Death by suicide occurs in a disproportionate percentage of individuals with anorexia nervosa (AN), with a standardized mortality ratio indicating a 57 fold greater risk of death from suicide relative to an age-matched cohort. These shocking statistics speak to the incapacitating, perplexing, and isolating nature of AN, a severe psychiatric illness that negatively impacts the biological, emotional, and psychosocial functioning of both the affected individual and her or his family. Longitudinal studies indicate impaired social functioning increases risk for fatal outcomes. Social impairment persists and affects quality of life even after recovery. Despite this knowledge, very little is known about social information processing in AN. Careful study of social cognition in AN may elucidate impaired processes that may influence outcome and therapeutic efficacy: difficulty forming therapeutic alliances, disturbances in body image, impaired empathy, and dearth of secure attachments. Symptoms of autistic spectrum disorders (ASD), particularly in cognitive domains that impact social cognition, are overrepresented in individuals with chronic AN and persist after recovery. In contrast, eating disturbances in ASD are widely acknowledged, but are seldom the topic of systematic inquiry. Relative to AN, social information processing in ASD is well characterized and may help to inform the characterization of these domains in AN. The goals of this investigation are: 1) to provide a detailed characterization of the behavioral, visual, and neurocognitive processes that subserve social information processing in AN; 2) to differentiate the contribution of low weight status on these deficits by characterizing changes over the course of illness, 3) to compare the neurocircuitry of social cognition in relation to females with high functioning autism; and 4) to develop a new paradigm for assessing social information processing during parent and child interactions across emotionally valanced conditions. We will achieve these goals using a battery of neuropsychological and social cognitive measures, fMRI while viewing dynamic facial affective stimuli, and eye-tracking while viewing social information processing tasks. Sophisticated methodologies that characterize the cognitive processes that underlie social information processing deficits and map onto functional neurocircuits may greatly enhance our knowledge of the pathophysiology of AN and may open new avenues for effective treatment development. ? ? ?
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