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1.1 Hyperhomocysteinaemia In 1997, when we were designing our clinical study, hyperhomocysteinaemia was considered to be a potential independent cardiovascular risk factor. A variety of underlying causes, i.e. inherited enzyme defects, renal insufficiency, and acquired defects in homocysteine metabolism, had been discovered. Since B vitamins and folic acid are relevant cofactors for metabolizing homocysteine, their combined treatment had been proved to significantly lower homocysteine plasma concentrations. However, the impact of combined B vitamin treatment on cardiovascular disease had been considered controversial.

cardiovascular research

Reloaded: ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inaemia: effects of L-arginine and B vitamins: AUTHORS' RETROSPECTIVE