Gene-environment interaction can be detected by both quantitative genetic analyses and molecular studies of specific genetic variation (gene polymorphisms). Among the former, for instance, the heritability of body mass (body mass index) has been found lower among men who engage in vigorous exercise than in the less physically active (McCaffery et al, 2009), and the heritability of hypertension appears to rise with higher levels of educational attainment (McCaffery et al, 2008). Molecular studies of gene-stress interaction are more common than quantitative genetic studies, though, and these generally fall into two categories: (1) those that examine how naturally occurring stressors moderate genetic influences on aspects of disease risk and, in psychiatric genetics, liability to psychopathologies of mood or conduct; and (2) studies examining the genetic modulation of physiological responses to acute psychological stressors, as manipulated experimentally. The latter investigations add to a longstanding focus of research in behavioral medicine on psy-chophysiological reactivity as a possible risk factor for disease (Krantz and Manuck, 1984; Manuck, 1994; Marsland et al, 2002). Candidate genetic variation in these studies commonly targets genes encoding components of neurotrans-mitter systems acting in the brain or peripherally (e.g., enzymes effecting synthesis, release and reuptake, receptor activation, or metabolism), as well as intracellular signaling molecules, hormonal influences on gene expression (e.g., steroid receptors), and other elements of systemic physiology (e.g., inflammatory cytokines and other immune parameters). In the following sections, we discuss selected literatures involving genetic interactions with life events or other natural stressors and experimental studies of genetically modulated physiological responses to laboratory stressors.
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