Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, Texas, USA.
Program in Neuroscience, Florida State University, Tallahassee, Florida, USA.
Int J Eat Disord. 2024 Jul;57(7):1510-1517. doi: 10.1002/eat.24183. Epub 2024 Mar 6.
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.
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.
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.
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.
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.
暴食谱系障碍（BESD）涉及伴随失控感的大量进食发作，发生在体重横跨整个身体质量指数（BMI）谱的个体中。虽然研究将 BESD 与外周炎症联系起来，但该文献受到研究力量不足的限制，并且未能控制可能独立于饮食失调（特别是升高的身体肥胖和抑郁）促进炎症的混杂变量。我们的研究在患有 BESD 和无饮食障碍对照的女性样本中检查了血浆白细胞介素-6（IL-6），这是外周炎症的标志物，同时控制了 BMI、身体肥胖和抑郁。
参与者（N=94）包括患有 BESD（n=73）或无饮食障碍（n=21）的女性，她们在一项更大的研究中完成了结构化临床访谈，选择代表两组中从体重不足到肥胖的 BMI 类别。通过酶联免疫吸附试验处理空腹血液样本以测量血浆 IL-6 浓度。除了评估血浆 IL-6 组间差异外，探索性分析还检查了 IL-6 与 BESD 的生物学和临床标志物之间的关联。
与对照组相比，患有 BESD 的女性血浆 IL-6 水平显著升高，而 BMI、肥胖或抑郁并不能解释这一差异。血浆 IL-6 与血浆瘦素浓度、饮食障碍严重程度的临床评估以及参与者最大的自我报告的进食发作呈正相关。
外周炎症与 BESD 中独立于体重、肥胖和抑郁的饮食失调具体相关。未来的研究应该探究神经炎症在改变的进食行为中的潜在作用。
本研究首次证明，炎症表现为血浆 IL-6 浓度升高，与 BESD 中饮食失调的独特相关。更好地了解免疫因素是否有助于饮食失调，可以帮助确定新的干预生物学靶点。
