A Systematic Review of Molecular Hydrogen Therapy in Cancer Management

Abstract

Background: Cancer remains a challenging target to cure, with present therapeutic methods unable to exhibit restorative outcomes without causing severe negative effects. Molecular hydrogen (H2) has been reported to be a promising adjunctive therapy for cancer treatment, having the capability to induce anti-proliferative, anti-oxidative, pro-apoptotic and anti-tumoural effects. This review summarises the findings from various articles on the mechanism, treatment outcomes, and overall effectiveness of H2 therapy on cancer management.

Methods: Using Cochrane, PubMed, and Google Scholar as the search engines, full-text articles in the scope of the study, written in English and within 10 years of publication were selected.

Results: Out of the 677 articles, 27 articles fulfilled the eligibility criteria, where data was compiled into a table, outlining the general characteristics and findings. Throughout the different forms of H2 administration, study design and types of cancers reported, outcomes were found to be consistent.

Conclusion: From our analysis, H2 plays a promising therapeutic role as an independent therapy as well as an adjuvant in combination therapy, resulting in an overall improvement in survivability, quality of life, blood parameters, and tumour reduction. Although more comprehensive research is needed, given the promising outcomes, H2 is worth considering for use as a complement to current cancer therapy.

Keywords: Anti-tumour; cancer; complementary therapy; molecular hydrogen; oxidative stress.

Figure 1

PRISMA Flow Diagram for the Systematic Review of Molecular Hydrogen Research on Cancer in the Past 10 Years

Figure 2

Activation of PPAR pathway inducing fatty acid oxidation (diagram created using BioRender software). Under normal circumstances, PPARɑ up-regulates the peroxisomal β-oxidation by increasing the expression of the enzyme AOX, which facilitates the conversion of Acyl-CoA. However, when subjected to HRW, the hydrogen group lowers the activation of PPARɑ, resulting in the reduced expression of AOX. VLCFA very-long-chain fatty acid, HW hydrogen water, PPARα peroxisome proliferator-activated receptor alpha, AOX acyl-coenzyme A oxidase, FAD flavin adenine dinucleotide, O2 oxygen, H2O2 hydrogen peroxide