A 2025 rodent study integrated metabolomics and lipidomics analyses to investigate how sulforaphane treats a Helicobacter pylori infection:

“Helicobacter pylori (H. pylori) is a microaerobic Gram-negative bacterium that colonizes the gastric mucosa. Approximately half of the global population is infected with this bacterium, and it is classified as a group 1 carcinogen.

However, H. pylori infection does not typically present with obvious symptoms in the early stages, making it difficult to detect. Daily dietary interventions may be a relatively effective method for its prevention and treatment.

This study established an H. pylori-infected mouse model, to which sulforaphane was orally administered. H. pylori-low-dose and H. pylori-high-dose represent 4 weeks of gavage with 5 mg/kg/d and 20 mg/kg/d of sulforaphane after H. pylori colonization.

Metabolomics and lipidomics analysis of the effects of sulforaphane treatment on mouse serum. Stacked bar chart of the metabolites regulated by (A) low-dose and (B) high-dose sulforaphane treatment compared to the differential metabolites between the control group and H. pylori group.

Results showed that H. pylori infection significantly altered host amino acid and lipid levels, specifically manifested as abnormal serum glycerophospholipids and metabolic imbalances of amino acids, bile acids, glycerophospholipids, ceramides, and peptides in the liver. Sulforaphane treatment reversed these metabolic abnormalities, with high-dose sulforaphane exhibiting more prominent regulatory effects.

High-dose sulforaphane effectively restored hepatic metabolic disorders of amino acids, bile acids, and lipids, and ameliorated abnormal serum glycerophospholipid profiles. Regulation of key pathways such as glycine metabolism and glutathione metabolism constitutes an important basis for sulforaphane’s anti-H. pylori infection effects.

This study provides a comprehensive metabolic basis for understanding the role of sulforaphane as a dietary intervention in preventing and managing H. pylori-associated gastric diseases and lays a foundation for subsequent clinical translational research.”

https://www.mdpi.com/1422-0067/26/16/7791 “Therapeutic Effects of Sulforaphane on Helicobacter pylori-Infected Mice: Insights from High-Coverage Metabolomics and Lipidomics Analyses of Serum and Liver”

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A human equivalent to this study’s low sulforaphane dose is (5 mg x .081) x 70 kg = 28 mg, which is achievable by eating broccoli sprouts every day. Quadrupling 28 mg to a human equivalent of the study’s high sulforaphane dose would involve additional supplementation.

Another way to support this study’s glycine metabolism findings without high-dose sulforaphane is to supplement betaine (trimethylglycine) so that the body requires less choline-to-glycine synthesis. A synergistic effect can be achieved with taurine supplementation that enhances cysteine availability for the tripeptide (glutamate, cysteine, and glycine) glutathione synthesis by requiring less cysteine-to-taurine synthesis.