Hydrogen-rich water reduces serum LDL-cholesterol levels and improves HDL functionScientific Research
Hydrogen-rich water decreases serum LDL-cholesterol levels and improves HDL function in patients with potential metabolic syndrome
Abstract
We found that hydrogen (dihydro; H2) had beneficial lipid-lowering effects in Syrian golden hamsters fed a high-fat diet. The aim of this study was to describe the effect of H2-enriched water (0.9-1.0 L/day) on serum lipoprotein levels, composition, and bioactivity in 20 patients with underlying metabolic syndrome. Serum analysis showed that drinking H2-enriched water for 10 weeks reduced serum total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol (LDL-C) levels. Western blot analysis showed that serum apolipoprotein (apo) B100 and apoE were significantly reduced. Furthermore, we found that H2 significantly improved HDL function, assessed in four independent ways, i) preventing LDL oxidation, ii) inhibiting tumor necrosis factor (TNF)-α-induced adhesion of monocytes to endothelial cells , iii) stimulated cholesterol efflux from macrophage foam cells and iv) protected endothelial cells from TNF-α-induced apoptosis. In addition, we found that drinking H2-enriched water resulted in an increase in the antioxidant enzyme superoxide dismutase, and a decrease in serum total thiobarbituric acid-reactive substances and LDL. In conclusion, H2-rich hydration can reduce serum LDL-C and ApoB levels, improve HDL function impaired by dyslipidemia, and reduce oxidative stress, which may play a positive role in preventing possible metabolic syndrome.
Results
Taken together, our data suggest that in vivo administration of H2-water appears to reduce serum TC and LDL-C levels and improve HDL function in patients with underlying metabolic syndrome, suggesting that H2 could be used as a new drug for treatment or control. Disorders of lipid metabolism.
References
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DOI: 10.1194
Published on: 20130107
Hydrogen-rich water decreases serum LDL-cholesterol levels and improves HDL function in patients with potential metabolic syndrome
Abstract
We found that hydrogen (dihydro; H2) had beneficial lipid-lowering effects in Syrian golden hamsters fed a high-fat diet. The aim of this study was to describe the effect of H2-enriched water (0.9-1.0 L/day) on serum lipoprotein levels, composition, and bioactivity in 20 patients with underlying metabolic syndrome. Serum analysis showed that drinking H2-enriched water for 10 weeks reduced serum total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol (LDL-C) levels. Western blot analysis showed that serum apolipoprotein (apo) B100 and apoE were significantly reduced. Furthermore, we found that H2 significantly improved HDL function, assessed in four independent ways, i) preventing LDL oxidation, ii) inhibiting tumor necrosis factor (TNF)-α-induced adhesion of monocytes to endothelial cells , iii) stimulated cholesterol efflux from macrophage foam cells and iv) protected endothelial cells from TNF-α-induced apoptosis. In addition, we found that drinking H2-enriched water resulted in an increase in the antioxidant enzyme superoxide dismutase, and a decrease in serum total thiobarbituric acid-reactive substances and LDL. In conclusion, H2-rich hydration can reduce serum LDL-C and ApoB levels, improve HDL function impaired by dyslipidemia, and reduce oxidative stress, which may play a positive role in preventing possible metabolic syndrome.
Results
Taken together, our data suggest that in vivo administration of H2-water appears to reduce serum TC and LDL-C levels and improve HDL function in patients with underlying metabolic syndrome, suggesting that H2 could be used as a new drug for treatment or control. Disorders of lipid metabolism.
References
Nat. Med. 2007; 13: 688-694
PLoS ONE. 2013; 8: e53913
Nutr. Res. 2008; 28: 137-143
C. R. Acad. Sci. III. 2001; 324: 719-724
Atherosclerosis. 2012; 221: 55-65
Metabolism. 2012; 61: 794-800
J. Clin. Invest. 2004; 114: 1752-1761
JAMA. 2008; 299: 2287-2293
JAMA. 2002; 287: 356-359
Circulation. 2004; 109: 433-438
Rev. Med. Inst. Mex. Seguro Soc. 2012; 50: 301-306
Trends Cardiovasc. Med. 2001; 11: 155-161
Metabolism. 2010; 59: 653-657
J. Lipid Res. 2004; 45: 1169-1196
Clin. Nutr. 2005; 24: 16-31
FEBS Lett. 2009; 583: 2157-2159
J. Biol. Chem. 1993; 268: 27406-27412
J. Atheroscler. Thromb. 2000; 7: 152-158
J. Clin. Invest. 1999; 103: 907-914
Atherosclerosis. 1998; 136: 51-57
Circulation. 1999; 99: 2317-2322
J. Biol. Chem. 1996; 271: 30647-30655
Proc. Natl. Acad. Sci. USA. 1981; 78: 7545-7549
J. Cell Sci. 1990; 95: 481-485
Biochem. Biophys. Res. Commun. 2008; 377: 1195-1198
Curr. Pharm. Des. 2008; 14: 338-351
Ann. Pharmacother. 1992; 26: 1109-1117
Proc. Natl. Acad. Sci. USA. 1986; 83: 8370-8374
Am. J. Med. 1977; 62: 707-714
Pharmacol. Rev. 2006; 58: 342-374
