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01-07-2015 | Empirical Research | Uitgave 7/2015

Journal of Youth and Adolescence 7/2015

The Dopamine D2 Receptor Polymorphism (DRD2 TaqIA) Interacts with Maternal Parenting in Predicting Early Adolescent Depressive Symptoms: Evidence of Differential Susceptibility and Age Differences

Tijdschrift:
Journal of Youth and Adolescence > Uitgave 7/2015
Auteurs:
Wenxin Zhang, Yanmiao Cao, Meiping Wang, Linqin Ji, Liang Chen, Kirby Deater-Deckard

Abstract

Most gene-environment interaction research on depression has largely focused on negative environment and to a lesser extent on positive environment. Moreover, to date few studies have directly examined G × E at different periods in development, particularly during early adolescence. The present study addressed these issues by examining the concurrent and prospective longitudinal effects of maternal parenting, DRD2 TaqIA polymorphism, and their interaction on adolescent depressive symptoms in a sample of 1026 Chinese adolescents (M age  = 11.33 ± 0.47 years at T1, 50.3 % girls) in a three-wave longitudinal study from age 11 to 13. Results indicated that maternal positive and negative parenting significantly concurrently predicted adolescent depressive symptoms at all three waves, whereas TaqIA polymorphism had no main effect on depressive symptoms. TaqIA polymorphism interacted with negative parenting in predicting concurrent depressive symptoms at age 11 and 12. A1 carriers were more susceptible to negative parenting compared to A2A2 homozygotes, such that adolescents carrying A1 alleles experiencing high negative parenting reported more depressive symptoms but fared better when experiencing low negative parenting. However, the interaction became nonsignificant at age 13, indicating the interaction of TaqIA polymorphism and maternal parenting may vary with development. Also, there was no G × E effect on longitudinal change in depression. The findings provided evidence in support of the differential susceptibility hypothesis and shed light on the potential for dynamic change in gene-environment interactions over development.

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