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1H NMR- based metabolomics approaches as non-invasive tools for diagnosis of endometriosis A Comparative Study of Blood Levels of Manganese, Some Macroelements and Heavy Metals in Obese and Non-Obese Polycystic Ovary Syndrome Patients A Comparative Study of the Gut Microbiota Associated With Immunoglobulin a Nephropathy and Membranous Nephropathy A comparative study of the gut microbiota in immune-mediated inflammatory diseases-does a common dysbiosis exist? A comprehensive analysis of breast cancer microbiota and host gene expression A comprehensive analysis of breast cancer microbiota and host gene expression A cross-sectional analysis about bacterial vaginosis, high-risk human papillomavirus infection, and cervical intraepithelial neoplasia in Chinese women A cross-sectional pilot study of birth mode and vaginal microbiota in reproductive-age women A metabonomics approach as a means for identification of potentialbiomarkers for early diagnosis of endometriosis A More Diverse Cervical Microbiome Associates with Better Clinical Outcomes in Patients with Endometriosis: A Pilot Study A Multi-Omic Systems-Based Approach Reveals Metabolic Markers of Bacterial Vaginosis and Insight into the Disease A New Approach to Polycystic Ovary Syndrome: The Gut Microbiota A Review of the Anti-inflammatory Properties of Clindamycin in the Treatment of Acne Vulgaris A Systematic Review and Meta-Analysis of Premenstrual Syndrome with Special Emphasis on Herbal Medicine and Nutritional Supplements. Adherence to the Mediterranean Diet, Dietary Patterns and Body Composition in Women with Polycystic Ovary Syndrome (PCOS)

H pylori

March 10, 2025

Helicobacter pylori, a bacterium that colonizes the human stomach, is primarily known for its pathogenic role, particularly in causing peptic ulcers, chronic gastritis, and its association with gastric cancer. However, research has also suggested that H. pylori infection may have protective roles against other diseases. The concept of H. pylori exerting protective effects against certain […]

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Last Updated: March 10, 2025

Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.

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.

feedOverview
Gastroesophageal Reflux Disease (GERD) and Barrett’s Esophagus
Asthma and Allergic Conditions
Obesity and Metabolic Syndrome
Our Hypothesis
Theoretical Basis:
Considerations:
Controversies
feedInterventions
feedReferences

Overview

Helicobacter pylori, a bacterium that colonizes the human stomach, is primarily known for its pathogenic role, particularly in causing peptic ulcers, chronic gastritis, and its association with gastric cancer. However, research has also suggested that H. pylori infection may have protective roles against other diseases. The concept of H. pylori exerting protective effects against certain conditions arises from its longstanding co-evolution with humans, suggesting potential beneficial aspects to this relationship. Here are some areas where H. pylori has been proposed to have protective effects:

Gastroesophageal Reflux Disease (GERD) and Barrett’s Esophagus

Several studies have indicated that individuals infected with H. pylori, especially those harboring strains expressing the cytotoxin-associated gene A (CagA), have a lower risk of developing GERD and its complications, such as Barrett’s esophagus and esophageal adenocarcinoma. The proposed mechanism is that H. pylori-induced gastritis leads to decreased gastric acid secretion, reducing acid reflux into the esophagus and thus lowering the risk of GERD and its complications.

Asthma and Allergic Conditions

Epidemiological studies have suggested an inverse relationship between H. pylori infection and the prevalence of asthma and other allergic conditions. This observation is often discussed in the context of the “hygiene hypothesis,” which proposes that reduced exposure to infectious agents in childhood can increase susceptibility to allergic diseases by suppressing the natural development of the immune system. H. pylori, as a component of the human microbiota in more traditional living environments, may play a role in the maturation of the immune system in a way that protects against allergic diseases.

Obesity and Metabolic Syndrome

There is some evidence to suggest that H. pylori infection may be inversely associated with obesity and components of the metabolic syndrome. The mechanism behind this protective effect is not well-understood but may involve H. pylori-related alterations in hormones such as ghrelin and leptin, which play key roles in regulating appetite and metabolism.

Our Hypothesis

H. pylori relies on not one but two nickel-dependent enzymes, namely H2-uptake hydrogenase, and urease, for colonization and survival in the harsh, acidic environment of the stomach. These enzymes are crucial for neutralizing gastric acid (via urease) and utilizing hydrogen (via hydrogenase), thereby supporting H. pylori‘s potential pathogenicity and persistence.

We hypothesize that Helicobacter pylori may confer protection against various diseases such as Gastroesophageal Reflux Disease (GERD), Barrett’s Esophagus, asthma, allergic conditions, and obesity/metabolic syndrome, through nickel competition occurring in the upper gastrointestinal tract.

Theoretical Basis:

Nickel Utilization: The high requirement for nickel by H. pylori to activate its urease and hydrogenase enzymes could theoretically lead to competition for available nickel in the gastrointestinal tract, potentially limiting the growth of other nickel-dependent bacteria associated with the pathogenesis of inflammatory conditions like GERD and Barrett’s Esophagus, Asthma and Allergic Conditions, and Obesity and Metabolic Syndrome.

Considerations:

While this hypothesis could contribute to our understanding of H. pylori‘s complex role in human health and disease, it is speculative and would require substantial empirical evidence to be validated. The interplay between H. pylori, nickel availability, and the microbiome’s impact on disease risk involves intricate biochemical and ecological dynamics that are not fully understood. Moreover, the beneficial effects hypothesized would need to be carefully weighed against the well-documented pathogenic potential of H. pylori, including its role in peptic ulcer disease and gastric cancer.

Controversies

While the potentially protective role of H. pylori is intriguing, it is crucial to balance against the well-documented risks of H. pylori infection, including peptic ulcer disease and gastric cancer. The decision to eradicate H. pylori must consider the individual patient’s risk factors, clinical presentation, and the broader epidemiological context.

Furthermore, the idea of H. pylori exerting protective effects is still subject to debate and ongoing research. The relationship between H. pylori and human health exemplifies the complex interplay between humans and their microbiota, where a pathogen in one context may have beneficial effects in another. Ultimately, while H. pylori has been associated with certain protective effects against other diseases, its role as a pathogen with serious health consequences cannot be overlooked. Future research is necessary to continue to elucidate the complex roles of H. pylori in human health and disease.

Interventions

InterventionFindings
Low-Nickel DietIncorporating a low-nickel diet into the standard triple therapy for H. pylori infection can significantly enhance eradication rates. This dietary adjustment undermines the bacterium’s urease activity, which depends on nickel to neutralize stomach acid, thereby increasing H. pylori’s vulnerability to antibiotics like amoxicillin. [1] Nickel is crucial for H. pylori survival, activating urease for metabolism and colonization. HpNikR regulates urease expression in response to nickel levels, suggesting a nickel-free diet (NFD) may aid H. pylori eradication. A 52-patient trial compared NFD + triple therapy (LAC) vs. LAC alone. H. pylori eradication was significantly higher with NFD + LAC (84.6% vs. 46.1%, P <0.01). All regimens were well tolerated, with no dropouts. Further trials are needed to validate these findings. [2]
Green and Black Tea (Camellia sinensis)Animal studies suggest green tea catechins reduce H. pylori colony counts and inhibit growth, preventing gastric inflammation. No clinical trials exist, but a study on 150 dyspeptic patients found lower H. pylori infection rates in those consuming green/black tea weekly (45.2% vs. 64.8%), with logistic regression confirming a significant correlation (OR 0.45, 95% CI 0.21-0.95).[3]
Black Cumin (Nigella sativa)Nigella sativa exhibits anti-inflammatory, antioxidative, and antimicrobial effects, including potential H. pylori suppression via thymoquinone, thymol, and carvacrol. In a study of 88 patients, 2 g/day N. sativa plus omeprazole achieved a 66.7% eradication rate, statistically comparable to triple therapy. A second trial found adding 2 g/day N. sativa to bismuth-based quadruple therapy significantly improved H. pylori eradication (P = 0.01) and quality of life (P <0.05).[4]
HoneyHoney consumption was linked to a lower H. pylori infection rate (50.6% vs. 70.8%) in a study of 150 dyspeptic patients. A systematic review of 53 in vitro studies confirmed honey’s anti-H. pylori effects, with ≥10% concentration being effective. A trial combining N. sativa (6 g/day) and honey (12 g/day) for 14 days in 14 participants resulted in a 57.1% eradication rate and significantly reduced dyspeptic symptoms (P = 0.005). The mixture was well tolerated, with one dropout due to mild diarrhea.[5]
Cranberry (Vaccinium macrocarpon)Cranberry inhibits H. pylori adhesion and colonization. In a 271-infant trial, cranberry juice or Lactobacillus johnsonii La1 improved H. pylori eradication (14.9–22.9% vs. 1.5% control, P <0.01), but no additive effect was seen when combined. A 522-participant study found high-proanthocyanidin cranberry juice (44 mg twice daily for 8 weeks) reduced H. pylori infection by 20% (P <0.05). Encapsulated cranberry powder was ineffective. Cranberry juice was well tolerated.[6]
Mastic Gum (Pistacia lentiscus)Mastic gum may reduce H. pylori colonization, possibly due to its acidic fractions.
In a randomized trial, 350 mg and 1.05 g mastic gum (3x/day) achieved 30% and 38% eradication, respectively. Pantoprazole + mastic gum had no effect, while triple therapy had a 77% eradication rate (P = 0.01). Mastic gum was well tolerated with no dropouts. [7]
Licorice (Glycyrrhiza glabra)Licorice has antioxidant, anti-inflammatory, and anti-H. pylori properties, including DNA gyrase inhibition. In a 60-patient trial, licorice-based quadruple therapy achieved a 67% eradication rate, comparable to bismuth-based therapy (57%, P > 0.05), suggesting licorice as a potential bismuth substitute. A 120-patient study found licorice + triple therapy significantly improved H. pylori eradication (83.3% vs. 62.5%, P <0.05).[8]
Cinnamon Extract (Cinnamomum verum)Cinnamon extract inhibits H. pylori growth via eugenol, carvacrol, cinnamaldehyde, and antimicrobial effects. In a 15-patient pilot study, 40 mg cinnamon extract (2x/day for 28 days) had mixed effects on H. pylori colonization, with some reductions but overall increased UBT readings.
A 98-patient trial found cinnamon + antibiotics significantly improved H. pylori eradication (73.47% vs. 53.06%, P = 0.036) compared to antibiotics alone. Cinnamon was well tolerated.[9]
Polyunsaturated Fatty AcidsPolyunsaturated fatty acids (PUFAs) exhibit anti-H. pylori and anti-inflammatory effects, inhibiting Interleukin-8, mRNA, and protein expression in infected cells. In a 40-patient trial, despite higher PUFA intake, no significant changes were observed in H. pylori eradication or prostaglandin levels after six weeks. However, in a 15-patient trial using 2 g/day fish oil + black currant seed oil for 8 weeks showed 53% eradication of H. pylori. Further studies are needed to confirm efficacy.[10]

References

  1. Nickel Free-Diet Enhances the Helicobacter pylori Eradication Rate: A Pilot Study.. Campanale, M., Nucera, E., Ojetti, V. et al.. (Dig Dis Sci. 2014.)
  2. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  3. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  4. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  5. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  6. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  7. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  8. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  9. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)
  10. A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.. Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.. (IJ Pharmaceutical Research. 2022.)

Campanale, M., Nucera, E., Ojetti, V. et al.

Nickel Free-Diet Enhances the Helicobacter pylori Eradication Rate: A Pilot Study.

Dig Dis Sci. 2014.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

Saeed AbdiSara AtaeiMaede AbroonPantea Majma SanayeMohammad AbbasinazariAmir Farrokhianet al.

A Comprehensive Review of the Role of Complementary and Dietary Medicines in Eradicating Helicobacter pylori.

IJ Pharmaceutical Research. 2022.

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A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Class)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Family)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Genus)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Kingdom)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Order)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Phylum)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Species)