Molecular Hydrogen as a medical gas for the treatment of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: possible efficacy based on a literature review, by Shin-ichi Hirano, Yusuke Ichikawa, Bunpei Sato, Yoshiyasu Takefuji and Fumitake Satoh in Front. Neurol., 11 April 2022 [doi.org/10.3389/fneur.2022.841310]
Review article:
Conclusion:
Since H2 ameliorates mitochondrial dysfunction, we herein reviewed the literature for the anti-fatigue effects of H2 in animal studies and human clinical trials. The findings of the literature review suggested that H2 exerts anti-fatigue effects, and that these effects may involve not only the direct scavenging of mitochondria-generated ROS by H2, but also its antioxidant and anti-inflammatory effects through the regulation of gene expression.
Molecular hydrogen =H2 = dihydrogen = hydrogen gas
Since mitochondrial dysfunction is also involved in the etiology of ME/CFS, the literature review also suggested that the anti-fatigue effects of H2 in animal and human clinical studies indicate a possible ameliorative effect of H2 on ME/CFS. Since “long COVID” or “post COVID,” the “sequelae” of COVID-19, may be similar to ME/CFS, there is an urgent need to develop precise therapies and substances for ME/CFS. H2 gas may be an effective medical gas for the treatment of ME/CFS.
A possible mechanism by which H2 ameliorates mitochondrial dysfunction in ME/CFS patients.
Review abstract:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disorder that is characterized by fatigue that persists for more than 6 months, weakness, sleep disturbances, and cognitive dysfunction. There are multiple possible etiologies for ME/CFS, among which mitochondrial dysfunction plays a major role in abnormal energy metabolism.
The potential of many substances for the treatment of ME/CFS has been examined; however, satisfactory outcomes have not yet been achieved. The development of new substances for curative, not symptomatic, treatments is desired. Molecular hydrogen (H2) ameliorates mitochondrial dysfunction by scavenging hydroxyl radicals, the most potent oxidant among reactive oxygen species. Animal experiments and clinical trials reported that H2 exerted ameliorative effects on acute and chronic fatigue.
Therefore, we conducted a literature review on the mechanism by which H2 improves acute and chronic fatigue in animals and healthy people and showed that the attenuation of mitochondrial dysfunction by H2 may be involved in the ameliorative effects.
Although further clinical trials are needed to determine the efficacy and mechanism of H2 gas in ME/CFS, our literature review suggested that H2 gas may be an effective medical gas for the treatment of ME/CFS.
