Context Despite nutrition information and guidelines that advise against depriving
diabetic patients of the potential benefit of moderate alcohol intake against
cardiovascular events, the association between alcohol consumption and risk
of cardiovascular outcomes in diabetic individuals has not been determined.
Objective To examine the relationship between alcohol intake and coronary heart
disease (CHD) mortality in persons with older-onset diabetes.
Design Population-based, prospective cohort study conducted from 1984 through
1996, with a follow-up of up to 12.3 years.
Setting and Participants A total of 983 older-onset diabetic individuals (mean [SD] age, 68.6
[11.0] years; 45.2% male; 98.5% white) were interviewed about their past-year
intake of alcoholic beverages during the 1984-1986 follow-up examination of
a population-based study of diabetic persons in southern Wisconsin.
Main Outcome Measure Time to mortality from CHD by category alcohol intake.
Results Alcohol use was inversely associated with risk of CHD mortality in older-onset
diabetic subjects. The CHD mortality rates for never and former drinkers were
43.9 and 38.5 per 1000 person-years, respectively, while the rates for those
with alcohol intakes of less than 2, 2 to 13, and 14 or more g/d were 25.3,
20.8, and 10.0 per 1000 person-years, respectively. Compared with never drinkers
and controlling for age, sex, cigarette smoking, glycosylated hemoglobin level,
insulin use, plasma C-peptide level, history of angina or myocardial infarction,
digoxin use, and the presence and severity of diabetic retinopathy, former
drinkers had a relative risk (RR) of 0.69 (95% confidence interval [CI], 0.43-1.12);
for those who drank less than 2 g/d (less frequent than 1 drink a week), the
RR was 0.54 (95% CI, 0.33-0.90); for 2 to 13 g/d, it was 0.44 (95% CI, 0.23-0.84);
and for 14 or more g/d (about 1 drink or more a day), it was 0.21 (95% CI,
0.09-0.48). Further adjustments for blood pressure, body mass index, education,
physical activity, diabetes duration, hypertension history, overt nephropathy,
peripheral neuropathy, lipid measures, or intake of medications such as aspirin
and antihypertensive agents did not change the associations observed.
Conclusion Our results suggest an overall beneficial effect of alcohol consumption
in decreasing the risk of death due to CHD in people with older-onset diabetes.
As reviewed in an earlier meta-analysis1
and reported in subsequent articles,2-14
numerous prospective epidemiological studies conducted with selected cohorts
and general populations and subgroups have reported a nearly consistent pattern
of a beneficial effect of modest levels of alcohol consumption, with reductions
in the risk of coronary heart disease (CHD) or death ranging from 20% to 60%.
Some mechanisms cited for the protective effect of moderate alcohol intake
include its antiatherogenic role in increasing the levels of high-density
lipoprotein cholesterol (HDL-C),15 its hemostatic
effects by decreasing platelet aggregation16
and increasing fibrinolytic activity,17,18
and its possible association with beneficial changes in insulin and glucose
metabolism.19-22
Despite nutrition information and guidelines for people with diabetes23-25 that advise against
depriving diabetic patients of the potential benefit of moderate alcohol intake
against ischemic heart disease23 or cardiovascular
mortality,24 to our knowledge, there has been
no prospective study of the association between alcohol consumption and cardiovascular
outcomes in diabetic individuals. Understanding this relationship is important,
given the high rates of morbidity and mortality due to CHD in type 2 diabetes
and the current evidence for the cardioprotective role of moderate alcohol
intake in general populations. Coronary heart disease remains the leading
cause of death in persons with type 2 diabetes, accounting for about 40% of
all deaths.26 It may be possible that the level
of protection, if any, from coronary events differs from that seen in generally
healthier cohorts because of the presence of more coexisting medical problems,
including the macrovascular and microvascular complications commonly seen
in diabetes, and the different exposures to medications used for such conditions.
The purpose of this study was to examine the association between alcohol consumption
and mortality due to CHD in persons with older-onset diabetes using a population-based
prospective study design.
Study Cohort and Procedures
The Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) has
been described in detail in earlier publications.27-34
Briefly, WESDR is a population-based study of diabetic persons that began
in 1980 by working with 99% of 457 physicians providing primary care for diabetic
patients in an 11-county area of southern Wisconsin. A total of 10,135 diabetic
persons were identified, of which a representative sample of 2990 was selected
for the baseline examination. This sample included all 1210 younger-onset
diabetic patients (diabetes diagnosed before age 30 years) and a probability
sample of 1780 older-onset diabetic persons (diabetes diagnosed after age
30 years), 824 of whom were taking insulin. Follow-up interviews and/or examinations
were conducted in 1984-1986, 1990-1992, and 1995-1996 to update information
on potential risk factors and relevant clinical events. The subject of this
study was the older-onset group, of which 1370 participated in the baseline
examination from 1980 to 1982. Of these, 1.5% refused to participate in the
1984-1986 follow-up examination, while 1.2% had an interview only, 0.4% were
lost to follow-up, and 24.8% of the original cohort had died.31
The analyses in this article were performed for the remaining 987 subjects
who returned for the follow-up examination done in 1984-1986, when information
on alcohol intake was first obtained. We excluded 4 individuals who had missing
information on alcohol consumption, leaving 983 older-onset diabetic persons
in the study cohort, 98.5% of whom were white, with characteristics shown
in Table 1.
Pertinent procedures in the 1984-1986 examination included standardized
methods for measuring height, weight, and blood pressure35;
dilating the pupils and taking stereoscopic color fundus photographs of 7
standard fields for determining the presence and severity of diabetic retinopathy36; administering a structured interview for information
on risk factors; taking urine samples for a semiquantitative determination
of urinary proteins (Labstix, Ames Division, Miles Inc, Elkhart, Ind); and
taking blood samples for standardized measurements of glycosylated hemoglobin37 and plasma C-peptide38
levels for the whole cohort and serum total cholesterol39,40
and HDL-C41 levels for a subset of the cohort.42 All procedures were performed in a mobile van in
or near the city in which the participants lived. The study was approved by
the institutional review board of the University of Wisconsin Medical School,
Madison.
Ascertainment and Computation of Alcohol Intake
During the 1984-1986 and 1990-1992 follow-up examinations, participants
were asked about their intake of alcoholic beverages. Questions included whether
participants had ever had any beer, wine, or liquor at any time during their
lives; whether they had at least 1 drink of beer, wine, or liquor in the past
year; and, if so, about how often they drank an alcoholic beverage. Additional
questions were asked about the number of servings consumed during the average
week of 12-oz (355-mL) bottles or cans of beer, 4-oz (118-mL) glasses of wine,
and 1.5-oz (44-mL) shots of liquor. From these, we computed the average total
amount of absolute alcohol consumed in grams per day, using an equation based
on a published national survey of alcohol consumption43:
average alcohol intake (grams per day)=1/7 × ([0.04B × 12] + [0.15W
× 4] + [0.45L × 1.5]) oz × 28.35 g/oz, where B, W, and L
are the numbers of servings consumed during an average week of beer, wine,
and liquor, respectively. Although we did not directly validate the alcohol
intake data, the rank correlations between our calculated levels of alcohol
intake using this equation and serum levels of HDL-C were statistically significant
in both examinations (1984-1986 and 1990-1992).
Deaths were ascertained from regular contact with study participants
and their relatives, designated contact persons, or physicians and from reviews
of daily newspaper obituaries. Identified deaths were confirmed with annual
requests for death certificate information made to the Section of Vital Statistics
of the Wisconsin Center for Health Statistics. The names of persons who had
been lost to follow-up, who had moved out of Wisconsin, or who were suspected
to be deceased were submitted for matching against Wisconsin death records
and the National Death Index. For each match made, a copy of the death certificate
was obtained from the appropriate state. Only deaths confirmed by death certificates
were included in the definition of CHD death. Persons who were thought to
be deceased but for whom a death certificate could not be located were considered
to be alive as of the last contact date they were known to be alive. Medical
conditions on the Wisconsin death certificates were coded by trained nosologists
in the Wisconsin Division of Health using the International
Classification of Diseases, Ninth Revision (ICD-9).44 Out-of-state certificates were
coded and processed in the same manner. Participants were considered to have
died of CHD if the underlying cause of death was assigned to ICD-9 codes 410 through 414.9. Although we did not validate this coding,
other studies have observed a relatively high validity of death certificates
that stated CHD as the cause of death.45,46
No codes for sudden death or other ill-defined and unknown causes were included
in our definition of CHD mortality.
Participants were grouped into the following categories based on the
amount of absolute alcohol they consumed in the past year, as reported in
the 1984-1986 examination: 0 g/d (all nondrinkers), less than 2 g/d (less
frequent than 1 drink per week), 2 to 13 g/d (at least 1 drink per week),
14 to 28 g/d (about 1-2 drinks per day), and more than 28 g/d (more than 2
drinks per day). Due to the possibility that abstainers of alcohol could have
stopped drinking because of the presence of comorbid conditions, persons with
an alcohol intake of 0 were further divided into 2 categories: lifetime abstainers
or never drinkers, who were used as the reference category, and former drinkers.
After examining the frequency distribution of all variables, the association
of alcohol intake with possible confounders was assessed by χ2
analysis and analysis of variance. Mortality rates were calculated as the
number of deaths from CHD divided by the total number of person-years accrued
for each cohort member, based on the length of follow-up (computed as the
number of days from the date of the 1984-1986 examination to the date of death,
date of last contact, or December 31, 1996, whichever was earliest). The relation
of alcohol consumption level and subsequent mortality due to CHD was examined
with Kaplan-Meier analysis.47 The log-rank
test48 was used to evaluate whether mortality
differed by groups of alcohol intake. Cox proportional hazards regression49 was used to assess associations adjusted for age
(as a continuous measure) and sex as well as those further controlled by factors
that could affect the risk of coronary events and those potentially related
to both mortality and alcohol intake. These included cardiovascular risk factors,
such as cigarette smoking (classified as never, former, current), systolic
and diastolic blood pressure, body mass index (calculated as weight in kilograms
divided by the square of height in meters), education (<12, 12, or >12
years), and physical activity (defined as engaging in regular physical activity ≥3
times per week); and diabetes-related variables, such as use of insulin, intake
of oral glucose-lowering agents, duration of diabetes, and levels of glycosylated
hemoglobin (grouped as <8.0%, 8.0%-9.9%, and ≥10.0%) and plasma C-peptide
(categorized as undetectable, 0.03-0.29, 0.30-0.89, 0.90-1.49, and ≥1.50
nmol/L). Other comorbid conditions (or their markers) examined included history
of hypertension (defined as systolic blood pressure of ≥160 mm Hg or diastolic
of ≥95 mm Hg, or taking antihypertensive medications), intake of antihypertensive
agents, history of angina or myocardial infarction, intake of digoxin, intake
of aspirin, the presence and severity of diabetic retinopathy (grouped into
none, mild to early nonproliferative, moderate to severe nonproliferative,
and proliferative retinopathy, based on fundus photographs graded in masked
fashion using a modified Airlie House Classification system36,50,51),
presence of peripheral neuropathy symptoms (defined as loss of tactile sensation
in hands or feet or decreased ability to feel the hotness or coldness of things
touched), and presence of overt nephropathy (defined as having a urinary protein
concentration of ≥0.30 g/L as measured by a reagent strip, or a history
of dialysis or renal transplantation). Variables were progressively entered
in the regression models, which included age and sex, starting from cardiovascular
factors, to diabetes-related variables, and finally to comorbid conditions
or their markers. Variables that remained independently related to CHD mortality
were retained in the final model.
To examine the presence of effect modification, stratified analyses
were performed on subgroups of participants defined by specific variables,
including age (<69.6 vs ≥69.6 years, the median age for the cohort),
sex, cigarette smoking (never vs ever), insulin use, glycosylated hemoglobin
level (<9.1% vs ≥9.1%, the median value), aspirin intake, history of
hypertension, history of angina or myocardial infarction, and presence of
retinopathy, peripheral neuropathy symptoms, and overt nephropathy. Likelihood
ratio tests52 were used to check for interactions
in the proportional hazards models, which included cross-product terms for
these variables and each alcohol intake level.
Serum lipid levels are important risk factors for coronary events and
might influence our findings. Therefore, for the subset of the study cohort
for whom we had measurements of HDL-C, total cholesterol, and the ratio of
total cholesterol to HDL-C (n=451), we repeated our multivariate analyses
including each of these variables.
The assumption of proportionality for the Cox regression models was
tested and met. Hazard ratios were reported as relative risks (RRs) with 95%
confidence intervals (CIs). All P values were 2-tailed,
with values of .05 or less indicating statistical significance. The analyses
were performed using SAS Version 6.12 (SAS Institute Inc, Cary, NC).
Of the 983 persons eligible for follow-up, 10.9% were lifetime abstainers;
32.8% were former drinkers; and 34.6%, 11.9%, 6.1%, and 3.8% had alcohol intakes
of less than 2, 2 to 13, 14 to 28, and more than 28 g/d, respectively.
Not all potential risk factors were evenly distributed among the alcohol
intake groups (Table 1). Persons
with higher alcohol consumption were more likely to be younger, male, and
smokers, and to have higher diastolic blood pressure and education. Compared
with nondrinkers, drinkers were less likely to be sedentary and to be taking
insulin and tended to have relatively lower plasma C-peptide levels. No clear
patterns were observed for the other variables, although the rates of comorbid
conditions or complications (eg, history of CHD and hypertension, presence
of proliferative retinopathy and overt nephropathy) from nondrinkers as a
group to drinkers with increasing alcohol intake levels suggested V- or J-shaped
patterns (Table 1).
During follow-up of up to 12.3 years (7004 person-years), we identified 198
CHD deaths, 100 from acute myocardial infarction (ICD-9 code 410) and 98 from coronary atherosclerosis or chronic ischemic
heart disease (ICD-9 codes 414.0-414.9). The overall
CHD mortality rate for the study cohort was 28.3 per 1000 person-years. The
rates for never drinkers and former drinkers were 43.9 and 38.5 per 1000 person-years,
respectively, while the rates for those with alcohol intakes of less than
2, 2 to 13, 14 to 28, and more than 28 g/d were 25.3, 20.8, 9.8, and 10.4
per 1000 person-years, respectively. Because of the small number of cases
and the similar coronary mortality rates for moderate (14-28 g/d) and heavy
(>28 g/d) drinkers, we merged these 2 categories in subsequent analyses.
Compared with never drinkers, drinkers had significantly lower risks
for death due to CHD (Figure 1).
The age- and sex-adjusted RRs progressively decreased across increasing levels
of alcohol intake (Table 2). Additional
adjustments for significant cardiovascular factors, diabetes-related variables,
and comorbid conditions or markers, which included cigarette smoking, insulin
use, glycosylated hemoglobin level, plasma C-peptide level, history of angina
or myocardial infarction, digoxin use, and diabetic retinopathy severity,
showed that the associations for alcohol users remained significant. The RRs
were 0.54 (95% CI, 0.33-0.90), 0.44 (95% CI, 0.23-0.84), and 0.21 (95% CI,
0.09-0.48) for those with intake levels of less than 2, 2 to 13, and 14 or
more g/d, respectively (Table 2).
Further control for the presence of overt nephropathy (also significantly
related to CHD mortality in this cohort in the presence of all variables in
the earlier model) had little effect on the significant associations observed.
Results were also essentially unchanged with inclusions of other factors not
independently related to CHD death, such as blood pressure, body mass index,
education, physical activity, diabetes duration, hypertension history, peripheral
neuropathy symptoms, or intake of aspirin, antihypertensive drugs, or oral
hypoglycemic agents (data not shown). In all multivariate-adjusted models,
the RRs for former drinkers were generally 15% to 30% lower than lifetime
abstainers, although these data were not statistically significant (Table 2).
We examined variables, including
age, sex, smoking status, insulin use, glycosylated hemoglobin level, aspirin
intake, and hypertension history, for their potential to modify the negative
associations between alcohol intake and fatal CHD. None were statistically
significant (P>.05 for all) as interaction variables.
In earlier studies of general cohorts, there were concerns53,54
that current abstainers were more likely to have other comorbid conditions
such that a protective effect of modest alcohol intake was not apparent among
those who had no coexisting disease or history of serious illnesses. We tested
this hypothesis in our cohort of older-onset diabetic persons and found no
significant differences in the alcohol–CHD mortality relationship between
persons who had and did not have the diabetic complications of overt nephropathy,
any grade of retinopathy, symptoms of peripheral neuropathy (data not shown),
and history of angina or myocardial infarction (Table 3). Although some subgroup RRs were not statistically significant
because of smaller numbers, all RRs for alcohol drinkers compared with never
drinkers still showed lower risks, regardless of disease status.
Because serum lipid levels might
have influenced our findings, we performed similar analyses for 451 diabetic
persons, a subset of the older-onset diabetic cohort who had complete information
on HDL-C and total cholesterol levels. This subset, compared with those with
no data on serum lipids, showed no significant difference (P>.05) in the means, ranks, and age- and sex-adjusted proportions for
variables such as survival time, age, sex, cigarette smoking, education, physical
activity, body mass index, insulin use, diabetes duration, glycosylated hemoglobin
level, C-peptide level, blood pressure, proteinuria, peripheral neuropathy
symptoms, presence and severity of diabetic retinopathy, hypertension, and
history of angina, myocardial infarction, or stroke. Similar multivariate
models that included either HDL-C, total cholesterol, or the ratio of total
cholesterol to HDL-C still showed significantly lowered risks for the groups
with higher alcohol intake (Table 4).
We also examined the alcohol–CHD
mortality association using different alcohol intake categories as a reference,
finding consistently protective associations with regular drinking. For example,
using all abstainers (never and former drinkers combined) as the reference
category, the multivariate-adjusted RRs were 0.73 (95% CI, 0.52-1.02), 0.59
(95% CI, 0.35-0.998), and 0.28 (95% CI, 0.13-0.60) for those with alcohol
intakes of less than 2, 2 to 13, and 14 or more g/d, respectively (P for trend based on median value for each level=.002), with an overall
effect associated with any amount of drinking compared with abstinence equal
to 0.63 (95% CI, 0.46-0.86). Using infrequent drinkers (alcohol intake <2
g/d) as the reference, the adjusted RRs were 1.83 (95% CI, 1.11-3.02) for
never drinkers, 1.27 (95% CI, 0.89-1.81) for former drinkers, 0.80 (95% CI,
0.47-1.37) for drinkers of 2 to 13 g/d, and 0.38 (95% CI, 0.18-0.81) for drinkers
of 14 g/d or more.
Finally, we analyzed the relationship of alcohol
consumption and all-cause mortality. Controlling for the same variables (all
independently related to total mortality) listed in Table 2, the RRs were 0.74 (95% CI, 0.56-0.98) for former drinkers
and 0.64 (95% CI, 0.48-0.86), 0.47 (95% CI, 0.33-0.69), and 0.49 (95% CI,
0.33-0.74) for those with intake levels of less than 2, 2 to 13, and 14 or
more g/d, respectively.
In this population-based, prospective study, older-onset diabetic persons
who drank higher amounts of alcohol had a considerably reduced risk of death
due to CHD compared with never drinkers. Despite the initial differences in
some characteristics across alcohol intake groups at baseline, some of which
were expected and seen in studies involving healthier populations, the reductions
in risk were independent of and appeared similar across levels of known risk
factors related to CHD, survival, and diabetes.
Bias appeared
unlikely to substantially account for the observed associations. Differential
follow-up was unlikely, given the uniform and regular vital status follow-up
procedures used by staff masked to the exposure status in determining fatal
events. Although misclassification in our outcome could have occurred with
the use of death certificate data in assigning the underlying cause of death,
such information was collected without knowledge of the alcohol intake levels
reported in the study. Chance was possible but it appeared unlikely to materially
affect our findings, given the strength of the relationships we found. The
significant risk reductions among alcohol drinkers that remained from simpler
multivariate models to those adjusting for several covariates made it less
likely that the associations found were due to unmeasured factors. A strength
of the study was our ability to measure (using objective and standardized
procedures) and subsequently control for cardiovascular and diabetes-related
factors associated with survival.
Because of the self-reported
nature of our alcohol data and the lack of long-term information on alcohol
intake (such as a history of lifetime drinking ), misclassification of exposure
status was possible. For example, the former drinkers group could have included
former heavy drinkers, former moderate drinkers, and former infrequent drinkers
who reported not having any alcohol in the past year. Diabetes-related and
other comorbid conditions could also influence a patient's decision to alter
his/her drinking habits over time. We thus did similar analyses using updated
information on alcohol intake and other potential confounders among 533 older-onset
diabetic participants who were still alive and returned for the next follow-up
examination in 1990-1992, finding consistently protective associations in
alcohol drinkers compared with never drinkers (data not shown). Furthermore,
using a subset of the cohort who had information on serum lipids, we observed
a significant correlation between our calculated alcohol intake levels and
serum HDL-C concentrations. We likewise found, as expected, strong and direct
relationships with diastolic blood pressure and cigarette smoking, lending
further credence to the participants' reports of alcohol consumption.
In prior studies in general populations, concerns were raised53,54 that persons who reported abstaining
from alcohol use, which usually formed the reference group used in comparing
risks among groups of alcohol drinkers, did so because of coexisting medical
conditions that could account for the higher risks among nondrinkers. This
was unlikely in our study because we used the information on ever drinking
to identify our reference group of lifetime abstainers. (Separate analyses
using different subgroups as the reference category consistently showed lowered
risks among drinkers, especially regular drinkers.) We also observed similar
inverse associations for alcohol drinkers in subgroups defined by cardiovascular
risk factor status, such as age and sex, and the presence of certain diabetic
complications, with no evidence of interaction between alcohol consumption
and any of the subgroup variables we studied (although the power to detect
such interactions may be limited). Further analyses that excluded deaths occurring
in the earlier (eg, first 5) years of follow-up showed that the inverse relationship
between alcohol and fatal CHD remained (data not shown), refuting the argument
that abstainers might have a greater burden of ill health than drinkers because
of undiagnosed preexisting diseases. Overall, we found no strong evidence
that the higher death rates in abstainers were due to misclassification of
exposure status.
Our cohort did not exhibit a wide range of alcohol
consumption. Most participants were either nondrinkers or infrequent (ie,
less frequent than 1 drink per week) drinkers, with merely 1.8% of individuals
drinking more than 42 g/d (more than 3 drinks per day). This restricted our
evaluation to a relatively tight range of alcohol use, especially any inference
regarding heavy drinking. However, despite the limited range and the greater
proportion of abstainers found in our diabetic cohort compared with general
populations, we were still able to consistently find protective, graded associations
from infrequent drinkers to regular drinkers of about 1 drink or more per
day. Regarding the apparent negative relationship with infrequent drinking
(alcohol intake <2 g/d), the exact reasons for this observation are not
known, given the lack of a strong biologic evidence for this association in
diabetic patients. It is possible that infrequent drinking was a marker of
other health-related behaviors or that some individuals in this subgroup underreported
their consumption. The lack of information on the onset or duration of alcohol
use and its possible relationship with the onset or duration of medical conditions
prevented us from further differentiating the health status of regular drinkers,
infrequent drinkers, former drinkers, and lifelong abstainers. It is also
possible that regular drinkers were constitutionally healthier than never
drinkers, regardless of the presence of any medical comorbidities. Another
limitation was our inability to assess the role of diet, genetic determinants,
and other lipid and hemostatic factors, which may modify or confound any relationship
between alcohol and CHD mortality in diabetic individuals.
The
consistency of our results with those of others who studied healthier populations,
showing an apparent protective effect of moderate alcohol consumption on the
risk of coronary events, is notable. Given the current lack of epidemiological
data on the relationship of alcohol intake to CHD deaths in people with diabetes,
our findings provide evidence of such a relationship in persons largely known
to have more advanced atherosclerotic and other complications compared with
nondiabetic individuals. Moreover, the lowered risk associated with increasing
alcohol intake levels found in this diabetic cohort appear greater than those
found in many general population studies (up to 80% vs 20%-60%). This may
suggest a possibly greater synergism or potentiation of the antiatherogenic,
hemostatic, and/or glucose metabolism–related effects of alcohol consumption
in people with older-onset diabetes. This is also consistent with the perception
that the benefit of alcohol seems greatest in individuals (such as those with
type 2 diabetes) at higher risk of cardiovascular mortality.24
Our results are not inconsistent with the current guidelines regarding
alcohol consumption for people with diabetes, namely, "the same precautions
regarding the use of alcohol that apply to the general public also apply to
people with diabetes."25(pS44) Daily intakes
of no more than 1 drink for women and no more than 2 drinks for men have been
recommended.55 Although our population-based
cohort consisted of older-onset diabetic persons with characteristics that
varied in terms of the presence of coexistent medical problems and diabetic
complications, as well as use of insulin and other medications, we were not
able to assess the acute risks (associated with higher alcohol consumption)
of hyperglycemia, hypoglycemia, or other short-term complications in the presence
of other medical problems seen in diabetes. More importantly, policies regarding
long-term, moderate consumption of alcohol specifically for the prevention
of CHD in older-onset diabetic patients cannot be made and should await the
results of additional prospective studies, including those with a sizable
number of newly diagnosed diabetic women and men and those using incident
disease measures and multiple long-term assessments of alcohol intake. Such
results must also be carefully and thoroughly reviewed in the light of further
findings on the possible risks of other noncardiac end points, such as stroke
and hypertension, in people with diabetes.
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