Elsevier

Physiology & Behavior

Volume 122, 2 October 2013, Pages 56-61
Physiology & Behavior

CCK response in bulimia nervosa and following remission

https://doi.org/10.1016/j.physbeh.2013.08.014Get rights and content

Highlights

  • Prior findings in bulimia nervosa indicate an abnormal response of the satiety hormone CCK

  • Unknown if altered functioning is cause, consequence or maintenance factor in binge eating

  • Implications of study are CCK responsivity may normalize in those who remit from bulimia

Abstract

The core defining features of bulimia nervosa (BN) are repeated binge eating episodes and inappropriate compensatory (e.g., purging) behavior. Previous studies suggest an abnormal post-prandial response in the satiety-signaling peptide cholecystokinin (CCK) in persons with BN. It is unknown whether this altered response persists following remission or if it may be a potential target for 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 study prospectively evaluated the plasma CCK response and corresponding eating behavior-related ratings (e.g., satiety, fullness, hunger, urge to binge and vomit) in individuals with BN-purging subtype (n = 10), RBN-purging subtype (n = 14), and healthy controls (CON, n = 13) at baseline, + 15, + 30, and + 60 min following the ingestion of a standardized liquid test meal.

Subject groups did not significantly differ in CCK response to the test meal. A significant relationship between CCK response and satiety ratings was observed in the RBN group (r = .59, p < .05 two-tailed). A new and unanticipated finding in the BN group was a significant relationship between CCK response and ratings of “urge to vomit” (r = .86, p < .01, two-tailed).

Unlike previous investigations, CCK response did not differ in BN and CON groups. Thus the role of symptom severity remains an area of further investigation. Additionally, findings suggest that in this sample, CCK functioning following remission from BN-purging subtype is not different from controls. It remains unknown whether or not CCK functioning may be a protective or liability factor in the stabilization and recovery process. Replication studies utilizing a larger sample size are needed to further elucidate the role of CCK in recovery from BN and its potential target of related novel treatment strategies.

Introduction

Bulimia nervosa (BN) is a chronic and debilitating eating disorder characterized by repeated binge eating episodes followed by inappropriate compensatory (e.g., purging) behavior to prevent weight gain. The underlying pathophysiologic mechanisms that contribute to this aberrant behavior are complex and poorly understood. Individuals with BN report altered perceptions in hunger, fullness, and satiety [1]. Laboratory studies have shown that cholecystokinin (CCK) response, a satiety producing gastric hormone, following a meal is decreased in individuals with active BN when compared to matched healthy controls [2], [3], [4].

To date, investigations have not examined CCK function following remission of BN. To help evaluate the extent to which post-prandial (after a meal) CCK normalizes following remission of BN, this study examined CCK responses following a test-meal in persons with active BN, remitted BN (RBN), and healthy controls (CON).

Is there a significant difference in post-prandial CCK response and satiety ratings among persons with active BN, RBN, and healthy controls?

H1

Subjects with BN will have a significantly blunted post-prandial plasma CCK response compared to the RBN and CON groups.

H2

Post-prandial plasma CCK response will be significantly positively correlated with post-prandial visual analog measures of satiety in the RBN and CON groups.

Section snippets

Subjects

Participants included a convenience sample of women with RBN (n = 14), BN (n = 10), and healthy controls (CON; n = 13). Subject group inclusion criteria are as follows:

  • All subjects: 1) age 18–45 years; 2) body mass index (BMI) between 19 and 26 kg/m2; 3) gender, female; 4) in good medical health; 5) free of known medical conditions or medication treatment (except for birth control); and 6) free of alcohol use for 72 h prior to study.

  • BN: 1) Diagnostic and Statistical Manual of Mental Disorders 4th Text —

Subject characteristics

The overall sample age was 22.5 ± 5.0 years with a BMI of 22.5 ± 2.2 kg/m2. The racial/ethnic composition of the sample was 71.1% white, 7.9% Black/African American, 18.4% Asian/Pacific Islander, 2.6% American Indian or Alaska Native, and 7.9% Hispanic, Latino or Spanish.

The average binge and purge (vomit) frequency among the BN group was 4.9 ± 2.7 episodes per week. Similarly, the RBN group reported binge and purge frequency during active illness to average 6.8 ± 4.6 episodes per week. There was no

Discussion

This is the first study to compare post-prandial CCK response and subjective ratings of satiety from a group of individuals who have remitted from bulimia nervosa (RBN) to those with the active illness (BN) and healthy (CON). Previous studies found that CCK is abnormal in BN in comparison to healthy CON [21] These former results implied that an altered CCK response may be a possible cause, consequence, and or maintenance factor for binge eating in individuals suffering from BN. To observe the

Conclusions

Results extend the understanding of the post-prandial CCK response in those who have remitted from BN. The implications of this study are that CCK responsivity in those who remit from binge and vomit behavior appears similar to controls. While this study does not offer particular guidance concerning possible changes in CCK response that might occur with remission, it does indicate that previous findings of a blunted response in the BN population may be a state versus trait related phenomenon.

Role of funding sources

Sponsor involvement was limited to providing funding for the study.

Disclosure statement

Dr. Hannon-Engel, Dr. Filin, and Dr. Wolfe report no financial, personal, or other relationships with other people or organizations that could inappropriately influence this work.

Acknowledgments

The authors wish to acknowledge the contributions of Drs. Katherine Gregory and Catherine Yetter Read, and the Clinical Research Center nursing staff at the Beth Israel Deaconess Medical Center in this project. This study was supported by a Ruth L. Kirschstein National Research Service Award fellowship from the NIH/National Institute of Nursing Research Grant #F31NR010453 and Grant Number UL1 RR025758 — Harvard Clinical and Translational Science Center, from the National Center for Research

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