Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors
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Abstract Objective: To summarise quantitatively the association between moderate alcohol intake and biological markers of risk of coronary heart disease and to predict how these changes would lower the risk. Design: Meta-analysis of all experimental studies that assessed the effects of moderate alcohol intake on concentrations of high density lipoprotein cholesterol, apolipoprotein A I, fibrinogen, triglycerides, and other biological markers previously found to be associated with risk of coronary heart disease. Participants: Men and women free of previous chronic disease and who were not dependent on alcohol Studies were included in which biomarkers were assessed before and after participants consumed up to 100 g of alcohol a day. Interventions: Alcohol as ethanol, beer, wine, or spirits. Main outcome measures: Changes in concentrations of high density lipoprotein cholesterol, apolipoprotein A I, Lp(a) lipoprotein, triglycerides, tissue type plasminogen activator activity, tissue type plasminogen activator antigen, insulin, and glucose after consuming an experimental dose of alcohol for 1 to 9 weeks; a shorter period was accepted for studies of change in concentrations of fibrinogen, factor VII, von Willebrand factor, tissue type plasminogen activator activity, and tissue type plasminogen activator antigen. Results: 61 data records were abstracted from 42 eligible studies with information on change in biological markers of risk of coronary heart disease. An experimental dose of 30 g of ethanol a day increased concentrations of high density lipoprotein cholesterol by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A I by 8.82 mg/dl (7.79 to 9.86), and triglyceride by 5.69 mg/dl (2.49 to 8.89). Several haemostatic factors related to a thrombolytic profile were modestly affected by alcohol On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease. Conclusions: Alcohol intake is causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors. Key messages Results from observational studies provide strong evidence that moderate alcohol intake lowers risk of coronary heart disease Short term trials of alcohol intake show significant changes in concentrations of lipids and clotting factors The changes in concentrations of high density lipoprotein cholesterol, fibrinogen, and triglycerides associated with an intake of 30 g of alcohol a day should reduce risk of coronary disease by 24.7% Alcohol intake may be causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors
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Excess alcohol consumption, particularly in individuals with pre-existing hypertriglyceridemia, is associated with marked triglyceride elevation, often ≥250 mg/dL.
“Excess alcohol consumption, particularly in individuals with pre-existing hypertriglyceridemia, is associated with marked triglyceride elevation, often ≥250 mg/dL, and can precipitate hypertriglyceridemic pancreatitis (93,98).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [93]
The Triglycerides section (page unavailable) reports that alcohol intake increased triglycerides, but by an average of only 5.69 mg/dL at 30 g/day. Alcohol and other factors (page unavailable) says the studies were mostly in young, healthy people with low baseline triglycerides. The paper does not establish marked elevations of ≥250 mg/dL with excess consumption, particularly in people with pre-existing hypertriglyceridemia. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAlcohol consumption of 1 ounce per day is estimated to correspond to a 5% to 10% higher concentration of triglycerides in drinkers versus nondrinkers.
“Alcohol consumption of 1 ounce per day is estimated to correspond to a 5% to 10% higher concentration of triglycerides in drinkers versus nondrinkers (93,94).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [93]
Excess alcohol consumption can precipitate hypertriglyceridemic pancreatitis.
“Excess alcohol consumption, particularly in individuals with pre-existing hypertriglyceridemia, is associated with marked triglyceride elevation, often ≥250 mg/dL, and can precipitate hypertriglyceridemic pancreatitis (93,98).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [93]
The Triglycerides section reports a small increase in triglycerides with moderate alcohol intake. A search of our copy for pancreatitis and excessive alcohol consumption found no passage addressing whether excess drinking can precipitate hypertriglyceridemic pancreatitis. No page number was available for the indexed passage. (LLM, conf=0.74)
Experimental — accuracy not yet measuredRed yeast rice preparations providing 5-10 mg monacolin K once daily produce a clinically relevant cholesterol reduction of up to 20%.
“A clinically relevant hypocholesterolaemic effect (up to a 20% reduction) has been observed with RYR preparations providing an o.d. [once daily (omni die)] dose of 5-10 mg monacolin K [145].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [145]
Alcohol intake has a major negative impact on triglyceride levels; in individuals with hypertriglyceridaemia even a small amount can raise triglycerides, while in the general population detrimental effects occur only above moderate consumption (10-30 g/day).
“Alcohol intake has a major negative impact on TG levels.While in individuals with HTG even a small amount of alcohol can induce a further elevation of TG concentrations, in the general population alcohol exerts detrimental effects on TG levels only if the intake exceeds what is considered a moderate consumption (up to 1-2 drinks/day corresponding to 10-30 g/day).74”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [74]
Alcohol intake has a major impact on triglyceride levels.
“Alcohol intake has a major impact on TG levels.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [152]
In the general population, alcohol has harmful effects on triglycerides only when intake is excessive.
“in the general population alcohol exerts detrimental effects on TG levels only if the intake is excessive. 152,177”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [152]
In people with hypertriglyceridaemia, even a small amount of alcohol can further elevate triglyceride concentrations.
“While in individuals with HTG even a small amount of alcohol can induce a further elevation of TG concentrations”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [152]
In individuals with hypertriglyceridaemia, even small amounts of alcohol can further elevate triglycerides; in the general population, detrimental effects occur only with excessive intake.
“While in individuals with HTG even a small amount of alcohol can induce a further elevation of TG concentrations, in the general population alcohol exerts detrimental effects on TG levels only if the intake is excessive.152,177”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [152]
Alcohol abuse may be associated with hypertriglyceridemia; nearly 1 in 5 hospitalized alcoholics have triglyceride levels exceeding 250 mg/dL.
“In contrast, alcohol abuse may be associated with hypertriglyceridemia; nearly 1 in 5 hospitalized alcoholics have triglyceride levels exceeding 250 mg/dL.450”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [450]
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“…effect of moderate alcohol consumption involve an increase in the levels of alcohol metabolites, such as acetaldehyde and acetate (Sarkola et al. 2002); an increase in high-density lipoprotein (HDL)4 (Rimm et al. 1999); and the anti-inflammatory effects of alcohol consumption (Imhof et al. 2001).”
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- Authors
- Rimm, E. B., Williams, P., Fosher, K., Criqui, M., & Stampfer, M. J.
- Affiliations
- Harvard University (US)
- Corresponding author
- Rimm, E. B
- Venue
- BMJ
- Publisher
- BMJ
- Published
- 1999-12-11
- Volume
- 319
- Issue
- 7224
- Pages
- 1523-1528
- ISSN
- 0007-1447 (ISSN-L)
- 0959-8138
- 1468-5833
- PMC
- PMC28294
- OpenAlex
- W1969728057
- Cited by
- 1,360
- References
- 57
- Citations by year
- 2026: 19 · 2025: 16 · 2024: 26 · 2023: 24 · 2022: 26 · 2021: 50 · 2020: 29 · 2019: 45 · 2018: 50 · 2017: 48 · 2016: 42 · 2015: 52 · 2014: 47 · 2013: 68 · 2012: 83
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- BMJ (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Risk Factors
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- moderate drinking, coronary heart disease risk, HDL cholesterol, apolipoprotein A-I, triglycerides, fibrinogen, hemostatic factors, tissue plasminogen activator, alcohol dose-response, cardiovascular risk markers, ethanol
- MeSH terms
- Alcohol Drinking, Cardiovascular Diseases, Female, Homeostasis, Humans, Lipids, Cholesterol, HDL, Male, Prospective Studies, Risk Factors, Triglycerides, Biomarkers, Apolipoprotein A-I
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