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Cardiovascular benefits and risks of moderate alcohol consumption

Cardiovascular benefits and risks of moderate alcohol consumption
Literature review current through: Jan 2024.
This topic last updated: Nov 16, 2021.

INTRODUCTION — Excessive alcohol use can lead to a variety of adverse effects including liver disease, heart failure (HF), increased cancer risk, neurologic complications, and unintentional injuries. Balanced against these deleterious effects is the observation that, compared with abstinence or heavy drinking, moderate alcohol intake may have sex-specific health benefits, particularly in regard to cardiovascular disease (CVD) and diabetes.

The cardiovascular benefits and risks of alcohol consumption will be reviewed here. A general review of the risk and benefits of alcohol consumption is presented separately. (See "Overview of the risks and benefits of alcohol consumption".)

DEFINITIONS

Moderate drinking — The 2020 to 2025 Dietary Guidelines for Americans define moderate drinking as having up to one drink per day for females and up to two drinks per day for males (table 1) [1]. This definition refers to the amount of alcohol consumed on any single day and is not intended as an average over several days. The definition of the dose (grams of alcohol) which provides protection from all-cause mortality or specific cardiovascular outcomes has been challenged [2].

Standard drink — Definitions of a "standard drink" differ, both within and between countries (figure 1) [3,4]. The Global Burden of Disease Study defined a standard drink as 10 grams of pure ethyl alcohol consumed daily [2]. However, in the United States, a standard drink contains 14 grams (0.6 fluid ounces) of pure alcohol, and around the world the standard drink ranges from as few as 8 grams of alcohol to as many as 20 grams of alcohol [3,5,6]. (See "Overview of the risks and benefits of alcohol consumption", section on 'Standard drink size'.)

Beverage type — Available data do not clearly support a definitive conclusion regarding the differential benefits of various beverage types. However, it is generally accepted that the type of alcohol is not as important a factor as the amount of alcohol consumed and the pattern of intake [7-9].

However, the French paradox that coronary heart disease (CHD) mortality is lower in France than would be expected from the high national prevalence of smoking and saturated fat intake has been attributed to frequent red wine consumption [10]. Red wine contains phenolic and flavonoid substances that have antithrombotic and antioxidant properties [11,12]. Additionally, wine intake has been associated with improvements in heart rate variability [13], which could contribute to improved prognosis for CHD [11,14].

Data from clinical studies vary on whether the type of alcoholic beverage is a factor in the cardioprotective effect of alcohol, with some suggesting that all alcoholic beverages afford cardioprotective benefits [15], while others report that the cardioprotection is strongest for wine [16,17].

A dose-response relationship on risk of vascular events was seen for both wine and beer, but the relationship was stronger for wine. A J-shaped relationship was again observed between alcohol dose and total mortality [16,17].

One systematic review found that all beverage types are associated with lower rates of CHD [18].

A meta-analysis of 13 cohort studies, including 209,418 people, reported a strong and statistically significant benefit for moderate consumption of both beer and wine, although the effect was stronger for wine (32 versus 22 percent relative risk [RR] reduction) [17]. A dose-response relationship was seen for both wine and beer with vascular risk, but the relationship was stronger for wine. A J-shaped relationship was again observed for alcohol dose and total mortality.

ADVICE TO PATIENTS REGARDING ALCOHOL USE — Our approach to advising patients about the benefits of alcohol as part of a strategy to reduce cardiovascular disease (CVD) risk is as follows:

Individuals who are not currently drinking, or those who have a personal preference to avoid alcohol, should not be advised to consume alcohol solely for the purpose of CVD risk reduction.

Patients who have an underlying medical condition that precludes alcohol use (eg, alcohol use disorder, liver disease, etc) should not be advised to consume alcohol.

Patients who choose to drink moderate amounts of alcohol, such as those who drink alcohol less than one unit per day (or less than 15 g per day) [19] or less than 100 g per week [20] may experience benefits for their health.

Caution is necessary when promoting the beneficial effects of alcohol for cardiovascular risk reduction. The absolute benefits of alcohol consumption are unclear in the absence of randomized controlled trials. There is little agreement regarding the upper limit of alcohol consumption that correlates with cardiovascular benefit, nor are there good data about which group of individuals might benefit from different levels of alcohol at no additional risk. (See 'Effect of alcohol on cardiovascular risk' below.)

The potential cardiovascular benefit of moderate alcohol intake must be balanced against the effect of alcohol on other disorders, such as cirrhosis and cancer, and the total alcohol-attributable deaths [21,22]. The net risk-benefit balance associated with moderate alcohol consumption will vary in different age groups and populations. As an example, alcohol intake increases the risk for breast cancer in females [21]. For a young woman with a low risk for coronary disease, the increased risk related to alcohol intake and breast cancer might outweigh any potential cardiovascular benefits. (See "Overview of the risks and benefits of alcohol consumption", section on 'Breast cancer'.)

PROPOSED MECHANISMS OF BENEFIT — Factors responsible for the apparent cardiovascular benefits of light to moderate alcohol intake are uncertain. A meta-analysis evaluated 42 clinical studies with information about biochemical markers assessed before and after consumption of ethanol [23]. The following beneficial changes, which were noted with an experimental dose of 30 grams of ethanol per day, would be estimated to reduce the risk of coronary heart disease (CHD) by 25 percent:

Serum apolipoprotein A-I increased by 8.8 mg/dL

Plasma fibrinogen concentration decreased by 7.5 mg/dL

Tissue-type plasminogen activator (tPA) concentration increased by 1.25 ng/mL

Serum triglycerides increased by 5.7 mg/dL (potentially detrimental rather than beneficial)

For many decades, light to moderate alcohol intake was proposed as a way to increase serum high-density lipoprotein (HDL) cholesterol and thereby reduce cardiovascular risk. While an increase of serum HDL cholesterol by 4 mg/dL or (0.1 mmol/L) may occur following light to moderate alcohol intake, it should not be expected [23]. An updated meta-analysis found similar results, finding a dose response for increased HDL cholesterol levels and similar responses for the other markers listed above [24,25]. However, strategies directed at raising HDL cholesterol as a means of reducing cardiovascular events have failed in multiple clinical trials [26]. (See "HDL cholesterol: Clinical aspects of abnormal values".)

However, the effects of alcohol on various HDL functional measures requires further exploration. In Mendelian randomization studies, self-reported alcohol intakes of Japanese adults were linearly related to increases in HDL particle numbers and decreases in low-density lipoprotein (LDL) particle numbers [27]. Still, others propose that the cardioprotective effects of alcohol may be related to the metabolite, acetate, and its interaction with the adipocyte free fatty acid receptor 2 to elicit an antilipolytic effect [28]. Changes in HDL cholesterol are markers of lower CHD risk but not a target of nonpharmacologic or pharmacologic therapy [26]. (See "Pathogenesis of type 2 diabetes mellitus".)

Antioxidant effects — Red wine and two of its antioxidants, but not other sources of alcohol, also prevent the activation of mononuclear cell nuclear factor kappa B, a redox-sensitive transcription factor that is involved in various processes that may contribute to atherosclerosis [29]. In another study, use of antioxidants N-acetylcysteine and resveratrol from wine inhibited macrophage reactive oxygen species production and facilitated cell migration through restoration of focal adhesion kinase activity [30].

Further study of the dynamic modeling of arterial lesions by dietary or other lifestyle behaviors is warranted. Endothelial progenitor cells are mobilized into circulation when vascular repair and neovascularization are needed. Red wine and a major constituent of red wine, resveratrol, slow endothelial progenitor cell senescence through a protein kinase B (Akt) dependent mechanism [31]. When 14 healthy volunteers consumed 250 mL of red wine for 21 consecutive days, apoptosis of endothelial progenitor cells was reduced and their migration and proliferation were significantly improved [29]. These findings may contribute to the mechanism of cardiovascular protection observed with regular, moderate consumption of red wine.

Enhanced insulin sensitivity — Consuming moderate amounts of alcohol has been shown to enhance insulin sensitivity and glucose utilization for the subsequent 12 to 24 hours [32]. Fasting and postprandial insulin concentrations are reduced with two drinks per day, and insulin sensitivity is also improved in randomized controlled trials [33]. The mechanism by which insulin sensitivity is enhanced by alcohol is not entirely known but may involve suppression of fatty acid release from adipose tissue and improved glucose metabolism [28,34]. A more detailed discussion of this subject is presented separately. (See "Overview of the risks and benefits of alcohol consumption", section on 'Diabetes mellitus'.)

Antithrombotic effects — Alcohol has antithrombotic activities that may contribute to the observed reduction in CHD. These include modification of platelet function and of other components of the clotting system and fibrinolysis [11,12].

Platelet aggregation is inhibited by the same quantities of alcohol that reduce CHD risk [35]; this effect may persist for six hours after a single alcohol drink, even when the blood alcohol level has returned to baseline [36].

Fibrinolysis also may be induced by moderate alcohol intake (three to seven drinks per week) and may contribute to the cardiovascular benefit. Reduced levels of plasminogen activator inhibitor (PAI) activity, fibrinogen, plasma viscosity, von Willebrand factor, factor VII, and increased concentrations of tissue-type plasminogen activator (tPA) have been described [37,38].

By contrast, a higher intake of alcohol (7 to 21 drinks per week) is associated with impaired fibrinolytic potential, manifested by higher levels of PAI antigen-1 and tPA antigen [37].

Antiinflammatory effects — There appears to be an inverse relationship between levels of inflammatory markers and mild to moderate alcohol intake.

Patients with moderate alcohol consumption have lower concentrations of C-reactive protein (CRP) than those who consume occasional or no alcohol [39]. In the PRINCE study, which correlated self-reported alcohol intake with CRP levels in 2833 subjects (41 percent with a history of cardiovascular disease [CVD]), there was a progressive decline in CRP levels with increasing alcohol intake, from 2.6 mg/L for less than one drink per month to 1.6 mg/L for five to seven drinks per week.

A study of alcohol intake and inflammatory markers in a biracial cohort of 2574 older people (aged 70 to 79 years) identified a J-shaped relationship between alcohol intake and both interleukin (IL) 6 and CRP levels [40]. Compared with people who drank one to seven drinks per week, people who never drank or who drank eight or more drinks per week were more likely to have high levels of IL-6 and CRP. However, in a subsequent study from the same population, the benefit of light to moderate alcohol intake on cardiac events and mortality persisted even after adjustment for levels of CRP and IL-6, leading to questions of the role of antiinflammatory properties as a mechanism of cardioprotection [41].

EFFECT OF ALCOHOL ON CARDIOVASCULAR RISK

Overview — No long-term randomized trials of alcohol consumption have been performed. The available evidence is from observational studies (including meta-analyses of numerous studies) that typically compare the characteristics of alcohol users with nonusers. As such, the apparent effect of alcohol is subject to confounding. As one example, moderate alcohol use is more common among those of higher socioeconomic status, thereby introducing the likelihood of confounding by factors associated with higher socioeconomic status [42,43].

Evidence from trend analyses by the National Health and Examination Survey (NHANES) over a 15-year period (1999 to 2014) linked to the United States mortality registry in 2015 suggest that alcohol use has increased and that use above the recommended limits by the Dietary Guidelines for Americans was associated with enhanced all-cause and cause-specific mortality risk, ranging from 39 to 126 percent [44].

Several prospective cohort studies suggest that light to moderate alcohol consumption decreases the risk of coronary heart disease (CHD) by 40 to 70 percent, compared with drinking no alcohol or with heavy alcohol intake [7].

A 2011 meta-analysis of 84 observational studies found that, relative to nondrinkers, alcohol drinkers had a relative risk (RR) of 0.75 (95% CI 0.70-0.80) for cardiovascular disease (CVD) mortality, 0.75 (95% CI 0.68-0.81) for CHD mortality, and 0.71 (95% CI 0.66-0.77) for incident CHD [45]. This protective effect has been found in multiple groups, including individuals without CHD at baseline [20], those with risk factors for CHD [22,46], and adults over age 65 [47].

In a pooled analysis of nearly 600,000 patients from three major cohorts in which the comparisons are made for current drinkers, the risk of myocardial infarction (MI) was lowest in the patients whose consumption was greater than 0 but less than 100 grams per week (figure 2) [20].

A population-based cohort study from the United Kingdom followed close to two million adults ≥30 years old who were free from CVD [48]. At a median follow-up of six years, 5.9 percent of these individuals had received a cardiovascular diagnosis. Non-drinking compared with moderate drinking was associated with an increased risk of multiple CVD outcomes, including unstable angina, MI, CHD death, heart failure (HF), ischemic stroke, and peripheral arterial disease, whereas heavy drinking was generally associated with worse cardiovascular outcomes.

However, in a cross-sectional study of over 2000 drinkers in Russia, levels of high-sensitivity cardiac troponin T, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity C-reactive protein (CRP) were greater among those receiving treatment for alcohol problems than in the general population, and greater alcohol intake was associated with higher NT-proBNP and CRP levels across all drinkers, without a protective effect among light to moderate drinkers [49].

Cardiovascular mortality — Many studies have found that moderate alcohol consumption is associated with a specific reduction in cardiovascular mortality [45,50,51]. However, other results show no benefit on all-cause mortality [2,20,52]. Additionally, heavy alcohol consumption (six or more drinks per day) or binge drinking increases the risk for many medical conditions, including sudden cardiac death [2,53]. (See "Overview of sudden cardiac arrest and sudden cardiac death".)

Patients without known CVD — Findings from representative studies of patients without known CVD include the following:

Data collected over nine iterations of the National Health Interview Study (NHIS), a representative United States sample, including 10,000 cardiovascular deaths, reveal an inverse association with cardiovascular mortality and light and moderate alcohol consumption [50]. Compared with lifetime abstainers, the RR of CVD was 0.69 and 0.62 for light and moderate drinkers, respectively. Similarly, after 13 waves of NHIS (including death index records in 2011), compared with lifetime abstainers, the RR of CVD was 0.74 (95% CI 0.69-0.80) and 0.71 (95% CI 0.64-0.78) for light and moderate drinkers, respectively (figure 2) [46].

In a combined analysis of three large-scale data sources (Emerging Risk Factor Collaboration, European Prospective Investigation into Cancer and Nutrition [EPIC] – Cardiovascular Disease, and United Kingdom Biobank) of 19 high-income countries and across 83 prospective studies, 599,912 current drinkers were followed for a minimum of one year and a median of 7.5 years [20]. The main analyses focused on current drinkers whose baseline alcohol intakes were defined in grams consumed per week. There was a J-shaped association for CVD outcomes. After adjustment for age, sex, smoking, and history of diabetes, the amount of alcohol consumed had positive associations with all disease subtypes except for MI, and associations were stronger for fatal versus nonfatal events. For CVD subtypes other than MI, there was no definitive threshold below which lower alcohol intakes ceased being associated with lower risk of disease. For MI, the association was inverse and stronger for non-fatal than fatal associations (figure 3).

What if middle-aged adults initiate moderate alcohol consumption in an attempt to lower CVD risk? Initiation of moderate drinking in adults aged 45 to 64 years was associated with a 40 percent decrease in risk of cardiovascular events (odds ratio [OR] 0.62, 95% CI 0.41-0.94) over four years in a cohort of prior nondrinkers participating in the Atherosclerosis Risk in Communities (ARIC) survey [54].

By contrast, the cardioprotection of light to moderate alcohol intake is not universally seen. In a meta-analysis using 694 data sources of individual and population-level alcohol consumption from 592 prospective and retrospective studies, which included 28 million individuals aged 15 to 49 years, 12.2 percent of male deaths and 3.8 percent of female deaths were attributed to alcohol use [2]. The protective effects of alcohol consumption on CVD were complex in populations aged 50 years and older; these associations were influenced by sex, age, and socio-demographic status. For men residing in countries with high or low socio-demographic index (SDI), light to moderate alcohol consumption had a protective effect on ischemic heart disease. For females in high SDI regions, there were protective effects of alcohol on diabetes beyond 60 years of age. In a sensitivity analysis that explored the weighted influence for various health outcomes, the only protective effect of alcohol was observed in populations where diabetes and ischemic heart disease comprised more than 60 percent of total deaths. In at least two other pooled analyses, the cardioprotective influence of light to moderate alcohol consumption was not observed [52,55].

Patients with known CVD — Moderate alcohol intake also appears to be beneficial in patients with known CVD. A 2010 meta-analysis of eight prospective studies, including 16,351 patients with a history of CVD, found a J-shaped curve between alcohol consumption and cardiovascular mortality, with a maximal protection (22 percent decreased risk) for consumption of 26 g per day of alcohol, equivalent to slightly less than two glasses of alcohol daily [56]. In a subsequent study of 1818 men from the Health Professionals Follow-up Study with prior MI, a U-shaped relationship between alcohol consumption and mortality (both all-cause and cardiovascular) was seen, with the greatest benefit for alcohol consumption between 10 and 30 grams per day, compared with abstinence (for all-cause mortality, hazard ratio [HR] 0.66, 95% CI 0.51-0.86; for cardiovascular mortality, HR 0.58, 95% CI 0.39-0.84). [57].

However, binge drinking in patients with a history of MI is associated with increased mortality [58].

Coronary heart disease — Similar to the benefit on total CVD mortality, moderate alcohol consumption is associated with a reduced risk of CHD in all adults [15,59-61].

Binge drinking, however, increases the risk for CHD [62,63]. As one example, in a pooled meta-analysis of case-control studies, the RR for fatal and nonfatal MI was 1.45 (95% CI 1.24-1.70) comparing those who reported irregular heavy drinking (≥5 drinks per occasion or intoxication at least monthly) with those who did not [62].

Hypertension — Multiple studies have shown an association between excess alcohol intake and the development of hypertension [64-66]. However, light to moderate alcohol consumption may be beneficial in reducing the risk of hypertension.

In a review of 32 trials of alcohol consumption in healthy persons, alcohol had a biphasic effect on blood pressure in the hours after consumption [67]. Although both medium- (14 to 28 grams) and high-dose alcohol (greater than 30 grams) decreased blood pressure within six hours of consumption, high-dose alcohol produced an increase in blood pressure after 12 hours.

In a meta-analysis of 36 trials, a decrease in alcohol intake reduced blood pressure in people who drank more than two drinks per day; however, a reduction was not seen in those consuming two or fewer drinks per day [68]. In patients who consumed six or more drinks per day, a 50 percent decrease in alcohol intake resulted in a 5.5 mmHg (95% CI 4.3-6.7) reduction in systolic blood pressure and a 4 mmHg (95% CI 3.2-4.7) reduction in diastolic blood pressure. (See "Definition, risk factors, and evaluation of resistant hypertension".)

On the other hand, moderate alcohol intake appears to have a cardioprotective effect, even in patients with preexisting hypertension [69,70]. A 2014 meta-analysis of nine cohort studies including over 390,000 patients with hypertension found that, compared with abstainers or occasional drinkers, those who consumed 8 to 10 grams of alcohol per day had a decreased risk for all-cause mortality (RR 0.82, 95% CI 0.76-0.88) [70].

Heart failure — Chronic consumption of large amounts of alcohol may lead to alcohol-induced cardiomyopathy. This condition is discussed separately. (See "Alcohol-induced cardiomyopathy".)

By comparison, light to moderate alcohol intake may protect against the development of HF [71,72]. Among 7686 subjects initially free of HF or coronary disease prospectively followed in the Framingham Heart Study, the risk of HF in men was significantly lower at all levels of alcohol consumption, whereas among females, the consumption of one to seven drinks per week was also associated with a lower risk of HF [73].

A related issue is the effect of light to moderate alcohol intake in patients with left ventricular (LV) dysfunction. The SOLVD study evaluated this issue in an analysis of 6797 patients with an ejection fraction of 35 percent or less [74]. When compared with nondrinkers, light to moderate drinkers (1 to 14 drinks per week) with ischemic LV dysfunction had a lower all-cause mortality (7.2 versus 9.4 deaths/100 person-years), particularly death from MI. Alcohol had no significant effect on mortality in patients with a nonischemic cardiomyopathy.

In patients with diabetes mellitus — Light to moderate alcohol consumption appears to protect against development of CHD and the risk of coronary death in adults with diabetes [75-77].

In the Health Professionals Follow-up Study of 2419 men with type 2 diabetes over the age of 30, moderate alcohol intake was associated with a lower risk for CHD [77]. Alcohol also protects against the risk of CHD death in patients with diabetes. Among 2790 men with diabetes in the Physicians' Health Study who were free of MI, cancer, or liver disease at baseline, those men with diabetes who consumed alcohol on a weekly or daily basis had a significantly lower risk of death from CHD compared with those who rarely or never consumed alcohol (adjusted RR 0.67 and 0.42) [75].

Among 5103 females in the Nurses' Health Study with a diagnosis of diabetes at ≥30 years of age who were free of CHD, stroke, or cancer at baseline, the adjusted RR for nonfatal or fatal CHD for diabetic females reporting a daily intake of 0.1 to 4.9 grams of alcohol (<0.5 drinks) or ≥5.0 grams (≥0.5 drinks) was 0.72 and 0.45, respectively, compared with abstainers [76]. (See "Prevalence of and risk factors for coronary heart disease in patients with diabetes mellitus".)

In addition, moderate alcohol consumption may lower the risk of developing type 2 diabetes, as reported in a meta-analyses of 15 prospective cohort studies [78]. (See "Overview of the risks and benefits of alcohol consumption", section on 'Diabetes mellitus'.)

Stroke risk — Different studies have reported disparate outcomes regarding the impact of light to moderate alcohol intake on stroke risk.

Moderate alcohol intake (up to two glasses per day) has been associated with a decreased risk of ischemic stroke in most studies [45,79-82].

In a combined analysis of three large-scale data sources (Emerging Risk Factor Collaboration, European Prospective Investigation into Cancer and Nutrition [EPIC] – Cardiovascular Disease, and United Kingdom Biobank) of 19 high-income countries and across 83 prospective studies, 599,912 current drinkers were followed for a minimum of one year and a median of 7.5 years (figure 4) [20]. The amount of alcohol had a positive, nearly linear relationship with stroke (HR 1.14, 95% CI 1.10-1.17), both ischemic and hemorrhagic.

In a cohort study of 38,156 male health professionals published subsequent to this meta-analysis, light alcohol consumption (<10 g/day) had no effect on the risk of ischemic stroke (RR 0.99, 95% CI 0.72-1.37) [80]. Consumption of more than two drinks daily (>29.9 g per day) appeared to be associated with an increased risk of ischemic stroke (RR 1.42, 95% CI 0.97-2.09). Data collected over 26 years (>1,695,000 person-years) from the Nurses' Health Study found that, compared with abstainers, the risk of stroke was decreased in females who drank less than 15 g/day of alcohol (RR 0.83, 95% CI 0.75-0.92 for <5 g per day and RR 0.79, 95% CI 0.70-0.90 for 5.0 to 14.9 g per day) [82]. There was no difference between the incidence of ischemic or hemorrhagic stroke.

Binge drinking (≥6 drinks in one session for males, or ≥4 drinks for females) was associated with increased risk for all strokes (HR 1.85) and for ischemic strokes (HR 1.99) [83].

Peripheral artery disease — Alcohol appears to reduce the risk of peripheral artery disease (PAD) among apparently healthy people. Moderate alcohol intake (one to two drinks per day in males and 0.5 to 1.0 drinks per day in females) also reduces the risk of intermittent claudication [84]. It is difficult to account for the influences of dietary pattern and alcohol consumption on disease outcomes, although the PREDMED study examined the risk of developing PAD in their trial participants; nearly 50 percent had type 2 diabetes. Moderate alcohol consumption, non-smoking, physical activity, and following a Mediterranean diet pattern were inversely associated with incident PAD [85].

The effects of alcohol on risk for abdominal aortic aneurysm are discussed in detail elsewhere. (See "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm", section on 'Food and alcohol consumption'.)

Atrial fibrillation — Both heavy binge drinking and heavy chronic alcohol use have been reported to increase the incidence of atrial fibrillation (AF), while chronic moderate alcohol use does not appear to increase the incidence of AF. Evidence suggests there is no benefit from light to moderate alcohol intakes with respect to incident AF [86]. Even ablation treatment for AF is less successful amongst moderate and heavy drinkers [87]. (See "Epidemiology, risk factors, and prevention of atrial fibrillation", section on 'Alcohol'.)

Advice from professional societies — There is uncertainty as to whether the available data support encouraging middle-aged adults, with or without CHD, who do not drink or who drink only occasionally to take up regular drinking [3,7,88-91].

In 2001, an American Heart Association (AHA) Science Advisory reached the following conclusion [92]: "Moderate intake of alcoholic beverages (one to two drinks per day) is associated with a reduced risk of CHD in populations… Despite the biologic plausibility and observational data in this regard, it should be kept in mind that these are insufficient to prove causality… Without a large-scale, randomized, clinical end point trial of wine intake, there is little current justification to recommend alcohol (or wine specifically) as a cardioprotective strategy."

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) indicates that "individuals who are not currently drinking should not be encouraged to drink solely for health reasons, because the basis for health improvements has not yet been established as deriving from alcohol itself" [93].

A 2016 report from the Department of Health in the United Kingdom states that "people who do not drink any alcohol at all should not be recommended to start drinking in the interests of their health" [94].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alcohol consumption".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Beyond the Basics topics (see "Patient education: Risks and benefits of alcohol (Beyond the Basics)")

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), under the National Institutes of Health (NIH) maintains an active website for the general public (www.niaaa.nih.gov/alcohol-health). Patient information specific to the interaction of alcohol intake and the effect on the body is available within this site (www.niaaa.nih.gov/alcohol-health/alcohols-effects-body).

SUMMARY AND RECOMMENDATIONS

The 2020 to 2025 Dietary Guidelines for Americans define moderate drinking as having up to one drink per day for females and up to two drinks per day for males. Definitions of a "standard drink" differ, both within and between countries, with a standard drink containing from as few as 8 grams of alcohol to as many as 20 grams of alcohol. (See 'Definitions' above.)

Moderate alcohol consumption most likely reduces the risk of myocardial infarction (MI) through its effects on insulin sensitivity, thrombotic activity, and inflammation. (See 'Proposed mechanisms of benefit' above.)

It is uncertain whether wine is more cardioprotective than other types of alcohol; however, it is likely that the type of alcohol is not as important as the amount of alcohol consumed and the pattern of intake. (See 'Beverage type' above.)

No long-term randomized trials of alcohol consumption have been performed. Most studies have found that light to moderate alcohol consumption is associated with a specific reduction in cardiovascular mortality, with several prospective cohort studies suggesting that light to moderate alcohol consumption decreases the risk of coronary heart disease (CHD) compared with drinking no alcohol or with heavy alcohol intake. However, other data have challenged this potential benefit on CHD risk and CHD mortality, and no level of drinking has shown to be beneficial for other cardiovascular disease (CVD) risks (eg, stroke, hypertension, heart failure [HF], etc). (See 'Effect of alcohol on cardiovascular risk' above.)

Our approach to advising patients about the benefits of alcohol as part of a strategy to reduce CVD risk is as follows (see 'Advice to patients regarding alcohol use' above):

Individuals who are not currently drinking, or those who have a personal preference to avoid alcohol, should not be advised to consume alcohol solely for the purpose of CVD risk reduction.

Patients who have an underlying medical condition that precludes alcohol use (eg, alcohol use disorder, liver disease, etc) should not be advised to consume alcohol and seek counseling, if needed, to abstain from alcohol.

Patients who choose to drink moderate amounts of alcohol, such as those who drink alcohol less than one unit per day (or less than 15 g per day) or less than 100 g per week, may experience benefits for their health.

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Topic 2784 Version 53.0

References

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