use in isolation. However, environmental risk factors are often related to one another, and there is no unified framework for measuring or modeling cumulative risk in gene-by-environment interaction studies. A corollary to this point is that to understand gene-by-environment interactions for clinical outcomes across development—an approach that is important for creating effective early preventive-intervention efforts—holistic models of the environment will need to incorporate a developmental perspective. For example, exposure to risk factors later in development may be offset by experiencing protective factors earlier in development (and vice versa) (Rönkä, Oravala, & Pulkkinen, 2002; Salvatore, Haydon, Simpson, & Collins, 2013; Sroufe, Egeland, & Kreutzer, 1990). Bronfenbrenner's (1979) classic ecological model, which conceptualizes the environment as a series of transactional, nested environments that both affect and are affected by one another, provides a useful heuristic for what we are suggesting. Translating this conceptual model into an empirical one is critical for moving beyond “candidate environments” toward an integrative, developmentally sensitive understanding of how multiple, nested environments are likely to interface with genetic predispositions to predict the onset and course of clinical disorders. Psychologists are in a strong position to contribute to these efforts.
