Poster #63 - Cortisol Stress Reactivity Moderating the Effects of Community Violence Exposure and Social Support on Depression

• In Event: 1-005 - Poster Session 01
  In Poster Session: PS 01 Section - Developmental Psychopathology

Integrative Statement

Community violence exposure is associated with multiple negative outcomes such as depression and behavioral problems (Hammack, 2004). Social support is linked with better adjustment outcomes due to lower stress responses (Heinrichs, 2003). According to the differential susceptibility theory, greater stress reactivity may render some individuals more susceptible to the effects of both positive and negative environmental influences (Ellis, 2011; Obradovic, 2010). Stress reactivity may be indicated by cortisol, a marker of HPA axis activity (Granger et al., 2012). However, few studies have examined differential susceptibility to both positive and negative environmental influences using cortisol stress reactivity. This study examined whether cortisol stress reactivity moderated the effects of community violence exposure and social support on depression in adolescents. We hypothesized that the effects of both violence exposure and social support on depression would be stronger for youth with greater cortisol response to stress.
The present study included 79 adolescents (50% female; 95% African American) who participated in two waves of a longitudinal study at average ages of 13 and 15 years. Youth reported on their exposure to community violence, social support, and depressive symptoms. Cortisol stress reactivity was measured as the Area Under the Curve for three salivary cortisol assessments corresponding to baseline, peak stress, and recovery on the Trier Social Stress Test. Linear regression analyses tested the effects of community violence exposure, social support, and cortisol reactivity to stress at age 13 on depressive symptoms at age 15. Interactions of cortisol reactivity with violence exposure and social support were used to test the differential susceptibility hypothesis.
Results indicated that depressive symptoms were stable across time (β= .43). Social support predicted lower depressive symptoms over time (β= -.23; p<.05), and violence exposure predicted more depression over time (β= .29; p<.05). The interactions of cortisol stress reactivity with violence exposure and social support were not significant (β= .18 and β= -.13 respectively, p>.05).
Cortisol stress reactivity did not indicate differential susceptibility to either positive or negative environmental influences. It is possible that cortisol reactivity to social stress in the lab is not a valid measure of differential susceptibility, which has typically been assessed with specific genetic polymorphisms. The results of the study were limited by generally small cortisol response to the stress task, as well as small sample size which may not have provided enough statistical power to test the complex hypotheses. Future research should examine the possible moderating effects of cortisol stress reactivity in larger and more diverse samples (e.g., including youth from urban, suburban, and rural areas). These results suggest that preventing adolescents’ exposure to community violence and increasing their social support may be beneficial in preventing an increase in depressive symptoms.

Authors

• Victoria Swaine, Auburn University
  Presenting Author

• Catheryn Orihuela, University of Alabama at Birmingham
  Non-Presenting Author

• Jonathan Adams, University of Alabama at Birmingham
  Non-Presenting Author

• Sylvie Mrug, University of Alabama at Birmingham
  Non-Presenting Author