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The developmental progression of age 14 behavioral disinhibition, early age of sexual initiation, and subsequent sexual risk-taking behavior / Diana R. SAMEK in Journal of Child Psychology and Psychiatry, 55-7 (July 2014)
[article]
Titre : The developmental progression of age 14 behavioral disinhibition, early age of sexual initiation, and subsequent sexual risk-taking behavior Type de document : Texte imprimé et/ou numérique Auteurs : Diana R. SAMEK, Auteur ; William G. IACONO, Auteur ; Margaret A. KEYES, Auteur ; Marina EPSTEIN, Auteur ; Marina A. BORNOVALOVA, Auteur ; Matt MCGUE, Auteur Article en page(s) : p.784-792 Langues : Anglais (eng) Mots-clés : Behavior genetics behavioral disinhibition externalizing disorder gender differences sexual behavior Index. décimale : PER Périodiques Résumé : Background Research has demonstrated a consistent relationship between early sexual experience and subsequent sexual risk-taking behaviors. We hypothesized that this relationship is due to a general predisposition toward behavioral disinhibition (BD), and that relationships among BD, early sex, and subsequent risky sexual behavior may be influenced by common genetic influences for males and common environmental influences for females. Methods A prospective sample of 1,512 same-sex adolescent twins (50.2% female) was used. Adolescent BD was measured by clinical symptom counts of conduct disorder, oppositional defiant disorder, and self-reported delinquent behavior (age 14). Age of sexual initiation was defined as first age of consensual oral or penetrative sex (mean age ~17). Adult risky sexual behavior was defined by sexual behaviors under the influence of drugs and alcohol and number of casual sexual partners in the past year (age 24). Results Multivariate analyses showed evidence for substantial common genetic variance among age 14 BD, age at sexual initiation, and adult risky sexual behavior for males, but not females. There was no significant difference in the degree of common environmental influence on these variables for females compared to males. Notably, age of sexual initiation was not significantly correlated with age 24 risky sexual behavior for females. Conclusion The relationship between early sex and later risky sex can be better understood through a general liability toward BD, which is influenced primarily by genetic factors for males. The association between age 14 BD and age of sexual initiation was influenced through a combination of genetic and environmental factors for females; however, age of sexual initiation does not appear to be a salient predictor of adult women's sexual risk-taking behavior. Findings suggest that prevention programs aimed at reducing sexual risk behavior might target youth exhibiting BD by age 14, particularly males. More research is needed on what predicts adult sexual risk-taking behavior for females. En ligne : http://dx.doi.org/10.1111/jcpp.12176 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=235
in Journal of Child Psychology and Psychiatry > 55-7 (July 2014) . - p.784-792[article] The developmental progression of age 14 behavioral disinhibition, early age of sexual initiation, and subsequent sexual risk-taking behavior [Texte imprimé et/ou numérique] / Diana R. SAMEK, Auteur ; William G. IACONO, Auteur ; Margaret A. KEYES, Auteur ; Marina EPSTEIN, Auteur ; Marina A. BORNOVALOVA, Auteur ; Matt MCGUE, Auteur . - p.784-792.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 55-7 (July 2014) . - p.784-792
Mots-clés : Behavior genetics behavioral disinhibition externalizing disorder gender differences sexual behavior Index. décimale : PER Périodiques Résumé : Background Research has demonstrated a consistent relationship between early sexual experience and subsequent sexual risk-taking behaviors. We hypothesized that this relationship is due to a general predisposition toward behavioral disinhibition (BD), and that relationships among BD, early sex, and subsequent risky sexual behavior may be influenced by common genetic influences for males and common environmental influences for females. Methods A prospective sample of 1,512 same-sex adolescent twins (50.2% female) was used. Adolescent BD was measured by clinical symptom counts of conduct disorder, oppositional defiant disorder, and self-reported delinquent behavior (age 14). Age of sexual initiation was defined as first age of consensual oral or penetrative sex (mean age ~17). Adult risky sexual behavior was defined by sexual behaviors under the influence of drugs and alcohol and number of casual sexual partners in the past year (age 24). Results Multivariate analyses showed evidence for substantial common genetic variance among age 14 BD, age at sexual initiation, and adult risky sexual behavior for males, but not females. There was no significant difference in the degree of common environmental influence on these variables for females compared to males. Notably, age of sexual initiation was not significantly correlated with age 24 risky sexual behavior for females. Conclusion The relationship between early sex and later risky sex can be better understood through a general liability toward BD, which is influenced primarily by genetic factors for males. The association between age 14 BD and age of sexual initiation was influenced through a combination of genetic and environmental factors for females; however, age of sexual initiation does not appear to be a salient predictor of adult women's sexual risk-taking behavior. Findings suggest that prevention programs aimed at reducing sexual risk behavior might target youth exhibiting BD by age 14, particularly males. More research is needed on what predicts adult sexual risk-taking behavior for females. En ligne : http://dx.doi.org/10.1111/jcpp.12176 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=235 Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development / K. Paige HARDEN in Journal of Child Psychology and Psychiatry, 56-12 (December 2015)
[article]
Titre : Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development Type de document : Texte imprimé et/ou numérique Auteurs : K. Paige HARDEN, Auteur ; Megan W. PATTERSON, Auteur ; Daniel A. BRILEY, Auteur ; Laura E. ENGELHARDT, Auteur ; Natalie KRETSCH, Auteur ; Frank D. MANN, Auteur ; Jennifer L. TACKETT, Auteur ; Elliot M. TUCKER-DROB, Auteur Article en page(s) : p.1370-1379 Langues : Anglais (eng) Mots-clés : Antisocial behavior aggression rule-breaking puberty adolescence behavior genetics Index. décimale : PER Périodiques Résumé : Background Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. Method Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (?12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. Results Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. Conclusions Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression. En ligne : http://dx.doi.org/10.1111/jcpp.12419 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273
in Journal of Child Psychology and Psychiatry > 56-12 (December 2015) . - p.1370-1379[article] Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development [Texte imprimé et/ou numérique] / K. Paige HARDEN, Auteur ; Megan W. PATTERSON, Auteur ; Daniel A. BRILEY, Auteur ; Laura E. ENGELHARDT, Auteur ; Natalie KRETSCH, Auteur ; Frank D. MANN, Auteur ; Jennifer L. TACKETT, Auteur ; Elliot M. TUCKER-DROB, Auteur . - p.1370-1379.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 56-12 (December 2015) . - p.1370-1379
Mots-clés : Antisocial behavior aggression rule-breaking puberty adolescence behavior genetics Index. décimale : PER Périodiques Résumé : Background Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. Method Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (?12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. Results Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. Conclusions Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression. En ligne : http://dx.doi.org/10.1111/jcpp.12419 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273 Visual Disengagement: Genetic Architecture and Relation to Autistic Traits in the General Population / Monica SIQUEIROS SANCHEZ in Journal of Autism and Developmental Disorders, 50-6 (June 2020)
[article]
Titre : Visual Disengagement: Genetic Architecture and Relation to Autistic Traits in the General Population Type de document : Texte imprimé et/ou numérique Auteurs : Monica SIQUEIROS SANCHEZ, Auteur ; Erik PETTERSSON, Auteur ; Daniel P KENNEDY, Auteur ; Sven BÖLTE, Auteur ; Paul LICHTENSTEIN, Auteur ; Brian M. D'ONOFRIO, Auteur ; Terje FALCK-YTTER, Auteur Article en page(s) : p.2188-2200 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders Autistic traits Behavior genetics Gap-overlap task Visual disengagement Index. décimale : PER Périodiques Résumé : Visual disengagement has been hypothesized as an endophenotype for autism. In this study we used twin modelling to assess the role of genetics in basic measures of visual disengagement, and tested their putative association to autistic traits in the general population. We used the Gap Overlap task in a sample of 492 twins. Results showed that most of the covariance among eye movement latencies across conditions was shared and primarily genetic. Further, there were unique genetic contributions to the Gap condition, but not to the Overlap condition-i.e. the one theorized to capture visual disengagement. We found no phenotypic association between autistic traits and disengagement, thus not supporting the hypothesis of visual disengagement as an endophenotype for autistic traits. En ligne : http://dx.doi.org/10.1007/s10803-019-03974-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=425
in Journal of Autism and Developmental Disorders > 50-6 (June 2020) . - p.2188-2200[article] Visual Disengagement: Genetic Architecture and Relation to Autistic Traits in the General Population [Texte imprimé et/ou numérique] / Monica SIQUEIROS SANCHEZ, Auteur ; Erik PETTERSSON, Auteur ; Daniel P KENNEDY, Auteur ; Sven BÖLTE, Auteur ; Paul LICHTENSTEIN, Auteur ; Brian M. D'ONOFRIO, Auteur ; Terje FALCK-YTTER, Auteur . - p.2188-2200.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 50-6 (June 2020) . - p.2188-2200
Mots-clés : Autism spectrum disorders Autistic traits Behavior genetics Gap-overlap task Visual disengagement Index. décimale : PER Périodiques Résumé : Visual disengagement has been hypothesized as an endophenotype for autism. In this study we used twin modelling to assess the role of genetics in basic measures of visual disengagement, and tested their putative association to autistic traits in the general population. We used the Gap Overlap task in a sample of 492 twins. Results showed that most of the covariance among eye movement latencies across conditions was shared and primarily genetic. Further, there were unique genetic contributions to the Gap condition, but not to the Overlap condition-i.e. the one theorized to capture visual disengagement. We found no phenotypic association between autistic traits and disengagement, thus not supporting the hypothesis of visual disengagement as an endophenotype for autistic traits. En ligne : http://dx.doi.org/10.1007/s10803-019-03974-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=425 Maltreatment-associated neurodevelopmental disorders: a co-twin control analysis / Lisa DINKLER in Journal of Child Psychology and Psychiatry, 58-6 (June 2017)
[article]
Titre : Maltreatment-associated neurodevelopmental disorders: a co-twin control analysis Type de document : Texte imprimé et/ou numérique Auteurs : Lisa DINKLER, Auteur ; Sebastian LUNDSTROM, Auteur ; Ruchika GAJWANI, Auteur ; Paul LICHTENSTEIN, Auteur ; Christopher GILLBERG, Auteur ; Helen MINNIS, Auteur Article en page(s) : p.691-701 Langues : Anglais (eng) Mots-clés : Child maltreatment child abuse neurodevelopmental disorders behavior genetics co-twin control design Index. décimale : PER Périodiques Résumé : Background Childhood maltreatment (CM) is strongly associated with psychiatric disorders in childhood and adulthood. Previous findings suggest that the association between CM and psychiatric disorders is partly causal and partly due to familial confounding, but few studies have investigated the mechanisms behind the association between CM and neurodevelopmental disorders (NDDs). Our objective was to determine whether maltreated children have an elevated number of NDDs and whether CM is a risk factor for an increased NDD ‘load’ and increased NDD symptoms when controlling for familial effects. Methods We used a cross-sectional sample from a population-representative Swedish twin study, comprising 8,192 nine-year-old twins born in Sweden between 1997 and 2005. CM was defined as parent-reported exposure to emotional abuse/neglect, physical neglect, physical abuse, and/or sexual abuse. Four NDDs were measured with the Autism–Tics, AD/HD, and other comorbidities inventory. Results Maltreated children had a greater mean number of NDDs than nonmaltreated children. In a co-twin control design, CM-discordant monozygotic twins did not differ significantly for their number of NDDs, suggesting that CM is not associated with an increased load of NDDs when genetic and shared environmental factors are taken into account. However, CM was associated with a small increase in symptoms of attention-deficit/hyperactivity disorder and autism spectrum disorder in CM-discordant MZ twins, although most of the covariance of CM with NDD symptoms was explained by common genetic effects. Conclusions Maltreated children are at higher risk of having multiple NDDs. Our findings are, however, not consistent with the notion that CM causes the increased NDD load in maltreated children. Maltreated children should receive a full neurodevelopmental assessment, and clinicians should be aware that children with multiple NDDs are at higher risk of maltreatment. En ligne : http://dx.doi.org/10.1111/jcpp.12682 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=308
in Journal of Child Psychology and Psychiatry > 58-6 (June 2017) . - p.691-701[article] Maltreatment-associated neurodevelopmental disorders: a co-twin control analysis [Texte imprimé et/ou numérique] / Lisa DINKLER, Auteur ; Sebastian LUNDSTROM, Auteur ; Ruchika GAJWANI, Auteur ; Paul LICHTENSTEIN, Auteur ; Christopher GILLBERG, Auteur ; Helen MINNIS, Auteur . - p.691-701.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 58-6 (June 2017) . - p.691-701
Mots-clés : Child maltreatment child abuse neurodevelopmental disorders behavior genetics co-twin control design Index. décimale : PER Périodiques Résumé : Background Childhood maltreatment (CM) is strongly associated with psychiatric disorders in childhood and adulthood. Previous findings suggest that the association between CM and psychiatric disorders is partly causal and partly due to familial confounding, but few studies have investigated the mechanisms behind the association between CM and neurodevelopmental disorders (NDDs). Our objective was to determine whether maltreated children have an elevated number of NDDs and whether CM is a risk factor for an increased NDD ‘load’ and increased NDD symptoms when controlling for familial effects. Methods We used a cross-sectional sample from a population-representative Swedish twin study, comprising 8,192 nine-year-old twins born in Sweden between 1997 and 2005. CM was defined as parent-reported exposure to emotional abuse/neglect, physical neglect, physical abuse, and/or sexual abuse. Four NDDs were measured with the Autism–Tics, AD/HD, and other comorbidities inventory. Results Maltreated children had a greater mean number of NDDs than nonmaltreated children. In a co-twin control design, CM-discordant monozygotic twins did not differ significantly for their number of NDDs, suggesting that CM is not associated with an increased load of NDDs when genetic and shared environmental factors are taken into account. However, CM was associated with a small increase in symptoms of attention-deficit/hyperactivity disorder and autism spectrum disorder in CM-discordant MZ twins, although most of the covariance of CM with NDD symptoms was explained by common genetic effects. Conclusions Maltreated children are at higher risk of having multiple NDDs. Our findings are, however, not consistent with the notion that CM causes the increased NDD load in maltreated children. Maltreated children should receive a full neurodevelopmental assessment, and clinicians should be aware that children with multiple NDDs are at higher risk of maltreatment. En ligne : http://dx.doi.org/10.1111/jcpp.12682 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=308 Simulated nonlinear genetic and environmental dynamics of complex traits / Michael D. HUNTER in Development and Psychopathology, 35-2 (May 2023)
[article]
Titre : Simulated nonlinear genetic and environmental dynamics of complex traits Type de document : Texte imprimé et/ou numérique Auteurs : Michael D. HUNTER, Auteur ; Kevin L. MCKEE, Auteur ; Eric TURKHEIMER, Auteur Article en page(s) : p.662-677 Langues : Anglais (eng) Mots-clés : behavior genetics dynamical systems GWAS heritability simulation Index. décimale : PER Périodiques Résumé : Genetic studies of complex traits often show disparities in estimated heritability depending on the method used, whether by genomic associations or twin and family studies. We present a simulation of individual genomes with dynamic environmental conditions to consider how linear and nonlinear effects, gene-by-environment interactions, and gene-by-environment correlations may work together to govern the long-term development of complex traits and affect estimates of heritability from common methods. Our simulation studies demonstrate that the genetic effects estimated by genome wide association studies in unrelated individuals are inadequate to characterize gene-by-environment interaction, while including related individuals in genome-wide complex trait analysis (GCTA) allows gene-by-environment interactions to be recovered in the heritability. These theoretical findings provide an explanation for the ''missing heritability'' problem and bridge the conceptual gap between the most common findings of GCTA and twin studies. Future studies may use the simulation model to test hypotheses about phenotypic complexity either in an exploratory way or by replicating well-established observations of specific phenotypes. En ligne : http://dx.doi.org/10.1017/S0954579421001796 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=504
in Development and Psychopathology > 35-2 (May 2023) . - p.662-677[article] Simulated nonlinear genetic and environmental dynamics of complex traits [Texte imprimé et/ou numérique] / Michael D. HUNTER, Auteur ; Kevin L. MCKEE, Auteur ; Eric TURKHEIMER, Auteur . - p.662-677.
Langues : Anglais (eng)
in Development and Psychopathology > 35-2 (May 2023) . - p.662-677
Mots-clés : behavior genetics dynamical systems GWAS heritability simulation Index. décimale : PER Périodiques Résumé : Genetic studies of complex traits often show disparities in estimated heritability depending on the method used, whether by genomic associations or twin and family studies. We present a simulation of individual genomes with dynamic environmental conditions to consider how linear and nonlinear effects, gene-by-environment interactions, and gene-by-environment correlations may work together to govern the long-term development of complex traits and affect estimates of heritability from common methods. Our simulation studies demonstrate that the genetic effects estimated by genome wide association studies in unrelated individuals are inadequate to characterize gene-by-environment interaction, while including related individuals in genome-wide complex trait analysis (GCTA) allows gene-by-environment interactions to be recovered in the heritability. These theoretical findings provide an explanation for the ''missing heritability'' problem and bridge the conceptual gap between the most common findings of GCTA and twin studies. Future studies may use the simulation model to test hypotheses about phenotypic complexity either in an exploratory way or by replicating well-established observations of specific phenotypes. En ligne : http://dx.doi.org/10.1017/S0954579421001796 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=504