Conflict of interest statement: No conflict declared.
The interacting effect of the BDNF Val66Met polymorphism and stressful life events on adolescent depression is not an artifact of gene–environment correlation: evidence from a longitudinal twin study
Article first published online: 12 JUL 2013
© 2013 The Authors. Journal of Child Psychology and Psychiatry © 2013 Association for Child and Adolescent Mental Health.
Journal of Child Psychology and Psychiatry
Special Issue: Gene- environment interplay in child psychology and psychiatry: challenges and ways forward
Volume 54, Issue 10, pages 1066–1073, October 2013
How to Cite
Chen, J., Li, X. and McGue, M. (2013), The interacting effect of the BDNF Val66Met polymorphism and stressful life events on adolescent depression is not an artifact of gene–environment correlation: evidence from a longitudinal twin study. Journal of Child Psychology and Psychiatry, 54: 1066–1073. doi: 10.1111/jcpp.12099
- Issue published online: 5 SEP 2013
- Article first published online: 12 JUL 2013
- Manuscript Accepted: 3 MAY 2013
- Chinese Academy of Sciences. Grant Number: KSCX2-EW-J-8
- Institute of Psychology. Grant Number: Y0CX351S01
- National Natural Science Foundation of China. Grant Number: 31170993
- Key Laboratory of Mental Health
- depressive symptoms;
- BDNF Val66Met polymorphism;
- stressful life events;
- gene–environment interaction;
- gene–environment correlation
Confounding introduced by gene–environment correlation (rGE) may prevent one from observing a true gene–environment interaction (G × E) effect on psychopathology. The present study investigated the interacting effect of the BDNF Val66Met polymorphism and stressful life events (SLEs) on adolescent depression while controlling for the rGE by two means: separating pure environmental factors (independent SLEs) from the environmental factors under partial genetic control (dependent SLEs) and adopting a prospective longitudinal design.
A total of 780 pairs of Chinese twins, aged 11–17 years (mean = 13.6, SD = 1.8) at intake, were followed up twice. Self-reported depression symptoms at Time 1 and Time 2 were assessed by the Children's Depression Inventory (CDI). SLEs occurring between Time 1 and Time 2 were assessed by a self-reported checklist. SLEs were differentiated into independent and dependent ones and were validated by heritability analyses using twin design. The interacting effects between the BDNF Val66Met polymorphism and numbers of SLEs (total SLEs and independent SLEs) on intraindividual change of depression symptoms were examined.
After controlling for sex, age, age square, and Time 1 depression, both total SLEs × BDNF Val66Met genotype and independent SLEs × BDNF Val66Met genotype significantly predicted Time 2 depression. Val allele carriers (Val/Val and Val/Met) were more susceptible to the detrimental effects of stress.
There is a true G × E effect underlying the observed interaction between BDNF Val66Met polymorphism and environmental stress on depression.