RESUMO
OBJECTIVE: Binge-eating spectrum disorders (BESD) involve large eating episodes accompanied by a sense of loss of control that occur in individuals with body weights spanning the full body mass index (BMI) spectrum. While research links BESD with peripheral inflammation, this literature is limited by underpowered studies and a failure to control for confounding variables that could promote inflammation independent of dysregulated eating, specifically elevated body adiposity and depression. Our study examined plasma interleukin-6 (IL-6), a marker of peripheral inflammation, in a sample of women with BESD and non-eating disorder controls, controlling for BMI, body adiposity, and depression. METHOD: Participants (N = 94) included women with BESD (n = 73) or no eating disorder (n = 21) who completed structured clinical interviews in a larger study, selected to represent BMI categories ranging from underweight to obese in both groups. Fasting blood samples were processed for plasma IL-6 concentration via enzyme-linked immunosorbent assays. In addition to assessing group differences in plasma IL-6, exploratory analyses examined associations between IL-6 and biological and clinical markers of BESD. RESULTS: Significantly elevated plasma IL-6 was found in women with BESD, relative to controls, that was not accounted for by BMI, adiposity, or depression. Plasma IL-6 was positively correlated with plasma leptin concentration, clinical assessments of eating disorder severity, and participants' largest self-reported eating episode. DISCUSSION: Peripheral inflammation is specifically linked to presence of dysregulated eating independently from weight, adiposity, and depression in BESD. Future research should probe the potential role of neuroinflammation in altered eating behavior. PUBLIC SIGNIFICANCE: This study provides the first demonstration that inflammation, characterized by elevated plasma IL-6 concentration, is uniquely associated with dysregulated eating in a transdiagnostic group of individuals with BESD. A better understanding of whether immune factors contribute to dysregulated eating could help identify novel biological targets for intervention.