Hydrogen Water Prevents Bone Death from Steroid Medications
- Authors
- Yuanming An, Lizhen Zheng, Shi'an Zhang, Haozhi Zhang, Yuantao Zhang, Hongwei Shao, Wenxue Tong, Ziyi Chen, Hao Yao, Zhenkang Wen, Xu Shunxiang, Ye Li, Qinyu Tian, Liming Cheng, Wei Sun, Lin Wei, Jiankun Xu
- Journal
- Biomaterials
- Year
- 2025
- DOI
- 10.1016/j.biomaterials.2025.123428
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Steroid-Associated Osteonecrosis
- Body System
- Skeletal
TL;DR
Drinking hydrogen-rich water (HRW) helps prevent bone damage and reduces bad cholesterol in mice treated with high doses of steroids.
Key Finding
Hydrogen-rich water prevented steroid-induced bone death in mice by activating a cellular pathway (ACOD1-itaconate) that reduced bone cell death, improved bone structure, and shifted immune cells toward an anti-inflammatory state.
Summary
This mouse study tested whether hydrogen-rich water could prevent bone death (osteonecrosis) caused by steroid medications. Mice given high-dose steroids and treated with hydrogen-rich water showed better bone health, improved blood vessel formation, lower cholesterol levels, and reduced inflammation compared to untreated mice. The protective effects appeared to work through a specific cellular pathway called ACOD1-itaconate.
Practical Takeaway
While this is early evidence from mouse studies suggesting hydrogen water may help prevent steroid-related bone damage, human studies are needed before any health claims can be made. The study does not report how long treatment lasted or other practical details needed to assess real-world applicability. Anyone taking steroids should discuss bone health strategies with their doctor rather than relying on unproven interventions.
Abstract
Steroid-associated osteonecrosis (SAON) remains a challenging clinical condition as there are few effective preventive measures. This study investigates the effects of hydrogen (H2) administrated via saturated hydrogen-rich water (HRW) in mice received high dose of glucocorticoids (for inducing SAON model). Here we find that HRW treatment significantly reduces osteocyte apoptosis, improves deteriorated trabecular architecture, increases osteoblast numbers and the bone formation, while decreases osteoclast numbers and the bone resorption. Additionally, HRW-treated mice exhibit improved serum lipid profiles, including decreased levels of low-density lipoprotein (LDL), triglycerides (TG), and total cholesterol (T-CHO), as well as reduced lipid accumulation. HRW treatment also enhances blood perfusion and increases formation of type H vessels in SAON mice. We further demonstrate that HRW shifts the polarization of macrophages from M1 to M2 phenotype and suppresses inflammatory marker TNF-α. RNA sequencing data and subsequent validation reveal that HRW upregulates ACOD1 mRNA and protein levels in bone tissues. The protective effects of HRW are mimicked by supplementation with the itaconate derivative dimethyl itaconate in a dose-dependent manner, highlighting the importance of the ACOD1-itaconate pathway in the prevention of SAON by HRW. These findings indicate that HRW ameliorates SAON by modulating the ACOD1-itaconate pathway, presenting a novel avenue for the cost-effective prevention of osteonecrosis.