Beyond behavior: neural and cognitive alterations in eating disorders-a systematic review

Eating disorders (EDs), particularly Anorexia Nervosa (AN) and Bulimia Nervosa (BN), are complex psychiatric conditions marked by alterations in cognition, emotional regulation, and interoception. Accumulating evidence suggests that these behavioral features are underpinned by structural and functional brain abnormalities.

This systematic review aims to synthesize recent neuroimaging findings, particularly resting-state functional MRI and functional connectivity studies on cognitive and neural alterations in eating disorders (EDs).

Following PRISMA guidelines (PROSPERO: CRD42025648023), we systematically searched PubMed and APA PsycINFO for studies published between 2014 and 2024. Twelve studies met inclusion criteria and were assessed for quality and risk of bias using GRADE, RoB 2.0, and ROBINS-I tools. The included studies investigated both adolescent and adult populations, allowing consideration of developmental and illness stage-related aspects.

Altered brain activity and connectivity patterns were consistently reported in individuals with AN and BN, particularly in the cortico-striatal-thalamic system (CSTS), default mode network (DMN), and interhemispheric circuits. Cognitive flexibility deficits were associated with abnormal neural activation despite preserved behavioral performance, suggesting compensatory mechanisms. Insular dysfunction persisted after weight restoration, and altered responses to reward and social cues were linked to symptom persistence.

EDs are underpinned by widespread neural dysregulation involving not only circuits traditionally associated with food intake and reward, but also higher-order large-scale networks supporting cognitive control, interoception, self-referential processing, and emotion regulation. Multimodal neuroimaging studies underscore the necessity for individualized, neurobiologically informed interventions targeting the cognitive control, affect regulation, and reward processing deficits characteristic of EDs. Findings across adolescent and adult samples highlight both state-dependent and potentially developmentally mediated neural alterations, underscoring the relevance of large-scale network connectivity across illness stages.