ACNP 56th Annual Meeting: Poster Session I, December 4, 2017
Post-traumatic stress disorder (PTSD) is a stress-related psychiatric disorder that is associated with increased risk for type 2 diabetes mellitus (T2DM). However, the biological mechanisms by which PTSD increases risks for T2DM remain unclear. A growing body of data suggests that dysregulation of the stress axis, including altered glucocorticoid sensitivity and innate immune activity, may act to disrupt glycemic control in trauma-exposed individuals with PTSD. To evaluate the association
... n PTSD, glycemic regulation, neuroendocrine function and immune activity, we examined associations between PTSD diagnosis and PTSD symptom severity and metabolic, glucocorticoid, and immune biomarkers in trauma-exposed women with T2DM. Methods: We recruited a sample of (N = 63) African-American women with T2DM and high rates of lifetime trauma exposure from the primary care and diabetes specialty clinic waiting rooms of Grady Memorial Hospital, a large county hospital and level 1 trauma center in Atlanta, Georgia. PTSD diagnosis and PTSD symptom severity were determined using the Clinician-Administered PTSD Scale (CAPS). A fasting blood sample was collected and a study physician performed a general medical assessment for each participant. Blood was assayed for hemoglobin A1c (HbA1c) and calculation of average estimated glucose (AEG) concentrations. Peripheral blood mononuclear cells (PBMCs) were extracted and assayed for nuclear factor-κB (NF-κB) pathway activity and monocyte glucocorticoid sensitivity (expressed as dexamethasone [DexIC50]) using previously validated methods. Results: Women with current PTSD had significantly higher levels of HbA1c (p = 0.006) and AEG (p = 0.008) compared to women without PTSD. Furthermore, DexIC50 (p = 0.003) and NF-κB pathway activity (p = 0.013) were increased significantly in women with PTSD as compared to women without PTSD. PTSD symptom severity was predictive of higher DexIC50 (r = 0.27; p = 0.05), denoting decreased glucocorticoid sensitivity), higher HbA1c (r = 0.28; p = 0.024), higher AEG (r = 0.27; p = 0.033), and higher NF-κB pathway activity (r = 0.38; p = 0.023). Increased NF-κB pathway activity was associated with higher HbA1c (r = 0.34; p = 0.05), but not with DexIC50 (r = 0.023; p = 0.91). Conclusions: PTSD diagnosis and PTSD symptom severity are positively associated with worsened glycemic regulation in African-American women with T2DM. In addition, PTSD diagnosis and PTSD symptom severity are also positively associated with increased monocyte glucocorticoid resistance and increased innate immune activity. These data suggest mechanisms of shared pathophysiology and risk connecting PTSD and T2DM which are both significant public health problems. Increased understanding of shared pathophysiology between stress-related psychiatric and medical disorders such as PTSD and T2DM may lead to novel approaches to prevention and progression of disease and argues for improved integration of care for psychiatric and medical disorders.