Because the additive genetic and nonshared environmental variance of EXT was moderated, the size of the genetic (rA) and nonshared environmental (rE) correlations (i.e., the G-E correlations) also varied with levels of the environmental risk factor (this situation holds even if only the unique variance of EXT is moderated)38,39. As results were consistent across the environmental moderators, we discuss results for mother-child relationship problems as an illustrative example. At low levels of mother-child relationship problems (-2 SD), the rA with EXT was large (.78), but declined as levels of mother-child relationship problems increased (rA = .44 and .29 at 0 SD and +2 SD, respectively). Results for the rE were similar though of lesser magnitude (rE = .31, .16, and .10 at levels of mother-child relationship problems of -2 SD, 0 SD, and +2 SD, respectively). This indicates that as environmental adversity increases, EXT and mother-child relationship problems share less genetic and environmental variance. The uncoupling points to a true environmental effect or social causation process on the inherited vulnerability to EXT, an effect that is most pronounced in the context of extreme environmental adversity38.
