Zinc in Inflammatory Bowel Disease: Biological Functions, Clinical Associations and Therapeutic Uncertainty

Zinc deficiency is reported in up to half of patients with inflammatory bowel disease (IBD), yet interpreting a low serum zinc concentration can be challenging. Zinc is an essential micronutrient with important roles in epithelial barrier integrity, immune regulation and cellular signalling, providing biological plausibility that deficiency could contribute to intestinal inflammation. Observational studies have associated low serum zinc with adverse outcomes, including hospitalisation, surgery and relapse, particularly in Crohn’s disease. However, both systemic inflammation and hypoalbuminaemia reduce circulating zinc concentrations, raising uncertainty as to whether low zinc represents a true deficiency, a marker of active disease or a potentially modifiable contributor to inflammation. This narrative review examines the mechanistic, observational and interventional evidence linking zinc with IBD. Experimental studies support effects on tight-junction integrity, mucus production, Paneth cell function and immune signalling. Despite this biological rationale and the associations seen in observational studies, evidence that zinc supplementation improves IBD-related outcomes remains limited. Existing studies are small, heterogeneous and often rely on surrogate outcomes, while oral supplementation has not consistently improved clinical or inflammatory endpoints. Zinc deficiency should be identified and corrected as part of nutritional care in IBD but serum zinc concentrations should be interpreted in the context of underlying inflammation, and the benefit of routine zinc monitoring remains uncertain. Well-designed prospective trials are needed to determine whether correcting zinc deficiency improves objective IBD outcomes.