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Insufficient Evidence to Justify Treatment

Colin Baigent, BM BCh, FRCP; Robert Clarke, MD, FRCP

JAMA. 2007;298:1212-1214.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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

Many observational epidemiological studies have reported that cases with coronary heart disease (CHD) or stroke have higher homocysteine levels compared with age and sex-matched controls. In 1995, a meta-analysis of observational studies, involving a total of 2297 CHD cases, indicated that a 5 µmol/L higher homocysteine level was associated with about a 70% increase in the risk of CHD.² These studies were mainly retrospective in design, however, and were unable to exclude the possibility that . . . [Full Text of this Article]

Author Affiliations: Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford, England.

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