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A key characteristic of eating disorders is atypical activity in the amygdala. However, risk factors for the development of eating disorder symptomology (EDS) and their underlying neural mechanisms are not well understood in non-clinical populations. We examined the role of amygdala reactivity to negative facial emotions in anorexia nervosa symptomology (ANS) and bulimia nervosa symptomology (BNS) using a classical face-matching task and an inter-subject representational similarity analysis (IS-RSA). Behavioral analyses showed a sequential-mediation effect, tracing a path from greed personality trait → depression → body dysmorphic disorder → EDS/ANS. Imaging analyses revealed that individuals with high EDS had decreased amygdala reactivity and altered activation patterns in the amygdala and visual pathways when processing angry faces. We found that variations in amygdala activation and its connectivity with the visual pathway mediated the effect of depression on EDS/ANS, but not BNS. Individuals with similar EDS showed similar spontaneous brain activity patterns, especially in regions associated with the default mode network, frontal-parietal network, visual network (VIS), and attention network. We also observed sequence-mediation effects, e.g., depression → VIS → body dysmorphic disorder → EDS/ANS, but not BNS. These findings highlight the role of amygdala activation in understanding eating disorders and the potential influence of greed personality traits and depression on disordered eating symptoms through the amygdala-visual pathway connection in non-clinical populations.
A key characteristic of eating disorders is atypical activity in the amygdala. However, risk factors for the development of eating disorder symptomology (EDS) and their underlying neural mechanisms are not well understood in non-clinical populations. We examined the role of amygdala reactivity to negative facial emotions in anorexia nervosa symptomology (ANS) and bulimia nervosa symptomology (BNS) using a classical face-matching task and an inter-subject representational similarity analysis (IS-RSA). Behavioral analyses showed a sequential-mediation effect, tracing a path from greed personality trait → depression → body dysmorphic disorder → EDS/ANS. Imaging analyses revealed that individuals with high EDS had decreased amygdala reactivity and altered activation patterns in the amygdala and visual pathways when processing angry faces. We found that variations in amygdala activation and its connectivity with the visual pathway mediated the effect of depression on EDS/ANS, but not BNS. Individuals with similar EDS showed similar spontaneous brain activity patterns, especially in regions associated with the default mode network, frontal-parietal network, visual network (VIS), and attention network. We also observed sequence-mediation effects, e.g., depression → VIS → body dysmorphic disorder → EDS/ANS, but not BNS. These findings highlight the role of amygdala activation in understanding eating disorders and the potential influence of greed personality traits and depression on disordered eating symptoms through the amygdala-visual pathway connection in non-clinical populations.
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