High Prevalence of Nickel Allergy in an Overweight Female Population: A Microbial Metallomics Commentary Original paper

What was studied?

This pilot observational study assessed two interconnected phenomena: (1) the prevalence of nickel allergy in an overweight Italian population and (2) the impact of a normocaloric, Low-Nickel Diet (LNiD) on BMI and waist circumference in nickel-sensitive individuals. The authors sought to evaluate whether nickel hypersensitivity is more common in overweight individuals and whether nickel restriction could offer metabolic benefits.

Who was studied?

The study involved 87 overweight adults (BMI > 26 kg/m²), predominantly female (72 of 87). Participants were screened for nickel allergy via standard patch testing. Among these, 43 women and 2 men tested positive and were advised to follow a low-nickel diet (80–100 µg/day). A 6-month follow-up was completed by 24 allergic overweight women, whose BMI, waist circumference, and body fat percentage were tracked as outcome variables.

Most Important Findings

The prevalence of nickel allergy in overweight women was 59.7%, substantially higher than the 12.5% seen in the general female population. In those with both metabolic syndrome and liver steatosis, the prevalence rose to 61.1%. A normocaloric, Low-Nickel Diet (LNiD) significantly reduced BMI (by 4.2 units), waist circumference (by 11.7 cm), and body fat percentage (by 5.1%) in the adherent cohort, all with p-values <0.001.

From a microbial perspective, the authors speculated that elevated dietary nickel may promote the growth or activity of nickel-dependent bacteria. This observation aligns with emerging concepts in microbial metallomics: many gut microbes use nickel as a catalytic cofactor in key enzymes such as urease, [NiFe]-hydrogenase, and glyoxalase I—enzymes directly linked to microbial virulence, stress response, and survival in host environments. Helicobacter pylori, for instance, hoards nickel to support its colonization of the gastric mucosa. The authors even referenced studies suggesting that a low-nickel diet enhances H. pylori eradication.

This pilot study opens the door to consider nickel-dependence as a defining functional trait in specific gut microbial populations associated with obesity. Excess nickel intake may act as a selective pressure that favors nickelophilic organisms, which in turn may modulate host immunity and metabolism. Moreover, nickel-selective dysbiosis may represent an unrecognized microbial signature in overweight individuals, particularly women with metabolic syndrome and liver steatosis.

IL-17, a cytokine elevated in both obesity and nickel hypersensitivity, provides a mechanistic bridge. Nickel-specific T cells produce IL-17, and menopausal estrogen deficiency further upregulates this cytokine. Taken together, a nickel-driven Th17 inflammatory axis may amplify gut inflammation and metabolic disruption through both host immune mechanisms and microbial activation pathways.

Greatest Implications

The data suggest that overweight women, especially those with comorbid metabolic dysfunction, may harbor nickel-selective microbial communities contributing to obesity through metallomic and immunologic pathways. Clinically, this highlights the need to screen for nickel allergy in metabolic and obesity management settings and suggests that nickel restriction may serve as a dual-purpose intervention, addressing both allergic and metabolic symptoms. From a microbiome signatures perspective, this study supports the inclusion of nickel-dependent microbial traits as part of a broader metallomic signature for obesity and metabolic syndrome. Interventions like a Low-Nickel Diet (LNiD) or nickel chelators (e.g., lactoferrin or dimethylglyoxime (DMG) may represent microbiome-targeted strategies that alter not only dietary exposure but microbial composition and activity. Further metagenomic and metallomic analyses are warranted to define nickel-dependent microbial associations and their causal contributions to the obese phenotype.