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The Potential of Hydrogen for Improving Mental Disorders.

水素分子が精神疾患に与える影響の可能性に関するレビュー

review not specified not assessed

Abstract

Following the landmark 2007 report by Ohsawa et al. demonstrating that H2 gas reduced infarct volume in a rat cerebral infarction model—at least partly through hydroxyl radical scavenging—research interest expanded to encompass H2's anti-inflammatory and anti-apoptotic properties alongside its antioxidant effects. Mental disorders, defined by disturbances in mood, cognition, and behavior, currently lack reliable preventive strategies, and existing pharmacological agents carry efficacy limitations and adverse effects. Accumulating evidence links elevated oxidative and inflammatory stress to the pathophysiology of these conditions. This review consolidates recent findings on H2's effects in mental health-related conditions, examines proposed biomedical mechanisms, and discusses the potential of H2 as a novel approach for individuals affected by psychiatric disorders.

Mechanism

H2 selectively scavenges hydroxyl radicals and peroxynitrite, while also exerting anti-inflammatory and anti-apoptotic effects, thereby potentially mitigating the oxidative and inflammatory stress implicated in the pathophysiology of mental disorders.

Bibliographic

Authors
Satoh Y
Journal
Curr Pharm Des
Year
2021
PMID
33185151
DOI
10.2174/1381612826666201113095938

Tags

Disease:認知機能低下 うつ・不安 Mechanism:アポトーシス抑制 ヒドロキシルラジカル消去 炎症抑制 酸化ストレス 活性酸素種

Delivery context

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 33185151. https://h2-papers.org/en/papers/33185151
Source: PubMed PMID 33185151