The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
mechanistically homocysteine will um inhibit the clearance of something called symmetric uh and asymmetric dimethyl Arginine have you heard of these things sdma and adma so adma and sdma uh regulate nitric oxide synthes and homocystine impairs their clearance and therefore when you have high levels of homocystine it per it results ultimately an impaired nitric oxide synthes and therefore low lower nitric oxide
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one inhibits the synthesis and the other enhances the catabolism of arginine so the end of the day you're gonna have less and less nitric oxide
because homocysteine really inhibits the clearance of a DM NS team and that's very clear when you correct it which would therefore screw up nitric oxide production yes so it brings even oxidation into the process would disturb that process - so if Pro oxidative state if hyper homocysteine emia is adversarial to the vasculature that's one of the pathways in which it is