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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Gastrointest Oncol. Mar 15, 2026; 18(3): 117083
Published online Mar 15, 2026. doi: 10.4251/wjgo.v18.i3.117083
Dietary factors in Helicobacter pylori-negative early gastric cancer: Risk, protection, and mechanistic insights
Di Fan, Rui-Jia Li, Chu-Yan Guo, Yan Jiao
Di Fan, Anesthesia Recovery Room, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Rui-Jia Li, Chu-Yan Guo, Department of Gastrointestinal Surgery, General Surgery Center, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Yan Jiao, Department of Hepatobiliary and Pancreatic Surgery, General Surgery Center, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Author contributions: Jiao Y and Fan D contributed to conceptualization; Fan D, Guo CY, and Li RJ contributed to the writing of the original draft; Jiao Y contributed to the methodology, revised the manuscript, and supervised the study; Guo CY and Li RJ contributed to the literature review and assisted in formal analysis and visualization. All authors approved the final version to publish.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Yan Jiao, Department of Hepatobiliary and Pancreatic Surgery, General Surgery Center, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun 130021, Jilin Province, China. jiaoyan@jlu.edu.cn
Received: November 28, 2025
Revised: December 14, 2025
Accepted: January 4, 2026
Published online: March 15, 2026
Processing time: 104 Days and 18 Hours
Abstract

Helicobacter pylori (H. pylori)-negative early gastric cancer (GC) is an emerging clinical and epidemiological challenge that cannot be explained by the classical H. pylori-driven carcinogenic pathway. Growing evidence indicates that dietary factors play a critical role in modulating gastric mucosal integrity, inflammation, and carcinogenic progression in the absence of H. pylori infection. High salt intake and processed foods, particularly those rich in nitrates and nitrites, are associated with mucosal injury, oxidative stress, and endogenous N-nitroso compound formation, thereby increasing early GC risk. In contrast, diets rich in fruits, vegetables, antioxidants, and dietary fiber exert protective effects by reducing oxidative DNA damage, attenuating chronic inflammation, and supporting a favorable gastric microenvironment. Mediterranean and prudent dietary patterns, characterized by plant-based foods, polyphenols, and unsaturated fatty acids, show inverse associations with GC risk independent of H. pylori status. While vitamins C and E demonstrate consistent protective trends, evidence regarding vitamin D remains inconclusive due to population heterogeneity. Emerging studies using the dietary inflammatory index further suggest that pro-inflammatory diets may promote H. pylori-negative gastric carcinogenesis. This minireview summarizes current evidence and highlights key mechanistic gaps to inform targeted prevention strategies in high-risk populations.

Keywords: Helicobacter pylori-negative; Early gastric cancer; Dietary risk factors; Dietary patterns; Dietary inflammatory index

Core Tip: Diet plays a critical role in the development of Helicobacter pylori (H. pylori)-negative early gastric cancer. High salt intake and processed foods increase carcinogenic risk, while fruits, vegetables, antioxidants, dietary fiber, and Mediterranean-style dietary patterns provide protective effects independent of H. pylori status. Understanding these dietary influences is essential for improving prevention strategies and refining risk assessment in H. pylori-negative populations.