Hydrogen for Hearing Loss, COPD, Stroke

Dr. Weeks’ Comment: Hydrogen is fundamental and essential for life and vitality.  Here we reveal its ability to lengthen telomeres and enhance anti-aging . But did you know it protect neurological function, such as preventing hearing loss as well as helping in post stroke situations. Here below is some new research to consider as you and I optimize our health and vitality.

 

HEARING LOSS

Hydrogen: a novel strategy for preventing and treating hearing loss

Jin, Ling#; Tan, Shiwang#; Lai, Ju#; Fan, Kai#; Zhou, Shican; Wang, Yang; Yu, Shaoqing*

Medical Gas Research ():10.4103/mgr.MEDGASRES-D-25-00274, April 11, 2026. | DOI: 10.4103/mgr.MEDGASRES-D-25-00274
 

Abstract

Sensorineural hearing loss, often caused by irreversible damage to cochlear hair cells, is primarily mediated by oxidative stress triggered by aging, noise exposure, or ototoxic agents. Conventional treatments such as hearing aids or cochlear implants have limitations in accessibility and efficacy. Hydrogen (H2), a selective antioxidant with anti-inflammatory and anti-apoptotic properties, has demonstrated protective effects on various organ systems. This review evaluates the therapeutic potential of H2 in preventing and treating sensorineural hearing loss and aims to inform future research directions. In preclinical models of sensorineural hearing loss, H2 administration via inhalation, injection, or drinking water reduces reactive oxygen species accumulation, protects cochlear hair cells, and improves functional hearing markers (auditory brainstem response and distortion product otoacoustic emission). Clinical trials have shown that H2 inhalation improves hearing thresholds in patients with radiotherapy-induced hearing loss and idiopathic sudden sensorineural hearing loss. No serious side effects have been observed. H2‘s high diffusion capacity and selective reactive oxygen species-scavenging properties support its role as a promising therapeutic for sensorineural hearing loss. While animal data are robust and initial clinical outcomes encouraging, further large-scale studies are warranted to validate efficacy, optimize delivery methods, and establish clinical protocols.

 

COPD

. 2026 May 20;21(1):20261438. doi: 10.1515/med-2026-1438

A narrative review of hydrogen therapy for COPD: aging-related insights

PMCID: PMC13186515  PMID: 42164762

Abstract

Objectives

Molecular hydrogen (H2) exhibits selective antioxidant, anti-inflammatory, and anti-senescence properties that may provide therapeutic benefits for chronic obstructive pulmonary disease (COPD), particularly in aging populations where oxidative stress and chronic inflammation are prominent. Given the increasing burden of aging-related COPD and the emerging biological effects of molecular hydrogen, we hypothesized that H2 therapy may exert beneficial effects by modulating oxidative stress, inflammation, and aging pathways.

Conclusions

H2 therapy shows consistent antioxidative, anti-inflammatory, and anti-senescence effects across preclinical and clinical settings, suggesting potential as an adjunctive treatment for COPD in aging populations. Further large-scale, long-term trials are warranted to confirm efficacy, optimize dosage, and clarify mechanistic pathways.

 

STROKE

Research ArticleVolume 35, Issue 6108645June 2026Open acces

Hydrogen gas inhalation alleviated cerebral ischemia/reperfusion injury by regulating mitophagy in SH-SY5Y cells and mice via PTEN-induced kinase 1/Parkin pathway

Abstract

Background

Cerebral ischemia–reperfusion injury (CIRI) causes severe neuronal damage following restoration of cerebral blood flow, and mitochondrial dysfunction acts as a core pathological driver of this process. Molecular hydrogen (H₂) has exhibited promising neuroprotective effects in multiple neurological disease models, yet it remains unclear whether H2 alleviates CIRI by modulating mitophagy and its upstream regulatory signaling pathways.

Results

In vivo experiments demonstrated that H₂ inhalation markedly alleviated neurological deficits, reduced cerebral infarct volume and histopathological damage, inhibited neuronal apoptosis, and promoted mitophagy in MCAO/R mice. In SH-SY5Y cells, H₂ treatment significantly improved cell viability, attenuated oxidative stress and mitochondrial dysfunction, and enhanced mitophagy via activation of the PINK1/Parkin pathway. Mechanistically, H₂ maintained cellular redox homeostasis, cleared damaged mitochondria, upregulated the Nrf2/HO-1 antioxidant pathway, and suppressed NF-κB-mediated inflammatory signaling. Notably, inhibition of Nrf2 with ML385 significantly reversed the mitochondrial protective and anti-apoptotic effects of H₂ in OGD/R-exposed cells.

Conclusion

Our findings revealed that H2 exerts significant neuroprotective effects against CIRI by attenuating oxidative stress, inhibiting neuronal apoptosis, and improving mitochondrial function. These effects are closely associated with the activation of the Nrf2/PINK1/Parkin-mediated mitophagy pathway, highlighting H₂ as a potential therapeutic method for CIRI.

 

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