A genome‐wide approach to children's aggressive behavior: The EAGLE consortium
Open accessAbstract
Individual differences in aggressive behavior emerge in early childhood and predict persisting behavioral problems and disorders. Studies of antisocial and severe aggression in adulthood indicate substantial underlying biology. However, little attention has been given to genome‐wide approaches of aggressive behavior in children. We analyzed data from nine population‐based studies and assessed aggressive behavior using well‐validated parent‐reported questionnaires. This is the largest sample exploring children's aggressive behavior to date (N = 18,988), with measures in two developmental stages (N = 15,668 early childhood and N = 16,311 middle childhood/early adolescence). First, we estimated the additive genetic variance of children's aggressive behavior based on genome‐wide SNP information, using genome‐wide complex trait analysis (GCTA). Second, genetic associations within each study were assessed using a quasi‐Poisson regression approach, capturing the highly right‐skewed distribution of aggressive behavior. Third, we performed meta‐analyses of genome‐wide associations for both the total age‐mixed sample and the two developmental stages. Finally, we performed a gene‐based test using the summary statistics of the total sample. GCTA quantified variance tagged by common SNPs (10–54%). The meta‐analysis of the total sample identified one region in chromosome 2 (2p12) at near genome‐wide significance (top SNP rs11126630, P = 5.30 × 10−8). The separate meta‐analyses of the two developmental stages revealed suggestive evidence of association at the same locus. The gene‐based analysis indicated association of variation within AVPR1A with aggressive behavior. We conclude that common variants at 2p12 show suggestive evidence for association with childhood aggression. Replication of these initial findings is needed, and further studies should clarify its biological meaning. © 2015 Wiley Periodicals, Inc.
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From 2011, genome-wide association studies started to be published, although the sample size remained relatively small (n < 1000) until 2016.
“From 2011, genome-wide association studies started to be published, although the sample size remained relatively small (n < 1000) until 2016 [35].”
From Genetics of child aggression, a systematic review (2024) · cites this paper as [35]
The Introduction cites a 2011 GWAS of hostility and anger traits in adolescents, supporting the starting year. But it reports N = 1,780 for that study and N = 2,930 for a 2013 study of children—both above 1,000 before 2016. Page numbers are not available in the supplied copy. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe review found converging evidence for a role of AVPR1A in child aggression coming from genome-wide association, epigenomic, and candidate gene studies.
“Nonetheless, we found converging evidence for a role of AVPR1A in child aggression coming from genome-wide association [35], epigenomic [126], and candidate gene [101] studies.”
From Genetics of child aggression, a systematic review (2024) · cites this paper as [35]
The largest GWAS of aggression, performed by the EAGLE consortium, reported association with one SNP, rs11126630, at a suggestive significance level (p = 5.3e−08).
“The largest GWAS, which was performed by the Early Genetics and Lifecourse Epidemiology (EAGLE) consortium (http://research.lunenfeld.ca/eagle/), reported association with one SNP, rs11126630, at a suggestive significance level (p = 5.3e−08).”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [13]
Among the classical candidate genes evaluated in the EAGLE dataset, only AVPR1A showed a nominal association with aggression (p = 1.6e−03).
“Among the “classical” candidates evaluated in the EAGLE dataset, only one gene, AVPR1A, encoding the arginin vasopressin receptor 1A, showed a nominal association with aggression (p = 1.6e−03) [13].”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [13]
The EAGLE GWAS meta-analysis of children's aggression and Tielbeek's GWAS of antisocial behavior (64% adult) do not show genetic correlation.
“Furthermore, the EAGLE GWAS meta-analysis of children’s aggression [13] and the Tielbeek’s GWAS of antisocial behavior (64% adult) [47] do not show genetic correlation.”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [13]
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- Authors
- Pappa, I., St Pourcain, B., Benke, K., Cavadino, A., Hakulinen, C., Nivard, M. G., Nolte, I. M., Tiesler, C. M. T., Bakermans‐Kranenburg, M. J., Davies, G. E., Evans, D. M., Geoffroy, M., Grallert, H., Groen‐Blokhuis, M. M., Hudziak, J. J., Kemp, J. P., Keltikangas‐Järvinen, L., McMahon, G., Mileva‐Seitz, V. R., Motazedi, E., Power, C., Raitakari, O. T., Ring, S. M., Rivadeneira, F., Rodriguez, A., Scheet, P. A., Seppälä, I., Snieder, H., Standl, M., Thiering, E., Timpson, N. J., Veenstra, R., Velders, F. P., Whitehouse, A. J. O., Smith, G. D., Heinrich, J., Hypponen, E., Lehtimäki, T., Middeldorp, C. M., Oldehinkel, A. J., Pennell, C. E., Boomsma, D. I., & Tiemeier, H.
- Affiliations
- Erasmus MC (NL)
- Medical Research Council Integrative Epidemiology Unit University of Bristol Bristol United Kingdom
- Johns Hopkins University (US)
- Queen Mary University of London (GB)
- University of Helsinki (FI)
- Amsterdam Neuroscience (NL)
- University Medical Center Groningen (NL)
- Helmholtz Munich (DE)
- Leiden University (NL)
- Avera Institute for Human Genetics (US)
- Translational Research Institute (AU)
- Douglas Mental Health University Institute (CA)
- Amsterdam Public Health (NL)
- University of Vermont (US)
- Erasmus University Rotterdam (NL)
- University College London (GB)
- University of Turku (FI)
- University of Bristol (GB)
- Erasmus MC - Sophia Children’s Hospital (NL)
- Imperial College London (GB)
- The University of Texas MD Anderson Cancer Center (US)
- Tampere University (FI)
- University of Groningen (NL)
- The Kids Research Institute Australia (AU)
- School of Pedagogical and Educational Sciences Erasmus University Rotterdam Rotterdam The Netherlands
- The University of Western Australia (AU)
- Vrije Universiteit Amsterdam (NL)
- Corresponding author
- Tiemeier, Henning
- ORCID
- Pappa, Irene
- Benke, Kelly
- Cavadino, Alana
- Hakulinen, Christian
- Nivard, Michel G.
- Nolte, Ilja M.
- Bakermans‐Kranenburg, Marian J.
- Evans, David M.
- Geoffroy, Marie‐Claude
- Grallert, Harald
- Hudziak, James J.
- Kemp, John P.
- Keltikangas‐Järvinen, Liisa
- Mileva‐Seitz, Viara R.
- Motazedi, Ehsan
- Power, Christine
- Raitakari, Olli T.
- Ring, Susan M.
- Rivadeneira, Fernando
- Rodriguez, Alina
- Scheet, Paul A.
- Seppälä, Ilkka
- Snieder, Harold
- Standl, Marie
- Thiering, Elisabeth
- Timpson, Nicholas J.
- Veenstra, René
- Velders, Fleur P.
- Whitehouse, Andrew J. O.
- Smith, George Davey
- Heinrich, Joachim
- Lehtimäki, Terho
- Middeldorp, Christel M.
- Oldehinkel, Albertine J.
- Pennell, Craig E.
- Boomsma, Dorret I.
- Tiemeier, Henning
- Venue
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
- Publisher
- Wiley
- Published
- 2015-06-18
- Volume
- 171
- Issue
- 5
- Pages
- 562-572
- ISSN
- 1552-4841 (ISSN-L)
- 1552-485X
- OpenAlex
- W2128939801
- Cited by
- 195
- References
- 58
- Citations by year
- 2026: 1 · 2025: 13 · 2024: 13 · 2023: 11 · 2022: 14 · 2021: 29 · 2020: 42 · 2019: 21 · 2018: 23 · 2017: 18 · 2016: 8 · 2015: 2
- FWCI
- 11.62
- Type
- journal article
- Language
- en
- Open access
- green
- pure.amsterdamumc.nl
- Locations
- American Journal of Medical Genetics Part B Neuropsychiatric Genetics (publishedVersion)
- PubMed (publishedVersion)
- Explore Bristol Research (publishedVersion)
- Pure Amsterdam UMC (submittedVersion, cc-by)
- UWA Profiles and Research Repository (University of Western Australia) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Diva portal (Dalarna University Library) (submittedVersion, other-oa)
- Leiden Repository (Leiden University) (submittedVersion)
- eScholarship@McGill (McGill) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Site cant be reached (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- VU Research Portal (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (VICI grant no. 453-09-003)
- Sophia Foundation for Scientific Research (SKZ Foundation) (SSWO no.491)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Psychopathy, Forensic Psychiatry, Sexual Offending
- Keywords
- child aggression, aggression, genetic association, AVPR1A, additive genetic variance, early childhood, middle childhood, early adolescence, GCTA, quasi-Poisson regression
- MeSH terms
- Adolescent, Aggression, Behavior, Child, Female, Genetics, Behavioral, Humans, Male, Surveys and Questionnaires, Genetic Variation, Receptors, Vasopressin, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Association Studies
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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