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Systematic review reveals shared brain factors in eating disorders and obesity, suggesting overlapping vulnerabilities.
Eating disorders (EDs) and obesity have traditionally been conceptualized as distinct entities, yet accumulating evidence points to overlapping vulnerabilities spanning genetic, neurobiological, behavioral and psychological domains. Shared risk factors suggest convergent mechanisms, particularly in impulse control, reward processing, emotion regulation and body-image representation. In this scenario, functional near-infrared spectroscopy (fNIRS) offers a clinically accessible tool to examine cortical activity, although findings remain dispersed across heterogeneous studies. A systematic search of PubMed, Scopus and Ovid Embase identified peer-reviewed fNIRS studies in individuals with anorexia nervosa, bulimia nervosa, binge eating disorder and obesity. Eligible studies included at least one clinical group, reported original data and applied fNIRS to assess cortical responses. From 990 records, 26 studies met inclusion criteria. Eighteen studies incorporated healthy controls, while eight investigated clinical samples only. Across case-control comparisons, consistent alteration emerged in the prefrontal cortex (PFC). Obesity and binge eating disorders were associated with attenuated PFC activation during inhibitory control, decision-making and food-related paradigms, whereas bulimia nervosa showed condition-dependent alterations linked to loss-of-control symptoms. Findings in anorexia nervosa were mixed, with reduced activation during executive tasks but heightened responses to socially or emotionally salient stimuli. Broader ED samples showed blunted frontal and temporal activation during verbal fluency. Evidence highlights the PFC as a transdiagnostic hub of altered activity in EDs and obesity, consistent with overlapping vulnerabilities. Disorder-specific profiles underscore context-dependent modulation. Standardized, large-scale studies are needed to clarify the utility of fNIRS in delineating common and distinct neural substrates across the ED-obesity spectrum.
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Collantoni et al. (2026) studied this question.
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