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A Functional Medicine H. Pylori Treatment Protocol

Medically reviewed by 
 
A Functional Medicine H. Pylori Treatment Protocol

Helicobacter pylori (H. pylori) is a bacteria that resides in the digestive tracts of over two-thirds of the world's population. For most, H. pylori infection is asymptomatic, but for a small percentage, serious consequences can occur due to the inflammation that this bacteria induces in the lining of the stomach and small intestine. Gastritis, ulcers, and, rarely, cancer can be caused by untreated H. pylori infection. This article will discuss testing and treatment recommendations for a successful functional medicine protocol for patients experiencing upper digestive symptoms associated with H. pylori.

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What is H. Pylori?

H. pylori is a spiral-shaped bacteria that most commonly causes infection in the stomach but can reside anywhere in the gastrointestinal (GI) tract. Up to 75% of the world's population has H. pylori bacteria in their guts, but most do not have associated illnesses. In susceptible people, H. pylori can cause peptic ulcer disease (PUD), gastritis, and stomach cancer. (1)

What Causes H. Pylori?

It is not clear how H. pylori is spread, but it appears that transmission typically occurs during childhood through fecal-oral and oral-oral modes of transmission. Person-to-person transmission within the same family is prevalent. Evidence suggests that H. pylori is harbored in dental plaque and may serve as a reservoir of infection. Environmental contamination of water and food products may also allow H. pylori to gain access to the stomach. (3, 7)

Factors associated with high infection rates include increasing age, African-American or Hispanic race, and living in crowded conditions or a developing country (2, 4).

Hyperchlorhydria, the presence of excess stomach acid in the stomach, is protective against H. pylori infection. Hypochlorhydria, or low stomach acid, fosters a more welcoming stomach environment so that H. pylori can more easily adhere to the stomach wall. Conditions that can cause hypochlorhydria include atrophic gastritis, pernicious anemia, and hypothyroidism. Aging and using proton pump inhibitors (PPIs) also reduce stomach acid levels.

Symptoms of H. Pylori

H. pylori burrows into the lower portion of the stomach and has many virulence factors that induce inflammation within the stomach lining. H. pylori produces urease to convert urea to ammonia, neutralizing stomach acid, which is antibacterial. Ammonia raises stomach pH and inflames the cells that line the stomach. H. pylori's proteolytic enzymes degrade the stomach's protective mucus layer, increasing the bacteria's damaging effects. (3)

Additionally, H. pylori secretes vacuole-forming cytotoxin (VacA) and cytotoxin-associated antigen (CagA). VacA and CagA are cytotoxic proteins with immune-activating properties, responsible for inducing cell death of the cells lining the stomach and causing stomach ulcers and cancers. (3)

H. pylori produces no symptoms in 90% of people with the bacteria. When signs and symptoms do occur, they are related to gastritis (inflammation of the stomach lining) and ulcers caused by the bacteria. H. pylori is the most common cause of PUD: 95% of patients with duodenal ulcers and 80% of patients with gastric ulcers are infected. Eradication of H. pylori in patients with PUD resolves associated symptoms and prevents recurrence. Gastritis is another common presentation of H. pylori infection; virtually all patients infected with H. pylori who undergo an endoscopic biopsy will have histological gastritis. (2)

The most common symptoms caused by H. pylori include (1, 4, 5)

  • Abdominal and stomach aching and burning
  • Gas and bloating
  • Loss of appetite and nausea
  • Frequent burping
  • Heartburn, reflux, or GERD
  • Unintentional weight loss
  • Vomiting
  • Black or bloody stools caused by bleeding ulcers

Functional Medicine Labs to Test for Root Cause of H. Pylori

Per the American College of Gastroenterology (ACG), testing for H. pylori should be performed in patients with an active or past history of PUD, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, gastric cancer, and dyspepsia (stomach upset or indigestion) (6).

Endoscopy is used to culture and biopsy the stomach mucosa for a rapid urease test or histologic staining. Because of the invasive nature of these tests, endoscopy is not recommended solely for diagnosing H. pylori and is only performed if indicated for other reasons.

The most common testing methods for diagnosing H. pylori infection and confirming eradication include the urea breath test and stool antigen testing. A serum IgG antibody test is an accepted method for screening in patients with PUD but is never recommended over breath or stool testing for eradication testing. (6)

The GI-MAP utilizes PCR technology to detect and quantify the growth of microbes contributing to gut dysbiosis and illness. This stool test also includes other markers of digestion, absorption, GI inflammation, and immune function to evaluate digestive health and function comprehensively. The GI-MAP is a popular stool test to order when specifically interested in H. pylori screening because it includes testing for H. pylori virulence factors and antibiotic susceptibility, which help to guide decision-making regarding the treatment of the infection.

Other Lab Tests to Check

Blood work, including a CBC, CMP, iron panel, and vitamin B12, can screen for common nutrient deficiencies and complications secondary to hypochlorhydria.

Hypothyroidism and pernicious anemia can predispose an individual to H. pylori infection by causing hypochlorhydria. A thyroid panel measuring TSH, free T4, and free T3 can diagnose hypothyroidism. The presence of intrinsic factor and anti-parietal cell antibodies suggest pernicious anemia.

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Conventional Treatment for H. Pylori

The ACG recommends offering antibiotic therapy to all patients who test positive for active H. pylori infection. Conventional treatment recommendations should consider the patient's history of penicillin allergy and macrolide exposure, the patient's ability to adhere to a multi-drug regimen, and the sensitivity of the regional H. pylori strain to the combination of antibiotics administered. (6)

Standard first-line protocols for the treatment of H. pylori include (6):

  • Clarithromycin triple therapy: PPI, clarithromycin, and amoxicillin or metronidazole for 14 days
  • Bismuth quadruple therapy: PPI, bismuth, tetracycline, and metronidazole or tinidazole for 10-14 days
  • Concomitant therapy: PPI, clarithromycin, amoxicillin, and metronidazole or tinidazole for 10-14 days

Functional Medicine Treatment Protocol for H. Pylori

Natural eradication of H. pylori is possible when combining multiple natural agents. Nonprescription therapy gives patients alternative options to antibiotic treatment, usually has fewer side effects than antibiotics, and is less likely to cause treatment resistance. Natural protocols are typically implemented for 4-8 weeks before reassessing.

Nutrition for H. Pylori

There is no one universally suggested diet for the eradication of H. pylori. Preliminary research suggests a low-nickel diet increases eradication rates in patients receiving conventional antibiotic therapy, but additional research is required to confirm this result.

Generally, a well-balanced, whole-food diet is recommended to prevent nutritional deficiencies commonly associated with H. pylori infection. Nutrients to emphasize in the diet for those with H. pylori include vitamins B12, C, E, and iron. (3)

Botanical Medicine for H. Pylori

Mastic gum which is the resin of the mastic bush (Pistacia lentiscus) native to the Mediterranean region is a medicinal remedy used for centuries for its antioxidant, anti-inflammatory, and anti-ulcer properties. Many laboratory studies confirm these properties and suggest that mastic gum has potent bactericidal actions against H. pylori, which human studies have supported. (8)

Plant compounds called polyphenols have potent anti-inflammatory and antioxidant properties and have been shown to inhibit the growth of H. pylori. A 2023 systematic review with meta-analysis concluded that the polyphenols in curcumin, cranberry, garlic, licorice, and broccoli are effective in eradicating H. pylori infection. (9)

Licorice and the sulforaphane extracted from broccoli have additional healing properties that can benefit patients with H. pylori (9). Not only has research shown licorice's effectiveness at eradicating H. pylori, but it also confirms the healing of ulcers in patients with H. pylori-induced PUD. Similar anti-inflammatory and anti-cancer effects are produced by sulforaphane in the stomach cells of patients with H. pylori-induced gastritis (8).

Berberine is a plant alkaloid with strong antimicrobial properties against bacteria, fungi, and parasites. Research has compared the use of berberine in quadruple therapy for H. pylori eradication to the conventional bismuth quadruple therapy protocol and has found it to be a comparable safe, effective alternative.

Nutritional Supplements for H. Pylori

Lactoferrin is an iron-binding protein found in mammalian milk that enhances immunity during pathogenic infection. Given its ability to improve the efficacy of multidrug eradication protocols, lactoferrin should be considered as an adjunct to any H. pylori eradication protocol.

N-Acetylcysteine (NAC) is the antioxidant precursor to glutathione. NAC can destroy bacterial biofilms, which plays a role in H. pylori colonization and resistance to antibiotic therapy. Adding NAC to eradication therapy can enhance treatment efficacy and should especially be considered in patients with a previous history of failed antibiotic treatment. (10)

Betaine hydrochloride (HCl) is commonly used as a supplemental digestive aid to replace stomach acid and reacidify the stomach environment. Betaine HCl can be supplemented with meals to support healthy digestion, while H. pylori is being eradicated. Caution should be used in patients with gastritis or active PUD, as HCl can aggravate preexisting stomach irritation and worsen digestive symptoms.

Probiotics improve the outcome of antibiotic treatment of H. pylori infection by reducing the side effects of antibiotic therapy and increasing the eradication rate of H. pylori. Lactobacillus and Bifidobacterium probiotics, Saccharomyces boulardii, and soil-based probiotics have all been effectively used with conventional eradication therapy protocols (11, 12).

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Summary

H. pylori is a bacteria that commonly colonizes the gastrointestinal tract and, for a small percentage of these people, will cause negative consequences, including gastritis, ulcers, and stomach cancer. Treatment is recommended for symptomatic patients for disease remission and recurrence prevention, but conventional antibiotic therapy requires multiple drug agents, given H. pylori's resistance to treatment. Side effects associated with multidrug regimens lead many people to search for alternative avenues for eradication. Specialty testing can provide insight into the severity of the infection and antibiotic resistance to guide therapy recommendations for successful H. pylori eradication. Many evidence-based natural agents are effective in H. pylori eradication, used in conjunction with one another or with conventional therapy.

The information provided is not intended to be a substitute for professional medical advice. Always consult with your doctor or other qualified healthcare provider before taking any dietary supplement or making any changes to your diet or exercise routine.
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Lab Tests in This Article

References

1. H. Pylori Infection: How Do You Get, Causes, Symptoms, Tests & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/21463-h-pylori-infection

2. Meurer, L.N., & Bower, D.J. (2002). Management of Helicobacter pylori infection. American Family Physician, 65(7), 1327–1336.

3. Öztekin, M., Yılmaz, B., Ağagündüz, D., et al. (2021). Overview of Helicobacter pylori Infection: Clinical Features, Treatment, and Nutritional Aspects. Diseases, 9(4), 66. https://doi.org/10.3390/diseases9040066

4. Helicobacter pylori (H. pylori) infection - Symptoms and causes - Mayo Clinic. (2022, May 5). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171

5. Helicobacter Pylori. (2019, November 19). Johns Hopkins Medicine. https://www.hopkinsmedicine.org/health/conditions-and-diseases/helicobacter-pylori

6. Chey, W.D., Leontiadis, G.I., Howden, C.W., et al. (2017). ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. The American Journal of Gastroenterology, 112(2), 212–239. https://doi.org/10.1038/ajg.2016.563

7. Kayali, S., Manfredi, M., Gaiani, F., et al. (2018). Helicobacter pylori, transmission routes and recurrence of infection: state of the art. Acta Bio-Medica : Atenei Parmensis, 89(8-S), 72–76. https://doi.org/10.23750/abm.v89i8-s.7947

8. Murali, M.R., Naveen, S.V., Son, C., et al. (2014). Current knowledge on alleviating Helicobacter pylori infections through the use of some commonly known natural products: bench to bedside. Integrative Medicine Research, 3(3), 111–118. https://doi.org/10.1016/j.imr.2014.04.001

9. Wang, Q., Feng, P., Li, Y., et al. (2023). Effect of polyphenol compounds on Helicobacter pylori eradication: a systematic review with meta-analysis. BMJ Open, 13(1), e062932. https://doi.org/10.1136/bmjopen-2022-062932

10. Makipour, K., & Friedenberg, F.K. (2011). The Potential Role of N-Acetylcysteine for the Treatment of Helicobacter pylori. Journal of Clinical Gastroenterology, 45(10), 841–843. https://doi.org/10.1097/mcg.0b013e31822be4d6

11. Feng, J., Wang, F., Qiu, X., et al. (2017). Efficacy and safety of probiotic-supplemented triple therapy for eradication of Helicobacter pylori in children: a systematic review and network meta-analysis. European Journal of Clinical Pharmacology, 73(10), 1199–1208. https://doi.org/10.1007/s00228-017-2291-6

12. Wang, F., Feng, J., Chen, P., et al. (2017). Probiotics in Helicobacter pylori eradication therapy: Systematic review and network meta-analysis. Clinics and Research in Hepatology and Gastroenterology, 41(4), 466–475. https://doi.org/10.1016/j.clinre.2017.04.004

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