Chronic gastritis (CG), particularly when associated with Helicobacter pylori (H. pylori) infection, is a significant precursor to gastric cancer (GC), a leading cause of cancer-related deaths worldwide. The persistent inflammation in CG, driven by factors such as H. pylori, induces oxidative stress and DNA damage in gastric epithelial cells, which can lead to malignant transformation. Atrophic gastritis, a form of CG, can be categorized into autoimmune and H. pylori-associated types, both of which increase the risk of GC development, particularly when compounded by external factors like smoking and dietary habits. This manuscript explores the pathophysiological mechanisms underlying CG and its progression to GC, highlighting the critical role of metabolomics in advancing our understanding of these processes. Metabolomics, the comprehensive study of metabolites, offers a novel approach to identifying biomarkers that could facilitate early detection and improve the accuracy of GC diagnosis and prognosis. The analysis of metabolic alterations, particularly in glucose, lipid, and amino acid metabolism, reveals distinct biochemical pathways associated with the progression from benign gastritis to malignancy. Integrating metabolomic profiling with traditional diagnostic methods can revolutionize GC management, enabling more personalized treatment strategies and improving clinical outcomes. However, significant challenges remain, including the need to validate biomarkers across diverse populations and standardize metabolomic techniques. Future research should address these challenges to fully realize the potential of metabolomics in early GC detection and treatment, ultimately aiming to reduce the global burden of this deadly disease.