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Research · Food and drink

Alcohol

Older cohorts linked light drinking to fewer heart attacks and deaths than not drinking. A 2023 analysis correcting for former drinkers found no lower death, and genetic studies found no protection against stroke. Alcohol is linked to cancers of the mouth, throat, esophagus, breast and liver, to cirrhosis, and to higher blood pressure.

Add to Bio HackChecked 2026-11-13
Status
A food, not a regulated health product. The Dietary Guidelines for Americans, 2025-2030 say to consume less alcohol for better overall health, and name pregnant women, people recovering from alcohol use disorder and people taking medicines that interact with alcohol among the groups they say to avoid it completely [1].
Also called
alcoholic drinks, ethanol, wine, red wine, beer, spirits, liquor, booze, a drink a day, moderate drinking, light drinking, binge drinking, nightcap
Studied for
heart health, longer life, a drink a day, HDL cholesterol, relaxation, stress, falling asleep, red wine for the heart

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Shown to help1

Reported risks13

What it was studied for, and what was found

Shown to help1

Moderate

HDL cholesterol in trials

Shown to raise HDL cholesterol by about 0.09 mmol/L in trials of adults without heart disease, with no change in triglycerides.

Compared with periods without alcohol [9]

The numbers and sources
Effect
Alcohol raised HDL cholesterol (mean difference 0.094 mmol/L, 95% CI 0.064 to 0.123), apolipoprotein A1 (0.101 g/L, 95% CI 0.073 to 0.129) and adiponectin, with a dose-response for HDL. It lowered fibrinogen (-0.20 g/L) and did not change triglycerides. Results were similar for wine, beer and spirits [9].
Population
44 interventional studies of 13 markers in adults without known cardiovascular disease [9].
Sources
[9]
Caveats
These are blood markers, not heart attacks. The review calls them indirect support for a protective effect [9], while genetic studies of heart disease found none (see above).

Mixed results3

Moderate

Death from any cause and the light drinking debate

Mixed results: older pooled cohorts linked drinking to 13% lower death than not drinking, while a 2023 analysis correcting for former drinker bias found no lower risk.

Compared with non-drinkers [2]; lifetime nondrinkers [3]; current drinkers of more than 0 and up to 100 g a week [4]

The numbers and sources
Effect
Pooled cohorts found lower death from all causes in drinkers than non-drinkers (RR 0.87, 95% CI 0.83 to 0.92) [2]. Across 107 cohorts, after adjusting for former drinker bias and study quality, death did not differ between lifetime nondrinkers and occasional drinkers of under 1.3 g a day (RR 0.96, 95% CI 0.86 to 1.06) or low-volume drinkers of 1.3 to 24 g a day (RR 0.93, P = 0.07). Risk rose at 45 to 64 g a day (RR 1.19) and 65 g or more (RR 1.35), and female drinkers overall had higher risk than female lifetime nondrinkers (RR 1.22) [3]. Among current drinkers only, death was lowest at about 100 g a week or less. Against drinkers of up to 100 g a week, those drinking over 350 g a week had 4 to 5 years shorter life expectancy at age 40 [4]. A global analysis put the lowest-risk intake at 0 to 0.6 standard drinks a day for people aged 15 to 39, and 0.1 to 1.9 for people 40 and older, varying by region [5].
Population
84 prospective cohorts [2]. 4,838,825 participants and 425,564 deaths in 107 cohorts [3]. 599,912 current drinkers without cardiovascular disease in 83 studies from 19 high-income countries [4]. Disease rates for 204 countries [5].
Sources
[2], [3], [4], [5]
Caveats
All observational. Many cohorts count "sick quitters", former drinkers who cut down or stopped for health reasons, among non-drinkers, which makes drinkers look healthier by comparison. Adjusting for this removed the lower risk [3]. Light drinkers also have other healthier habits, and adjusting for them weakened the apparent benefit in a UK cohort [6].
Moderate

Heart attack and coronary heart disease

Mixed results: cohorts linked drinking to about 29% less coronary heart disease than non-drinking, but genetic studies found no protection and some found higher risk.

Compared with non-drinkers [2]; each 100 g a week less, among current drinkers [4]; genetically predicted lower intake [7][8][6]

The numbers and sources
Effect
Drinkers had less incident coronary heart disease (RR 0.71, 95% CI 0.66 to 0.77) and less coronary death (RR 0.75, 95% CI 0.68 to 0.81) than non-drinkers, lowest at 1 to 2 drinks a day [2]. Among current drinkers, each 100 g a week was linked to slightly lower heart attack risk (HR 0.94, 95% CI 0.91 to 0.97) [4]. In Chinese men, self-reported drinking of about 100 g a week showed a U-shaped link with heart attack, but genetically predicted intake was not linked to it (RR 0.96 per 280 g a week, 95% CI 0.78 to 1.18) [7]. A gene variant tied to drinking 17.2% less was linked to lower odds of coronary heart disease (OR 0.90, 95% CI 0.84 to 0.96) [8]. In UK adults, genetically predicted intake was linked to 1.4-fold higher coronary artery disease risk per standard deviation, with minimal rise at light intake [6].
Population
84 cohorts [2]. 599,912 current drinkers [4]. 512,715 Chinese adults, 161,498 genotyped [7]. 261,991 people of European descent in 56 studies [8]. 371,463 UK Biobank participants [6].
Sources
[2], [4], [7], [8], [6]
Caveats
Cohorts share the sick quitter and lifestyle problems above. Mendelian randomization uses genes that set drinking levels to sidestep those problems, and its results disagree with the cohorts. Genetic studies have their own limits, such as genes acting through other paths.
Moderate

Falling asleep

Shown to shorten time to fall asleep only at about five standard drinks, in pooled studies of healthy adults. REM sleep fell even at two drinks.

Compared with a no-alcohol condition the abstract does not describe [10]

The numbers and sources
Effect
Shorter sleep onset and quicker deep sleep appeared only after a high dose of 0.85 g per kg or more, about five standard drinks. REM sleep was delayed and shortened from a low dose of 0.50 g per kg or less, about two drinks, worsening with dose. Effects on total sleep time, sleep efficiency and waking during the night were too uncertain to determine [10].
Population
Healthy adults in 27 studies [10].
Sources
[10]
Caveats
Laboratory nights after a set dose. The review notes faster sleep onset at high doses likely worsens later REM disruption [10].

Amounts studied

Studies count standard drinks of about 12 g of pure alcohol [11][12]. The largest mortality analysis grouped people as occasional drinkers (more than 0 to under 1.3 g a day), low-volume (1.3 to 24 g), and up to 65 g or more a day [3]. The pooled current-drinker analysis used 100 g a week, 12.5 UK units, as its unit [4]. Light drinking in the cancer review meant up to 1 drink a day [13]. Sleep studies used low doses of 0.50 g per kg or less and high doses of 0.85 g per kg or more [10]. Blood pressure trials gave single doses under 14 g, 14 to 28 g, or over 30 g [14].

Risks

Reported risks12

StrongHow often is not known

Cancer

Linked to higher risk of cancers of the mouth, throat, esophagus, bowel, larynx, liver and breast, rising with dose. Breast cancer rose 5% at up to one drink daily.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Against non-drinkers and occasional drinkers, heavy drinkers had higher risk of oral and pharyngeal cancer (RR 5.13), esophageal squamous cell cancer (4.95), laryngeal (2.65), liver (2.07), breast (1.61) and colorectal cancer (1.44), with clear dose-response for most [15]. Against non-drinkers, light drinking of up to 1 drink a day was linked to oropharyngeal cancer (RR 1.17, 95% CI 1.06 to 1.29), esophageal squamous cell cancer (RR 1.30, 95% CI 1.09 to 1.56) and female breast cancer (RR 1.05, 95% CI 1.02 to 1.08), and not to bowel, liver or larynx cancer [13].
Population
572 studies with 486,538 cancer cases [15]. 222 articles with about 92,000 light drinkers and 60,000 non-drinkers with cancer [13].
Sources
[15], [13]
Caveats
Observational, though consistent across hundreds of studies and with clear dose-response. Lymphomas were less common in drinkers [15].
StrongHow often is not known

Liver cirrhosis

Linked to sharply higher cirrhosis risk with heavy drinking, 12 to 25 times in women at 5 or more drinks a day. Women had higher risk at the same intake.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Against long-term abstainers, 1 drink a day was linked to higher cirrhosis risk in women and not in men. At 5 to 6 drinks a day the relative risk was 12.44 (95% CI 6.65 to 23.27) in women and 3.80 (95% CI 0.85 to 17.02) in men, and at 7 or more 24.58 in women and 6.93 in men. Occasional drinkers had no higher risk [16]. An earlier review of 17 studies found the same amount carried higher risk in women, and a larger effect on cirrhosis death than on cirrhosis illness [17].
Population
2,629,272 participants with 5,505 cirrhosis cases in 9 studies [16]. 17 cohort and case-control studies [17].
Sources
[16], [17]
Caveats
Observational. Heterogeneity pointed to other factors, such as genes, weight and drinking pattern [16].
ModerateHow often is not known

Higher blood pressure with regular drinking

Trials found cutting down lowered blood pressure only in people drinking over two drinks a day, 5.5 mmHg systolic at six or more. Genetic studies linked intake to higher pressure.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
In trials, cutting alcohol by about half lowered systolic pressure by 5.50 mmHg (95% CI 4.30 to 6.70) and diastolic by 3.97 mmHg in people drinking 6 or more drinks a day. In people drinking 2 or fewer drinks a day, cutting down did not significantly lower blood pressure [11]. In Chinese men, genetically predicted alcohol intake was strongly linked to higher systolic pressure [7]. In UK adults, genetically predicted intake was linked to 1.3-fold higher risk of hypertension per standard deviation [6].
Population
2,865 participants, 2,464 of them men, in 36 trials lasting at least 7 days [11]. 161,498 genotyped Chinese adults [7]. 371,463 UK adults [6].
Sources
[11], [7], [6]
Caveats
Most trial participants were men [11].
ModerateHow often is not known

Blood pressure and heart rate in the hours after drinking

Shown to lower blood pressure for up to 12 hours after drinking and raise it after 13 hours at high doses. Heart rate rose about 5 beats a minute.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Against placebo, 14 to 28 g of alcohol lowered systolic pressure by 5.6 mmHg (95% CI 3.0 to 8.3) and diastolic by 4.0 mmHg within 6 hours, and raised heart rate by 4.6 beats a minute. Over 30 g lowered systolic pressure by 3.5 mmHg within 6 hours and by 3.7 mmHg at 7 to 12 hours, then raised it by 3.7 mmHg (95% CI 2.3 to 5.1) and diastolic by 2.4 mmHg 13 hours or more later. Heart rate stayed raised for up to 24 hours after high doses [14].
Population
767 participants in 32 randomized trials, mostly healthy men, mean age 33 [14].
Sources
[14]
Caveats
Single doses. The authors note the findings apply mainly to healthy men [14].
ModerateHow often is not known

Stroke

Linked to higher stroke risk in a pooled analysis of current drinkers and in genetic studies, which found no protective effect at moderate intake.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Among current drinkers, each 100 g a week was linked to higher stroke risk (HR 1.14, 95% CI 1.10 to 1.17), heart failure (HR 1.09) and fatal hypertensive disease (HR 1.24) [4]. In Chinese men, genetically predicted intake was linked to higher risk of intracerebral hemorrhage (RR 1.58 per 280 g a week, 95% CI 1.36 to 1.84) and ischemic stroke (RR 1.27, 95% CI 1.13 to 1.43), with no U-shaped dip. Self-reported moderate drinking had looked protective in the same cohort [7]. Against non-drinkers, pooled cohorts found no difference in incident stroke (RR 0.98, 95% CI 0.91 to 1.06) [2].
Population
599,912 current drinkers [4]. 512,715 Chinese adults, 161,498 genotyped [7]. 17 cohorts for incident stroke [2].
Sources
[4], [7], [2]
Caveats
Few women in the Chinese cohort drank, so the genetic results are for men [7].
LimitedHow often is not known

Atrial fibrillation

One trial found atrial fibrillation returned in 53% of regular drinkers who abstained against 73% who kept drinking, over 6 months.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Drinkers of 10 or more drinks a week with atrial fibrillation were randomized to abstain or continue. Recurrence was 37 of 70 (53%) with abstinence and 51 of 70 (73%) with usual drinking (HR 0.55, 95% CI 0.36 to 0.84), and time spent in atrial fibrillation was lower with abstinence [12].
Population
140 adults, 85% men, mean age 62, at 6 Australian hospitals [12].
Sources
[12]
Caveats
One open-label trial in people who already had atrial fibrillation. The rate is recurrence in people with the condition who kept drinking.
ModerateHow often is not known

Less REM sleep

Shown to delay and shorten REM sleep from about two standard drinks, worsening with dose, in pooled studies of healthy adults.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Disruption of REM sleep began at 0.50 g per kg or less, about two standard drinks, and grew with higher doses [10].
Population
Healthy adults in 27 studies [10].
Sources
[10]
Caveats
Laboratory studies of single nights.
ModerateHow often is not known

Sleep apnea

Linked to 25% higher risk of sleep apnea at higher alcohol intake, in pooled observational studies.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Higher against lower alcohol consumption was linked to sleep apnea (RR 1.25, 95% CI 1.13 to 1.38, I² 82%) [18].
Population
21 studies of adults [18].
Sources
[18]
Caveats
Observational, with high heterogeneity and evidence of publication bias [18].
LimitedHow often is not known

Interaction with opioids and sedatives

One small trial found alcohol deepened oxycodone's slowing of breathing by a further 19%. Alcohol was involved in about a fifth of US opioid and benzodiazepine deaths.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Oxycodone 20 mg cut resting breathing by 28%, and an alcohol infusion reaching 1 g/L cut it by a further 19%, with more pauses in breathing. Older volunteers were more affected [19]. In US data from 2010, alcohol was involved in 22.1% of opioid pain reliever deaths and 21.4% of benzodiazepine deaths [20]. Alcohol was involved in 14.7% of all opioid overdose deaths in 2017 [21]. A review lists opioids, benzodiazepines, barbiturates and sleep medicines among drugs whose effects on the brain alcohol enhances [22].
Population
12 young and 12 older opioid-naive volunteers [19]. US emergency visits and deaths in 13 states [20]. 399,230 US opioid deaths from 1999 to 2017 [21].
Sources
[19], [20], [21], [22]
Caveats
Death records show alcohol was involved, not that it caused the death.
LimitedHow often is not known

Interaction with acetaminophen and NSAID pain relievers

FDA requires over-the-counter acetaminophen labels to warn of severe liver damage, and NSAID labels of stomach bleeding, with 3 or more drinks every day.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Federal labeling rules require acetaminophen products to warn that severe liver damage may occur with 3 or more alcoholic drinks every day while using the product, and NSAID products to warn that the chance of severe stomach bleeding is higher with 3 or more drinks a day [23]. A review states that alcohol enhances the breakdown of acetaminophen into a toxic product [22].
Population
US labeling regulation [23]. Narrative review [22].
Sources
[23], [22]
Caveats
The regulation states the warning and gives no rate.
LimitedHow often is not known

Interaction with warfarin

Limited evidence: in people taking warfarin, alcohol misuse and heavy episodic drinking were linked to about twice the odds of major bleeding, in one case-control study.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Screening positive for moderate or severe alcohol misuse (OR 2.10, 95% CI 1.08 to 4.07) and drinking 5 or more drinks on an occasion (OR 2.36, 95% CI 1.24 to 4.50) were linked to major bleeding [24]. A review states that acute drinking may raise warfarin's effect by slowing its breakdown, while chronic drinking may lower it [22].
Population
265 people with major bleeding and 305 without, all taking warfarin, mean age 70 [24].
Sources
[24], [22]
Caveats
One case-control study of misuse, not of light drinking.
LimitedHow often is not known

Interaction with metformin and other diabetes medicines

Case reports: lactic acidosis in people taking metformin after heavy drinking. A review lists low blood sugar with sulfonylureas and alcohol.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
A 65-year-old man taking metformin, with normal kidney function, developed lactic acidosis after excessive drinking, and the authors review earlier cases [25]. A review states that alcohol raises the risk of low blood sugar with chlorpropamide, glyburide and tolbutamide, and that metformin may raise blood lactic acid after drinking [22].
Population
One patient and earlier case reports [25]. Narrative review [22].
Sources
[25], [22]
Caveats
Case reports give no rate. Across US drinkers, 41.5% used a prescription medicine that interacts with alcohol, and 77.8% of drinkers aged 65 or older [26].

Mixed results1

ModerateStudied in womenHow often is not known

Fibroids

Mixed results: a 2026 pooled analysis found no overall link between drinking and fibroids, while an earlier one linked current drinking to 33% higher odds.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
Across 13 studies (135,370 women, 9,944 with fibroids), ever drinking was not linked to fibroids against never drinking (OR 1.04, 95% CI 0.86 to 1.26), and across 9 studies (3,375,571 women) neither was current drinking (OR 1.09, 95% CI 0.91 to 1.32). Odds were higher in studies from China (OR 3.48, 95% CI 1.29 to 9.43) and in studies that confirmed fibroids clinically or surgically (OR 1.18, 95% CI 1.00 to 1.39) [27]. An earlier review found ever drinking not linked (OR 1.12, 95% CI 0.94 to 1.34) and current drinking linked to higher odds (OR 1.33, 95% CI 1.01 to 1.76), from 2 studies [28].
Population
Women in 13 studies for ever drinking and 9 for current drinking [27]; 5 studies, 2 of them for current drinking [28].
Sources
[27], [28]
Caveats
Observational. The authors describe the studies as heterogeneous and the evidence as limited [27]. Both reviews come from the same group, and the later one includes the earlier studies. Drinkers differ from nondrinkers in other habits, so confounding is possible.

Claims tested and not found

  1. That light drinking lengthens life. After adjusting for former drinker bias, occasional and low-volume drinkers had no lower death than lifetime nondrinkers across 107 cohorts [3].
  2. That moderate drinking protects against stroke. Genetically predicted intake showed no protective dip and a steady rise in stroke risk in 161,498 Chinese adults [7].
  3. That a nightcap improves sleep. Pooled studies found faster sleep onset only at about five drinks, REM sleep reduced from about two, and no clear effect on total sleep [10].
  4. That light drinking carries no cancer risk. Up to one drink a day was linked to higher risk of breast, oropharyngeal and esophageal cancer [13].

Sources

  1. US Department of Agriculture and US Department of Health and Human Services. Dietary Guidelines for Americans, 2025-2030. realfood.gov. 2026. https://cdn.realfood.gov/DGA.pdf
  2. Ronksley PE, Brien SE, Turner BJ, et al. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. 2011. https://doi.org/10.1136/bmj.d671
  3. Zhao J, Stockwell T, Naimi T, et al. Association Between Daily Alcohol Intake and Risk of All-Cause Mortality: A Systematic Review and Meta-analyses. JAMA Network Open. 2023. https://doi.org/10.1001/jamanetworkopen.2023.6185
  4. Wood AM, Kaptoge S, Butterworth AS, et al. Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies. The Lancet. 2018. https://doi.org/10.1016/s0140-6736(18)30134-x
  5. GBD 2020 Alcohol Collaborators. Population-level risks of alcohol consumption by amount, geography, age, sex, and year: a systematic analysis for the Global Burden of Disease Study 2020. The Lancet. 2022. https://doi.org/10.1016/s0140-6736(22)00847-9
  6. Biddinger KJ, Emdin CA, Haas ME, et al. Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease. JAMA Network Open. 2022. https://doi.org/10.1001/jamanetworkopen.2022.3849
  7. Millwood IY, Walters RG, Mei XW, et al. Conventional and genetic evidence on alcohol and vascular disease aetiology: a prospective study of 500 000 men and women in China. The Lancet. 2019. https://doi.org/10.1016/s0140-6736(18)31772-0
  8. Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. BMJ. 2014. https://doi.org/10.1136/bmj.g4164
  9. Brien SE, Ronksley PE, Turner BJ, et al. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011. https://doi.org/10.1136/bmj.d636
  10. Gardiner C, Weakley J, Burke LM, et al. The effect of alcohol on subsequent sleep in healthy adults: A systematic review and meta-analysis. Sleep Medicine Reviews. 2025. https://doi.org/10.1016/j.smrv.2024.102030
  11. Roerecke M, Kaczorowski J, Tobe SW, et al. The effect of a reduction in alcohol consumption on blood pressure: a systematic review and meta-analysis. The Lancet Public Health. 2017. https://doi.org/10.1016/s2468-2667(17)30003-8
  12. Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol Abstinence in Drinkers with Atrial Fibrillation. The New England Journal of Medicine. 2020. https://doi.org/10.1056/nejmoa1817591
  13. Bagnardi V, Rota M, Botteri E, et al. Light alcohol drinking and cancer: a meta-analysis. Annals of Oncology. 2013. https://doi.org/10.1093/annonc/mds337
  14. Tasnim S, Tang C, Musini VM, Wright JM. Effect of alcohol on blood pressure. Cochrane Database of Systematic Reviews. 2020. https://doi.org/10.1002/14651858.cd012787.pub2
  15. Bagnardi V, Rota M, Botteri E, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. British Journal of Cancer. 2015. https://doi.org/10.1038/bjc.2014.579
  16. Roerecke M, Vafaei A, Hasan OSM, et al. Alcohol Consumption and Risk of Liver Cirrhosis: A Systematic Review and Meta-Analysis. The American Journal of Gastroenterology. 2019. https://doi.org/10.14309/ajg.0000000000000340
  17. Rehm J, Taylor B, Mohapatra S, et al. Alcohol as a risk factor for liver cirrhosis: a systematic review and meta-analysis. Drug and Alcohol Review. 2010. https://doi.org/10.1111/j.1465-3362.2009.00153.x
  18. Simou E, Britton J, Leonardi-Bee J. Alcohol and the risk of sleep apnoea: a systematic review and meta-analysis. Sleep Medicine. 2018. https://doi.org/10.1016/j.sleep.2017.12.005
  19. van der Schrier R, Roozekrans M, Olofsen E, et al. Influence of Ethanol on Oxycodone-induced Respiratory Depression: A Dose-escalating Study in Young and Elderly Individuals. Anesthesiology. 2017. https://doi.org/10.1097/aln.0000000000001505
  20. Jones CM, Paulozzi LJ, Mack KA. Alcohol involvement in opioid pain reliever and benzodiazepine drug abuse-related emergency department visits and drug-related deaths, United States, 2010. MMWR Morbidity and Mortality Weekly Report. 2014. https://pubmed.ncbi.nlm.nih.gov/25299603/
  21. Tori ME, Larochelle MR, Naimi TS. Alcohol or Benzodiazepine Co-involvement With Opioid Overdose Deaths in the United States, 1999-2017. JAMA Network Open. 2020. https://doi.org/10.1001/jamanetworkopen.2020.2361
  22. Weathermon R, Crabb DW. Alcohol and medication interactions. Alcohol Research and Health. 1999. https://pubmed.ncbi.nlm.nih.gov/10890797/
  23. US Food and Drug Administration. Over-the-counter drug products containing internal analgesic/antipyretic active ingredients; required warnings and other labeling. Code of Federal Regulations, 21 CFR 201.326. https://www.ecfr.gov/current/title-21/chapter-I/subchapter-C/part-201/subpart-G/section-201.326
  24. Roth JA, Bradley K, Thummel KE, et al. Alcohol misuse, genetics, and major bleeding among warfarin therapy patients in a community setting. Pharmacoepidemiology and Drug Safety. 2015. https://doi.org/10.1002/pds.3769
  25. Yamagishi H, Sekiguchi N, Hirano A, et al. Metformin-associated Lactic Acidosis Induced by Excessive Alcohol Consumption. Internal Medicine. 2024. https://doi.org/10.2169/internalmedicine.2707-23
  26. Breslow RA, Dong C, White A. Prevalence of alcohol-interactive prescription medication use among current drinkers: United States, 1999 to 2010. Alcoholism, Clinical and Experimental Research. 2015. https://doi.org/10.1111/acer.12633
  27. Salmeri N, Cipriani S, Ricci E, et al. A Systematic Review and Meta-analysis on Alcohol Consumption and Uterine Fibroids: An Update from 2017. The Journal of Nutrition. 2026. https://doi.org/10.1016/j.tjnut.2026.101465
  28. Chiaffarino F, Cipriani S, Ricci E, et al. Alcohol consumption and risk of uterine myoma: A systematic review and meta analysis. PLOS ONE. 2017. https://doi.org/10.1371/journal.pone.0188355

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