The Western diet, characterized by high intake of saturated fat, sugar, and salt, is associated with elevated inflammation and chronic disease risk. Few studies have investigated molecular mechanisms linking diet and inflammation; however, a small number of randomized controlled trials suggest that consuming an anti-inflammatory diet (i.e., a primarily plant-based diet rich in monounsaturated fat and lean protein) decreases proinflammatory gene expression. The current study investigated the association between everyday diet and proinflammatory gene expression, as well as the extent to which central adiposity and social involvement modulate risk. Participants were healthy middle-aged and older adults (N=105) who completed a food frequency questionnaire and reported how many close social roles they have. Anthropometric measurements and blood samples also were collected; gene expression data were analyzed from LPS-stimulated peripheral blood mononuclear cells for interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. The inflammatory potential of each participant's diet was calculated using the Dietary Inflammatory Index (DII®). Participants with higher DII® scores, indicating a more proinflammatory diet, had greater IL-6 (b = -0.02, SE = 0.008, p = .01), IL-1 β (b = -0.01, SE = 0.006, p = .03), and TNF-α (b = -0.01, SE = 0.005, p = .04) gene expression if they had a smaller sagittal abdominal diameter (SAD); effects were not seen among those with higher SADs. Social involvement served a protective role, such that participants with smaller SADs had greater IL-6 (b = 0.01, SE = 0.004, p = .049) and IL-1β (b = 0.01, SE = 0.003, p = .045) gene expression only if they had less social involvement; there was no effect of diet on gene expression among those who reported greater social participation. Results are the first to demonstrate a link between self-reported diet and proinflammatory gene expression. Importantly, the effect of diet on gene expression depended upon both body fat composition and social participation, both of which have previously been linked directly with proinflammatory gene expression and inflammation.

中文翻译：

---

促炎饮食与健康、非肥胖成年人的炎症基因表达有关：社会关系可以防止风险吗？

西方饮食的特点是摄入大量饱和脂肪、糖和盐，与炎症和慢性疾病风险升高有关。很少有研究调查饮食和炎症之间的分子机制。然而，少数随机对照试验表明，食用抗炎饮食（即富含单不饱和脂肪和瘦肉蛋白的主要以植物为基础的饮食）会降低促炎基因的表达。目前的研究调查了日常饮食与促炎基因表达之间的关联，以及中枢性肥胖和社会参与调节风险的程度。参与者是健康的中老年人（N=105），他们完成了食物频率问卷并报告了他们有多少亲密的社会角色。还收集了人体测量数据和血液样本；从 LPS 刺激的外周血单核细胞中分析白细胞介素 (IL)-6、IL-1β 和肿瘤坏死因子 (TNF)-α 的基因表达数据。使用膳食炎症指数 (DII®) 计算每个参与者饮食的潜在炎症。DII® 评分较高的参与者表明饮食促炎性更强，IL-6 (b = -0.02, SE = 0.008, p = .01)、IL-1 β (b = -0.01, SE = 0.006, p = .03) 和 TNF-α (b = -0.01, SE = 0.005, p = .04) 基因表达，如果他们的矢状腹径 (SAD) 较小；在具有较高 SAD 的患者中未观察到影响。社会参与起到了保护作用，因此具有较小 SAD 的参与者具有较高的 IL-6（b = 0.01，SE = 0.004，p = .049）和 IL-1β（b = 0.01，SE = 0.003，p = . 045）只有当他们的社会参与较少时才能表达基因；在报告更多社会参与的人中，饮食对基因表达没有影响。结果首次证明了自我报告的饮食与促炎基因表达之间存在联系。重要的是，饮食对基因表达的影响取决于体脂组成和社会参与，这两者以前都与促炎基因表达和炎症直接相关。