Keirns Natalie G, Keirns Bryant H, Tsotsoros Cindy E, Layman Harley M, Stout Madison E, Sciarrillo Christina M, Emerson Sam R, Byrd-Craven Jennifer, Krems Jaimie Arona, Pearl Rebecca L, Tomiyama A Janet, Hawkins Misty A W
Division of Cardiology, The Miriam Hospital, Lifespan.
Department of Nutrition and Health Science, Ball State University.
Stigma Health. 2025 Aug;10(3):567-571. doi: 10.1037/sah0000487. Epub 2023 Oct 16.
Weight stigma is a chronic stressor and may contribute to cardiometabolic health risk. This pilot study tests an experimental protocol exploring acute inflammation as a potential biological mechanism connecting weight stigma and disease risk. Preliminary effect sizes and protocol feasibility were assessed. Women (=44, 68% white) with overweight/obesity ( =33.2±6.7 kg/m) were randomized to either weight stigma (=22) or control (=22) stress reactivity tasks. Serum cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α, interferon [IFN]-γ) were measured at baseline and serially over 90 minutes via peripheral intravenous catheter (PIVC) to assess inflammatory responses. The absolute change (Δ; baseline-to-peak) and incremental area under the curve (AUC) were calculated for all outcomes. Within the weight stigma group, pre/post-task increases in IL-6 (=.20, =.365), TNF-α (=.43, =.047), and IFN-γ (=.078, =.48) were consistent with small effects. Within the control group, only IL-6 increased and displayed a medium effect (=.62, =.004). When comparing weight stigma versus control, the between-group difference in ΔTNF-α displayed a small effect (=.21, =.495), consistent with a greater TNF-α increase in weight stigma. Similarly, a small effect size was observed for weight stigma displaying greater ΔIFN-γ (=.46, =.153) and IFN-γ AUC (=.27, =.502) versus control. Experimental procedures were feasible to conduct with minimal attrition/data loss. Based on the small effect sizes observed in this pilot study, the impact of weight stigma on acute inflammatory responses warrants further investigation in larger samples. Use of in-lab weight stigma stress tasks with repeated blood draws via PIVC was supported as a feasible future protocol.
体重羞辱是一种慢性应激源,可能会增加心血管代谢健康风险。这项试点研究测试了一种实验方案,探索急性炎症作为连接体重羞辱和疾病风险的潜在生物学机制。评估了初步效应大小和方案可行性。将超重/肥胖(体重指数=33.2±6.7kg/m²)的女性(n=44,68%为白人)随机分为体重羞辱组(n=22)或对照组(n=22),进行应激反应任务。通过外周静脉导管(PIVC)在基线和90分钟内连续测量血清细胞因子(白细胞介素[IL]-6、肿瘤坏死因子[TNF]-α、干扰素[IFN]-γ),以评估炎症反应。计算所有结果的绝对变化(Δ;基线至峰值)和曲线下增量面积(AUC)。在体重羞辱组中,任务前后IL-6(效应大小=0.20,P=0.365)、TNF-α(效应大小=0.43,P=0.047)和IFN-γ(效应大小=0.078,P=0.48)的增加与小效应一致。在对照组中,只有IL-6增加并显示出中等效应(效应大小=0.62,P=0.004)。比较体重羞辱组和对照组时,ΔTNF-α的组间差异显示出小效应(效应大小=0.21,P=0.495),与体重羞辱组中TNF-α的更大增加一致。同样,与对照组相比,体重羞辱组显示出更大的ΔIFN-γ(效应大小=0.46,P=0.153)和IFN-γ AUC(效应大小=0.27,P=0.502),观察到小效应大小。实验程序可行,损耗/数据丢失最小。基于该试点研究中观察到的小效应大小,体重羞辱对急性炎症反应的影响值得在更大样本中进一步研究。通过PIVC进行重复采血的实验室体重羞辱应激任务被支持作为一种可行的未来方案。