News
New study shows significant effect of Quatrefolic® in lowering Homocysteine Serum Levels
10 November 2016
A recently new published study (Mazza et al., Nutraceutical approaches to homocysteine lowering in hypertensive subjects at low cardiovascular risk: a multicenter, randomized clinical trial. J Biol Regul Homeost Agents. 2016) has investigated the efficacy of Quatrefolic® (400 mcg of Quatrefolic® plus B6, and B12 BID) in lowering homocysteine serum levels (HCys) versus a conventional vitamin supplementation with highly dosed folic acid (5 mg/day) in hypertensive subjects at low cardiovascular risk.
The treatment was significantly effective and the ideal HCys level was reached in 55.8% of cases in the Quatrefolic® group, and it was significantly higher than in controls.
No side effects were observed in either treatment group. Homocysteinemia is widely accepted as an independent risk factor for coronary, cerebral, and peripheral vascular diseases.
Focus on Homocysteine & Homocysteinemia
Homocysteine is a metabolite of methionine metabolism in the one-carbon metabolism, often referred to as the methylation cycle, and exists at a critical biochemical intersection – between S-adenosylmethionine, the indispensable ubiquitous methyl donor, and 5-MTHF and vitamins B12[1].
Homocysteinemia may be caused by several nutritional deficiencies other than B12, including vitamin B6 and folate deficiencies[2], and decreasing plasma total homocysteine by providing nutritional cofactors for its metabolism has been shown to reduce the risk of cardiovascular events.
High blood levels of homocysteine signal a breakdown in this vital process, resulting in far-reaching biochemical and life consequences. As a matter of fact, the link between homocysteine and cardiovascular disease is well established especially in the elderly[3]. High Hcys concentrations inhibit the proliferation of vascular endothelial cells[4], decrease the antioxidant activity of superoxide dismutase on endothelial cell surfaces, and impair endothelial function[5] They are also implicated in the pathophysiology of essential hypertension[6]. Hyperhomocysteinemia exerts its deleterious vascular effects through the production of free-reactive oxygen species that cause oxidative stress[7] as a result of antioxidant/prooxidant imbalance and probably also by inhibition of intracellular glutathione peroxidase[8,9].
References:
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Altern Med Rev. 2003 Feb;8(1):7-19 The methionine-homocysteine cycle and its effects on cognitive diseases. Miller AL1.
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Johnson MA. If High Folic Acid Aggravates Vitamin B12 Deficiency What Should Be Done About It? Nutr Rev 2007; 65: 451-458.
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Kazemi MS, Eshraghian K, Omrani G, Lankarani KB,Hosseini E. Homocysteine level and coronary artery disease. Angiology 2006; 57:9-14.
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Wang H, Yoshizumi M, Lai K, et al. Inhibition of growth and p21ras methylation in vascular endothelial cells by homocysteine but not cysteine. J Biol Chem. 1997;272:25380–25385.
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Yamamoto M, Hara H, Adachi T. Effect of homocysteine on the binding of extracellular-super-oxide dismutase to the endothelial cell surface. FEBS Lett. 2000;486:159–162.
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Rodrigo R, Passalacqua W, Araya J, et al. Implications of oxidative stress and homocysteine in the pathophysiology of essential hypertension. J Cardiovasc Pharmacol. 2003;42:453–461.
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Welch GN, Loscalzo J. Homocysteine and atherothrombosis N Engl J Med. 1998;338:1042–1050.
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Schnabel R, Lackner KJ, Rupprecht HJ, et al. Glutathione peroxidase-1 and homocysteine for cardiovascular risk prediction. J Am Coll Cardiol. 2005;45:1631–1637.
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Caruso R, Campolo J, Sedda V, De Chiara B, Dellanoce C, Baudo F, Tonini A, Parolini M, Cighetti G, Parodi O (2006) Effect of homocysteine lowering by 5-methyltetrahydrofolate on redox status in hyperhomocysteinemia. J Cardiovasc Pharmacol 47:549–555
