Evidence that gene-environment correlations are important to anxiety and depression comes from a range of twin and family designs. Because such correlations essentially refer to the co-occurrence of genetic and environmental effects on phenotypic variation, support for these correlations primarily involves demonstrating that an environmental risk variable also shows genetic influence. Many environmental predictors of anxiety and depression, such as negative life events and aspects of the parent-child relationship, have been found to show genetic effects (Lau, Rijsdijk, & Eley, in press; Pike, McGuire, Hetherington, Reiss, & Plomin, 1996; Saudino, Pedersen, Lichtenstein, McClearn, & Plomin, 1997). Moreover, such genetic effects also overlap with genes that are implicated in outcome measures of emotional symptoms. This indicates that genetic risks for these phenotypes may in part be expressed through an exposure to environmental risk, and this exposure has been suggested to arise in three ways: "passive," "evocative," or "active" processes (Scarr & McCartney, 1983).
Passive gene-environment correlation arises when the parental genetic makeup influences both the child's genotype and the rearing environment provided for the child. For example, a child may inherit his or her mother's depressogenic genes, together with being exposed to a repertoire of negative parenting styles. Evocative processes apply when a child's genetic propensities elicit, through cognitive variables or temperamental traits, certain reactions from other people. Thus infants who are frequently crying and irritable may evoke more negative responses from their parents than cheerful, smiling babies may. Finally, active types of gene-environment correlation occur when individuals select, modify, or construct their experiences based on genetically mediated dispositions, such as personality traits. Sociable youngsters may choose to spend more of their time with other children, thus increasing the levels of social contact in their environment, while inhibited children may spend more time in isolation and thus may experience increased feelings of loneliness.
As yet, it is fairly difficult to distinguish among these three types of geneenvironment correlations at an analytical level, and often only an overall effect can be demonstrated. However, it has been suggested that such correlation processes may be expressed at different points in development: Passive forms may be more salient during infancy and early childhood, whereas evocative and active processes may become more important as children begin to experience environments outside the family and play a more active role in shaping their own experiences. One study that has explored these developmental trends included a comparison of the relative contribution of genetic and environmental factors to the relationship between negative life events and depression in two different age groups (8-11 and 12-17 years) (Rice, Harold, & Thapar, 2003). Their results showed that genes did play a larger role in this association in the older adolescent sample compared to the child sample, thus suggesting that active gene-environment correlation becomes a stronger influence on depression symptoms across development. These increased effects could also potentially account for the larger genetic effects found during adolescence by previous studies.
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