Genetics and crime: Integrating new genomic discoveries into psychological research about antisocial behavior Show others and affiliations
Number of Authors: 16 2018 (English) In: Psychological Science, ISSN 0956-7976, E-ISSN 1467-9280, Vol. 29, no 5, p. 791-803Article in journal (Refereed) Published
Abstract [en]
Drawing on psychological and sociological theories of crime causation, we tested the hypothesis that genetic risk for low educational attainment (assessed via a genome-wide polygenic score) is associated with criminal offending. We further tested hypotheses of how polygenic risk relates to the development of antisocial behavior from childhood through adulthood. Across the Dunedin and Environmental Risk (E-Risk) birth cohorts of individuals growing up 20 years and 20,000 kilometers apart, education polygenic scores predicted risk of a criminal record with modest effects. Polygenic risk manifested during primary schooling in lower cognitive abilities, lower self-control, academic difficulties, and truancy, and it was associated with a life-course-persistent pattern of antisocial behavior that onsets in childhood and persists into adulthood. Crime is central in the nature-nurture debate, and findings reported here demonstrate how molecular-genetic discoveries can be incorporated into established theories of antisocial behavior. They also suggest that improving school experiences might prevent genetic influences on crime from unfolding.
Place, publisher, year, edition, pages New York: Cambridge University Press, 2018. Vol. 29, no 5, p. 791-803
Keywords [en]
crime, genetics, antisocial behavior, longitudinal
National Category
Psychology
Identifiers URN: urn:nbn:se:oru:diva-113805 DOI: 10.1177/0956797617744542 ISI: 000432115000010 PubMedID: 29513605 Scopus ID: 2-s2.0-85044079330 OAI: oai:DiVA.org:oru-113805 DiVA, id: diva2:1859622
Note The E-Risk Study is funded by UK Medical Research Council (MRC) Grant G1002190. The Dunedin Multidisciplinary Health and Development Research Unit is funded by the New Zealand Health Research Council and the New Zealand Ministry of Business, Innovation and Employment. This research was supported by National Institute on Aging Grant AG032282, National Institute of Child Health and Human Development Grant HD077482, MRC Grant MR/P005918/1, the Jacobs Foundation, and the Avielle Foundation. Data support was provided by Duke’s Social Science Research Institute and North Carolina Biotechnology Center Grant 2016-IDG-1013. D. W. Belsky and C. L. Odgers are supported by fellowships from the Jacobs Foundation. A. L. Beckley is supported by a Forte Marie Curie International Fellowship.
2024-05-222024-05-222024-05-23 Bibliographically approved