How does homocysteine cause heart disease?
Homocysteinemia is widely accepted as an independent risk factor for coronary, cerebral, and peripheral vascular diseases. Molecular mechanisms of homocysteine-induced cellular dysfunction include increased inflammatory cytokine expression, altered nitric oxide bioavailability, induction of oxidative stress, activation of apoptosis, and defective methylation. High homocysteine levels in the blood can damage the lining of the arteries. High levels may also make the blood clot more easily than it should. This can increase the risk of blood vessel blockages.
Folate is an important regulator of Hcy metabolism.
Clinical studies report evidence that folate supplementation can reduce cardiovascular disease risk by lowering Hcy levels. In 2015, a meta-analysis showed that the elevated HCys level is an independent predictor for cardiovascular good health in the general population, and among elderly persons. Mazza et al. investigated the efficacy of Quatrefolic® (400 μg of Quatrefolic® plus B6, and B12) 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 (104 patients with HCys ≥15 μmol/l ). The result shows a significant HCys reduction in comparison with a baseline from 21.5 μmol/l to 10.0 μmol/l with the product containing Quatrefolic®. 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.
References
Mazza A. et al. Biol Regul Homeost Agents 2016
Fu Y. et al. Br J Pharmacol 2018; Peng H. et al.
J Zhejiang Univ Sci B. 2015
Ambrosino P. at al. Nutr Res. 2015
