Changes in guilt cognitions mediate the effect of trauma-informed guilt reduction therapy on PTSD and depression outcomes.

OBJECTIVE: Trauma-informed guilt reduction therapy (TrIGR), a six-session cognitive behavioral therapy targeting trauma-related guilt and distress, reduces guilt and symptoms of posttraumatic stress disorder (PTSD) and depression, yet little is known regarding how and why TrIGR may be effective. METHOD: This study examined treatment-related changes in avoidant coping and trauma-related guilt cognitions as possible mediators of treatment effects on PTSD and depression outcomes at 3- and 6-month follow-up. Data were from a randomized controlled trial for treatment of trauma-related guilt comparing TrIGR and supportive care therapy among 145 post-9/11 US veterans (Mage = 39.2 [8.1], 93.8% male). RESULTS: At pretreatment, most (86%) met PTSD criteria. Intent to treat analyses using parallel mediation models indicated changes in guilt cognitions, but not avoidant coping, mediated the effect of TrIGR on reducing PTSD severity at 3-month (a × b = -0.15, p < 0.01, 95% CI: [-0.24 to -0.06], p = 0.001) and 6-month (a × b = -0.17, 95% CI: [-0.26 to -0.07], p = 0.001) follow-up. Similarly, changes in guilt cognitions, but not avoidant coping, mediated the effect of TrIGR on reducing depression severity at 3-month (a × b = -0.10, 95% CI: [-0.18 to -0.02], p = 0.02) and 6-month (a × b = -0.11, 95% CI: [-0.20 to -0.03], p = 0.01) follow-up. CONCLUSIONS: Compared to guilt cognitions, changes in avoidant coping were less integral to downstream PTSD and depression symptom reduction. Guilt cognition change may be a salient active ingredient of PTSD and depression treatment for those with trauma-related guilt and a key therapy element to which providers should be attuned.

Real-world glycaemic outcomes in patients with type 1 diabetes using glucose sensors-Experience from a single centre in Dublin.

AIMS: To evaluate changes in glycated haemoglobin (HbA1 c) and sensor-based glycaemic metrics after glucose sensor commencement in adults with T1D. METHODS: We performed a retrospective observational single-centre study on HbA1 c, and sensor-based glycaemic data following the initiation of continuous glucose monitoring (CGM) in adults with T1D (n = 209). RESULTS: We observed an overall improvement in HbA1 c from 66 (59-78) mmol/mol [8.2 (7.5-9.3)%] pre-sensor to 60 (53-71) mmol/mol [7.6 (7.0-8.6)%] on-sensor (p < .001). The pre-sensor HbA1 c improved from 66 (57-74) mmol/mol [8.2 (7.4-8.9)%] to 62 (54-71) mmol/mol [7.8 (7.1-8.7)%] within the first year of usage to 60 (53-69) mmol/mol [7.6 (7.0-8.4)%] in the following year (n = 121, p < .001). RT-CGM-user had a significant improvement in HbA1 c (Dexcom G6; p < .001, r = 0.33 and Guardian 3; p < .001, r = 0.59) while a non-significant reduction was seen in FGM-user (Libre 1; p = .279). Both MDI (p < .001, r = 0.33) and CSII group (p < .001, r = 0.41) also demonstrated significant HbA1 c improvement. Patients with pre-sensor HbA1 c of ≥64 mmol/mol [8.0%] (n = 125), had attenuation of pre-sensor HbA1 c from 75 (68-83) mmol/mol [9.0 (8.4-9.7)%] to 67 (59-75) mmol/mol [8.2 (7.6-9.0)%] (p < .001, r = 0.44). Altogether, 25.8% of patients achieved the recommended HbA1 c goal of ≤53 mmol/mol and 16.7% attained the recommended ≥70% time in range (3.9-10.0 mmol/L). CONCLUSIONS: Our study demonstrated that minimally invasive glucose sensor technology in adults with T1D is associated with improvement in glycaemic outcomes. However, despite significant improvements in HbA1 c, achieving the recommended goals for all glycaemic metrics remained challenging.