| Summary: | Thesis advisor: Barbara E. Wolfe === The core defining features of bulimia nervosa (BN) are repeated binge eating episodes and compensatory purging behavior. The biobehavioral aspects of binge eating are complex and not fully understood. One area of recent interest is the role of the satiety-signaling peptide cholecystokinin (CCK). Previous research observed a blunted postprandial plasma CCK response in those with BN, therefore suggesting this may be a cause, consequence, or maintenance factor in binge eating. It is unknown whether this altered response is due to a state versus trait phenomenon, thus having implications in the development of clinical treatment strategies. To examine the nature of this altered response, this study assessed whether CCK normalizes following remission from BN (RBN). This biobehavioral study utilized a comparative design to prospectively evaluate the biological CCK response and the corresponding behavioral ratings of satiety and other eating-related sensations in individuals with BN (n=10), RBN (n =14), and healthy controls (CON, n=13). CCK and behavioral ratings were assessed at baseline, +15, +30, and +60 minutes following the ingestion of a standardized liquid test meal. The BN group's CCK response was blunted and approached significance (p =.052) when compared to the RBN and CON groups. As predicted the RBN and CON groups' CCK response did not significantly differ. This finding supports the premise that CCK may normalize following abstinence from binge and purge (vomit) episodes and that this is a state versus trait related phenomenon. A significant positive relationship between CCK response and ratings of satiety occurred in the RBN group only (r=.59, p<.05). A new and unanticipated finding in the BN group was a significant relationship (r=.86, p < .01, two-tailed) between their CCK response and urge to vomit. A greater urge to vomit was reported by those individuals who had increased CCK response. Therefore, it is unknown whether the normalization of CCK functioning is a protective or liability factor in the stabilization and recovery process. Replication studies utilizing a larger sample size are needed to understand the role of CCK in recovery and the subsequent development of novel treatment strategies for those suffering with BN. === Thesis (PhD) — Boston College, 2012. === Submitted to: Boston College. Connell School of Nursing. === Discipline: Nursing.
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