Symposia
Racial Trauma
Lorraine Benuto, Ph.D. (she/her/hers)
Associate Professor
DICE Center
reno, Nevada, United States
Jorge Cao Noa, M.S,
Graduate Student
University of Nevada Reno
Reno, NV, United States
Cossette A. Canovas, M.S. (she/her/hers)
Graduate Student
University of Nevada, Reno
Reno, NV, United States
Natalia Duda, B.A.
Graduate Student
University of Nevada, Reno
Truckee, CA, United States
Madison Thomasson, M.S,
Graduate Student
University of Nevada, Reno
Reno, NV, United States
People of color (POC) are exposed to overt racism and microaggressions, often daily. Because nonviolent experiences of racism do not meet the DSM-5-TR definition of a Criterion A trauma, POC who experience negative sequalae due to racism are not considered to have PTSD, despite evidence that racism produces PTSD-like symptoms, such as negative cognitions, difficulty coping, and lack of safety (Williams, 2024). Frequent exposure to racism may also lead to chronic stress, which may create persistent feelings of anxiety and hypervigilance. Researchers have assessed salivary cortisol (a marker of hypothalamic–pituitary–adrenal axis [HPA] response) and salivary alpha amylase (sAA; a marker of sympathetic nervous system [SNS] response) as potential biomarkers to assess neural hypervigilance (Yoon & Weierich, 2016).
To explore possible similarities and differences between PTSD and racial trauma, we examined HPA and SNS response to a trauma narrative among individuals with racial trauma (n = 17) and PTSD (n = 8). Participants rested for 10 minutes before providing a baseline saliva sample (T1). They then were asked to recall and recount, in detail, their traumatic memory (PTSD) or most prominent racial experiences (racial trauma) before a second (T2) saliva sample was taken (to analyze sAA). The third (T3) saliva sample was taken after 20 minutes (to analyze cortisol). Saliva samples were then sent to a lab for processing. sAA reactivity was determined by subtracting T1 from T2 concentrations, and cortisol reactivity was determined by subtracting T1 from T3 concentrations. We then conducted two independent sample t-tests to determine if there was a statistically significant difference between our groups.
Results indicated a significant difference for cortisol reactivity t(23) = -2.34, p = .05 but not sAA reactivity t(23) = -.62, p= .56. These results indicate that individuals with PTSD had greater cortisol reactivity (M = .02; SD = .19) than those with racial trauma (M = -.21; SD = .20); conversely, individuals with PTSD and racial trauma had similar sAA response patterns. These results indicate that individuals with PTSD and racial trauma may have similar SNS responses but that HPA responses may be more pronounced among individuals with PTSD. A possible explanation is that participants with racial trauma display a blunted cortisol response due to the chronic, ongoing nature of racism. In this presentation, we will further discuss the implications of our findings and how they set the foundation for understanding the underlying mechanisms of racial trauma.