Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain.
Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark.
Am J Clin Nutr. 2018 Apr 1;107(4):607-616. doi: 10.1093/ajcn/nqy002.
Chronic inflammation plays a critical role in the pathogenesis of the 2 major types of gastric cancer. Several foods, nutrients, and nonnutrient food components seem to be involved in the regulation of chronic inflammation.
We assessed the association between the inflammatory potential of the diet and the risk of gastric carcinoma, overall and for the 2 major subsites: cardia cancers and noncardia cancers.
A total of 476,160 subjects (30% men, 70% women) from the European Investigation into Cancer and Nutrition (EPIC) study were followed for 14 y, during which 913 incident cases of gastric carcinoma were identified, including 236 located in the cardia, 341 in the distal part of the stomach (noncardia), and 336 with overlapping or unknown tumor site. The dietary inflammatory potential was assessed by means of an inflammatory score of the diet (ISD), calculated with the use of 28 dietary components and their corresponding inflammatory scores. The association between the ISD and gastric cancer risk was estimated by HRs and 95% CIs calculated by multivariate Cox regression models adjusted for confounders.
The inflammatory potential of the diet was associated with an increased risk of gastric cancer. The HR (95% CI) for each increase in 1 SD of the ISD were 1.25 (1.12, 1.39) for all gastric cancers, 1.30 (1.06, 1.59) for cardia cancers, and 1.07 (0.89, 1.28) for noncardia cancers. The corresponding values for the highest compared with the lowest quartiles of the ISD were 1.66 (1.26, 2.20), 1.94 (1.14, 3.30), and 1.07 (0.70, 1.70), respectively.
Our results suggest that low-grade chronic inflammation induced by the diet may be associated with gastric cancer risk. This pattern seems to be more consistent for gastric carcinomas located in the cardia than for those located in the distal stomach. This study is listed on the ISRCTN registry as ISRCTN12136108.
慢性炎症在两种主要类型胃癌的发病机制中起着关键作用。一些食物、营养素和非营养性食物成分似乎参与了慢性炎症的调节。
我们评估了饮食的炎症潜能与胃癌风险之间的关系,总体上以及两个主要部位的风险:贲门癌和非贲门癌。
来自欧洲癌症与营养前瞻性调查(EPIC)研究的 476160 名受试者(30%为男性,70%为女性)进行了 14 年的随访,在此期间发现了 913 例胃癌新发病例,其中 236 例位于贲门,341 例位于胃远端(非贲门),336 例肿瘤部位重叠或未知。饮食的炎症潜能通过饮食炎症评分(ISD)来评估,该评分通过使用 28 种饮食成分及其相应的炎症评分来计算。通过多变量 Cox 回归模型调整混杂因素后,计算 HRs 和 95%CI 来估计 ISD 与胃癌风险之间的关系。
饮食的炎症潜能与胃癌风险增加相关。ISD 每增加 1SD,所有胃癌的 HR(95%CI)为 1.25(1.12,1.39),贲门癌为 1.30(1.06,1.59),非贲门癌为 1.07(0.89,1.28)。ISD 最高四分位数与最低四分位数相比,相应值分别为 1.66(1.26,2.20)、1.94(1.14,3.30)和 1.07(0.70,1.70)。
我们的结果表明,饮食引起的低度慢性炎症可能与胃癌风险相关。这种模式对于贲门癌似乎比对于胃远端癌更为一致。本研究已在 ISRCTN 注册处注册,注册号为 ISRCTN80115662。