Genetic and environmental architecture of violent victimisation across development and sex: A study of 4.5 million Nordic twins and siblings

Violent victimisation affects 1-4% of populations annually and constitutes a major risk factor for psychiatric morbidity and suicidal behaviours. However, the aetiological mechanisms underlying vulnerability to severe victimisation remain poorly understood. We examined genetic and environmental contributions to victimisation risk across development using nationwide family data from 4,458,368 individuals born in Sweden (1973-2004) and Finland (1970-2003). Violent victimisation was identified through hospital admissions and mortality records. Quantitative genetic models estimated additive genetic, shared environmental, and unique environmental influences across developmental periods, 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 (h2=70%, 95% CI 44-95%) with notable shared environmental contributions (c2=22%, 95% CI 9-35%). Adolescent-onset and adult-onset victimisation demonstrated lower heritability (h2=40-44%) with predominant unique environmental effects (e2=56-60%) and negligible shared environmental influence. Sex-limitation models revealed comparable heritability between sexes but moderate cross-sex genetic correlations (rg=0.77-0.78), indicating partially distinct genetic pathways. Violent victimisation therefore exhibits a developmentally dynamic genetic architecture, with heritability decreasing and unique environmental contributions increasing from childhood to adulthood. Partially sex-specific genetic pathways underscore the need for age- and sex-stratified genomic investigations.