Alcohol and Hypertension

An Update
Lawrence J. Beilin, Ian B. Puddey

iven 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.

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

Pattern of Drinking, Beverage Type, and

Effects on Hypertension Subtypes
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
disease2 and considered further in an accompanying editorial3

Received January 18, 2006; first decision January 26, 2006; revision accepted March 8, 2006.
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@uwa.edu.au
(Hypertension. 2006;47:1-4.)
2006 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org

DOI: 10.1161/01.HYP.0000218586.21932.3c

Hypertension

June 2006

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 controlabstinence 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 trinitrate
mediated 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-four hour 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
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 women13,14 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 hypertension6 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

Alcohol, the Metabolic Syndrome,

and Diabetes
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
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

Beilin and Puddey

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
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
al25 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

Alcohol and Hypertension

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).

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