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(Circulation. 2000;102:500.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Alcohol Consumption and Risk of Coronary Heart Disease by Diabetes Status
From the Division of Preventive Medicine (U.A.A., J.M.G., P.A.L., S.L., J.E.B., J.E.M.), Channing Laboratory (J.E.M.), and Cardiovascular Division (J.M.G.), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass; the Department of Epidemiology (J.E.B., J.E.M.) and Department of Nutrition (S.L.), Harvard School of Public Health, Boston, Mass; and Massachusetts Veterans Epidemiology Research and Information Center (J.M.G.), Veterans Affairs Medical Center, Brockton/West Roxbury, Mass. Dr Hennekens is visiting Professor of Medicine, and Epidemiology and Public Health at the University of Miami School of Medicine.
Correspondence to Umed A. Ajani, Division of Preventive Medicine, Brigham and Women’s Hospital, 900 Commonwealth Ave E, Boston, MA 02215-1204. E-mail uajani{at}rics.bwh.harvard.edu
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Abstract |
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Background—An inverse association between moderate alcohol consumption and coronary heart disease (CHD) has been observed in several epidemiological studies. To assess whether a similar association exists among diabetics, we examined the relation between light to moderate alcohol consumption and CHD in men with and without diabetes mellitus in a prospective cohort study.
Methods and Results—A total of 87 938 US physicians (2790 with diagnosed diabetes mellitus) who were invited to participate in the Physicians’ Health Study and were free of myocardial infarction, stroke, cancer, or liver disease at baseline were followed for an average of 5.5 years for death with CHD as the underlying cause. During 480 876 person-years of follow-up, 850 deaths caused by CHD were documented: 717 deaths among nondiabetic men and 133 deaths among diabetic men. Among men without diabetes at baseline, the relative risk estimates for those reporting rarely/never, monthly, weekly, and daily alcohol consumption were 1.00 (referent), 1.02, 0.82, and 0.61 (95% CI 0.49 to 0.78; P for trend <0.0001) after adjustment for age, aspirin use, smoking, physical activity, body mass index, and history of angina, hypertension, and high cholesterol. Among men with diabetes at baseline, the relative risk estimates were 1.00 (referent), 1.11, 0.67, and 0.42 (95% CI 0.23 to 0.77; P for trend=0.0019).
Conclusions—These results suggest that light to moderate alcohol consumption is associated with similar risk reductions in CHD among diabetic and nondiabetic men.
Key Words: alcohol • coronary disease • diabetes mellitus • risk factors
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Introduction |
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For the millions of people with diabetes mellitus, coronary heart disease (CHD) is a major cause of morbidity and mortality. A recent survey of a representative cohort of 14 734 US adults with diabetes, for example, found that CHD was listed on 69% of death certificates.1 Age-adjusted rates for CHD are substantially higher among diabetic men and women than among those without diabetes, and clinically apparent CHD appears at an earlier age among people with diabetes than it does in the general population.2 3 4
In general populations, epidemiological studies have consistently demonstrated an inverse association between moderate alcohol consumption and CHD incidence and mortality.5 6 7 8 9 The reduced risk of CHD associated with alcohol is believed to be due, at least in part, to the effect of alcohol on the lipid profile, including favorable increases in HDL cholesterol and its subfractions.10 Whether or not alcohol consumption has a similar association with CHD among individuals with diabetes, however, is a largely unexamined question. It has been suggested that alcohol increases sensitivity to insulin and has favorable effects on glucose metabolism.11 12 13 14 Yet, moderate alcohol consumption has been associated with decreased risk of type 2 diabetes mellitus in some15 16 16A but not all17 studies. Given this uncertainty, many patients with diabetes are advised to avoid alcohol.
To address this question, we examined the relation between alcohol intake and CHD mortality according to diabetes status in prospective data from the Physicians’ Health Study (PHS) enrollment cohort.
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Methods |
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Study Population
The PHS was a randomized, double-blind, placebo-controlled trial of low-dose aspirin (325 mg every other day) and ß-carotene (50 mg every other day) in the primary prevention of cardiovascular disease and cancer. Potentially eligible participants were male physicians living in the United States. In 1982 to 1983, letters of invitation, informed consent forms, and baseline questionnaires were mailed to 261 248 physicians listed on the American Medical Association’s mailing tape. By the end of December 1983, 104 353 completed questionnaires had been returned. After further evaluation, 16 415 men were excluded because of missing diabetes status (n=5290), missing alcohol data (n=3775), and history of myocardial infarction, stroke, cancer, or liver disease (n=11 959) at baseline, leaving a total of 87 938. This study includes these 87 938 respondents, of whom 21 852 were subsequently randomized in the trial.
Baseline Data
Information about alcohol consumption and several other risk
factors was collected at baseline. The physicians were asked how often
they usually consumed alcoholic beverages (beer, wine, liquor) and
offered 7 possible responses: rarely/never, 1 to 3 per month, 1 per
week, 2 to 4 per week, 5 to 6 per week, 1 per day, and 
2 per day. We
interpreted their responses to be the number of drinks consumed in the
specified time period. Information was also collected about other CHD
risk factors, including age, cigarette smoking (never, past, or
current, including number of cigarettes smoked per day for current
smokers), use of antihypertensive medications, systolic and
diastolic blood pressure, cholesterol level,
use of cholesterol-lowering medications, frequency of
vigorous exercise, and history of angina pectoris and diabetes
mellitus. Body mass index (kg/m2) was calculated
by means of self-reported weight and height. Participants were
considered diabetic if they reported a history of diabetes mellitus or
use of insulin or other antidiabetic medication.
End Points
Death was the primary end point that we determined for the
entire enrollment cohort. Deaths were identified through systematic
searches of the National Death Index for the entire enrollment cohort,
and death certificates were obtained for all cases to determine cause
of death. All deaths occurring before February 1, 1988, were
recorded. Trained nosologists who had no knowledge of cohort
members’ alcohol consumption status classified deaths by using the
first revision of the Ninth International Classification of Diseases
(ICD) in conjunction with the Automated Classification of Medical
Entities Decision Tables. Men for whom cause of death was classified as
ischemic heart disease and myocardial infarction (ICD codes
410-414) were classified as CHD deaths for this analysis.
Because the enrollment cohort was followed for mortality only, we could not identify incident cases of CHD. However, incidence information was available for the subset of respondents who were randomized into the PHS. These participants reported new diagnosis of CHD on annual questionnaires, which were then confirmed by medical record review. For this subgroup, the morbidity and mortality follow-up was >99% complete for >12 years (through December 31, 1995). In our secondary analyses, we evaluated incident CHD cases among the randomized subgroup.
Statistical Analysis
We used 4 categories of alcohol intake at baseline:
rarely/never, monthly (1 drink per month but <1 drink per week),
weekly (1 drink per week but <1 drink per day), and daily (1 drink
per day). For each physician, person-years of follow-up were counted
from the date the enrollment questionnaire was returned until January
31, 1988, or, in case of death, the date of death. We calculated
proportions and means of baseline risk factors for the 4 levels of
alcohol use and used proportional hazards models to compute
age-adjusted and multivariable-adjusted relative risk and 95%
confidence intervals for each category of alcohol use compared with the
reference category. Multivariate models were adjusted
for potential confounders by including terms for age, smoking (never,
past, current [<20 cigarettes/d, or 20 or more cigarettes/d]),
exercise (at least once per week), body mass index, current aspirin use
(at enrollment), history of angina, hypertension (reported
systolic blood pressure of 160 or diastolic blood
pressure of 95 or history of treatment for high blood pressure), and
high cholesterol (reported blood cholesterol
level of 260 or history of treatment for high
cholesterol). Initially, we did not adjust for history of
hypertension and high cholesterol in our models because
these variables may be considered predictors of death affected by
alcohol consumption.18 19 We did, however, add them in our
analyses because this did not materially change the results.
Analyses were repeated excluding the first 2 years of follow-up
to determine if there was any possible confounding of the association
between alcohol and death caused by changes in alcohol consumption
resulting from terminal stages of illness. We tested linear trends
across the categories of alcohol consumption by using alcohol intake as
an ordinal variable in the model. We also examined the association
of alcohol with incident CHD in the subgroup of the enrollment cohort
subsequently randomized in the PHS.
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Results |
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At baseline, about one quarter (29%) of the study population reported alcohol use of <1 drink per week; almost half (46%) reported weekly alcohol use (1 to 6 alcoholic beverages per week); and the remaining 25% reported daily alcohol use. Overall, alcohol consumption was light to moderate, with only 3% of the members of this cohort reporting alcohol consumption of >1 drink per day. Baseline characteristics of the subjects with and without diabetes are presented in Table 1
. Men
who reported higher levels of alcohol intake tended to be older, were
more likely to be former or current smokers, and tended to report more
physical activity, a history of hypertension, and higher aspirin
intake. Of the 87 938 respondents, 2790 (3.2%) reported having
diabetes mellitus. As expected, among those with diabetes, the
distribution of alcohol consumption was somewhat different, with 43%
reporting alcohol use of <1 drink per week, 35% reporting weekly
consumption, and the remaining 22% reporting daily consumption. At
study entry, those with diabetes were slightly older, were more likely
to be former or current smokers, were less physically active, and had a
higher prevalence of angina, hypertension, and high
cholesterol than those with no diagnosis of diabetes at
baseline.
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During an average follow-up period of 5.5 years (a total of 480 876
person-years), 3093 deaths were identified. CHD was the reported cause
of death in 850 cases: 717 among nondiabetics and 133 among diabetics.
The CHD deaths included 353 deaths from ischemic heart disease
and 497 from myocardial infarction. Relative risks for CHD mortality
are presented in Table 2.
Overall, there was a decreasing risk of CHD mortality with increasing
levels of alcohol intake (P<0.0001). Men reporting daily
consumption of alcohol were observed to have a 40% decreased risk of
CHD mortality compared with those reporting rarely or never drinking
alcohol.
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When examining the association between alcohol use and CHD mortality by
diabetes status, similar relations between alcohol use and CHD were
observed in both groups. For participants with no diabetes at baseline,
the relative risks were 1.00 (referent), 1.02, 0.82, and 0.61 (95% CI
0.49 to 0.78; P for trend <0.0001) for those consuming
alcohol rarely, monthly, weekly, and daily, respectively, after
adjusting for age, aspirin use, smoking, physical activity, body mass
index, history of angina, hypertension, and high
cholesterol. For those reporting diabetes at baseline, the
relative risks were 1.00 (referent), 1.11, 0.67, and 0.42 (95% CI 0.23
to 0.77; P for trend=0.0019) for increasing level of alcohol
intake after adjusting for the same variables (Table 2
). No
significant interaction was observed when we examined possible
modifications of this association by age (>60 years of age versus
60), body mass index (27.8 versus <27.8), cigarette smoking (ever
versus never), aspirin intake at baseline, or physical activity (at
least once per week versus less than once per week) among men with
diabetes.
Because the enrollment cohort was followed for mortality only, we could
not determine the relative risk for CHD incidence. We were able,
however, to examine this association in a subset of the enrollment
cohort: physicians who were randomized into the PHS. In this group of
21 852 men, the overall relative risks for any CHD diagnosis (defined
as cases of myocardial infarction plus cases of coronary artery
bypass graft or percutaneous transluminal
coronary angioplasty procedures) for the same 4 categories of
alcohol use were 1.00 (referent), 0.93, 0.89, and 0.67 (95% CI 0.57 to
0.78; P for trend <0.0001) after an average follow-up of 12
years and adjustment for age, randomized treatment, smoking, physical
activity, body mass index, parental history of myocardial infarction
before age 60 years, and personal history of angina, hypertension, high
cholesterol, and diabetes (Table 3). Similar associations were observed
among the nondiabetic men in this group. Among the relatively small
number of randomized PHS participants who reported having diabetes at
baseline (n=510), those reporting daily alcohol consumption had a
relative risk for CHD incidence of 0.66 (95% CI 0.38 to 1.16) compared
with those reporting rarely or never drinking alcohol. These relative
risks, however, did not reach statistical significance, perhaps because
of the small sample size of diabetics within this subpopulation.
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Discussion |
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These prospective data indicate that low-to-moderate consumption of alcohol is associated with a decreased risk of CHD mortality in men with diabetes, just as it is among men without diabetes, and that there are comparable risk reductions for CHD mortality in both groups.
Despite the prevalence of diabetes and the impact of CHD among people
with diabetes, few studies have examined the possible relation between
alcohol and CHD in diabetic populations. One case-control study of risk
factors for CHD among diabetics reported alcohol consumption as a
predictor of CHD.20 However, alcohol consumption data were
not clearly reported and were included in the models as a binary
variable only. In contrast, a small (n=232) prospective population
study of the impact of cardiovascular risk factors on
CHD mortality among diabetic men reported no association between
alcohol abuse and CHD.21 Our findings are
consistent with 2 more recent studies. A preliminary report
from Switzerland regarding 287 patients with type 2 diabetes mellitus
recruited for a multinational study of vascular disease in diabetes
sponsored by the World Health Organization showed that alcohol intake
was associated with decreased risk of death from ischemic heart
disease among men with type 2 diabetes (Exp[Coef]: 0.90 (95% CI 0.81
to 0.995; P=0.039) (P. Diem et al, data presented at
59th Scientific Session of American Diabetes Association, 1999). In
addition, data from the Wisconsin Epidemiologic Study of Diabetic
Retinopathy showed a 55% to 75% reduction in risk of
death caused by CHD in people with older-onset diabetes and who
consumed 14 g of alcohol per day (
1 drink per
day).22
Our findings are also consistent with those from the Nurses’
Health Study, in which an 50% reduction in risk of CHD was observed
among diabetic participants of that large cohort (C. Solomon, personal
communication).22A
Several plausible biological mechanisms have been proposed to explain the inverse association between alcohol and CHD among general populations. In addition to increasing the levels of HDL cholesterol and its subfractions,10 23 alcohol has also been shown to decrease platelet aggregation24 25 and increase fibrinolytic activity.26 These hypothesized mechanisms could be even more important in a diabetic population, in which dyslipidemia and coagulation disorders are more prevalent than they are in a general population. In addition, hyperinsulinemia, which is common among diabetics, has been implicated as an important risk factor for CHD,27 and light to moderate alcohol consumption has been reported to lower fasting insulin levels,12 28 29 which could decrease the risk of CHD.
Our study has several strengths. Its large sample size provides sufficient power to detect true differences. The prospective design minimizes differential misclassification of exposure status, and the relatively homogenous group minimizes confounding by factors such as socioeconomic status, educational background, and access to and quality of medical care.
Potential limitations of the study also must be considered. Misclassification of outcome is possible when using death certificate data to determine cause of death. However, the end points in this study were ascertained without prior knowledge of alcohol use, making nonrandom misclassification unlikely. As in most other alcohol-related studies, we used self-reported alcohol consumption; other approaches are generally not practical in large cohort studies such as this.30 Health professionals generally provide reliable reports of alcohol use,31 32 though random misclassification of alcohol intake is possible if the physicians in this study generally underreported or underestimated their alcohol intake. This type of misclassification could have led to underestimation of any true protective association of light to moderate alcohol intake and CHD if heavier drinkers underreported to a greater extent than light or moderate drinkers. We used a single measure of alcohol consumption and did not account for any change in alcohol intake over time. This could also lead to some misclassification, although drinking patterns among middle-aged and older subjects tend to be stable over time.33 We did not collect information on type of alcoholic beverage consumed and thus cannot compare separately the risks and benefits of wine, beer, or liquor consumption. Moreover, if healthier subjects tended to consume light to moderate amounts of alcohol, or if alcohol consumption was a marker of overall healthy behavior, a "healthy worker effect" cannot be ruled out.
It has been suggested that the reduced risk of cardiovascular disease observed among drinkers in studies of alcohol consumption can be partly explained by increased risk among ex-drinkers who stopped drinking because of comorbid conditions and who are included with the nondrinkers.34 Although we were unable to exclude recent ex-drinkers, we did exclude any physician who reported a history of myocardial infarction, stroke, cancer, or liver disease. Furthermore, studies of alcohol and cardiovascular mortality have reported no difference in results with and without excluding recent ex-drinkers.35
Another potential limitation of our study is generalizability. The study participants were relatively healthy men who consumed low-to-moderate amounts of alcohol. Therefore, results may not be generalizable to other populations with less healthy risk factor profiles or to those consuming higher amounts of alcohol. Although our results are not generalizable to women, this concern is minimized by findings similar to ours from the Nurses’ Health Study, a large cohort of women. Finally, residual confounding is possible but unlikely because adjustment for potential confounders did not materially change the results.
In the PHS enrollment cohort, distribution of alcohol consumption among all participants and those with diabetes showed a greater proportion of diabetic participants reporting rarely/never drinking alcohol, suggesting that the participants may have changed their alcohol consumption in response to diabetes. It is also possible that some clinicians may routinely discourage low-to-moderate alcohol consumption among those with diabetes. This may be due to a potential risk of alcohol-induced hypoglycemia, which can be minimized by consuming alcohol in moderation and in conjunction with meals. Current guidelines from the American Diabetes Association state that "[if] used in moderation and with food, however, blood glucose levels are not affected by the ingestion of alcohol when diabetes is well controlled."36
In conclusion, results from this prospective cohort study suggest that light to moderate alcohol consumption is associated with a similar degree of reduction in risk of CHD mortality among men with diabetes as it is among men in the general population. Our results are limited to those consuming low-to-moderate amounts of alcohol and cannot be generalized to those consuming heavy amounts. Furthermore, these results should be interpreted with caution and require confirmation in other cohorts of diabetics. In light of major clinical and public health problems associated with heavy drinking, recommendations regarding alcohol use must be made on an individual basis after carefully assessing the risks and benefits of any changes in drinking behavior.
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Acknowledgments |
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This study was supported by National Institutes of Health grants HL-42441, HL-34595, and CA-40360. Dr Lotufo is the recipient of a fellowship (97-02424-8) from FAPESP (Fundação de Amparo a Pesquisa do Estado de São Paulo), São Paulo, Brazil. We are grateful to all dedicated and conscientious physicians who participated in this study. We also thank Patrick Skerrett for his expert assistance. One of the authors (U.A.A.) has received past support from the Alcohol Beverage Medical Research Foundation for an unrelated project.
Received December 15, 1999; revision received March 1, 2000; accepted March 4, 2000.
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 R. R. Zilkens, V. Burke, G. Watts, L. J. Beilin, and I. B. Puddey The Effect of Alcohol Intake on Insulin Sensitivity in Men: A randomized controlled trial Diabetes Care, March 1, 2003; 26(3): 608 - 612. [Abstract] [Full Text] [PDF]
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A. D. Mooradian Cardiovascular Disease in Type 2 Diabetes Mellitus: Current Management Guidelines Arch Intern Med, January 13, 2003; 163(1): 33 - 40. [Abstract] [Full Text] [PDF]
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D. E. Cooper, D. C. Goff Jr., R. A. Bell, D. Zaccaro, E. J. Mayer-Davis, and A. J. Karter Is Insulin Sensitivity a Causal Intermediate in the Relationship Between Alcohol Consumption and Carotid Atherosclerosis?: The Insulin Resistance and Atherosclerosis Study Diabetes Care, August 1, 2002; 25(8): 1425 - 1431. [Abstract] [Full Text] [PDF]
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 L. Djousse, R. H. Myers, M. A. Province, S. C. Hunt, J. H. Eckfeldt, G. Evans, J. M. Peacock, and R. C. Ellison Influence of Apolipoprotein E, Smoking, and Alcohol Intake on Carotid Atherosclerosis: National Heart, Lung, and Blood Institute Family Heart Study Stroke, May 1, 2002; 33(5): 1357 - 1361. [Abstract] [Full Text] [PDF]
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 T. P. Gavin and P. D. Wagner Acute ethanol increases angiogenic growth factor gene expression in rat skeletal muscle J Appl Physiol, March 1, 2002; 92(3): 1176 - 1182. [Abstract] [Full Text] [PDF]
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M. J. Franz, J. P. Bantle, C. A. Beebe, J. D. Brunzell, J.-L. Chiasson, A. Garg, L. A. Holzmeister, B. Hoogwerf, E. Mayer-Davis, A. D. Mooradian, et al. Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications Diabetes Care, January 1, 2002; 25(1): 148 - 198. [Full Text] [PDF]
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 M. Tanasescu, F. B. Hu, W. C. Willett, M. J. Stampfer, and E. B. Rimm Alcohol consumption and risk of coronary heart disease among men with type 2 diabetes mellitus J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1836 - 1842. [Abstract] [Full Text] [PDF]
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 L M Hines and E B Rimm Moderate alcohol consumption and coronary heart disease: a review Postgrad. Med. J., December 1, 2001; 77(914): 747 - 752. [Full Text] [PDF]
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 A. L. Klatsky Should Patients With Heart Disease Drink Alcohol? JAMA, April 18, 2001; 285(15): 2004 - 2006. [Full Text] [PDF]
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 K. H. Johnson, M. Bazargan, and E. G. Bing Alcohol Consumption and Compliance Among Inner-city Minority Patients With Type 2 Diabetes Mellitus Arch Fam Med, November 1, 2000; 9(10): 964 - 970. [Abstract] [Full Text] [PDF]
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W. S. Weintraub Alcohol Consumption, Diabetes, and Coronary Disease : An Epidemiological Perspective Circulation, August 1, 2000; 102(5): 489 - 490. [Full Text] [PDF]
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