Hermine H.M. Maes1, Michael C. Neale1, Judy L. Silberg1, Lindon J. Eaves1
The prevalence of conduct disorder (CD) increases during adolescence, particularly in males. Various forms of the disorder have been described, "adolescent-limited" and "life course persistent" (T.E. Moffit, 1993, Psychol Rev, 100:674-701). We hypothesize that their genetic etiologies are distinct. In the Virginia Twin Study of Adolescent Behavioral Development, data on conduct disorder symptoms were collected using the Child and Adolescent Psychiatric Assessment (CAPA) from 1,226 male twins between the ages of 8 and 16. Second wave data were available on 929 twins. Raw data on one or two-year interval data were used to fit developmental genetic models, including common factor, simplex and growth curve models, allowing for age changes in genetic effects on rate of change in CD symptoms over the age range. A linear growth curve model provided the most parsimonious fit to the data. This model included genetic and environmental factors on the intercept and slope, as well as on the residual variances. The overall picture of the genetic control of developmental change in CD is consistent with Moffit's model. We found two genetically distinct components affecting the development of CD. The linear component, has initially small genetic effects that increase with age ("life-course persistent"). The second component creates a burst of genetic variability in mid-adolescence ("adolescent-limited").
Address: Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Box 980003, Richmond, VA 23298. Tel: 804 828 8145 Fax: 804 828 8801 Email: hmaes@hsc.vcu.edu Web URL: http://www.vipbg.vcu.edu
1Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Box 980003, Richmond, VA 23298. 2Supported by NIH Grants MH45268 and RR08123