Hydrogen-rich water supplementation demonstrates potential protective effects in chronic high-altitude disease patients by downregulating inflammation and cytokine-related gene pathways, with molecular analysis identifying six key hub genes involved in the therapeutic mechanism. While oxidative stress and inflammatory markers showed non-significant downward trends after 60 days of HRW treatment, the genomic evidence suggests hydrogen-rich water may serve as a novel adjuvant therapy for managing CHAD. Further research with larger sample sizes and longer intervention periods is warranted to establish clinical efficacy and optimize therapeutic protocols.
Plain-Language Summary
This study tested whether hydrogen-rich water could help people with chronic high-altitude disease (a condition caused by living at high elevations where the body experiences oxidative stress—cellular damage from unstable molecules—and inflammation). Forty-three patients drank either hydrogen-rich water or regular water for 60 days. Researchers found that hydrogen-rich water appeared to reduce inflammation-related genes and showed a downward trend in inflammatory markers, though the changes were not statistically significant.
Abstract
Chronic high-altitude disease (CHAD) is primarily driven by oxidative damage and inflammation. Hydrogen-rich water (HRW) is a novel functional food with demonstrated antioxidant and anti-inflammatory properties. However, its potential effects on inflammation and oxidative stress in CHAD remain unexplored. In this study, 50 participants with CHAD were recruited and assigned to the HRW or placebo water (PW) group for 60 days. After seven participants were lost to follow-up, 43 participants (HRW, n = 23; PW, n = 20) completed the intervention and were included in the analysis. Oxidative stress indicators and inflammation-related immune cells were evaluated before and after treatment, and transcriptional profiles of all participants were analyzed to determine the potential mechanism of HRW in CHAD. Baseline characteristics did not differ significantly between the two groups. Enrichment analysis showed that differentially expressed genes in the PW group between pre- and post-intervention were predominantly associated with inflammation- and cytokine-related pathways, whereas HRW treatment significantly downregulated these pathways. By integrating weighted gene co-expression network analysis and protein-protein interaction network analysis we identified six hub genes, including tumor necrosis factor, interleukin-1 beta, C-C motif chemokine ligand 3, C-C motif chemokine ligand 3-like 1, C-C motif chemokine ligand 4-like 2, and radiation-inducible immediate-early response 3. Furthermore, measurements of oxidative stress and inflammatory markers indicated a non-significant downward trend in oxidative stress and inflammation in patients with CHAD after HRW intake for 60 days. These results suggest the potential protective role of HRW in CHAD, providing a novel adjuvant therapy for CHAD.
