Dietary inflammatory potential, genetic predisposition, and incidence of Crohn's disease and ulcerative colitis.

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2025-05-01 DOI:10.1186/s12986-025-00934-z

Ji-Mei Gu, Miao Zhao, Jie Zhu, Hao-Wei Tao, Xiao-Ping Shao, Li-Qiang Qin, Yang-Yang Ge, Guo-Chong Chen

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引用次数: 0

Abstract

Background: Evidence for a potential link between dietary inflammatory potential and inflammatory bowel disease is limited, and the moderating role of genetic susceptibility remains to be assessed.

Objective: To evaluate energy-adjusted dietary inflammatory index (E-DII) for the associations with incident Crohn's disease (CD) and ulcerative colitis (UC) and the role of genetic susceptibility.

Methods: A total of 205,706 UK Biobank participants who were aged 39-72 years and had no known CD or UC at baseline (2006-2010) were included. The E-DII score was calculated based on energy-adjusted average intakes of 33 food or nutrient items derived from up to five 24-hour dietary recalls. Multivariable Cox regression models were used estimate hazard ratios (HRs) with 95% confidence interval (CI) for incident CD and UC.

Results: During a median 12.3 years of follow-up, 382 incident CD and 798 incident UC cases were ascertained. A higher E-DII score was not associated with risk of CD (HR _{Q4 VS. Q1} = 1.28, 95% CI: 0.94-1.74; P-trend = 0.09) or UC (HR _{Q4 VS. Q1} = 1.10, 95% CI: 0.90-1.36; P-trend = 0.17). There was an interaction between the E-DII and the polygenic risk score (PRS) for CD on incident CD (P-interaction = 0.023), with an association only among participants with a high PRS (HR _{Q4 VS. Q1} = 1.64, 95% CI: 1.03-2.61) (P-interaction = 0.023). As compared with the participants with a low PRS for CD and a low E-DII score, participants with high levels of both scores had a particularly higher risk of CD (HR = 3.12; 95% CI: 1.74-5.60).

Conclusions: The association of dietary inflammatory potential with incident CD appears to be amplified by high genetic susceptibility to CD.

查看原文本刊更多论文

饮食炎症潜能、遗传易感性和克罗恩病和溃疡性结肠炎的发病率。

背景：饮食炎症与炎症性肠病之间的潜在联系的证据有限，遗传易感性的调节作用仍有待评估。目的：评价能量调节饮食炎症指数（E-DII）与克罗恩病（CD）和溃疡性结肠炎（UC）发病的关系及其遗传易感性的作用。方法：共纳入205,706名英国生物银行参与者，年龄在39-72岁之间，基线时（2006-2010年）没有已知的CD或UC。E-DII评分是根据33种食物或营养项目的能量调整平均摄入量计算的，这些食物或营养项目来自最多5次24小时饮食召回。使用多变量Cox回归模型估计CD和UC事件的95%可信区间（CI）的风险比（hr）。结果：在中位12.3年的随访中，确定了382例CD和798例UC。较高的E-DII评分与CD风险无关(HR Q4 VS. Q1 = 1.28, 95% CI: 0.94-1.74；P-trend = 0.09)或UC (HR Q4 VS. Q1 = 1.10, 95% CI: 0.90-1.36；p趋势= 0.17)。E-DII与多基因风险评分（PRS）之间存在交互作用（P-interaction = 0.023），仅在高PRS的参与者之间存在关联（HR Q4 VS. Q1 = 1.64, 95% CI: 1.03-2.61）（P-interaction = 0.023）。与低CD PRS和低E-DII评分的参与者相比，两项评分均较高的参与者患CD的风险特别高(HR = 3.12；95% ci: 1.74-5.60)。结论：饮食炎症与乳糜泻事件的关联似乎被乳糜泻的高遗传易感性所放大。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.