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(Hypertension. 2004;44:805.)
© 2004 American Heart Association, Inc.

Editorial Commentary

Alcohol-Associated Hypertension

When One Drinks Makes a Difference

From the Kaiser Permanente Medical Center, Oakland, Calif.

Correspondence to Arthur L. Klatsky, Kaiser Permanente Medical Center, 280 West MacArthur Boulevard, Oakland, CA 94611. E-mail hartmavn@pacbell.net or arthur.klatsky@kp.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The high prevalence of systemic hypertension (HTN) and its progressive association with multiple adverse sequelae¹ confer great potential importance on any modifiable trait influencing blood pressure (BP). Established modifiable factors include obesity and sodium intake. Less solidly established are physical inactivity and low potassium or calcium intake. With a relationship to HTN seen nearly unanimously in a substantial number of observational cross-sectional and prospective studies, alcohol drinking has become a major focus of interest in recent decades as a modifiable HTN risk factor.^2–3 Even low estimates of 5% or 7% of HTN attributable to alcohol imply that there are more patients with HTN caused by alcohol than by conventional causes of remediable secondary HTN.³

Present in both sexes and several ethnic groups, the alcohol–HTN association is independent of a number of potential confounders including nutritional factors.^2–3 Available evidence suggests substantial regression of HTN in several days with alcohol abstinence. Although heavier alcohol intake (2 drinks daily) has been more consistently related, an alcohol–BP relationship with lighter drinking in some studies raises a possibility of great potential pubic health importance. Most observational analyses used average amount of alcohol consumed daily as the alcohol measure, with presumed underestimation of alcohol amount by some heavier drinkers impairing definition of a threshold dose level.³ To add further confusion, a few studies show lower pressures in light drinkers than in abstainers, perhaps especially in women.³

Lack of a proven mechanism limits causal interpretation of the alcohol–HTN link. There are other unresolved issues, including: (1) . . . [Full Text of this Article]

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