This article reviews concepts and principles of trauma-informed care and trauma-informed practice for those with eating disorders (EDs). EDs are not universally recognized to be associated with traumatic events, despite substantial research evidence indicating that individuals with EDs report very high rates of childhood maltreatment, other lifetime traumatic events, as well as adverse consequences from trauma. Using national representative samples, higher prevalence rates of PTSD and other trauma-related comorbidities have been reported in those with EDs, particularly those with bulimic symptoms (binge eating and/or purging). Evidence suggests that those prone to develop EDs appear to be especially sensitive to the effects of stress/adversity and have high rates of premorbid anxiety disorders, personality traits, and neuropsychological features that predispose them to PTSD and its symptoms. This article also reviews some of the important principles for treating individuals with EDs comorbid for PTSD and other trauma-related disorders, including the necessity of moving beyond sequential treatment to the development of integrated treatment protocols. Integration of existing evidence-based treatments, including family therapy, cognitive behavioral therapy, dialectical behavior therapy, cognitive processing therapy, prolonged exposure, and eye movement desensitization reprocessing are recommended. Recent research suggests that ED clinicians view integrated treatment for individuals with ED and PTSD as a top priority, yet they have several concerns about administering such a treatment. As trauma-informed care is embraced by all clinicians and treatment programs that assess and treat eating and related disorders, better outcomes are anticipated.

Eating disorders (EDs) and posttraumatic stress disorder (PTSD) are highly comorbid, yet there are no proven integrative treatment modalities for ED-PTSD. In clinical trials, MDMA-assisted therapy (MDMA-AT) has shown marked success in the treatment of PTSD and may be promising for ED-PTSD. Ninety individuals with severe PTSD received treatment in a double-blind, placebo-controlled pivotal trial of MDMA-AT. In addition to the primary (Clinician-Administered PTSD Scale) and secondary (Sheehan Disability Scale) outcome measures, the Eating Attitudes Test 26 (EAT-26) was administered for pre-specified exploratory purposes at baseline and at study termination. The study sample consisted of 58 females (placebo = 31, MDMA = 27) and 31 males (placebo = 12, MDMA = 19) (n = 89). Seven participants discontinued prior to study termination. At baseline, 13 (15%) of the 89 individuals with PTSD had total EAT-26 scores in the clinical range (≥20), and 28 (31.5%) had total EAT-26 scores in the high-risk range (≥11) despite the absence of active purging or low weight. In completers (n = 82), there was a significant reduction in total EAT-26 scores in the total group of PTSD participants following MDMA-AT versus placebo (p = .03). There were also significant reductions in total EAT-26 scores in women with high EAT-26 scores ≥11 and ≥ 20 following MDMA-AT versus placebo (p = .0012 and p = .0478, respectively). ED psychopathology is common in individuals with PTSD even in the absence of EDs with active purging and low weight. MDMA-AT significantly reduced ED symptoms compared to therapy with placebo among participants with severe PTSD. MDMA-AT for ED-PTSD appears promising and requires further study.

Objective: There is little information about the pharmacological treatment of avoidant and restrictive food intake disorder (ARFID), a challenging feeding disorder associated with marked impairment and developmental arrest. This brief clinical report seeks to fill this gap. Methods: A retrospective chart review of nine patients with ARFID treated in an eating disorder (ED) program (residential, partial hospital, and intensive outpatient levels of care) with adjunctive olanzapine was undertaken. Results: The mean initial and final olanzapine doses were 0.9 + 0.63 mg/day and 2.8 + 1.47 mg/day, respectively. There was a statistically significant difference in weight gain pre- versus post-olanzapine treatment (3.3 ± 7.3 lbs vs. 13.1 ± 7.9 lbs [2.99 ± 6.62 lb SI vs. 11.88 ± 7.17 lb SI], paired t-test (p < 0.04, t = −2.48). Clinically, adjunctive olanzapine was helpful for not only weight gain but also reduction of associated anxious, depressive, and cognitive symptoms. Clinical Global Impressions scale scores indicated marked improvement in patients receiving adjunctive olanzapine. Conclusion: These cases illustrate that judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms in ARFID patients. Future randomized, placebo-controlled studies in ARFID are warranted.