Alcohol Consumption and Risk of Ischemic Stroke

The Framingham Study

Luc Djouss, MD; R. Curtis Ellison, MD; Alexa Beiser, PhD; Amy Scaramucci, MPH;
Ralph B. DAgostino, PhD; Philip A. Wolf, MD

Background and PurposeStroke is a major cause of death in the United States. The association between alcohol
consumption and ischemic stroke (IS) remains controversial.
MethodsWe used data collected on participants in the Framingham Study to assess the association between total alcohol
intake and type of alcoholic beverage and development of IS, overall and according to age.
ResultsA total of 196 men and 245 women developed IS during three 10-year follow-up periods. In the categories of
never drinkers, drinkers of 0.1 to 11, 12 to 23, and 24 g/d of ethanol (a typical drink is 12 g of ethanol), and former
drinkers of 0.1 to 11 and 12 g/d, crude incidence rates of IS were 6.5, 5.9, 4.9, 5.0, 6.7, and 17.8 cases per 1000
person-years, respectively, for men and 5.9, 4.1, 4.1, 4.3, 8.3, and 7.1, respectively, for women. Overall, compared with
never drinkers in a multivariate Cox regression, current alcohol consumption was not related significantly to IS in either
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sex. Former drinking of 12 g/d of alcohol was associated with a 2.4 times higher risk of IS among men but not among
women. When stratified by age, alcohol intake was associated with lower risk of IS among subjects aged 60 to 69 years.
In beverage-specific analysis, only wine consumption was related to a decreased risk of IS.
ConclusionsOur data showed no significant association between total alcohol and IS overall but showed a protective
effect of alcohol among subjects aged 60 to 69 years. (Stroke. 2002;33:907-912.)
Key Words: alcohol drinking beer cerebrovascular accident stroke, ischemic wine

S troke remains one of the major causes of death in the

United States and is associated with a substantial
economic burden.1 Epidemiological studies have been
inconsistent on the relation of total alcohol and type of
alcoholic beverage to stroke.2 4 While some studies have
suggested an increased risk of stroke with alcohol in-
take,59 there is evidence that consumption of small to
moderate amounts of alcohol may be associated with lower
risk of ischemic stroke (IS).3,10 16 The protective effect of
alcohol on blood vessels may be mediated through the
effects of alcohol on lipid peroxidation and coagulation.17
Little is known about type of alcoholic beverage and the
risk of IS. Some studies have reported that wine consump-
tion, but not beer or spirits intake, was related to a lower
risk of stroke.10,18 Beer, wine, and spirits could have
different effects on cardiovascular disease from other
substances contained in these beverages, such as polyphe-
nols with antioxidant properties that may influence cardio-
vascular pathophysiology.13,19,20 In the present study we
assessed the relation of total alcohol consumption and type
of alcoholic beverage to IS, overall and according to age.
Subjects and Methods
The Framingham Study is a population-based cohort study of 5209
subjects that started in 1948 in Framingham, Mass. After the first
examination in 1948 1952, participants have been reexamined
biennially. Detailed descriptions of the Framingham Study have been
published previously.21,22 Informed consent was obtained repeatedly
from study participants, and the study protocol was approved by the
Institutional Review Board of the Boston University School of
Medicine.
Assessment of Alcohol Consumption
Data on alcohol have been collected at examinations 2, 7, 9, 12 to 15,
and 17 and at all subsequent examinations with the use of standard-
ized questionnaires. At each of these examinations, each participant
was asked if he/she had consumed alcohol in the past 12 months. If
the answer was affirmative, the average weekly number of drinks
consumed over the past year for spirits, beer, and wine was recorded.
For this study, a drink was defined as 360 mL of beer containing
12.6 g of alcohol, 120 mL of wine containing 13.2 g of alcohol, or
37.5 mL of 80 proof spirits (approximately 40% ethanol by volume)
containing 15 g of alcohol. At each examination, total alcohol was
computed as the sum of ethanol contents in beer, wine, and spirits
consumed. We used alcohol information from the second examina-
tion to classify former drinkers; thus, follow-up for the present
analyses began with examination 7.

Received October 15, 2001; final revision received December 14, 2001; accepted December 17, 2001.
From the Section of Preventive Medicine and Epidemiology, Boston University School of Medicine (L.D., R.C.E, P.A.W.); Department of
Epidemiology and Biostatistics, Boston University School of Public Health (A.B., A.S.); and Department of Mathematics, Boston University (R.B.DA.),
Boston, Mass.
Correspondence to Luc Djouss, MD, MPH, Boston University School of Medicine, 715 Albany St, Room B-612, Boston, MA 02118. E-mail
ldjousse@bu.edu
2002 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org

907
 908 Stroke April 2002
Outcome
Stroke events were detected by review of interim Framingham Heart
Study examinations, daily surveillance of all admissions to the local
hospital, and scrutiny of outside hospital records. For all potential
cases of stroke, a panel of 3 investigators (including a neurologist)
reviewed all medical records, radiographic images, a medical his-
tory, and findings from physical examinations performed at the
Framingham Study to determine whether a stroke has occurred. In
addition, since 1968, whenever possible, the Framingham Study
neurologists have examined subjects in the hospital at the time of
acute stroke. A detailed description of the stroke assessment in the
Framingham Study has been published previously.23 Stroke events
were categorized with previously published criteria as atherothrom-
botic brain infarction, cerebral embolus, intraparenchymal hemor-
rhage, or subarachnoid hemorrhage.24 Because of the small number
of nonischemic strokes (n63), the present study was limited to IS.
Other Variables
Cigarette smoking information was obtained through a standardized
questionnaire. Subjects were asked if they smoked cigarettes in the
past year, and, if the answer was affirmative, the number of
cigarettes smoked per day was recorded. Resting blood pressure was
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measured twice by a physician according to a standard protocol,
using a mercury sphygmomanometer and appropriately sized cuff.
Subjects were asked about antihypertensive medications during each
examination. Diabetes mellitus was defined as a history of physician-
diagnosed diabetes mellitus or current treatment with hypoglycemic
medications. Prevalent coronary heart disease was ascertained by
standard protocols described previously.21,25 Height and weight were
measured at every examination. Body mass index was computed as
weight in kilograms divided by the square of height in meters. Atrial
fibrillation and left ventricular hypertrophy were assessed through
the review of standard 12-lead ECGs obtained at each visit.
Statistical Methods
Since alcohol consumption and/or the number of cigarettes smoked
per day might change over time, a pooling method using subsequent
10-year follow-up periods (nonoverlapping) was used. For each
10-year period, information on alcohol intake and other covariates
collected at the beginning of the follow-up period was used. Thus,
alcohol consumption at the beginning of each of the three 10-year
periods (at examinations 7, 12, and 17) was used as exposure in the
pooled data. Of the 9628 person-observations, 457 were excluded for
the following reasons: missing information on alcohol (n44),
inability to determine former drinking status (n138), or prevalent
stroke or history of transient ischemic attack (n275). The final data
set consisted of 9171 person-observations. Each subject could
contribute to 1 (n1110), 2 (n1203), or 3 (n1885) observations
in the analyses if he/she was free of stroke at the beginning of each
10-year period.
For the initial 10-year follow-up period, each nondrinking partic-
ipant at examination 7 was classified as former nondrinker or
former drinker on the basis of his/her reported alcohol consump-
tion at examination 2. For subsequent follow-up periods, previous
drinking status was based on alcohol data recorded at all examina-
tions preceding the beginning of the period. We classified subjects as
never drinkers, current drinkers of 0.1 to 11, 12 to 23, and 24 g/d,
and former drinkers of 0.1 to 11 and 12 g/d. Similar point estimates
were obtained for current drinkers of 24 to 35 and 35 g/d, and
therefore we collapsed these categories. We calculated person-years
of follow up as the time from the beginning of each follow-up period
to the occurrence of either (1) IS; (2) loss to follow-up; or (3) death,
hemorrhagic stroke, or end of the 10-year period.
Age is an important determinant of stroke and also relates strongly
to alcohol consumption. This is especially true for the elderly (aged
70 years), who may be in nursing homes or other facilities that
limit their access to alcohol. Therefore, we examined the risk of IS
overall as well as by age categories (50, 50 to 59, 60 to 69, 70
years). Within each sex, we fitted a Cox model to estimate the
association of alcohol consumption to IS. The first model adjusted
for age only. The full model controlled for age, diabetes mellitus
(yes/no), smoking categories, and body mass index. Additional
adjustment for blood pressure, left ventricular hypertrophy (yes/no),
atrial fibrillation (yes/no), antihypertensive treatment (yes/no), and
prevalence of coronary heart disease (yes/no) at the beginning of
each interval did not alter the results. Both sexes were combined for
age-specific analyses. Since there were few cases of IS (n8) in the
category 50 years, this stratum was dropped in the stratified
analysis. Assumptions for the proportional hazard models were
tested and were met.
To assess the association between beverage-specific alcohol and
IS, we classified subjects as never or current drinkers for each type
of beverage. We excluded former drinkers in this secondary analysis.
In addition to the aforementioned covariates, the effects of each
beverage type were adjusted for the other 2 beverages (by using 3
indicator variables for the 3 types of beverage in the same model).
Thus, while controlling for the intake of other beverages, we
evaluated whether each specific type affected the risk of IS differ-
ently from other beverages.
Results
Table 1 presents the baseline characteristics of the study
participants, according to alcohol consumption. During the
three 10-year follow-up periods, 196 men and 245 women
developed IS. As shown in Table 2, crude incidence rates
among men were lowest in those consuming 12 to 23 g/d of
ethanol (4.9/1000 person-years) and highest in the former
heavier drinker category (17.8/1000 person-years). For
women, the lowest incidence rates were in women consuming
0.1 to 11 g/d and 12 to 23 g/d of ethanol (4.1 and 4.1 cases per
1000 person-years, respectively) and highest in former drink-
ers. In the multivariate model, alcohol consumption was not
significantly associated with IS in either sex (Table 2).
Among men who were former heavy drinkers, the risk of IS
was 2.4 times greater that that of never drinkers among men,
but no increase in risk was seen among women (Table 2).
Table 3 presents combined data for men and women
stratified by age. A protective effect of alcohol intake on the
risk of IS was observed in the age category of 60 to 69 years
but not in the age groups of 50 to 59 and 70 years.
Compared with never drinkers, the multivariate relative risks
(95% CI) for 60 to 69 year-old subjects were 0.5 (0.3 to 0.8),
0.3 (0.2 to 0.7), 0.5 (0.3 to 0.9), 0.5 (0.3 to 0.8), and 1.2 (0.6
to 2.4) for the categories of drinkers of 0.1 to 11, 12 to 23, and
24 g/d and former drinkers of 0.1 to 11 and 12 g/d,
respectively (Table 3). These results were not altered when
additional risk factors were included in the model.
In a secondary analysis, we assessed the effects of beer,
wine, and spirits on the risk of IS. There were 115 cases of IS
(23 128 person-years) among wine drinkers compared with
213 cases (34 179 person-years) for nondrinkers of wine. For
beer drinkers, 101 cases of IS were registered (18 590
person-years) compared with 227 cases among nondrinkers
of beer (38 718 person-years). Corresponding numbers for
spirits drinkers were 205 cases (38 749 person-years) and 123
cases of IS (18 559 person-years) among subjects who did not
consume spirits. In multivariate analysis, we observed a
borderline association of current wine drinking on IS (hazard
ratio0.8 [95% CI, 0.6 to 1.0]) but no effects for beer (hazard
ratio1.0 [95% CI, 0.8 to 1.4]) or spirits (hazard ratio0.9
[95% CI, 0.7 to 1.2]) on the risk of IS.
 Djouss et al Alcohol and Stroke 909

TABLE 1. Baseline Characteristics of Participants in the Framingham Study

Total Ethanol, g/d

Former Drinkers Current Drinkers

Never 0.111 12 0.111 1223 24

Men (n273) (n341) (n159) (n1161) (n568) (n1369)
Ethanol, g/d 0 4.83.3 17.33.5 58.544.7
Age, y 61.810.4 65.510.2 64.19.6 60.910.0 61.010.0 59.99.5
Body mass index, kg/m2 26.03.5 26.83.7 26.43.6 26.63.6 26.63.4 26.63.4
Systolic BP, mm Hg 138.921.5 139.620.9 135.421.5 136.419.1 136.619.4 140.920.5
Diastolic BP, mm Hg 82.711.2 81.411.2 78.012.4 82.610.4 82.410.7 85.311.9
Current smoking, % 27.6 28.9 39.1 35.4 36.8 48.9
Diabetes mellitus, % 12.8 13.2 15.1 10.6 10.9 8.9
Coronary disease, % 17.2 26.7 23.3 15.6 15.1 13.3
LVH, % 4.8 6.5 7.6 4.9 5.6 4.8
Atrial fibrillation, % 1.8 4.1 5.7 2.2 3.0 2.1
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Antihypertensive agents, % 13.9 23.7 18.9 14.5 16.5 16.0

Women (n1042) (n833) (n133) (n2073) (n507) (n712)
Ethanol, g/d 0 4.13.0 17.13.2 43.630.8
Age, y 63.910.6 66.810.2 67.810.1 60.79.9 61.810.0 58.69.2
Body mass index, kg/m2 26.95.2 26.55.0 26.45.3 26.04.4 25.23.9 24.33.7
Systolic BP, mm Hg 145.724.3 140.921.8 137.118.7 138.923.0 140.222.7 139.822.9
Diastolic BP, mm Hg 83.611.6 78.910.2 78.311.2 81.610.9 81.711.5 83.111.1
Current smoking, % 13.8 24.9 26.6 30.0 36.9 55.0
Diabetes mellitus, % 10.1 13.0 18.1 5.5 6.3 5.2
Coronary disease, % 10.7 16.0 6.0 7.9 5.7 4.2
LVH, % 4.8 5.4 9.1 3.2 2.6 4.4
Atrial fibrillation, % 2.5 2.2 3.0 1.1 2.0 1.4
Antihypertensive agents, % 25.7 35.5 37.1 20.4 21.2 18.7
BP indicates blood pressure; LVH, left ventricular hypertrophy. Values are meanSD unless specified otherwise. Median (range) of ethanol in the
highest categories: 46.2 (24.1 to 623.7) g/d for men and 33.9 (24.0 to 571.2) g/d for women.

Discussion may be different among older subjects than among younger

Our study found that when all ages were combined, total
alcohol consumption was not significantly associated with IS.
However, a protective effect of alcohol intake was observed
among subjects aged 60 to 69 years. In addition, unlike beer
and spirits, wine consumption was suggestive of a reduced
risk of IS.
Epidemiological studies have been inconsistent on the
association between alcohol and the risk of stroke. Some
prospective studies have documented the J- or U-shaped
relation between alcohol and the risk of stroke,3,10,12,15,16,26,27
with the estimated magnitude of effect averaging approxi-
mately 30% risk reduction for light to moderate drinking. In
contrast, several case-control studies28,29 and cohort stud-
ies8,9,30 did not find an association between alcohol consump-
tion and IS. Some epidemiological studies have reported an
increased risk of IS with recent moderate and heavy alcohol
consumption.31,32
We found a protective effect of alcohol on IS only among
subjects aged 60 to 69 years. We do not have a biological
explanation for these findings and can only speculate. First,
differential dietary and lifestyle habits across age groups may
partially account for the findings. Second, access to alcohol
ones. Third, the drinking patterns may vary with age.
Younger age, for example, could be associated with un-
healthy drinking habits such as binge drinking; heavy drink-
ing has been associated with increased risk of IS.32 Fourth,
the observed association may be due to chance.
Few studies have examined the association between the
type of alcoholic beverage and ischemic stroke. We found a
borderline significant protective effect of wine on IS in this
study. This suggests that substances other than ethanol may
be important in preventing atherosclerosis.13,20,33 In the
Copenhagen City Heart Study, consumption of 3 to 5 glasses
of wine or beer, but not spirits, was associated with a 56% or
28% reduction, respectively, in death from cardiovascular
and cerebrovascular disease.13 Truelsen et al18 reported that
only wine intake was associated with a reduction of the risk
of stroke. In a case-control study, wine consumption was
found to be associated with lower odds of IS (odds ra-
tio0.55 [95% CI, 0.31 to 0.98]) among young women,34 but
beer (odds ratio0.92 [95% CI, 0.53 to 1.61]) or spirits (odds
ratio1.35 [95% CI, 0.73 to 2.49]) consumption did not show
a significant effect.34 Our beverage-specific findings are
consistent with these previous studies.
 910 Stroke April 2002

TABLE 2. Risk and Hazard Ratio of IS According to Total Ethanol Intake Among Participants
of the Framingham Study
Incidence Rate,
Cases/1000 Age-Adjusted Multivariate Adjusted
Ethanol, g/d Case/Person-Years Person-Years Hazard Ratio Hazard Ratio*
Men
Never 15/2300 6.5 1.0 1.0
0.111 59/10 035 5.9 1.0 (0.61.7) 0.8 (0.41.5)
1223 24/4910 4.9 0.8 (0.41.6) 0.7 (0.41.4)
24 60/12 042 5.0 0.9 (0.51.6) 0.8 (0.41.5)
Former (0.111) 18/2703 6.7 0.8 (0.41.6) 0.8 (0.41.6)
Former (12) 20/1127 17.8 2.6 (1.35.1) 2.4 (1.24.8)
Women
Never 54/9186 5.9 1.0 1.0
0.111 77/19 034 4.1 0.9 (0.61.3) 0.9 (0.61.3)
1223 19/4670 4.1 0.8 (0.51.4) 0.8 (0.51.4)
24 28/6517 4.3 1.2 (0.71.9) 0.9 (0.51.5)
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Former (0.111) 59/7151 8.3 1.1 (0.81.6) 1.0 (0.71.5)

Former (12) 8/1129 7.1 1.0 (0.52.0) 0.8 (0.41.7)
Values in parentheses are 95% CI.
*Adjusted for age, body mass index, smoking, and diabetes mellitus.

Varying results from studies on the alcohol-IS relation can
be partially explained by methodological issues: few studies
have separated former drinkers from lifetime abstainers but
have used all current nondrinkers as the referent group. As
seen in our results, further distinction between former light
and former heavier drinkers appears to be important since
these categories may have different risks for IS. In addition,
classification of the amount of alcohol consumed has varied
across studies, making it difficult to compare studies with
different cut points of alcohol exposure. In many studies,

TABLE 3. Risk and Hazard Ratio of IS According to Age and Total Ethanol Intake Among
Participants of the Framingham Study
Incidence Rate, Age- and
Cases/1000 Sex-Adjusted Multivariate-Adjusted
Ethanol, g/d Case/Person-Years Person-Years Hazard Ratio Hazard Ratio*
50 59 y
Never 4/3028 1.3 1.0 1.0
0.111 14/9267 1.5 1.1 (0.43.4) 1.4 (0.44.4)
1223 5/2951 1.7 1.2 (0.34.4) 1.5 (0.46.3)
24 20/6486 3.1 2.1 (0.76.4) 2.2 (0.67.5)
Former (0.111) 6/2058 2.9 2.1 (0.67.6) 2.3 (0.68.5)
Former (12) 2/546 3.7 2.4 (0.413.3) 1.6 (0.214.9)
6069 y
Never 34/4094 8.3 1.0 1.0
0.111 53/9978 5.3 0.6 (0.40.9) 0.5 (0.30.8)
1223 14/3373 4.2 0.4 (0.20.8) 0.3 (0.20.7)
24 40/6171 6.5 0.6 (0.41.0) 0.5 (0.30.9)
Former (0.111) 18/3902 4.6 0.5 (0.30.9) 0.5 (0.30.8)
Former (12) 14/843 16.6 1.7 (0.93.3) 1.2 (0.62.4)
70 y
Never 30/2912 10.3 1.0 1.0
0.111 63/4989 12.6 1.3 (0.82.0) 1.2 (0.71.8)
1223 24/1719 14.0 1.3 (0.82.3) 1.3 (0.72.3)
24 27/2340 11.5 1.1 (0.71.9) 1.0 (0.51.8)
Former (0.111) 53/3194 16.6 1.5 (1.02.4) 1.4 (0.82.2)
Former (12) 12/670 17.9 1.7 (0.93.3) 1.7 (0.83.3)
Values in parentheses are 95% CI.
*Adjusted for age, sex, body mass index, smoking, and diabetes mellitus.

alcohol exposure has been assessed only at baseline, and it
has been shown that there is a tendency for alcohol consump-
tion to decrease with aging.35 Ignoring the changes in
drinking habits with time could lead to misclassification of
alcohol intake and bias the estimate of effect.
Our study has some limitations: (1) We were not able to
identify binge drinkers, who may have a different risk of IS
than regular moderate drinkers. Binge drinking has been
associated with raised systolic and diastolic blood pressure36
and could thus increase the risk of stroke. (2) Despite a
standardized questionnaire, underreporting of alcohol intake
by the study participants may have biased our results. (3) We
were unable to control confounding by dietary factors since
we did not collect adequate data on diet among subjects used
in these analyses. The large number of subjects, the use of
standardized protocols, and the repeated data collection are
strengths of this study.
Alcohol may protect against atherosclerosis by decreasing
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lipoprotein(a),37 increasing HDL cholesterol,38,39 or inhibiting
LDL oxidation. Alcohol consumption is also associated with
decreased platelet aggregation,40 decreased fibrinogen lev-
els,41 increased concentration of tissue plasminogen activa-
tor,42,43 and enhanced insulin sensitivity.44 Wine also contains
phenolic compounds with antioxidant properties,45 and con-
sumption of polyphenols from other sources is associated
with a decreased risk of cardiovascular disease.46
In conclusion, our study found no significant association
between moderate alcohol consumption and IS in the overall
population but found a protective effect among subjects aged
60 to 69 years. Wine, but not beer or spirits, appeared to be
protective against IS.
Acknowledgment
This study was supported by the National Heart, Lung, and Blood
Institute, National Institutes of Health (contract N01-HC-38038).
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 Alcohol Consumption and Risk of Ischemic Stroke: The Framingham Study
Luc Djouss, R. Curtis Ellison, Alexa Beiser, Amy Scaramucci, Ralph B. D'Agostino and Philip
A. Wolf

Stroke. 2002;33:907-912
Downloaded from http://stroke.ahajournals.org/ by guest on April 8, 2017

doi: 10.1161/hs0402.105245
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 2002 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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An erratum has been published regarding this article. Please see the attached page for:
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 Correction
In Alcohol Consumption and Risk of Ischemic Stroke: The Framingham Study by Djouss et
al,1 one source of funding was inadvertently omitted. The complete Acknowledgment should read
as follows:

This study was supported in part by grant NS17950 from the National Institute of Neurological
Diseases and Stroke, National Institutes of Health, and by contract HC38038 from the National
Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

The authors apologize for this error.

1
[Correction for Vol 33, Number 4, April 2002. Pages 907912.]
(Stroke. 2002;33:1727.)
2002 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org

1727