Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Gastroenterology. 2020 Sep;159(3):873-883.e1. doi: 10.1053/j.gastro.2020.05.011. Epub 2020 May 7.
BACKGROUND & AIMS: Inflammation is a potential mechanism through which diet modulates the onset of inflammatory bowel disease. We analyzed data from 3 large prospective cohorts to determine the effects of dietary inflammatory potential on the risk of developing Crohn's disease (CD) and ulcerative colitis (UC).
We collected data from 166,903 women and 41,931 men in the Nurses' Health Study (1984-2014), Nurses' Health Study II (1991-2015), and Health Professionals Follow-up Study (1986-2012). Empirical dietary inflammatory pattern (EDIP) scores were calculated based on the weighted sums of 18 food groups obtained via food frequency questionnaires. Self-reported CD and UC were confirmed by medical record review. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).
We documented 328 cases of CD and 428 cases of UC over 4,949,938 person-years of follow-up. The median age at IBD diagnosis was 55 years (range 29-85 years). Compared with participants in the lowest quartile of cumulative average EDIP score, those in the highest quartile (highest dietary inflammatory potential) had a 51% higher risk of CD (HR 1.51; 95% CI 1.10-2.07; P = .01). Compared with participants with persistently low EDIP scores (at 2 time points, separated by 8 years), those with a shift from a low to high inflammatory potential of diet or persistently consumed a proinflammatory diet had greater risk of CD (HR 2.05; 95% CI 1.10-3.79 and HR 1.77; 95% CI 1.10-2.84). In contrast, dietary inflammatory potential was not associated with the risk of developing UC (P = .62).
In an analysis of 3 large prospective cohorts, we found dietary patterns with high inflammatory potential to be associated with increased risk of CD but not UC.
炎症是饮食调节炎症性肠病发病的潜在机制。我们分析了 3 项大型前瞻性队列研究的数据，以确定饮食炎症潜能对克罗恩病（CD）和溃疡性结肠炎（UC）发病风险的影响。
我们收集了护士健康研究（1984-2014 年）、护士健康研究 II（1991-2015 年）和健康专业人员随访研究（1986-2012 年）中 166903 名女性和 41931 名男性的数据。基于通过食物频率问卷获得的 18 种食物组的加权和计算经验性饮食炎症模式（EDIP）评分。通过病历回顾确认 CD 和 UC 病例。使用 Cox 比例风险模型计算风险比（HR）和 95%置信区间（CI）。
在 4949938 人年的随访中，我们记录了 328 例 CD 和 428 例 UC。IBD 诊断的中位年龄为 55 岁（范围 29-85 岁）。与累积平均 EDIP 评分最低四分位的参与者相比，最高四分位（最高饮食炎症潜能）的 CD 风险高 51%（HR 1.51；95%CI 1.10-2.07；P =.01）。与持续低 EDIP 评分的参与者相比（在 2 个时间点，间隔 8 年），饮食炎症潜能从低到高或持续摄入促炎饮食的参与者 CD 风险更高（HR 2.05；95%CI 1.10-3.79 和 HR 1.77；95%CI 1.10-2.84）。相反，饮食炎症潜能与 UC 发病风险无关（P =.62）。
在对 3 项大型前瞻性队列的分析中，我们发现高炎症潜能的饮食模式与 CD 风险增加相关，但与 UC 无关。
