Genome-wide Association Meta-analysis of Childhood and Adolescent Internalizing Symptoms
To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and...
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| Published in | Journal of the American Academy of Child and Adolescent Psychiatry Vol. 61; no. 7; pp. 934 - 945 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.07.2022
Elsevier BV |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0890-8567 1527-5418 1527-5418 |
| DOI | 10.1016/j.jaac.2021.11.035 |
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| Abstract | To investigate the genetic architecture of internalizing symptoms in childhood and adolescence.
In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.
The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.
Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. |
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| AbstractList | ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.MethodIn 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.ResultsThe meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.ConclusionGenetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. Objective To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. Method In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. Results The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Conclusion Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. To investigate the genetic architecture of internalizing symptoms in childhood and adolescence.OBJECTIVETo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.METHODIn 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.RESULTSThe meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.CONCLUSIONGenetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence. MethodIn 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. ResultsThe meta-analysis of overall internalizing symptoms (INT overall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, n effective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). Additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (| rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range | rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. ConclusionGenetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. Objective: To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. Method: In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. Results: The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, n(effective) = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (vertical bar r(g)vertical bar > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range vertical bar r(g)vertical bar = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Conclusion: Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. The meta-analysis of overall internalizing symptoms (INT ) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, n = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|r | > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |r | = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. |
| Author | Wang, Carol Wall, Tamara L. Plomin, Robert Thiering, Elisabeth Allegrini, Andrea G. Munafò, Marcus R. Peterson, Roseann E. Harden, K. Paige Palviainen, Teemu Henders, Anjali K. Brown, Sandra A. Rose, Richard J. Whitehouse, Andrew J.O. Evans, Luke M. Klump, Kelly L. Hagenbeek, Fiona A. Karhunen, Ville Hopfer, Christian Nolte, Ilja M. Rivadeneira, Fernando Williams, Gail M. Kuja-Halkola, Ralf Reynolds, Chandra Benyamin, Beben Tong, Xiaoran Ehli, Erik A. Vuoksimaa, Eero Alemany, Silvia Sallis, Hannah M. Andreassen, Ole A. Lundström, Sebastian Oldehinkel, Albertine J. Snieder, Harold van Beijsterveldt, Catharina E. Boomsma, Dorret I. Standl, Marie Mamun, Abdullah Lehtimäki, Terho Harris, Kathleen Mullan Kaprio, Jaakko Rimfeld, Kaili Lichtenstein, Paul Ip, Hill F. Ystrøm, Eivind Mallard, Travis T. Marrington, Shelby Hakulinen, Christian Ask, Helga Maes, Hermine H. Pennell, Craig E. Adkins, Daniel E. Middeldorp, Christel M. Korhonen, Tellervo Burt, S. Alexandra Jiang, Chang Hypponen, Elina Heinrich, Joachim Dick, Danielle M. Larsson, Henrik Keltikan |
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| Keywords | molecular genetics anxiety depression repeated measures genetic epidemiology |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 content type line 14 ObjectType-Feature-3 ObjectType-Evidence Based Healthcare-1 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 Conceptualization: Bartels, Middeldorp Supervision: Hammerschlag, Bartels, Middeldorp Formal analysis: Jami, Hammerschlag, Allegrini, Benyamin, Border, Diemer, Jiang, Karhunen, Y. Lu, Q. Lu, Mallard, Mishra, Nolte, Palviainen, Peterson, Sallis, Shabalin, Tate, Thiering, Vilor-Tejedor, Wang, Zhou Funding acquisition: Middeldorp Methodology: Jami, Hammerschlag, Ip, Nivard, Bartels, Middeldorp Writing – original draft: Jami, Bartels, Middeldorp Data curation: Q. Lu, Adkins, Alemany, Ask, Chen, Corley, Ehli, Evans, Havdahl, Hagenbeek, Hakulinen, Henders, Hottenga, Korhonen, Mamun, Marrington, Neumann, Rimfeld, Rivadeneira, Silberg, van Beijsterveldt, Vuoksimaa, Whipp, Tong, Andreassen, Boomsma, Brown, Burt, Copeland, Dick, Harden, Harris, Hartman, Heinrich, Hewitt, Hopfer, Hypponen, Jarvelin, Kaprio, Keltikangas-Järvinen, Klump, Krauter, Kuja-Halkola, Larsson, Lehtimäki, Lichtenstein, Lundstrom, Maes, Magnus, Munaf€ o, Najman, Njølstad, Oldehinkel, Pennell, Plomin, Reichborn-Kjennerud, Reynolds, Rose, Smolen, Snieder, Stallings, Standl, Sunyer, Tiemeier, Wadsworth, Wall, Whitehouse, Williams, Ystrøm Writing – review and editing: Jami, Hammerschlag, Ip, Allegrini, Benyamin, Border, Diemer, Jiang, Karhunen, Y. Lu, Q. Lu, Mallard, Mishra, Nolte, Palviainen, Peterson, Sallis, Shabalin, Tate, Thiering, Vilor-Tejedor, Wang, Zhou, Adkins, Alemany, Ask, Chen, Corley, Ehli, Evans, Havdahl, Hagenbeek, Hakulinen, Henders, Hottenga, Korhonen, Mamun, Marrington, Neumann, Rimfeld, Rivadeneira, Silberg, van Beijsterveldt, Vuoksimaa, Whipp, Tong, Andreassen, Boomsma, Brown, Burt, Copeland, Dick, Harden, Harris, Hartman, Heinrich, Hewitt, Hopfer, Hypponen, Jarvelin, Kaprio, Keltikangas-Järvinen, Klump, Krauter, Kuja-Halkola, Larsson, Lehtimäki, Lichtenstein, Lundström, Maes, Magnus, Munafò, Najman, Njølstad, Oldehinkel, Pennell, Plomin, Reichborn- Kjennerud, Reynolds, Rose, Smolen, Snieder, Stallings, Standl, Sunyer, Tiemeier, Wadsworth, Wall, Whitehouse, Williams, Ystrøm, Nivard, Bartels, Mid-deldorp Author Contributions |
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| Snippet | To investigate the genetic architecture of internalizing symptoms in childhood and adolescence.
In 22 cohorts, multiple univariate genome-wide association... ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence. MethodIn 22 cohorts, multiple univariate genome-wide... ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.MethodIn 22 cohorts, multiple univariate genome-wide... To investigate the genetic architecture of internalizing symptoms in childhood and adolescence.OBJECTIVETo investigate the genetic architecture of... Objective To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. Method In 22 cohorts, multiple univariate genome-wide... Objective: To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. Method: In 22 cohorts, multiple univariate... |
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| SubjectTerms | Adolescent Adolescents Adult Adults Age Aggression Anorexia Anxiety Anxiety - genetics Associations Attention Deficit Disorder with Hyperactivity - genetics Attention deficit hyperactivity disorder Autism Autistic Disorder - genetics behavioral-problems Bipolar Disorder Child Child development Child, Preschool Childhood Children Comorbidity Consortia depression Depression - genetics Eating disorders Estimates Fathers Genes Genetic analysis genetic epidemiology genetics Genome-wide association studies Genome-Wide Association Study Genomes Genomics Heritability Humans Hyperactivity Insomnia Internalization Internalizing disorders Loneliness Longitudinal studies major depressive disorder Mental depression Mental disorders Meta-analysis molecular molecular genetics Obsessive compulsive disorder Pediatrics Polymorphism, Single Nucleotide prevalence Psychiatric/Mental Health Psychiatry Psychology psychopathology Psykiatri Quality control questionnaire repeated measures risk Sample size Schizophrenia Single-nucleotide polymorphism Sleep disorders Sleep Initiation and Maintenance Disorders - genetics Statistics Subsets Teachers Well being Within-subjects design Young Children |
| Title | Genome-wide Association Meta-analysis of Childhood and Adolescent Internalizing Symptoms |
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