PTSD AND DIABETES: A TWO-WAY STREET IN METABOLIC AND MENTAL HEALTH

Background

Posttraumatic stress disorder (PTSD) is linked with metabolic disturbance and increased risk of Type 2 diabetes (DM2). While mounting evidence suggests that trauma is linked to downstream disruption of both brain and metabolic processes, mechanisms explaining the connection between PTSD and DM2 have yet to be defined. Conventional risk factors for worsening DM2 such as obesity, poor diet, and sedentary lifestyle are treatment targets in patients with DM2 but the role that these risks play in the poor glycemic control and associated medical comorbidities seen in the PTSD population remains unclear. Here we examine the commonly hypothesized risk factors influencing the strength and directionality of the relationship between PTSD and DM2 severity in traumatized black women with DM2.

Methods

We examined the relationships among PTSD severity (Clinician-Administered PTSD Scale, CAPS), glycemic control (A1c), age, smoking, body mass index (BMI), depression (Beck Depression Inventory, BDI) and medications in trauma-exposed Black women with DM2 recruited from an urban hospital between 2013-2015 (n=95) as a part of the Grady Trauma Project. Missing data were handled with multiple imputation (mice package, R). The relationship between PTSD severity and glycemic control, along with the influence of common risk factors, was assessed using lasso regression (glmnet package, R) performed on each imputed dataset. Mediation analysis tested whether BMI or depression mediated associations between PTSD severity and glycemic control.

Results

Lasso regression identified BDI, ACE inhibitor/ARB/beta blocker use, and CAPS severity as predictors in the final model predicting A1c. In pooled linear regression analyses across imputed datasets, overall model fit was modest, and none of these predictors were statistically significant. Lasso regression in the reverse direction selecting predictors of PTSD severity yielded BMI, BDI, ACE inhibitor/ARB use, and A1c for the final model predicting CAPS severity. In pooled analyses, model fit was substantially stronger and BDI emerged as the only statistically significant predictor (p < 0.05). Mediation analyses indicated that BDI, but not BMI, significantly mediated the effect of A1c on CAPS severity, as well as to a lesser extent the reverse relationship, the causal effect of CAPS severity on A1c.

Conclusion

In this examination of the relationships between PTSD and DM2 severity, CAPS severity and A1c were found to be bidirectionally correlated in lasso regression models, with BDI emerging as a significant predictor and mediator of these relationships. BMI was not found to be a mediator in either direction. These results suggest a possible reciprocal relationship between PTSD and DM2, where worsening of either condition may drive worsening of the other, resulting in a vicious cycle where treating one condition in isolation may not be sufficient to prevent increased overall morbidity and mortality. Further research should include physiological interventions to ascertain directionality in these relationships more definitively.

References

Dixon HD, Michopoulos V, Gluck RL, Mendoza H, Munoz AP, Wilson JG, Powers A, Schwartz AC, Umpierrez GE, Gillespie CF. Trauma exposure and stress-related disorders in African-American women with diabetes mellitus. Endocrinol Diabetes Metab. 2020 Jan 14;3(2):e00111. doi: 10.1002/edm2.111. PMID: 32318631;