a1 Oregon Social Learning Center
a2 University of Oregon
a3 Brown University
a4 Wayne State University
a5 University of Kentucky
a6 University of Miami
a7 Research Triangle Institute
a8 University of Tennessee
a9 Eunice Kennedy Shriver National Institute of Child Health and Human Development
The negative effects of prenatal substance exposure on neurobiological and psychological development and of early adversity are clear, but little is known about their combined effects. In this study, multilevel analyses of the effects of prenatal substance exposure and early adversity on the emergence of neurobehavioral disinhibition in adolescence were conducted. Neurobehavioral disinhibition has previously been observed to occur frequently in multiproblem youth from high-risk backgrounds. In the present study, neurobehavioral disinhibition was assessed via behavioral dysregulation and poor executive function composite measures. Data were drawn from a prospective longitudinal investigation of prenatal substance exposure that included 1,073 participants followed from birth through adolescence. The results from latent growth modeling analyses showed mean stability but significant individual differences in behavioral dysregulation and mean decline with individual differences in executive function difficulties. Prior behavioral dysregulation predicted increased executive function difficulties. Prenatal drug use predicted the emergence and growth in neurobehavioral disinhibition across adolescence (directly for behavioral dysregulation and indirectly for executive function difficulties via early adversity and behavioral dysregulation). Prenatal drug use and early adversity exhibited unique effects on growth in behavioral dysregulation; early adversity uniquely predicted executive function difficulties. These results are discussed in terms of implications for theory development, social policy, and prevention science.
(Online publication July 15 2011)
Support for this research was provided by the following grants and cooperative agreements: DA024117, DA024128, DA024119, DA024118, and DA023920, NIDA, US PHS; HD021385, HD02786, HD027904, HD021397; HD-2-3159, and HD045894, NICHD, US PHS; and MH078105 and MH059780, NIMH, US PHS. The authors thank Matthew Rabel for editorial assistance.