Distal-to-proximal etiologically relevant variables associated with the general (p) and specific factors of psychopathology / Melissa VOS ; Odilia M. LACEULLE ; Charlotte VRIJEN ; Camiel M. VAN DER LAAN ; Ilja M. NOLTE ; Catharina A. HARTMAN in Journal of Child Psychology and Psychiatry, 65-10 (October 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1340-1354 Titre : Distal-to-proximal etiologically relevant variables associated with the general (p) and specific factors of psychopathology Type de document : Texte imprimé et/ou numérique Auteurs : Melissa VOS, Auteur ; Odilia M. LACEULLE, Auteur ; Charlotte VRIJEN, Auteur ; Camiel M. VAN DER LAAN, Auteur ; Ilja M. NOLTE, Auteur ; Catharina A. HARTMAN, Auteur Article en page(s) : p.1340-1354 Langues : Anglais (eng) Mots-clés : Psychopathology Index. décimale : PER Périodiques Résumé : Background The general factor of psychopathology, often denoted as p, captures the common variance among a broad range of psychiatric symptoms. Specific factors are co-modeled based on subsets of closely related symptoms. This paper investigated the extent to which wide-ranging genetic, personal, and environmental etiologically relevant variables are associated with p and specific psychopathology factors. Methods Using data from four waves (ages 11?19) of TRAILS, we modeled a bifactor model of p and four specific factors [internalizing, externalizing, ADHD, Autism Spectrum Disorder (ASD)]. Next, we examined the associations of 19 etiologically relevant variables with these psychology factors using path models that organized the variables according to the distal-to-proximal risk principle. Results Collectively, the etiologically relevant factors, including temperament traits, accounted for 55% of p's variance, 46% in ADHD, 35% in externalizing, 19% in internalizing, and 7% in ASD. The low 7% is due to insufficient unique variance in ASD indicators that load more strongly on p. Excluding temperament, variables accounted for 29% variance in p, 9% ADHD, 14% EXT, 7% INT, and 4% ASD. Most etiologically relevant factors were generic, predicting p. In addition, we identified effects on specific factors in addition to effects on p (e.g., parental SES, executive functioning); only effects on specific factors (e.g., parental rejection); opposite effects on different factors [e.g., diurnal cortisol (high INT but low EXT, p); developmental delay (high ASD and p but low EXT)]. Frustration, family functioning, parental psychopathology, executive functioning, and fearfulness had strong effects on p. Conclusions (1) Strong generic effects on p suggest that etiologically relevant factors and psychopathology tend to cluster in persons. (2) While many factors predict p, additional as well as opposite effects on specific factors indicate the relevance of specific psychopathology factors in understanding mental disorder. (3) High frustration, neurodevelopmental problems, and a disadvantaged family environment primarily characterize p. En ligne : https://doi.org/10.1111/jcpp.13979 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535 [article] Distal-to-proximal etiologically relevant variables associated with the general (p) and specific factors of psychopathology [Texte imprimé et/ou numérique] / Melissa VOS, Auteur ; Odilia M. LACEULLE, Auteur ; Charlotte VRIJEN, Auteur ; Camiel M. VAN DER LAAN, Auteur ; Ilja M. NOLTE, Auteur ; Catharina A. HARTMAN, Auteur . - p.1340-1354. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1340-1354 Mots-clés : Psychopathology Index. décimale : PER Périodiques Résumé : Background The general factor of psychopathology, often denoted as p, captures the common variance among a broad range of psychiatric symptoms. Specific factors are co-modeled based on subsets of closely related symptoms. This paper investigated the extent to which wide-ranging genetic, personal, and environmental etiologically relevant variables are associated with p and specific psychopathology factors. Methods Using data from four waves (ages 11?19) of TRAILS, we modeled a bifactor model of p and four specific factors [internalizing, externalizing, ADHD, Autism Spectrum Disorder (ASD)]. Next, we examined the associations of 19 etiologically relevant variables with these psychology factors using path models that organized the variables according to the distal-to-proximal risk principle. Results Collectively, the etiologically relevant factors, including temperament traits, accounted for 55% of p's variance, 46% in ADHD, 35% in externalizing, 19% in internalizing, and 7% in ASD. The low 7% is due to insufficient unique variance in ASD indicators that load more strongly on p. Excluding temperament, variables accounted for 29% variance in p, 9% ADHD, 14% EXT, 7% INT, and 4% ASD. Most etiologically relevant factors were generic, predicting p. In addition, we identified effects on specific factors in addition to effects on p (e.g., parental SES, executive functioning); only effects on specific factors (e.g., parental rejection); opposite effects on different factors [e.g., diurnal cortisol (high INT but low EXT, p); developmental delay (high ASD and p but low EXT)]. Frustration, family functioning, parental psychopathology, executive functioning, and fearfulness had strong effects on p. Conclusions (1) Strong generic effects on p suggest that etiologically relevant factors and psychopathology tend to cluster in persons. (2) While many factors predict p, additional as well as opposite effects on specific factors indicate the relevance of specific psychopathology factors in understanding mental disorder. (3) High frustration, neurodevelopmental problems, and a disadvantaged family environment primarily characterize p. En ligne : https://doi.org/10.1111/jcpp.13979 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535

Gene-environment interplay in externalizing behavior from childhood through adulthood / Tina KRETSCHMER in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1206-1213 Titre : Gene-environment interplay in externalizing behavior from childhood through adulthood Type de document : Texte imprimé et/ou numérique Auteurs : Tina KRETSCHMER, Auteur ; Charlotte VRIJEN, Auteur ; Ilja Maria NOLTE, Auteur ; Jasmin WERTZ, Auteur ; Catharina A. HARTMAN, Auteur Année de publication : 2022 Article en page(s) : p.1206-1213 Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Antisocial Personality Disorder/genetics  Child  Child Behavior  Genetic Predisposition to Disease  Humans  Longitudinal Studies  Multifactorial Inheritance  Prospective Studies  Externalising disorder  family functioning  gene-environment interaction (GxE)  molecular genetics Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic and environmental influences on externalizing problems are often studied separately. Here, we extended prior work by investigating the implications of gene-environment interplay in childhood for early adult externalizing behavior. Genetic nurture would be indicated if parents' genetic predisposition for externalizing behavior operates through the family environment in predicting offspring early adult externalizing behavior. Evocative gene-environment correlation would be indicated if offspring genetic predisposition for externalizing behavior operates through child externalizing behavior in affecting the family environment and later early adult externalizing behavior. METHOD: Longitudinal data from seven waves of the TRacking Adolescents' Individual Lives Survey, a prospective cohort study of Dutch adolescents followed from age 11 to age 29 (n at baseline=2,734) were used. Child externalizing behavior was assessed using self and parent reports. Family dysfunction was assessed by parents. Early adult externalizing behavior was assessed using self-reports. Genome-wide polygenic scores for externalizing problems were constructed for mothers, fathers, and offspring. RESULTS: Offspring polygenic score and child behavior each predicted early adult externalizing problems, as did family dysfunction to a small extent. Parents' polygenic scores were not associated with offspring's early adult externalizing behavior. Indirect effect tests indicated that offspring polygenic score was associated with greater family dysfunction via child externalizing behavior (evocative gene-environment correlation) but the effect was just significant and the effect size was very small. Parents' polygenic scores did not predict family dysfunction, thus the data do not provide support for genetic nurture. CONCLUSIONS: A very small evocative gene-environment correlation was detected but effect sizes were much more pronounced for stability in externalizing behavior from childhood through early adulthood, which highlights the necessity to intervene early to prevent later problems. En ligne : http://dx.doi.org/10.1111/jcpp.13652 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Gene-environment interplay in externalizing behavior from childhood through adulthood [Texte imprimé et/ou numérique] / Tina KRETSCHMER, Auteur ; Charlotte VRIJEN, Auteur ; Ilja Maria NOLTE, Auteur ; Jasmin WERTZ, Auteur ; Catharina A. HARTMAN, Auteur . - 2022 . - p.1206-1213. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1206-1213 Mots-clés : Adolescent  Adult  Antisocial Personality Disorder/genetics  Child  Child Behavior  Genetic Predisposition to Disease  Humans  Longitudinal Studies  Multifactorial Inheritance  Prospective Studies  Externalising disorder  family functioning  gene-environment interaction (GxE)  molecular genetics Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic and environmental influences on externalizing problems are often studied separately. Here, we extended prior work by investigating the implications of gene-environment interplay in childhood for early adult externalizing behavior. Genetic nurture would be indicated if parents' genetic predisposition for externalizing behavior operates through the family environment in predicting offspring early adult externalizing behavior. Evocative gene-environment correlation would be indicated if offspring genetic predisposition for externalizing behavior operates through child externalizing behavior in affecting the family environment and later early adult externalizing behavior. METHOD: Longitudinal data from seven waves of the TRacking Adolescents' Individual Lives Survey, a prospective cohort study of Dutch adolescents followed from age 11 to age 29 (n at baseline=2,734) were used. Child externalizing behavior was assessed using self and parent reports. Family dysfunction was assessed by parents. Early adult externalizing behavior was assessed using self-reports. Genome-wide polygenic scores for externalizing problems were constructed for mothers, fathers, and offspring. RESULTS: Offspring polygenic score and child behavior each predicted early adult externalizing problems, as did family dysfunction to a small extent. Parents' polygenic scores were not associated with offspring's early adult externalizing behavior. Indirect effect tests indicated that offspring polygenic score was associated with greater family dysfunction via child externalizing behavior (evocative gene-environment correlation) but the effect was just significant and the effect size was very small. Parents' polygenic scores did not predict family dysfunction, thus the data do not provide support for genetic nurture. CONCLUSIONS: A very small evocative gene-environment correlation was detected but effect sizes were much more pronounced for stability in externalizing behavior from childhood through early adulthood, which highlights the necessity to intervene early to prevent later problems. En ligne : http://dx.doi.org/10.1111/jcpp.13652 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

Genetic confounding in bullying research: Causal claims revisited / Charlotte VRIJEN in Development and Psychopathology, 36-3 (August 2024)  

Public ISBD [article]  inDevelopment and Psychopathology > 36-3 (August 2024) . - p.1219-1230 Titre : Genetic confounding in bullying research: Causal claims revisited Type de document : Texte imprimé et/ou numérique Auteurs : Charlotte VRIJEN, Auteur ; Ilja M. NOLTE, Auteur ; Albertine J. OLDEHINKEL, Auteur ; René VEENSTRA, Auteur ; Tina KRETSCHMER, Auteur Article en page(s) : p.1219-1230 Langues : Anglais (eng) Mots-clés : bullying  externalizing problems  genetic confounding  internalizing problems Index. décimale : PER Périodiques Résumé : Bullying research has shown repeatedly that victims of bullying have an increased risk for later internalizing problems and bullies have an increased risk for later externalizing problems. Bullying involvement is often, either explicitly or implicitly, presented as part of a causal mechanism for maladjustment. However, genetic vulnerability may confound the reported associations. This study examined to what extent genetic vulnerability can account for the reported associations between bullying involvement (age 11-14) and later internalizing and externalizing problems (age 16), using data from the TRacking Adolescents' Individual Lives Survey (n = 1604). Because polygenic scores capture only a fraction of the total genetic effect, they were extrapolated to the size of single-nucleotide polymorphism and twin heritability estimates to examine genetic confounding while controlling for (hypothetical) polygenic scores that fully capture the genetic effect. Genetic vulnerability for internalizing and externalizing problems confounded, respectively, the association between bullying victimization and later internalizing problems, and the association between bullying perpetration and later externalizing problems. As such, this study showcases a method that can be broadly used to assess the magnitude of genetic confounding. Caution is, however, warranted in interpreting particularly the less straightforward extrapolations of polygenic scores to the size of twin heritability estimates. En ligne : https://dx.doi.org/10.1017/S0954579423000445 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 [article] Genetic confounding in bullying research: Causal claims revisited [Texte imprimé et/ou numérique] / Charlotte VRIJEN, Auteur ; Ilja M. NOLTE, Auteur ; Albertine J. OLDEHINKEL, Auteur ; René VEENSTRA, Auteur ; Tina KRETSCHMER, Auteur . - p.1219-1230. Langues : Anglais (eng) in Development and Psychopathology > 36-3 (August 2024) . - p.1219-1230 Mots-clés : bullying  externalizing problems  genetic confounding  internalizing problems Index. décimale : PER Périodiques Résumé : Bullying research has shown repeatedly that victims of bullying have an increased risk for later internalizing problems and bullies have an increased risk for later externalizing problems. Bullying involvement is often, either explicitly or implicitly, presented as part of a causal mechanism for maladjustment. However, genetic vulnerability may confound the reported associations. This study examined to what extent genetic vulnerability can account for the reported associations between bullying involvement (age 11-14) and later internalizing and externalizing problems (age 16), using data from the TRacking Adolescents' Individual Lives Survey (n = 1604). Because polygenic scores capture only a fraction of the total genetic effect, they were extrapolated to the size of single-nucleotide polymorphism and twin heritability estimates to examine genetic confounding while controlling for (hypothetical) polygenic scores that fully capture the genetic effect. Genetic vulnerability for internalizing and externalizing problems confounded, respectively, the association between bullying victimization and later internalizing problems, and the association between bullying perpetration and later externalizing problems. As such, this study showcases a method that can be broadly used to assess the magnitude of genetic confounding. Caution is, however, warranted in interpreting particularly the less straightforward extrapolations of polygenic scores to the size of twin heritability estimates. En ligne : https://dx.doi.org/10.1017/S0954579423000445 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538

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