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

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

Interplay between genetic risk and the parent environment in adolescence and substance use in young adulthood: A TRAILS study / Joëlle A. PASMAN in Development and Psychopathology, 35-1 (February 2023)  

Public ISBD [article]  inDevelopment and Psychopathology > 35-1 (February 2023) . - p.396-409 Titre : Interplay between genetic risk and the parent environment in adolescence and substance use in young adulthood: A TRAILS study Type de document : Texte imprimé et/ou numérique Auteurs : Joëlle A. PASMAN, Auteur ; Koen SMIT, Auteur ; Wilma A. M. VOLLEBERGH, Auteur ; Ilja M. NOLTE, Auteur ; Catharina A. HARTMAN, Auteur ; Abdel ABDELLAOUI, Auteur ; Karin J. H. VERWEIJ, Auteur ; Dominique MACIEJEWSKI, Auteur ; Jacqueline M. VINK, Auteur Article en page(s) : p.396-409 Langues : Anglais (eng) Mots-clés : Gene*Environment interaction  genetic nurturing  parenting  smoking  substance use Index. décimale : PER Périodiques Résumé : Many adolescents start using tobacco, alcohol, and cannabis. Genetic vulnerability, parent characteristics in young adolescence, and interaction (GxE) and correlation (rGE) between these factors could contribute to the development of substance use. Using prospective data from the TRacking Adolescent Individuals' Lives Survey (TRAILS; N = 1,645), we model latent parent characteristics in young adolescence to predict young adult substance use. Polygenic scores (PGS) are created based on genome-wide association studies (GWAS) for smoking, alcohol use, and cannabis use. Using structural equation modeling we model the direct, GxE, and rGE effects of parent factors and PGS on young adult smoking, alcohol use, and cannabis initiation. The PGS, parental involvement, parental substance use, and parent-child relationship quality predicted smoking. There was GxE such that the PGS amplified the effect of parental substance use on smoking. There was rGE between all parent factors and the smoking PGS. Alcohol use was not predicted by genetic or parent factors, nor by interplay. Cannabis initiation was predicted by the PGS and parental substance use, but there was no GxE or rGE. Genetic risk and parent factors are important predictors of substance use and show GxE and rGE in smoking. These findings can act as a starting point for identifying people at risk. En ligne : https://doi.org/10.1017/S095457942100081X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=500 [article] Interplay between genetic risk and the parent environment in adolescence and substance use in young adulthood: A TRAILS study [Texte imprimé et/ou numérique] / Joëlle A. PASMAN, Auteur ; Koen SMIT, Auteur ; Wilma A. M. VOLLEBERGH, Auteur ; Ilja M. NOLTE, Auteur ; Catharina A. HARTMAN, Auteur ; Abdel ABDELLAOUI, Auteur ; Karin J. H. VERWEIJ, Auteur ; Dominique MACIEJEWSKI, Auteur ; Jacqueline M. VINK, Auteur . - p.396-409. Langues : Anglais (eng) in Development and Psychopathology > 35-1 (February 2023) . - p.396-409 Mots-clés : Gene*Environment interaction  genetic nurturing  parenting  smoking  substance use Index. décimale : PER Périodiques Résumé : Many adolescents start using tobacco, alcohol, and cannabis. Genetic vulnerability, parent characteristics in young adolescence, and interaction (GxE) and correlation (rGE) between these factors could contribute to the development of substance use. Using prospective data from the TRacking Adolescent Individuals' Lives Survey (TRAILS; N = 1,645), we model latent parent characteristics in young adolescence to predict young adult substance use. Polygenic scores (PGS) are created based on genome-wide association studies (GWAS) for smoking, alcohol use, and cannabis use. Using structural equation modeling we model the direct, GxE, and rGE effects of parent factors and PGS on young adult smoking, alcohol use, and cannabis initiation. The PGS, parental involvement, parental substance use, and parent-child relationship quality predicted smoking. There was GxE such that the PGS amplified the effect of parental substance use on smoking. There was rGE between all parent factors and the smoking PGS. Alcohol use was not predicted by genetic or parent factors, nor by interplay. Cannabis initiation was predicted by the PGS and parental substance use, but there was no GxE or rGE. Genetic risk and parent factors are important predictors of substance use and show GxE and rGE in smoking. These findings can act as a starting point for identifying people at risk. En ligne : https://doi.org/10.1017/S095457942100081X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=500

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