Yousaf, Hagen, Mitchell, Ghareeb, Fang, Correa, Zinn, Gayam 2021 — Low-nickel diet and gastroesophageal reflux disease: a pilot study
This Indian Journal of Gastroenterology pilot trial from West Virginia University Departments of Dermatology, Internal Medicine, and Clinical and Translational Science tests whether a low-nickel diet reduces GERD symptoms in refractory patients and whether epicutaneous patch testing to nickel predicts diet responsiveness. 20 patients with refractory GERD (measured by GERD-HRQL) underwent patch testing and an 8-week low-nickel diet. The headline finding: 19 of 20 patients (95 percent) had GERD-HRQL symptom-severity reduction at 8 weeks; the response was not predicted by patch-test positivity. The implication challenges the standard clinical framework that nickel sensitivity (and the therapeutic relevance of low-Ni diet) tracks with positive patch testing.
Key numbers
| Outcome | Result |
|---|---|
| GERD-HRQL responders at 8 weeks | 19 of 20 (95 percent) |
| Patch-test-positive responders | Did not differ from patch-test-negative responders |
| Endoscopic improvement | Documented in the responder cohort |
Both patch-test-positive and patch-test-negative GERD patients responded to the low-nickel diet, suggesting nickel-related GI symptoms are not exclusively mediated through type IV (delayed-type hypersensitivity) immune mechanisms. This is a major finding for the SNAS-vs-broader-nickel-sensitivity debate.
Methods (brief)
Single-site prospective pilot study. Inclusion: refractory GERD by GERD-HRQL. Intervention: 8-week low-nickel diet (Italian Allergological Society protocol). Pre- and post- patch testing to nickel sulfate at standard concentration. GERD-HRQL and Bravo pH testing where applicable.
Implications
- Certification: Demonstrates that low-nickel-diet benefits extend beyond patch-test-positive nickel-allergic individuals, broadening the population for whom dietary Ni reduction is clinically meaningful. Relevant to HMTc Ni-threshold rationale for broader vulnerable populations than the EFSA-acute-LOAEL framework recognizes.
- Microbiome / GI: Plausible mechanism is Ni-driven H. pylori virulence (companion to Campanale 2014) plus Ni-driven barrier dysfunction (Ghosh 2024).
- Courses: Standard recent reference for nickel and refractory GERD.