More than simply accumulating examples of moderation of genetic influence by environmental factors, efforts have been made to integrate this work into theoretical frameworks surrounding the etiology of different clinical conditions. This is critical if science is to advance beyond individual observations to testable broad theories. A 2005 review paper by Shanahan and Hofer suggested four processes by which social context may moderate the relative importance of genetic effects (Shanahan & Hofer 2005). The environment may (a) trigger or (b) compensate for a genetic predisposition, (c) control the expression of a genetic predisposition, or (d ) enhance a genetic predisposition (referring to the accentuation of “positive” genetic predispositions). These processes are not mutually exclusive and can represent different ends of a continuum. For example, the interaction between genetic susceptibility and life events may represent a situation whereby the experience of life events triggers a genetic susceptibility to depression. Conversely, “protective” environments, such as marriage-like relationships and low stress levels, can buffer against or reduce the impact of genetic predispositions to depressive problems. Many different processes are likely involved in the
