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.
so ADM a and s dma are things that we use to look at endothelial health they inhibit nitric oxide synthase so when a DM a and SEMA are elevated you're inhibiting nitric oxide synthase synthase you have less nitric oxide produced in the endothelium you're more prone obviously to constriction
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you can look at things like homocysteine we also look at something called asymmetric dimethyl arginine or ADM a and SDM a which are inhibitors of nitric oxide synthase
We also look at something called asymmetric dimethyl arginine or ADMA and SDMA, which are inhibitors of nitric oxide synthase.
there's at least reasonable mechanistic data to suggest that high amounts of symmetric and asymmetric dimethyl Arginine impaired the enzyme nitric oxide synthes which produces nitric oxide which leads to vasodilation