Context Moderate alcohol consumption has been shown to be
protective for coronary heart disease, but the relationship between
moderate alcohol consumption and ischemic stroke is more controversial.
Objective To determine the association between alcohol
consumption and risk of ischemic stroke.
Design Population-based case-control study conducted between July
1993 and June 1997.
Setting Multiethnic population in northern Manhattan, New York,
NY, aged 40 years or older.
Patients and Other Participants Cases (n=677) had first
ischemic stroke and were matched to community controls (n=1139)
derived through random digit dialing by age, sex, and race/ethnicity.
Mean ± SD age of cases was 70.0 ± 12.7 years; 55.8% were women;
19.5% were white, 28.4% black, and 50.7% Hispanic.
Main Outcome Measure First ischemic stroke (fatal or nonfatal).
Results Moderate alcohol consumption, up to 2 drinks per day, was
significantly protective for ischemic stroke after adjustment for
cardiac disease, hypertension, diabetes, current smoking, body mass
index, and education (odds ratio [OR], 0.51; 95% confidence interval
[CI], 0.39-0.67). This protective effect of alcohol consumption was
detected in both younger and older groups, in men and women, and in
whites, blacks, and Hispanics. In a quadratic model of stroke risk,
increased risk of ischemic stroke was statistically significant among
those consuming 7 or more drinks per day (OR, 2.96; 95% CI,
1.05-8.29).
Conclusions Moderate alcohol consumption was independently
associated with a decreased risk of ischemic stroke in our elderly,
multiethnic, urban subjects, while heavy alcohol consumption had
deleterious effects. Our data support the National Stroke Association
Stroke Prevention Guidelines regarding the beneficial effects of
moderate alcohol consumption.
Several
case-control and prospective cohort studies have shown that moderate
alcohol consumption has a protective effect on the risk of cardiac
mortality and myocardial infarction.1-3 The effect of
moderate alcohol consumption on stroke is controversial. While several
case-control4,5 and prospective cohort6-9
studies have shown that alcohol consumption has a direct dose-dependent
effect on the risk of hemorrhagic stroke, the data on infarction, which
accounts for approximately 80% of all strokes, are contradictory. Some
studies suggest that moderate consumption confers a protective effect
on the risk of ischemic stroke in certain
populations,8,10-16 while studies in other populations find
no beneficial effect.6,17-28 It has been speculated
that there is a differential effect of alcohol dependent on
race/ethnicity since studies in white
populations10-12,14,15 have found a protective effect,
while those in Asian populations9,18,23,27,28 have not.
Among blacks, some studies have found a protective
effect,13 while others have not.21 No study has
addressed the relationship between alcohol and stroke among Hispanics.
To help clarify the relationship of alcohol consumption to ischemic
stroke among different racial/ethnic groups, we undertook a
population-based case-control study in a multiethnic, elderly population.
The Northern Manhattan Stroke Study (NOMASS) is a population-based
study designed to determine stroke incidence, risk factors, and
prognosis in a multiethnic, urban population. Northern Manhattan
consists of the area in New York City north of 145th Street, south of
218th Street, bordered on the west by the Hudson River and on the east
by the Harlem River. In 1990, nearly 260,000 people lived in the
community with 40% older than 39 years and a racial/ethnic mixture
consisting of 20% black, 63% Hispanic, and 15% white
residents.29
Cases eligible for this population-based case-control study were
prospectively enrolled if they met the following criteria: (1)
diagnosed as having first cerebral infarction after July 1, 1993; (2)
older than 39 years at onset of stroke; and (3) resident in northern
Manhattan in a household with a telephone. Patients with intracerebral
or subarachnoid hemorrhage or transient ischemic attack, defined as
neurologic deficits lasting less than 24 hours and no ischemic infarct
found on brain imaging, were excluded. Patients with fatal or nonfatal
infarcts were enrolled. The methods of case detection in NOMASS have
been described previously.30 The study was approved by the
institutional review boards at Columbia-Presbyterian Medical Center and
other primary hospitals, and all participants provided written informed
consent.
The methods of control recruitment and enrollment have
been described in a previous publication.31 Random digit dialing of approximately 16,000 households was performed by
Audits and Surveys, Inc, New York, NY. Community controls were enrolled
if they (1) had never been diagnosed as having stroke, (2) were older
than 39 years, and (3) resided in northern Manhattan for 3 months or
longer in a household with a telephone. Ninety-four percent of those
contacted by telephone provided responses to a telephone survey that
included questions about alcohol use, smoking, hypertension, and other
risk factors. Of those who provided answers to the telephone survey,
70% participated in an in-person interview and examination. For
this analysis, 2 concurrent control participants were prospectively
selected and matched to stroke cases by age within 5 years, sex, and
race/ethnicity. For those stroke cases for whom additional, individual
matched controls were not available (8%), matching to controls already
used was permitted.
Index Evaluation of Cases and Controls
Data were collected through interviews of cases and controls by trained
research assistants, medical record review, physical and neurologic
examination by the study physicians, in-person measurements, and
fasting blood specimens for lipid and glucose measurements, as
described elsewhere.31 In-person
evaluations of cases and
controls were performed at the medical center or at home for those who
could not come in person or who had a nonhospitalized stroke (6% were
done at home). When possible, data were obtained directly from
participants using the standardized data collection instruments. When
the participant was unable to provide answers, a proxy knowledgeable
about the participant's history was interviewed. Stroke-free controls
were interviewed in person and evaluated in the same manner as cases.
Direct participant data were obtained from 70% of cases and 99% of
controls.
Standardized questions were adapted from the Behavioral Risk Factor
Surveillance System32 by the
Centers for Disease Control
and Prevention regarding the following conditions: hypertension,
diabetes, hypercholesterolemia, peripheral vascular disease, transient
ischemic attack, cigarette smoking, and cardiac conditions such as
myocardial infarction, coronary artery disease, angina, congestive
heart failure, atrial fibrillation, other arrhythmias, and valvular
heart disease. Standard techniques were used to measure blood pressure,
height, weight, and fasting glucose level as described in prior
publications.33 Fasting lipid panels,
including total cholesterol, low-density lipoprotein cholesterol, high-density
lipoprotein (HDL) cholesterol, and triglyceride, were measured using an
automated spectrometer (Hitachi 705, Boehringer, Mannheim, Germany). In
60% of cases the blood was drawn within 72 hours of admission.
Hypertension, diabetes mellitus, and body mass index (BMI) were defined
as in prior publications.31,33
Alcohol Consumption Assessment
Alcohol use was assessed through structured in-person interviews using
questions adapted from the National Cancer Institute food frequency
questionnaire developed by Block et al34 and the food frequency questionnaire of Willett et al.35 The questions were modified to provide a defined frequency response set, as in the
Willett questionnaire.35,36 Inquiries were made about
consumption of 3 different forms of alcohol (wine, beer, and liquor)
both during the past year and on average during the participant's
drinking lifetime. The defined responses regarding frequency allowed 9
possibilities ranging from never to 7 or more drinks per day for each
beverage type. The responses for each beverage type were then summed to
obtain a total overall quantity. A standard drink was considered to be
120 mL of wine, 360 mL of beer, and 45 mL of liquor. In addition, an
alcoholism screening questionnaire containing 4 structured questions
(CAGE)37 and questions about binge drinking and
hospitalizations for alcohol-related illness were asked to assess for
pathologic drinking patterns for which food frequency questionnaires
may be less sensitive.38,39
Statistical analysis was performed using SAS software (SAS Institute,
Cary, NC). Our main analyses used average daily alcohol consumption
during the past year. The frequency and quantity of alcohol consumed
were examined in cases and controls. The mean daily quantity of alcohol
consumed by each participant was calculated as drinks per day,
regardless of beverage type. For the matched data, conditional logistic
regression was used to calculate unadjusted odds ratios (ORs) for the 9
drinking frequency categories, with those who had abstained during the
past year as the reference group. After exploring the magnitude and
direction of the effect estimate for individual frequency categories,
alcohol consumption was divided into 4 categories: (1) reference: no
drinks during the past year; (2) moderate: at least 1 drink per year up
to 2 drinks per day; (3) intermediate: more than 2 but fewer than 5
drinks per day; and (4) heavy: 5 or more drinks per day. Multivariate
conditional logistic regression was used to calculate the ORs and 95%
confidence intervals (95% CIs) for alcohol consumption and stroke after
adjustment for the potential confounding risk factors (hypertension,
diabetes, cardiac disease, current smoking, education, and BMI).
Adjusted analyses were performed overall and stratified by age, sex,
and race/ethnicity. A separate analysis was performed after controlling
for HDL among the participants who had this measurement performed.
Because of the small number of individuals (24 cases and 18 controls)
who drank 5 or more drinks per day, alcohol consumption was also
modeled continuously using a quadratic formula to increase the power to
detect an effect among those in higher categories of alcohol consumption.
Further analyses were conducted to evaluate the effects of the type of
alcoholic beverage, average lifetime alcohol use, and former heavy
drinking. Participants who drank at least 1 drink per month but no more
than 2 per day were divided into 4 categories depending on their
predominant beverage type. Those who drank 1 type of drink at least
monthly were considered predominant drinkers of that beverage type
(wine, beer, or liquor), as long as they drank both of the other 2
beverage types less often than monthly. Those who drank more than 1
beverage type monthly were considered combination drinkers.
Substudies were undertaken to assess construct validity and proxy
reliability of the alcohol assessments. Among a random sample of stroke
cases and their proxies, test-retest and proxy reliability of the
alcohol consumption questionnaire was analyzed. To evaluate whether
using proxy responses led to bias in estimates of the OR, an additional
analysis was performed restricted to nonproxy data. Control selection
bias was evaluated using the telephone survey alcohol response data.
The log (OR) of being selected as a control dependent on alcohol
consumption status was calculated and added to the model log (OR) to
correct for potential selection bias.40,41 The CIs for
these bias-corrected estimates were calculated using a selection model
estimated from the telephone survey data rather than a known selection
model. A method for the calculation of the CIs that adjusts for the
estimated selection model is not yet available in the statistical
literature and may produce CIs wider than those reported here. All
tests were 2 sided, and significance was accepted at the P=.05 level.
Over 4.0 years, 688 ischemic stroke patients were enrolled in this
population-based case-control study. For this analysis, 677 cases
(98.5%) were used; 11 cases were excluded because of lack of available
data on alcohol consumption. The 30-day case-fatality rate among
enrolled cases was 4.9%, and the mean ± SD and median National
Institutes of Health Stroke Scores (range, 0-43) were 7.6 ± 6.8 and
5.0, respectively. The 677 ischemic stroke cases were matched by age,
sex, and race/ethnicity using expanded strata where necessary, as
described above, to 1139 controls. Among stroke cases, the mean ± SD
age was 70.0 ± 12.7 years. There were 55.8% women, and 19.5% of the
subjects were non-Hispanic white, 28.4% non-Hispanic black, 50.7%
Hispanic (black or white), and 1.4% other. The ethnic distribution of
our Hispanic case population was 62.7% Dominican, 15.6% Puerto Rican,
11.5% Cuban, and 10.3% other. Cases were more likely to have
hypertension, cardiac disease, and diabetes mellitus, and controls were
more likely to have a high school education (Table 1).
The distribution of alcohol use among our elderly control group showed
that the majority of the population did not drink alcohol or drank only
in moderation (Table 2). Among
controls, 53.1% stated they did not drink any alcohol over the
preceding year, and an additional 40.7% drank up to 2 drinks per day
on average. Controls who participated in person had a similar frequency
of diabetes, cardiac disease, and current smoking but were more
likely to be overweight and less likely to have hypertension than those
subjects who did not participate in person based on analyses of
telephone response data. No significant relationship existed between
moderate or heavy drinking and the likelihood of in-person evaluation,
but the likelihood of in-person
participation was increased among subjects who consumed
intermediate quantities of alcohol.
The reliability and validity of our alcohol assessment tool were
good in our sample. Test-retest reliability among 37 stroke-free
participants demonstrated good correlation (Pearson
R=0.62; P<.001). The reliability of proxy
respondents among 16 stroke cases was also good (Pearson
R=0.81; P<.001). Construct validity of the
alcohol assessment was measured by comparing responses to the alcohol
frequency questions with responses to the CAGE questions and other
questions about drinking history. A significant association between
alcohol frequency responses and CAGE questionnaire responses was
demonstrated (χ2 for linear trend, P<.001).
Results were similar for other questions about problem drinking.
Our case-control analyses, matched by age, sex, and
race/ethnicity but unadjusted for other variables, demonstrated that
moderate average daily alcohol consumption in the preceding year was
protective against ischemic stroke. Those drinking at least 1 drink per
year but less than 1 per month, at least 1 drink per month but less
than 1 per day, and at least 1 but no more than 2 drinks per day all
had similar risks of ischemic stroke (Table 2) and were combined into 1
group, moderate drinkers, for further analyses. Those drinking up to 2
drinks per day had a statistically significantly reduced risk of
ischemic stroke compared with those who were not current drinkers, the
reference group (unadjusted OR, 0.58; 95% CI, 0.35-0.94; Table 3). The protective effect of moderate
alcohol consumption persisted after adjusting for hypertension,
diabetes, cardiac disease, current smoking, education, and BMI
(adjusted OR, 0.51; 95% CI, 0.39-0.67). These effects were similar in
analyses restricted to nonproxy data. Our telephone survey response
data were used to further adjust our estimates for potential control
selection bias attributable to differences among alcohol consumption
between controls who participated in person and the base population.
The protective effect of moderate alcohol use persisted with a new
adjusted OR of 0.55 (95% CI, 0.42-0.72).
The protective effect of alcohol consumption in our subjects was not
explained by an elevation in HDL levels. The independent protective
effect of moderate alcohol use remained after HDL was added to our
model in an analysis among the 1458 participants (92.2% of study
sample) with HDL data (adjusted OR, 0.53; 95% CI, 0.28-1.0;
P=.048). No interaction of HDL with moderate drinking was
found.
The protective effect of moderate alcohol consumption was demonstrated
in subgroup analyses based on age, sex, and race/ethnicity (Table 4). No significant interaction was found
between age, sex, or race/ethnicity and alcohol consumption. There were
differences in consumption in the control group according to age, sex,
and race/ethnicity (Table 4).
Intermediate quantities of alcohol also demonstrated a trend toward
protection (adjusted OR, 0.58; 95% CI, 0.33-1.03; Table 3). After
correction for selection bias, however, the OR for the intermediate
group, in whom selection bias was greatest, increased from 0.58 to
0.77. Heavy drinking (≥5 drinks per day) was
associated with an increased risk of stroke (OR, 1.63; 95% CI,
0.74-3.62), with minimal change (OR, 1.55; 95% CI, 0.70-3.43) after
adjusting for selection bias. The relationship between alcohol
consumption and stroke fit a quadratic model. The results
(Figure 1) demonstrated a J-shaped
relationship between alcohol consumption and stroke risk, with a
statistically significant increase in stroke risk among those drinking
7 or more drinks per day (OR for those drinking 7 drinks per day, 2.96;
95% CI, 1.05-8.29).
We found no differential protective effects among the types of
alcoholic beverages. Our sample of moderate drinkers was subdivided
into 4 groups based on predominant drink type: 17.2% drank
predominantly wine, 17.2% beer, and 30.2% liquor; 35.3% were
classified as combination drinkers. On average, those who were
predominantly wine drinkers consumed less alcohol than those who drank
beer or liquor or were combination drinkers (Table 5). A similar protective effect of drinking
up to 2 drinks per day in each of the 4 beverage categories was observed.
To address the possibility that those stroke patients not currently
drinking may in fact represent individuals who curtailed their drinking
because of early symptoms of cerebrovascular disease, we performed a
separate analysis using those identified as lifetime abstainers as the
reference group. The protective effects of moderate average daily
alcohol consumption in the preceding year persisted (adjusted OR, 0.43;
95% CI, 0.31-0.58). Average daily alcohol consumption over the
participant's lifetime was analyzed in the subset of 62.6% of
participants in whom these data were collected (372 cases and 623
controls). The protective effect of moderate average lifetime drinking
was similar to that of drinking over the preceding year when compared
with lifetime abstainers (258 cases, 307 controls; adjusted OR, 0.54;
95% CI, 0.38-0.78). Those who during their lifetime drank 5 or more
drinks per day but were currently drinking 2 or fewer drinks per day
(ie, reformed heavy drinkers, 24 cases, 26 controls) did not have a
significantly increased stroke risk (OR, 0.66; 95% CI, 0.31-1.41).
Our results demonstrate a protective effect of moderate alcohol
consumption on ischemic stroke risk in a multiethnic, elderly
population. Moderate consumption—up to 2 drinks of liquor, 2 cans of
beer, or 2 glasses of wine per day—was protective with an OR of 0.5.
This protective effect of moderate alcohol consumption persisted after
adjusting for other stroke risk factors and was found in younger and
older participants, men and women, and in whites, blacks, and
Hispanics. In addition, we found that very heavy alcohol consumption—7
or more drinks per day—was associated with an increased risk of
ischemic stroke.
The protective relationship between moderate alcohol
consumption and coronary artery disease has been well studied and
confirmed in several case-control and cohort studies.1-3 A
meta-analysis of the data found a summary relative risk of 0.83 for
moderate drinkers compared with lifetime abstainers.1 The
relationship of alcohol consumption to stroke risk is more
controversial, partly because many studies fail to distinguish between
hemorrhagic and ischemic stroke. Many studies have shown an increased
risk of hemorrhagic stroke associated with increasing alcohol
consumption in a dose-dependent fashion.4-9 Those studies
that have investigated alcohol as a risk factor for ischemic stroke
have found conflicting results and have not agreed on the optimal
protective dose of alcohol.6,8,10-26 Our finding of a
protective effect of moderate drinking agrees with several case-control
studies of the relationship between ischemic stroke and
alcohol,10-12,14-16 conducted predominantly among white
subjects. Other case-control studies of ischemic stroke found possible
trends toward a protective effect of alcohol24 but failed to confirm an independent relationship between ischemic stroke and
alcohol.17,20,25 In a study mostly among black
participants, current weekly alcohol consumption was associated with an
increased risk for cerebral infarction but failed to be significant
after controlling for confounding by smoking and
hypertension.21
Among prospective cohort studies, 2 have found a protective
relationship between moderate drinking and ischemic
stroke.8,13 The US Nurses' Health Study found a protective
effect of moderate alcohol consumption (up to 1.2 drinks per day) on
ischemic stroke among women.8 In a study using an
administrative database, all levels of alcohol consumption were
associated with a decreased risk of hospitalization for ischemic stroke
in both men and women, but a stronger protective effect was found in
blacks than in whites.13 Other cohort studies looking
specifically at ischemic stroke6,19,22 have failed to
confirm this relationship. Many prospective studies have analyzed total
stroke (approximately 80% of which is ischemic) and found a protective
effect of moderate drinking,26,42-46 while others have not.
Some of these studies, however, did not classify drinkers by quantity
consumed or relied on data about alcohol abuse only.
No study among Japanese subjects has shown a protective effect of
alcohol,9,18,23,27,28 suggesting that alcohol's effect on
stroke risk may vary by race/ethnicity. Recent data also suggest there
may be different subgroups among American blacks, some of whom may
share the risk factor profiles typical of white
populations.47 Our finding of a protective relationship
between moderate alcohol consumption and ischemic stroke in blacks,
unlike other studies, may reflect underlying differences between our
black population and those examined in other studies.21
Hispanics have rarely been enumerated separately in stroke and
cardiovascular epidemiologic studies, and our study is the first to
find a protective relationship between moderate alcohol and ischemic
stroke in this racial/ethnic subgroup. Like blacks, Hispanics comprise
a heterogeneous group. The northern Manhattan Hispanic population is
predominantly from the Dominican Republic and may be quite different
from the Mexican Americans of the southwestern United States. Our study
is also different from others in that it allows study of different
racial/ethnic groups living in the same community and thereby may
minimize the environmental effects seen when racial/ethnic groups from
separate communities are studied.
The protective effect of alcohol on heart disease appears to be
partially mediated by the increase in HDL-2 and HDL-3 associated with
alcohol consumption.2,3,48,49 The relative importance of
HDL in mediating alcohol's effect on stroke has not been well studied;
none of the other studies correlated alcohol intake, HDL, and stroke.
In our analyses, much of the protective effect of alcohol on stroke
risk was independent of HDL. Data from NOMASS using repeated measures
of lipid levels at intervals after acute stroke, moreover, suggest that
the level of HDL is not significantly altered by acute
stroke.50 In other studies,51 serum lipid
levels decreased slightly after stroke, but HDL remained relatively
more constant than other lipid or lipoprotein fractions. Other
potential alcohol-induced protective mechanisms that were not evaluated
in our study include decreased platelet aggregability, increased
prostacyclin-thromboxane ratios, and a decrease in fibrinogen
levels.21,52
Some investigators have suggested that certain types of alcoholic
beverages, particularly wine, are more protective than
others.53,54 We investigated whether any differential
protective effect by beverage type exists and found that wine, beer,
and liquor all had approximately the same effect, although in our study
wine drinkers consumed less alcohol. This is in accord with most other
studies of the protective effect of alcohol on coronary artery
disease.3,48
Our data did not permit us to distinguish
between consumption of red wine and white wine.
In our study, a quadratic model demonstrated that there is a
J-shaped relationship between alcohol consumption and risk of ischemic
stroke. Drinking 7 or more drinks daily is associated with a
statistically significant increased risk of ischemic stroke. Because of
the small number of subjects who reported drinking heavily, however, we
are obliged to interpret these results with caution. Nonetheless, these
observations are consistent with those of several other studies that
have found higher doses of alcohol to be a risk factor for ischemic
stroke10,12,14,18,23,26,55 and extend these observations to
a multiethnic population. We were also able to demonstrate that former
heavy drinkers who decrease their drinking to no more than 2 drinks per
day do not maintain an increased risk of stroke.
Proposed mechanisms for the increased risk of ischemic stroke among
those who drink heavily include hypertension, alcohol-induced
cardiomyopathy, and atrial fibrillation.52 Our data show that the increased risk persists even after controlling for potential
mediators such as hypertension and cardiac disease, suggesting there
may be other unidentified mechanisms by which excessive alcohol use
leads to an increased risk of stroke. Other possible mechanisms include
cerebral vasoconstriction and spasm,56 arterial dissection associated with trauma, hyperviscosity due to dehydration, increased
platelet reactivity,57,58 and
hyperhomocysteinemia.59
The methodological problems of the study of alcohol as a risk factor
for stroke have been reviewed by others.24,42,60 Not all
studies are consistent in their definitions of moderate alcohol
consumption. We defined our category of moderate alcohol consumption
based on the similarity in risk of ischemic stroke observed among those
in subcategories of drinking up to 2 drinks per day. We chose 2 drinks
per day as the upper limit of moderate consumption because this
quantity has been accepted by several investigators13,42,45
and also because this is a commonly encountered, clinically meaningful
quantity.
In case-control studies, control selection can lead to a variety of
biases. The use of community-based controls, as in our study, probably
gives the best estimate of the underlying prevalence of an exposure, as
long as study participation is not related to alcohol use. Our
telephone survey response analyses did not demonstrate a significant
bias with regard to alcohol use, and where a trend toward bias existed,
it spared moderate and heavy drinking groups. Moreover, no significant
changes in the associations of either moderate or heavy drinking with
stroke risk were found when we corrected for selection biases. In
addition, data available from the US Census29 indicate that, on other markers of socioeconomic status, such as education, our
control sample is similar to that of the underlying population. In our
control group older than 40 years, 79.3% of whites, 63.3% of blacks,
and 23.2% of Hispanics completed high school, and the US Census data
from northern Manhattan for all age groups indicate that 90.7%,
72.3%, and 43.5%, respectively, completed high school. Our stroke
cases, furthermore, should be representative of the spectrum of stroke
in the underlying population. We included both mild, nonhospitalized
stroke cases and severe fatal strokes, and our results should therefore be
generalizable to most populations of stroke patients.
Recall bias may also affect case-control studies, but it would have to
be postulated that the bias operated in different directions among
moderate and heavy drinkers since a J-shaped relationship was found.
Moreover, measurement of alcohol consumption was assessed using
structured in-person interviews, a method used and validated in other
large epidemiologic studies.61,62 Our construct validity
analysis suggested a good correlation between other measures of problem
drinking and drinking more than 5 drinks per day, quantities for which
food frequency questionnaires may be less sensitive.38,39
One of the major methodological weaknesses of any epidemiologic studies
of alcohol and stroke is the bias attributable to the "sick
quitter" hypothesis: persons who are ill or experiencing early,
preclinical symptoms of disease may decrease their usual alcohol
consumption.42 Assessment of current or recent alcohol exposure may underestimate true lifetime alcohol exposure and lead to a
misclassification of exposure status. Moreover, people tend to drink
less as they age.63 Therefore, assessment
of current alcohol use in an elderly population is likely to systematically
underestimate lifetime exposure. We attempted to minimize this
potential misclassification in several ways. First, we performed our
analysis using 2 different reference groups, those who were not current
drinkers and lifetime abstainers, and obtained similar results. Second,
we used as our measure of alcohol exposure both consumption during the
past year and average lifetime consumption and found a similar
protective effect. Third, we controlled for other confounding
diseases that may have both predisposed an individual to stroke and led
to a decrease in alcohol consumption.
In conclusion, our study demonstrates that moderate alcohol consumption
may have important health benefits in terms of reducing the risk of
ischemic stroke, particularly in an elderly, urban, multiethnic
population. These benefits, of course, need to be weighed against the
overall risk of morbidity and mortality due to excess alcohol
consumption. Additionally, our study supports the advice that heavy
drinkers can decrease their risk of ischemic stroke by decreasing or
discontinuing their alcohol intake. While no study has shown benefit in
recommending alcohol consumption to those who do not drink, our data
support the view, endorsed by the National Stroke Association in its
Stroke Prevention Guidelines,64 that, among those who are moderate drinkers, continued consumption may provide a reduction of
ischemic stroke risk.
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