(Stroke. 2001;32:591.)
© 2001 American Heart Association, Inc.
AHA Science Advisory |
| Introduction |
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| Epidemiological Association of Wine Intake and Cardiovascular Disease |
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A synthesis of the observational studies is difficult because of wide variations in methodology, measurement error in alcohol consumption, and biological variability in response to alcohol consumption (which tends to underestimate effect). Moreover, consumption may vary over time, and this is often not taken into consideration in observational studies. Consumption of alcohol is associated with age, race, smoking, ethnic background, and education level. Wine drinkers tend to be less fat, to exercise more, and to drink with meals. Statistical modeling that includes potential confounders does not mitigate the beneficial effect of alcohol consumption on CHD. Furthermore, the residual protective effect of wine may be due to unmeasured factors or differences between drinkers and nondrinkers that cannot be adequately controlled for in statistical analyses. Because of these limitations, epidemiological data can be considered to be supportive of the alcohol-CHD hypothesis, but not definitive. More data are needed to clarify the effects of specific types of beverages in diverse populations.
The mortality rate from CHD in France is perhaps half the rate in the United States despite similar intakes of animal fats.10 This has been coined the "French paradox." When potential confounders and differences in reporting are taken into consideration, the gap is narrowed but probably not eliminated. Regional variation in CHD rates and risk factors in both the United States and France makes a simple explanation for the paradox unlikely. Nevertheless, one explanation for the lower risk of CHD among the French is an increased intake of wine, especially red wine.11 An inverse association between moderate consumption of alcoholic beverages (1 to 2 glasses per day) and CHD has been documented. However, data regarding the specific effects of red wine are less consistent, possibly for the reasons discussed above. Moreover, the protective effect appears to be influenced by whether the wine is consumed with meals.4 This hypothesis deserves further investigation, because the pattern of consumption of alcoholic beverages may be a marker for other lifestyle factors related to CHD risk.7 A number of dietary factors, such as consumption of fresh fruits, vegetables, and fish and reduced intake of milk products, differ between European populations and can be readily associated with reduced CHD risk.12 13
| The Biological Basis for a Protective Effect of Alcohol and Red Wine |
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How Does Alcohol Ingestion Change
Lipoproteins?
Alcohol leads to 2 well-established changes in
lipoproteins; wine, as a source of alcohol, has no other known effects.
Like any other source of carbohydrates, alcohol can increase plasma
triglyceride levels and can serve as a source of excess calories. In
patients with underlying hypertriglyceridemia, the triglyceride
elevations can be
marked.24 25 The
association between alcohol-related hypertriglyceridemia and
exacerbation of pancreatitis is well known. The source of the increase
in triglyceride is an increase in triglyceride production and secretion
in very-low-density lipoprotein (VLDL). The best-known effect of
alcohol is to increase circulating levels of high-density lipoprotein
(HDL) cholesterol. One to 2 drinks per day increase HDL by
12% on
average.26 This increase is
similar to that seen with several other interventions, including
exercise programs27 and
fibric acid medications. Niacin therapy is a more effective method to
raise HDL and leads to an
20% increase in HDL cholesterol.
Approximately half of the beneficial effects of alcohol on
cardiovascular disease have been ascribed to the increase in HDL
cholesterol.1 No clinical
trials have provided verification that alcohol can be used to increase
HDL cholesterol levels. In contrast, treatment of patients with low HDL
with statins as primary
prevention28 and with fibric
acids as secondary
prevention29 has been shown
to be beneficial.
Do Wine and Other Alcoholic Beverages Have
Significant Antithrombotic Actions?
For light to moderate intakes (up to 60 mL of alcohol
per day), the answer appears to be yes. Numerous studies have shown
statistically significant decreases in platelet aggregation (measured
in vitro) associated with the consumption of alcoholic
beverages.30 However,
controversy surrounds the issue of whether some forms of alcoholic
beverages, particularly red wine, are more effective than others. There
is some evidence that resveratrol and other polyphenolic compounds
found in red wine can have an independent and additive effect on the
reduction of platelet
aggregation.31 32 33
Other studies34 suggest that
most of the effects on platelets can be explained by the alcohol
component of the beverage. Primarily on the basis of in vitro studies,
inhibition of prostaglandin synthesis has been determined to be the
apparent mechanism by which alcoholic beverages decrease platelet
aggregation; aspirin works by a similar mechanism. Less well studied
than the effects on platelets are the effects of alcoholic beverages on
other aspects of coagulation. For example, there are occasional reports
of potentially beneficial effects of alcohol or resveratrol on plasma
fibrinogen levels
(decreased34 ) and cellular
tissue factor levels (also
decreased35 ), but more data
are needed to adequately evaluate these and related findings. Overall,
light to moderate consumption of any type of alcohol-containing
beverage appears to reduce platelet aggregation and thereby provides an
antithrombotic benefit similar to that of
aspirin.
| Adverse Effects of Alcohol Ingestion |
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Hypertension
There are more than 50 cross-sectional and 10
prospective epidemiological population-based studies that have
demonstrated a direct association of alcohol intake and hypertension in
men and women of different ages and races. Data from the Nurses Heath
Study37 demonstrate that
>20 g of alcohol per day (2 drinks) in women who are between 30 and 55
years of age is associated with a linear increase in the incidence of
hypertension. In men, alcohol consumption exceeding 20 g/d is also
linked to the development of hypertension; however, the increase in
blood pressure relative to the level of alcohol consumption is less
linear. In the Kaiser Permanente
study,38 men and women
drinking 6 to 8 drinks/d had a 9.1-mm Hg higher systolic blood
pressure and 5.6-mm Hg higher diastolic blood pressure than
nondrinkers. Daily intake of more than moderate amounts of alcoholic
beverages is a clear risk factor for the development of hypertension.
Patients who are hypertensive should avoid alcoholic
beverages.
Stroke
There appears to be consensus that long-term heavy
alcohol consumption (>60 g/d) increases an individuals risk for all
stroke subtypes, especially intracerebral and subarachnoid hemorrhage.
The effects of moderate alcoholic beverage consumption (<2 drinks/d)
are less clear because of conflicting reports. Some
studies39 suggest that
moderate alcohol consumption may decrease the risk of ischemic stroke
in specific populations, whereas
others40 have not found a
protective association between alcohol intake and stroke. There may be
numerous variables, such as race/ethnicity, age, sex, drinking
patterns, and beverage type, that interact with the effects of alcohol
on stroke risk. Data remain inconclusive in this area, and therefore
specific recommendations are difficult to
formulate.
| What Conclusions Can We Make About a Protective Effect of Wine Against Heart Disease? |
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| Footnotes |
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This statement is being published in the January 23, 2001, issue of Circulation.
| References |
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