Neuroendocrine Mechanisms Underlying Perimenopausal Risk for Trauma-Related Hyperarousal in Black Women

总结

Summary The cumulative rate of repeated trauma exposure is greater in Black communities of urban, low socioeconomic status and is associated with increased prevalence of adverse, posttraumatic mental health outcomes, including posttraumatic stress disorder (PTSD). PTSD is associated with trauma-related hyperarousal (TRH) and dysregulated fear responses that are dependent upon brain regions that modulate responses to threat, including the amygdala and the ventromedial prefrontal cortex. One biological factor that confers increased risk for TRH is female sex. While rigorous studies have shown that low levels of the steroid hormone estradiol (E2) are associated with increased risk for TRH and hyper-sensitivity to threat in trauma-exposed women, these prior studies compared women who naturally differed from one another in E2 levels regardless of reproductive status/stage. Thus, further work is needed to determine how changes in E2 over the menopausal transition increase vulnerability to TRH and hyper-reactivity to threat in trauma-exposed women. The current study is well positioned to address this gap in knowledge given our recruitment of perimenopausal Black women from a high trauma risk population. The proposed research will combine clinical interviews, fear psychophysiology, neuroimaging, and neuroendocrinology to examine how the perimenopause and changes in E2 levels over time influence TRH and responsivity to threat. Investigating how neuroendocrine changes during the menopausal transition influence fear psychophysiology and amygdala reactivity to threat to impact TRH is critical for the identification, assessment, and treatment of these symptoms during the perimenopause in women, especially Black women, who experience disproportionately higher rates of cumulative trauma exposure and PTSD.