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An Adoption Study of the Development of Early Substance Use: The Joint Roles of Genetic Influences, Prenatal Risk, Rearing Environment, and Pubertal Maturation

Jenae Neiderhiser headshot

PI: Jenae Neiderhiser

NIH R01DA045108
Administered in: College of the Liberal Arts

Abstract:

The proposed research will clarify how heritable risks and prenatal and postnatal environments work together with hormonal changes to influence the development of risk for early substance use (SU) and related problems in adolescence. Understanding the development of SU problems is a vital health concern due to the economic costs of dealing with SU related injury, illness, death, crime, and lost productivity. Pathways and interactions by which genes, prenatal exposures, hormones, and key postnatal factors (parenting, marital, and peer processes) influence the development of SU are not fully understood, in part because studies have not adequately considered these influences together. The proposed research is highly innovative by using and expanding on an existing prospective longitudinal adoption study, the Early Growth and Development Study (EGDS) to address the dearth of research combining heritable, prenatal, hormone, and postnatal influences. This application is timely, directly addressing PA-15-110, which emphasizes using genetically informative approaches to expand research on the interplay of genetic and environmental factors in the genesis and course (e.g., developmental trajectories) of substance use disorders and comorbid conditions. The EGDS is a longitudinal study of children adopted at birth as well as their birth and adoptive parents (N = 561 linked triads), assessed in two cohorts. We propose to collect new data from both cohorts into adolescence on SU milestones, behavioral risk for SU, and pubertal development. We will use existing and newly collected data to: (SA1) estimate the unique contributions of heritable risk, prenatal exposure, and postnatal environmental influences on trajectories of child behaviors from infancy to adolescence that increase risk for SU; (SA2) examine the mediating role of prenatal exposures for transmitting heritable influences on trajectories of behavioral risk for SU; (SA3) examine the mediating role of pubertal development for transmitting heritable, prenatal and postnatal environmental influences on trajectories of behavioral risk for SU; and (SA4) examine moderation of early and biological influences by postnatal rearing environment (GxE, prenatal environment x E, endocrine development x E) to elucidate the possible interactions among genetic, prenatal, hormone, and postnatal environment in influencing child risk behaviors. This study will help to advance knowledge of the development of adolescent SU, will help clarify which children are at greatest risk for developing SU and related behaviors early in adolescence, and to indicate which influences are most salient for SU development given multiple other influences. The prospective, longitudinal, genetically-informed investigation using the EGDS sample is uniquely poised to achieve these aims, which are critical for gaining a more precise understanding of factors influencing the developmental course of SU that can be used to improve prevention efforts.


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