BACKGROUND: Longitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior. METHOD: Analyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study. RESULTS: The following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood ('life-course persistent'); (2) a shared-environmental effect beginning in adolescence ('adolescent-onset'); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior. CONCLUSIONS: Overall, these etiological findings are consistent with predictions from Moffitt's developmental theory of antisocial behavior. The genetic effect at puberty at ages 12-15 is also consistent with a genetically mediated influence on the timing of puberty affecting the expression of genetic differences in antisocial outcomes.
BACKGROUND: Longitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior. METHOD: Analyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study. RESULTS: The following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood ('life-course persistent'); (2) a shared-environmental effect beginning in adolescence ('adolescent-onset'); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior. CONCLUSIONS: Overall, these etiological findings are consistent with predictions from Moffitt's developmental theory of antisocial behavior. The genetic effect at puberty at ages 12-15 is also consistent with a genetically mediated influence on the timing of puberty affecting the expression of genetic differences in antisocial outcomes.
Authors: Avshalom Caspi; Joseph McClay; Terrie E Moffitt; Jonathan Mill; Judy Martin; Ian W Craig; Alan Taylor; Richie Poulton Journal: Science Date: 2002-08-02 Impact factor: 47.728
Authors: Jeffrey J Wood; Sarah D Lynne-Landsman; David A Langer; Patricia A Wood; Shaunna L Clark; J Mark Eddy; Nick Ialongo Journal: Child Dev Date: 2011-12-21
Authors: Christopher J Hopwood; S Alexandra Burt; John C Markowitz; Shirley Yen; M Tracie Shea; Charles A Sanislow; Carlos M Grilo; Emily B Ansell; Thomas H McGlashan; John G Gunderson; Mary C Zanarini; Andrew E Skodol; Leslie C Morey Journal: J Psychiatr Res Date: 2008-09-12 Impact factor: 4.791
Authors: T Reichborn-Kjennerud; N Czajkowski; E Ystrøm; R Ørstavik; S H Aggen; K Tambs; S Torgersen; M C Neale; E Røysamb; R F Krueger; G P Knudsen; K S Kendler Journal: Psychol Med Date: 2015-06-08 Impact factor: 7.723