Indirect Effects of Racial Discrimination on Health Outcomes Through Prefrontal Cortical White Matter Integrity.

BACKGROUND: Racial discrimination is consistently associated with adverse health outcomes and has been linked to structural decrements in brain white matter. However, it is unclear whether discrimination-related neuroplastic changes could indirectly affect health outcomes. Our goal was to evaluate indirect associations of racial discrimination on health outcomes through white matter microstructure in a sample of trauma-exposed Black women. METHODS: A trauma study in an urban hospital setting recruited 79 Black women who received a history and physical examination to assess medical disorders (compiled into a summed total of disorder types). Participants reported on experiences of racial discrimination and underwent diffusion tensor imaging; fractional anisotropy values were extracted from white matter pathways previously linked to racial discrimination (corpus callosum, including the body and genu; anterior cingulum bundle; and superior longitudinal fasciculus) and entered into mediational models. RESULTS: Indirect effects of racial discrimination on medical disorders through left anterior cingulum bundle fractional anisotropy were significant (ß = 0.07, SE = 0.04, 95% CI [0.003, 0.14]) after accounting for trauma and economic disadvantage. Indirect effects of racial discrimination on medical disorders through corpus callosum genu fractional anisotropy were also significant (ß = 0.08, SE = 0.04, 95% CI [0.01, 0.16]). CONCLUSIONS: Racial discrimination may increase risk for medical disorders via neuroplastic effects on microstructural integrity of stress-sensitive prefrontal white matter tracts. Racial discrimination-related changes in these tracts may affect health behaviors, which, in turn, influence vulnerability for medical disorders. These data highlight the connections between racial discrimination, prefrontal white matter connections, and incidence of medical disorders in Black Americans.

Subjective Social Status Is Associated with Dysregulated Eating Behaviors and Greater Body Mass Index in an Urban Predominantly Black and Low-Income Sample.

BACKGROUND: Higher subjective social status (SSS) or a person's perception of their social standing is related to better health outcomes, but few studies examined SSS in relation to obesity. Emotional eating and food addiction have been linked to obesity. Some studies indicated that manipulating SSS may lead to altered food intake, but the relationship between SSS and dysregulated eating, such as emotional eating and food addiction (FA), has not been examined. The goal of this study was to examine the associations between SSS in the community and the larger society, dysregulated eating (emotional eating and FA), and body mass index (BMI) in a majority racial minority sample. METHODS: The participants (N = 89; 93% Black, 86% women, and 56% with obesity; 72% income lower than USD 2000), recruited from a publicly funded hospital in Atlanta, GA, completed the MacArthur Scale, Dutch Eating Behaviors Questionnaire, Yale Food Addiction Scale, Beck Depression Inventory, PTSD Symptom Checklist, and demographics questionnaire. RESULTS: Twenty-two percent of the sample met the criteria for FA; those with FA had significantly higher BMI than those without (p = 0.018). In the hierarchical linear regression, the SSS community (but not in society) predicted higher severity of emotional eating (ß = 0.26, p = 0.029) and FA (ß = 0.30, p = 0.029), and higher BMI (ß = 0.28, p = 0.046), independent from depression and PTSD symptoms. CONCLUSIONS: The findings indicate that, among Black individuals with predominantly low income in the U.S., perceived role in their community is associated with eating patterns and body mass. Given the small sample size, the results should be interpreted with caution.

The renin-angiotensin pathway in posttraumatic stress disorder: angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are associated with fewer traumatic stress symptoms.

OBJECTIVE: Posttraumatic stress disorder (PTSD) is a debilitating stress-related illness associated with trauma exposure. The peripheral and central mechanisms mediating stress response in PTSD are incompletely understood. Recent data suggest that the renin-angiotensin pathway, essential to cardiovascular regulation, is also involved in mediating stress and anxiety. In this study, the authors examined the relationship between active treatment with blood pressure medication, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), and PTSD symptom severity within a highly traumatized civilian medical population. METHOD: Cross-sectional, observational data were analyzed from a larger study; patients were recruited from Grady Memorial Hospital's outpatient population from 2006 to November 2010. Multivariable linear regression models were fit to statistically evaluate the independent association of being prescribed an ACE inhibitor or ARB with PTSD symptoms, using a subset of patients for whom medical information was available (n = 505). Categorical PTSD diagnosis was assessed using the modified PTSD Symptom Scale (PSS) based on DSM-IV criteria, and PTSD symptom severity (the primary outcome of interest) was measured using the PSS and Clinician Administered PTSD Scale. RESULTS: A significant association was determined between presence of an ACE inhibitor/ARB medication and decreased PTSD symptoms (mean PSS score 11.4 vs 14.9 for individuals prescribed vs not prescribed ACE inhibitors/ARBs, respectively [P = .014]). After adjustment for covariates, ACE inhibitor/ARB treatment remained significantly associated with decreased PTSD symptoms (P = .044). Notably, other blood pressure medications, including ß-blockers, calcium channel blockers, and diuretics, were not significantly associated with reduced PTSD symptoms. CONCLUSIONS: These data provide the first clinical evidence supporting a role for the renin-angiotensin system in the regulation of stress response in patients diagnosed with PTSD. Further studies should examine whether available medications targeting this pathway should be considered for future treatment and potential protection against PTSD symptoms.

Posttraumatic stress disorder is a risk factor for metabolic syndrome in an impoverished urban population.

OBJECTIVE: Metabolic syndrome is associated with elevated risk for cardiovascular disease and diabetes and has increased prevalence in low-income African Americans, which constitutes a significant health disparity. The mechanisms responsible for this disparity remain unclear; the current study investigated the relationship between posttraumatic stress disorder (PTSD) and metabolic syndrome. METHOD: We assessed childhood and adult trauma history, major depressive disorder, PTSD and the components of metabolic syndrome in an urban population. We recruited 245 low-socioeconomic-status, primarily African American subjects from general medical clinics in an inner-city hospital. RESULTS: Trauma exposure was extremely prevalent, with 90.6% of subjects reporting at least one significant trauma and 18.8% of subjects meeting criteria for current PTSD. Metabolic syndrome was also prevalent in this population (33.2%), with significantly higher rates among patients with current PTSD (47.8%, P<.05). After controlling for demographics, smoking history, antipsychotic use, depression and exercise, current PTSD remained the only significant predictor of metabolic syndrome (P=.006). CONCLUSIONS: PTSD is associated with increased rates of metabolic syndrome within a traumatized, impoverished urban population. Further studies should investigate if PTSD treatment may reduce the rates of metabolic syndrome, improve overall health outcomes and decrease health care disparities in minority populations.