Evidence of comorbid relations between substance use, abuse and dependence and depressive symptomatology and/or disorder has been found in both clinical and epidemiologic studies of adolescents am adults (Birmaher et al., 1996). Concurrent estimates of comorbidity range from 11% to 32% among youth, with depression ranking second to conduct disorder in association with substance use disorder. Lifetime comorbidity estimates approach 50%. Although adolescent onset of either disorder is associated with deleterious long term outcomes, adolescents most at risk are those who display a combination of symptoms. This application proposes to utilize two existing data sets, both longitudinal, to elucidate the nature of the comorbid relations between substance use and depressive symptomatology. Data from one study covers the period from adolescence to young adulthood over a 19-year time span with 14 assessments. The second dataset covers a ten-year period of time beginning in early adulthood with five assessments. Each of the studies employed a multimethod, multisource approach to assessing both intra- and interpersonal functioning as well as a comprehensive set of developmentally relevant contextual variables.
The aims of the proposed work are as follows: 1) Model the reciprocal relations between depression and substance use/abuse from adolescence into adulthood; 2) Test the hypothesis, derived from the theory of cumulative continuity (Caspi and Elder, 1988), that the relations between depression and substance emerge as a function of an accumulation of adverse life events that arise consequent to problems in either domain (i.e., depression or substance use) and subsequently function as vulnerability factors for the emergence of difficulties in the other domain; and 3) Examine hypothesized moderating influences, both intrapersonal and contextual, on the relations between depression and substance use. The results may have significant implications for the treatment and prevention of substance use and depression in adolescence and young adulthood. In particular, evidence that elucidates the sequential relations between the two would provide guidance in targeting at risk populations for preventive interventions. Relatedly, this targeting would be further refined through the identification of moderating factors that distinguish individuals at particular risk for secondary problems from those who are at less risk. Finally, a thorough understanding of the mechanisms connecting these two disorders would inform the development of preventive interventions.
