The eating disorder bulimia nervosa is characterized by periodic binge- eating usually followed by self-induced vomiting or laxative abuse. These symptoms clearly are related to alterations in meal size and meal patterning. With remarkably few exceptions, information relevant to meal termination is relayed to the central nervous system via the vagus nerve. We therefore hypothesize that an approach to the pathophysiology of bulimia nervosa is through studies of the neurocircuitry and neurochemistry of these satiety mechanisms. In addition to mediating short-term satiety, a rapidly growing body of literature suggests that the vagus Is also involved in modulating nociceptive information. Accordingly, the hypothesis that vagally- activated satiety mechanisms are abnormal in bulimia nervosa would predict that a related alteration in nociception might also be evident in this clinical group. In our initial study of 27 bulimia women and 31 age and sex matched controls, nociceptive thresholds, both pain detection and pain tolerance, were found to be significantly elevated in patients with an active diagnosis of bulimia nervosa compared to controls. Our Initial studies suggest that this effect- may be specific to nociceptive responsivity, since the ability to perceive an innocuous sensory stimulus did not differ between groups. In this application, we propose to further investigate this finding. Sensory processing (both tactile thresholds and pain responsivity) will be characterized in detail in a control population and in patients with either bulimia nervosa or with a psychiatric diagnosis which is frequently co-morbid with bulimia nervosa. We will also study this phenomena over the course of the binge/purge cycle, and in recovered bulimic patients. Regardless of the etiology of bulimia nervosa, we believe that the profound alterations in nutrient intake that characterize this disorder may affect, and in turn be affected by peripheral and central nervous system neurotransmission. Identification of alterations in nervous system function may lead to improved treatment.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK052291-04
Application #
2444176
Study Section
Clinical Neuroscience and Biological Psychopathology Review Committee (CNBP)
Project Start
1993-08-01
Project End
1999-06-30
Budget Start
1997-07-01
Budget End
1998-06-30
Support Year
4
Fiscal Year
1997
Total Cost
Indirect Cost
Name
University of Minnesota Twin Cities
Department
Psychiatry
Type
Schools of Medicine
DUNS #
168559177
City
Minneapolis
State
MN
Country
United States
Zip Code
55455
Faris, Patricia L; Hofbauer, Randall D; Daughters, Randall et al. (2008) De-stabilization of the positive vago-vagal reflex in bulimia nervosa. Physiol Behav 94:136-53
Faris, Patricia L; Eckert, Elke D; Kim, Suck-Won et al. (2006) Evidence for a vagal pathophysiology for bulimia nervosa and the accompanying depressive symptoms. J Affect Disord 92:79-90
Stephan, Elke; Pardo, Jose V; Faris, Patricia L et al. (2003) Functional neuroimaging of gastric distention. J Gastrointest Surg 7:740-9
Raymond, N C; Eckert, E D; Hamalainen, M et al. (1999) A preliminary report on pain thresholds in bulimia nervosa during a bulimic episode. Compr Psychiatry 40:229-33
Hartman, B K; Faris, P L; Kim, S W et al. (1997) Treatment of bulimia nervosa with ondansetron. Arch Gen Psychiatry 54:969-70