Individuals with homocystinuria, a rare genetic disorder associated with markedly elevated plasma homocysteine levels (ie, 100-300 μmol/L [to convert to mg/dL, divide by 7.397]—at least 10 times higher than the general population), experience rapidly progressive atherosclerosis and associated thromboembolic events in early adulthood. This observation prompted the “homocysteine hypothesis” that moderately elevated homocysteine levels might be of causal relevance to cardiovascular disease in the general population.1
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