Eating Disorders
Alexandra D. Convertino, M.S.
Graduate Student
San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology
San Diego, California
Aaron J. Blashill, Ph.D.
Professor
San Diego State University
San Diego, California
The association between comorbid posttraumatic stress disorder (PTSD) symptoms and eating disorder (ED) symptoms is understudied. While many people experience traumatic events, only a small percentage of these individuals meet criteria for PTSD. When examining individuals with an ED, however, the prevalence of those also diagnosed with PTSD increases significantly. Individuals diagnosed with PTSD and an ED are more likely to drop out of ED treatment and less likely to maintain symptom reduction after treatment as compared to their undiagnosed peers. Understanding the complex symptom relationships between PTSD and EDs may be key to addressing this comorbidity clinically. Previous network analyses have been conducted, but with smaller sample sizes and different ED symptom measures. The current study explored the associations between symptoms of EDs (i.e., EPSI) and PTSD (i.e., PCL-5) in a sample of undergraduate students in order to identify salient relationships that may maintain the comorbidity. Cross-sectional network analysis was conducted in a sample of undergraduates (N=1301) to identify bridge symptoms (association across symptom clusters) and core symptoms. The ED symptom body dissatisfaction (strength = 1.54) and the PTSD symptom negative alterations in cognition and mood (strength = 1.32) were the strongest symptoms in the network, and significantly stronger (p > .05) than all other nodes except the PTSD symptom hyperarousal (strength = 0.77). The strongest bridge node was the PTSD symptom hyperarousal (bridge strength = 0.31), which was significantly stronger than all other nodes (p > .05). The strongest edges between PTSD and ED nodes were between hyperarousal and binge eating (part r = .09), purging (part r = .09), restriction (part r = .06), and muscle building (part r = .04). These edges were not significantly different from each other, but stronger than other edges in the network (p > .05). Findings suggest that the ED symptom body dissatisfaction and the PTSD symptom negative alterations in cognitions and mood may be highly influential in the ED-PTSD network due to their relatedness to all other symptoms. The pathways linking hyperarousal and eating disordered behaviors suggest that the comorbidity may be partially maintained through an affect regulation function of binge eating, purging, restriction, and muscle building. Clinicians are therefore encouraged to consider how interacting symptom clusters may impact treatment efficacy. Research on integrated protocols for PTSD and EDs are in their infancy but are worth considering to address this complex comorbidity.