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Eva Lonn, MD, MSc, FRCPC

JAMA. 2008;299(17):2086-2087.

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

In 1969, McCully first proposed that homocysteine, an amino acid produced during catabolism of methionine, causes arterial and venous atherothrombotic disease.¹ This theory was based on observations that children with extreme elevations of plasma homocysteine concentrations due to inborn errors of metabolism also had premature atherothrombotic disease. While the genetic disorders associated with homocystinuria are rare, these conditions provide an in vivo human model for vascular injury associated with exposure to high homocysteine concentrations. Subsequent in vitro and in vivo studies confirmed that in experimental settings, homocysteine can cause atherothrombosis by promoting oxidative stress, endothelial cell damage, endothelial dysfunction, inflammation, thrombosis, and cell proliferation.²

Epidemiological studies have in general demonstrated associations between elevated homocysteine levels and increased risk of coronary heart disease (CHD) and even stronger associations with increased risk of stroke. A meta-analysis of early cross-sectional and retrospective case-control studies suggested that plasma homocysteine . . . [Full Text of this Article]

Author Affiliation: Department of Medicine and Population Health Research Institute, McMaster University, Hamilton, Ontario, Canada.

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