Center for Education and Drug Abuse Research (CEDAR): Etiological and Prospective Family Study in Southwestern Pennsylvania, Baseline and Follow-Up Data, 1990-2014

Résumé 0

The Center for Education and Drug Abuse Research (CEDAR) conducted research on 775 families enrolled in the Center's prospective investigations into the etiology of substance use disorder (SUD). The pro-bands are men with lifetime presence/absence of SUD consequent to use of an illicit drug who have a 10-12 year old biological son or daughter. The biological children of SUD men are assigned to the high average risk (HAR) group whereas offspring of men without SUD, having neither axis 1 disorder ("normal") nor SUD psychiatric disorder, are assigned to the low average risk (LAR) group. A second control group (Psych control) was also collected, in whom the fathers had a lifetime DSM-III-R diagnosis of any psychiatric disorder not related to substance use. The sample sizes are as follows: HAR = 344, LAR = 350, and Psych = 81. The children had follow-up evaluations conducted at ages 12-14, 16, 19, and annually thereafter until age 30. CEDAR has already shown that they can predict in 10-12 year old youth cannabis use disorder by age 22 with approximately 70 percent accuracy, thereby substantiating the paradigm, subject recruitment strategy, and measurement protocols. Multidisciplinary research was conducted on family members (father, mother, children) with the objective of elucidating the genetic, bio-behavioral, and environmental factors on development of SUD consequent to use of illegal drugs. Research protocols are organized into three thematically connected research modules (Neurogenetics, Developmental Psychopathology, and Translation) linking etiology and prevention. The research components thus align with the NIH Roadmap model such that basic science informs clinical research leading to prevention guided by an understanding of etiology. In addition to module-level research, faculty also participate in three organizational aims: (1) Devise a practical scale to quantify the transmissible liability to SUD; (2) Empirically test a bio-psychological theory of SUD etiology focusing on off-time maturation leading to psychological dysregulation predisposing to SUD; and, (3) Delineate SUD liability variants within an ontogenetic framework.