To Örebro University

Previous research has shown that genetic factors are important in the stability of psychopathic personality from ages 17–24 years (D. M. Blonigen, B. M. Hicks, R. F. Krueger, C. J. Patrick, W. G. Iacono, 2006, Journal of Abnormal Psychology, 85–95) and ages 16–19 years (M. Forsman, P. Lichtenstein, H. Andershed, H. Larsson, 2008, Journal of Abnormal Psychology, 606–17). However, these studies did not examine the developmental trajectory of psychopathy, and they only evaluated psychopathy at two time points. The present study examined to what extent genetic and environmental effects influence initial level and change in psychopathic personality measured on three time. The USC Twin Study of Risk Factors for Antisocial Behavior is a longitudinal study of >600 twin pairs born 1990–1996 (L. A. Baker, M. Barton, D. I. Lozano, A. Raine, J. H. Fowler, 2006, Twin Research, 933–40). Psychopathic personality in the twins were assessed with the Child Psychopathy Scale (D. R. Lynam, 1997, Journal of Abnormal Psychology, 425–38) which was administered in interview format to the twins and their caregivers when the twins were aged 9–10 years, 11–14 years and 15–18 years old: N= 1,441 twins. Phenotypic Latent Growth Curve models were fit in MPlus (L. K. Muthén & B. O. Muthén, 1998–2007, Los Angeles, CA). Age variation within each wave of assessment is a powerful design for examining genetic and environmental influences on level and change (J. J. McArdle, 2006, Twin Research, 343–59) and was fit using Proc Mixed (SAS Institute, 2005). For both parent and self-report ratings of psychopathic traits, the best-fitting phenotypic growth model was a linear model, indicating significant growth in psychopathic traits, decreasing over time on average in parent reported ratings and increasing over time in youth selfreported ratings. For parent reports, slope variation was significant, suggesting that individuals have different trajectories. For youth-self-reports the slope variation was non-significant, suggesting that every-one is changing in a similar way. Next, the genetic and environmental etiology of individual differences in both level and change in psychopathic traits was investigated. A full model was fit which included growth variation, and where non-shared environment, shared environment, and additive genetic variation contributed to both intercept and slope. For both parent and self-reported ratings of psychopathic traits, an AE model was the most parsimonious model. For parent reports: the intercept variance due to additive genetic effects was 90% and the non-shared environment was 10%, the slope variance due to genetic effects was 51% and the non-shared environment was 49%. For youth self-reports, intercept variance due to genetic effects was 67% and the non-shared environment was 33%, the slope variance due to additive genetic effects was 27% and the non-shared environment was 73%. These longitudinal data demonstrate that genetic influences are important in both level and change in psychopathic personality, based on bothparental and self-reports. A significant growth across age was found. Interestingly, the slope was negative when examining parental ratings of psychopathic personality traits indicating a reduction in these traits whereas, the slope was positive when examining youth self-reports, indicating an increase in these traits.