Dépouillements

Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward / Stephen A. PETRILL in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1029-1029 Titre : Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward Type de document : Texte imprimé et/ou numérique Auteurs : Stephen A. PETRILL, Auteur ; Christopher W. BARTLETT, Auteur ; Clancy BLAIR, Auteur Article en page(s) : p.1029-1029 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This special issue in the Journal of Child Psychology and Psychiatry presents several invited articles examining gene–environment interplay in child development and psychopathology. Models of gene–environment interplay have been exhaustively discussed in the literature, including an important contribution by Rutter, Moffitt and Caspi (2006) published in this journal. En ligne : http://dx.doi.org/10.1111/jcpp.12133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward [Texte imprimé et/ou numérique] / Stephen A. PETRILL, Auteur ; Christopher W. BARTLETT, Auteur ; Clancy BLAIR, Auteur . - p.1029-1029. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1029-1029 Index. décimale : PER Périodiques Résumé : This special issue in the Journal of Child Psychology and Psychiatry presents several invited articles examining gene–environment interplay in child development and psychopathology. Models of gene–environment interplay have been exhaustively discussed in the literature, including an important contribution by Rutter, Moffitt and Caspi (2006) published in this journal. En ligne : http://dx.doi.org/10.1111/jcpp.12133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Maternal warmth and directiveness jointly moderate the etiology of childhood conduct problems / S. Alexandra BURT in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1030-1037 Titre : Maternal warmth and directiveness jointly moderate the etiology of childhood conduct problems Type de document : Texte imprimé et/ou numérique Auteurs : S. Alexandra BURT, Auteur ; Ashlea M. KLAHR, Auteur ; Michael C. NEALE, Auteur ; Kelly L. KLUMP, Auteur Article en page(s) : p.1030-1037 Langues : Anglais (eng) Mots-clés : Child conduct problems  GxE  maternal directiveness or control  maternal warmth Index. décimale : PER Périodiques Résumé : Background Prior studies exploring gene–environment interactions (GxE) in the development of youth conduct problems (CP) have focused almost exclusively on single-risk experiences, despite research indicating that the presence of other risk factors and or the absence of protective factors can accentuate the influence of a given risk factor on CP. The goal of the current study was to fill this gap in the literature, evaluating whether risky and protective aspects of parenting might combine to jointly moderate the etiology of CP. Methods The sample consisted of 500 child twin pairs from the Michigan State University Twin Registry (MSUTR). Child CP was assessed using multiple informant reports. Maternal warmth and directiveness were assessed via videotaped dyadic interactions between mothers and each of their twins. Results Biometric GxE analyses revealed that directiveness and warmth did appear to jointly moderate the etiology of CP. In particular, shared environmental influences were accentuated by colder, less directive or ‘less engaged’ mothering, whereas genetic influences were strongest when the child was experiencing warmer, more directive or ‘more authoritative’ mothering. Conclusions Such findings serve to highlight the synergistic effects of risky and protective experiences on child outcomes. They also provide additional empirical support for the bioecological form of GxE, which postulates that, in some cases, genetic influences may be most strongly expressed in the presence of low-risk environments. En ligne : http://dx.doi.org/10.1111/jcpp.12095 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Maternal warmth and directiveness jointly moderate the etiology of childhood conduct problems [Texte imprimé et/ou numérique] / S. Alexandra BURT, Auteur ; Ashlea M. KLAHR, Auteur ; Michael C. NEALE, Auteur ; Kelly L. KLUMP, Auteur . - p.1030-1037. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1030-1037 Mots-clés : Child conduct problems  GxE  maternal directiveness or control  maternal warmth Index. décimale : PER Périodiques Résumé : Background Prior studies exploring gene–environment interactions (GxE) in the development of youth conduct problems (CP) have focused almost exclusively on single-risk experiences, despite research indicating that the presence of other risk factors and or the absence of protective factors can accentuate the influence of a given risk factor on CP. The goal of the current study was to fill this gap in the literature, evaluating whether risky and protective aspects of parenting might combine to jointly moderate the etiology of CP. Methods The sample consisted of 500 child twin pairs from the Michigan State University Twin Registry (MSUTR). Child CP was assessed using multiple informant reports. Maternal warmth and directiveness were assessed via videotaped dyadic interactions between mothers and each of their twins. Results Biometric GxE analyses revealed that directiveness and warmth did appear to jointly moderate the etiology of CP. In particular, shared environmental influences were accentuated by colder, less directive or ‘less engaged’ mothering, whereas genetic influences were strongest when the child was experiencing warmer, more directive or ‘more authoritative’ mothering. Conclusions Such findings serve to highlight the synergistic effects of risky and protective experiences on child outcomes. They also provide additional empirical support for the bioecological form of GxE, which postulates that, in some cases, genetic influences may be most strongly expressed in the presence of low-risk environments. En ligne : http://dx.doi.org/10.1111/jcpp.12095 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture / Gordon T. HAROLD in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1038-1046 Titre : Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture Type de document : Texte imprimé et/ou numérique Auteurs : Gordon T. HAROLD, Auteur ; Leslie D. LEVE, Auteur ; Douglas BARRETT, Auteur ; Kit ELAM, Auteur ; Jenae M. NEIDERHISER, Auteur ; Misaki N. NATSUAKI, Auteur ; Daniel S. SHAW, Auteur ; David REISS, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.1038-1046 Langues : Anglais (eng) Mots-clés : ADHD  parenting  gene-environment correlation  adoption Index. décimale : PER Périodiques Résumé : Background Families of children with attention deficit hyperactivity disorder (ADHD) report more negative family relationships than families of children without ADHD. Questions remain as to the role of genetic factors underlying associations between family relationships and children's ADHD symptoms, and the role of children's ADHD symptoms as an evocative influence on the quality of relationships experienced within such families. Utilizing the attributes of two genetically sensitive research designs, the present study examined associations between biologically related and nonbiologically related maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. The combined attributes of the study designs permit assessment of associations while controlling for passive genotype-environment correlation and directly examining evocative genotype-environment correlation (rGE); two relatively under examined confounds of past research in this area. Methods A cross-sectional adoption-at-conception design (Cardiff IVF Study; C-IVF) and a longitudinal adoption-at-birth design (Early Growth and Development Study; EGDS) were used. The C-IVF sample included 160 mothers and children (age 5–8 years). The EGDS sample included 320 linked sets of adopted children (age 6 years), adoptive-, and biologically related mothers. Questionnaires were used to assess maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. A cross-rater approach was used across measures of maternal behavior (mother reports) and child ADHD symptoms (father reports). Results Significant associations were revealed between rearing mother ADHD symptoms, hostile parenting behavior, and child ADHD symptoms in both samples. Because both samples consisted of genetically unrelated mothers and children, passive rGE was removed as a possible explanatory factor underlying these associations. Further, path analysis revealed evidence for evocative rGE processes in the longitudinal adoption-at-birth study (EGDS) from biologically related maternal ADHD symptoms to biologically unrelated maternal hostile parenting through early disrupted child behavior (impulsivity/activation), with maternal hostile parenting and disrupted child behavior associated with later child ADHD symptoms, controlling for concurrent adoptive mother ADHD symptoms. Conclusions Results highlight the importance of genetically influenced child ADHD-related temperamental attributes on genetically unrelated maternal hostility that in turn links to later child ADHD symptoms. Implications for intervention programs focusing on early family processes and the precursors of child ADHD symptoms are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12100 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture [Texte imprimé et/ou numérique] / Gordon T. HAROLD, Auteur ; Leslie D. LEVE, Auteur ; Douglas BARRETT, Auteur ; Kit ELAM, Auteur ; Jenae M. NEIDERHISER, Auteur ; Misaki N. NATSUAKI, Auteur ; Daniel S. SHAW, Auteur ; David REISS, Auteur ; Anita THAPAR, Auteur . - p.1038-1046. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1038-1046 Mots-clés : ADHD  parenting  gene-environment correlation  adoption Index. décimale : PER Périodiques Résumé : Background Families of children with attention deficit hyperactivity disorder (ADHD) report more negative family relationships than families of children without ADHD. Questions remain as to the role of genetic factors underlying associations between family relationships and children's ADHD symptoms, and the role of children's ADHD symptoms as an evocative influence on the quality of relationships experienced within such families. Utilizing the attributes of two genetically sensitive research designs, the present study examined associations between biologically related and nonbiologically related maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. The combined attributes of the study designs permit assessment of associations while controlling for passive genotype-environment correlation and directly examining evocative genotype-environment correlation (rGE); two relatively under examined confounds of past research in this area. Methods A cross-sectional adoption-at-conception design (Cardiff IVF Study; C-IVF) and a longitudinal adoption-at-birth design (Early Growth and Development Study; EGDS) were used. The C-IVF sample included 160 mothers and children (age 5–8 years). The EGDS sample included 320 linked sets of adopted children (age 6 years), adoptive-, and biologically related mothers. Questionnaires were used to assess maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. A cross-rater approach was used across measures of maternal behavior (mother reports) and child ADHD symptoms (father reports). Results Significant associations were revealed between rearing mother ADHD symptoms, hostile parenting behavior, and child ADHD symptoms in both samples. Because both samples consisted of genetically unrelated mothers and children, passive rGE was removed as a possible explanatory factor underlying these associations. Further, path analysis revealed evidence for evocative rGE processes in the longitudinal adoption-at-birth study (EGDS) from biologically related maternal ADHD symptoms to biologically unrelated maternal hostile parenting through early disrupted child behavior (impulsivity/activation), with maternal hostile parenting and disrupted child behavior associated with later child ADHD symptoms, controlling for concurrent adoptive mother ADHD symptoms. Conclusions Results highlight the importance of genetically influenced child ADHD-related temperamental attributes on genetically unrelated maternal hostility that in turn links to later child ADHD symptoms. Implications for intervention programs focusing on early family processes and the precursors of child ADHD symptoms are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12100 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Expanding the environment: gene × school-level SES interaction on reading comprehension / Sara A. HART in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1047-1055 Titre : Expanding the environment: gene × school-level SES interaction on reading comprehension Type de document : Texte imprimé et/ou numérique Auteurs : Sara A. HART, Auteur ; Brooke SODEN, Auteur ; Wendy JOHNSON, Auteur ; Christopher SCHATSCHNEIDER, Auteur ; Jeanette TAYLOR, Auteur Article en page(s) : p.1047-1055 Langues : Anglais (eng) Mots-clés : Reading comprehension  G × E interaction  school-level SES  bioecological model Index. décimale : PER Périodiques Résumé : Background Influential work has explored the role of family socioeconomic status (SES) as an environmental moderator of genetic and environmental influences on cognitive outcomes. This work has provided evidence that socioeconomic circumstances differentially impact the heritability of cognitive abilities, generally supporting the bioecological model in that genetic influences are greater at higher levels of family SES. The present work expanded consideration of the environment, using school-level SES as a moderator of reading comprehension. Methods The sample included 577 pairs of twins from the Florida Twin Project on Reading, Behavior and Environment. Reading comprehension was measured by the Florida Comprehensive Achievement Test (FCAT) Reading in third or fourth grade. School-level SES was measured by the mean Free and Reduced Lunch Status (FRLS) of the schoolmates of the twins. Results The best-fitting univariate G × E moderation model indicated greater genetic influences on reading comprehension when fewer schoolmates qualified for FRLS (i.e., ‘higher’ school-level SES). There was also an indication of moderation of the shared environment; there were greater shared environmental influences on reading comprehension at higher school-level SES. Conclusions The results supported the bioecological model; greater genetic variance was found in school environments in which student populations experienced less poverty. In general, ‘higher’ school-level SES allowed genetic and probably shared environmental variance to contribute as sources of individual differences in reading comprehension outcomes. Poverty suppresses these influences. En ligne : http://dx.doi.org/10.1111/jcpp.12083 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Expanding the environment: gene × school-level SES interaction on reading comprehension [Texte imprimé et/ou numérique] / Sara A. HART, Auteur ; Brooke SODEN, Auteur ; Wendy JOHNSON, Auteur ; Christopher SCHATSCHNEIDER, Auteur ; Jeanette TAYLOR, Auteur . - p.1047-1055. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1047-1055 Mots-clés : Reading comprehension  G × E interaction  school-level SES  bioecological model Index. décimale : PER Périodiques Résumé : Background Influential work has explored the role of family socioeconomic status (SES) as an environmental moderator of genetic and environmental influences on cognitive outcomes. This work has provided evidence that socioeconomic circumstances differentially impact the heritability of cognitive abilities, generally supporting the bioecological model in that genetic influences are greater at higher levels of family SES. The present work expanded consideration of the environment, using school-level SES as a moderator of reading comprehension. Methods The sample included 577 pairs of twins from the Florida Twin Project on Reading, Behavior and Environment. Reading comprehension was measured by the Florida Comprehensive Achievement Test (FCAT) Reading in third or fourth grade. School-level SES was measured by the mean Free and Reduced Lunch Status (FRLS) of the schoolmates of the twins. Results The best-fitting univariate G × E moderation model indicated greater genetic influences on reading comprehension when fewer schoolmates qualified for FRLS (i.e., ‘higher’ school-level SES). There was also an indication of moderation of the shared environment; there were greater shared environmental influences on reading comprehension at higher school-level SES. Conclusions The results supported the bioecological model; greater genetic variance was found in school environments in which student populations experienced less poverty. In general, ‘higher’ school-level SES allowed genetic and probably shared environmental variance to contribute as sources of individual differences in reading comprehension outcomes. Poverty suppresses these influences. En ligne : http://dx.doi.org/10.1111/jcpp.12083 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Schooling and variation in the COMT gene: the devil is in the details / Daniel B. CAMPBELL in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1056-1065 Titre : Schooling and variation in the COMT gene: the devil is in the details Type de document : Texte imprimé et/ou numérique Auteurs : Daniel B. CAMPBELL, Auteur ; Johanna BICK, Auteur ; Carolyn M. YRIGOLLEN, Auteur ; Maria LEE, Auteur ; Antony JOSEPH, Auteur ; Joseph T. CHANG, Auteur ; Elena L. GRIGORENKO, Auteur ; LEARNING DISABILITIES PROJECT ZAMBIA,, Auteur Article en page(s) : p.1056-1065 Langues : Anglais (eng) Mots-clés : Schooling  nonverbal intelligence  the COMT gene  haplotype analysis  haplo.glm  interaction effects Index. décimale : PER Périodiques Résumé : Background Schooling is considered one of the major contributors to the development of intelligence within societies and individuals. Genetic variation might modulate the impact of schooling and explain, at least partially, the presence of individual differences in classrooms. Method We studied a sample of 1,502 children (mean age = 11.7 years) from Zambia. Approximately 57% of these children were enrolled in school, and the rest were not. To quantify genetic variation, we investigated a number of common polymorphisms in the catechol-O-methyltransferase (COMT) gene that controls the production of the protein thought to account for 60% of the dopamine degradation in the prefrontal cortex. Results Haplotype analyses generated results ranging from the presence to absence of significant interactions between a number of COMT haplotypes and indicators of schooling (i.e., in- vs. out-of-school and grade completed) in the prediction of nonverbal intelligence, depending on the parameter specification. However, an investigation of the distribution of corresponding p-values suggested that these positive results were false. Conclusions Convincing evidence that the variation in the COMT gene is associated with individual differences in nonverbal intelligence either directly or through interactions with schooling was not found. p-values produced by the method of testing for haplotype effects employed here may be sensitive to parameter settings, invalid under default settings, and should be checked for validity through simulation. En ligne : http://dx.doi.org/10.1111/jcpp.12120 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Schooling and variation in the COMT gene: the devil is in the details [Texte imprimé et/ou numérique] / Daniel B. CAMPBELL, Auteur ; Johanna BICK, Auteur ; Carolyn M. YRIGOLLEN, Auteur ; Maria LEE, Auteur ; Antony JOSEPH, Auteur ; Joseph T. CHANG, Auteur ; Elena L. GRIGORENKO, Auteur ; LEARNING DISABILITIES PROJECT ZAMBIA,, Auteur . - p.1056-1065. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1056-1065 Mots-clés : Schooling  nonverbal intelligence  the COMT gene  haplotype analysis  haplo.glm  interaction effects Index. décimale : PER Périodiques Résumé : Background Schooling is considered one of the major contributors to the development of intelligence within societies and individuals. Genetic variation might modulate the impact of schooling and explain, at least partially, the presence of individual differences in classrooms. Method We studied a sample of 1,502 children (mean age = 11.7 years) from Zambia. Approximately 57% of these children were enrolled in school, and the rest were not. To quantify genetic variation, we investigated a number of common polymorphisms in the catechol-O-methyltransferase (COMT) gene that controls the production of the protein thought to account for 60% of the dopamine degradation in the prefrontal cortex. Results Haplotype analyses generated results ranging from the presence to absence of significant interactions between a number of COMT haplotypes and indicators of schooling (i.e., in- vs. out-of-school and grade completed) in the prediction of nonverbal intelligence, depending on the parameter specification. However, an investigation of the distribution of corresponding p-values suggested that these positive results were false. Conclusions Convincing evidence that the variation in the COMT gene is associated with individual differences in nonverbal intelligence either directly or through interactions with schooling was not found. p-values produced by the method of testing for haplotype effects employed here may be sensitive to parameter settings, invalid under default settings, and should be checked for validity through simulation. En ligne : http://dx.doi.org/10.1111/jcpp.12120 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

The interacting effect of the BDNF Val66Met polymorphism and stressful life events on adolescent depression is not an artifact of gene–environment correlation: evidence from a longitudinal twin study / Jie CHEN in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1066-1073 Titre : The interacting effect of the BDNF Val66Met polymorphism and stressful life events on adolescent depression is not an artifact of gene–environment correlation: evidence from a longitudinal twin study Type de document : Texte imprimé et/ou numérique Auteurs : Jie CHEN, Auteur ; Xinying LI, Auteur ; Matt MCGUE, Auteur Article en page(s) : p.1066-1073 Langues : Anglais (eng) Mots-clés : Adolescent  depressive symptoms  BDNF Val66Met polymorphism  stressful life events  gene–environment interaction  gene–environment correlation Index. décimale : PER Périodiques Résumé : Background Confounding introduced by gene–environment correlation (rGE) may prevent one from observing a true gene–environment interaction (G × E) effect on psychopathology. The present study investigated the interacting effect of the BDNF Val66Met polymorphism and stressful life events (SLEs) on adolescent depression while controlling for the rGE by two means: separating pure environmental factors (independent SLEs) from the environmental factors under partial genetic control (dependent SLEs) and adopting a prospective longitudinal design. Methods A total of 780 pairs of Chinese twins, aged 11–17 years (mean = 13.6, SD = 1.8) at intake, were followed up twice. Self-reported depression symptoms at Time 1 and Time 2 were assessed by the Children's Depression Inventory (CDI). SLEs occurring between Time 1 and Time 2 were assessed by a self-reported checklist. SLEs were differentiated into independent and dependent ones and were validated by heritability analyses using twin design. The interacting effects between the BDNF Val66Met polymorphism and numbers of SLEs (total SLEs and independent SLEs) on intraindividual change of depression symptoms were examined. Results After controlling for sex, age, age square, and Time 1 depression, both total SLEs × BDNF Val66Met genotype and independent SLEs × BDNF Val66Met genotype significantly predicted Time 2 depression. Val allele carriers (Val/Val and Val/Met) were more susceptible to the detrimental effects of stress. Conclusions There is a true G × E effect underlying the observed interaction between BDNF Val66Met polymorphism and environmental stress on depression. En ligne : http://dx.doi.org/10.1111/jcpp.12099 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] The interacting effect of the BDNF Val66Met polymorphism and stressful life events on adolescent depression is not an artifact of gene–environment correlation: evidence from a longitudinal twin study [Texte imprimé et/ou numérique] / Jie CHEN, Auteur ; Xinying LI, Auteur ; Matt MCGUE, Auteur . - p.1066-1073. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1066-1073 Mots-clés : Adolescent  depressive symptoms  BDNF Val66Met polymorphism  stressful life events  gene–environment interaction  gene–environment correlation Index. décimale : PER Périodiques Résumé : Background Confounding introduced by gene–environment correlation (rGE) may prevent one from observing a true gene–environment interaction (G × E) effect on psychopathology. The present study investigated the interacting effect of the BDNF Val66Met polymorphism and stressful life events (SLEs) on adolescent depression while controlling for the rGE by two means: separating pure environmental factors (independent SLEs) from the environmental factors under partial genetic control (dependent SLEs) and adopting a prospective longitudinal design. Methods A total of 780 pairs of Chinese twins, aged 11–17 years (mean = 13.6, SD = 1.8) at intake, were followed up twice. Self-reported depression symptoms at Time 1 and Time 2 were assessed by the Children's Depression Inventory (CDI). SLEs occurring between Time 1 and Time 2 were assessed by a self-reported checklist. SLEs were differentiated into independent and dependent ones and were validated by heritability analyses using twin design. The interacting effects between the BDNF Val66Met polymorphism and numbers of SLEs (total SLEs and independent SLEs) on intraindividual change of depression symptoms were examined. Results After controlling for sex, age, age square, and Time 1 depression, both total SLEs × BDNF Val66Met genotype and independent SLEs × BDNF Val66Met genotype significantly predicted Time 2 depression. Val allele carriers (Val/Val and Val/Met) were more susceptible to the detrimental effects of stress. Conclusions There is a true G × E effect underlying the observed interaction between BDNF Val66Met polymorphism and environmental stress on depression. En ligne : http://dx.doi.org/10.1111/jcpp.12099 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Gene variants associated with antisocial behaviour: a latent variable approach / Mary Jane BENTLEY in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1074-1085 Titre : Gene variants associated with antisocial behaviour: a latent variable approach Type de document : Texte imprimé et/ou numérique Auteurs : Mary Jane BENTLEY, Auteur ; Haiqun LIN, Auteur ; Thomas V. FERNANDEZ, Auteur ; Maria LEE, Auteur ; Carolyn M. YRIGOLLEN, Auteur ; Andrew J. PAKSTIS, Auteur ; Liliya KATSOVICH, Auteur ; David L. OLDS, Auteur ; Elena L. GRIGORENKO, Auteur ; James F. LECKMAN, Auteur Article en page(s) : p.1074-1085 Langues : Anglais (eng) Mots-clés : Antisocial behaviour  latent variable analysis  shared variance  co-action of gene variants Index. décimale : PER Périodiques Résumé : Objective The aim of this study was to determine if a latent variable approach might be useful in identifying shared variance across genetic risk alleles that is associated with antisocial behaviour at age 15 years. Methods Using a conventional latent variable approach, we derived an antisocial phenotype in 328 adolescents utilizing data from a 15-year follow-up of a randomized trial of a prenatal and infancy nurse-home visitation programme in Elmira, New York. We then investigated, via a novel latent variable approach, 450 informative genetic polymorphisms in 71 genes previously associated with antisocial behaviour, drug use, affiliative behaviours and stress response in 241 consenting individuals for whom DNA was available. Haplotype and Pathway analyses were also performed. Results Eight single-nucleotide polymorphisms (SNPs) from eight genes contributed to the latent genetic variable that in turn accounted for 16.0% of the variance within the latent antisocial phenotype. The number of risk alleles was linearly related to the latent antisocial variable scores. Haplotypes that included the putative risk alleles for all eight genes were also associated with higher latent antisocial variable scores. In addition, 33 SNPs from 63 of the remaining genes were also significant when added to the final model. Many of these genes interact on a molecular level, forming molecular networks. The results support a role for genes related to dopamine, norepinephrine, serotonin, glutamate, opioid and cholinergic signalling as well as stress response pathways in mediating susceptibility to antisocial behaviour. Conclusions This preliminary study supports use of relevant behavioural indicators and latent variable approaches to study the potential ‘co-action’ of gene variants associated with antisocial behaviour. It also underscores the cumulative relevance of common genetic variants for understanding the aetiology of complex behaviour. If replicated in future studies, this approach may allow the identification of a ‘shared’ variance across genetic risk alleles associated with complex neuropsychiatric dimensional phenotypes using relatively small numbers of well-characterized research participants. En ligne : http://dx.doi.org/10.1111/jcpp.12109 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Gene variants associated with antisocial behaviour: a latent variable approach [Texte imprimé et/ou numérique] / Mary Jane BENTLEY, Auteur ; Haiqun LIN, Auteur ; Thomas V. FERNANDEZ, Auteur ; Maria LEE, Auteur ; Carolyn M. YRIGOLLEN, Auteur ; Andrew J. PAKSTIS, Auteur ; Liliya KATSOVICH, Auteur ; David L. OLDS, Auteur ; Elena L. GRIGORENKO, Auteur ; James F. LECKMAN, Auteur . - p.1074-1085. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1074-1085 Mots-clés : Antisocial behaviour  latent variable analysis  shared variance  co-action of gene variants Index. décimale : PER Périodiques Résumé : Objective The aim of this study was to determine if a latent variable approach might be useful in identifying shared variance across genetic risk alleles that is associated with antisocial behaviour at age 15 years. Methods Using a conventional latent variable approach, we derived an antisocial phenotype in 328 adolescents utilizing data from a 15-year follow-up of a randomized trial of a prenatal and infancy nurse-home visitation programme in Elmira, New York. We then investigated, via a novel latent variable approach, 450 informative genetic polymorphisms in 71 genes previously associated with antisocial behaviour, drug use, affiliative behaviours and stress response in 241 consenting individuals for whom DNA was available. Haplotype and Pathway analyses were also performed. Results Eight single-nucleotide polymorphisms (SNPs) from eight genes contributed to the latent genetic variable that in turn accounted for 16.0% of the variance within the latent antisocial phenotype. The number of risk alleles was linearly related to the latent antisocial variable scores. Haplotypes that included the putative risk alleles for all eight genes were also associated with higher latent antisocial variable scores. In addition, 33 SNPs from 63 of the remaining genes were also significant when added to the final model. Many of these genes interact on a molecular level, forming molecular networks. The results support a role for genes related to dopamine, norepinephrine, serotonin, glutamate, opioid and cholinergic signalling as well as stress response pathways in mediating susceptibility to antisocial behaviour. Conclusions This preliminary study supports use of relevant behavioural indicators and latent variable approaches to study the potential ‘co-action’ of gene variants associated with antisocial behaviour. It also underscores the cumulative relevance of common genetic variants for understanding the aetiology of complex behaviour. If replicated in future studies, this approach may allow the identification of a ‘shared’ variance across genetic risk alleles associated with complex neuropsychiatric dimensional phenotypes using relatively small numbers of well-characterized research participants. En ligne : http://dx.doi.org/10.1111/jcpp.12109 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Predicting outcomes following cognitive behaviour therapy in child anxiety disorders: the influence of genetic, demographic and clinical information / Jennifer L. HUDSON in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1086-1094 Titre : Predicting outcomes following cognitive behaviour therapy in child anxiety disorders: the influence of genetic, demographic and clinical information Type de document : Texte imprimé et/ou numérique Auteurs : Jennifer L. HUDSON, Auteur ; Kathryn J. LESTER, Auteur ; Cathryn M. LEWIS, Auteur ; Maria TROPEANO, Auteur ; Cathy CRESWELL, Auteur ; David A. COLLIER, Auteur ; Peter J. COOPER, Auteur ; Heidi J. LYNEHAM, Auteur ; Talia MORRIS, Auteur ; Ronald M. RAPEE, Auteur ; Susanna ROBERTS, Auteur ; Jennifer A. DONALD, Auteur ; Thalia C. ELEY, Auteur Article en page(s) : p.1086-1094 Langues : Anglais (eng) Mots-clés : CBT  G × E  anxiety disorders  child anxiety disorders Index. décimale : PER Périodiques Résumé : Background Within a therapeutic gene by environment (G × E) framework, we recently demonstrated that variation in the Serotonin Transporter Promoter Polymorphism; 5HTTLPR and marker rs6330 in Nerve Growth Factor gene; NGF is associated with poorer outcomes following cognitive behaviour therapy (CBT) for child anxiety disorders. The aim of this study was to explore one potential means of extending the translational reach of G × E data in a way that may be clinically informative. We describe a ‘risk-index’ approach combining genetic, demographic and clinical data and test its ability to predict diagnostic outcome following CBT in anxious children. Method DNA and clinical data were collected from 384 children with a primary anxiety disorder undergoing CBT. We tested our risk model in five cross-validation training sets. Results In predicting treatment outcome, six variables had a minimum mean beta value of 0.5:5HTTLPR, NGF rs6330, gender, primary anxiety severity, comorbid mood disorder and comorbid externalising disorder. A risk index (range 0–8) constructed from these variables had moderate a predictive ability (AUC = .62–.69) in this study. Children scoring high on this index (5–8) were approximately three times as likely to retain their primary anxiety disorder at follow-up as compared with those children scoring 2 or less. Conclusion Significant genetic, demographic and clinical predictors of outcome following CBT for anxiety-disordered children were identified. Combining these predictors within a risk index could be used to identify which children are less likely to be diagnosis-free following CBT alone and require longer or enhanced treatment. The ‘risk-index’ approach represents one means of harnessing the translational potential of G × E data. En ligne : http://dx.doi.org/10.1111/jcpp.12092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Predicting outcomes following cognitive behaviour therapy in child anxiety disorders: the influence of genetic, demographic and clinical information [Texte imprimé et/ou numérique] / Jennifer L. HUDSON, Auteur ; Kathryn J. LESTER, Auteur ; Cathryn M. LEWIS, Auteur ; Maria TROPEANO, Auteur ; Cathy CRESWELL, Auteur ; David A. COLLIER, Auteur ; Peter J. COOPER, Auteur ; Heidi J. LYNEHAM, Auteur ; Talia MORRIS, Auteur ; Ronald M. RAPEE, Auteur ; Susanna ROBERTS, Auteur ; Jennifer A. DONALD, Auteur ; Thalia C. ELEY, Auteur . - p.1086-1094. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1086-1094 Mots-clés : CBT  G × E  anxiety disorders  child anxiety disorders Index. décimale : PER Périodiques Résumé : Background Within a therapeutic gene by environment (G × E) framework, we recently demonstrated that variation in the Serotonin Transporter Promoter Polymorphism; 5HTTLPR and marker rs6330 in Nerve Growth Factor gene; NGF is associated with poorer outcomes following cognitive behaviour therapy (CBT) for child anxiety disorders. The aim of this study was to explore one potential means of extending the translational reach of G × E data in a way that may be clinically informative. We describe a ‘risk-index’ approach combining genetic, demographic and clinical data and test its ability to predict diagnostic outcome following CBT in anxious children. Method DNA and clinical data were collected from 384 children with a primary anxiety disorder undergoing CBT. We tested our risk model in five cross-validation training sets. Results In predicting treatment outcome, six variables had a minimum mean beta value of 0.5:5HTTLPR, NGF rs6330, gender, primary anxiety severity, comorbid mood disorder and comorbid externalising disorder. A risk index (range 0–8) constructed from these variables had moderate a predictive ability (AUC = .62–.69) in this study. Children scoring high on this index (5–8) were approximately three times as likely to retain their primary anxiety disorder at follow-up as compared with those children scoring 2 or less. Conclusion Significant genetic, demographic and clinical predictors of outcome following CBT for anxiety-disordered children were identified. Combining these predictors within a risk index could be used to identify which children are less likely to be diagnosis-free following CBT alone and require longer or enhanced treatment. The ‘risk-index’ approach represents one means of harnessing the translational potential of G × E data. En ligne : http://dx.doi.org/10.1111/jcpp.12092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders / Sarah J. LEWIS in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Titre : Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders Type de document : Texte imprimé et/ou numérique Auteurs : Sarah J. LEWIS, Auteur ; Caroline RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur Article en page(s) : p.1095-1108 Langues : Anglais (eng) Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders [Texte imprimé et/ou numérique] / Sarah J. LEWIS, Auteur ; Caroline RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur . - p.1095-1108. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults / Samuel L. WOLOCK in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1109-1119 Titre : Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults Type de document : Texte imprimé et/ou numérique Auteurs : Samuel L. WOLOCK, Auteur ; Andrew YATES, Auteur ; Stephen A. PETRILL, Auteur ; Jason W. BOHLAND, Auteur ; Clancy BLAIR, Auteur ; Ning LI, Auteur ; Raghu MACHIRAJU, Auteur ; Kun HUANG, Auteur ; Christopher W. BARTLETT, Auteur Article en page(s) : p.1109-1119 Langues : Anglais (eng) Mots-clés : Genetics  environment  brain development  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Numerous studies have examined gene × environment interactions (G × E) in cognitive and behavioral domains. However, these studies have been limited in that they have not been able to directly assess differential patterns of gene expression in the human brain. Here, we assessed G × E interactions using two publically available datasets to assess if DNA variation is associated with post-mortem brain gene expression changes based on smoking behavior, a biobehavioral construct that is part of a complex system of genetic and environmental influences. Methods We conducted an expression quantitative trait locus (eQTL) study on two independent human brain gene expression datasets assessing G × E for selected psychiatric genes and smoking status. We employed linear regression to model the significance of the Gene × Smoking interaction term, followed by meta-analysis across datasets. Results Overall, we observed that the effect of DNA variation on gene expression is moderated by smoking status. Expression of 16 genes was significantly associated with single nucleotide polymorphisms that demonstrated G × E effects. The strongest finding (p = 1.9 × 10?11) was neurexin 3-alpha (NRXN3), a synaptic cell–cell adhesion molecule involved in maintenance of neural connections (such as the maintenance of smoking behavior). Other significant G × E associations include four glutamate genes. Conclusions This is one of the first studies to demonstrate G × E effects within the human brain. In particular, this study implicated NRXN3 in the maintenance of smoking. The effect of smoking on NRXN3 expression and downstream behavior is different based upon SNP genotype, indicating that DNA profiles based on SNPs could be useful in understanding the effects of smoking behaviors. These results suggest that better measurement of psychiatric conditions, and the environment in post-mortem brain studies may yield an important avenue for understanding the biological mechanisms of G × E interactions in psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults [Texte imprimé et/ou numérique] / Samuel L. WOLOCK, Auteur ; Andrew YATES, Auteur ; Stephen A. PETRILL, Auteur ; Jason W. BOHLAND, Auteur ; Clancy BLAIR, Auteur ; Ning LI, Auteur ; Raghu MACHIRAJU, Auteur ; Kun HUANG, Auteur ; Christopher W. BARTLETT, Auteur . - p.1109-1119. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1109-1119 Mots-clés : Genetics  environment  brain development  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Numerous studies have examined gene × environment interactions (G × E) in cognitive and behavioral domains. However, these studies have been limited in that they have not been able to directly assess differential patterns of gene expression in the human brain. Here, we assessed G × E interactions using two publically available datasets to assess if DNA variation is associated with post-mortem brain gene expression changes based on smoking behavior, a biobehavioral construct that is part of a complex system of genetic and environmental influences. Methods We conducted an expression quantitative trait locus (eQTL) study on two independent human brain gene expression datasets assessing G × E for selected psychiatric genes and smoking status. We employed linear regression to model the significance of the Gene × Smoking interaction term, followed by meta-analysis across datasets. Results Overall, we observed that the effect of DNA variation on gene expression is moderated by smoking status. Expression of 16 genes was significantly associated with single nucleotide polymorphisms that demonstrated G × E effects. The strongest finding (p = 1.9 × 10?11) was neurexin 3-alpha (NRXN3), a synaptic cell–cell adhesion molecule involved in maintenance of neural connections (such as the maintenance of smoking behavior). Other significant G × E associations include four glutamate genes. Conclusions This is one of the first studies to demonstrate G × E effects within the human brain. In particular, this study implicated NRXN3 in the maintenance of smoking. The effect of smoking on NRXN3 expression and downstream behavior is different based upon SNP genotype, indicating that DNA profiles based on SNPs could be useful in understanding the effects of smoking behaviors. These results suggest that better measurement of psychiatric conditions, and the environment in post-mortem brain studies may yield an important avenue for understanding the biological mechanisms of G × E interactions in psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Gene–environment interactions in genome-wide association studies: current approaches and new directions / Stacey J. WINHAM in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1120-1134 Titre : Gene–environment interactions in genome-wide association studies: current approaches and new directions Type de document : Texte imprimé et/ou numérique Auteurs : Stacey J. WINHAM, Auteur ; Joanna M. BIERNACKA, Auteur Article en page(s) : p.1120-1134 Langues : Anglais (eng) Mots-clés : Gene–environment interaction  gene-level  pathway  gene-set  data-mining Index. décimale : PER Périodiques Résumé : Background Complex psychiatric traits have long been thought to be the result of a combination of genetic and environmental factors, and gene–environment interactions are thought to play a crucial role in behavioral phenotypes and the susceptibility and progression of psychiatric disorders. Candidate gene studies to investigate hypothesized gene–environment interactions are now fairly common in human genetic research, and with the shift toward genome-wide association studies, genome-wide gene–environment interaction studies are beginning to emerge. Methods We summarize the basic ideas behind gene–environment interaction, and provide an overview of possible study designs and traditional analysis methods in the context of genome-wide analysis. We then discuss novel approaches beyond the traditional strategy of analyzing the interaction between the environmental factor and each polymorphism individually. Results Two-step filtering approaches that reduce the number of polymorphisms tested for interactions can substantially increase the power of genome-wide gene–environment studies. New analytical methods including data-mining approaches, and gene-level and pathway-level analyses, also have the capacity to improve our understanding of how complex genetic and environmental factors interact to influence psychologic and psychiatric traits. Such methods, however, have not yet been utilized much in behavioral and mental health research. Conclusions Although methods to investigate gene–environment interactions are available, there is a need for further development and extension of these methods to identify gene–environment interactions in the context of genome-wide association studies. These novel approaches need to be applied in studies of psychology and psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12114 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Gene–environment interactions in genome-wide association studies: current approaches and new directions [Texte imprimé et/ou numérique] / Stacey J. WINHAM, Auteur ; Joanna M. BIERNACKA, Auteur . - p.1120-1134. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1120-1134 Mots-clés : Gene–environment interaction  gene-level  pathway  gene-set  data-mining Index. décimale : PER Périodiques Résumé : Background Complex psychiatric traits have long been thought to be the result of a combination of genetic and environmental factors, and gene–environment interactions are thought to play a crucial role in behavioral phenotypes and the susceptibility and progression of psychiatric disorders. Candidate gene studies to investigate hypothesized gene–environment interactions are now fairly common in human genetic research, and with the shift toward genome-wide association studies, genome-wide gene–environment interaction studies are beginning to emerge. Methods We summarize the basic ideas behind gene–environment interaction, and provide an overview of possible study designs and traditional analysis methods in the context of genome-wide analysis. We then discuss novel approaches beyond the traditional strategy of analyzing the interaction between the environmental factor and each polymorphism individually. Results Two-step filtering approaches that reduce the number of polymorphisms tested for interactions can substantially increase the power of genome-wide gene–environment studies. New analytical methods including data-mining approaches, and gene-level and pathway-level analyses, also have the capacity to improve our understanding of how complex genetic and environmental factors interact to influence psychologic and psychiatric traits. Such methods, however, have not yet been utilized much in behavioral and mental health research. Conclusions Although methods to investigate gene–environment interactions are available, there is a need for further development and extension of these methods to identify gene–environment interactions in the context of genome-wide association studies. These novel approaches need to be applied in studies of psychology and psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12114 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Confirmatory and competitive evaluation of alternative gene-environment interaction hypotheses / Jay BELSKY in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1135-1143 Titre : Confirmatory and competitive evaluation of alternative gene-environment interaction hypotheses Type de document : Texte imprimé et/ou numérique Auteurs : Jay BELSKY, Auteur ; Michael PLUESS, Auteur ; Keith F. WIDAMAN, Auteur Article en page(s) : p.1135-1143 Langues : Anglais (eng) Mots-clés : Gene-environment interaction  diathesis-stress  differential susceptibility  child care  DRD4 Index. décimale : PER Périodiques Résumé : Background Most gene-environment interaction (GXE) research, though based on clear, vulnerability-oriented hypotheses, is carried out using exploratory rather than hypothesis-informed statistical tests, limiting power and making formal evaluation of competing GXE propositions difficult. Method We present and illustrate a new regression technique which affords direct testing of theory-derived predictions, as well as competitive evaluation of alternative diathesis-stress and differential-susceptibility propositions, using data on the moderating effect of DRD4 with regard to the effect of childcare quality on children's social functioning. Results Results show that (a) the new approach detects interactions that the traditional one does not; (b) the discerned GXE fit the differential-susceptibility model better than the diathesis-stress one; and (c) a strong rather than weak version of differential susceptibility is empirically supported. Conclusion The new method better fits the theoretical ‘glove’ to the empirical ‘hand,’ raising the prospect that some failures to replicate GXE results may derive from standard statistical approaches being less than ideal. En ligne : http://dx.doi.org/10.1111/jcpp.12075 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Confirmatory and competitive evaluation of alternative gene-environment interaction hypotheses [Texte imprimé et/ou numérique] / Jay BELSKY, Auteur ; Michael PLUESS, Auteur ; Keith F. WIDAMAN, Auteur . - p.1135-1143. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1135-1143 Mots-clés : Gene-environment interaction  diathesis-stress  differential susceptibility  child care  DRD4 Index. décimale : PER Périodiques Résumé : Background Most gene-environment interaction (GXE) research, though based on clear, vulnerability-oriented hypotheses, is carried out using exploratory rather than hypothesis-informed statistical tests, limiting power and making formal evaluation of competing GXE propositions difficult. Method We present and illustrate a new regression technique which affords direct testing of theory-derived predictions, as well as competitive evaluation of alternative diathesis-stress and differential-susceptibility propositions, using data on the moderating effect of DRD4 with regard to the effect of childcare quality on children's social functioning. Results Results show that (a) the new approach detects interactions that the traditional one does not; (b) the discerned GXE fit the differential-susceptibility model better than the diathesis-stress one; and (c) a strong rather than weak version of differential susceptibility is empirically supported. Conclusion The new method better fits the theoretical ‘glove’ to the empirical ‘hand,’ raising the prospect that some failures to replicate GXE results may derive from standard statistical approaches being less than ideal. En ligne : http://dx.doi.org/10.1111/jcpp.12075 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Commentary: Study of gene–environment interplay – a lesson in how to keep oneself busy for the foreseeable future / Essi VIDING in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1144-1146 Titre : Commentary: Study of gene–environment interplay – a lesson in how to keep oneself busy for the foreseeable future Type de document : Texte imprimé et/ou numérique Auteurs : Essi VIDING, Auteur Article en page(s) : p.1144-1146 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Psychologists and psychiatrists have long been aware that individuals differ in their response to environmental stressors. It is equally apparent that whilst positive or corrective environmental factors help some individuals, others seem to benefit little, if at all. To make the matters even more interesting (at least for a researcher who is hoping for a long and painstaking road of scientific discovery), it is not safe to assume that environments operate entirely independently of the study participants. En ligne : http://dx.doi.org/10.1111/jcpp.12129 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Commentary: Study of gene–environment interplay – a lesson in how to keep oneself busy for the foreseeable future [Texte imprimé et/ou numérique] / Essi VIDING, Auteur . - p.1144-1146. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1144-1146 Index. décimale : PER Périodiques Résumé : Psychologists and psychiatrists have long been aware that individuals differ in their response to environmental stressors. It is equally apparent that whilst positive or corrective environmental factors help some individuals, others seem to benefit little, if at all. To make the matters even more interesting (at least for a researcher who is hoping for a long and painstaking road of scientific discovery), it is not safe to assume that environments operate entirely independently of the study participants. En ligne : http://dx.doi.org/10.1111/jcpp.12129 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Commentary: Missing heritability, polygenic scores, and gene–environment correlation / Robert PLOMIN in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1147-1149 Titre : Commentary: Missing heritability, polygenic scores, and gene–environment correlation Type de document : Texte imprimé et/ou numérique Auteurs : Robert PLOMIN, Auteur Article en page(s) : p.1147-1149 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This special issue amply fulfils its aim of moving the study of gene × environment (GE) interplay forward constructively and creatively, exploiting contributions from diverse disciplines. Rather than discussing the many interesting findings and methods in this special issue, I will comment on two cross-cutting issues – one about genes and the other about the environment – that came to mind as I read these articles. En ligne : http://dx.doi.org/10.1111/jcpp.12128 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Commentary: Missing heritability, polygenic scores, and gene–environment correlation [Texte imprimé et/ou numérique] / Robert PLOMIN, Auteur . - p.1147-1149. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1147-1149 Index. décimale : PER Périodiques Résumé : This special issue amply fulfils its aim of moving the study of gene × environment (GE) interplay forward constructively and creatively, exploiting contributions from diverse disciplines. Rather than discussing the many interesting findings and methods in this special issue, I will comment on two cross-cutting issues – one about genes and the other about the environment – that came to mind as I read these articles. En ligne : http://dx.doi.org/10.1111/jcpp.12128 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Commentary: Gene by environment interplay and psychopathology – in search of a paradigm / Joel T. NIGG in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1150-1152 Titre : Commentary: Gene by environment interplay and psychopathology – in search of a paradigm Type de document : Texte imprimé et/ou numérique Auteurs : Joel T. NIGG, Auteur Article en page(s) : p.1150-1152 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The articles in this Special Issue (SI) extend research on G×E in multiple ways, showing the growing importance of specifying kinds of G×E models (e.g., bioecological, susceptibility, stress-diathesis), incorporation of sophisticated ways of measuring types of G×E correlations (rGE), checking effects of statistical artifact, exemplifying an impressive range of quantitative and biological methodologies, and pointing to clearly needed next-step studies such as summarizing across many genes in gene sets (Bentley et al.) or in genome-wide pathway based approaches to G×E (Winham Biernacka) and prediction of clinical outcomes (Rapee et al.). As a group, they document nicely that gene × environment research has come of age. What is the import of this? Does it represent a major new development in our field, or merely an incremental change of a framework that remains fundamentally unchanged? En ligne : http://dx.doi.org/10.1111/jcpp.12134 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Commentary: Gene by environment interplay and psychopathology – in search of a paradigm [Texte imprimé et/ou numérique] / Joel T. NIGG, Auteur . - p.1150-1152. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1150-1152 Index. décimale : PER Périodiques Résumé : The articles in this Special Issue (SI) extend research on G×E in multiple ways, showing the growing importance of specifying kinds of G×E models (e.g., bioecological, susceptibility, stress-diathesis), incorporation of sophisticated ways of measuring types of G×E correlations (rGE), checking effects of statistical artifact, exemplifying an impressive range of quantitative and biological methodologies, and pointing to clearly needed next-step studies such as summarizing across many genes in gene sets (Bentley et al.) or in genome-wide pathway based approaches to G×E (Winham Biernacka) and prediction of clinical outcomes (Rapee et al.). As a group, they document nicely that gene × environment research has come of age. What is the import of this? Does it represent a major new development in our field, or merely an incremental change of a framework that remains fundamentally unchanged? En ligne : http://dx.doi.org/10.1111/jcpp.12134 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212