ; T. Michael O'SHEA, Auteur ; Rashelle J. MUSCI, Auteur ; program collaborators for Environmental influences on Child Health OUTCOMES, Auteur . - p.551-569. Langues : Anglais (eng) in Autism Research > 15-3 (March 2022) . - p.551-569 Index. décimale : PER Périodiques Résumé : Abstract Given inconsistent evidence on preconception or prenatal tobacco use and offspring autism spectrum disorder (ASD), this study assessed associations of maternal smoking with ASD and ASD-related traits. Among 72 cohorts in the Environmental Influences on Child Health Outcomes consortium, 11 had ASD diagnosis and prenatal tobaccosmoking (n = 8648). and 7 had Social Responsiveness Scale (SRS) scores of ASD traits (n = 2399). Cohorts had diagnoses alone (6), traits alone (2), or both (5). Diagnoses drew from parent/caregiver report, review of records, or standardized instruments. Regression models estimated smoking-related odds ratios (ORs) for diagnoses and standardized mean differences for SRS scores. Cohort-specific ORs were meta-analyzed. Overall, maternal smoking was unassociated with child ASD (adjusted OR, 1.08; 95% confidence interval [CI], 0.72 1.61). However, heterogeneity across studies was strong: preterm cohorts showed reduced ASD risk for exposed children. After excluding preterm cohorts (biased by restrictions on causal intermediate and exposure opportunity) and small cohorts (very few ASD cases in either smoking category), the adjusted OR for ASD from maternal smoking was 1.44 (95% CI, 1.02 2.03). Children of smoking (versus non-smoking) mothers had more ASD traits (SRS T-score+2.37 points, 95% CI, 0.73 4.01 points), with results homogeneous across cohorts. Maternal preconception/prenatal smoking was consistently associated with quantitative ASD traits and modestly associated with ASD diagnosis among sufficiently powered United States cohorts of non-preterm children. Limitations resulting from self-reported smoking and unmeasured confounders preclude definitive conclusions. Nevertheless, counseling on potential and known risks to the child from maternal smoking is warranted for pregnant women and pregnancy planners. Lay Summary Evidence on the association between maternal prenatal smoking and the child's risk for autism spectrum disorder has been conflicting, with some studies reporting harmful effects, and others finding reduced risks. Our analysis of children in the ECHO consortium found that maternal prenatal tobacco smoking is consistently associated with an increase in autism-related symptoms in the general population and modestly associated with elevated risk for a diagnosis of autism spectrum disorder when looking at a combined analysis from multiple studies that each included both pre- and full-term births. However, this study is not proof of a causal connection. Future studies to clarify the role of smoking in autism-like behaviors or autism diagnoses should collect more reliable data on smoking and measure other exposures or lifestyle factors that might have confounded our results. En ligne : https://doi.org/10.1002/aur.2665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

Sensitive periods and other timing hypotheses in developmental psychopathology: A tutorial / Kylie K. HARRALL ; Deborah H. GLUECK ; Elysia Poggi DAVIS ; Keith E. MULLER ; Dana DABELEA ; Jenalee R. DOOM in Development and Psychopathology, 37-4 (October 2025)  

Public ISBD [article]  inDevelopment and Psychopathology > 37-4 (October 2025) . - p.1721-1729 Titre : Sensitive periods and other timing hypotheses in developmental psychopathology: A tutorial Type de document : texte imprimé Auteurs : Kylie K. HARRALL, Auteur ; Deborah H. GLUECK, Auteur ; Elysia Poggi DAVIS, Auteur ; Keith E. MULLER, Auteur ; Dana DABELEA, Auteur ; Jenalee R. DOOM, Auteur Article en page(s) : p.1721-1729 Langues : Anglais (eng) Mots-clés : Development  longitudinal modeling  methods  sensitive periods  tutorial Index. décimale : PER Périodiques Résumé : Researchers often aim to assess whether repeated measures of an exposure are associated with repeated measures of an outcome. A question of particular interest is how associations between exposures and outcomes may differ over time. In other words, researchers may seek the best form of a temporal model. While several models are possible, researchers often consider a few key models. For example, researchers may hypothesize that an exposure measured during a sensitive period may be associated with repeated measures of the outcome over time. Alternatively, they may hypothesize that the exposure measured immediately before the current time period may be most strongly associated with the outcome at the current time. Finally, they may hypothesize that all prior exposures are important. Many analytic methods cannot compare and evaluate these alternative temporal models, perhaps because they make the restrictive assumption that the associations between exposures and outcomes remains constant over time. Instead, we provide a tutorial describing four temporal models that allow the associations between repeated measures of exposures and outcomes to vary, and showing how to test which temporal model is best supported by the data. By finding the best temporal model, developmental psychopathology researchers can find optimal windows for intervention. En ligne : https://dx.doi.org/10.1017/S0954579424001299 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=567 [article] Sensitive periods and other timing hypotheses in developmental psychopathology: A tutorial [texte imprimé] / Kylie K. HARRALL, Auteur ; Deborah H. GLUECK, Auteur ; Elysia Poggi DAVIS, Auteur ; Keith E. MULLER, Auteur ; Dana DABELEA, Auteur ; Jenalee R. DOOM, Auteur . - p.1721-1729. Langues : Anglais (eng) in Development and Psychopathology > 37-4 (October 2025) . - p.1721-1729 Mots-clés : Development  longitudinal modeling  methods  sensitive periods  tutorial Index. décimale : PER Périodiques Résumé : Researchers often aim to assess whether repeated measures of an exposure are associated with repeated measures of an outcome. A question of particular interest is how associations between exposures and outcomes may differ over time. In other words, researchers may seek the best form of a temporal model. While several models are possible, researchers often consider a few key models. For example, researchers may hypothesize that an exposure measured during a sensitive period may be associated with repeated measures of the outcome over time. Alternatively, they may hypothesize that the exposure measured immediately before the current time period may be most strongly associated with the outcome at the current time. Finally, they may hypothesize that all prior exposures are important. Many analytic methods cannot compare and evaluate these alternative temporal models, perhaps because they make the restrictive assumption that the associations between exposures and outcomes remains constant over time. Instead, we provide a tutorial describing four temporal models that allow the associations between repeated measures of exposures and outcomes to vary, and showing how to test which temporal model is best supported by the data. By finding the best temporal model, developmental psychopathology researchers can find optimal windows for intervention. En ligne : https://dx.doi.org/10.1017/S0954579424001299 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=567

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