Chronic gastritis is one of the most common infections worldwide, with estimates indicating more than half of the global population currently have this disease to some degree.¹ Helicobacter pylori (H. pylori) infection is acknowledged to be the source of the disease in the majority of cases, causing progressive damage to the mucosal barrier which, in turn, leads to the development of various gastric disorders ranging from mild discomfort to more serious conditions such as peptic and duodenal ulcers, mucosa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma.^2,3 Increasing evidence demonstrates that normalisation of the gastric mucosa can occur with eradication of H. pylori.⁴

It has been suggested that one of the mechanisms via which H. pylori promotes gastritis is by inducing chronic oxidative stress in gastrointestinal mucosa, thereby causing mucosal injury.² BroccoPhane® is a concentrated broccoli extract standardised to sulforaphane, which is a potent inducer of phase 2 detoxification enzymes via Nrf2-Keap 1-depedent mechanisms, and has been shown to mitigate various kinds of oxidative stresses.⁵ H. pylori is able to colonise the acidic environment of the stomach via the production of large amounts of urease, which neutralises gastric acid and provides ammonia for bacterial protein synthesis.⁶ Sulforaphane has been shown to markedly inhibit urease activity and hence, the viability of H. pylori.² Sulforaphane extracted from the broccoli sprout is 10 to 100 times more effective in activating phase 2 enzymes than that from mature broccoli.⁷

Clinical trials with H. pylori-infected human subjects who consume broccoli sprout have shown that sulforaphane may have both a direct antibacterial effect on H. pylori, leading to reduced gastritis, as well as having an indirect (systemic) effect by induction of cytoprotective enzymes in the gastric mucosa.^2,8 In one study, fifty H. pylori-positive volunteers were randomised to receive either 70g/day of sulforaphane-rich 3-day-old broccoli sprouts (BS) (sulforaphane content approximately 6 μmol/g, which delivers a quantity of sulforaphane equivalent to between two and three servings of broccoli per day) or 70 g/day of alfalfa sprouts (AS), which don’t contain sulforaphane or other isothiocyanates.

At the end of the 8-week trial period and compared to baseline, intervention with broccoli sprouts, but not with placebo (AS), significantly decreased the levels of urease measured by the urea breath test and H. pylori stool antigen, both of which are biomarkers of H. pylori colonisation. Serum pepsinogen I and II (PGI/PGII) levels (used as a more robust indicator of change in gastric Inflammation) were also significantly reduced in the BS group but not in placebo, when compared to baseline. A significant increase in the pepsinogen I/II ratio is considered a reliable biomarker for successful H. pylori eradication.⁹ The ratio of PGI to PGII increased significantly during the intervention in the BS group, with no change seen in the AS group. Biomarker values recovered to their original levels 2-6 months after treatment was discontinued indicating that BS treatment reduced H. pylori colonisation and associated gastric inflammation, but did not result in complete eradication long term.

These findings highlight the need for practitioners to consider the beneficial role of dietary and supplemental sources of sulforaphane as part of an overall treatment protocol in supporting patients with gastric dysbiosis as a result of H. pylori infection.

Practitioners should consider the following treatment approaches:

• Consider a supplement for at least 8 weeks which includes a high dose and concentrated broccoli extract standardised to sulforaphane (eg. Broccophane® which is 10 to 100 times more effective in activating phase 2 enzymes than that from mature broccoli) to reduce colonisation and attenuate gastritis in pylori infections.
• Educate patients to incorporate more vegetables from the cruciferous family into their diet, as they are rich in the active component sulforaphane, as well as other nutrients and fibre to support liver detoxification and gastrointestinal function. 
• For local gut inflammation and to support the structural integrity of the GIT include high dose glutamine in combination with a prebiotic (i.e. inulin, Larch arabinogalactans, pectin, kiwi fruit).
• Educate patients on diet and lifestyle habits that negatively affect gastrointestinal health, such as an increased intake of highly processed foods and alcohol, cigarette smoking, eating on the run or when stressed, and not chewing their food adequately.

 

References

1. Sipponen, P. and H.I. Maaroos, Chronic gastritis. Scand J Gastroenterol, 2015. 50(6): p. 657-67.
2. Yanaka, A., Role of Sulforaphane in Protection of Gastrointestinal Tract Against H. pylori and NSAID-Induced Oxidative Stress. Curr Pharm Des, 2017. 23(27): p. 4066-4075.
3. Ayala, G., et al., Exploring alternative treatments for Helicobacter pylori infection. World Journal of Gastroenterology, 2014. 20(6): p. 1450-1469.
4. Lahner, E., M. Carabotti, and B. Annibale, Treatment of Helicobacter pylori infection in atrophic gastritis. World Journal of Gastroenterology, 2018. 24(22): p. 2373-2380.
5. Chang, Y.W., et al., The Effects of Broccoli Sprout Extract Containing Sulforaphane on Lipid Peroxidation and Helicobacter pylori Infection in the Gastric Mucosa. Gut and Liver, 2015. 9(4): p. 486-493.
6. Graham, D.Y. and M. Miftahussurur, Helicobacter pylori urease for diagnosis of Helicobacter pylori infection: A mini review. Journal Of Advanced Research, 2018. 13: p. 51-57.
7. Fahey, J.W., Y. Zhang, and P. Talalay, Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proc Natl Acad Sci U S A, 1997. 94(19): p. 10367-72.
8. Yanaka, A., et al., Dietary sulforaphane-rich broccoli sprouts reduce colonization and attenuate gastritis in Helicobacter pylori-infected mice and humans. Cancer Prev Res (Phila), 2009. 2(4): p. 353-60.
9. Osumi, H., et al., A significant increase in the pepsinogen I/II ratio is a reliable biomarker for successful Helicobacter pylori eradication. PLoS One, 2017. 12(8): p. e0183980-e0183980.