Zinc in Inflammatory Bowel Disease: Biological Functions, Clinical Associations and Therapeutic Uncertainty
- 1Department of Gastroenterology, St George’s University Hospitals NHS Foundation Trust, London SW17 0QT, UK
- 2Institute of Infection and Immunity, City St George’s, University of London, London SW17 0RE, UK
- 3School of Immunology and Microbial Sciences, King’s College London, Strand, London WC2R 2LS, UK
Abstract
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.
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BibTeX
@article{hall2026zinc,
title = {{Zinc in Inflammatory Bowel Disease: Biological Functions, Clinical Associations and Therapeutic Uncertainty}},
author = {Richard Hall and Michael Colwill and Aaron S. Bancil and Kamal V. Patel and Sailish Honap and Andrew Poullis},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18213575},
url = {https://www.mdpi.com/2072-6643/18/21/3575},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Zinc in Inflammatory Bowel Disease: Biological Functions, Clinical Associations and Therapeutic Uncertainty
AU - Richard Hall
AU - Michael Colwill
AU - Aaron S. Bancil
AU - Kamal V. Patel
AU - Sailish Honap
AU - Andrew Poullis
PY - 2026
DA - 2026/10/29
JO - Nutrients
DO - 10.3390/nu18213575
UR - https://www.mdpi.com/2072-6643/18/21/3575
AB - 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.
SN - 2072-6643
ER -