非アルコール性脂肪性肝疾患に対する水素・酸素吸入の無作為化プラセボ対照臨床試験
A 13-week randomized, placebo-controlled trial enrolling 43 subjects with NAFLD evaluated the effects of hydrogen/oxygen inhalation on metabolic and hepatic parameters. Inhalation improved serum lipid profiles and liver enzyme levels, with significant reductions in liver fat content by ultrasound and CT imaging observed particularly in moderate-to-severe cases. Complementary animal experiments using a methionine- and choline-deficient diet-induced mouse model of NASH demonstrated improvements in systemic inflammation and liver histology, accompanied by enhanced hepatic autophagy; chloroquine administration abolished these benefits. In AML-12 hepatocyte cultures, 20% hydrogen suppressed palmitic acid-induced intracellular lipid accumulation, an effect partially reversed by the autophagy inhibitor 3-methyladenine. These findings collectively suggest that autophagy activation is a key mechanism underlying the hepatoprotective effects of hydrogen/oxygen inhalation in NAFLD.
Hydrogen/oxygen inhalation appears to activate hepatocyte autophagy, thereby reducing intracellular lipid accumulation and attenuating hepatic inflammation and histological damage. Blockade of autophagy with chloroquine or 3-methyladenine abolished these protective effects, supporting autophagy as the primary mechanistic pathway.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/35734974