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(Hypertension. 2006;47:1035.)
© 2006 American Heart Association, Inc.
Hypertension Highlights |
From the Royal Perth Hospital Unit (L.J.B.), School of Medicine & Pharmacology, and the Faculty of Medicine and Dentistry and Health Sciences (I.B.P.), University of Western Australia, Australia.
Correspondence to Lawrence J. Beilin, Professor of Medicine, Royal Perth Hospital Unit, School of Medicine & Pharmacology, University of Western Australia, Level 4, Medical Research Foundation Bldg, Rear, 50 Murray St, Perth, Western Australia, Australia. E-mail Lawrie.Beilin{at}uwa.edu.au
| Introduction |
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The more recent cross-sectional studies have concentrated on the effects of pattern of drinking and the consumption of alcohol with or without food, beverage type, and the relative effects of alcohol on hypertension subtypes.
| Pattern of Drinking, Beverage Type, and Effects on Hypertension Subtypes |
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The possible effects of individual alcoholic beverages on blood pressure continue to arouse interest. However, the previously cited study from western New York3 found no consistent beverage-specific associations with hypertension risk in North Americans drinking beer, wine, or spirits. A cross-sectional study in Chinese men that examined the associations between alcohol intake and isolated systolic, combined systolic and diastolic, and isolated diastolic hypertension found that those in the highest alcohol intake category (
30 drinks/week) were twice as likely as nondrinkers to have any of these hypertensive subtypes with population attributable risks of 13.9%, 13.4% and 12.0%, respectively.6 In this Chinese study,6 liquor drinking was associated with a higher odds ratio of isolated systolic hypertension, but this finding was probably because the liquor drinkers generally drank more alcohol. Another study grouped Japanese male workers7 on the basis of their total consumption of beer, sake, shochu (traditional Japanese spirits), whiskey, or wine. Blood pressure was highest in the shochu group but an analysis adjusting for total alcohol consumption resulted in disappearance of this difference. The interest in the effects of specific beverages has been evoked in part by the so-called French Paradox of a relatively low incidence of coronary disease in France despite a high intake of saturated fat, a phenomenon that has been attributed to the consumption of red wine.8 It has also been suggested that wine drinkers may be protected from the blood pressureraising effects of regular moderate to heavy alcohol consumption, perhaps because of antioxidant and vasodilator effects of polyphenolic flavonoids improving endothelial function.9 In our opinion, these suggestions have been laid to rest in a randomized crossover trial10 that confirmed suggestions from population studies that moderate alcohol consumption raises blood pressure regardless of source. In that study, normotensive men showed similar elevations of awake ambulatory systolic blood pressure and heart rate after 4 weeks of either beer or red wine (40-g ethanol equivalent per day) compared with a control-abstinence period. De-alcoholized red wine had no effect on blood pressure, and neither this beverage nor alcohol containing red wine had any effect on flow or glyceryl trinitratemediated dilation. It was concluded that results from population studies suggesting differential effects of red wine compared with other beverages on blood pressure were most likely because of confounding lifestyle differences in wine drinkers. Twenty-fourhour endothelin-1 excretion was increased with beer and wine drinking, leading to the suggestion that this might reflect increased vascular endothelin-1 production as at least a contributor to the pressor effects of alcohol.10
A systematic review11 of alcohol intervention studies confirmed the previous findings of an initial meta-analysis by Xin et al12 with similar estimates for the effect of alcohol restriction to reduce systolic and diastolic blood pressure by 2.7 mm Hg and 1.4 mm Hg, respectively. However, these authors also compared data from studies that used conventional clinic or office review of blood pressure with those that incorporated ambulatory or home blood pressure monitoring, highlighting biphasic effects of alcohol on blood pressure with an early presumably vasodilator effect of alcohol leading to a reduction in blood pressure (in the immediate hours after exposure) and a later effect (the next day) of raising blood pressure.
| Effects on Large Vessel Structure and Function |
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| Alcohol, the Metabolic Syndrome, and Diabetes |
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glutamyltransferase (
GT) levels seen in hypertensive subjects were caused alcohol. In this 6-year longitudinal study,
GT levels within the normal range were associated with incident hypertension in both drinkers and nondrinkers, but only in participants who were above median measures of fatness. The authors interpreted these findings to indicate that serum
GT may predict hypertension among individuals with increased central fat distribution, with fatty liver representing an important underlying mechanism for the association. A closely related area of interest concerns the possible link between alcohol consumption, diabetes, and the metabolic syndrome. Alcohol has been linked not only to an increase in blood pressure but to several other elements of this syndrome, in particular the increase in triglyceride levels, central adiposity, and elevated uric acid. However, alcohol simultaneously acts to increase HDL-cholesterol levels, so whether it makes any significant contribution to the metabolic syndrome has remained controversial. In the 1998 Korean National Health and Nutrition Examination Survey19 the consumption of >30 g alcohol/d was associated with an increase in blood pressure in men, a high blood glucose in women, and higher triglycerides in both men and women, whereas for both sexes and across all alcohol consumption categories there was a significant increase in HDL-cholesterol. Despite these contrasting effects on different components, overall there was a doseresponse relationship between increasing alcohol intake and the odds of having the metabolic syndrome. In contrast, a report on 4510 white participants from the National Heart and Blood Institute Family Heart Study in the United States, after careful adjustment for confounders including education, diet, and physical activity,20 actually found a substantially reduced prevalence of the syndrome across all beverage types compared with "never drinkers" (odds ratio down to 0.32 for wine drinkers only). Data from the Third National Health and Nutrition Examination Survey21 also suggested alcohol consumption was inversely associated with the prevalence of several components of the syndrome, low-serum HDL cholesterol, elevated serum triglycerides, high waist circumference, and hyperinsulinemia, a finding that was strongest among whites and among beer and wine drinkers. These contrasting results from several different population studies suggest that any overall effects of alcohol on the metabolic syndrome are probably dictated by a number of competing and confounding influences, such as volume and type of alcohol consumed, gender, race, and ethnicity. Therefore, an effect of alcohol to induce hypertension and the metabolic syndrome by impairing insulin resistance is doubtful. This is supported by a randomized controlled alcohol intervention trial involving a reduction of alcohol consumption by 80% for 4 weeks in regular moderate drinkers,22 which was unable to detect any effect of changing alcohol on glucose or insulin homeostasis. | Safe Levels of Drinking for Hypertensive People in the Context of Alcohol and the Global Burden of Hypertensive Disease |
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Further data on the relative benefits and risks of light to moderate alcohol consumption in hypertensive patients was provided from a study of total and cardiovascular mortality in a population of 14 125 men derived from the Physicians Health Study cohort and identified with a history of past or current treatment for hypertension.27 There were 1018 deaths during the study period, and about half of these were cardiovascular. Compared with individuals who reported that they rarely or never drank alcohol they found that those who reported monthly, weekly, or daily consumption had increasingly significant trends for reduced total and cardiovascular mortality. The beneficial effects of light to moderate drinking were seen regardless of whether blood pressure levels were above or below 140/90 mm Hg. However, the finding that consumption of as little as a single alcoholic drink monthly could reduce overall cardiovascular risk by 18% strongly suggests confounding from an unmeasured effect modifier. In this regard, nondrinkers have recently been characterized as an inappropriate comparison group for such studies that overestimate any beneficial effect of alcohol as a result.28 Similar confounding was probably also operative in a new study from France29 that involved a 13- to 21-year follow-up of 36 583 initially healthy middle-aged men. Moderate wine drinkers (their definition <60 g alcohol/d) had lower risks of deaths from all causes at all levels of systolic blood pressure. No significant reduction in all-cause mortality was seen in heavier drinkers or in those who consumed predominantly beer or spirits. Unmeasured confounding may have included dietary differences that differentiate beer, wine, and spirits drinkers as well as marked lifestyle differences, including patterns of alcohol consumption, that are likely to have impacted on many disease processes contributing to total mortality.30 The most recent study measuring cardiovascular outcomes in drinking hypertensive people was in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study cohort,31 which found that in drinkers there was no decrease in composite cardiovascular risk when being treated with losartan compared with atenolol because a decrease in the incidence of myocardial infarction in the drinkers was offset by an increase in the risk of stroke.
In terms of the overall significance of the effects of alcohol to elevate blood pressure, an analysis from the landmark World Health Organization Global Burden of Disease 2000 Comparative Risk Analysis study32 assessed the risks and benefits of alcohol by region and then globally and attributed 16% of all hypertensive disease to alcohol. To add to the controversy concerning "safe" levels of drinking, Jackson et al33 concluded that issues of bidirectional confounding in population studies had been underestimated in relation to alcohol and coronary heart disease and that any benefits of moderate alcohol consumption on coronary disease were likely to be outweighed by harmful effects (ie, there was "probably no free lunch").
Received January 18, 2006; first decision January 26, 2006; accepted March 8, 2006.
| References |
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