Examining Protective-Stabilizing Effects of Family-Centered Prevention on Biological Indicators of Stress

Chronic stressors influence on psychosocial functioning and drug use and abuse has long been recognized (Miller, Chen, & Parker, 2009). But recently it has become evident that stress exposure has even further-reaching consequences, in the form of heightened vulnerability to common medical illnesses across the life course (Shonkoff, Boyce, & McEwen, 2009).  Indeed, children raised in stressful contexts go on to have elevated levels of infectious, respiratory, metabolic, and cardiovascular diseases in adulthood, independent of traditional risk factors for these conditions (Cohen, Janicki-Deverts, Chen, & Mathews, 2010). However, not all children and adolescents who grow up with high levels of stress exposure go on to develop medical problems as adults (Chen, & Miller, 2011). One route to resilience to health problems is supportive family environments.  While we know that involved and supportive family environments can offset risks for drug use and psychosocial problems, there is emerging evidence that family relationships can favorably mold the stress-response tendencies of vulnerable children (Gunnar & Quevedo, 2007). In fact, parental warmth and support may help mitigate the wear and tear that cumulative life stress places on children's and adolescents' physiology (Brody et al 2012, 2013). Most research to date, on the protective effects of family processes, however, consists of observational studies, making it difficult to draw causal inferences about the connection between family support and health-related endpoints.  Few studies have investigated whether family-centered preventive interventions designed to deter drug use and risky behaviors can also lead to changes in the biological pathways associated with health outcomes.  As a proof of principle for this conjecture, the results of two studies will be presented that illustrate the stress-buffering effects of family-centered drug use prevention programs on biological outcomes (catecholamine levels and telomere length) that forecast the development of chronic disease. In the first study, participants  in the Strong African American Families (SAAF) prevention  trial who, at age 11, were living in risky family environments  evinced higher catecholamines levels at age 20,if they were in the control condition, but not if they were in the SAAF condition.  The second study showed that participants in the Adults in the Making (AIM) prevention trial who were living in nonsupportive family environments at age 17, had shorter telomere lengths (TL)( a biological indicator of cellular aging and stress exposure) at age 22,if they were in the control condition but not if they were in the AIM condition.