Cortisol Reactivity to the Trier Social Stress Test in African Americans with Childhood Violence Exposure

• In Event: Successes and Challenges Adapting the Trier Social Stress Test for Remote, Diverse, and fMRI Populations

Abstract

Exposure to violence impacts multiple aspects of development, including stress reactivity. Stress engages the hypothalamic pituitary adrenal (HPA) axis, which produces cortisol. A substantial body of research has utilized the Trier Social Stress Test (TSST) as a model for examining responses to social stress. This research has predominantly included Caucasian American participants without extensive exposure to violence. Less is known about other populations, particularly those with childhood violence exposure. A handful of studies indicate that childhood adversity is associated with decreased cortisol reactivity during the TSST. Based on these findings, we hypothesized that cortisol would decrease from baseline to post-TSST in a sample of African Americans with childhood violence exposure. We also hypothesized that violence exposure and post-traumatic stress symptoms (PTSS) would be associated with the magnitude of this decrease.

We examined cortisol reactivity as measured from saliva samples collected before the TSST was introduced (baseline), immediately post-TSST, and 20min after the TSST (recovery) in a sample of N=266 African Americans (137 female) aged 18 to 22 years from a birth cohort study conducted in Detroit, Michigan. Participants completed the My Exposure to Violence scale, a 31-item measure of trauma exposure, and the Million Clinical Multiaxial Inventory, a 175-item measure of psychopathology symptoms. The median number of exposures to violence was 15; just 4.2% of participants had none.

A repeated-measures analysis of variance indicated significant change in cortisol levels across the three time points, F(2,265) = 23.18, p < .0001. Cortisol decreased from baseline to post-TSST, F(1,265) = 77.85, p < .001, followed by a marginal increase from post-TSST to recovery, F(1,265) = 3.36, p = .072. There were not significant associations between violence exposure or PTSS and the decrease from baseline to post-TSST, both ps > .24, or the increase from post-TSST to recovery, both ps > .65. Given that sexual violence may have amplified physiological effects versus other types of violence exposure, we conducted an exploratory analysis to ascertain whether participants with (n = 39) versus without (n = 220) prior sexual violence exposure had different recovery patterns, as measured by cortisol at recovery. The exposed group had lower cortisol at recovery than the unexposed group, t(1.37) = 1.37, p = .032.

We observed cortisol reductions from baseline to post-TSST and blunted recovery that was not modulated by total violence exposure or PTSS symptom severity. We also found preliminary evidence that sexual violence, an interpersonal trauma that is linked to severe psychological outcomes, may prolong this blunting effect. These results indicate that cortisol response to social stressors may be unique in populations with high levels of childhood violence exposure. Future analyses will add to these findings by examining the impact of early caregiving and timing of violence exposure on cortisol reactivity. These findings highlight the importance of further research into how threat exposures during development, as well as specific types of violence, impact the HPA axis in diverse populations to confer later risk or resilience.

Authors

• Anais Fern Stenson, Wayne State University
  Presenting Author

• Lisa Chiodo, University of Massachusetts Amherst
  Non-Presenting Author

• Virginia Delaney-Black, Wayne State University School of Medicine
  Non-Presenting Author

• Tanja Jovanovic, Wayne State University
  Non-Presenting Author