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Auteur Matt MCGUE
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Documents disponibles écrits par cet auteur (24)
Faire une suggestion Affiner la rechercheAntisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction / Diana R. SAMEK in Development and Psychopathology, 29-1 (February 2017)
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[article]
Titre : Antisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction Type de document : texte imprimé Auteurs : Diana R. SAMEK, Auteur ; Brian M. HICKS, Auteur ; Margaret A. KEYES, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur Article en page(s) : p.155-172 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : AbstractGene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene–environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior. En ligne : http://dx.doi.org/10.1017/s0954579416000109 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298
in Development and Psychopathology > 29-1 (February 2017) . - p.155-172[article] Antisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction [texte imprimé] / Diana R. SAMEK, Auteur ; Brian M. HICKS, Auteur ; Margaret A. KEYES, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur . - p.155-172.
Langues : Anglais (eng)
in Development and Psychopathology > 29-1 (February 2017) . - p.155-172
Index. décimale : PER Périodiques Résumé : AbstractGene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene–environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior. En ligne : http://dx.doi.org/10.1017/s0954579416000109 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298 Changes in genetic and environmental influences on the development of nicotine dependence and major depressive disorder from middle adolescence to early adulthood / Erin C. TULLY in Development and Psychopathology, 22-4 (November 2010)
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Titre : Changes in genetic and environmental influences on the development of nicotine dependence and major depressive disorder from middle adolescence to early adulthood Type de document : texte imprimé Auteurs : Erin C. TULLY, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur Année de publication : 2010 Article en page(s) : p.831-848 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other. En ligne : http://dx.doi.org/10.1017/s0954579410000490 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=110
in Development and Psychopathology > 22-4 (November 2010) . - p.831-848[article] Changes in genetic and environmental influences on the development of nicotine dependence and major depressive disorder from middle adolescence to early adulthood [texte imprimé] / Erin C. TULLY, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur . - 2010 . - p.831-848.
Langues : Anglais (eng)
in Development and Psychopathology > 22-4 (November 2010) . - p.831-848
Index. décimale : PER Périodiques Résumé : This longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other. En ligne : http://dx.doi.org/10.1017/s0954579410000490 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=110 Close relationships and depression: A developmental cascade approach / Rebecca J. GOODMAN in Development and Psychopathology, 31-4 (October 2019)
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Titre : Close relationships and depression: A developmental cascade approach Type de document : texte imprimé Auteurs : Rebecca J. GOODMAN, Auteur ; Diana R. SAMEK, Auteur ; Sylia WILSON, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur Article en page(s) : p.1451-1465 Langues : Anglais (eng) Mots-clés : depression developmental cascade interpersonal relationships longitudinal research major depressive disorder problematic relationships Index. décimale : PER Périodiques Résumé : Previous research has shown that problematic parent-child, peer, and romantic partner relationships are associated with an increased likelihood for major depressive disorder (MDD). Less research has evaluated the developmental unfolding of how these interpersonal relationship features are both an antecedent versus a consequence of MDD symptoms from adolescence through young adulthood. These gaps were evaluated using a large community sample (N = 1,127; 54% female, 96% white) via a developmental cascade model. Results showed support for significant antecedent effects, as greater parent-child relationship problems at ages 11 and 17 predicted rank-order increases in MDD symptoms at ages 14 and 20. Supporting a developmental cascade of problematic social relationships, greater parent-child relationship problems at ages 11 and 14 also predicted greater subsequent rank-order increases in antisocial peer affiliation at ages 14 and 17. Greater affiliation to antisocial peers at age 20 predicted greater rank-order increases in romantic relationship problems at age 24, which in turn predicted greater MDD symptoms at age 29. Cross-effects were generally small (betas = .16), illustrating other factors may be relevant to the development or consequences of MDD. Nonetheless, findings support the importance of efforts to strengthen social support networks to offset risk as well as potentially treat depression. En ligne : http://dx.doi.org/10.1017/s0954579418001037 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=406
in Development and Psychopathology > 31-4 (October 2019) . - p.1451-1465[article] Close relationships and depression: A developmental cascade approach [texte imprimé] / Rebecca J. GOODMAN, Auteur ; Diana R. SAMEK, Auteur ; Sylia WILSON, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur . - p.1451-1465.
Langues : Anglais (eng)
in Development and Psychopathology > 31-4 (October 2019) . - p.1451-1465
Mots-clés : depression developmental cascade interpersonal relationships longitudinal research major depressive disorder problematic relationships Index. décimale : PER Périodiques Résumé : Previous research has shown that problematic parent-child, peer, and romantic partner relationships are associated with an increased likelihood for major depressive disorder (MDD). Less research has evaluated the developmental unfolding of how these interpersonal relationship features are both an antecedent versus a consequence of MDD symptoms from adolescence through young adulthood. These gaps were evaluated using a large community sample (N = 1,127; 54% female, 96% white) via a developmental cascade model. Results showed support for significant antecedent effects, as greater parent-child relationship problems at ages 11 and 17 predicted rank-order increases in MDD symptoms at ages 14 and 20. Supporting a developmental cascade of problematic social relationships, greater parent-child relationship problems at ages 11 and 14 also predicted greater subsequent rank-order increases in antisocial peer affiliation at ages 14 and 17. Greater affiliation to antisocial peers at age 20 predicted greater rank-order increases in romantic relationship problems at age 24, which in turn predicted greater MDD symptoms at age 29. Cross-effects were generally small (betas = .16), illustrating other factors may be relevant to the development or consequences of MDD. Nonetheless, findings support the importance of efforts to strengthen social support networks to offset risk as well as potentially treat depression. En ligne : http://dx.doi.org/10.1017/s0954579418001037 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=406 Confirming the etiology of adolescent acting-out behaviors: an examination of observer-ratings in a sample of adoptive and biological siblings / S. Alexandra BURT in Journal of Child Psychology and Psychiatry, 52-5 (May 2011)
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Titre : Confirming the etiology of adolescent acting-out behaviors: an examination of observer-ratings in a sample of adoptive and biological siblings Type de document : texte imprimé Auteurs : S. Alexandra BURT, Auteur ; Ashlea M. KLAHR, Auteur ; Martha A. RUETER, Auteur ; Matt MCGUE, Auteur ; William G. IACONO, Auteur Année de publication : 2011 Article en page(s) : p.519-526 Langues : Anglais (eng) Mots-clés : Shared environment antisocial behavior adoption design observer-ratings Index. décimale : PER Périodiques Résumé : Background: A recent meta-analysis revealed moderate shared environmental influences (C) on most forms of child and adolescent psychopathology (Burt, 2009), including antisocial behavior. Critically, however, the research analyzed in this meta-analysis relied largely on specific informant-reports (and particularly parent and child reports), each of which is subject to various sources of rater bias. Observer-ratings of children’s behaviors avoid many of these biases, and are thus well suited to verify the presence of C. Given this, we sought to buttress the evidence supporting C in two key ways. First, we sought to confirm that C contributes to observer-ratings in a sample of adoptive siblings, as similarity between adoptive siblings constitutes a ‘direct’ estimate of C. Second, we sought to confirm that these shared environmental influences persist across informants (i.e., the effects are not specific to the rater or the context in question).
Methods: The current study examined the etiology of observer-ratings of acting-out behaviors, as well as sources of etiological overlap across observer-ratings, adolescent self-report and maternal-report in sample of over 600 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS).
Results: Results revealed moderate and significant shared environmental influences on observer-ratings (31%), as well as on the other informant-reports (20–23%). Moreover, a portion of these effects overlapped across measures (C correlations ranged from .32 to .34).
Conclusions: Such findings argue against passive gene–environment correlations (rGE) and rater bias as primary explanations for earlier findings of C on antisocial behavior, and in this way, offer a critical extension of prior work indicating that the role of shared environmental influences on child and adolescent antisocial behavior was dismissed too soon.En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02334.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121
in Journal of Child Psychology and Psychiatry > 52-5 (May 2011) . - p.519-526[article] Confirming the etiology of adolescent acting-out behaviors: an examination of observer-ratings in a sample of adoptive and biological siblings [texte imprimé] / S. Alexandra BURT, Auteur ; Ashlea M. KLAHR, Auteur ; Martha A. RUETER, Auteur ; Matt MCGUE, Auteur ; William G. IACONO, Auteur . - 2011 . - p.519-526.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 52-5 (May 2011) . - p.519-526
Mots-clés : Shared environment antisocial behavior adoption design observer-ratings Index. décimale : PER Périodiques Résumé : Background: A recent meta-analysis revealed moderate shared environmental influences (C) on most forms of child and adolescent psychopathology (Burt, 2009), including antisocial behavior. Critically, however, the research analyzed in this meta-analysis relied largely on specific informant-reports (and particularly parent and child reports), each of which is subject to various sources of rater bias. Observer-ratings of children’s behaviors avoid many of these biases, and are thus well suited to verify the presence of C. Given this, we sought to buttress the evidence supporting C in two key ways. First, we sought to confirm that C contributes to observer-ratings in a sample of adoptive siblings, as similarity between adoptive siblings constitutes a ‘direct’ estimate of C. Second, we sought to confirm that these shared environmental influences persist across informants (i.e., the effects are not specific to the rater or the context in question).
Methods: The current study examined the etiology of observer-ratings of acting-out behaviors, as well as sources of etiological overlap across observer-ratings, adolescent self-report and maternal-report in sample of over 600 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS).
Results: Results revealed moderate and significant shared environmental influences on observer-ratings (31%), as well as on the other informant-reports (20–23%). Moreover, a portion of these effects overlapped across measures (C correlations ranged from .32 to .34).
Conclusions: Such findings argue against passive gene–environment correlations (rGE) and rater bias as primary explanations for earlier findings of C on antisocial behavior, and in this way, offer a critical extension of prior work indicating that the role of shared environmental influences on child and adolescent antisocial behavior was dismissed too soon.En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02334.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121 Confluence of genes, environment, development, and behavior in a post Genome-Wide Association Study world / Scott I. VRIEZE in Development and Psychopathology, 24-4 (November 2012)
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Titre : Confluence of genes, environment, development, and behavior in a post Genome-Wide Association Study world Type de document : texte imprimé Auteurs : Scott I. VRIEZE, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur Année de publication : 2012 Article en page(s) : p.1195-1214 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This article serves to outline a research paradigm to investigate main effects and interactions of genes, environment, and development on behavior and psychiatric illness. We provide a historical context for candidate gene studies and genome-wide association studies, including benefits, limitations, and expected payoffs. Using substance use and abuse as our driving example, we then turn to the importance of etiological psychological theory in guiding genetic, environmental, and developmental research, as well as the utility of refined phenotypic measures, such as endophenotypes, in the pursuit of etiological understanding and focused tests of genetic and environmental associations. Phenotypic measurement has received considerable attention in the history of psychology and is informed by psychometrics, whereas the environment remains relatively poorly measured and is often confounded with genetic effects (i.e., gene–environment correlation). Genetically informed designs, which are no longer limited to twin and adoption studies thanks to ever-cheaper genotyping, are required to understand environmental influences. Finally, we outline the vast amount of individual difference in structural genomic variation, most of which remains to be leveraged in genetic association tests. Although the genetic data can be massive and burdensome (tens of millions of variants per person), we argue that improved understanding of genomic structure and function will provide investigators with new tools to test specific a priori hypotheses derived from etiological psychological theory, much like current candidate gene research but with less confusion and more payoff than candidate gene research has to date. En ligne : http://dx.doi.org/10.1017/S0954579412000648 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=182
in Development and Psychopathology > 24-4 (November 2012) . - p.1195-1214[article] Confluence of genes, environment, development, and behavior in a post Genome-Wide Association Study world [texte imprimé] / Scott I. VRIEZE, Auteur ; William G. IACONO, Auteur ; Matt MCGUE, Auteur . - 2012 . - p.1195-1214.
Langues : Anglais (eng)
in Development and Psychopathology > 24-4 (November 2012) . - p.1195-1214
Index. décimale : PER Périodiques Résumé : This article serves to outline a research paradigm to investigate main effects and interactions of genes, environment, and development on behavior and psychiatric illness. We provide a historical context for candidate gene studies and genome-wide association studies, including benefits, limitations, and expected payoffs. Using substance use and abuse as our driving example, we then turn to the importance of etiological psychological theory in guiding genetic, environmental, and developmental research, as well as the utility of refined phenotypic measures, such as endophenotypes, in the pursuit of etiological understanding and focused tests of genetic and environmental associations. Phenotypic measurement has received considerable attention in the history of psychology and is informed by psychometrics, whereas the environment remains relatively poorly measured and is often confounded with genetic effects (i.e., gene–environment correlation). Genetically informed designs, which are no longer limited to twin and adoption studies thanks to ever-cheaper genotyping, are required to understand environmental influences. Finally, we outline the vast amount of individual difference in structural genomic variation, most of which remains to be leveraged in genetic association tests. Although the genetic data can be massive and burdensome (tens of millions of variants per person), we argue that improved understanding of genomic structure and function will provide investigators with new tools to test specific a priori hypotheses derived from etiological psychological theory, much like current candidate gene research but with less confusion and more payoff than candidate gene research has to date. En ligne : http://dx.doi.org/10.1017/S0954579412000648 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=182 Exploring the possibility of parents’ broad internalizing phenotype acting through passive gene–environment correlations on daughters’ disordered eating / Shannon M. O’CONNOR in Development and Psychopathology, 34-5 (December 2022)
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PermalinkGene–environment correlation in the development of adolescent substance abuse: Selection effects of child personality and mediation via contextual risk factors / Brian M. HICKS in Development and Psychopathology, 25-1 (February 2013)
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PermalinkGene–environment interplay in internalizing disorders: consistent findings across six environmental risk factors / Brian M. HICKS in Journal of Child Psychology and Psychiatry, 50-10 (October 2009)
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PermalinkGenetic and environmental influences on the codevelopment among borderline personality disorder traits, major depression symptoms, and substance use disorder symptoms from adolescence to young adulthood / Marina A. BORNOVALOVA in Development and Psychopathology, 30-1 (February 2018)
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PermalinkIdentifying childhood characteristics that underlie premorbid risk for substance use disorders: Socialization and boldness / Brian M. HICKS in Development and Psychopathology, 26-1 (February 2014)
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PermalinkLongitudinal effects and environmental moderation of ALDH2 and ADH1B gene variants on substance use from age 14 to 40 / Gretchen R.B. SAUNDERS in Development and Psychopathology, 34-5 (December 2022)
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PermalinkMediating pathways from childhood ADHD to adolescent tobacco and marijuana problems: roles of peer impairment, internalizing, adolescent ADHD symptoms, and gender / Irene J. ELKINS in Journal of Child Psychology and Psychiatry, 59-10 (October 2018)
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PermalinkMendelian randomization: A novel test of the gateway hypothesis and models of gene–environment interplay / Daniel E. IRONS in Development and Psychopathology, 19-4 (Fall 2007)
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PermalinkMothers’ maximum drinks ever consumed in 24 hours predicts mental health problems in adolescent offspring / Stephen M. MALONE in Journal of Child Psychology and Psychiatry, 51-9 (September 2010)
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PermalinkPersonality, romantic relationships, and alcohol use disorder symptoms in adolescence and young adulthood: An evaluation of personality × social context interplay / Diana R. SAMEK in Development and Psychopathology, 32-3 (August 2020)
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