The good news from researchers is that you can lower your risk of stomach cancer by eating broccoli which contains a chemical that fights Helicobacter pylori (H. pylori) infections. One of the most common bacterial infections worldwide, these infections are a major cause of stomach cancer.

Jed Fahey, Sc. D., Johns Hopkins and colleagues report in the April issue of Cancer Prevention Research that infected Japanese patients, who ate broccoli sprouts every day for eight weeks, showed significantly lower levels of urease, a H. pylori infection bio-marker, in comparison to those under control to eat alfalfa.

In a mouse study carried out simultaneously, researchers found eating broccoli, which contains sulforaphane, also led to reduced bacterial colonization, with the researchers saying: 'The complementary mouse and human evidence suggests that sulforaphane may have a direct antibacterial effect on H. pylori, leading to reduced gastritis.'

A phytochemical, sulforaphane has powerful anti-bacterial effects against H. pylori infection, which is known to cause peptic ulcers and stomach cancer. In addition, sulforaphane also has anti-oxidative and anti-inflammatory effects via Nrf2, the transcription factor.

Researchers, to be able to document the compound's effects, randomized 48-H. pylori-infected Japanese patients, giving them either 70-gms of uncooked broccoli sprouts or alfalfa sprouts for eight weeks. Unlike broccoli, alfalfa lacks sulforaphanes.

At enrollment, H. pylori levels were measured via standard breath, serum, and stool tests, and again at four weeks, followed by eight weeks.

While, those who ate alfalfa showed no significant changes in urea levels, researchers found significantly lower levels of urea at eight weeks across all three tests, in those who ate broccoli every day, with their urea levels returning to baseline two months after they stopped eating broccoli on a daily basis.

Researchers also found broccoli to have reduced levels of pepsinogens I and II, the bio-markers for gastric inflammation.

In the accompanying animal study, a high-salt diet was given to infected mice to exaggerate the effects of H. pylori, showed reduced corpus gastritis and gastric mucosal inflammation when fed broccoli, with wild mice also showing a reduction in H. pylori colonization, though mice lacking the gene for Nrf2 (transcription factor), responsible for regulating the effects of sulforaphanes, showed no such reductions.

Researchers say this finding provides 'strong support for the integral role of the Nrf2 mechanism in protection against H. pylori-induced inflammation and gastritis,' and while more investigation is required, they concluded sulforaphane 'has promise both as an anti-bacterial agent directed against H. pylori and as a dietary preventive agent against the development of human gastric cancer.'