Gene-Environment Correlation Linking Depressed Mood During Adolescence with Later Victimization in College and at Work

• In Event: 1-072 - Gene-Environment Correlations As Critical Influences on Children’s Social Relationships

Integrative Statement

The Stress Generation Hypothesis of Depression (SGHD; Hammen, 2006) postulates that depression symptoms may not only result from stressful experiences, but may also foster the occurrence of new—particularly social—stress. Supporting this notion, depression-related cognitions and behaviors are among the most important risk factors of peer victimization during adolescence (Reijntjes et al., 2010). It is unclear, however, whether a persistent tendency for depression-related cognitions and behaviors during adolescence also increases the risk of victimization later in life (e.g., in college or at work). When true experiments are not possible to test causal links, genetically informed designs provide a more comprehensive test of transactional processes between individual, heritable characteristics and environmental experiences than studies using singleton samples (Moffit, 2005). Since depressive symptoms are partly genetically influenced (Rice, 2009), evidence of a Gene-Environment Correlation (rGE) between genetic risks associated with depression symptoms during adolescence and later victimization experiences at work or in college would offer strong support of the SGHD.

To address this issue, the present study used a longitudinal, genetically informed design based on self-reports from 151 Monozygotic and 117 same-sex Dizygotic twin pairs (49% girls). Depression symptoms were assessed from grade 6 (age 12) through the end of high school (age 17). Victimization experiences in college and at work were assessed at age 19 years. Depressive symptom scores were averaged across all measurement times and victimization scores at age 19 were averaged across college and work contexts.

Depression symptoms in adolescence were positively correlated with victimization experiences at age 19 (r=0.26, p<.000). ACE modeling using a Cholesky decomposition (Neale, 2004) was performed to estimate the genetic and/or environmental influences underlying this covariation (see Figure 1). Genetic effects explained 56% of the variance of depression symptoms in adolescence and 29% of the variance of victimization at age 19, with the remaining variances explained by environmental influences unique to each individual. Importantly, 11% of the genetic effects on victimization at age 19 stemmed from genetic influences related to depression symptoms in adolescence (rGE=.33). Moreover, 5% of the environmental effects on victimization at age 19 stemmed from environmental influences related to depression symptoms in adolescence (rEE=.23).

The observed rGE concords with an evocative gene-environment correlation and with previous reports that a genetic vulnerability for depression is associated with an increased risk of adverse life events (Jaffee & Price, 2007). Our findings show that these adverse experiences may include being bullied by others even later in life. However, the observed rEE indicates that environmentally influenced depression symptoms in adolescence also predict victimization in college or at work later on. Part of these environmental influences may come from previous victimization during adolescence. Indeed, there is evidence that increased depression symptoms partly mediate the continuation of victimization from adolescence to young adulthood (Brendgen & Poulin, 2018). Together, these findings support the notion of a bidirectional relation between depression and stress postulated by the SGHD. They also highlight the importance of reducing depression symptoms before vulnerable youths become caught in a spiral of long-lasting abuse.

Authors

• Mara Brendgen, University of Quebec at Montreal
  Presenting Author

• Frank Vitaro, University of Montreal
  Non-Presenting Author

• Ginette Dionne, Laval University
  Non-Presenting Author

• Michel Boivin, Laval University
  Non-Presenting Author