Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Department of Biostatistics, University of Alabama at Birmingham School of Public Health, Birmingham, AL, USA.
J Nutr. 2019 Dec 1;149(12):2206-2218. doi: 10.1093/jn/nxz165.
Chronically higher inflammation, which may partly result from diet and lifestyle, is implicated in risk for multiple chronic diseases. The dietary inflammatory index (DII) and empirical dietary inflammatory pattern (EDIP), developed to characterize dietary contributions to systemic inflammation, have several limitations. There are no scores to characterize contributions of lifestyle to inflammation.
To reflect dietary/lifestyle contributions to inflammation, we developed novel, inflammation biomarker panel-weighted, dietary (DIS) and lifestyle (LIS) inflammation scores in a subset (n = 639) of the Reasons for Geographic and Racial Differences in Stroke Study (REGARDS) cohort.
We selected a priori 19 food groups and 4 lifestyle characteristics to comprise the DIS and LIS, respectively. We calculated the components' weights based on their strengths of association with an inflammation biomarker score [comprising high-sensitivity C-reactive protein (hsCRP), IL-6, IL-8, and IL-10] using multivariable linear regression. The sums of the weighted components constitute the scores, such that higher scores reflect, on balance, more proinflammatory exposures. We calculated the DIS, LIS, DII, and EDIP with cross-sectional data from the remaining REGARDS cohort ( n = 14,210 with hsCRP measurements) and 2 other study populations with hsCRP and/or an 8-component inflammation biomarker panel, and investigated their associations with circulating inflammation biomarker concentrations using multivariable logistic regression.
In REGARDS, those in the highest relative to the lowest DIS, LIS, DII, and EDIP quintiles had statistically significant 1.66-, 4.29-, 1.56-, and 1.32-fold higher odds of a high hsCRP concentration (>3 mg/dL), respectively (all P-trend < 0.001). Those in the highest relative to the lowest joint DIS/LIS quintile had a statistically significant 7.26-fold higher odds of a high hsCRP concentration. Similar findings were noted in the other 2 validation populations.
Our results support that dietary and lifestyle exposures collectively contribute substantially to systemic inflammation, and support the use of our novel DIS and LIS.
长期高水平的炎症,部分可能源于饮食和生活方式,与多种慢性疾病的发病风险相关。饮食炎症指数(DII)和经验性饮食炎症模式(EDIP)被开发出来以描述饮食对全身炎症的贡献,但它们有几个局限性。目前还没有评分来描述生活方式对炎症的贡献。
为了反映饮食/生活方式对炎症的贡献,我们在 REGARDS 队列的一个亚组(n=639)中开发了新的、基于炎症生物标志物的饮食(DIS)和生活方式(LIS)炎症评分。
我们分别选择了 19 种食物组和 4 种生活方式特征来组成 DIS 和 LIS。我们使用多变量线性回归根据它们与炎症生物标志物评分(包括高敏 C 反应蛋白 [hsCRP]、IL-6、IL-8 和 IL-10)的关联强度来计算成分的权重。加权成分的总和构成了评分,因此,更高的评分反映了更具促炎作用的暴露。我们使用 REGARDS 队列中剩余的横断面数据(n=14210 人,有 hsCRP 测量值)和另外两个有 hsCRP 和/或 8 个炎症生物标志物组合的研究人群计算了 DIS、LIS、DII 和 EDIP,并使用多变量逻辑回归研究了它们与循环炎症生物标志物浓度的关系。
在 REGARDS 中,与最低 DIS、LIS、DII 和 EDIP 五分位数相比,最高五分位数的个体发生高 hsCRP 浓度(>3mg/dL)的比值比分别为 1.66、4.29、1.56 和 1.32(所有 P 趋势<0.001)。与最低 DIS/LIS 五分位数相比,最高五分位数的个体发生高 hsCRP 浓度的比值比为 7.26。在另外两个验证人群中也观察到了类似的发现。
我们的结果支持饮食和生活方式暴露共同对全身炎症有很大贡献,并支持使用我们新的 DIS 和 LIS。