title: Supplementation of hydrogen-rich water improves lipid and glucose metabolism in patients with type 2 diabetes or impaired glucose tolerance.
abstract: Oxidative stress is recognized widely as being associated with various disorders including diabetes, hypertension, and atherosclerosis. It is well established that hydrogen has a reducing action. We therefore investigated the effects of hydrogen-rich water intake on lipid and glucose metabolism in patients with either type 2 diabetes mellitus (T2DM) or impaired glucose tolerance (IGT). We performed a randomized, double-blind, placebo-controlled, crossover study in 30 patients with T2DM controlled by diet and exercise therapy and 6 patients with IGT. The patients consumed either 900 mL/d of hydrogen-rich pure water or 900 mL of placebo pure water for 8 weeks, with a 12-week washout period. Several biomarkers of oxidative stress, insulin resistance, and glucose metabolism, assessed by an oral glucose tolerance test, were evaluated at baseline and at 8 weeks. Intake of hydrogen-rich water was associated with significant decreases in the levels of modified low-density lipoprotein (LDL) cholesterol (ie, modifications that increase the net negative charge of LDL), small dense LDL, and urinary 8-isoprostanes by 15.5% (P < .01), 5.7% (P < .05), and 6.6% (P < .05), respectively. Hydrogen-rich water intake was also associated with a trend of decreased serum concentrations of oxidized LDL and free fatty acids, and increased plasma levels of adiponectin and extracellular-superoxide dismutase. In 4 of 6 patients with IGT, intake of hydrogen-rich water normalized the oral glucose tolerance test. In conclusion, these results suggest that supplementation with hydrogen-rich water may have a beneficial role in prevention of T2DM and insulin resistance.
authors.affiliation: Kajiyama Clinic, Kyoto 615-0035, Japan.
authors.forename: Sizuo
authors.initials: S
authors.lastname: Kajiyama
authors.forename: Goji
authors.initials: G
authors.lastname: Hasegawa
authors.forename: Mai
authors.initials: M
authors.lastname: Asano
authors.forename: Hiroko
authors.initials: H
authors.lastname: Hosoda
authors.forename: Michiaki
authors.initials: M
authors.lastname: Fukui
authors.forename: Naoto
authors.initials: N
authors.lastname: Nakamura
authors.forename: Jo
authors.initials: J
authors.lastname: Kitawaki
authors.forename: Saeko
authors.initials: S
authors.lastname: Imai
authors.forename: Koji
authors.initials: K
authors.lastname: Nakano
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Ohta
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Adachi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Obayashi
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D019587:Dietary Supplements; D004311:Double-Blind Method; D005260:Female; D018149:Glucose Intolerance; D005951:Glucose Tolerance Test; D006801:Humans; D006859:Hydrogen / Q000378:metabolism / Q000494:pharmacology*; D050356:Lipid Metabolism / Q000187:drug effects* / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D016896:Treatment Outcome; D014867:Water / Q000494:pharmacology*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D014867:Water; D006859:Hydrogen