Hypertension. 2006;47:1035-1038
Published online before print April 3, 2006,
doi: 10.1161/01.HYP.0000218586.21932.3c
(Hypertension. 2006;47:1035.)
© 2006 American Heart Association, Inc.
Alcohol and Hypertension
An Update
Lawrence J. Beilin;
Ian B. Puddey
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
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Introduction
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Given the social significance of alcohol worldwide it is not
surprising that there is continuing strong interest in the relation
between alcohol and hypertension. Recent research continues
to address unresolved questions concerning the balance between
the medical hazards and the cardiovascular benefits of alcohol,
the possible significance of different types of beverage, the
role of different drinking patterns for cardiovascular morbidity
and mortality, and mechanisms underlying the pressor effects
of ethanol. These issues all need to be considered in the context
of social aspects of drinking and effects on noncardiovascular
morbidity and mortality. Epidemiologic data relating the type
or quantity of alcohol consumption to blood pressure or cardiovascular
disease needs to be viewed with circumspection from a number
of viewpoints. First, heavier drinkers or problems drinkers
are far less likely to participate in surveys than others. Second,
alcohol consumption past or present is notoriously underreported.
Third, drinking patterns are difficult to quantify and often
not reported at all. The type, quantity, and pattern of drinking
are all highly correlated with socioeconomic and other lifestyle
behaviors,
1 many of which may not be measured or not measured
accurately enough for adequate adjustments in statistical models.
A relation between average weekly alcohol consumption, blood
pressure level, and hypertension prevalence has been consistent
worldwide and continues to be studied in different populations
to evaluate its contribution in relation to other risk factors.
However, because of the above issues some caveats should be
put on interpretation of data where authors emphatically imply
causal relationships from statistical associations.
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.
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Pattern of Drinking, Beverage Type, and Effects on Hypertension Subtypes
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The relationship between the pattern of alcohol drinking and
the risk of hypertension was addressed in a cross-sectional
study of 2609 New Yorkers free from other cardiovascular disease
2 and considered further in an accompanying editorial
3 in which
some of the key issues surrounding the topic were discussed.
Compared with lifetime abstainers, those who reported drinking
on a daily basis or apart from food had a significantly higher
risk of hypertension, but this effect disappeared after accounting
for the amount of alcohol consumed in the previous 30 days.
When current drinkers only were studied and adjustment made
for the amount of alcohol consumed in the previous 30 days,
the risk of being hypertensive increased (64%) only in those
who said they drank without food. Preference for any one type
of beverage did not influence the association but the important
potential confounder of dietary habits was not assessed. Nevertheless
this finding was consistent with an earlier study of Italian
wine drinkers coming from a different cultural background,
4 and a follow-up in that population showed drinking alcohol outside
of meals was associated with higher risk of death from all causes
and cardiovascular disease. Similar relationships were seen
between drinking outside of meals or snacks and increased risk
of myocardial infarction in a recent case control study in men.
5
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.
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Effects on Large Vessel Structure and Function
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How might alcohol exert its coronary protective effects over
and above influences on high-density lipoprotein (HDL) cholesterol,
platelet function, and fibrinogen and in the face of adverse
effects on blood pressure and homocysteine metabolism? Cross-sectional
data from Holland described an inverse or J-shaped relation
between alcohol intake and measures of aortic stiffness in middle-aged
and older men and pre- and postmenopausal women
13,14 but not
in younger men.
15 They recognized that these results might be
confounded by other lifestyle factors but suggested that if
they were causally linked direct effects of alcohol to improve
vascular compliance might contribute to any cardioprotective
effect. As discussed in an accompanying editorial,
16 the findings
are not easy to reconcile with the association of alcohol with
isolated systolic hypertension
6 nor with a 9-year longitudinal
study showing an association between alcohol consumption and
increased aortic stiffness in middle-aged Japanese men who were
initially free of aortic stiffness.
17
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Alcohol, the Metabolic Syndrome, and Diabetes
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The nature of the association between liver enzymes, body fat
distribution, alcohol consumption, and the risk of hypertension
has been explored further in the Western New York longitudinal
study of 1455 men and women.
18 It had been assumed that the
increased

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 Survey
19 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 Survey
21 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.
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Safe Levels of Drinking for Hypertensive People in the Context of Alcohol and the Global Burden of Hypertensive Disease
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On the basis of coronary protective effects of red wine, Bulpitt
posed the question "How many alcoholic drinks might benefit
an older person with hypertension?"
23 Largely using meta-analyses
from general population studies, he concluded that hypertensive
patients aged >60 years who drank >16 drinks a week should
be advised to reduce their consumption. This is broadly in accord
with international guidelines on the management of hypertension.
Some of the pitfalls of limiting the focus to coronary artery
disease were discussed in an accompanying editorial.
24 Care
also needs to be taken in extrapolating data quantitatively
across cultures with widely differing coronary rates and social
circumstances. Connor et al
25 showed how some ethnic communities
living within Westernized populations, such as Maoris in New
Zealand, show a far higher burden from death, disease, and disability
from alcohol. In Japan stroke remains the most common cause
of cardiovascular death, coronary deaths are relatively low,
and there is a linear relation between alcohol consumption and
hemorrhagic stroke. Youthfulness carries an increased share
of hazards associated with alcohol caused by drinking patterns,
risky behaviors, and greater periods of exposure to alcohol-related
liver disease and cancers, and the age dependence of alcohol
risks and benefits has been well illustrated by Jackson and
Beaglehole.
26
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.
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