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). 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.
Results: Women with current PTSD had significantly higher levels of HbA1c ( p=0.006) and AEG ( p=0.008) compared to women without PTSD. Peripheral blood mononuclear cells (PBMCs) were extracted and assayed for nuclear factor-κB (NF-κB) pathway activity and monocyte glucocorticoid sensitivity (expressed as dexamethasone ) using previously validated methods. Blood was assayed for hemoglobin A1c (HbA1c) and calculation of average estimated glucose (AEG) concentrations.
A fasting blood sample was collected and a study physician performed a general medical assessment for each participant. PTSD diagnosis and PTSD symptom severity were determined using the Clinician-Administered PTSD Scale (CAPS). 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.
To evaluate the association between 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. 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. However, the biological mechanisms by which PTSD increases risks for T2DM remain unclear.
Part 1: All Financial Involvement with a pharmaceutical or biotechnology company, a company providing clinical assessment, scientific, or medical products or companies doing business with or proposing to do business with ACNP over past 2 years (Calendar Years 2014–Present) Part 2: Income Sources & Equity of $10,000 per year or greater (Calendar Years 2014 - Present): List those financial relationships which are listed in part one and have a value greater than $10,000 per year, OR financial holdings that are listed in part one and have a value of $10,000 or greater as of the date of disclosure Part 3: Financial Involvement with a pharmaceutical or biotechnology company, a company providing clinical assessment, scientific, or medical products or companies doing business with or proposing to do business with ACNP which constitutes more than 5% of personal income (Calendar Years 2014 - Present) Part 4: Grants from pharmaceutical or biotechnology company, a company providing clinical assessment, scientific, or medical products directly, or indirectly through a foundation, university, or any other organization (Calendar Years 2014 - Present) Part 5: My primary employer is a pharmaceutical/biotech/medical device company.Īsterisks in the author lists indicate presenter of the abstract at the annual meeting.Įmory University School of Medicine, Atlanta, Georgia, United Statesīackground: Post-traumatic stress disorder (PTSD) is a stress-related psychiatric disorder that is associated with increased risk for type 2 diabetes mellitus (T2DM). Individual contributor disclosures may be found within the abstracts. Sponsorship Statement: Publication of this supplement is sponsored by the ACNP.
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