Abstract
Proponents of cholesterol as a risk factor for stroke usually support their argument by citing evidence from clinical trials of the beneficial effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (“statins”) in reducing stroke risk among people with prior cardiovascular disease. Although such studies may provide some supportive evidence, causation can really only be established between a risk factor and a disease when certain criteria are met.1 These include the criteria that the association between the risk factor and the disease must be temporal and biologically plausible. Although there may be little or no debate about whether cholesterol is a biologically plausible risk factor for stroke or that high cholesterol levels precede (rather than follow) stroke, some of the other criteria are more ambiguous. These other “guidelines for causation” are discussed below: There have been numerous major prospective epidemiological studies of cholesterol and the risk of stroke. However, at best, the …
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