mediated through neighborhood or school variables (Gershoff and Aber, 2006).
Similarly, biological factors may mediate the effects of psychosocial risk and protective factors, and conversely psychosocial risk and protective factors may moderate the effects of biological risk factors. For example, Davies, Sturge-Apple, and colleagues (2007) found that diminished cortisol reactivity mediated the relationship between children’s exposure to interparental conflict and the development of externalizing problems over a two-year time period. Research has also identified interactions between genetic and environmental factors to predict disorder (see Chapter 5). However, intervention trials that include genetic or other biological information in the design or analysis of the trial are just beginning to emerge. For example, Brody, Kogan, and colleagues (2008) tested whether a psychosocial intervention to improve parent–child communication of parents in rural poor African American families would moderate the effect of genetic risk due to the presence of a specific variant of the serotonin transporter gene on their children’s initiation of alcohol use, binge drinking, marijuana use, and sexual intercourse in early adolescence. As predicted, they found that program participation moderated the relationship between genetic risk and high-risk behavior; youth at genetic risk who did not receive the intervention had significantly greater increases in risk behavior initiation (1.91 versus .90 on the risk index) from pretest than youth at genetic risk who were assigned to the program.
In addition to identifying direct or indirect associations between risk and protective factors and outcomes of interest, it is also important for the development of interventions to understand the processes by which these effects occur (Luthar and Cicchetti, 2000). Conceptually, several different mechanisms have been proposed. Rutter (1987), for example, discussed five processes by which the effects of risk factors could be reduced: (1) by altering the experience of the risk factor (e.g., by coping); (2) by altering exposure to the risk factor (e.g., by parental monitoring of child involvement with antisocial peers); (3) by averting negative chain reactions (e.g., when harsh parenting leads to child oppositional behavior, which leads to increased conflict); (4) by strengthening protective factors (e.g., self-esteem, adaptive control beliefs); and (5) by turning points, which change the total context and provide new opportunities for development (e.g., moving from institutional care to a positive school environment). Each of these processes may be targeted by preventive interventions.
Evaluations of mediators and moderators of preventive interventions also enable the development of more efficient prevention programs (Brown and Liao, 1999). For example, a meta-analysis of school-based programs for the prevention of problem behavior, such as substance use and delinquency, found that program effects on two theoretical mediators (bond-