Supplementation of hydrogen-rich water improves lipid and glucose metabolism in patients with type 2 diabetes or impaired glucose tolerance
Kajiyama S, Hasegawa G, Asano M, Hosoda H, Fukui M, Nakamura N, Kitawaki J, Imai S, Nakano K, Ohta M, Adachi T, Obayashi H, Yoshikawa T. · Nutrition research (New York, N.Y.). 2008;28(3):137–143.
Study at a glance
A small crossover trial found changes in selected blood-fat and oxidation markers. Fasting glucose, HbA1c and insulin resistance did not significantly improve. An exploratory six-person glucose-tolerance finding does not establish diabetes prevention.
Human
30 people with mild type 2 diabetes managed by diet/exercise and six with impaired glucose tolerance. Eighteen men and eighteen women; age 58.6 ± 4.7 years, BMI 23.4 ± 3.5 kg/m². Twelve used stable antihypertensive medicines and three low-dose lipid medicines.
900 mL/day purified hydrogen water for eight weeks, supplied by I’rom Pharmaceutical in unlabelled 300 mL aluminum pouches. · Dissolved H₂ 1.2 ± 0.1 mg/L; pH 6.7 ± 0.1; dissolved O₂ 0.8 ± 0.2 mg/L.
Two eight-week periods separated by twelve weeks.
Within the hydrogen period, modified electronegative LDL changed from 8.4 ± 7.2 to 7.1 ± 5.6 (15.5%, P < 0.01), small-dense LDL from 1.05 ± 0.25 to 0.99 ± 0.17 mmol/L (5.7%, P < 0.05), and urinary 8-isoprostane from 257 ± 154 to 240 ± 127 pg/mg creatinine (6.6%, P < 0.05). Placebo changes were nonsignificant; precise placebo-adjusted estimates/interaction P values and confidence intervals were not supplied. Fasting glucose, insulin, HOMA-IR, HbA1c, total/HDL/LDL cholesterol, RLP, triglycerides, free fatty acids, homocysteine, leptin, resistin, hsCRP, BMI and blood pressure did not significantly change. Oxidized LDL P = 0.0567, EC-SOD P = 0.0871 and adiponectin P = 0.0577 were nonsignificant. Four of six IGT participants changed to normal OGTT classification; two-hour glucose 9.36 ± 0.91 to 7.33 ± 1.17 mmol/L (P = 0.0010), one-hour insulin 270.1 ± 206.9 to 423.8 ± 246.2 pmol/L (P = 0.0329), insulinogenic index unchanged. No placebo-period OGTT comparator was shown. In ten healthy volunteers, breath H₂ after 300 mL peaked at 56.8 ± 27.8 ppm at 15 minutes and returned to baseline 11.2 ± 6.5 ppm at 150 minutes; this is not universal tissue-retention time.
Small selected population, many surrogate endpoints, limited allocation and carryover/sequence detail. Table significance markers are within-period comparisons. No demonstrated diabetes-prevention, cardiovascular or other patient-important benefit.
What kind of evidence is this?
Human
Randomized, double-blind, placebo-controlled crossover trial in Japan, with two eight-week periods separated by a twelve-week washout.
Metabolic and lipid health
H₂-rich water
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
30 people with mild type 2 diabetes managed by diet/exercise and six with impaired glucose tolerance. Eighteen men and eighteen women; age 58.6 ± 4.7 years, BMI 23.4 ± 3.5 kg/m². Twelve used stable antihypertensive medicines and three low-dose lipid medicines.
36 participants received both conditions, not 72 independent participants. Six formed the exploratory impaired-glucose-tolerance subgroup. A separate breath-kinetics substudy involved ten healthy fasting volunteers; they are not added to the therapeutic trial sample. Separate attrition accounting was not reported.
Two eight-week periods separated by twelve weeks.
900 mL/day purified hydrogen water for eight weeks, supplied by I’rom Pharmaceutical in unlabelled 300 mL aluminum pouches.
Hydrogen-rich water
Dissolved H₂ 1.2 ± 0.1 mg/L; pH 6.7 ± 0.1; dissolved O₂ 0.8 ± 0.2 mg/L.
900 mL/day placebo purified water for eight weeks; twelve-week washout. Diet plans, weekly diaries, four-week activity/condition checks and unchanged medicines.
Outcomes and reported result
Multiple lipid, glucose, oxidation and insulin-resistance biomarkers; no single primary endpoint explicitly declared. OGTT was reported before/after hydrogen water in the six-person subgroup.
Within the hydrogen period, modified electronegative LDL changed from 8.4 ± 7.2 to 7.1 ± 5.6 (15.5%, P < 0.01), small-dense LDL from 1.05 ± 0.25 to 0.99 ± 0.17 mmol/L (5.7%, P < 0.05), and urinary 8-isoprostane from 257 ± 154 to 240 ± 127 pg/mg creatinine (6.6%, P < 0.05). Placebo changes were nonsignificant; precise placebo-adjusted estimates/interaction P values and confidence intervals were not supplied. Fasting glucose, insulin, HOMA-IR, HbA1c, total/HDL/LDL cholesterol, RLP, triglycerides, free fatty acids, homocysteine, leptin, resistin, hsCRP, BMI and blood pressure did not significantly change. Oxidized LDL P = 0.0567, EC-SOD P = 0.0871 and adiponectin P = 0.0577 were nonsignificant. Four of six IGT participants changed to normal OGTT classification; two-hour glucose 9.36 ± 0.91 to 7.33 ± 1.17 mmol/L (P = 0.0010), one-hour insulin 270.1 ± 206.9 to 423.8 ± 246.2 pmol/L (P = 0.0329), insulinogenic index unchanged. No placebo-period OGTT comparator was shown. In ten healthy volunteers, breath H₂ after 300 mL peaked at 56.8 ± 27.8 ppm at 15 minutes and returned to baseline 11.2 ± 6.5 ppm at 150 minutes; this is not universal tissue-retention time.
Main-text methods, results, limitations and declarations were reviewed. Source versions, missing information and conflicting findings are stated in this record.
No dedicated systematic adverse-event results were identified; absent reporting does not establish absence of harm.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Small selected population, many surrogate endpoints, limited allocation and carryover/sequence detail. Table significance markers are within-period comparisons. No demonstrated diabetes-prevention, cardiovascular or other patient-important benefit.
Limited to the population/model and protocol described above. These findings do not provide a treatment, concentration or device recommendation.
No dedicated funding statement identified. Acknowledgments thank Hiroshige Itakura for guidance; I’rom Pharmaceutical supplied the water.
No dedicated competing-interest declaration identified.
Cochrane RoB 2 crossover variant · reported metabolic biomarker results
Cannot be fully assessed — abstract only
The abstract confirms a randomized double-blind placebo-controlled crossover design, but does not provide enough detail for domain-level judgements or carryover and period-effect checks.
Randomization reported; sequence generation and concealment unavailable. · Double blinding reported; deviations and adherence unavailable. · Missing-data handling unavailable. · Laboratory outcomes are less subjective, but measurement procedures are unavailable. · Protocol, analysis plan, carryover assessment and full outcome reporting are unavailable.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 19083400 · DOI: 10.1016/j.nutres.2008.01.008
Complete final journal article, Nutrition Research 28(3), 137–143, seven pages, hosted by NuLifeSciences.
AI-assisted editorial review of the available main full text, 29 October 2026. No independent clinical or statistical assessment has been performed.
Pages 137–143: Introduction; Methods 2.1–2.6; Results 3.1–3.2; Tables 1–3 and Figures 1–2/captions; Discussion; Acknowledgment and references.
AI-assisted editorial review of the available main full text, 29 October 2026. Complete final journal article, Nutrition Research 28(3), 137–143, seven pages, hosted by NuLifeSciences.
No registration reported in the article.
29 October 2026
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