Despite food fortification, vitamin B12 deficiency endures, now driven chiefly by malabsorption rather than inadequate intake. Pernicious anemia, the end‑stage of autoimmune atrophic gastritis, emerges as the principal cause and is increasingly linked to modifiable diet. Evidence from clinical, epidemiological, and mechanistic studies shows that salt‑, fat‑ and nitrosamine‑rich diets elevate gastric pH, suppress gastric–pancreatic proteases and inflame mucosa, blocking the release of cobalamin from food. Concurrent deficits of zinc, vitamin D and other micronutrients erode antioxidant defenses and immune tolerance, hastening parietal‑cell loss and intrinsic‑factor failure, while ultra‑processed foods drive microbiome shifts that bias Th2‑mediated autoimmunity. These converging insults disrupt two critical steps—enzymatic liberation of B12 and intrinsic‑factor–dependent uptake—spanning reversible gastritis to irreversible pernicious anemia. Preliminary interventions suggest that diet optimization and micronutrient repletion can restore gastric enzyme activity and lower parietal‑cell antibodies, positioning targeted nutrition as a low‑cost adjunct, or occasional alternative, to lifelong parenteral B12 therapy. Rigorous prospective and randomised studies are now needed.