Overview

Nickel (Ni) is a ubiquitous trace metal present in soil, water, foods, and many consumer products.^[1] While Nickel has no known essential biochemical role in humans, it is required by numerous microorganisms for key enzymes that influence metabolism and virulence.^[2] Concurrently, Nickel is among the most common allergens in humans, capable of eliciting T-cell-mediated contact dermatitis and systemic immune reactions in sensitized individuals. ^[3][4] These dual effects of Nickel – supporting microbial pathogenicity and triggering immune dysfunction – form the basis for the Low‑Nickel diet (LNiD) as a therapeutic strategy. A low-nickel diet (LNiD) aims to reduce dietary Ni intake (typically from ~200–600 μg/day down to <50 μg/day) in order to starve Ni-dependent microbes and mitigate Ni-driven immune inflammation.^[5] This review summarizes the mechanistic rationale of the Low-nickel diet (LNiD), spanning microbial metabolism and immune modulation, and compiles evidence for its clinical benefits across multiple conditions.

Foods to Avoid on a Low-Nickel Diet

Implementing a LNiD requires understanding which foods and exposures are high in nickel. Nickel is pervasive in plant-based foods, especially whole grains, legumes, nuts, and seeds, as well as certain seafood and cocoa products. Below is a breakdown of sources:

Foods to Include on a Low-Nickel Diet

Nickel, Immunity, and Barrier Function

In parallel to its microbial effects, dietary nickel influences the immune system, especially in Ni-sensitized individuals. Nickel is a highly sensitizing allergen: approximately 15–20% of people in industrialized countries are allergic to nickel. Classically, Ni allergy manifests as allergic contact dermatitis (ACD) after skin contact (a type IV hypersensitivity). However, many Ni-allergic patients also experience systemic symptoms (eczema flares, itch, urticaria, or GI distress) upon oral Ni exposure – a condition termed Systemic Nickel Allergy Syndrome (SNAS). ^[6][7] In SNAS, Ni acts as a dietary trigger of both cutaneous and gastrointestinal inflammation. Mechanistic studies show that Ni ingestion skews the immune response toward a Th2 profile in susceptible individuals, on top of the Th1/Th17 response typical of contact dermatitis. ^[8]

What are the immunopathological mechanisms of nickel exposure?

Nickel-Induced Effects and Relevance of a Low-Nickel Diet (LNID)

Nickel in the diet can act as an immunological Trojan horse. In Ni-sensitized individuals, it incites a combination of Th1/Th17 (cell-mediated) and Th2 (allergic) inflammation. SNAS patients experience eczema flares, rashes, and gastrointestinal distress due to Ni ingestion, and improvement is typically seen when Ni is removed from the diet. ^[9][10] The low-nickel diet is both a diagnostic tool and a treatment in such cases: symptom improvement on LNiD and recurrence on re-exposure confirms Ni as the culprit. Even in those not formally diagnosed with SNAS, subclinical Ni sensitivity or Ni-induced mast cell/eosinophil activation might underlie conditions like irritable bowel syndrome IBS, GERD, or chronic fatigue, and LNiD reduces the overall inflammatory burden.

Immunopathological Mechanism	Nickel-Induced Effects and LNiD Relevance
Th2 Cytokine Elevation	In SNAS patients, oral nickel challenge elevates Th2 cytokines—especially IL-5, along with IL-4 and IL-13—driving eosinophilic inflammation, as seen in some duodenal biopsies. Nickel desensitization reverses this pattern, reducing IL-5/IL-13 and increasing IL-10. The marked IL-5 response implicates eosinophils in Ni-induced GI symptoms, resembling food allergy or eosinophilic esophagitis.[11]
T Cell Trafficking to Gut	In Ni-allergic individuals, oral nickel exposure mobilizes CD4⁺CD45RO⁺ memory T cells to the gut, driving local inflammation and symptoms such as pain, diarrhea, and bloating. LNiD removes the trigger, resolving symptoms and likely allowing T cells to recirculate or become quiescent. CD8⁺ involvement is possible but less documented.[12]
Barrier Dysfunction	Nickel-induced inflammation impairs epithelial barrier integrity, likely through Th2 cytokines (IL-4, IL-13, IL-33) known to disrupt tight junctions and increase permeability.[13] In SNAS, this may exacerbate “leaky gut,” allowing antigen translocation and amplifying immune activation. Ni also acts as a chemical irritant, generating ROS and cellular stress that further destabilize tight junctions. Common symptoms like brain fog or fatigue after Ni-rich meals may stem from this barrier disruption. Thus, a low-nickel diet may restore epithelial integrity by simply removing the inflammatory stimulus.
Innate Immune Activation	Nickel’s allergenicity is partly due to its ability to activate innate immunity: Ni²⁺ binds directly to human TLR4 on dendritic cells, triggering an NF-κB–driven inflammatory cascade. [14] Acting as a “danger signal,” Ni provokes cytokine release (e.g., IL-1β, TNFα) even in the absence of pathogens, priming adaptive responses and skewing immunity toward Th2. In the gut, this can drive pain, motility changes, and inflammation. A low-nickel diet may blunt this innate activation by removing the Ni trigger.
Systemic Immune Effects	Chronic Ni exposure has been linked to broader immune disturbances. For example, a significantly higher prevalence of Ni hypersensitivity has been observed in conditions like chronic fatigue syndrome (CFS) and fibromyalgia. One study found 36% of women with CFS had positive Ni patch tests, compared to 19% of controls (p<0.05). [15] This raises the possibility that Ni-driven immune activation (or cross-reactive metal ions) could contribute to systemic symptoms like fatigue, perhaps via persistent cytokine release or neuroimmune interactions. Reducing Ni burden with a low-nickel diet might therefore alleviate some systemic symptoms in a subset of patients, though more research is needed in these domains.

Consequences of Excessive Dietary Nickel

Excessive nickel in the gut (whether from diet or environmental exposure) can perturb the composition and function of the microbiome. Ni is a heavy metal that, at high concentrations, can be toxic to some microbes and select for Ni-resistant strains. At sub-toxic levels, Ni preferentially enables the growth of organisms that possess Ni-dependent machinery or robust metal efflux systems. Dysbiosis associated with high Ni intake has been observed in patients with SNAS and related disorders.^[16] In summary, nickel excess is associated with gut dysbiosis, whereas nickel restriction fosters microbial rebalance and symbiosis. The LNiD not only removes a direct inflammatory trigger but also creates conditions for a healthier microbiome – with increased diversity of Ni-independent commensals and reduction of Ni-dependent pathobionts. This microbiome shift likely contributes to the clinical efficacy of LNiD, as a more balanced microbiota can improve barrier function, nutrient processing, and immune regulation.

What are the impacts of a Low-Nickel Diet on the Microbiome ?

Nickel excess is associated with gut dysbiosis, whereas nickel restriction fosters microbial rebalance and symbiosis. The LNiD not only removes a direct inflammatory trigger but also creates conditions for a healthier microbiome – with increased diversity of Ni-independent commensals and reduction of Ni-dependent pathobionts. This microbiome shift likely contributes to the clinical efficacy of LNiD, as a more balanced microbiota can improve barrier function, nutrient processing, and immune regulation.

Microbiome Feature/Mechanism	Nickel Effects and LNiD Impact
Microbial Dysbiosis	In a cohort of SNAS patients with GI symptoms, all were found to have gut dysbiosis as measured by urinary indican and skatole levels (metabolic markers of intestinal microbial imbalance). [17] “Fermentative” dysbiosis (overgrowth of gas-producing, carbohydrate-fermenting bacteria) was the most common pattern, followed by mixed dysbiosis. These patients most likely had an overabundance of bacteria that thrive on a high-plant nickel-rich diet or can tolerate Ni. Notably, many high-Ni foods (whole grains, legumes) are FODMAP-rich and could fuel fermentative dysbiosis, compounding symptoms like bloating.[18]
Microbial Rebalancing with LNiD	A 3-month low-Ni diet in SNAS patients significantly reduced Ni sensitivity and normalized urinary indican/skatole levels, indicating microbiome rebalancing.[19] When paired with targeted probiotics (Lactobacillus or Bifidobacterium based on dysbiosis type), eubiosis restoration was even more effective . These results suggest Ni restriction enhances conditions for beneficial microbes to reestablish, especially with probiotic support.[20]
Nickel and Pathobionts	High Ni may favor the bloom of pathobionts – commensal microbes with opportunistic pathogenic traits. For instance, Proteobacteria (a phylum containing E. coli, Klebsiella, etc.) often harbor Ni enzymes and metal resistance genes; Ni could promote their expansion at the expense of more sensitive genera like Bifidobacterium.[21] Additionally, environmental heavy metal exposure is known to co-select for antibiotic resistance genes in bacteria. Chronic dietary Ni might thus encourage a microbiome with greater antibiotic resistance and inflammatory potential (due to concurrent heavy metal resistance mechanisms). Lowering Ni could reduce this selective pressure, possibly decreasing the reservoir of antibiotic resistance in the gut over time.[22]
Metabolic Changes	The gut microbiome of someone consuming a Ni-rich diet (e.g. high in whole grains, soy, cocoa) might produce different metabolic outputs. Methylglyoxal (MG) is a microbial and host metabolite that can cause inflammation if not detoxified; Ni-dependent GloI in gut bacteria could neutralize MG, perhaps allowing bacteria to ferment more aggressively without self-harm. A LNiD could lead to accumulation of MG in Ni-requiring bacteria, inhibiting their growth – effectively a form of metabolic brake on overactive fermentation. This is speculative but aligns with the observation that fermentative dysbiosis improved on LNiD.[23]
Symbiotic Effects	By curbing Ni-requiring microbes (typically pro-inflammatory species), LNiD may indirectly reduce intestinal inflammation, further helping beneficial microbes to flourish. Many Lactobacilli and Bifidobacteria do not utilize Ni; instead, they might even benefit from Ni reduction because it handicaps their competitors. The net result is a microbiome shift that parallels symptom improvement. For example, in a study of refractory celiac patients with persistent IBS-like symptoms, 80% of gastrointestinal and extra-intestinal symptoms improved after 3 months on a low-nickel diet, strongly suggesting that the diet modulated the underlying microbiota or immune triggers. Indeed, those patients had a high prevalence of Ni-related allergic mucositis and responded dramatically to Ni elimination. [24]

Clinical Conditions Improved with a Low‑Nickel Diet

Robust clinical evidence for LNiD has emerged in a variety of conditions, especially those straddling dermatology and gastroenterology. Below we outline key conditions where LNiD is clinically validated or suggested, along with the pathophysiological links to nickel:

Condition	Findings
Systemic Nickel Allergy Syndrome (SNAS)	Systemic Nickel Allergy Syndrome (SNAS) is the prototypical indication for LNiD. Patients with a history of Ni contact allergy experience systemic symptoms—eczema, GI distress, brain fog, and itching—after consuming Ni-rich foods. A Ni-restricted diet (<50 μg/day) for 1–2 months leads to symptom resolution in most cases. Diagnosis is confirmed by symptom recurrence within 24–48 h following a supervised oral Ni challenge (1.25–5 mg Ni sulfate). [25] In one study, 64% of nickel-sensitive dermatitis patients improved short-term on LNiD, with 44% maintaining benefit at 1–2 years. Those with moderate patch-test reactivity respond better than those with strong reactivity.[26] LNiD minimizes antigen exposure and halts both skin and gut inflammation.[27]
Refractory Eczema and Allergic Dermatitis	In nickel-allergic individuals with chronic or vesicular eczema—particularly when unexplained by contact exposures—dietary Ni may be a contributing factor. Veien et al. (1993) found that a significant subset improved on LNiD,[28] and case reports have documented resolution of hand eczema with Ni avoidance, especially in vesicular forms.[29] Clues include dermatitis flares after Ni-rich foods (e.g. chocolate, soy, whole grains) or systemic rashes (e.g. baboon syndrome). LNiD is often paired with other interventions like Ni avoidance and disulfiram chelation. While not all eczema cases are Ni-responsive, a 1–2 month LNiD trial is a low-risk strategy in Ni-sensitized patients with refractory dermatitis.[30]
Irritable Bowel Syndrome (IBS)	Nickel allergy is increasingly recognized as a contributor to IBS, particularly via allergic contact mucositis that mimics IBS symptoms such as bloating, abdominal pain, and altered bowel.[31] Over 30% of the general population is estimated to have subclinical Ni ACM, potentially overlapping with IBS diagnoses.[32] IBS patients show a higher prevalence of Ni hypersensitivity than controls, and a low-nickel diet (LNiD) has been shown to significantly improve GI symptoms in pilot studies.[33] Borghini et al. also found LNiD effective in IBS-like symptoms in endometriosis.[35] In celiac patients with persistent IBS-like complaints despite a gluten-free diet, 19.6% had Ni allergy, and all improved on LNiD, with >80% symptom relief and significant GSRS score reductions.[36] These results highlight dietary Ni as an underdiagnosed trigger for IBS, particularly in Ni-sensitive individuals. A history of metal allergy or symptom flares after high-Ni foods should raise suspicion; diagnosis can be confirmed with patch testing or oral mucosa patch test (Ni omPT). In confirmed cases, a LNiD can yield broad symptom relief, including in those misdiagnosed with refractory celiac disease.
Gastroesophageal Reflux Disease (GERD)	Nickel has emerged as a potential contributor to GERD via both allergic and non-allergic mechanisms. Ni allergy appears more prevalent in GERD patients than the general population, and many GERD trigger foods (e.g. chocolate, coffee, nuts, whole grains) are high in Ni—possibly exacerbating symptoms via LES relaxation, mucosal irritation, or neurogenic inflammation.[37] In a 2021 pilot study, 95% of GERD patients (19/20) experienced symptom reduction after 8 weeks on a low-nickel diet (LNiD).[38] Notably, symptom improvement occurred regardless of Ni patch test status, suggesting that LNiD benefits may extend beyond classical allergy. GERD-HRQL scores improved significantly, supporting the idea that Ni restriction could mitigate reflux via multiple pathways. Clinically, LNiD may be especially helpful for refractory GERD patients, even in the absence of confirmed Ni allergy.
Chronic Fatigue Syndrome (CFS) and Fibromyalgia	Nickel exposure has been linked to chronic fatigue syndrome (CFS) and fibromyalgia through its potential to drive systemic inflammation and immune activation. Ni allergy was detected in 36% of CFS patients vs 19% of controls (p < 0.05), and many patients with unexplained fatigue or myalgia report symptom improvement after reducing dietary heavy metals.[39] Nickel may contribute to fatigue via chronic innate immune activation (e.g., TLR4-mediated cytokine release) or oxidative stress. Nickel hypersensitivity often overlaps with other metal allergies (e.g., mercury), which have also been implicated in fatigue and autoimmune phenomena.[40] While large trials are lacking, small studies and case reports suggest that identifying Ni allergy and implementing a low-nickel diet (LNiD), along with removal of Ni-containing dental materials or supplements when applicable, can improve fatigue and pain. Given its safety and biologic plausibility, LNiD is a reasonable option in select patients with refractory fatigue or fibromyalgia.[41]
Endometriosis with IBS-like symptoms	Endometriosis often presents with IBS-like symptoms and systemic complaints such as fatigue and allergies. A 2020 open-label study found a high prevalence of nickel allergic contact mucositis (Ni ACM) among women with endometriosis and gastrointestinal symptoms. After 2–3 months on a low-nickel diet (LNiD), participants experienced significant relief in both GI and gynecological symptoms. These findings suggest that nickel hypersensitivity may contribute to gut dysfunction in endometriosis and that dietary Ni restriction can reduce inflammatory burden and improve quality of life. Given endometriosis’ inflammatory and immune-mediated features, clinicians should consider Ni allergy testing and LNiD in patients with refractory digestive complaints. This supports the broader view that LNiD may benefit syndromes characterized by immune and gut dysregulation, beyond classical SNAS.[42]
Helicobacter pylori Infection	Helicobacter pylori depends on Ni-containing enzymes—urease and [NiFe] hydrogenase—for survival in the gastric environment. A pilot study by Campanale et al. showed that adding a Low-nickel diet to standard triple therapy significantly increased H. pylori eradication rates (85% vs 46%).[43] This approach may also be relevant to other conditions hallmarked by urease-positive pathogens that require nickel (e.g., Proteus, Ureaplasma). Clinically, initiating a low-Ni diet during H. pylori treatment may enhance antibiotic efficacy by depriving the bacterium of its essential cofactor. This represents a novel, non-pharmacologic strategy to weaken microbial virulence through targeted dietary manipulation.

Research Feed

References

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