Abstract

BackgroundBulimia nervosa (BN) is a complex psychiatric illness that includes binge-purge behaviors and a belief that one’s value as a person depends on body shape and weight. Social pressure strongly influences the development and maintenance of BN, but how this manifests neurobiologically within an individual remains unknown. We used a computational psychiatry approach to evaluate neural mechanisms underlying social interactions in BN. MethodsBehavioral and functional magnetic resonance imaging data were collected from 24 women with BN and 26 healthy comparison women using an iterated social exchange game. Data were sorted round by round based on whether the mathematically computed social signals indicated an improving (positive reciprocity) or deteriorating (negative reciprocity) relationship for each participant. ResultsSocial interactions with negative reciprocity resulted in more negative behavioral responses and stronger neural activations in both cortical and subcortical regions in women with BN than healthy comparison women. No behavioral or neural differences were observed for interactions demonstrating positive reciprocity, suggesting a very specific form of psychopathology in BN: amplification of negative self-relevant social interactions. Cortical activations (e.g., temporoparietal junction and dorsolateral prefrontal cortex) did not covary with mood symptoms, while subcortical activations (e.g., amygdala and dorsal striatum) were associated with acute psychopathology. ConclusionsThese data provide a first step toward a mechanistic neuropsychological model of aberrant social processing in BN, demonstrating how a computational psychiatric approach can elucidate neural mechanisms for complex psychiatric illnesses. Future treatments for BN may include targeting neural regions that support these negative biases in social perceptions.

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