Serotonin transporter gene moderates the development of emotional problems among children following bullying victimization.
Journal Article (Journal Article)
Objective
Bullying is the act of intentionally and repeatedly causing harm to someone who has difficulty defending him- or herself, and is a relatively widespread school-age phenomenon. Being the victim of bullying is associated with a broad spectrum of emotional problems; however, not all children who are bullied go on to develop such problems.Method
We tested the hypothesis that the relationship between bullying victimization and emotional problems was moderated by variation in the serotonin transporter (5-HTT) gene in 2,232 British children comprising the Environmental Risk (E-Risk) study cohort.Results
Our data supported the hypothesis that children's bullying victimization leads to their developing emotional problems, and that genetic variation in the 5-HTTLPR moderates this relationship. Specifically, frequently bullied children with the SS genotype were at greater risk for developing emotional problems at age 12 than were children with the SL or LL genotype. Furthermore, we demonstrated that this genetic moderation persisted (a) after controlling for children's previctimization emotional problems by assessing intraindividual change in problems between ages 5 and 12 years, and (b) after controlling for other risk factors shared by children growing up in the same family by comparing emotional problems in twins discordant for bullying victimization.Conclusions
These findings are further evidence that the 5-HTTLPR moderates the risk of emotional disturbance after exposure to stressful events.Full Text
Duke Authors
Cited Authors
- Sugden, K; Arseneault, L; Harrington, H; Moffitt, TE; Williams, B; Caspi, A
Published Date
- August 2010
Published In
Volume / Issue
- 49 / 8
Start / End Page
- 830 - 840
PubMed ID
- 20643316
Pubmed Central ID
- PMC2908591
Electronic International Standard Serial Number (EISSN)
- 1527-5418
International Standard Serial Number (ISSN)
- 0890-8567
Digital Object Identifier (DOI)
- 10.1016/j.jaac.2010.01.024
Language
- eng