Development & Malleability from Childhood to Adulthood

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Abstract The central purpose of the proposed study is to extend through ages 31-35 an examination of normal and pathogenic development and the impact of two, universal, first grade, preventive interventions on the distal targets of: antisocial behavior, substance abuse/dependence, psychiatric symptoms/disorders, high risk sexual behavior, and successful adaptation to the relevant developmental demands of the educational, work, romantic relationships, and family (both family of procreation and origin/orientation) social fields/contexts. This study capitalizes on the scientific value of 1) a prospective, developmental epidemiological prevention trial involving a population (N = 798) of urban, predominately African-American young adults, who began first grade in the fall of 1993 in 9 elementary schools in predominantly low to lower middle-income Baltimore areas96. Participants and teachers were randomly assigned to one of two universal, elementary school-based, preventive interventions, or a control condition. Both interventions—the Family School Partnership (FSP) and Classroom- Centered (CC)--targeted aggressive-coercive behavior and poor academic achievement as antecedents of the distal outcomes elaborated above. Annual data on these outcomes and their hypothesized phenotypic moderators and mediators, including participant, family, peer group, school, and neighborhood characteristics, have been collected from 1st grade through age 26. DNA was obtained in early adulthood, which has allowed examination of the interplay between genetic and phenotypic factors in explaining variation in developmental and intervention outcomes. The proposed annual assessments will allow a more precise assessment of the timing and sequencing of the interplay of phenotypic and genetic influences, including the interventions, on successful adaptation to the relevant developmental challenges between the ages of 31-35. Similarly, we will continue to study the role of phenotypic and genetic factors and the impact of the interventions on the development and course of substance use/abuse/dependence, psychiatric symptoms/disorders, antisocial behavior/disorder, and high risk sexual behavior through young adulthood. Finally, we will also assess potential epigenetic effects in terms of change in telomere length and telomerase activity as a function of accumulative stress over time and the interventions as moderators of the stress/telomere relationship. The knowledge accrued over the course of the proposed assessments should serve to inform the nature, targets, and timing of our future preventive intervention efforts.