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. Author manuscript; available in PMC: 2023 Oct 1.
Published in final edited form as: Am J Med. 2022 May 14;135(10):1213–1230.e3. doi: 10.1016/j.amjmed.2022.04.021

Alcohol Consumption and Cardiovascular Health

Chayakrit Krittanawong a,b, Ameesh Isath c, Robert S Rosenson d,e, Muzamil Khawaja b, Zhen Wang d,e,f,g, Sonya E Fogg h, Salim S Virani a,b, Lu Qi i, Yin Cao j, Michelle T Long k, Christy C Tangney l, Carl J Lavie m
PMCID: PMC9529807  NIHMSID: NIHMS1819660  PMID: 35580715

Abstract

BACKGROUND:

Studies evaluating alcohol consumption and cardiovascular diseases have shown inconsistent results.

METHODS:

We performed a systematic review of peer-reviewed publications from an extensive query of Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from database inception to March 2022 for all studies that reported the association between alcohol consumption in terms of quantity (daily or weekly amounts) and type of beverage (wine, beer or spirit) and cardiovascular disease events.

RESULTS:

The study population included a total of 1,579,435 individuals based on 56 cohorts from several countries. We found that moderate wine consumption defined as 1–4 drinks per week was associated with a reduction in risk for cardiovascular mortality when compared with beer or spirits. However, higher risk for cardiovascular disease mortality was typically seen with heavier daily or weekly alcohol consumption across all types of beverages.

CONCLUSIONS:

It is possible that the observational studies may overestimate the benefits of alcohol for cardiovascular disease outcomes. Although moderate wine consumption is probably associated with low cardiovascular disease events, there are many confounding factors, in particular, lifestyle, genetic, and socioeconomic associations with wine drinking, which likely explain much of the association with wine and reduced cardiovascular disease events. Further prospective study of alcohol and all-cause mortality, including cancer, is needed.

Keywords: Alcohol consumption, Beer consumption, Cardiovascular disease, Liquor consumption, Wine consumption

INTRODUCTION

The US Department of Agriculture 2015 to 2025 Dietary Guidelines for Americans1 define moderate drinking as having up to 1 drink per day for women and up to 2 drinks per day for men. Alcohol consumption above the recommended limits was associated with higher all-cause and cause-specific mortality risk (39%–126%).2 Alcohol may contain polyphenols, amino acids, and minerals,3 although the content varies considerably among types of alcohol (beer vs red wine vs white wine vs spirit). A complete understanding of these complex mechanisms in human health is limited. Several studies have shown that alcohol consumption has a J-shaped or biphasic relationship with cardiovascular disease.4,5 In a recent report, analyses suggest that any quantity of alcohol has a deleterious effect on cancer risk.4 Our study is unique in that it relies on data culled from more than 1 million individuals. We include both alcoholic beverage quantity (daily or weekly amounts) and type of beverage (wine, beer, or spirits) in relation to cardiovascular disease events. Additionally, very few meta-analyses have included spirits when the association of alcohol is examined in relation to these cardiovascular disease outcomes.

METHODS

We performed a systematic review of peer-reviewed publications from an extensive query of Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from database inception to March 2022. Search strategy included MESH headings and keywords related to alcohol and cardiovascular disease (Supplementary Material, available online). We identified studies based on appropriate types of study (observational study, prospective cohort study, randomized controlled trial, or case control design) and the exposure (alcohol consumption). We were unable to perform meta-analysis of the results due to tremendous heterogeneity among the included studies related to intervention, comparison, outcomes, and timing. Instead, we qualitatively synthesized the results and summarized key features and characteristics (eg, study populations, design, interventions, outcomes, and conclusions) of the included studies.

RESULTS

After exclusions in our initial electronic search, we identified and reviewed a total of 56 studies related to alcohol consumption and cardiovascular outcomes. Most common adjustments were age, body mass index, hypertension, and diabetes. As for alcoholic beverages and the relationship with developing coronary artery disease, 19 total studies were included for a total of 1,009,067 individuals; 51.1% were men (Table 1). Studies were published since 1986 and included a diverse group of participants from countries all over the world. Most of the studies were prospective, but several were case-control studies or cross-sectional. Results were variable across these cohorts, but there was a notable pattern of significantly lower hazard ratios (HRs) for coronary artery disease in low to moderate alcohol consumers (defined by weekly and daily consumption thresholds) across all categories of alcoholic beverages.

Table 1.

Included Studies for Alcohol Consumption and CAD

First Author Year Country Number of Participants Men Type of Study Age, Years Follow-Up Type of Drink Comparison OutcomeHR (95% CI)
Bos68 2010 Netherlands 10,530 0 Prospective – 9.4 y White wine 5–29.9 vs 0–4.9 g/wk 0.96 (0.76–1.21)
White wine 30–69.9 vs 0–4.9 g/wk 1.1 (0.74–1.66)
White wine >70 vs 0–4.9 g/wk 0.96 (0.59–1.57)
Red wine 5–29.9 vs 0–4.9 g/wk 0.74 (0.56–0.97)
Red wine 30–69.9 vs 0–4.9 g/wk 0.77 (0.52–1.14)
Red wine >70 vs 0–4.9 g/wk 0.71 (0.43–1.16)
Beer 5–29.9 vs 0–4.9 g/wk 1 (0.68–1.49)
Beer 30–69.9 vs 0–4.9 g/wk 0.84 (0.49–1.43)
Liquor 5–29.9 vs 0–4.9 g/wk 1.04 (0.76–1.41)
Liquor 30–69.9 vs 0–4.9 g/wk 0.93 (0.61–1.41)
Liquor >70 vs 0–4.9 g/wk 1.17 (0.82–1.69)
Fortified wine 5–29.9 vs 0–4.9 g/wk 1.03 (0.8–1.33)
Fortified wine 30–69.9 vs 0–4.9 g/wk 1.01 (0.67–1.52)
Fortified wine >70 vs 0–4.9 g/wk 0.85 (0.6–1.19)
White wine, red wine, beer, liquor, fortified wine 0–4.9 g/wk vs lifetime abstainer 0.98 (0.76–1.27)
White wine, red wine, beer, liquor, fortified wine 5–29.9 g/wk vs lifetime abstainer 0.75 (0.57–0.98)
White wine, red wine, beer, liquor, fortified wine 30–69.9 g/wk vs lifetime abstainer 0.92 (0.68–1.24)
White wine, red wine, beer, liquor, fortified wine 70–139.9 g/wk vs lifetime abstainer 0.72 (0.52–1.01)
White wine, red wine, beer, liquor, fortified wine ≥ 140 g/wk vs lifetime abstainer 0.65 (0.46–0.9)
Brenner69 2001 Germany 791 267 cases Case control 57.7 cases
 55.8 control		 Wine, beer, mixed Drinkers vs nondrinkers 0.55 (0.37–0.83)
Beer only Beer only vs nondrinkers 0.5 (0.3–0.84)
Wine only Wine only vs nondrinkers 0.95 (0.57–1.59)
Mixed Mixed vs nondrinkers 0.42 (0.27–0.66)
Wine, beer, mixed ≤ 125 g/wk vs nondrinkers 0.56 (0.36–0.86)
Wine, beer, mixed > 125 g/wk vs nondrinkers 0.55 (0.35–0.86)
Foerster70 2009 Switzerland 5769 2574 Cross-sectional
 I would delete		 52.5 ± 10.6 – Wine, beer, spirits Did not include as mean ± SE ()
Gigleux71 2006 Canada 1966 1966 Prospective IHD-free men - 56 ± 7
 IHD cases - 59 ± 7		 13 y Wine, beer, spirits ≥15.2 vs <1.3 g/d 0.51 (0.33–0.8)
Wine, beer, spirits 5.5–15.1 vs <1.3 g/d 0.81 (0.55–1.21)
Wine, beer, spirits 1.3–5.4 vs <1.3 g/d 0.87 (0.6–1.27)
Klatsky72 1986 US 85,001 37,605 Prospective cohort – 5y Wine, beer, liquor Ex-drinkers vs abstainers 0.99 (0.72–1.36)
Wine, beer, liquor <1 drink/mo vs abstainers 0.93 (0.74–1.18)
Wine, beer, liquor <1 drink/d, >l drink/mo vs abstainers 0.65 (0.51–0.82)
Wine, beer, liquor 1–2 drinks/d vs abstainers 0.55 (0.42–0.72)
Wine, beer, liquor 3–5 drinks/d vs abstainers 0.54 (0.38–0.76)
Wine, beer, liquor 6–8 drinks/d vs abstainers 0.52 (0.26–1.05)
Wine, beer, liquor >9 drinks/d vs abstainers 0.47 (0.15–1.49)
Beer Beer vs liquor 1.01 (0.69–1.46)
Wine Wine vs liquor 0.89 (0.64–1.24)
Klatsky73 1997 US 128,934 56,730 Prospective cohort 40.6 6 y Red wine, beer, Liquor, white wine ALL drinkers (>1 drink/mo vs abstainers) 0.79 (0.71–0.88)
<1 drink/d vs abstainers 0.93 (0.8–1.09)
1–2 drinks/d vs abstainers 0.77 (0.65–0.91)
≥3 drinks/d vs abstainers 0.71 (0.59–0.86)
ALL drinkers (>1 drink/mo vs abstainers) 0.76 (0.65–0.89)
<1 drink/d vs abstainers 0.83 (0.7–0.98)
1–2 drinks/d vs abstainers 0.64 (0.52–0.79)
≥3 drinks/d vs abstainers 0.6 (0.42–0.85)
Marques-Vidai74 2004 France, Northern Ireland 9750 9750 Prospective cohort Divided by alcohol and country 5 y Wine, beer, spirits, cider 0–128 mL pure ethanoL/wk vs none 0.74 (0.45–1.21)
Wine, beer, spirits, cider 128–265 mL pure ethanoL/wk vs none 0.65 (0.39,1.08)
Wine, beer, spirits, cider 265–441 mL pure ethanoL/wk vs none 0.48 (0.28–0.81)
Wine, beer, spirits, cider ≥441 mL pure ethanoL/wk vs none 0.37 (0.22–0.64)
Wine, beer, spirits, cider 0–128 mL pure ethanoL/wk vs none 0.67 (0.36–1.27)
Wine, beer, spirits, cider 128–265 mL pure ethanoL/wk vs none 0.81 (0.46–1.46)
Wine, beer, spirits, cider 265–441 mL pure ethanoL/wk vs none 0.88 (0.5–1.54)
Wine, beer, spirits, cider ≥441 mL pure ethanoL/wk vs none 0.7 (0.38–1.29)
Wine Wine vs none 0.89 (0.82–0.98)
Beer Beer vs none 0.94 (0.74–1.01)
Spirits Spirits vs none 1.04 (0.83–1.43)
Wine, beer, spirits, cider TotaL alcohol vs none 0.96 (0.84–0.97)
Wine Wine vs none 0.33 (0.11–0.96)
Beer Beer vs none 0.99 (0.89–1.07)
Spirits Spirits vs none 1.03 (0.93–1.22)
Wine, beer, spirits, cider TotaL alcohol vs none 0.99 (0.92–1.06)
Wine, beer, spirits Alcohol vs no alcohol 1.001 (1–1.003)
Wine, beer, spirits Drinker group 1 (<15 g/d) vs nondrinkers 0.61 (0.4–0.94)
Wine, beer, spirits Drinker group 2 (≥15 g/d) vs nondrinkers 0.68 (0.41–1.12)
Wine, beer, spirits Drinker group 1 (<15 g/d) vs Lifetime abstainer 0.61 (0.39–0.95)
Wine, beer, spirits Drinker group 2 (≥15 g/d) vs Lifetime abstainer 0.67 (0.39–1.14)
Wine, beer, spirits Drinker group 1 (<15 g/d) vs occasionaL drinker 0.71 (0.42–1.19)
Wine, beer, spirits Drinker group 2 (≥15 g/d) vs occasionaL drinker 0.75 (0.46–1.23)
Wine, beer, spirits Former drinker vs Lifetime abstainer 0.97 (0.56–1.71)
Rimm76 1991 US 44,059 44,059 Prospective cohort 0 g/d
 0.1–5 g/d
 5.1–30 g/d
 >30 g/d		 72,290 person-years Wine, beer, spirits 0.1–5 g/d vs 0 g/d 0.99 (74–1.33)
5.1–30 g/d vs 0 g/d 0.74 (0.56–0.97)
>30 g/d vs 0 g/d 0.53 (0.35–0.79)
Roy99 2010 India 8930 8930 Cross-sectional
 I would delete		 Alcohol users - 42.8 ± 11.0
 Nonusers- 42.8 ± 11.1		 – Wine, beer, spirits Alcohol users vs nonusers 1.4 (1–1.9)
Wine, beer, spirits Occasional users (less than once a week) vs nonusers 1.2 (0.8–1.6)
Wine, beer, spirits Regular users (once or more in a week) vs nonusers 1.6 (1–2.2)
Wine, beer, spirits Past users (quit at least 6 months ago) vs nonusers 2.1 (1.1–3)
Local spirits Local spirits vs none 1.8 (1–2.6)
Branded spirits Branded spirits vs none 1.5 (0.9–2.2)
Wine, beer, spirits <14 g/d vs no alcohol 1.3 (1.2–1.5)
Wine, beer, spirits 14–28 g/d vs no alcohol 1.6 (1–2.3)
Wine, beer, spirits >28 g/d vs no alcohol 2 (1.2–2.6)
Schutte111 2020 UK 446,439 206,088 Prospective cohort 56.4 ± 8.1 7.05 y Beer/cider Beer/cider vs other alcohol drinkers 1.12 (0.99–1.26)
Champagne/white wine Champagne/white wine vs other alcohol drinkers 0.84 (0.72–0.98)
Red wine Red wine vs other alcohol drinkers 0.88 (0.77–0.99)
Spirits Spirits vs other alcohol drinkers 1.17 (1.02–1.35)
Snow100 2009 Canada 1154 580 Prospective cohort – 10 y Wine, beer, spirits 0.65–5.77 g vs <0.65 g/d 1.66 (0.2–13.92)
5.78–18.1 g vs <0.65 g/d
>18.1 g vs <0.65 g/d 0.44 (0.04–4.59)
>18.1 (heavy) episodic vs <0.65 g/d 4.13 (1.46–11.62)
0.65–5.77 g vs <0.65 g/d 0.98 (0.4–2.37)
5.78–18.1 g vs <0.65 g/d 0.75 (0.29–1.95)
>18.1 g vs <0.65 g/d 0.28 (0.08–0.93)
>18.1 (heavy) episodic vs <0.65 g/d 1.76 (0.81–3.82)
0.65–2.92 g vs <0.65 g/d 1.13 (0.07–18.39)
2.93–9.15 g vs <0.65 g/d 2.95 (0.29–29.69)
>9.15 g vs <0.65 g/d 1.96 (0.17–22.19)
>9.15 g (heavy) episodic vs <0.65 g/d 1.09 (0.99–1.19)
0.65–2.92 g vs <0.65 g/d 1.35 (0.51–3.57)
2.93–9.15 g vs <0.65 g/d 2.12 (0.82–5.48)
>9.15 g vs <0.65 g/d 0.44 (0.09–2.02)
>9.15 g (heavy) episodic vs <0.65 g/d 0 (0–∞)
Song101 2018 US 156,728 142,622 Prospective cohort 65.3 ± 12.1 2.9 y Wine, beer, spirits Former drinkers vs never drinkers 1.02 (0.92–1.13)
≤6 g/d vs never drinkers 0.83 (0.74–0.93)
>6–12g/d vs never drinkers 0.77 (0.67–0.87)
>12–24g/d vs never drinkers 0.71 (0.62–0.81)
 >24–36g/d vs never drinkers 0.62 (0.51–0.76)
>36–48 g/d vs never drinkers 0.58 (0.46–0.74)
AUD/heavy drinkers (>48 g/d) vs never drinkers 0.95 (0.85–1.06)
Stampfer77 1988 US 87,526 0 Prospective cohort 34–59 334,382 person-years Wine, beer, spirits <1.5 g/d vs 0 g/d 0.7 (0.5–1.1)
1.5–4.9 g/d vs 0 g/d 0.5 (0.4–0.8)
5–14.9 g/d vs 0 g/d 0.5 (0.4–0.8)
15–24.9 g/d vs 0 g/d 0.6 (0.3–1.1)
>25 g/d vs 0 g/d 0.6 (0.3–1)
Wannamethee78 1999 UK 7272 7272 Prospective cohort 40–59 16.8 y Wine, beer, spirits None vs occasional (<1 unit per week) 1.03 (0.78–1.37)
Wine, beer, spirits Light (1–15 units per week) vs occasional 0.76 (0.64–0.91)
Wine, beer, spirits Moderate (16–42 units per week), vs occasional 0.78 (0.65–0.94)
Wine, beer, spirits Heavy (more than 6 units per day) vs occasional 0.75 (0.59–0.95)
Beer Regular drinker vs occasional drinker 0.78 (0.63–0.97)
Spirits Regular drinker vs occasional drinker 0.57 (0.39–0.85)
Beer and spirits Regular drinker vs occasional drinker 0.75 (0.5–1.1)
Wine Regular drinker vs occasional drinker 0.92 (0.51–1.67)
Wine/sherry, beer, spirits Regular drinker vs occasional drinker 1.23 (0.54–2.79)
Spirits, beer Spirits vs beer in occasional and regular drinkers 1.07 (0.9–1.26)
Wine, beer Wine vs beer in occasional and regular drinkers 0.82 (0.64–1.04)
Wellmann79 2004 Germany 2710 1345 Prospective cohort 35–64 10 y in men
 10.1 in women		 Wine, beer, spirits 0.1–19.9 g/d vs 0 g/d 0.34 (0.17–0.69)
20.0–39.9 g/d vs 0 g/d 0.43 (0.22–0.81)
40.0–79.9 g/d vs 0 g/d 0.7 (0.4–1.22)
>80.0 g/d vs 0 g/d 0.33 (0.12–0.89)
Quitter vs nondrinker 0.78 (0.32–1.87)
Starter vs nondrinker 0.32 (0.09–1.18)
Constant drinker 0.1–19.9 g/d vs nondrinker 0.29 (0.12–0.7)
Constant drinker 20.0–39.9 g/d vs nondrinker 0.39 (0.17–0.87)
Constant drinker 40.0–79.9 g/d vs nondrinker 0.6 (0.29–1.24)
Constant drinker >80.0g/d vs nondrinker 0.29 (0.1–0.86)
Woodward80 1995 Scotland Cross-sectional 40–59 – Wine, beer, spirits 1–7 Units/wk vs 0 0.99 (0.7–1.41)
8–15 Units/wk vs 0 0.99 (0.69–1.42)
16–29 Units/wk vs 0 0.97 (0.66–1.43)
>30 Units/wk vs 0 1.04 (0.67–1.61)
1–2 Units/wk vs 0 0.57 (0.36–0.91)
3–5 Units/wk vs 0 0.62 (0.41–0.96)
6–9 Units/wk vs 0 0.74 (0.47–1.15)
>10 Units/wk vs 0 0.61 (0.37–1.01)
Keil81 1997 Germany 2087 1074 Prospective cohort 45–64 7.9 y Beer Drinkers vs nondrinkers 0.55 (0.29–1.02)
0.1–19.9 g/d vs nondrinkers 0.54 (0.24–1.2)
20–39.9 g/d vs nondrinkers 0.48 (0.21–1.09)
40–79.9 g/d vs nondrinkers 0.63 (0.3–1.29)
>80 g/d vs nondrinkers 0.48 (0.18–1.28)
Biddinger82 202 UK 371,463 172,400 Cohort 57.0 ± 7.9 ∼ 6 y Wine, beer, spirits Light drinkers vs none 1.7 (1.2– 2.3)
Moderate drinkers vs none 1.7 (1.1–2.7)
Heavy drinkers vs none 2.1 (1.1– 3.9)
Abuse drinkers vs none 5.7 (2.4–13.5)
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AUD = alcohol use disorder; CAD = coronary artery disease; IHD = ischemic heart disease; CI - Confidence interval.

Table 2 summarizes alcohol consumption and the association with myocardial infarction (238,273 individuals). Most of these studies demonstrated a significantly lower HR for myocardial infarction in individuals with moderate to higher levels of alcohol consumption for all 3 types of beverages.

Table 2.

Included Studies for Alcohol Consumption and Myocardial Infarction

First Author Year Country Number of Participants Men Type of Study Age, Years Follow-Up Type of Drink Comparison OutcomesHR (95% CI)
Gigleux71 2006 Canada 1966 1966 Prospective – 13 y Wine, beer, spirits ≥15.2 vs <1.3 g/d 0.51 (0.33–0.8)
5.5–15.1 vs <1.3 g/d 0.81 (0.55–1.21)
1.3–5.4 vs <1.3 g/d 0.87 (0.6–1.27)
Klatsky72 1986 US 85,001 37,605 Prospective cohort – 5 y Wine, beer, spirits Ex-drinkers vs abstainers 1.19 (NR-NR)
<1 drink/mo vs abstainers 0.97 (NR-NR)
< 1 drink/d, > l drink/mo vs abstainers 0.72 (NR-NR)
1–2 drinks/d vs abstainers 0.54 (NR-NR)
3–5 drinks/d vs abstainers 0.38 (NR-NR)
6–8 drinks/d vs abstainers 0.7 (NR-NR)
>9 drinks/d vs abstainers 0.31 (NR-NR)
Marques-Vidal74 2004 France, Northern Ireland 9750 9750 Prospective cohort – 5y Wine, beer, spirits, cider 0–128 mL pure ethanol/wk vs none 0.54 (0.29–1.02)
128–265 mL pure ethanol/wk vs none 0.45 (0.23–0.87)
265–441 mL pure ethanol/wk vs none 0.37 (0.19–0.73)
≥ 441 mL pure ethanol/wk vs none 0.26 (0.13–0.54)
0–128 mL pure ethanol/wk vs none 0.62 (0.27–1.45)
128–265 mL pure ethanol/wk vs none 0.69 (0.31–1.52)
265–441 mL pure ethanol/wk vs none 0.56 (0.25–1.28)
≥441 mL pure ethanol/wk vs none 0.43 (0.17–1.09)
Wine Wine vs none 0.88 (0.78–1)
Beer Beer vs none 0.89 (0.58–0.99)
Spirits Spirits vs none 1.09 (0.95–1.58)
Wine, beer, spirits, cider Total alcohol vs none 0.95 (0.8–0.98)
Wine Wine vs none 0.18 (0.03–1.29)
Beer Beer vs none 0.97 (0.81–1.08)
Spirits Spirits vs none 1.01 (0.84–1.26)
Wine, beer, spirits, cider Total alcohol vs none 0.98 (0.85–1.06)
Park75 2017 Korea 8330 3936 Prospective cohort 40–49 y, n = 3876 (46.5%)
 50–59 y, n = 2220 (26.7%)
 60–69 y, n = 2234 (26.8%)		 10 y Wine, beer, spirits Drinker group 1 (<15 g/d) vs nondrinkers 0.44 (0.21–0.92)
Drinker group 2 (≥15 g/d) vs nondrinkers 0.42 (0.19–0.93)
Drinker group 1 (<15 g/d) vs lifetime abstainer 0.41 (0.19–0.9)
Drinker group 2 (≥15 g/d) vs lifetime abstainer 0.39 (0.16–0.91)
Drinker group 1 (<15 g/d) vs occasional drinker 0.65 (0.29–1.45)
Drinker group 2 (≥15 g/d) vs occasional drinker 0.51 (0.23–1.12)
Former drinker vs lifetime abstainer 0.84 (0.35–1.98)
Rimm57 1991 US 44,059 44,059 Prospective cohort 0 g/d
 0.1–5 g/d
 5.1–30 g/d
 >30 g/d		 72,290 person-years Wine, beer, spirits 0.1–5 g/d vs 0 g/d 0.99 (0.65–1.51)
5.1–30 g/d vs 0 g/d 0.71 (0.47–1.06)
>30 g/d vs 0 g/d 0.65 (0.37–1.31)
Stampfer77 1988 US 87,526 0 Prospective cohort 34–59 334,382 person-years Wine, beer, spirits <1.5 g/d vs 0 g/d 0.7 (0.5–1.1)
1.5–4.9 g/d vs 0 g/d 0.5 (0.4–0.8)
5–14.9 g/d vs 0 g/d 0.5 (0.4–0.8)
15–24.9 g/d vs 0 g/d 0.6 (0.3–1.1)
>25 g/d vs 0 g/d 0.6 (0.3–1)
Kauhanen93 1997 Finland 1641 1641 Prospective cohort 6 or more 50.4 (6.0)
 3–5 51.2 (5.6)
 <3 52.4 (5.0)		 7.7 y Beer 6 or more vs <3 bottles 0.96 (0.39–2.35)
Beer 3–5 bottles vs <3 bottles 1.28 (0.85–1.93)
Biddinger62 2022 UK 371,463 172,400 Cohort 57.0 ± 7.9 ∼ 6 y Wine, beer, spirits Light drinkers vs none 1.3 (0.89– 2.11)
Moderate drinkers vs none 2.6 (1.39– 4.94)
Heavy drinkers vs none 1.8 (0.78– 4.30)
Abuse drinkers vs none 7.3 (2.28–23.84)
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Table 3 summarizes the association between alcohol consumption and cardiovascular disease mortality (570,368 individuals with mean follow-up 11.7 years). For studies that evaluated low-moderate amounts of weekly or daily alcohol (wine, beer, or spirits) consumption, there were significantly lower risk ratios/HRs for cardiovascular disease mortality. Regardless of the specific alcoholic beverage included in the studies, the risk for cardiovascular disease mortality remained lower. Only a handful of studies noted a significantly higher risk for mortality that was associated with either heavier weekly alcohol consumption (either wine, beer, or spirits) or a history of alcohol consumption in the past. Direct comparisons of alcoholic beverages and the effects on cardiovascular disease mortality within the same cohort showed that moderate wine consumption has a 25% reduction in risk for cardiovascular mortality when compared with beer or spirits (HR 0.75; 95% confidence interval, 0.59–0.96) (Table 3). Higher risk for cardiovascular disease mortality was typically seen with heavier daily or weekly alcohol consumption, across all types of beverages.

Table 3.

Included Studies for Alcohol Consumption and Cardiovascular Mortality

First Author Year Country Number of Participants Men Type of Study Age, Years Follow-Up Type of Drink Comparison Outcome HR (95% CI)
Behrens83 2011 Sweden 49,259 0 Prospective – 713,295 person-years Wine, beer, spirits 0.1–1.4 g/d vs 0 g/d 0.76 (0.48–1.2)
1.5–4.9 g/d vs 0 g/d 0.57 (0.36–0.91)
5.0–9.9 g/d vs 0 g/d 0.85 (0.52–1.38)
10.0+ g/d vs 0 g/d 0.55 (0.27–1.12)
0.1–19.9g/d vs 0 g/d 0.69 (0.46–1.01)
Berberian84 1994 Netherlands 1620 760 Prospective survey based – 10 y Wine, beer, spirits Occasional (<1 time a week) vs no drinks and ex-drinkers 0.23 (0.07–0.73)
Frequent (one time a week or more) vs no drinks and ex-drinkers 0.61 (0.26–1.38)
Daily alcohol vs no drinks and ex-drinkers 0.37 (0.13–1)
Bertoia85 2012 US 93,676 0 Prospective – 3 y Wine, beer, spirits Never drinker vs 0.1–5 g 1.85 (0.86–3.98)
Former drinker vs 0.1–5 g 0.92 (0.47–1.81)
5.1–10 g vs 0.1–5 g 0.64 (0.38–1.1)
10.1–30 g vs 0.1–5 g 0.86 (0.55–1.32)
>30 g vs 0.1–5 g 0.83 (0.42–1.64)
Dai86 2015 US 843 843 Prospective 48 ± 3.1 41 y Wine, beer, spirits Per 10-g increment in alcohol intake 0.97 (0.94–1.01)
Deev87 1998 Russia, US 8164 3808 Prospective – 13 y Wine, beer, spirits Had at least 1 drink last year but none last week vs nondrinker 0.76 (0.47–1.22)
0 < g last week ≤ 12 vs nondrinker 0.54 (0.35–0.84)
12 < g last week ≤ 24 vs nondrinker 0.39 (0.23–0.67)
> 24 g last week vs nondrinker 0.48 (0.3–0.77)
Had at least 1 drink last year but none last week vs nondrinker 0.76 (0.48–1.18)
0 < g last week ≤ 12 vs nondrinker 0.79 (0.51–1.21)
12 < g last week ≤ 24 vs nondrinker 0.68 (0.42–1.11)
> 24 g last week vs nondrinker 0.98 (0.62–1.56)
Had at least 1 drink last year but none last week vs nondrinker 0.51 (0.31–0.82)
0 < g last week ≤ 6 vs nondrinker 0.45 (0.27–0.75)
> 6 g last week vs nondrinker 0.38 (0.23–0.62)
Had at least 1 drink last year but none last week vs nondrinker 0.78 (0.53–1.14)
0 < g last week < 6 vs nondrinker 0.63 (0.37–1.06)
> 6 g last week vs nondrinker 1.2 (0.54–2.65)
Diem88 2003 Switzerland 287 162 Prospective 46.2 ± 5.9 12.6 ± 0.6 y Wine, beer, spirits 1–15 g/d vs 0 g/d 0.87 (0.25–2.52)
16–30 g/d vs 0 g/d 0 (0–0.92)
>30 g/d vs 0 g/d 0.37 (0.01–2.42)
Grabas89 2016 Netherlands 1919 1599 67.0 [IQR 12.5] 2.2 y [IQR 2.0] Wine, beer, spirits 0 units/wk vs 1–14 units/wk 1.42 (0.84–2.38)
15–21 units/wk vs 1–14 units/wk 1.63 (0.8–3.29)
>21 units/wk vs 1–14 units/wk 1.7 (0.94–3.06)
Harriss90 2007 Australia 38,200 15,156 Prospective cohort 40–69; grouped by sex and drinking 11.4 y Wine, beer, spirits Former drinkers vs lifetime abstainers 2.58 (1.51–4.41)
Occasional drinkers (<10 g/wk) vs lifetime abstainers 1.65 (0.92–2.96)
1.43–20 g/d vs lifetime abstainers 1.39 (0.92–2.09)
>20–40 g/d vs lifetime abstainers 1.01 (0.63–1.63)
>40 g/d vs lifetime abstainers 1.27 (0.79–2.04)
Former drinkers vs lifetime abstainers 1.25 (0.57–2.74)
Occasional drinkers (<10 g/wk) vs lifetime abstainers 1.07 (0.6–1.89)
1.43–20 g/d vs lifetime abstainers 0.82 (0.5–1.34)
>20–40 g/d vs lifetime abstainers 1.03 (0.62–1.72)
>40 g/d vs lifetime abstainers 0.43 (0.19–0.95)
Hemandez-Hemandez91 2015 Spain 14651 – Prospective cohort No total cohort mean age; grouped by drinking 9.7 y Wine, beer, spirits Abstainers vs MADP score high (7–9) 1.91 (0.52–6.98)
MADP score
 Low (0–2) vs high (7–9)		 3.35 (0.77–14.5)
MADP score
 Low (0–2) vs high (7–9)		 2.64 (1.11–6.23)
Alcohol intake low vs moderate 1.53 (0.64–3.81)
Alcohol intake high vs moderate 3.24 (0.93–11.65)
Regular vs distributed 1.07 (0.39–2.88)
Concentrated vs distributed 0.50 (0.15–1.68)
Yes vs no 1.62 (0.65–4.12)
No vs yes 1.08 (0.46–2.62)
With meals, no vs yes 1.40 (0.62–3.27)
No vs yes 0.89 (0.43–1.91)
Excess vs no excess 1.68 (0.73–4.08)
Hoffmeister92 1999 Germany 15,400 7677 Prospective cohort 25–69 6.9 y Wine, beer, spirits 1–20 vs 0 g/d 0.42 (0.2–9)
21–40 vs 0 g/d 0.72 (0.34–1.53)
40–80 vs 0 g/d 0.73 (0.31–1.74)
>80 vs 0 g/d 0.35 (0.05–2.67)
1–20 vs 0 g/d 0.68 (0.25–1.86)
21–40 vs 0 g/d 1.62 (0.51–5.16)
40–80 vs 0 g/d 1.38 (0.3–6.28)
Kauhanen93 1997 Finland 1641 1641 Prospective cohort 6 or more 50.4 (6.0)
 3–5 51.2 (5.6)
 <3 (reference group) 52.4 (5.0)		 7.7 y Beer 6 or more vs <3 bottles 7.05 (1.93–25.67)
3–5 bottles vs <3 bottles 2.4 (0.95–6.06)
Laatikainen94 2003 Finland 5092 5092 Prospective cohort Drinkers with heavy pattern - 42.1 (10.5)
 No heavy drinking occasions - 45.5 (11.2)		 7.3 y Wine, beer, spirits Heavy drinkers vs other drinkers 1.77 (1.01–3.08)
Malyutina96 2002 Russia 6502 6502 Prospective cohort 25–64 9.5 y Wine, beer, spirits Nondrinkers vs none 1.55 (1.16–2.09)
<40 g vs none 0.71 (0.42–1.22)
40–79 g vs none 0.78 (0.53–1.15)
80–119 g vs none 0.85 (0.57–1.27)
120–159 g vs none 1.25 (0.81–1.95)
≥160 g vs none 0.91 (0.65–1.29)
Mukamal95 2010 US 10670 – Prospective cohort – 5 y Wine, beer, spirits Lifelong infrequent drinker vs never drinker 0.96 (0.89–1.03)
Former drinker vs never drinker 1.02 (0.94–1.11)
Light (≤3 drinks/wk) vs never drinker 0.71 (0.61–0.83)
Moderate (>3–7 drinks/wk for women and >3–14 drinks/wk for men) vs never drinker 0.65 (0.53–0.79)
Heavy (>7 drinks/wk for women and 0.96 (0.83–1.11)
>14 drinks/wk for men) vs never drinker
Mukamal97 2001 US 1913 1318 Prospective cohort Abstainers - 65 (12)
 <7 – 60 (12)
 >7 – 57 (12)		 3.8 y Wine, beer, spirits <7 drinks/wk vs abstainers 0.75 (0.55–1.02)
≥7 drinks/wk vs abstainers 0.67 (0.41–1.17)
Pai98 2012 US 1818 1818 Prospective cohort 40–75 20 y Wine, beer, spirits 0.1–9.9 g/d vs 0 g/d 0.74 (0.54–1.02)
10.0–29.9 g/d vs 0 g/d 0.58 (0.39–0.84)
≥30.0 g/d vs 0 g/d 0.98 (0.6–1.6)
Renaud114 2004 Europe 36,583 Prospective cohort Abstainers 47.98 ± 5.692
 Wine drinkers 48.39 ± 5.69
 Other drinkers 47.28 ± 5.55		 13–21 y Wine Moderate wine drinkers (<60 g alcohol/d and no beer) vs abstainers 0.755 (0.591–0.965)
Wine drinkers of ≥60 g/d vs abstainers 0.971 (0.748–1.261)
Moderate other drinkers (<60 g alcohoL/d) vs abstainers 0.853 (0.631–1.153)
Other drinkers of ≥60 g/d vs abstainers 0.951 (0.729–1.241)
Renaud113 1998 Europe 34,014 34014 Prospective cohort 48.87 418,068 person-years Wine, beer, spirits 1–21 g/d vs 0-OccasionaLy 0.83 (0.55–1.25)
22–32 g/d vs 0-OccasionaLy 0.65 (0.45–0.95)
33–54 g/d vs 0-OccasionaLy 0.72 (0.52–1)
55–76 g/d vs 0-OccasionaLy 0.73 (0.48–1.1)
77–128 g/d vs 0-OccasionaLy 0.67 (0.48–0.94)
>128 g/d vs 0-OccasionaLy 0.75 (0.48–1.18)
Rimm112 1991 US 44,059 44059 Prospective cohort 0 g/d
 0.1–5 g/d
 5.1–30 g/d
 >30 g/d		 72,290 person-years Wine, beer, spirits 0.1–5 g/d vs 0 g/d 1.1 (0.52–2.36)
5.1–30 g/d vs 0 g/d 0.71 (0.34–1.49)
>30 g/d vs 0 g/d 0.66 (0.24–1.82)
Stampfer77 1988 US 87,526 0 prospective cohort 34–59 334,382 person-years Wine, beer, spirits <1.5 g/d vs 0 g/d 0.7 (0.2–1.7)
1.5–4.9 g/d vs 0 g/d 0.2 (0.1–0.6)
5–14.9 g/d vs 0 g/d 0.3 (0.1–0.9)
15–24.9 g/d vs 0 g/d 0.2 (0.03–1.2)
>25 g/d vs 0 g/d 0.6 (0.2–1.9)
Streppel110 2009 Netherlands 1373 1373 Prospective cohort 49 ± 6 40 y Wine, beer, spirits >0 to 20 g/d vs 0 0.7 (0.55–0.89)
>20 g/d vs 0 0.83 (0.56–1.22)
>0 to 20 g/d vs 0 0.92 (0.58–1.46)
>0 to 20 g/d vs 0 0.81 (0.48–1.35)
>20 g/d vs 0 0.78 (0.09–6.73)
>0 to 20 g/d vs 0 1.44 (0.72–2.86)
>20 g/d vs 0 0.93 (0.2–4.32)
Suhonen109 1987 Finland 4532 4532 Prospective cohort 40–64 2 y for SCD (5 y total) Wine, beer, spirits Alcohol consumers vs abstainers 2.5 (1.1–5.9)
Theobald108 2000 Sweden 1828 – Prospective cohort 18–65 22y Wine Wine vs no wine drinker 0.49 (0.28–0.9)
Beer vs no beer drinker 1.15 (0.67–1.99)
Spirits vs no spirits drinker 0.88 (0.48–1.59)
Ex-drinkers vs 1–49 gram/wk 3.05 (1.37–6.77)
Lifelong abstainers vs 1–49 g/wk 1.09 (0.48–2.48)
50–139 g/wk vs 1–49 g/wk 1.39 (0.8–2.42)
140+ g/wk vs 1–49 g/wk 1.77 (0.77–4.08)
Trevisan107 2001 Italy 15,649 8980 Prospective cohort 30–59 7 y Wine Wine with meals vs Nondrinkers 0.5 (0.33–0.74)
Wine outside meals vs Nondrinkers 0.81 (0.45–1.43)
Wine + liquor vs Nondrinkers 0.62 (0.38–1.03)
Tverdal106 2017 Norway 115,592 53,819 Prospective cohort 40–44 16 y Wine, beer, spirits Men - 0, not teetotal vs teetotal 0.53 (0.37–0.77)
Men - >0-<0.5 units/d vs teetotal 0.43 (0.29–0.63)
Men - 0.5-<1.0 units/d vs teetotal 0.4(0.28–0.59)
Men - 1.0-<1.5 units/d vs teetotal 0.48 (0.32–0.71)
Men - 1.5-<2.0 units/d vs teetotal 0.46 (0.3–0.71)
Men - 2.0-<3.0 units/d vs teetotal 0.38 (0.23–0.62)
Men - 3.0-<4.0 units/d vs Teetotal 0.51 (0.27–0.95)
Men - 4.0+ units/d vs teetotal 0.48 (0.23–1)
Women - 0, not teetotal vs teetotal 0.63 (0.38–1.06)
Women - >0-<0.5 units/d vs teetotal 0.54 (0.31–0.94)
Women - 0.5-<1.0 units/d vs teetotal 0.61 (0.34–1.09)
Women - 1.0-<1.5 units/d vs teetotal 0.61 (0.29–1.32)
Women - 1.5-<2.0 units/d vs teetotal 0.4(0.14–1.18)
Women - 2.0-<3.0 units/d vs teetotal 0.23 (0.03–1.72)
Women - 3.0-<4.0 units/d vs teetotal 0.85 (0.11–6.39)
Waśkiewicz105 2004 Poland 5352 2686 Prospective cohort Male
 abstainers 52.8
 1 tertile 51.6
 2 tertile 48.6
 3 tertile 47.2
 Female
 abstainers 53
 1 tertile 50.9
 2 tertile 48.7
 3 tertile 46		 56,261.9 person-years Wine, beer, spirits 1 tertile (mean alcohol intake - 1.1 g/d) vs abstainers 0.584 (0.369–0.924)
2 tertile (mean alcohol intake - 3.9 g/d) vs abstainers 0.588 (0.366–0.944)
3 tertile (mean alcohol intake - 28.2 g/d) vs abstainers 0.6 (0.364–0.989)
1 tertile (mean alcohol intake - 0.2 g/d) vs abstainers 0.581 (0.339–0.996)
2 tertile (mean alcohol intake - 0.4 g/d) vs abstainers 0.432 (0.228–0.817)
3 tertile (mean alcohol intake - 2.8 g/d) vs abstainers 0.329 (0.135–0.804)
Yuan104 1997 China 18,244 18,244 Prospective cohort 45–64 6.7 y Wine, beer, spirits 1–28 drinks/wk vs nondrinkers 0.64 (0.41–0.998)
>28 drinks/wk vs nondrinkers 0.88 (NR-NR)
Hart103 1999 Sweden 5766 5766 Prospective cohort 35–64 5141 person- years Wine, beer, spirits 1–7 units/wk vs none 1.13 (0.9–1.42)
8–14 units/wk vs none 0.79 (0.61–1.01)
15–21 units/wk vs none 1.06 (0.81–1.38)
22–34 units/wk vs none 1.01 (0.77–1.34)
≥35 units/wk vs none 1 (0.75–1.35)
Suadicani102 2008 Denmark 3022 3022 Prospective cohort 63 y (range, 53–74) 16 y Wine 1–8 drinks/wk vs 0 drinks of wine/wk 0.7 (0.5–0.98)
>8 drinks/wk vs 0 drinks of wine/wk 0.9 (0.6–1.2)
1–8 drinks/wk vs alcohol abstainers 0.6 (0.4–0.96)
>8 drinks/wk vs alcohol abstainers 0.7 (0.5–1.2)
Wannamethee78 1999 UK 7272 7272 Prospective cohort 40–59 16.8 y Spirits, beer Spirits vs beer in occasional and regular drinkers 1.02 (0.83–1.25)
Wine vs beer in occasional and regular drinkers 0.71 (0.52–0.98)
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IQR = interquartile range; MADP = Mediterranean alcohol-drinking pattern; SCD = Sudden Coronary Death; CI - Confidence interval.

DISCUSSION

Beer Consumption and Cardiovascular Outcomes

Beer contains a wide variety of nonalcoholic components (eg, compounds derived from benzoic and cinnamic acids, catechins, procyanidins, humulones, and prenilchalcones)6,7 that differ from those in red wine, which has amino acids, minerals, and polyphenols (phenolic acid, prenylated chalcones, flavonoids, catechins). It also has been observed that xanthohumol inhibited the oxidation of low-density lipoprotein (LDL) in vitro induced by Cu2+,8 as well as lipid peroxidation of liver microsomes in rats.9

Moderate beer consumption (1 drink/d for women and 1–2 drinks/d for men) perhaps reduces cardiovascular risks due to a mechanism of prevention of LDL oxidation and induction of cholesterol efflux from macrophages, a process considered a first step in the reverse cholesterol transport pathway.10,11 Beer can also influence high-density lipoprotein (HDL)-induced cholesterol efflux, increase ABCA1-mediated cholesterol efflux,12 enhance the antioxidant capacity of HDL, elevate plasma HDL cholesterol (HDL-c) levels,13,14 and acutely improve arterial properties.15 Non-alcoholic-related beer components protect against hyperlipidemia-induced coronary endothelial dysfunction by counteracting vascular oxidative damage and preserving the Akt/endothelial nitric oxide synthase pathway.16 The anti-inflammatory mechanisms of the bioactive compounds of beer are mainly due to the inhibition of inducible nitric oxide synthase and the inhibition of the activity of cyclooxygenase 1.6,17

One study reported that low-moderate beer consumption is associated with HDL efflux capacity.18 In a randomized control trial, moderate beer consumption for 4 weeks raised HDL-c levels by a mean of 2.2 mg/dL in individuals with an LDL-c <130 mg/dL;19 circulating HDL quality was improved already in the 4-week period by rendering HDL particles functionally active to prevent LDL oxidation and facilitate cell-cholesterol efflux. However, regular beer intake increased the plasma gamma-glutamyl transferase levels in 15% of subjects because beer is primarily metabolized in the liver using enzyme alcohol dehydrogenase,20 and therefore, patients with liver disease or at risk for liver injury (eg, those with nonalcoholic fatty liver disease or chronic hepatitis) should avoid beer consumption. One meta-analysis demonstrated that alcohol is a major risk factor for liver cirrhosis, with risk increasing exponentially.21 Moreover, women may be at higher risk compared with men, even with little alcohol consumption. Additionally, alcohol consumption has a causal association with cancers of the oral cavity, pharynx, larynx, esophagus, lungs, liver, colon, rectum, and, in women, the breast. However, some studies did not find the association between alcohol consumption and cancers.

Wine Consumption and Cardiovascular Outcomes

Wine can be classified into white wine and red wine for evaluation in studies and because of different mechanisms for cardioprotective benefits. In the 1980s, the French paradox was observed due to low cardiovascular disease mortality (primarily from coronary artery disease) despite high intake of dietary cholesterol and saturated fat.22,23 There was also the indirect observation that the French population consumed red wine with their diet, which was mostly high in saturated fat, and this correlation between wine and cardiovascular disease protection was attributed to the consumption of red wine.24 Red wine primarily contains polyphenols, which are a combination of both flavonoids (eg, anthocyanins and flavan-3-ols) and nonflavonoids (eg, resveratrol, cinnamates, and gallic acid). In fact, flavonoids such as Flavan-3-ols are the most abundant and contain up to 50% of the total phenolic constituents.25 Wine promotes cardiovascular health via multiple mechanisms. These include polyphenols lowering plasma concentrations of pro-oxidant and inflammatory molecules and leukocyte adhesion molecules, improving homeostasis model assessment of insulin resistance values and blood pressure, reducing phospholipids oxidation, modulating cell signaling pathways, reducing platelet aggregation,26–28 decreasing highly sensitive C-reactive protein, as well as concentrations of monocyte and endothelial adhesion molecules.29,30 St Leger et al31 reported a negative correlation between alcohol consumption and ischemic heart disease deaths, and attributed this observation predominantly to wine. Several explanations for the French paradox have been postulated,24 with epidemiologists presenting strong correlations in favor of wine (both white and red), with other scientific literature criticizing these observations. Compared with beer or spirits, consumption of wine has been independently associated with improvements in heart rate variability, a marker of autonomic balance.32 In the CASCADE trial, in individuals with slow ethanol metabolizers (alcohol dehydrogenase alleles carriers ADH1B*1), wine consumption is associated with better glycemic control (eg, fasting plasma glucose, homeostatic model assessment of insulin resistance, and hemoglobin A1c) compared with individuals with fast ethanol metabolizers (homozygous ADH1B*2).33 Indeed, studies on wine consumption and cardiovascular disease are primarily based on observational studies. There is the risk of bias from confounding factors (eg, socioeconomic status, neighborhood, culture, physical activity, exercise) or unmeasured confounding (eg, genetics, gut microbiome).

Red Wine Consumption and Cardiovascular Outcomes

Compared with white wine, red wine has an approximately 10-fold higher polyphenolic content due to red wine’s grape fermentation.34 Unfortunately, few studies directly compare the different effects on cardiovascular health of red wine vs white wine.

Red wine promotes cardiovascular health via mechanisms of polyphenols, improved endothelial function, and increased circulating endothelial progenitor cells and nitric oxide levels.35 Red wine has higher levels of bioflavonoids (with antioxidant, antiplatelet, and antiendothelin-1 effects),36 polyphenolic mixtures such as flavonoids (eg, catechin/epicatechin/quercetin, procyanidins, and anthocyanins), polymeric tannins, and resveratrol (eg, 3,5,4′-trihydroxystilbene).37 In general, red wine contains abundant polyphenols and is, perhaps, considered a crucial polyphenol source in the diet.38 Red wine may be associated with increased HDL-c,39,40 improved insulin resistance28,41 and oxidative stress,42,43 and downregulated serum concentrations of CD40 antigen, CD40 ligand, interleukin-16, monocyte chemotactic protein-1, and vascular cell adhesion molecule-1.26 It also can reduce the propensity of LDL to undergo lipid peroxidation.44 In addition, a recent study found that people who drank red wine had increased gut microbiota diversity (a sign of gut health) compared with non-red-wine drinkers, as well as an association with lower levels of obesity and ‘bad’ cholesterol.45

Although alcohol increases triglyceride levels, very low-density lipoprotein production, and triglyceride enrichment of HDL, little is known about alcohol’s effect on lipoprotein (a). In the CASCADE trial, 224 abstainers with type 2 diabetes were randomized to consume red wine, white wine, or mineral water for 2 years.33 This long-term randomized controlled trial among well-controlled diabetics found that initiating moderate red wine is associated with increased HDL-c levels by 2.0 mg/dL and decreased the total cholesterol-to-HDL-c ratio by 27%. Moreover, red wine is associated with a reduction in components of the metabolic syndrome by 34%, compared with the changes in the water group. In fact, some studies performed in women observed that daily doses of 15–20 g of alcohol such as red wine were sufficient to elicit anti-inflammatory effects similar to those observed in men who consumed higher doses of wine.46

White Wine Consumption and Cardiovascular Outcomes

Compared with red wine, studies in white wine are inconclusive, and its mechanism for cardiovascular benefits is unclear. Clinical trials have suggested that white wine, particularly aged white wine, could promote cardiovascular health via various mechanisms. These include repair and maintenance of endothelial integrity, antioxidative and antiatherogenic effects, an increase in HDL-c, increase in paraoxonase-1 and glutathione peroxidase, reduced glutathione levels, a decrease in superoxide dismutase activity, and a decrease in oxidation protein products and thiobarbituric acid reactive substance concentrations.47 However, one non-placebo-controlled trial suggests that regular daily white wine consumption could potentially lead to a proatherogenic increase in homocysteine concentrations.48 There were, however, limitations in this study, such as the number of participants in each drinking pattern group (wine and beer drinkers). The difference in protective effect between red wines and white wines is perhaps due to the polyphenolic ratio. However, one study suggested that tyrosols (relatively unknown active compounds identified in white wines), along with known compounds such as caffeic acid, and shikimic acids, could potentially explain the biological mechanisms and association between white wine and cardiovascular disease.49 Some studies suggested that wine acutely improves endothelial function in patients with coronary artery disease, and a moderate daily intake of white wine with dinner can have antioxidative and cardioprotective effects.50,51 However, there are also studies that have reported no differences in the effects of red and white wines on endothelial function.50 Further research is needed to compare directly between red wine and white wine consumption on cardiovascular disease effects. Methodology to stratify confounders (eg, subgroup analysis) or identify unknown confounders using machine learning is needed in alcohol research.

Liquor/Other Alcohol Consumption and Cardiovascular Outcomes

There is no study directly on liquor or distilled spirits and the associations with cardiovascular disease outcomes. Liquor or spirits such as gin and vodka do not have a significant number of polyphenols or other nonalcoholic compounds with purported cardiovascular benefits. Therefore, data are relatively limited. One longitudinal study indicated that the use of spirits at least once a week may be associated with a slightly reduced risk of acute myocardial infarction among coronary artery disease-free men aged 30–59 years, but has no impact on total mortality compared with men using less spirits.52 Several studies on spirit consumption and vascular risk found no J-shaped correlation.53–56 No statistically significant association with vascular events was apparent for the intake of spirits up to 60 g/d, which is the maximum dose investigated in the 10 studies included in this meta-analysis. Indeed, several studies noted that spirit consumption mostly occurred as binge drinking (defined as the consumption of 3 or more drinks within 1–2 hours) and was restricted to only a few days per week. This may explain the absence of association between moderate spirit consumption and cardiovascular disease benefit in the present review and in a previous study.57 There are limited studies on the subtypes of liquor (whiskey, gin, rum, tequila) and cardiovascular disease. Researchers assessed whether consumption of 100 mL of whisky or red wine by healthy male subjects increased plasma total phenol content and antioxidant capacity. They found that consumption of phenolic-containing alcoholic beverages transiently raised total phenol concentration and enhanced the antioxidant capacity of plasma.58 This is compatible with suggestions that moderate alcohol usage and increased antioxidant intake decrease the risk of coronary heart disease.

Overall, although head-to-head comparisons between classes of alcoholic beverages are very limited, there may be underlying cardiovascular benefits from moderate alcohol consumption. However, further studies with confounder correction are needed to dissect this potential association before serious recommendations can be made. However, due to the many health risks linked to alcohol consumption (ie, dementia, alcohol use disorder, liver cirrhosis),21 no long-term randomized trials of alcohol consumption have been performed.59

Limitations

There are significant limitations of the present study. Most meta-analyses fit linear models ignoring the J shape, or did not use nondrinkers as the reference. First, the included studies are confounded by diet. For example, wine consumption is more often a component of the Mediterranean diet, while beer/liquor intake is more commonly accompanied by diets rich in oily and fried foods.60,61 Second, there is no genetic factor.62 A recent mendelian randomization study showed evidence of a causal relationship between higher alcohol consumption and an increased risk of stroke and peripheral artery disease.63 The causal role of alcohol consumption for other cardiovascular diseases requires further research. Third, there is no drink pattern adjusted. Although some studies adjusted, the direction and magnitude of the effects of adjustment need to be further explored. Studies show that binge drinking is associated with increased coronary artery disease risk,64 while alcohol is most cardioprotective when consumed prior to or during a meal.65 For example, studies showed that wine drinkers who participated in this study reported a healthier diet than did drinkers of beer or spirits.66,67 Fourth, a lack of behavioral pattern adjustment is a limitation. For example, the Finnish study found that in their study population, men who drank spirits also regularly smoked.52 Fifth, most importantly, there were no adjustments for socioeconomic status. For example, a recent study suggested that coincident, favorable lifestyle factors attenuated the observational benefits of modest alcohol intake.62 Moreover, it is likely that any particular benefit of wine over beer and spirits is prone to confounding by diet and socioeconomic status.66 Sixth, a limitation of many cohort studies is that they only have baseline estimates of alcohol intake, which may change over time. Finally, it is possible that the observational studies overestimate the benefits of alcohol for cardiovascular disease outcomes. Case-control and cross-sectional studies typically are more prone to bias and reverse causation. In fact, there is increasing concern about an increased risk of breast cancer and other cancers with even moderate alcohol intake. Further meta-analysis in alcohol and all-cause mortality is needed.

CONCLUSIONS

In individuals without liver disease, low to moderate amounts of weekly or daily alcohol consumption may be beneficial to cardiovascular health. Specifically, strong evidence has suggested that low-moderate amounts of weekly or daily red wine consumption may be particularly associated with low cardiovascular events. However, the relationship between alcohol consumption and cardiovascular disease appears to be biphasic and have a J-shape association. Heavy alcohol consumption could be harmful. Further prospective studies with correction of potential confounders (eg, lifestyle factors, socioeconomic status) are urgently needed. Further clinical trials, if able to be undertaken safely, are warranted to adequately determine the effect of alcohol consumption on cardiovascular disease.

Supplementary Material

1

CLINICAL SIGNIFICANCE.

  • It is possible that the observational studies may overestimate the benefits of alcohol for cardiovascular disease outcomes.

  • Moderate wine consumption may be associated with low cardiovascular disease events.

  • There are many confounding factors, in particular, lifestyle, genetic, and socioeconomic associations with wine drinking, which likely explain much of the association with wine and reduced cardiovascular disease events.

  • Further prospective study of alcohol and all-cause mortality, including cancer, is needed.

ACKNOWLEDGMENTS

The authors would like to thank Dr. JoAnn E. Manson, MD, DrPH, MACP (Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, Mass), Dr. Kenneth J. Mukamal, MD (Beth Israel Deaconess Medical Center, Harvard Medical School and Harvard TH Chan School of Public Health, Boston, Mass), and Dr. Meir Stampfer, MD, DrPH (Harvard T.H. Chan School of Public Health) for their suggestions and comments on this article.

Footnotes

Conflicts of Interest: Dr. Krittanawong discloses the following relationships – Member of the American College of Cardiology Solution Set Oversight Committee, the American Heart Association Committee of the Council on Genomic and Precision Medicine, and the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Performance Measures, The Lancet Digital Health (Advisory Board), European Heart Journal Digital Health (Editorial board), Journal of the American Heart Association (Editorial board), JACC: Asia (Section Editor), The Journal of Scientific Innovation in Medicine (Associate Editor), and Frontiers in Cardiovascular Medicine (Associate Editor). Dr. Rosenson receives research funding to his institution from Amgen, Arrowhead, Lilly, NIH, Novartis, Regeneron; consulting fees from Amgen, Lilly, Novartis, Regeneron, non-promotional speaking fees from Amgen, Kowa; royalties from Wolters Kluwer for UpToDate, and has stock holdings in MediMergent LLC. Dr. Virani discloses the following Grant support: Department of Veterans Affairs, World Heart Federation, Tahir and Jooma Family. Honorarium: American College of Cardiology (Associate Editor for Innovations, ACC.org). Steering Committee: Patient and Provider Assessment of Lipid Management (PALM) registry at Duke Clinical Research Institute (no financial remuneration). Dr. Qi is supported by grants from the National Heart, Lung, and Blood Institute (HL071981, HL034594, HL126024), the National Institute of Diabetes and Digestive and Kidney Diseases (DK115679, DK091718, DK100383, DK078616), the Fogarty International Center (TW010790), Tulane Research Centers of Excellence Awards. Dr. Qi is also supported by P30DK072476 and NIGMS P20GM109036. Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases K23 DK113252, the Doris Duke Charitable Foundation Grant #2019085, Gilead Sciences Research Scholars Award, Echosens Corporation, the Boston University. Dr. Tangney is an UpTodate consultant. Other authors have no disclosure.

SUPPLEMENTARY DATA

Supplementary data to this article can be found online at https://doi.org/10.1016/j.amjmed.2022.04.021.

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Supplementary Materials

1
NIHMS1819660-supplement-1.pdf (36.7KB, pdf)

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