a1 Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States of America.
a2 Department of Public Health, University of Helsinki, Helsinki, Finland; Department of Mental Health, National Public Health Institute, Helsinki, Finland.
a3 Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States of America; Department of Public Health, University of Helsinki, Helsinki, Finland. firstname.lastname@example.org
We enrolled more than 3500 same-sex twins from 5 consecutive Finnish birth cohorts into a longitudinal study as each cohort reached age 16. Twins completed the Psychopathic Deviate (Pd) Scale of the Minnesota Multiphasic Personality Inventory at baseline, Sensation Seeking Scale items as each cohort reached age 17, and later, at average ages 18.5 and 25, the Rutgers Alcohol Problem Index (RAPI). Using raw maximum likelihood estimation, we fit a Cholesky model to the 4 variables assessed at 4 ages across the 4 twin types; we estimated genetic and environmental influences on the stability of alcohol problems across development and the genetic and environmental contributions to predictive correlations between adolescent personality and later alcohol-related behavior problems. With one exception, the phenotypic, genetic, and environmental correlations were very similar for males and females. The exception was that the lagged associations of Pd and RAPI reflect a higher genetic correlation among males than females and a higher environmental correlation among females than males. Our analyses suggest that developmental changes underlying variation in alcohol problems from late adolescence to early adulthood differ for males and females. In males, the main change is decreased variation due to shared environmental effects; the magnitude of genetic effects is stable over time, and the high genetic correlation, .95, suggests that the same genetic influences are important at both ages. Among females, in contrast, genetic influences decline in magnitude from age 18 to 25, and at least part of the genetic effect evident at age 25 differs from the genetic effect evident at age 18.
(Received March 10 2006)
(Accepted November 13 2006)
c1 Address for correspondence: Richard J. Rose, Department of Psychological and Brain Sciences, Indiana University, 1011 East 10th Street, Bloomington, IN 47405, USA.