Diets That Promote Colon Inflammation Associate With Risk of Colorectal Carcinomas That Contain Fusobacterium nucleatum - PubMed (original) (raw)
. 2018 Oct;16(10):1622-1631.e3.
doi: 10.1016/j.cgh.2018.04.030. Epub 2018 Apr 24.
Fred K Tabung 2, Xuehong Zhang 3, Jonathan A Nowak 4, Zhi Rong Qian 5, Tsuyoshi Hamada 6, Daniel Nevo 7, Susan Bullman 8, Kosuke Mima 6, Keisuke Kosumi 6, Annacarolina da Silva 6, Mingyang Song 9, Yin Cao 10, Tyler S Twombly 6, Yan Shi 11, Hongli Liu 12, Mancang Gu 13, Hideo Koh 6, Wanwan Li 6, Chunxia Du 6, Yang Chen 6, Chenxi Li 14, Wenbin Li 6, Raaj S Mehta 15, Kana Wu 16, Molin Wang 17, Aleksander D Kostic 18, Marios Giannakis 19, Wendy S Garrett 20, Curtis Hutthenhower 21, Andrew T Chan 22, Charles S Fuchs 23, Reiko Nishihara 24, Shuji Ogino 25, Edward L Giovannucci 26
Affiliations
- PMID: 29702299
- PMCID: PMC6151288
- DOI: 10.1016/j.cgh.2018.04.030
Diets That Promote Colon Inflammation Associate With Risk of Colorectal Carcinomas That Contain Fusobacterium nucleatum
Li Liu et al. Clin Gastroenterol Hepatol. 2018 Oct.
Abstract
Background & aims: Specific nutritional components are likely to induce intestinal inflammation, which is characterized by increased levels of interleukin 6 (IL6), C-reactive protein (CRP), and tumor necrosis factor-receptor superfamily member 1B (TNFRSF1B) in the circulation and promotes colorectal carcinogenesis. The inflammatory effects of a diet can be estimated based on an empiric dietary inflammatory pattern (EDIP) score, calculated based on intake of 18 foods associated with plasma levels of IL6, CRP, and TNFRSF1B. An inflammatory environment in the colon (based on increased levels of IL6, CRP, and TNFRSF1B in peripheral blood) contributes to impairment of the mucosal barrier and altered immune cell responses, affecting the composition of the intestinal microbiota. Colonization by Fusobacterium nucleatum has been associated with the presence and features of colorectal adenocarcinoma. We investigated the association between diets that promote inflammation (based on EDIP score) and colorectal cancer subtypes classified by level of F nucleatum in the tumor microenvironment.
Methods: We calculated EDIP scores based on answers to food frequency questionnaires collected from participants in the Nurses' Health Study (through June 1, 2012) and the Health Professionals Follow-up Study (through January 31, 2012). Participants in both cohorts reported diagnoses of rectal or colon cancer in biennial questionnaires; deaths from unreported colorectal cancer cases were identified through the National Death Index and next of kin. Colorectal tumor tissues were collected from hospitals where the patients underwent tumor resection and F nucleatum DNA was quantified by a polymerase chain reaction assay. We used multivariable duplication-method Cox proportional hazard regression to assess the associations of EDIP scores with risks of colorectal cancer subclassified by F nucleatum status.
Results: During 28 years of follow-up evaluation of 124,433 participants, we documented 951 incident cases of colorectal carcinoma with tissue F nucleatum data. Higher EDIP scores were associated with increased risk of F nucleatum-positive colorectal tumors (Ptrend = .03); for subjects in the highest vs lowest EDIP score tertiles, the hazard ratio for F nucleatum-positive colorectal tumors was 1.63 (95% CI, 1.03-2.58). EDIP scores did not associate with F nucleatum-negative tumors (Ptrend = .44). High EDIP scores associated with proximal F nucleatum-positive colorectal tumors but not with proximal F nucleatum-negative colorectal tumors (Pheterogeneity = .003).
Conclusions: Diets that may promote intestinal inflammation, based on EDIP score, are associated with increased risk of F nucleatum-positive colorectal carcinomas, but not carcinomas that do not contain these bacteria. These findings indicate that diet-induced intestinal inflammation alters the gut microbiome to contribute to colorectal carcinogenesis; nutritional interventions might be used in precision medicine and cancer prevention.
Keywords: Immunity; Microsatellite Instability; Nutrition; Red Meat.
Copyright © 2018 AGA Institute. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Disclosures: No other conflict of interest exists. The other authors declare that they have no conflicts of interest.
Figures
Figure 1
Flow diagram of study population. EDIP, empirical dietary inflammatory pattern.
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