How and Why Does the 5-HTTLPR Gene Moderate Associations Between Maternal Unresponsiveness and Children's Disruptive Problems?

Authors


  • This research was supported by the National Institute of Mental Health (R01 MH071256) and the Spunk Fund Inc. The authors are grateful to the children, parents, and community agencies who participated in this project. We would also like to thank Crista Crittenden, Mike Ripple, and the rest of the Mt. Hope Family Center staff who assisted on the project.

Correspondence concerning this article should be addressed to Patrick T. Davies, Department of Clinical and Social Sciences in Psychology, University of Rochester, Rochester, NY 14627. Electronic mail may be sent to patrick.davies@rochester.edu.

Abstract

This study tested the 5-HTTLPR gene as a moderator in the relation between maternal unresponsiveness and child externalizing symptoms in a disadvantaged, predominantly Black sample of two hundred and one 2-year-old children and their mothers. Using a multimethod, prospective design, structural equation model analyses indicated that maternal unresponsiveness significantly predicted increases in externalizing symptoms 2 years later only for children possessing the LL genotype. Moderation was expressed in a “for better” or “for worse” form hypothesized in differential susceptibility theory. In examining why the risk posed by maternal unresponsiveness differed across the 5-HTTLPR polymorphism, mediated moderation analyses showed that children's angry reactivity to maternal negativity partly accounted for the greater susceptibility of homozygous L carriers to variations in maternal unresponsiveness.

Ancillary