Articles in PresS. Am J Physiol Heart Circ Physiol (January 14, 2005). doi:10.1152/ajpheart.00868.2004
ANTIATHEROGENIC POTENTIAL OF RED WINE:
Clinician Update
FINAL ACCEPTED VERSION
MANUSCRIPT NUMBER: H-00868-2004.R1
Paul E. Szmitko, BSc
Subodh Verma, MD, PhD
Division of Cardiac Surgery
Toronto General Hospital
University of Toronto
Toronto, Ontario, Canada
Running title: Red Wine and Atherosclerosis
Corresponding Author
Subodh Verma, MD, PhD
Division of Cardiac Surgery
Toronto General Hospital
14EN-215, 200 Elizabeth Street
Toronto, Ontario, Canada M5G 2C4
Tel. (416) 340-4580
Fax (416) 782-0096
[email protected]
Copyright © 2005 by the American Physiological Society.
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ABSTRACT
Complications of atherosclerosis remain the leading cause of morbidity and mortality in
industrialized countries. Epidemiological studies have repeatedly demonstrated that moderate
alcohol intake has a beneficial effect on cardiovascular disease. The purpose of this review is to
examine the epidemiological and biological evidence supporting the intake of red wine as a
means of reducing atherosclerosis. Based on epidemiologic studies, moderate intake of alcoholic
beverages, including red wine, reduces the risk of cardiovascular, cerebrovascular and peripheral
vascular disease in populations. In addition to the favourable biological effects of alcohol on the
lipid profile, on hemostatic factors, and in reducing insulin resistance, the phenolic compounds in
red wine appear to interfere with the molecular processes underlying the initiation, progression
and rupture of atherosclerotic plaques. Whether red wine is more beneficial than other types of
alcohol remains unclear. Definitive data from a large-scale, randomized clinical end-point trial
of red wine intake would be required before physicians can advise patients to use wine as part of
preventative or medical therapies.
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Numerous epidemiologic studies have concluded that a moderate intake of alcohol is
associated with a reduced risk of morbidity and mortality secondary to atherosclerotic
complications. Ethanol intake from any type of alcoholic beverage appears beneficial (82), but
red wine seems to confer additional health benefits (44). The regular drinking of red wine has
been suggested as the explanation for the “French Paradox”, the relatively low incidence of
coronary atherosclerosis in France compared to other Western countries, despite the high intake
of saturated fat (75). The combination of ethanol and phenolic compounds in red wine is thought
to be responsible for the apparent protective effects (115). Despite numerous epidemiological
and biological studies, insufficient information exists to definitively recommend wine intake as a
therapeutic intervention to prevent or treat atherosclerotic disease. This review of red wine and
atherosclerosis will examine the epidemiology of atherosclerotic disease and alcohol, particularly
wine consumption, the beneficial biological effects on atherosclerosis derived from red wine
compounds, and the current medical recommendations regarding alcohol intake.
EPIDEMIOLOGY
Moderate alcohol consumption, defined as 1 to 2 drinks a day, has been suggested to
increase overall survival in a number of different population groups (12,37,43,49,97,114). One
standard drink is generally considered to be 1.5 oz of liquor, 5 oz of wine, or 12 oz of beer.
However, higher intakes of ethanol have been linked to increased mortality (12,97). Based on
these observations, the relation between alcohol intake and mortality is described as U- or Jshaped, in which abstainers or heavy drinkers do not, but moderate drinkers do, experience
alcohol’s protective effects (27,42). Furthermore, the benefits associated with light to moderate
drinking do not extend to all patient groups and are most apparent in middle-aged men and
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women, especially those who are at increased risk for cardiovascular disease (37,114). Thus, the
reduction in total mortality is generally attributed to a reduction in atherosclerotic risk.
Atherosclerosis, a dynamic and progressive disease arising from the combination of
endothelial dysfunction and inflammation (56,86), manifests itself clinically when it involves the
coronary arteries, the extracranial carotid arteries or the vasculature of the lower extremities.
Moderate consumption of wine and other alcoholic beverages appear to reduce the risk of
morbidity and mortality related to the presentation of atherosclerotic disease.
Coronary Heart Disease
Epidemiological evidence confirms an association between moderate alcohol intake and a
reduced risk of coronary heart disease (CHD) in populations. A meta-analysis (19) of 51
epidemiological studies concluded that alcohol’s protective effects were most pronounced at
moderate doses. The risk of CHD decreased by approximately 20% (Relative Risk [RR]=0.80,
95% Confidence Interval [CI]: 0.78-0.83) when 0 to 2 drinks of alcohol were consumed per day
(19). The lower risk of CHD in moderate drinkers has been observed in a variety of patient
populations, including apparently healthy adults (4,13,65), patients with a history of myocardial
infarction (MI) (26,68), and diabetic patients (2,20,92,99).
Results from the Health Professionals Follow-up Study suggest that the consumption of
alcohol at least 3 to 4 days per week is inversely associated with the risk of MI (65). 38 077
male health professionals, who were free of cardiovascular disease at baseline, were followed for
12 years. After taking into account the confounding factors of age, smoking status, body-mass
index (BMI), use of aspirin, exercise, family history and presence of hypertension or diabetes,
the consumption of alcohol 3 to 4 days per week decreased the risk of MI by 32% (RR=0.68,
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95%CI: 0.55-0.84), regardless of the type of alcoholic beverage consumed. Results from the
Physicians’ Health Study confirm that moderate alcohol consumption decreases the risk for MI
(RR=0.65, 95%CI: 0.52-0.81) (13), and further suggest protection against angina (RR=0.69,
95%CI: 0.59-0.81) (13) and sudden cardiac death (RR=0.21, 95%CI: 0.08-0.56) (4) in apparently
healthy males. Self-reported moderate alcohol consumption in the year prior to MI, among
patients in the Onset Study, was associated with reduced mortality following infarction (52,67).
In this prospective cohort study, patients who consumed 7 or more alcoholic drinks per week had
lower cardiovascular mortality compared with abstainers (2.4 vs 6.3 deaths per 100 person-years;
hazard ratio [HR]: 0.38, 95% CI: 0.25-0.55) (67). Finally, moderate alcohol consumption also
appears to lower the risk of congestive heart failure based on findings in the Framingham cohort
(116).
The cardioprotective benefits derived from alcohol extend to patients at increased risk for
mortality from CHD, namely patients with diabetes or those who have already suffered from an
MI. Atherosclerosis causes most of the death and much of the disability in patients with diabetes
(8). Light to moderate alcohol consumption appears to be associated with a lower risk of type 2
diabetes mellitus (DM) among both younger women (113) and middle-aged men (3), possibly
due to beneficial effects on insulin sensitivity (24). In healthy postmenopausal women who were
randomized to consume 0 to 30 g of alcohol per day (approximately 2 to 3 drinks per day) for 8
weeks as part of a controlled diet, 30 g/day of alcohol significantly increased insulin sensitivity
by 7.2% and reduced fasting insulin concentration by 19.2% (24). In addition to lowering the
risk of diabetes in healthy patients, alcohol use is also inversely associated with the risk of CHD
mortality in older-onset DM subjects (99), and in middle-aged diabetic men (2) and women (92).
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These observations suggest that moderate alcohol consumption by patients with DM is
associated with similar risk reductions in CHD as in nondiabetic subjects.
Patients who have suffered an MI may also potentially benefit from moderate alcohol
intake. Among male physicians with a history of MI, 2 to 3 drinks per week was associated with
lower mortality, having a relative risk of death of 0.7 compared to nondrinkers (68). Patients
within the Lyon Diet Heart Study who survived a recent MI and consumed about 2 drinks per
day had a reduction in cardiovascular complications by 59% compared to abstainers (26).
Cerebrovascular Disease
A recent meta-analysis reported that light to moderate alcohol consumption may be
protective against total and ischemic stroke (76). From 35 observational studies (19 cohort
studies) consumption of approximately 1 drink per day was associated with a reduced relative
risk of total stroke (RR=0.83, 95%CI: 0.75-0.91) and ischemic stroke (RR=0.80, 95%CI: 0.670.96) (76). However, the risk of stroke increased with heavier alcohol consumption. The
protective effect of moderate alcohol consumption on ischemic stroke appears to be quite
generalizable across diverse populations. The Northern Manhattan Stroke Study, a populationbased study designed to determine stroke incidence, risk factors and prognosis, reported that
consuming up to 2 drinks per day was significantly protective for ischemic stroke (odds ratio
0.51, 95%CI: 0.39-0.67) in elderly, multiethnic, urban subjects (87). Results from the US
Nurses’ Health Study suggested a protective relationship between moderate drinking and
ischemic stroke among middle-aged women (93), a finding that was paralleled in middle-aged
men participating in the Physicians’ Health Study (10). However, in the Framingham cohort,
alcohol intake was only associated with a lower risk of stroke among subjects aged 60 to 69
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years (33). Furthermore, alcohol consumption appears to be safe and may even reduce the risk
of cardiovascular mortality in men with preexisting cerebrovascular disease (CVD) (49).
Peripheral Arterial Disease
An association between moderate alcohol intake and decreased prevalence of peripheral
arterial disease (PAD) appears to exist based on epidemiological evidence. In the Physicians’
Health Study, daily drinkers (≥ 7 drinks/week) had a relative risk of PAD of 0.68 (95%CI: 0.520.89) as compared to individuals who consumed < 1 drink per week after controlling for age,
smoking status and treatment assignment (14). Intermittent claudication, the clinical hallmark of
PAD, developed less frequently in subjects in the Framingham Heart Study who consumed 1 to 2
drinks per day (34). Using a multivariate Cox regression model, the lowest intermittent
claudication risk emerged at levels of 13 to 24 g of ethanol per day (1 to 2 drinks/day) for men
and 7 to 12 g of ethanol per day (0.5 to 1 drink/day) in women (34). The inverse association
between alcohol consumption and PAD was also found in non-smoking men and women (106).
Even though the protective effect is present regardless of the type of alcoholic beverage
consumed, results from the Edinburgh Artery Study suggested that less severe peripheral arterial
insufficiency, as determined by a higher ankle-brachial pressure index, was more evident with
the consumption of wine than with spirits or beer (50).
Is Red Wine Better?
Based on epidemiological data, alcohol intake is associated with a reduction in CHD,
CVD and PAD. However, the lower rate of CHD in France as compared with other developed
countries suggested that the consumption of red wine provided superior vascular protection and
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explained this apparent French Paradox (21, 94). Support for a more pronounced
cardioprotective effect for red wine compared to other alcoholic beverages first emerged from
the Copenhagen Heart Study which was performed prospectively in 13 285 men and women over
12 years (44). The results from this study suggested that subjects with low to moderate intake of
wine had half the risk of dying from cardiovascular and cerebrovascular disease as those who
never drank wine. Beer and spirit drinkers did not experience this advantage. These results were
reinforced when the same group performed pooled cohort studies in which the type of alcohol
consumed, smoking status, educational level, physical activity, and BMI were assessed at
baseline (43). Compared with nondrinkers, light drinkers who avoided wine had a RR for death
from all causes of 0.90 (95%CI: 0.82-0.99) while those who drank wine had a RR of 0.66
(95%CI: 0.55-0.77) (43). The authors concluded that wine intake may have a beneficial effect
on all cause mortality that is additive to the protection afforded by alcohol. The additional
benefit of wine as compared to other alcoholic beverages is supported by a meta-analysis of wine
intake in relation to vascular risk (30). Pooling the data from 13 studies involving 209 418
subjects, the risk reduction of vascular disease associated with wine intake was 32%, greater than
the risk reduction for beer consumption which was determined to be 22% (30). However, other
studies and reviews have failed to see wine’s dominant effect (81). A large prospective cohort
study among 128 934 adult members of a Northern California prepaid health care program
concluded that moderate consumption of any form of alcohol reduced cardiovascular risk
without any major additional benefits associated with drinking red wine (53,54).
Explanations for these contradictory results may include differences in the risk factor
patterns among beer, spirit and wine drinkers (82), the pattern of alcohol consumption, the
presence of other confounding lifestyle factors, or alternatively, differences in the type of wine
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consumed. European, but not American, studies have generally found a greater reduction in
cardiovascular risk associated with red wine consumption compared with other alcoholic
beverages (107). Recent research suggests that red wines differ in their vasodilating ability
based on the type of grape and the country of origin (107,109), suggesting that the type of red
wine consumed may influence the apparent protective effect that is conferred. Furthermore,
wine drinkers tend to have a healthier diet (98) and are generally members of higher socioeconomic groups (69) compared to beer or spirit drinkers, factors that may influence the
interpretation of previous reports. Most of the epidemiological studies to date fail to clearly
define the type of alcohol consumed and the circumstances under which it is consumed, for
example regularly only with meals or exclusively as weekend binges. As Mann et al (61) point
out, rather than using “alcohol consumption” authors would be more accurate in saying
“alcoholic beverage consumption” since beer, wine and spirits contain substances other than pure
ethanol that may exert beneficial or harmful health effects. It may be the balance between these
beneficial and harmful attributes that help explain the differences observed among population
groups, and more importantly, in individual patients. Therefore, future studies should focus on
clearly differentiating between the types of alcoholic beverages consumed, identifying
confounding factors that exist including socio-economic status and diet, and assessing the pattern
of consumption to assist with dispelling the confusion that exists within the current literature
regarding specific beverage effects.
VASCULAR DISEASE AND THE BENEFICIAL EFFECTS OF RED WINE
Epidemiological studies provide the initial evidence suggesting moderate wine
consumption is associated with a reduction in cardiovascular risk. A second type of evidence
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related to biologic plausibility lends support to these observations (40). A series of in vitro and
in vivo studies suggest that the polyphenolic compounds in red wine, in addition to ethanol, may
play an active role in limiting the initiation and progression of atherosclerosis (See Figure 1).
Polyphenolic substances in wine are usually subdivided into two groups, the flavonoids and nonflavonoids (100). The most common flavonoids in red wine are flavonols such as quercetin, and
flavon-3-ols such as tannins and catechin, while among the non-flavonoids, resveratrol is best
known (100).
Promotion of Endothelial Function
The vascular endothelium, located at the interface of blood and tissue, is able to sense
changes in hemodynamic forces and blood-borne signals and react by synthesizing and releasing
vasoactive substances (102). Vascular homeostasis is maintained by a balance between
endothelium-derived relaxing and contracting factors. With disruption of this balance, mediated
by inflammatory and traditional cardiovascular risk factors, the vasculature becomes susceptible
to atheroma formation. Both the alcohol and polyphenolic compounds found in red wine appear
to favourably maintain endothelial function and thus, limit atherosclerosis.
Nitric oxide (NO) is the key endothelium-derived relaxing factor that plays a pivotal role
in the regulation of vascular tone and vasomotor function (64). NO protects against vascular
injury, inhibits leukocyte adhesion to the endothelium, and limits platelet aggregation (25,38).
However, in response to the traditional cardiovascular risk factors, such as hypertension, diabetes
and hypercholesterolemia, the endogenous defences of the vascular endothelium begin to break
down. The ethanol content of red wine, and especially its polyphenolic compounds, may be able
to limit this descent toward endothelial dysfunction by enhancing NO mediated vasodilation
(31). In vitro, ethanol appears to increase the expression of endothelial nitric oxide synthase and
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NO production in aortic endothelial cells (101). Red wine polyphenols, in particular resveratrol,
appear to further enhance endothelial NO synthase expression and activity and subsequent NO
release from endothelial cells (55,108,109). Red wine, and not white or rosé wines, inhibits
endothelin-1 (ET-1) synthesis (18), a potent vasoconstrictor that is seen as a key factor in the
development of vascular disease and atherosclerosis. These in vitro data have been supported by
results in humans, which suggest that the consumption of red wine, compared to white wine or
vodka, led to a greater increase in coronary flow-velocity reserve (90). Thus, this vasodilatory
effect appears to be enhanced by red wine’s polyphenolic components.
One of the most important alterations with regular alcohol consumption is an increase in
plasma levels of high density lipoprotein (HDL) (29,39). A meta-analysis examining the effect
of moderate alcohol intake, not differentiating between the type of alcoholic beverage consumed,
on lipids found that a 16.8% reduction in risk of CHD could be directly attributable to increased
HDL concentration from the consumption of 30 g of alcohol (~2.5 drinks) per day (83). One to 2
drinks per day of any alcoholic beverage increases HDL by ~12% on average (58). Alcohol has
been demonstrated to act directly on the liver by increasing the synthesis of apolipoprotein (apo)
A-I (23), and to enhance lipoprotein lipase activity (71), leading to enhanced formation of HDL
cholesterol. In human subjects, elevations in HDL cholesterol were believed to be related to the
alcohol induced increase in transport rates of the major HDL apolipoproteins apoA-I and –II
(29). Elevations in HDL may serve to shuttle low density lipoprotein (LDL) cholesterol back to
the liver for reprocessing, reducing the cholesterol available for endothelial activation and
atheroma formation. In addition to this alcohol mediated effect, red wine possesses antioxidant
activity.
Impairment of Plaque Initiation and Progression
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The oxidation of LDL cholesterol not only increases its uptake by macrophages resulting
in foam cell formation, but oxidized LDL (oxLDL) causes endothelial activation and changes its
biological characteristics in part by reducing the intracellular concentration of NO (17,57).
These changes promote fatty streak atheroma formation. Thus, if LDL oxidation is reduced,
atherosclerotic plaque formation may be decreased. The phenolic substances in red wine, and
not the alcohol component, have potent antioxidant properties which inhibit the formation of
oxLDL in vitro (35), as well as macrophage-mediated LDL oxidation (7). Some in vivo studies
in rabbits (22,116), hamsters (105), and mice (45) suggest that the antioxidant properties of wine
limit early atherosclerotic plaque formation and progression. However, a reduction in mature
atherosclerosis in apolipoprotein-E deficient mice was not observed with red wine treatment,
though less than 60% of these treated mice had measurable blood ethanol levels (9). Human
studies suggest that the consumption of red wine (62) or alcohol-free red wine (89) leads to a
significant increase in serum antioxidant activity, which may reduce the susceptibility of lowdensity lipoproteins to oxidation in vivo (70), limiting the extent of atheroma formation.
However, to date, the results from clinical trials assessing the use of antioxidant therapies to
reduce cardiovascular events have been disappointing. The Antioxidant Supplementation in
Atherosclerosis Prevention (ASAP) Study suggested that supplementation with a combination of
vitamin E and slow-release vitamin C slowed down ultrasonographically documented common
carotid artery atherosclerotic progression in hypercholesterolemic persons (88). However, other
studies, including large, randomized clinical trials such as HOPE and SU.VI.MAX, have failed
to see any cardiovascular benefit. One arm of the Heart Outcomes Prevention Evaluation
(HOPE) trial (60) evaluated the effects of vitamin E in patients at high risk for cardiovascular
events. Vitamin E had a neutral effect on the composite of myocardial infarction, stroke or
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cardiovascular death (relative risk = 1.03, 95% CI 0.88-1.21; P = 0.70), suggesting that the daily
administration of 400 IU vitamin E for an average of 4.5 years to high risk patients had no effect
on adverse cardiovascular outcomes. The Supplementation en Vitamines et Mineraux
Antioxidants (SU.VI.MAX) study (46) was a randomized, double-blind, placebo-controlled
primary prevention trial involving 13 017 French adults who took a single daily capsule of a
combination of 120 mg of ascorbic acid, 30 mg of vitamin E, 6 mg of beta carotene, 100 mg of
selenium, and 20 mg of zinc, or a placebo. The study, with a mean follow-up of 7.5 years, failed
to detect a difference in ischemic cardiovascular disease incidence or all-cause mortality between
the groups.
Inflammatory activation of the endothelium is marked by the increased expression of
adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), secondary to nuclear
factor-kappa B (NF-κB) transcriptional activity. Red wine inhibits NF-κB activation in
peripheral blood mononuclear cells (11) and in human endothelial cells (73), resulting in a down
regulation of VCAM-1 (16). Wine further limits monocyte migration into the arterial intima by
inhibiting the expression of monocyte chemotactic protein-1 (MCP-1). Fatty streak evolution
toward a complex lesion is typified by the proliferation of vascular smooth muscle cells
(VSMCs) and their migration toward the intima. Red wine polyphenols impair this progression,
inhibiting both VSMC migration (48) and proliferation (6,47,48,85). In addition to these
polyphenol mediated anti-inflammatory actions, alcohol itself may also attenuate atherosclerosis,
in part through an anti-inflammatory mechanism, by reducing plasma C-Reactive protein (CRP)
levels (5,91). The inflammatory marker CRP represents one of the strongest independent
predictors of vascular death in a number of settings (77-79) in which wine consumption may be
beneficial. CRP elicits a multitude of effects on endothelial biology favoring a
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proatherosclerotic phenotype (96) such as decreasing NO release (104), upregulating adhesion
molecules (103), and stimulating VSMC proliferation and migration (111). In the Pravastatin
Inflammation/CRP Evaluation Study, the moderate consumption of any alcoholic beverage, as
compared to no or only occasional alcohol intake, was associated with lower CRP plasma
concentrations (5).
Plaque Destabilization, Rupture and Thrombosis
Disruption of a vulnerable atherosclerotic plaque, upon exposure to hemodynamic
stresses, can trigger thrombosis culminating in acute myocardial infarction. Both the alcohol and
polyphenolic compounds in red wine appear to have antithrombotic action. Erosion of the
plaque surface, characterized by areas of endothelial cell desquamation, exposes a prothrombotic
surface, making subendothelial collagen, tissue factor (TF) and von Willebrand factor (vWF)
accessible to components in the circulation, resulting in coagulation and thrombin formation.
Overall, light-to-moderate alcohol consumers have lower levels of fibrinogen, vWF, and factor
VII, with wine drinkers additionally having lower plasminogen activator inhibitor antigen-1
levels (63,66), suggesting a reduction in hemostasis. Furthermore, any form of alcohol
consumption also increases antithrombin-III activity (84) and based on results from the
Physicians’ Health Study, is associated with increased tissue plasminogen activator
concentrations (80). In vitro, alcohol induced the expression of tissue-type plasminogen
activator in human endothelial cells, resulting in enhanced fibrinolytic activity (1). Both
resveratrol and quercetin have been demonstrated to decrease the expression of TF by activated,
human endothelial cells (32). The polyphenolic compounds in red wine also exert an effect on
platelet aggregation. Resveratrol and other polyphenolic compounds decrease platelet
aggregation, possibly by interfering with prostaglandin synthesis and ADP-mediated aggregation
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(28,72,112). Similarly, ethanol inhibits in vitro platelet secretion and aggregation, in part by
inhibiting phospholipase A2 secretion and activity (74,95). In vivo, platelet aggregation was
inhibited after purple grape juice consumption in healthy human volunteers, suggesting grape
derived flavonoids and not just ethanol, may contribute to red wine’s apparent antithrombotic
effect (36). (See Figure 2)
WILL A GLASS OF RED WINE A DAY KEEP ATHEROSCLEROSIS AT BAY?
Despite the observational data derived from epidemiological studies and the biological
plausibility from in vitro and in vivo experimental research, there is insufficient evidence to
encourage patients who do not drink to start consuming red wine as part of a strategy to protect
against atherosclerosis. In this era of evidence based medicine, a large-scale, randomized control
trial, assessing the effects of red wine intake versus a non-alcoholic placebo, would be required
to ensure that there is legitimacy to both the epidemiological and biological data (41). Only
based on the favorable results of such a study may physicians be justified in recommending the
consumption of red wine for cardiovascular protection. However, whether such a clinical trial is
ethical based on alcohol’s well-documented toxic effects is questionable. Too much alcohol
consumption has been shown repeatedly to contribute to cardiovascular disorders such as
alcoholic cardiomyopathy, high blood pressure and arrhythmias. Excessive alcohol use can lead
to liver cirrhosis, cancers, pancreatitis, neurological disorders, motor vehicle accidents and
addiction. Individuals with a personal or family history of alcohol abuse or liver disease should
avoid drinking alcohol. Nevertheless, many medical societies view light ethanol use as being
potentially beneficial to the cardiovascular system, though no formal recommendations for light
alcohol consumption are made (15,51,59). The American Heart Association recommends that
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alcohol use should be an item of discussion between the physician and the patient (41). It is
clear that physicians should continue to advise heavy drinkers to reduce consumption and to help
alcoholics overcome their addiction. Also, there is no justification to recommend alcohol
consumption as a preventative measure to non-drinkers considering there are several well proven
therapies for cardiovascular risk reduction such as exercise, smoking cessation, blood pressure
control and cholesterol lowering that do not have wine’s undesirable effects (40). For those
patients who are established moderate drinkers, based on the current knowledge, abstention
should not be enforced, but also, increasing alcohol consumption for the purposes of
cardioprotection is not justified. Hence, physicians should make individualized
recommendations about alcohol drinking for patients with or without the clinical manifestations
of atherosclerosis.
CONCLUSION
Even though there are numerous studies extolling the virtues of red wine and other
alcoholic beverages, there is insufficient clinical evidence to firmly conclude that the
consumption of wine prevents cardiovascular disease. Though biologically plausible and
epidemiologically convincing, the cardiovascular protection afforded by red wine will remain
unknown until a randomized, clinical trial is performed. Only then will it be known if red wine
is truly protective or if it deserves to be categorized with vitamin E in the cardiovascular
literature as a therapy that did not hold up in clinical trials (60). Thus, patients should not be
advised to drink wine for health, but rather, if they do drink moderately, to drink to health.
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Figure Legends
Figure 1:
Both the alcohol and phenolic components found in red wine are believed to decrease the risk of
atherosclerotic disease via several different mechanisms.
Figure 2:
In vitro and in vivo experimental research support the biological plausibility of red wine, both its
ethanol and phenolic compounds, as an inhibitor of atherosclerosis. Red wine may promote the
maintenance of a healthy endothelium, and inhibit atherosclerotic plaque formation, progression
and rupture.
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Figure 1
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Figure 2