Authors:

Jasrah Ali

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About Paper:

Post-traumatic stress disorder (PTSD), which can result from exposure to severe trauma, has been linked to heightened systemic inflammation and increased risk for metabolic disorders in adulthood [1]). Individuals with PTSD often exhibit dysregulated immune responses, including higher concentrations of inflammatory biomarkers such as high-sensitivity C-reactive protein (hsCRP). Systemic inflammation is associated with impaired glucose regulation and higher glycated hemoglobin (HbA 1c), a biomarker of long-term glycemic control [2]. However, few studies have examined whether PTSD history strengthens the association between inflammation and glycemic risk in adulthood. This study aims to investigate whether the association between systemic inflammation (hsCRP) and glycemic control (HbA1c) was moderated by a history of PTSD diagnosis. Data were analyzed from the "National Longitudinal Study of Adolescent to Adult Health (Add Health)" dataset (n = 12,297, 56.5% female). The mean HbA'1c level was 5.37% (SD= 0.91), while the mean hsCRP level was 4.06 mg/L (SD=6.33). PTSD history was not significantly associated with hemoglobin A1c (HbA1c; r= .007, p= .610) or high-sensitivity C-reactive protein (nsCRP; r= .004, p = .775). Hierarchical regression analyses controlling for race and gender similarly showed no significant main effects of PTSD on HbA 1c ( 026, p = .605) or hsCRP (b = .089, p = .801). However, hsCRP. was positively associated with HbA'1c (b = .029, p < .001), indicating that higher levels of systemic inflammation were related to poorer glycemic control independent of PTSD status. A moderation analysis controlling for race and gender testing whether PTSD history moderated the association between hsCRP and HbA'c was not statistically significant (b = -.354, 324). Future longitudinal research should examine how trauma exposure, inflammation, and metabolic health interact over time, including the timing, severity of PTSD symptoms, to inform interventions that target inflammation to reduce long-term cardiometabolic risk among trauma-exposed populations.

Source:

DePaul University

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Co-authors:

Jasrah Ali