(Stroke. 2002;33:890.)
© 2002 American Heart Association, Inc.
Editorial |
From the Department of Neurology, University of Wisconsin, Madison, Wis.
Correspondence to Douglas A. Dulli, MD, MS, University of Wisconsin Medical School, H6/534 Clinical Science Center, 600 Highland Ave, Madison, WI 53792. E-mail dulli@neurology.wisc.edu
As one reviews a study with a negative outcome, there may be a sense of the role of a medical examiner at an autopsy, particularly if the expectation was a positive result and the data were from the renowned Framingham Study. Was the cohort too small? Were assumptions or analyses of the study flawed? Or should the natural death of the null hypothesis be accepted, rather than merely not rejected? In their article, Djoussé et al have found no overall association of alcohol consumption to ischemic stroke, although some preventive benefit was noted in the 60-to-69 age group.1 This was a novel but proficient analysis, and the latest of many observational studies that have addressed this question. A "J-shaped" curve of alcohol use compared with ischemic stroke risk has been demonstrated in at least 2 large prospective studies2,3 and at least 2 case-control studies,4,5 showing a positive benefit in moderate alcohol consumption in ischemic stroke prevention.
Other studies have had negative results, particularly in Japanese cohorts, or have demonstrated the harm of excessive alcohol use, either chronically or as "binge" drinking. These studies have been very well reviewed by Camargo.6 There are difficulties measuring the exposure of alcohol, particularly with underreporting that occurs at higher levels of drinking. It is also difficult to control for the various confounders of alcohol exposure, including smoking, hypertension, age, and gender. Moreover, advancing age is associated with both higher risk of stroke and factors that alter or stop alcohol consumption, such as heart disease,
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