Abstract: Exposure to Violence during Adolescence Predicting Later Cortisol Response: Understanding Sex Differences (Society for Prevention Research 22nd Annual Meeting)

354 Exposure to Violence during Adolescence Predicting Later Cortisol Response: Understanding Sex Differences

Schedule:
Thursday, May 29, 2014
Columbia A/B (Hyatt Regency Washington)
* noted as presenting author
Sophie M. Aiyer, PhD, Postdoctoral Fellow, University of Michigan-Ann Arbor, Ann Arbor, MI
Justin E. Heinze, PhD, Research Scientist, University of Michigan-Ann Arbor, Ann Arbor, MI
Alison L. Miller, PhD, Assistant Professor, University of Michigan-Ann Arbor, Ann Arbor, MN
Andria Eisman, MPH, Doctoral Student, University of Michigan-Ann Arbor, Ann Arbor, MI
Sarah A. Stoddard, PhD, Assistant Professor, University of Michigan-Ann Arbor, Ann Arbor, MI
Marc A. Zimmerman, PhD, Professor and Department Chair, University of Michigan-Ann Arbor, Ann Arbor, MI
Introduction:

            The biological stress response is proposed as a key mechanism through which psychosocial stress can affect health. In addition, adolescence is a developmental period characterized by biological and hormonal changes. Thus, stressors experienced during adolescence may exert lasting influences on biological stress response, as well as brain structure and function.  Adolescence is also a period characterized by changes in risk exposure. In sum, biological stress response is a likely explanatory mechanism for the influence of exposure to environmental stressors during adolescence on negative neurobiological outcomes in adulthood.

            Although we know that chronic exposure to environmental stress during childhood is associated with adverse cortisol profiles, less is known about the specific role of violence, particularly during adolescence. Further, researchers have also reported sex differences in HPA axis functioning, yet the direction of these findings remains inconclusive. Previous research on stress regulation has also been largely cross-sectional, emphasizing the need to examine determinants of stress over time. 

Method:

            Using longitudinal data from a low-income, high-risk, predominantly African-American sample (n=398), we tested hypotheses about the influence of exposure to violence (ETV) during adolescence on cortisol profiles in early adulthood. We tested our hypotheses using a series of multi-level models. First, we examined whether cumulative exposure to violence (witnessing violence, violence victimization, and family physical conflict) in adolescence (mean age 17.8 years) predicted cortisol profiles in early adulthood (mean age 22.0 years). Based on previous findings regarding sex differences, we then stratified the sample by sex to examine whether the effect of violence exposure on cortisol response differed by sex. Finally, we tested interactions to determine whether the associations between exposure to violence predictors and cortisol outcomes were moderated by mother or father support.

Results:

            Focusing on a uniquely high-risk sample, we found that female participants exposed to violence during adolescence demonstrate signs of an attenuated stress response in early adulthood. Neither mother support nor father support moderated the effect of cumulative exposure to violence on cortisol responsivity.

Conclusions:

            We found evidence for the long-term neurobiological effects of cumulative violence exposure during mid-adolescence on cortisol response in early adulthood. Our results suggest that chronic exposure to violence can have lasting deleterious effects, which include physiological consequences. Prevention efforts designed to prevent maladaptive cortisol regulation in populations exposed to high rates of violence would be useful. Research is also needed to understand why exposure to violence during adolescence may be more detrimental to girls, compared with boys.