Review article
Alcohol and hypertension: a review

https://doi.org/10.1016/j.jash.2008.03.010Get rights and content

Abstract

In recent decades alcohol use has joined other correlates of hypertension (HTN), such as obesity and salt intake, as a major research focus about HTN risk factors. In cross-sectional and prospective epidemiologic studies, higher blood pressure (BP) has consistently been found among persons reporting usual daily intake of three standard-sized drinks or more. Although definitive mechanisms have not been established, several aspects of the data, including short and intermediate term experiments, suggest a causal relationship. Heavier drinking may, in fact, be the commonest cause of reversible HTN, and reduction of heavy alcohol intake plays an important public health role in HTN management. Additional to the mechanism, unresolved issues about the alcohol-BP relationship include whether there is a threshold dosage of alcohol for association with HTN, the sequelae of alcohol-associated HTN and the roles of interactions with gender, ethnicity, other lifestyle traits, drinking pattern, and choice of beverage. This article reviews these areas and includes new data about the beverage choice aspect.

Introduction

For 60 years a first report of increased hypertension (HTN) prevalence among heavy drinkers in World War 1 French servicemen1 was largely ignored. The topic reappeared in epidemiologic reports in the 1970s. In reviews over the past 20 years,2, 3, 4, 5, 6, 7, 8, 9 alcohol use has joined other HTN risk factors, such as obesity and salt intake, as a major focus of research. Persons reporting usual daily intake of three drinks or more have consistently been found to have higher blood pressure (BP). This alcohol-HTN association has been shown in both genders, several racial and ethnic groups, and across all adult ages. Some studies report a lower alcohol intake threshold for increased BP. Although mechanisms have not been established, substantial evidence, including clinical experiments, supports a causal relationship. Even the lowest published estimates of 5%3 or 7%10 of HTN attributable to alcohol drinking imply that there may be more patients with HTN due to alcohol than patients with remediable secondary HTN.11 Reduction of heavy alcohol intake lowers BP in some persons and in some heavy drinkers alcohol impairs response to HTN management.

Remaining issues about the alcohol-HTN relation include the following: 1) Possible physiological mechanisms, 2) whether the relation is linear or involves a threshold dosage of alcohol, 3) whether other dietary or behavioral factors modify the association, 4) whether drinking pattern (steady vs. intermittent) is a major factor, 5) whether beverage type (wine, liquor, or beer) is a factor, and 6) whether HTN in heavy drinkers carries the same sequelae as HTN in abstainers or light drinkers.

Definitions of these imprecise but widely used terms are variable and much debated. As is the case for “HTN” itself, all definitions are arbitrary. The operational definitions used for discussion of relations to HTN in this article take into account the level of drinking in epidemiologic studies above which net harm and increased BP are usually seen. Thus, less than three drinks per day is called “light” or “moderate” drinking, and three or more drinks per day “heavy” drinking. Gender, age, and individual factors lower the upper limit for some persons and raise it for others. In survey data, systematic “under-reporting” (lying) lowers the apparent threshold for harm from alcohol, because some heavy drinkers allege lighter drinking. This possible role of under-reporting in the alcohol-HTN relation will be discussed.

Although there are also various “standard drink” definitions, the amount of alcohol in the usual drink of wine, liquor, or beer is approximately the same. Because people think in terms of “drinks,” not milliliters or grams of alcohol, in this article alcohol intake is described in terms of drinks per day or week. When talking with patients, health professionals need to remember the importance of defining the size of drinks.

Section snippets

Cross-Sectional Studies — BP Level and Prevalence of Hypertension

Almost all of ≥100 cross-sectional studies show higher mean BPs and/or higher HTN prevalence with increasing alcohol drinking.2, 3, 4, 5, 6, 7, 8 Reports involve North American, European, Australian, and Japanese populations. In these analyses, the relation seems independent of adiposity, salt intake, education, cigarette smoking, and several other potential indirect explanations. Some studies show no increase in BP at light to moderate alcohol drinking, and several, especially in women, show a

Controlled Clinical Trials in Humans

The controlled clinical trial of Potter and Beevers25 was, to our knowledge, the first one to examine the effects of reduction of alcohol consumption upon BP. Using a crossover design in hospital, these investigators studied 16 hypertensive men with a usual intake of approximately 4 pints of British beer. Upon maintenance of alcohol consumption, baseline high BP levels were unchanged, but fell significantly when alcohol was withdrawn for 3 to 4 days. There were no post-withdrawal increases in

Experimental Data

Acceptance of a causal alcohol to HTN relationship is hindered by lack of an established biological explanation. Reviews2, 3, 4, 5, 6, 7, 8, 9 are cited because of space limitations and because the observation25, 35 of a “slow” (days) effect of alcohol upon BP raises question of the relevance of acute effects. Physiologic data about chronic effects of alcohol drinking related to BP may be difficult to interpret because of alcohol's diverse actions upon target organs that have a direct or

Sequelae of Alcohol-Associated Hypertension

If alcohol drinking plays a causal role in HTN, one would expect alcohol-associated HTN to result in the usual adverse health sequelae of increased BP, including coronary heart disease (CHD), stroke, heart failure, and renal failure. With renal failure possibly excepted, alcohol drinking has complex, independent relationships with each of these outcomes. Population-based studies show that light to moderate drinking is associated with lower CHD risk, possibly mediated by increased protective

Proportion of Hypertension Due to Alcohol

Because the contribution of alcohol to HTN in a given population depends substantially upon the drinking habits of the group, it is not surprising that estimates vary substantially. When men and women are combined, the estimates of HTN attributable to heavy drinking are in the 5% to 7% range.3, 10 The proportion is larger in men than women, because women are less likely to be heavy drinkers. Even with low estimates and using as the denominator a very conservative figure of 40 million

Conclusion

Cross-sectional and prospective observational, epidemiological studies establish an empiric relation of heavy intake of alcoholic beverages to increased BP. Clinical intervention trials support causality, but mechanisms remain unclear. Light to moderate alcohol intake is probably unrelated to increased BP. Choice of wine, beer, or liquor is not a factor, and sequelae of HTN are similar in abstainers and drinkers. Avoidance or moderation of heavy drinking has a role in HTN prevention and

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    Conflict of interest: none.

    Portions of the material in this article include research supported by the Alcoholic Beverage Medical Research Foundation, Inc, Baltimore, Maryland, the Community Service Program of The Kaiser Permanente Medical Care Program, and by the Robert Wood Johnson Foundation.

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