Abstract
Using data from the Longitudinal Study of Chinese Children and Adolescents (LSCCA), this study is the first to examine the roles of the dopamine D2 receptor (DRD2) gene polymorphisms (i.e., TaqIA and A241G) and maternal positive parenting at ages 10 and 11 years in the trajectories of depressive symptoms from early to mid-adolescence (ages 11 to 16 years). In a sample of 1090 Chinese adolescents (50% girls), three trajectories of depressive symptoms were identified: (i) low-stable (36.1%), (ii) moderate-increasing (44.5%), and (iii) high-increasing (19.4%). A241G AA homozygotes and youth exposed to lower levels of maternal positive parenting were both at increased odds to follow the high-increasing vs. low-stable trajectory. Moreover, the A241G polymorphism interacted with maternal positive parenting to distinguish the moderate-increasing trajectory from the high-increasing and the low-stable trajectories. For A241G G-allele carriers, but not AA homozygotes, exposure to high quality of maternal parenting decreased the odds to follow the high-increasing vs. moderate-increasing trajectory of depressive symptoms. For AA homozygotes, but not G-allele carriers, high quality of maternal parenting increased the odds to follow the low-stable vs. moderate-increasing trajectory. The DRD2 TaqIA polymorphism had neither a direct nor an interactive effect with maternal positive parenting on trajectory membership. The current findings highlight the importance of investigating gene-by-environment interactions (G × E) in trajectories of depressive symptoms over adolescence, and support a developmental versus static nature of G × E effects.
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Notes
The genetics subsample (N = 1090) did not differ from the full sample (N = 2164) on the vast majority of variables: gender and age of the child, age and educational levels of mother and father, family income, maternal positive parenting and depressive symptoms at ages 12, 13, 14, 15 and 16. Only slightly lower levels of depressive symptoms at age 11 existed in the genetics subsample versus the full sample (p < 0.05, mean difference − 0.34). In order to maintain consistency in sample size throughout the analyses, we chose to restrict all analyses (i.e., analyses about trajectories of depressive symptoms and predictors of trajectories) to the genetics subsample. In a follow-up analysis, we tested the consistency of our findings across the full sample (N = 2164) and genetics subsample (N = 1090). Three main findings are highlighted. First, the three-trajectory model identified in the genetics subsample was confirmed in the full sample: (i) low-stable (40.2%; B intercept = 0.86, SE = 0.11, p < 0.001), (ii) moderate-increasing (40.8%; B intercept = 1.64, SE = 0.06, p < 0.001; B linear = 0.12, SE = 0.01, p < 0.001), and (iii) high-increasing (19.0%; B intercept = 2.56, SE = 0.07, p < 0.001; B linear = 0.13, SE = 0.03, p < 0.001; B quadratic = −0.01, SE = 0.01, p < 0.01). The entropy was 0.90, and the mean posterior probabilities of trajectories ranged from 0.95 to 0.96, suggesting good classification precision. Second, we identified no significant differences between the availability of genetic data across the three trajectories (χ2 = 4.81, df = 2, p > 0.05). Third, the pattern of regression findings was replicated when we used the trajectories as identified in the full sample. Specifically, the meta-analytically derived A241G × parenting interactions remained statistically significant (high-increasing vs. moderate-increasing: OR = 1.85, 95% CI [1.22, 2.81], p < 0.01; moderate-increasing vs. low-stable: OR = 0.67, 95% CI [0.49, 0.93], p < 0.05), and they were similar in magnitude to the effects with trajectories obtained in the genetics subsample.
Given no within class variances in the LCGA model, the LCGA is less complex than the GGMM (General Growth Mixture Modeling). The LCGA is more likely to avoid convergence issues and increase overall model stability versus the GGMM (Jung and Wickrama 2008). Therefore, in line with previous research (Dekker et al. 2007; Fanti and Henrich 2010), the LCGA was selected.
Again, mothers of girls had both higher levels of maternal positive parenting than mothers of boys at ages 10 (t (998) = 3.31, p < 0.001) and 11 (t (1051) = 2.10, p < 0.05), which is in accordance with previous research in similar age groups (i.e., 10 and 11 ages) (Oldehinkel et al. 2006).
The multinomial logistic regressions in this study were estimated on assigning classes to their most likely class. This is mainly because the mean posterior probabilities in the three trajectories ranged from 0.96 to 0.98, suggesting very high estimate probabilities for belonging to each class (Brendgen et al. 2005; Castelao and Kröner-Herwig 2013; Mezulis et al. 2014; Stoolmiller et al. 2005).
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Acknowledgements
This study was supported by the National Natural Science Foundation of China (31271105 and 31671156) and the Specialized Research Fund for the Doctoral Program of Higher Education (20133704110001) to W. Z. M.J.B.K was supported by the European research Council (ERC AdG), the Gravitation program of the Dutch Ministry of Education, Culture, and Science and the Netherlands Organization for Scientific Research (NWO grant number 024.001.003). We thank the parents and adolescents who generously donated their time to our study, as well as the students who assisted in the data collection. We thank Marinus H. Van IJzendoorn, Leiden University, for his contributions to the data-analysis and his comments to earlier drafts of the paper.
Authors’ Contributions
W.Z., M.J.B.K., C.C., and L. J. conceived the study and its design; C.C., and L. J. participated in the data collection; C.C., J.R., A.v.d.V., and M.J.B.K. participated in the statistical analysis and the interpretation of the data; C.C., J.R., A.v.d.V., and M.J.B.K. drafted the manuscript. All authors read and approved the final manuscript.
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Cao, C., Rijlaarsdam, J., van der Voort, A. et al. Associations Between Dopamine D2 Receptor (DRD2) Gene, Maternal Positive Parenting and Trajectories of Depressive Symptoms from Early to Mid-Adolescence. J Abnorm Child Psychol 46, 365–379 (2018). https://doi.org/10.1007/s10802-017-0294-5
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DOI: https://doi.org/10.1007/s10802-017-0294-5