7. Project Summary/Abstract
Eating disorders are prevalent, costly, and deadly psychiatric illnesses. Current empirically-supported
interventions fail to achieve symptom remission in the majority of patients. Gastrointestinal (GI) distress (e.g.,
nausea, stomachache) is one barrier that contributes to poor adherence to the meal-related interventions that
comprise evidence-based treatments. The proposed R15 Academic Research Enhancement Award seeks to
test a causal model of GI distress in eating disorder maintenance. In this model, fear of food, eating, and
weight gain are hypothesized to cause GI distress through two direct mechanisms (i.e., by increasing
cholecystokinin and peptide YY gut peptide responses and by increasing perceived fullness due to biased
interoception) as well as through an indirect mechanism of fear-related increases in fullness via enhanced gut
peptide response. Specific Aim 1 will test fear as a contributor to GI distress using a within-subject test meal
paradigm wherein participants consume foods that they are told contains high or low fat content, but which are
actually identical. Specific Aim 2 will test the proposed direct and indirect mechanisms of GI distress. In
addition, a serial multiple mediation model will be conducted to explore fear as a cause of enhanced gut
peptide response and in turn, increases in fullness, GI distress, and urges to restrict food intake. To address
these aims, 152 women with eating disorders in the normal weight range who report postprandial GI distress
will participate in a test meal paradigm. Using a within-subjects crossover design, on two separate mornings,
participants will eat yogurt described as “high fat” and “low fat.” Although the “high fat” meal is designed to
activate fear of food, eating, and weight gain relative to the “low fat” meal, in actuality the meals will not differ
and will each contain 67% fat. Efficacy of this manipulation will be assessed using subjective ratings of fear
and skin conductance. In addition, gut peptide levels and subjective ratings of GI distress, fullness, and urges
to restrict food intake will be assessed before, during, and after the test meal. This study fills a fundamental
gap by being the first to experimentally test an integration of fear, enhanced gut peptide response, and biased
interoception in an eating disorder maintenance model. This study will make a significant contribution by
examining fear as a cause of GI distress. This will provide specific insight into how to adapt empirically-
supported interventions (i.e., exposure) for eating disorder patients who experience GI distress. Identifying
enhanced gut peptide response as the cause of fullness and GI distress will facilitate tailoring psychoeducation
and interoceptive exposures for eating disorder patients based upon symptoms. This study will shift current
clinical practice by identifying fear, gut peptide response, and fullness as potential symptom-based treatment
targets, with the potential to improve treatment outcomes by tailoring interventions to the symptom experience
of individual eating disorder patients. Consistent with the aims of the R15, this study will enhance the research
experiences of Ohio University students.
