Neural Response to Catecholamine Depletion in Subjects Suffering From Bulimia Nervosa in Their Past and Healthy Controls
Status:
Suspended
Trial end date:
2022-05-01
Target enrollment:
Participant gender:
Summary
Bulimia nervosa is a severe psychiatric disorder characterized by recurrent binge eating
episodes followed by inappropriate compensatory behavior to prevent weight gain such as
self-induced vomiting. With this project, the investigators want to investigate the role of
the neurotransmitter dopamine in bulimia nervosa. Dopamine is reported to have an important
influence on the neural reward system and is involved in the processing of gains and losses.
The reward system is functionally connected to the individual perception of rewards in the
environment. A previous study revealed that under catecholamine depletion including dopamine
depletion women suffering from bulimia nervosa in their past reported mild bulimic symptoms
and their reward processing became dysfunctional: their ability to use rewarding stimuli for
task solving was diminished.
The aim of this study is to investigate the role of reduced dopamine availability in the
development or maintaining of bulimia nervosa and in the dysfunctional processing of
rewarding stimuli and negative visual information. Therefore, the investigators hypothesize
that catecholamine depletion achieved by oral administration of alpha-methyl-paratyrosine
(AMPT) will induce mild bulimic symptoms in females suffering from bulimia nervosa in their
past. In addition, they will reveal dysfunctions in reward and emotional processing under
catecholamine depletion. Using functional magnetic resonance imaging, the investigators
propose that a reduced activation of the nucleus accumbens, a neural structure of the reward
system, will be the neural correlate of this dysfunctional reward processing. Furthermore,
the amygdala, a neural structure that is involved in emotional processing, will show a higher
activation under catecholamine depletion. Genetic factors additionally have an influence on
the dopaminergic system. Therefore, the investigators hypothesize that genetic factors, for
example the COMT val-158-met polymorphism may have an effect on the behavioral and neural
response to catecholamine depletion. In sum, this investigation may help to understand which
changes in reward and emotional processing may lead to a reoccurrence of bulimic symptoms.
In future, the findings of this study may help to develop individual pharmacological and
psychotherapeutical interventions to enhance the outcome of treatment.
Phase:
N/A
Details
Lead Sponsor:
University of Bern
Collaborators:
University Hospital Inselspital, Berne University of Zurich