Low‑Nickel Diet (LNiD)

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

May 18, 2025

A low-nickel diet (NiD) is a therapeutic dietary intervention that eliminates high-nickel foods, primarily plant-based sources such as legumes, nuts, whole grains, and cocoa, to reduce systemic nickel exposure. It is clinically validated for managing systemic nickel allergy syndrome (NAS) and nickel-induced eczema. Its relevance is well-established in microbiome modulation, with studies demonstrating clinical benefits in conditions such as endometriosis, fibromyalgia, irritable bowel syndrome, and ERD.

Research feed

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Last Updated: March 9, 2024

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 [file-8ise6rvvaqbqmlci4hmqzd]. 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] The benefit is immunologic, not metabolic—SNAS patients do not retain excess Ni; rather, they react immunologically to normal exposures. 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.^[34][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

July 29, 2020

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This study provides strong evidence that nickel-rich foods in a gluten-free diet can trigger or exacerbate IBS-like gastrointestinal and extraintestinal symptoms in a subset of celiac disease patients, even when the disease is in serological and histological remission. The findings highlight the importance of nickel sensitivity in the pathogenesis of these relapsing symptoms, suggesting that a low-nickel diet can be a valuable intervention to improve patient outcomes. The use of the nickel oral mucosa patch test (Ni omPT) was also validated as a reliable diagnostic tool for identifying nickel-sensitive patients.

What was studied?

The study investigated the prevalence and effects of nickel allergic contact mucositis (Ni ACM) in celiac disease (CD) patients who were on a proper gluten-free diet (GFD) but experienced a relapse of Irritable Bowel Syndrome (IBS)-like gastrointestinal and extraintestinal symptoms. The main goal was to determine whether nickel-rich foods in a gluten-free diet could trigger these symptoms and to evaluate the impact of a low-nickel diet (LNiD) on symptom reduction in these patients. This pilot study also explored the use of the nickel oral mucosa patch test (Ni omPT) to diagnose nickel sensitivity in these patients.

Who was studied?

The study involved 102 consecutive adult celiac disease patients (74 females, 28 males, mean age 42.3 ± 7.4 years) who had been on a gluten-free diet for at least 12 months and were in serological and histological remission of their disease. These patients were selected because they reported relapsing or persisting gastrointestinal and extraintestinal symptoms despite proper adherence to a GFD. After exclusions based on comorbid conditions like lactose intolerance and Helicobacter pylori infection, 20 patients (all female, age 23–65 years) were included in the final analysis.

What were the most important findings?

In a cohort of 20 patients with persistent symptoms despite adherence to a gluten-free diet (GFD), all tested positive for nickel sensitivity via the nickel oral mucosa patch test (Ni omPT), confirming a diagnosis of nickel allergic contact mucositis (Ni ACM). Following prolonged GFD, 83.3% of patients experienced a relapse of symptoms, including abdominal pain, bloating, loose stools, and fatigue, coinciding with high dietary nickel intake from nickel-rich gluten-free foods such as corn. Implementing a low-nickel diet (LNiD) for three months improved 83.4% of total symptoms, with 41.7% reaching statistical significance. Notably, 80% of gastrointestinal and 88.9% of extraintestinal symptoms improved, including significant relief from abdominal pain, swelling, fatigue, and dermatitis. Combining LNiD with GFD restored patients' well-being to levels comparable to those previously achieved by GFD alone, strongly implicating nickel sensitivity as the primary driver of symptom relapse.

What are thegreatest implications of this study?

This study provides strong evidence that nickel-rich foods in a gluten-free diet can trigger or exacerbate IBS-like gastrointestinal and extraintestinal symptoms in a subset of celiac disease patients, even when the disease is in serological and histological remission. The findings highlight the importance of nickel sensitivity (Ni ACM) in the pathogenesis of these relapsing symptoms, suggesting that a low-nickel diet (LNiD) can be a valuable intervention to improve patient outcomes. The use of the nickel oral mucosa patch test (Ni omPT) was also validated as a reliable diagnostic tool for identifying nickel-sensitive patients.

Clinically, these results imply that gastroenterologists should consider nickel sensitivity as a differential diagnosis in celiac patients who are non-responsive to a GFD and continue to experience symptoms. The integration of a low-nickel dietary approach alongside the GFD may become an essential part of managing non-responsive celiac disease with overlapping IBS-like symptoms. Further large-scale studies are needed to confirm these findings and refine dietary guidelines for managing nickel sensitivity in this population.

January 28, 2020

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What was studied?

This open-label pilot study investigated the prevalence of nickel allergic contact mucositis (Ni ACM) in women with endometriosis who presented with irritable bowel syndrome (IBS)-like symptoms and assessed the efficacy of a low-nickel diet (LNiD) in ameliorating gastrointestinal, extra-intestinal, and gynecological symptoms. The study aimed to determine whether nickel (Ni) sensitivity contributes to the symptom burden in endometriosis and whether dietary nickel restriction can serve as a therapeutic intervention.

Who was studied?

The study initially screened 83 women of reproductive age diagnosed with endometriosis via imaging or laparoscopy who also experienced at least three gastrointestinal symptoms scoring ≥5 on the Gastrointestinal Symptom Rating Scale (GSRS). After applying exclusion criteria (e.g., celiac disease, IgE-mediated food allergies), 47 patients remained eligible. Sixteen dropped out due to the dietary restrictions, leaving 31 who completed the study. Each participant underwent a nickel oral mucosa patch test (omPT) to identify Ni ACM. Of the 31 patients, 28 (90.3%) tested positive. All participants followed a low-Ni diet for three months, with symptoms reassessed using the GSRS at baseline (T0) and after the intervention (T1).

What were the most important findings?

Nickel ACM was highly prevalent among women with endometriosis and IBS-like symptoms, with 90.3% of study completers testing positive via omPT. All patients who adhered to a three-month low-nickel diet experienced statistically significant reductions in all 15 gastrointestinal symptoms, including bloating, abdominal pain, diarrhea, and constipation. Additionally, the LNiD led to meaningful improvements in seven extra-intestinal symptoms such as headache, fatigue, and joint pain, as well as in hallmark gynecological symptoms of endometriosis: chronic pelvic pain, dysmenorrhea, and dyspareunia. These improvements underscore a systemic role of nickel sensitivity in the symptomatology of endometriosis beyond localized pelvic pathology.

From a microbiome perspective, Ni ACM reflects a low-grade inflammatory response that disrupts mucosal immune regulation and intestinal barrier integrity—two key mechanisms implicated in microbial dysbiosis. Though microbiome composition was not directly assessed, the systemic inflammatory profile induced by dietary nickel may favor enrichment of nickel-tolerant pathobionts, including certain Gammaproteobacteria and urease-producing bacteria, while impairing barrier-supporting commensals. This aligns with broader hypotheses on the metallomic drivers of endometriosis-associated dysbiosis.

What are the greatest implications of this study?

This study provides compelling evidence that nickel hypersensitivity may be a clinically significant and previously underrecognized contributor to the gastrointestinal and systemic symptom burden in endometriosis. It positions Ni ACM not only as a comorbidity but as a potential driver of symptom exacerbation, offering a new lens through which to understand IBS-like manifestations in endometriosis. Importantly, the successful use of a targeted dietary intervention based on objective testing (omPT) introduces a personalized medicine framework that could improve quality of life while minimizing unnecessary dietary restrictions, such as those imposed by low-FODMAP diets. If validated in larger, randomized cohorts, the incorporation of nickel testing and dietary counseling into standard endometriosis management could represent a low-risk, high-reward clinical advance.

November 21, 2020

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What was studied?

This prospective pilot study investigated the therapeutic potential of a Low‑Nickel diet (LNiD) in patients with refractory gastroesophageal reflux disease (GERD) and explored whether epicutaneous patch testing for nickel (Ni) could predict dietary responsiveness. The researchers sought to determine whether dietary nickel contributes to GERD pathophysiology and whether identifying nickel sensitivity via patch testing can inform clinical decision-making.

Who was studied?

Twenty adult patients with a confirmed diagnosis of GERD were enrolled at a single site in West Virginia. All had persistent GERD symptoms despite at least three months of proton pump inhibitor (PPI) therapy and a GERD-HRQL score ≥30 at baseline. Patch testing was conducted using nickel sulfate and three additional common allergens (cobalt chloride, balsam of Peru, and cinnamic aldehyde), but patients were blinded to their patch test results until the end of the study. All participants adhered to a standardized low-nickel diet for eight weeks. GERD symptom severity was evaluated pre- and post-intervention using the validated GERD Health-Related Quality of Life (GERD-HRQL) questionnaire, which assesses heartburn, regurgitation, and overall symptom burden.

What were the most important findings?

Nineteen out of twenty participants (95%) reported substantial improvement in GERD symptoms after following the low-nickel diet. Mean total GERD-HRQL scores dropped by 27.05 points, while mean heartburn and regurgitation scores declined by 11.45 and 10.85 points, respectively—all statistically significant reductions (p <0.001). Improvements were consistent across participants, regardless of nickel patch test results. Although 3 participants (15%) tested positive for nickel sensitivity, their symptom improvement was only modestly different from those who tested negative. Importantly, the magnitude of symptom reduction was not significantly correlated with patch test status. Nearly half of participants (45%) reported being satisfied with their GERD symptoms post-intervention, a notable shift from the 95% dissatisfaction rate at baseline.

While the study did not measure microbiome parameters directly, the data suggest nickel may act as a dietary irritant that exacerbates esophageal inflammation independently of overt allergic sensitization. This opens the possibility that dietary nickel contributes to barrier disruption or mucosal immune activation along the upper gastrointestinal tract—mechanisms well-documented in nickel-induced contact mucositis and consistent with microbial shifts observed in conditions like irritable bowel syndrome IBS and H. pylori infection, both of which have been responsive to nickel restriction.

What are the greatest implications of this study?

This study establishes that a low-nickel diet may be a powerful non-pharmacologic intervention for GERD, even in patients unresponsive to standard therapy. The data challenge the assumption that only patients with demonstrable nickel allergy benefit from nickel restriction, suggesting that dietary nickel may provoke inflammation through mechanisms not captured by skin-based patch testing. This has important clinical implications: patch test–guided exclusion diets may miss a substantial subset of patients who stand to benefit from nickel reduction. The findings justify broader consideration of dietary nickel as a contributing factor in GERD and potentially other inflammatory gastrointestinal conditions. Importantly, the intervention had excellent adherence and tolerability, supporting its viability in routine care. Future randomized, controlled trials with larger sample sizes and microbial/metallomic profiling are warranted to validate these findings and explore underlying mechanisms.

January 28, 2020

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What Was Studied?

This pilot study investigated the prevalence of nickel (Ni) allergic contact mucositis (ACM) in women with endometriosis who experience gastrointestinal symptoms and evaluated the effects of a low-nickel diet on these symptoms. The study focused on assessing the gastrointestinal, extra-intestinal, and gynecological symptom reductions associated with Ni ACM and dietary interventions.

Who Was Studied?

The study enrolled 84 women of reproductive age diagnosed with endometriosis who reported significant gastrointestinal symptoms. Thirty-one participants completed the study, undergoing a diagnostic nickel oral mucosa patch test (omPT) and a subsequent three-month low-nickel diet intervention. Participants were evaluated using symptom questionnaires both at baseline and after dietary changes.

What Were the Most Important Findings?

The study found that 90.3% of participants tested positive for Ni ACM, suggesting a high prevalence of nickel sensitivity among women with endometriosis.Following three months of adhering to a low-nickel diet, significant reductions in all evaluated symptoms were reported. Gastrointestinal symptoms such as abdominal pain, bloating, and diarrhea showed marked improvement. Extra-intestinal symptoms, including fatigue and headaches, and gynecological symptoms such as pelvic pain and dysmenorrhea, also exhibited statistically significant decreases. These findings indicate that nickel sensitivity may contribute to the symptomatic burden of endometriosis, and dietary interventions targeting nickel can alleviate these issues.

The study suggests a potential mechanistic link between nickel exposure, immune responses, and the exacerbation of endometriosis symptoms. Major microbial associations (MMAs) relevant to this context include those influenced by dietary changes, although specific microbiome alterations were not detailed.

What Are the Greatest Implications of This Study?

This research highlights nickel sensitivity as a significant yet previously under-recognized contributor to gastrointestinal and systemic symptoms in endometriosis patients. The findings suggest that incorporating nickel sensitivity screening and low-nickel dietary recommendations could represent a transformative approach to symptom management in endometriosis. Although the sample size was small, the results offer strong preliminary evidence for revising dietary protocols in clinical practice to include low-nickel guidelines, potentially improving the quality of life for patients.

January 17, 2017

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What was studied?

This pilot study evaluated the prevalence of nickel (Ni) allergy in individuals diagnosed with irritable bowel syndrome (IBS) and investigated the clinical efficacy of a low-nickel diet (LNiD) in this population. Specifically, the authors assessed the impact of the dietary intervention on gastrointestinal symptoms, intestinal permeability, quality of life, and psychological status in Ni-sensitized IBS patients. It also analyzed how the severity of allergic skin reactions and IBS subtypes might influence changes in gut permeability during LNiD intervention.

Who was studied?

Twenty patients fulfilling Rome III criteria for IBS and exhibiting Ni sensitization (confirmed by positive patch test) were enrolled. These individuals had undergone a thorough exclusion process to rule out other organic gastrointestinal disorders, infections, or metabolic dysfunctions. The sample predominantly consisted of females, with most presenting the diarrhea-predominant (IBS-D) subtype. After baseline evaluation of intestinal permeability, psychological wellbeing, and gastrointestinal symptoms, participants followed a low-Ni diet for three months. Compliance was monitored via dietary diaries. Post-intervention assessments included repeated clinical questionnaires and permeability testing using ⁵¹Cr-EDTA for patients with initially elevated intestinal permeability. A control group of healthy subjects matched by age, sex, and socioeconomic background was included for comparison in permeability analysis.

What were the most important findings?

A strikingly high prevalence of nickel allergy was found among IBS patients, particularly in females. The LNiD significantly alleviated gastrointestinal symptoms (except vomiting) and improved general well-being scores (notably bodily pain and physical functioning). Despite improvements in symptoms, all participants continued to show elevated intestinal permeability post-intervention, suggesting persistent barrier dysfunction possibly due to chronic mucosal immune activation. Interestingly, intestinal permeability changes (Δ⁵¹Cr-EDTA) varied by IBS subtype and allergic response severity. Patients with stronger Ni skin reactivity (++/+++) were more likely to experience worsened barrier function, while those with IBS-M or IBS-U subtypes exhibited improvement. Psychometric testing revealed widespread psychological distress, especially anxiety, supporting the established association between IBS and affective dysregulation. These findings reinforce the concept of systemic nickel allergy syndrome (SNAS) as a relevant comorbidity in IBS and point toward immune-mediated mechanisms involving CD4+ T cell infiltration and Th2 cytokines as underlying contributors to both gastrointestinal and systemic symptoms.

From a microbiome perspective, although the study did not directly assess microbial composition, its findings implicate Ni-induced barrier dysfunction as a potential facilitator of microbial dysbiosis. The interplay between metal exposure, gut immune activation, and barrier integrity represents a critical axis in microbiome-host interaction and warrants further microbial profiling in future studies.

What are the greatest implications of this study?

This study identifies a potentially overlooked driver of IBS symptoms—nickel hypersensitivity—and provides preliminary but compelling evidence for dietary nickel restriction as a therapeutic intervention in select IBS patients. Its implications extend to redefining subgroups within IBS, informing personalized nutrition strategies, and advancing the study of metal-induced gut dysfunction as a contributor to microbial dysbiosis. Moreover, it highlights the need for integrative care models that address metal exposure, gut permeability, immune status, and psychological health concurrently. Given that low-Ni diets do not restrict FODMAPs, this study also challenges prevailing dietary paradigms in IBS management by introducing a non-FODMAP, immune-targeted approach with mechanistic plausibility.

January 1, 2001

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What was studied?

This study investigated the relationship between nickel allergy, cigarette smoking, and dietary nickel intake in women diagnosed with chronic fatigue syndrome (CFS) and muscle pain. The primary aim was to evaluate the prevalence of nickel allergy in this population and explore how smoking and dietary nickel may trigger or exacerbate symptoms.

Who was studied?

The study involved 204 women aged 21 to 73 years with chronic fatigue and muscle pain, meeting the criteria for fibromyalgia and chronic fatigue syndrome but with no signs of autoimmune disorders. The participants underwent immune stimulation therapy using a Staphylococcus vaccine for six months, and their nickel allergy history, smoking habits, and treatment responses were analyzed.

What were the most important findings?

The study found that 52% of the women had a history suggestive of nickel allergy, and 28% were habitual smokers. Nickel allergy and smoking significantly influenced treatment outcomes, with non-allergic, non-smoking participants showing the highest treatment success rates (39%), compared to only 6% in allergic smokers. Additionally, two case reports highlighted the impact of dietary and smoking changes: one participant improved after quitting smoking and reducing dietary nickel intake, while another experienced sustained symptom relief by following a low-nickel diet. Notably, nickel hypersensitivity was associated with increased fatigue and muscle pain symptoms triggered by dietary nickel or cigarette smoke, both of which contain trace amounts of the metal. The findings indicate that systemic nickel allergy, potentially exacerbated by smoking or high dietary nickel, may contribute to chronic fatigue and muscle pain.

What are the greatest implications of this study?

This research emphasizes the importance of recognizing nickel allergy as a potential factor in chronic fatigue syndrome and muscle pain. The interplay between nickel hypersensitivity, dietary nickel intake, and smoking could have significant clinical implications. Managing nickel exposure through dietary adjustments such as a low-nickel diet and smoking cessation may serve as a non-invasive strategy to alleviate symptoms in affected patients. Furthermore, the study underscores the need for broader awareness and diagnostic consideration of systemic nickel allergy in chronic fatigue-related conditions, particularly in women.

December 11, 2022

•

What Was Reviewed?

The paper titled "I Am the 1 in 10—What Should I Eat? A Research Review of Nutrition in Endometriosis" provides an extensive review of the role of nutrition in the management and progression of endometriosis. The authors systematically explore various dietary factors and interventions, including antioxidants, polyphenols, omega-3 fatty acids, a low-nickel diet, and the Mediterranean diet, among others, in relation to their effects on inflammation, hormonal modulation, and oxidative stress in endometriosis patients.

Who Was Reviewed?

The review primarily evaluated research studies involving women diagnosed with endometriosis. It integrated findings from human clinical trials, observational studies, and in vitro research to synthesize current evidence on nutritional influences on endometriosis-related symptoms and disease progression.

What Were the Most Important Findings?

The review highlighted that endometriosis is a chronic inflammatory and estrogen-dependent condition where dietary modifications can play a pivotal role. It emphasized the following:

Antioxidants and Polyphenols: Foods rich in antioxidants, such as fruits, vegetables, and specific compounds like resveratrol, demonstrated anti-inflammatory and pro-apoptotic effects in reducing endometriosis severity. Polyphenols, especially phytoestrogens, can modulate estrogen activity, impacting endometriotic lesion growth.

Dietary Fats: Omega-3 fatty acids were shown to reduce inflammation and dysmenorrhea, while high consumption of omega-6 and trans fats increased risks.

Specific Diets: The Mediterranean diet, with its anti-inflammatory properties, low-FODMAP and low-nickel diets showed potential benefits in reducing gastrointestinal and systemic symptoms. Gluten-free diets also alleviated pain in a subset of patients.

Dairy and Vitamin D: Dairy consumption, particularly calcium- and vitamin D-rich products, was associated with reduced endometriosis risk. Vitamin D showed immunomodulatory effects, improving inflammatory responses.

Red Meat and Iron Overload: Excessive red meat consumption elevated estrogen and prostaglandin levels, exacerbating endometriosis. The condition was also linked to iron overload in peritoneal fluid, contributing to oxidative stress and infertility.

What Are the Greatest Implications of This Review?

The findings underscore the potential for personalized dietary interventions in endometriosis management, emphasizing the integration of anti-inflammatory, low-toxin, and nutrient-rich foods. Clinicians can leverage these insights to recommend diets tailored to reduce inflammation, regulate estrogen metabolism, and mitigate oxidative stress, thereby improving quality of life and fertility outcomes for patients. Furthermore, the review reinforces the importance of microbiome-targeted dietary strategies in addressing endometriosis-related dysbiosis.

April 22, 2022

•

Microbes •

What was reviewed?

The paper reviewed the influence of nickel on intestinal microbiota disturbances, drawing on 59 scientific publications from the past 20 years. The analysis focused on nickel’s dual role as an essential element for microbial enzymatic reactions and a disruptor of gut microbiota, especially under conditions of excessive exposure or systemic nickel allergy syndrome (SNAS).

Who was reviewed?

The review encompassed research involving humans, animals, and microbial models. Specific attention was given to populations exposed to high levels of nickel, individuals with SNAS, and animal studies demonstrating changes in microbial communities under nickel exposure.

What were the most important findings?

Nickel acts as a cofactor for metalloenzymes like urease, hydrogenase, and [NiFe]-hydrogenase, essential for microbial survival. However, excess nickel promotes dysbiosis, characterized by reductions in beneficial taxa and increases in nickel-resistant bacteria. In humans with SNAS, the microbiota showed decreased levels of beneficial genera such as Bifidobacterium and Lactobacillus, known for their probiotic effects and urease activity, and increases in nickel-tolerant taxa, including Clostridiaceae and Bacillaceae. Similarly, animal studies indicated reduced Verrucomicrobia and Bacteroidetes while promoting Escherichia coli and Enterococcus.

Nickel exposure also leads to an increased abundance of Bacteroides fragilis, Bacteroidales S24-7, and Interstinimonas, with a concurrent decline in Firmicutes, disrupting the Firmicutes-to-Bacteroidetes ratio, a critical marker of gut health. This imbalance contributed to systemic inflammation and altered immune responses. Moreover, nickel-reliant pathogens, such as Helicobacter pylori, which require Ni2+-dependent enzymes like urease for colonization, further highlighted nickel’s role in microbial pathogenicity. Probiotic strains such as Lactobacillus fermentum demonstrated detoxifying effects by metabolizing nickel, suggesting their therapeutic potential.

What are the greatest implications of this review?

The findings reveal that nickel exposure significantly alters gut microbial ecology, driving dysbiosis and systemic inflammation in susceptible populations. The rise of nickel-tolerant taxa, coupled with the decline of protective bacteria, underscores nickel’s role as a disruptor of gut homeostasis, contributing to conditions like obesity and SNAS. Probiotic supplementation, particularly strains capable of nickel detoxification, and dietary restrictions like a low-nickel diet, have shown promise in mitigating these effects. This review highlights the urgent need for dietary nickel regulations and further clinical studies on therapeutic interventions targeting nickel-induced microbial dysbiosis.

References

Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
IL-33 and IL-4 impair barrier functions of human vascular endothelium via different mechanisms.. Chalubinski M, Wojdan K, Luczak E, Gorzelak P, Borowiec M, Gajewski A, Rudnicka K, Chmiela M, Broncel M.. (Vascul Pharmacol. 2015.)
Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel.. Schmidt M, Raghavan B, Müller V, Vogl T, Fejer G, Tchaptchet S, Keck S, Kalis C, Nielsen PJ, Galanos C, Roth J, Skerra A, Martin SF, Freudenberg MA, Goebeler M.. (Nat Immunol. 2010.)
Chronic fatigue syndrome and nickel allergy.. Marcusson JA, Lindh G, Evengård B.. (Contact Dermatitis. 1999.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
Bacterial Exposure to Nickel: Influence on Adhesion and Biofilm Formation on Orthodontic Archwires and Sensitivity to Antimicrobial Agents.. Pavlic A, Begic G, Tota M, Abram M, Spalj S, Gobin I.. (Materials (Basel). 2021.)
Bacterial Exposure to Nickel: Influence on Adhesion and Biofilm Formation on Orthodontic Archwires and Sensitivity to Antimicrobial Agents.. Pavlic A, Begic G, Tota M, Abram M, Spalj S, Gobin I.. (Materials (Basel). 2021.)
The Effects of Low-Nickel Diet Combined with Oral Administration of Selected Probiotics on Patients with Systemic Nickel Allergy Syndrome (SNAS) and Gut Dysbiosis.. Lombardi F, Fiasca F, Minelli M, Maio D, Mattei A, Vergallo I, Cifone MG, Cinque B, Minelli M.. (Nutrients. 2020 Apr 9;12(4):1040.)
Beneficial Effects of a Low-Nickel Diet on Relapsing IBS-Like and Extraintestinal Symptoms of Celiac Patients during a Proper Gluten-Free Diet: Nickel Allergic Contact Mucositis in Suspected Non-Responsive Celiac Disease. . Borghini R, De Amicis N, Bella A, Greco N, Donato G, Picarelli A.. (Nutrients. 2020; 12(8):2277.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Low nickel diet: an open, prospective trial.. Veien NK, Hattel T, Laurberg G.. (J Am Acad Dermatol. 1993.)
Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.. Braga M, Quecchia C, Perotta C, Timpini A, Maccarinelli K, Di Tommaso L, Di Gioacchino M.. (Int J Immunopathol Pharmacol. 2013 Jul-Sep;26(3):707-16.)
Low nickel diet: an open, prospective trial.. Veien NK, Hattel T, Laurberg G.. (J Am Acad Dermatol. 1993.)
Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
Beneficial Effects of a Low-Nickel Diet on Relapsing IBS-Like and Extraintestinal Symptoms of Celiac Patients during a Proper Gluten-Free Diet: Nickel Allergic Contact Mucositis in Suspected Non-Responsive Celiac Disease.. Borghini R, De Amicis N, Bella A, Greco N, Donato G, Picarelli A.. (Nutrients. 2020; 12(8):2277.)
Beneficial Effects of a Low-Nickel Diet on Relapsing IBS-Like and Extraintestinal Symptoms of Celiac Patients during a Proper Gluten-Free Diet: Nickel Allergic Contact Mucositis in Suspected Non-Responsive Celiac Disease.. Borghini R, De Amicis N, Bella A, Greco N, Donato G, Picarelli A.. (Nutrients. 2020; 12(8):2277.)
Irritable Bowel Syndrome and Nickel Allergy: What Is the Role of the Low Nickel Diet?. Rizzi A, Nucera E, Laterza L, Gaetani E, Valenza V, Corbo GM, Inchingolo R, Buonomo A, Schiavino D, Gasbarrini A.. (J Neurogastroenterol Motil. 2017)
Beneficial Effects of a Low-Nickel Diet on Relapsing IBS-Like and Extraintestinal Symptoms of Celiac Patients during a Proper Gluten-Free Diet: Nickel Allergic Contact Mucositis in Suspected Non-Responsive Celiac Disease.. Borghini R, De Amicis N, Bella A, Greco N, Donato G, Picarelli A.. (Nutrients. 2020; 12(8):2277.)
Irritable Bowel Syndrome-Like Disorders in Endometriosis: Prevalence of Nickel Sensitivity and Effects of a Low-Nickel Diet. An Open-Label Pilot Study.. Borghini R, Porpora MG, Casale R, Marino M, Palmieri E, Greco N, Donato G, Picarelli A.. (Nutrients. 2020)
Beneficial Effects of a Low-Nickel Diet on Relapsing IBS-Like and Extraintestinal Symptoms of Celiac Patients during a Proper Gluten-Free Diet: Nickel Allergic Contact Mucositis in Suspected Non-Responsive Celiac Disease.. Borghini R, De Amicis N, Bella A, Greco N, Donato G, Picarelli A.. (Nutrients. 2020; 12(8):2277.)
The effect of a low-nickel diet and nickel sensitization on gastroesophageal reflux disease: A pilot study.. Yousaf A, Hagen R, Mitchell M, Ghareeb E, Fang W, Correa R, Zinn Z, Gayam S.. (Indian J Gastroenterol. 2021)
The effect of a low-nickel diet and nickel sensitization on gastroesophageal reflux disease: A pilot study.. Yousaf A, Hagen R, Mitchell M, Ghareeb E, Fang W, Correa R, Zinn Z, Gayam S.. (Indian J Gastroenterol. 2021)
Chronic fatigue syndrome and nickel allergy.. Marcusson JA, Lindh G, Evengård B.. (Contact Dermatitis. 1999 .)
Mercury and nickel allergy: risk factors in fatigue and autoimmunity.. Sterzl I, Procházková J, Hrdá P, Bártová J, Matucha P, Stejskal VD.. (Neuro Endocrinol Lett. 1999.)
Chronic fatigue syndrome and nickel allergy.. Marcusson JA, Lindh G, Evengård B.. (Contact Dermatitis. 1999 .)
Irritable Bowel Syndrome-Like Disorders in Endometriosis: Prevalence of Nickel Sensitivity and Effects of a Low-Nickel Diet. An Open-Label Pilot Study.. Borghini R, Porpora MG, Casale R, Marino M, Palmieri E, Greco N, Donato G, Picarelli A.. (Nutrients. 2020)
Nickel free-diet enhances the Helicobacter pylori eradication rate: a pilot study.. Campanale M, Nucera E, Ojetti V, Cesario V, Di Rienzo TA, D'Angelo G, Pecere S, Barbaro F, Gigante G, De Pasquale T, Rizzi A, Cammarota G, Schiavino D, Franceschi F, Gasbarrini A.. (Dig Dis Sci. 2014.)

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Low‑Nickel Diet (LNiD)

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Overview

Foods to Avoid on a Low-Nickel Diet

Foods to Include on a Low-Nickel Diet

Nickel, Immunity, and Barrier Function

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

Consequences of Excessive Dietary Nickel

Clinical Conditions Improved with a Low‑Nickel Diet

Research Feed

What was studied?

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What are thegreatest implications of this study?

What was studied?

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What were the most important findings?

What are the greatest implications of this study?

What was studied?

Who was studied?

What were the most important findings?

What are the greatest implications of this study?

What Was Studied?

Who Was Studied?

What Were the Most Important Findings?

What Are the Greatest Implications of This Study?

What was studied?

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What are the greatest implications of this study?

What was studied?

Who was studied?

What were the most important findings?

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What Was Reviewed?

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References

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