2026/07/01 by Amir Sariaslan, Ralf Kuja‐Halkola, Ralf Kuja-Halkola +10
Psychology · Social Sciences · Biochemistry, Genetics and Molecular Biology · #Cognitive Abilities and Testing #Crime Patterns and Interventions #Forensic and Genetic Research
paper · doi:10.1016/j.jcrimjus.2026.102708
Violent victimisation affects 1–4% of populations annually and is associated with subsequent offending, repeat victimisation, and premature mortality, yet its aetiology remains poorly understood. We examined genetic and environmental contributions to victimisation risk across development using nationwide data from 5,296,997 individuals born in Sweden (1973–2004) and Finland (1970–2003), of whom 4,455,431 had at least one co-twin or co-sibling. Violent victimisation was identified through hospital admissions and mortality records. Quantitative genetic models estimated additive genetic, shared environmental, and unique environmental influences, with sex-limitation analyses examining sex-specific effects. Among 154,209 individuals (2.9%) with documented victimisation, familial aggregation was proportional to genetic relatedness (adjusted hazard ratios: 6.0 [95% CI 4.0–9.0] for monozygotic twins; 1.4 [95% CI 1.4–1.5] for paternal half-siblings). Aetiological architecture varied substantially across development. Childhood-onset victimisation showed high heritability (h 2 = 70%, 95% CI 44–95%) with notable shared environmental contributions (c 2 = 22%, 95% CI 9–35%). Adolescent-onset and adult-onset victimisation demonstrated lower heritability (h 2 = 40–44%) with predominant unique environmental effects (e 2 = 56–60%) and negligible shared environmental influence. Sex-limitation models revealed comparable heritability between sexes but moderate cross-sex genetic correlations (rA = 0.77–0.78), indicating partially distinct genetic pathways. A bivariate quantitative genetic model confirmed that clinically recorded and police-reported victimisation largely captured the same genetic liability (rA = 0.94; 95% CI 0.89–1.00), despite more moderate environmental overlap (rE = 0.40; 95% CI 0.37–0.43). Violent victimisation therefore exhibits a developmentally dynamic genetic architecture, with heritability decreasing and unique environmental contributions increasing from childhood to adulthood. The development of effective preventive interventions, and future aetiological research, may benefit from considering moderation by developmental stage and sex.