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Parent–child conflict as an etiological moderator of childhood conduct problems: an example of a ‘bioecological’ gene–environment interaction

  • S. A. Burt (a1) and K. L. Klump (a1)

Abstract

Background

Prior research has suggested that, consistent with the diathesis–stress model of gene–environment interaction (G × E), parent–child conflict activates genetic influences on antisocial/externalizing behaviors during adolescence. It remains unclear, however, whether this model is also important during childhood, or whether the moderation of child conduct problems by negative/conflictive parenting is better characterized as a bioecological interaction, in which environmental influences are enhanced in the presence of environmental risk whereas genetic influences are expressed most strongly in their absence. The current study sought to distinguish between these possibilities, evaluating how the parent–child relationship moderates the etiology of childhood-onset conduct problems.

Method

We conducted a series of ‘latent G by measured E’ interaction analyses, in which a measured environmental variable was allowed to moderate both genetic and environmental influences on child conduct problems. Participants included 500 child twin pairs from the Michigan State University Twin Registry (MSUTR).

Results

Shared environmental influences on conduct problems were found to be several-fold larger in those with high levels of parent–child conflict as compared with those with low levels. Genetic influences, by contrast, were proportionally more influential at lower levels of conflict than at higher levels.

Conclusions

Our findings suggest that, although the diathesis–stress form of G × E appears to underlie the relationship between parenting and conduct problems during adolescence, this pattern of moderation does not extend to childhood. Instead, results were more consistent with the bioecological form of G × E which postulates that, in some cases, genetic influences may be most fully manifested in the absence of environmental risk.

Copyright

Corresponding author

* Address for correspondence: S. A. Burt, Ph.D., Department of Psychology, Michigan State University, 107D Psychology Building, East Lansing, MI 48824 USA. (Email: burts@msu.edu)

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