Hydrogen Water May Help High-Altitude Sickness Patients

Authors
Journal
Food Research International
Year
DOI
10.1016/j.foodres.2025.117118
Study Type
Human
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Chronic High-Altitude Disease
Body System
Immune System

TL;DR

Drinking hydrogen-rich water for 60 days showed early signs of reducing inflammation and oxidative stress in people with chronic high-altitude disease.

Key Finding

Hydrogen-rich water treatment significantly downregulated inflammation and cytokine-related gene pathways in chronic high-altitude disease patients, whereas placebo water did not produce these molecular changes.

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.

Practical Takeaway

While this study suggests hydrogen-rich water may help manage chronic high-altitude disease at the genetic level, the actual improvements in inflammation and oxidative stress markers were small and not statistically significant. The study was also relatively small (43 participants) and short (60 days), so larger and longer studies are needed before drawing firm conclusions about whether hydrogen-rich water would meaningfully help people with this condition.

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.