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Commentary: Whither the epigenetics of child psychopathology? Some reflections provoked by Barker et al. (2018) / Edmund J. S. SONUGA-BARKE in Journal of Child Psychology and Psychiatry, 59-4 (April 2018)
[article]
Titre : Commentary: Whither the epigenetics of child psychopathology? Some reflections provoked by Barker et al. (2018) Type de document : Texte imprimé et/ou numérique Auteurs : Edmund J. S. SONUGA-BARKE, Auteur ; P. FEARON, Auteur Article en page(s) : p.323-326 Langues : Anglais (eng) Mots-clés : Epigenetics Index. décimale : PER Périodiques Résumé : Barker et al.'s. () review addresses one of the most fundamental questions in the fields of child psychology and psychiatry - How can adverse experiences shape development to a sufficient degree and in profound and enduring ways to create long term risk for later mental disorder and disability? In particular they discuss the plausibility of differential methylation as an epigenetic mechanism by which such exposures can become neuro-biologically embedded. Our commentary rises six question relating to key issues that need to be addressed as we search for definitive evidence from human studies that such mechanisms actually do make an important causal contribution to abnormal trajectories of development to disorder. En ligne : http://dx.doi.org/10.1111/jcpp.12906 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=353
in Journal of Child Psychology and Psychiatry > 59-4 (April 2018) . - p.323-326[article] Commentary: Whither the epigenetics of child psychopathology? Some reflections provoked by Barker et al. (2018) [Texte imprimé et/ou numérique] / Edmund J. S. SONUGA-BARKE, Auteur ; P. FEARON, Auteur . - p.323-326.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 59-4 (April 2018) . - p.323-326
Mots-clés : Epigenetics Index. décimale : PER Périodiques Résumé : Barker et al.'s. () review addresses one of the most fundamental questions in the fields of child psychology and psychiatry - How can adverse experiences shape development to a sufficient degree and in profound and enduring ways to create long term risk for later mental disorder and disability? In particular they discuss the plausibility of differential methylation as an epigenetic mechanism by which such exposures can become neuro-biologically embedded. Our commentary rises six question relating to key issues that need to be addressed as we search for definitive evidence from human studies that such mechanisms actually do make an important causal contribution to abnormal trajectories of development to disorder. En ligne : http://dx.doi.org/10.1111/jcpp.12906 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=353 Research Review: Intergenerational transmission of disadvantage: epigenetics and parents' childhoods as the first exposure / P. SCORZA in Journal of Child Psychology and Psychiatry, 60-2 (February 2019)
[article]
Titre : Research Review: Intergenerational transmission of disadvantage: epigenetics and parents' childhoods as the first exposure Type de document : Texte imprimé et/ou numérique Auteurs : P. SCORZA, Auteur ; C. S. DUARTE, Auteur ; A. E. HIPWELL, Auteur ; J. POSNER, Auteur ; A. ORTIN, Auteur ; Glorisa CANINO, Auteur ; C. MONK, Auteur Article en page(s) : p.119-132 Langues : Anglais (eng) Mots-clés : Development adversity early life experience endocrinology epigenetics gene-environment interaction stress Index. décimale : PER Périodiques Résumé : BACKGROUND: For decades, economists and sociologists have documented intergenerational transmission of socioeconomic disadvantage, demonstrating that economic, political, and social factors contribute to 'inherited hardship'. Drawing on biological factors, the developmental origins of adult health and disease model posits that fetal exposure to maternal prenatal distress associated with socioeconomic disadvantage compromises offspring's neurodevelopment, affecting short- and long-term physical and mental health, and thereby psychosocial standing and resources. Increasing evidence suggests that mother-to-child influence occurs prenatally, in part via maternal and offspring atypical HPA axis regulation, with negative effects on the maturation of prefrontal and subcortical neural circuits in the offspring. However, even this in utero timeframe may be insufficient to understand biological aspects of the transmission of factors contributing to disadvantage across generations. METHODS: We review animal studies and emerging human research indicating that parents' childhood experiences may transfer epigenetic marks that could impact the development of their offspring independently of and in interaction with their offspring's perinatal and early childhood direct exposures to stress stemming from socioeconomic disadvantage and adversity. RESULTS: Animal models point to epigenetic mechanisms by which traits that could contribute to disadvantage may be transmitted across generations. However, epigenetic pathways of parental childhood experiences influencing child outcomes in the next generation are only beginning to be studied in humans. With a focus on translational research, we point to design features and methodological considerations for human cohort studies to be able to test the intergenerational transmission hypothesis, and we illustrate this with existing longitudinal studies. CONCLUSIONS: Epigenetic intergenerational transmission, if at play in human populations, could have policy implications in terms of reducing the continuation of disadvantage across generations. Further research is needed to address this gap in the understanding of the perpetuation of compromised lives across generations. En ligne : http://dx.doi.org/10.1111/jcpp.12877 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=381
in Journal of Child Psychology and Psychiatry > 60-2 (February 2019) . - p.119-132[article] Research Review: Intergenerational transmission of disadvantage: epigenetics and parents' childhoods as the first exposure [Texte imprimé et/ou numérique] / P. SCORZA, Auteur ; C. S. DUARTE, Auteur ; A. E. HIPWELL, Auteur ; J. POSNER, Auteur ; A. ORTIN, Auteur ; Glorisa CANINO, Auteur ; C. MONK, Auteur . - p.119-132.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 60-2 (February 2019) . - p.119-132
Mots-clés : Development adversity early life experience endocrinology epigenetics gene-environment interaction stress Index. décimale : PER Périodiques Résumé : BACKGROUND: For decades, economists and sociologists have documented intergenerational transmission of socioeconomic disadvantage, demonstrating that economic, political, and social factors contribute to 'inherited hardship'. Drawing on biological factors, the developmental origins of adult health and disease model posits that fetal exposure to maternal prenatal distress associated with socioeconomic disadvantage compromises offspring's neurodevelopment, affecting short- and long-term physical and mental health, and thereby psychosocial standing and resources. Increasing evidence suggests that mother-to-child influence occurs prenatally, in part via maternal and offspring atypical HPA axis regulation, with negative effects on the maturation of prefrontal and subcortical neural circuits in the offspring. However, even this in utero timeframe may be insufficient to understand biological aspects of the transmission of factors contributing to disadvantage across generations. METHODS: We review animal studies and emerging human research indicating that parents' childhood experiences may transfer epigenetic marks that could impact the development of their offspring independently of and in interaction with their offspring's perinatal and early childhood direct exposures to stress stemming from socioeconomic disadvantage and adversity. RESULTS: Animal models point to epigenetic mechanisms by which traits that could contribute to disadvantage may be transmitted across generations. However, epigenetic pathways of parental childhood experiences influencing child outcomes in the next generation are only beginning to be studied in humans. With a focus on translational research, we point to design features and methodological considerations for human cohort studies to be able to test the intergenerational transmission hypothesis, and we illustrate this with existing longitudinal studies. CONCLUSIONS: Epigenetic intergenerational transmission, if at play in human populations, could have policy implications in terms of reducing the continuation of disadvantage across generations. Further research is needed to address this gap in the understanding of the perpetuation of compromised lives across generations. En ligne : http://dx.doi.org/10.1111/jcpp.12877 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=381 Parent Perspectives Towards Genetic and Epigenetic Testing for Autism Spectrum Disorder / Kayla E. WAGNER in Journal of Autism and Developmental Disorders, 50-9 (September 2020)
[article]
Titre : Parent Perspectives Towards Genetic and Epigenetic Testing for Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Kayla E. WAGNER, Auteur ; Jennifer B. MCCORMICK, Auteur ; Sarah BARNS, Auteur ; Molly CARNEY, Auteur ; Frank A. MIDDLETON, Auteur ; Steven D. HICKS, Auteur Article en page(s) : p.3114-3125 Langues : Anglais (eng) Mots-clés : Autism Bioethics Diagnosis Epigenetics Parent perspectives biomarkers in autism spectrum disorder that is assigned to The Research Foundation for the State University of New York, The Penn State Research Foundation and Quadrant Biosciences Inc., and licensed to Quadrant Biosciences Inc. SDH is a paid consultant for Quadrant Biosciences Inc. These conflicts of interest are actively managed by the Penn State College of Medicine. KW and SB are employees of Quadrant Biosciences Inc. Index. décimale : PER Périodiques Résumé : Examining community views on genetic/epigenetic research allows collaborative technology development. Parent perspectives toward genetic/epigenetic testing for autism spectrum disorder (ASD) are not well-studied. Parents of children with ASD (n?=?131), non-ASD developmental delay (n?=?39), and typical development (n?=?74) completed surveys assessing genetic/epigenetic knowledge, genetic/epigenetic concerns, motives for research participation, and attitudes/preferences toward ASD testing. Most parents (96%) were interested in saliva-based molecular testing for ASD. Some had concerns about privacy (14%) and insurance-status (10%). None (0%) doubted scientific evidence behind genetic/epigenetic testing. Most reported familiarity with genetics (88%), but few understood differences from epigenetics (19%). Child developmental status impacted insurance concerns (p?=?0.01). There is broad parent interest in a genetic/epigenetic test for ASD. It will be crucial to carefully consider and address bioethical issues surrounding this sensitive topic while developing such technology. En ligne : http://dx.doi.org/10.1007/s10803-019-03990-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=430
in Journal of Autism and Developmental Disorders > 50-9 (September 2020) . - p.3114-3125[article] Parent Perspectives Towards Genetic and Epigenetic Testing for Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Kayla E. WAGNER, Auteur ; Jennifer B. MCCORMICK, Auteur ; Sarah BARNS, Auteur ; Molly CARNEY, Auteur ; Frank A. MIDDLETON, Auteur ; Steven D. HICKS, Auteur . - p.3114-3125.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 50-9 (September 2020) . - p.3114-3125
Mots-clés : Autism Bioethics Diagnosis Epigenetics Parent perspectives biomarkers in autism spectrum disorder that is assigned to The Research Foundation for the State University of New York, The Penn State Research Foundation and Quadrant Biosciences Inc., and licensed to Quadrant Biosciences Inc. SDH is a paid consultant for Quadrant Biosciences Inc. These conflicts of interest are actively managed by the Penn State College of Medicine. KW and SB are employees of Quadrant Biosciences Inc. Index. décimale : PER Périodiques Résumé : Examining community views on genetic/epigenetic research allows collaborative technology development. Parent perspectives toward genetic/epigenetic testing for autism spectrum disorder (ASD) are not well-studied. Parents of children with ASD (n?=?131), non-ASD developmental delay (n?=?39), and typical development (n?=?74) completed surveys assessing genetic/epigenetic knowledge, genetic/epigenetic concerns, motives for research participation, and attitudes/preferences toward ASD testing. Most parents (96%) were interested in saliva-based molecular testing for ASD. Some had concerns about privacy (14%) and insurance-status (10%). None (0%) doubted scientific evidence behind genetic/epigenetic testing. Most reported familiarity with genetics (88%), but few understood differences from epigenetics (19%). Child developmental status impacted insurance concerns (p?=?0.01). There is broad parent interest in a genetic/epigenetic test for ASD. It will be crucial to carefully consider and address bioethical issues surrounding this sensitive topic while developing such technology. En ligne : http://dx.doi.org/10.1007/s10803-019-03990-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=430 Understanding environmental contributions to autism: Causal concepts and the state of science / I. HERTZ-PICCIOTTO in Autism Research, 11-4 (April 2018)
[article]
Titre : Understanding environmental contributions to autism: Causal concepts and the state of science Type de document : Texte imprimé et/ou numérique Auteurs : I. HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; P. KRAKOWIAK, Auteur Article en page(s) : p.554-586 Langues : Anglais (eng) Mots-clés : autism spectrum disorder causal inference diabetes environmental risk factors epigenetics gene-environment interaction nutrition pesticides pre- and peri-natal risk factors Index. décimale : PER Périodiques Résumé : The complexity of neurodevelopment, the rapidity of early neurogenesis, and over 100 years of research identifying environmental influences on neurodevelopment serve as backdrop to understanding factors that influence risk and severity of autism spectrum disorder (ASD). This Keynote Lecture, delivered at the May 2016 annual meeting of the International Society for Autism Research, describes concepts of causation, outlines the trajectory of research on nongenetic factors beginning in the 1960s, and briefly reviews the current state of this science. Causal concepts are introduced, including root causes; pitfalls in interpreting time trends as clues to etiologic factors; susceptible time windows for exposure; and implications of a multi-factorial model of ASD. An historical background presents early research into the origins of ASD. The epidemiologic literature from the last fifteen years is briefly but critically reviewed for potential roles of, for example, air pollution, pesticides, plastics, prenatal vitamins, lifestyle and family factors, and maternal obstetric and metabolic conditions during her pregnancy. Three examples from the case-control CHildhood Autism Risks from Genes and the Environment Study are probed to illustrate methodological approaches to central challenges in observational studies: capturing environmental exposure; causal inference when a randomized controlled clinical trial is either unethical or infeasible; and the integration of genetic, epigenetic, and environmental influences on development. We conclude with reflections on future directions, including exposomics, new technologies, the microbiome, gene-by-environment interaction in the era of -omics, and epigenetics as the interface of those two. As the environment is malleable, this research advances the goal of a productive and fulfilling life for all children, teen-agers and adults. Autism Res 2018, 11: 554-586. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: This Keynote Lecture, delivered at the 2016 meeting of the International Society for Autism Research, discusses evidence from human epidemiologic studies of prenatal factors contributing to autism, such as pesticides, maternal nutrition and her health. There is no single cause for autism. Examples highlight the features of a high-quality epidemiology study, and what comprises a compelling case for causation. Emergent research directions hold promise for identifying potential interventions to reduce disabilities, enhance giftedness, and improve lives of those with ASD. En ligne : http://dx.doi.org/10.1002/aur.1938 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358
in Autism Research > 11-4 (April 2018) . - p.554-586[article] Understanding environmental contributions to autism: Causal concepts and the state of science [Texte imprimé et/ou numérique] / I. HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; P. KRAKOWIAK, Auteur . - p.554-586.
Langues : Anglais (eng)
in Autism Research > 11-4 (April 2018) . - p.554-586
Mots-clés : autism spectrum disorder causal inference diabetes environmental risk factors epigenetics gene-environment interaction nutrition pesticides pre- and peri-natal risk factors Index. décimale : PER Périodiques Résumé : The complexity of neurodevelopment, the rapidity of early neurogenesis, and over 100 years of research identifying environmental influences on neurodevelopment serve as backdrop to understanding factors that influence risk and severity of autism spectrum disorder (ASD). This Keynote Lecture, delivered at the May 2016 annual meeting of the International Society for Autism Research, describes concepts of causation, outlines the trajectory of research on nongenetic factors beginning in the 1960s, and briefly reviews the current state of this science. Causal concepts are introduced, including root causes; pitfalls in interpreting time trends as clues to etiologic factors; susceptible time windows for exposure; and implications of a multi-factorial model of ASD. An historical background presents early research into the origins of ASD. The epidemiologic literature from the last fifteen years is briefly but critically reviewed for potential roles of, for example, air pollution, pesticides, plastics, prenatal vitamins, lifestyle and family factors, and maternal obstetric and metabolic conditions during her pregnancy. Three examples from the case-control CHildhood Autism Risks from Genes and the Environment Study are probed to illustrate methodological approaches to central challenges in observational studies: capturing environmental exposure; causal inference when a randomized controlled clinical trial is either unethical or infeasible; and the integration of genetic, epigenetic, and environmental influences on development. We conclude with reflections on future directions, including exposomics, new technologies, the microbiome, gene-by-environment interaction in the era of -omics, and epigenetics as the interface of those two. As the environment is malleable, this research advances the goal of a productive and fulfilling life for all children, teen-agers and adults. Autism Res 2018, 11: 554-586. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: This Keynote Lecture, delivered at the 2016 meeting of the International Society for Autism Research, discusses evidence from human epidemiologic studies of prenatal factors contributing to autism, such as pesticides, maternal nutrition and her health. There is no single cause for autism. Examples highlight the features of a high-quality epidemiology study, and what comprises a compelling case for causation. Emergent research directions hold promise for identifying potential interventions to reduce disabilities, enhance giftedness, and improve lives of those with ASD. En ligne : http://dx.doi.org/10.1002/aur.1938 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358 Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms / Erika M. MANCZAK in Development and Psychopathology, 35-1 (February 2023)
[article]
Titre : Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms Type de document : Texte imprimé et/ou numérique Auteurs : Erika M. MANCZAK, Auteur ; Samantha R. SCOTT, Auteur ; Summer N. MILLWOOD, Auteur Article en page(s) : p.109-118 Langues : Anglais (eng) Mots-clés : epigenetics methylation parenting psychopathology symptoms temperament Index. décimale : PER Périodiques Résumé : In an effort to elucidate new factors that may contribute to developmental psychopathology, the current study examined whether accelerated epigenetic aging at birth related to children's differential susceptibility to the effects of aversive parenting on early emerging mental health risk. Using data from a multiethnic birth cohort, the interaction between Horvath's methylation age in umbilical cord blood and hostile parenting behaviors was examined in relation to perceptions of infant's temperament at 6 months and to children's psychological symptoms at 3 years in 154 families. Results broadly revealed that children with higher levels of accelerated methylation aging evinced more unpredictable temperaments and more psychological symptoms if their mothers reported more hostile parenting, but showed fewer difficulties if mothers engaged in less hostile parenting; children with lower levels of accelerated methylation age did not show associations between hostility and temperament or psychological symptoms. Effects were not accounted for by gestational age at birth, demographic factors, or the distribution of cell subtypes. These findings suggest that accelerated epigenetic age may function as a form of differential susceptibility, signaling increased risk for psychopathology in more aversive contexts but decreased risk in less aversive early environments. Taken together, they point to a novel biological process to consider within risk for psychopathology. En ligne : https://doi.org/10.1017/S0954579421000614 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499
in Development and Psychopathology > 35-1 (February 2023) . - p.109-118[article] Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms [Texte imprimé et/ou numérique] / Erika M. MANCZAK, Auteur ; Samantha R. SCOTT, Auteur ; Summer N. MILLWOOD, Auteur . - p.109-118.
Langues : Anglais (eng)
in Development and Psychopathology > 35-1 (February 2023) . - p.109-118
Mots-clés : epigenetics methylation parenting psychopathology symptoms temperament Index. décimale : PER Périodiques Résumé : In an effort to elucidate new factors that may contribute to developmental psychopathology, the current study examined whether accelerated epigenetic aging at birth related to children's differential susceptibility to the effects of aversive parenting on early emerging mental health risk. Using data from a multiethnic birth cohort, the interaction between Horvath's methylation age in umbilical cord blood and hostile parenting behaviors was examined in relation to perceptions of infant's temperament at 6 months and to children's psychological symptoms at 3 years in 154 families. Results broadly revealed that children with higher levels of accelerated methylation aging evinced more unpredictable temperaments and more psychological symptoms if their mothers reported more hostile parenting, but showed fewer difficulties if mothers engaged in less hostile parenting; children with lower levels of accelerated methylation age did not show associations between hostility and temperament or psychological symptoms. Effects were not accounted for by gestational age at birth, demographic factors, or the distribution of cell subtypes. These findings suggest that accelerated epigenetic age may function as a form of differential susceptibility, signaling increased risk for psychopathology in more aversive contexts but decreased risk in less aversive early environments. Taken together, they point to a novel biological process to consider within risk for psychopathology. En ligne : https://doi.org/10.1017/S0954579421000614 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499 Annual Research Review: DNA methylation as a mediator in the association between risk exposure and child and adolescent psychopathology / Edward D. BARKER in Journal of Child Psychology and Psychiatry, 59-4 (April 2018)
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