Symposia
Eating Disorders
Kendra R. Becker, Ph.D.
Massachusetts General Hospital/Harvard Medical School
Boston, Massachusetts
Avery Van De Water, BS
Graduate Student
Brigham and Women's Hospital
Boston, Massachusetts
Katie Rozzell, BS
Doctoral Student
University of Hawai'i at Manoa
Honolulu, Hawaii
Nassim Tabri, PhD
Assistant Professor
Carleton University
Ottawa, Ontario, Canada
Lauren Breithaupt, PhD
Instructor
Massachusetts General Hospital/Harvard Medical School
bosotn, Massachusetts
Helen Burton Murray, PhD
Director, GI Behavioral health Program/Staff Psychologist
Massachusetts General Hospital/Harvard Medical School
boston, Massachusetts
Casey M. Stern, PhD
Clinical Research Coordinator
Massachusetts General Hospital
Boston, Massachusetts
Madhusmita Misra, MD, MPH
Division Chief, Pediatric Endocrinology
Massachusetts General Hospital/Harvard Medical School
Boston, Massachusetts
Lawson Elizabeth, MD
Director of the Interdisciplinary Oxytocin Research Program/Assistant Professor
Massachusetts General Hospital/Harvard Medical School
Boston, Massachusetts
Laura Holsen, PhD
Associate Professor
Brigham and Women's Hospital
boston, Massachusetts
Kamryn Eddy, PhD
Director of the Eating disorder clinical and research program/Associate professor
Massachusetts General Hospital/Harvard Medical School
boston, Massachusetts
Jennifer J. Thomas, Ph.D.
Psychologist
Massachusetts General Hospital
Boston, Massachusetts
Introduction. Avoidant/restrictive food intake disorder (ARFID) is characterized by severe limitations in diet (volume and/or variety) due to fear of aversive consequences, lack of interest in eating, and/or sensory sensitivity. Preliminary evidence from uncontrolled studies suggests that cognitive-behavioral therapy for ARFID (CBT-AR) may be beneficial, but neurobiological mechanisms remain unknown. Similar to findings in patients with anxiety and depression, the salience network (anterior cingulate cortex: ACC, amygdala, and orbitofrontal cortex: OFC) may be hyperactive in those with ARFID. Consistent with this, our team’s data demonstrate ACC hyperactivation in youth with ARFID compared to healthy controls (HC) in a validated visual food cue fMRI paradigm. Appetite-regulating hormones are also disrupted in youth with ARFID. Specifically, across ARFID presentations, fasting levels of anorexigenic cholecystokinin (CCK) are elevated compared to HC, possibly contributing to reduced appetite. We tested two primary hypotheses from pre- to post-treatment in a sample of children, adolescents and adults with ARFID, specifically that 1) food-related hyperactivation in the salience network would decrease and 2) fasting CCK levels would decrease. Methods. Participants with ARFID viewed images of food and of objects in a fasted state (n=14; Mage=16.6; 86% female) and underwent fasting blood draws for CCK (n=24; Mage=15.3; 36% female) pre-treatment and again post-treatment as part of a larger study on the efficacy of CBT-AR. Results. Participants showed reduced activation in the right ACC (MNI coordinates: 3, 53, 17; k(E)= 579, p(FWEcorr) = 0.013) pre- to post-treatment for the contrast of food versus objects. There were no significant pre- to post-treatment changes in amygdala or OFC activation. However, compared to those whose illness persisted, individuals who no longer met criteria for ARFID at post-treatment showed a trend for greater reductions in amygdala activation post-treatment (Mann-Whitney U Test, p=0.07; Figure 2). Fasting levels of CCK significantly decreased pre- to post-treatment (T(23) = 5.21, p < .001). Conclusions. This is the first study assessing potential neurobiological mechanisms of CBT for any primarily restrictive eating disorder. Although firm conclusions cannot be drawn without a randomized controlled design, our findings suggest that reduction in the hyperactive saliency circuitry and appetite regulating hormones may be candidate mechanisms through which CBT-AR exerts its effects.