Clin Mol Hepatol > Volume 29(Suppl); 2023 > Article
Oh, Sohn, and Cho: The effects of moderate alcohol consumption on non-alcoholic fatty liver disease


Non-alcoholic fatty liver disease (NAFLD) is accepted as a counterpart to alcohol-related liver disease because it is defined as hepatic steatosis without excessive use of alcohol. However, the definition of moderate alcohol consumption, as well as whether moderate alcohol consumption is beneficial or detrimental, remains controversial. In this review, the findings of clinical studies to date with high-quality evidence regarding the effects of moderate alcohol consumption in NAFLD patients were compared and summarized.


Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by serial progression from isolated steatosis to steatohepatitis, fibrosis, and cirrhosis [1]. NAFLD is associated with the metabolic conditions of insulin resistance, type 2 diabetes, and obesity [2]. Mirroring the obesity epidemic, the global prevalence of NAFLD among adults is estimated to be 23–25%, and has become a major global concern as a dominant cause of chronic liver disease with increases in obesity and type 2 diabetes [3–5]. In particular, as the proportion of young patients is increasing, the burden of disease is expected to rise, and long-term management strategies are needed [6,7].
NAFLD is defined as hepatic steatosis occurring in over 5% of hepatocytes without excessive use of alcohol, viral hepatitis, or autoimmune liver disease. NAFLD is considered the counterpart of alcohol-related liver disease (ARLD) [8-10]. NAFLD and ARLD share a common pathophysiological basis involving gut dysbiosis and subsequent changes. In addition, single nucleotide polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3), transmembrane 6 superfamily member 2 (TM6SF2), membrane bound O-acyltransferase domain containing 7 (MBOAT7), and 17-β hydroxysteroid dehydrogenase 13 gene (HSD17B13) are significant genetic risk factors for NAFLD and ARLD [11-15]. These two entities are difficult to distinguish because both histologically include a certain degree of steatosis, lobular inflammation, and ballooning [16]. However, NAFLD and ARLD are distinguished by excessive alcohol consumption based on history taking and questionnaires, however, the amount of safe alcohol consumption accepted as “non-alcoholic” is disputed. In previous studies, conflicting evidence on whether moderate alcohol consumption is protec tive or detrimental for development of NAFLD was reported [17,18].
In this review, the clinical results to date on the effects of moderate alcohol consumption in NAFLD patients were compared and summarized.


The effects of alcohol on patients appear over a long period of time, and because randomized control trials are difficult to perform, the effects can only be estimated using observational studies. Several definitions for significant alcohol consumption to date exist (Table 1).
The definition of moderate alcohol consumption adopted by most guidelines and previous studies is <21 units of alcohol per week for males and <14 units of alcohol per week for females. Some researchers adopt other definitions based on their needs [26-28], however, many experts recommend the above definition for comparison and objectivity of studies [29,30]. One unit of alcohol is usually 10 mL of pure alcohol but standard drink definitions vary worldwide from 8–20 g of alcohol [31]. Therefore, the definition used should be confirmed when reviewing previous research.


Although alcohol is a carcinogen with a well-known doserisk relationship [32,33], meta-analyses based on many previous studies have published results that moderate alcohol consumption showed a protective effect against NAFLD (Table 2).
Notably, Sookoian et al. [28] suggested that moderate alcohol consumption is associated with a significant protective effect against NAFLD (Table 2). Body mass index (BMI) was not a statistically significant confounding factor in meta-regression analysis (slope=0.01, P<0.44) but moderate alcohol consumption was more protective in women than men (53% in women, 30% in men). This result was consistent with the odds of having steatohepatitis (odds ratio [OR]=0.501, 95% confidence interval [CI]: 0.340–0.740, P<0.0005, I2=0%) without heterogeneity [28]. Cao et al. [26] showed similar results. In pooled ORs for the prevalence of NAFLD, low- and moderaterisk alcohol consumption consistently showed a protective effect regardless of sex or BMI (≥25 vs. <25). A similar conclusion was presented in a recent meta-analysis. The risk of alcohol consumption in advanced fibrosis in patients with NAFLD was evaluated in recent meta-analyses. In Wijarnpreecha et al. [27] and Wongtrakul et al. [34], moderate alcohol consumption was associated with a lower risk of advanced fibrosis and steatohepatitis with lower-to-intermediate heterogeneity, although their definitions of alcohol consumption differed (Table 2). Furthermore, NAFLD patients with moderate alcohol consumption had a lower mortality risk than lifelong abstainers (hazard ratio [HR]=0.85, 95% CI: 0.75–0.95, I2=64%).
Despite the above results, alcohol consumption does not guarantee a protective effect against the progression of cirrhosis [35-37]. In a large NAFLD cohort study in Korea, patients with low fibrosis-4 index (FIB-4) progressed to intermediate or high FIB-4 with light alcohol drinking (<10 g/day, adjusted HR=1.06, 95% CI: 0.98–1.16) and moderate alcohol drinking (10 to <20 g/day for women, 10 to <30 g/day for men, adjusted HR=1.29, 95% CI: 1.18–1.40) [38]. In a recent NAFLD cohort study, moderate amounts of alcohol intake in NAFLD patients increased the risk of type 2 diabetes and of advanced fibrosis with the synergistic effect of insulin resistance [39,40]. The longitudinal association between moderate use of alcohol (≤2 drinks/day) and histology findings on follow-up liver biopsy more than 1 year apart were evaluated in a previous study; non-drinkers had a greater mean reduction in steatosis grade (0.49 reduction) than moderate drinkers (0.30 reduction, P=0.04) and moderate drinkers had significantly lower odds of steatohepatitis resolution compared with nondrinkers (adjusted OR=0.32, 95% CI: 0.11–0.92, P=0.04) [41].
Alcohol is also a well-known primary cause for developing hepatocellular carcinoma (HCC) [42,43]. In a previous meta-analysis, the dose-risk curve indicated a linear relationship with the amount of alcohol consumed, estimated excess risk of 46% for 50 g/day and 66% for 100 g/day [44]. Furthermore, in a meta-analysis, the risk of HCC was reported to decrease after alcohol cessation by 6% to 7% a year [45]. In another meta-analysis, Wongtrakul et al. [34] narrowed the analysis target to only NAFLD patients with moderate alcohol consumption, showing a significant HR of 3.77 (95% CI: 1.75–8.15, I2=0%) for developing HCC.
Several disadvantages should be considered when interpreting the conflicting research results discussed above. Previous meta-analyses had several inherent limitations due to the design of the included studies. Almost all studies were cross-sectional in design, thus limiting establishment of causality of the observed factors associated with selection bias and reverse causality issues [46]. Even if the researchers used a well-designed survey tool such as Alcohol Use Disorders Identification Test and Cut, Annoyed, Guilty, and Eye, the results may be associated with recall bias. Population surveys can underestimate alcohol consumption by approximately 40–50% [47]. Drinking patterns as well as quantity can have an effect. For example, binge drinking affects lipid profile and liver function tests and aggravates liver fibrosis compared with non-binge drinking [48,49]. In several studies, moderate alcohol drinkers tended to have higher socio-economic status (SES) and were less obese than lifelong abstainers which may confound the association between alcohol consumption and NAFLD through interference from the interaction between NAFLD and obesity [50,51].


Gut microbiota

Confounding factors may exist that are not identified through history-taking or blood tests in routine clinic visits. In recent studies, consumption of alcohol and alcohol produced by the gut microbiome were shown to affect development of NAFLD. When blood alcohol concentration increases without significant alcohol consumption, autobrewery syndrome can be suspected. Some microbiota, particularly Proteobacteria (especially Klebsiella pneumoniae and Escherichia coli) can ferment dietary sugars into ethanol [52]. Engstler et al [53]. reported that patients with NAFLD, even children, have increased blood ethanol levels due to endogenously produced ethanol. Recently, Yuan et al. [54] found high-alcohol-producing K. pneumoniae (HiAlc Kpn) in the gut microbiome of up to 60% of NAFLD patients. When clinically isolated HiAlc Kpn was transferred into mice via fecal microbiota transplant, the recipient mice were observed to have NAFLD [54]. In another in vivo study using proteome and metabolome analyses, researchers showed that HiAlc Kpn catabolizes carbohydrates via the 2,3-butanediol fermentation pathway and a potential causative agent of NAFLD [55]. Therefore, the fecal microbiome in NAFLD patients should be considered a confounding factor.

Types of alcoholic beverages

Whether beer or wine is safer than liquor or distilled spirits regarding NAFLD has been questioned. The Centers for Disease Control and Prevention (CDC) revealed the amount of alcohol consumed is the most influential factor rather than the type of alcoholic drink [56]. In a cross-sectional study utilizing data from the NHANES III conducted in the United States from 1988 to 1994, suspected NAFLD (alanine transaminase >43 IU/L) was observed in 3.2% and 0.4% among 7,211 nondrinkers and 945 moderate wine drinkers (alcohol consumption <10 g/day), respectively, and the adjusted OR was 0.15 (95% CI: 0.05–0.49) [57]. In a recent study in which the association between fibrosis and type and pattern of alcohol consumption in a biopsy-proven NAFLD cohort was evaluated, moderate (<70 g/week) alcohol consumption, particularly wine in a non-binge manner, was associated with lower fibrosis in NAFLD patients. In an animal study using a NAFLD mouse model fed a high-fat diet, extended-maceration wine improved glucose tolerance and reduced hepatic fat accumulation. Pomace also improved insulin sensitivity and reduced hepatic triglycerides [58].
Recently, a randomized controlled trial was announced to evaluate the effects of beer on human gut microbiota. Marques et al. recruited 22 healthy men in Portugal who were assigned to drink 1 can of alcoholic or non-alcoholic lager each day for 4 weeks. Intestinal microbial diversity improved as determined based on the Shannon index [59], indicating that drinking beer once a day can improve intestinal microbiome diversity regardless of alcohol content. That result is simultaneously consistent and contradictory to previous studies in which the effects of beer on the microbiome were investigated. In a study in Mexico, an increase in gut microbiome diversity, especially the relative abundance of Bacteroidetes, was observed in healthy men and women who consumed 355 mL of non-alcoholic beer a day for 30 days. However, the same improvement was not observed in a separate group who drank 355 mL of beer with 4.9% alcohol content [60]. The above positive effects of fermented alcoholic beverages are presumably due to polyphenols, although additional evidence is needed.


Clinical data have not conclusively proven the effects of moderate alcohol consumption and the amount of safe alcohol consumption for NAFLD patients has not been determined. Moderate alcohol consumption in patients with NAFLD has various effects and conflicting results have been reported. Unregulated factors such as sex, age, ethnicity, obesity, comorbidities, genetic factors, incomplete study design, unclear endpoints, economic and social aspects, and underreporting alcohol use confound the results. Based on the basic medical principle of “first, do no harm”, recommending moderate drinking to NAFLD patients, especially those with comorbid diseases or advanced liver fibrosis, is premature. Additional longitudinal studies are expected to demonstrate the interactions between moderate alcohol consumption, effect of type/pattern of alcohol use, and SES based on NAFLD stage.


Authors’ contribution
HO, WS, and YKC contributed to the design and drafting of the manuscript.
Conflicts of Interest
The authors have no conflicts to disclose.

Table 1.
International definitions of clinically significant alcohol consumption
Organizations Definitions
NIAAA [19] (1 standard drink=14 g) Heavy alcohol use:
Male: >14 standard drinks/week
Female: >7 standard drinks/week
WHO [20] Low risk: Male <40 g/day, Female <20 g/day
Medium risk: Male 40–60 g/day, Female 20–40 g/day
High risk: Male >60 g/day, Female >40 g/day
NICE thresholds for liver cirrhosis assessment [21] Male: 50 units/week, Female: 35 units/week
AASLD [8], AACE [2], AGA [22] Male: >21 standard drinks/week, Female: >14 standard drinks/week (over a 2-year period preceding baseline liver histology)
EASL–EASD–EASO [9] Male: >30 g/day, Female: >20 g/day
EASL patient guideline [23] (1 unit equals 8 g of alcohol) Male: >21 units/week, Female: >14 units/week
APASL [24] Male: two standard drinks per day (i.e., 140 g ethanol per week)
Female: one standard drink per day (i.e., 70 g ethanol per week)
China [25] (during the past 12 months) Male: >210 g/week, Female: >140 g/week
KASL [10] Male: >210 g/week, Female: >140 g/week

NIAAA, National Institute on Alcohol Abuse and Alcoholism; WHO, World Health Organization; NICE, National Institute for Health and Care Excellence; AASLD, American Association for the Study of Liver Diseases; AACE, American Association of Clinical Endocrinology; AGA, American Gastroenterological Association; EASL, European Association for the Study of the Liver; EASD, European Association for the Study of Diabetes; EASO, European Association for the Study of Obesity; APASL, Asian Pacific Association for the Study of the Liver; KASL, Korean Association for the Study of the Liver.

Table 2.
Comparison of previous meta-analyses in which the effects of moderate alcohol consumption in NAFLD patients were assessed
Author Year Search Number of included studies Primary outcome Participants (n) Definition of moderate alcohol consumption Pooled OR (95% CI) Hetero geneity (I2)
Sookoian et al. [28] 2014 Unknown 8 studies NAFLD prevalence 43,175 <40 g/day 0.684 (0.580–0.806) NA
Cao et al. [26] 2016 Without restriction 13 cross-sectional studies, 2 cross-sectional following longitudinal studies, 1 cohort study NAFLD prevalence 76,608 WHO definition Light: 0.76 (0.72–0.80) 66%
Moderate: 0.75 (0.70–0.80) 82.7%
Wijarnpreecha et al. [27] 2021 February 2019 6 cross-sectional studies Prevalence of advanced liver fibrosis 8,936 <28 g/day for males Modest drinkers vs. nondrinkers: 0.51 (0.35–0.75) 47%
<14 g/day for females
Wongtrakul et al. [34] 2021 October 2020 14 cross-sectional or cohort studies Prevalence of steatohepatitis 14,435 210 g/week for males Steatohepatitis: 0.59 (0.45–0.78) 12%
140 g/week for females Advanced fibrosis: 0.59 (0.36–0.95) 75%

OR, odds ratio; CI, confidence interval; NAFLD, non-alcoholic fatty liver disease; WHO, World Health Organization.


non-alcoholic fatty liver disease
alcohol-related liver disease
body mass index
odds ratio
confidence interval
hazard ratio
fibrosis-4 index
hepatocellular carcinoma
socio-economic status
Alcohol Use Disorders Identification Test
HiAlc Kpn
high-alcohol-producing Klebsiella pneumoniae
alanine transaminase


1. Sheka AC, Adeyi O, Thompson J, Hameed B, Crawford PA, Ikramuddin S. Nonalcoholic steatohepatitis: a review. JAMA 2020;323:1175-1183 Erratum in: JAMA 2020;323:1619.
crossref pmid
2. Cusi K, Isaacs S, Barb D, Basu R, Caprio S, Garvey WT, et al. American Association of Clinical Endocrinology Clinical Practice Guideline for the diagnosis and management of nonalcoholic fatty liver disease in primary care and endocrinology clinical settings: Co-Sponsored by the American Association for the Study of Liver Diseases (AASLD). Endocr Pract 2022;28:528-562.
3. Lazarus JV, Mark HE, Anstee QM, Arab JP, Batterham RL, Castera L, et al.; NAFLD Consensus Consortium. Advancing the global public health agenda for NAFLD: a consensus statement. Nat Rev Gastroenterol Hepatol 2022;19:60-78.
4. Le MH, Yeo YH, Zou B, Barnet S, Henry L, Cheung R, et al. Forecasted 2040 global prevalence of nonalcoholic fatty liver disease using hierarchical bayesian approach. Clin Mol Hepatol 2022;28:841-850.
crossref pmid pmc pdf
5. Ng CH, Chan KE, Chin YH, Zeng RW, Tsai PC, Lim WH, et al. The effect of diabetes and prediabetes on the prevalence, complications and mortality in nonalcoholic fatty liver disease. Clin Mol Hepatol 2022;28:565-574.
crossref pmid pmc pdf
6. Paik JM, Golabi P, Younossi Y, Saleh N, Nhyira A, Younossi ZM. The growing burden of disability related to chronic liver disease in the United States: data from the global burden of disease study 2007-2017. Hepatol Commun 2021;5:749-759.
crossref pmid pmc pdf
7. Lee J, Kim T, Yang H, Bae SH. Prevalence trends of non-alcoholic fatty liver disease among young men in Korea: A Korean military population-based cross-sectional study. Clin Mol Hepatol 2022;28:196-206.
crossref pmid pmc pdf
8. Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology 2018;67:328-357.
crossref pmid pdf
9. European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol 2016;64:1388-1402.
crossref pmid
10. Kang SH, Lee HW, Yoo JJ, Cho Y, Kim SU, Lee TH, et al.; Korean Association for the Study of the Liver (KASL). KASL clinical practice guidelines: management of nonalcoholic fatty liver disease. Clin Mol Hepatol 2021;27:363-401.
crossref pmid pmc pdf
11. Ikejima K, Kon K, Yamashina S. Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights. Clin Mol Hepatol 2020;26:728-735.
crossref pmid pmc pdf
12. Pirola CJ, Sookoian S. Personalized medicine in nonalcoholic fatty liver disease. Clin Mol Hepatol 2022;28:935-938.
crossref pmid pmc pdf
13. Sookoian S, Pirola CJ. Genetics in non-alcoholic fatty liver disease: The role of risk alleles through the lens of immune response. Clin Mol Hepatol 2022 Dec 5;doi: 10.3350/cmh.2022.0318.
14. Kawaguchi T, Tsutsumi T, Nakano D, Eslam M, George J, Torimura T. MAFLD enhances clinical practice for liver disease in the Asia-Pacific region. Clin Mol Hepatol 2022;28:150-163.
crossref pmid pdf
15. Kim HY. Recent advances in nonalcoholic fatty liver disease metabolomics. Clin Mol Hepatol 2021;27:553-559.
crossref pmid pmc pdf
16. Ntandja Wandji LC, Gnemmi V, Mathurin P, Louvet A. Combined alcoholic and non-alcoholic steatohepatitis. JHEP Rep 2020;2:100101.
crossref pmid pmc
17. Choi JH, Sohn W, Cho YK. The effect of moderate alcohol drinking in nonalcoholic fatty liver disease. Clin Mol Hepatol 2020;26:662-669.
crossref pmid pmc pdf
18. Kwon I, Jun DW, Moon JH. Effects of moderate alcohol drinking in patients with nonalcoholic fatty liver disease. Gut Liver 2019;13:308-314.
crossref pmid
19. National Institute on Alcohol Abuse and Alcoholism (NIAAA). Drinking Levels Defined. NIAAA web site, <>. Accessed 31 Oct 2022.

20. World health organization (WHO). International Guide for Monitoring Alcohol Consumption and Related Harm. WHO web site, <>. Accessed 31 Oct 2022.

21. National Institute for Health and Care Excellence (NICE). Cirrhosis in over 16s: assessment and management. NICE web site, <>. Accessed 31 Oct 2022.

22. Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, et al.; American Gastroenterological Association; American Association for the Study of Liver Diseases; American College of Gastroenterologyh. The diagnosis and management of nonalcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology 2012;142:1592-1609 Erratum in: Gastroenterology 2012;143:503.
crossref pmid
23. Francque SM, Marchesini G, Kautz A, Walmsley M, Dorner R, Lazarus JV, et al. Non-alcoholic fatty liver disease: a patient guideline. JHEP Rep 2021;3:100322.
crossref pmid pmc
24. Wong VW, Chan WK, Chitturi S, Chawla Y, Dan YY, Duseja A, et al. Asia-Pacific Working Party on Non-alcoholic Fatty Liver Disease guidelines 2017-Part 1: Definition, risk factors and assessment. J Gastroenterol Hepatol 2018;33:70-85.
crossref pmid pdf
25. Fan JG, Wei L, Zhuang H; National Workshop on Fatty Liver and Alcoholic Liver Disease, Chinese Society of Hepatology, Chinese Medical Association; Fatty Liver Disease Expert Committee, Chinese Medical Doctor Association. Guidelines of prevention and treatment of nonalcoholic fatty liver disease (2018, China). J Dig Dis 2019;20:163-173.
crossref pdf
26. Cao G, Yi T, Liu Q, Wang M, Tang S. Alcohol consumption and risk of fatty liver disease: a meta-analysis. PeerJ 2016;4:e2633.
crossref pmid pmc pdf
27. Wijarnpreecha K, Aby ES, Panjawatanan P, Lapumnuaypol K, Cheungpasitporn W, Lukens FJ, et al. Modest alcohol consumption and risk of advanced liver fibrosis in nonalcoholic fatty liver disease: a systematic review and meta-analysis. Ann Gastroenterol 2021;34:568-574.
crossref pmid pmc
28. Sookoian S, Castaño GO, Pirola CJ. Modest alcohol consumption decreases the risk of non-alcoholic fatty liver disease: a metaanalysis of 43 175 individuals. Gut 2014;63:530-532.
crossref pmid
29. Aller R, Fernández-Rodríguez C, Lo Iacono O, Bañares R, Abad J, Carrión JA, et al. [Consensus document. Management of nonalcoholic fatty liver disease (NAFLD). Clinical practice guideline]. Gastroenterol Hepatol 2018;41:328-349. Spanish. Erratum in: Gastroenterol Hepatol 2018;41:475-476.

30. Sanyal AJ, Brunt EM, Kleiner DE, Kowdley KV, Chalasani N, Lavine JE, et al. Endpoints and clinical trial design for nonalcoholic steatohepatitis. Hepatology 2011;54:344-353.
crossref pmid
31. Alcohol Research: Current Reviews Editorial Staff. Drinking patterns and their definitions. Alcohol Res 2018;39:17-18.
pmid pmc
32. Bagnardi V, Rota M, Botteri E, Tramacere I, Islami F, Fedirko V, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer 2015;112:580-593.
crossref pmid pdf
33. Cao Y, Willett WC, Rimm EB, Stampfer MJ, Giovannucci EL. Light to moderate intake of alcohol, drinking patterns, and risk of cancer: results from two prospective US cohort studies. BMJ 2015;351:h4238.
crossref pmid pmc
34. Wongtrakul W, Niltwat S, Charatcharoenwitthaya P. The effects of modest alcohol consumption on non-alcoholic fatty liver disease: a systematic review and meta-analysis. Front Med (Lausanne) 2021;8:744713.
crossref pmid pmc
35. Rehm J, Taylor B, Mohapatra S, Irving H, Baliunas D, Patra J, et al. Alcohol as a risk factor for liver cirrhosis: a systematic review and meta-analysis. Drug Alcohol Rev 2010;29:437-445.
crossref pmid
36. Corrao G, Bagnardi V, Zambon A, Torchio P. Meta-analysis of alcohol intake in relation to risk of liver cirrhosis. Alcohol Alcohol 1998;33:381-392.
crossref pmid
37. Roerecke M, Vafaei A, Hasan OSM, Chrystoja BR, Cruz M, Lee R, et al. Alcohol consumption and risk of liver cirrhosis: a systematic review and meta-analysis. Am J Gastroenterol 2019;114:1574-1586.
crossref pmid pmc
38. Chang Y, Cho YK, Kim Y, Sung E, Ahn J, Jung HS, et al. Nonheavy drinking and worsening of noninvasive fibrosis markers in nonalcoholic fatty liver disease: a cohort study. Hepatology 2019;69:64-75.
crossref pmid pdf
39. Xu L, Xie J, Chen S, Chen Y, Yang H, Miao M, et al. Light-tomoderate alcohol consumption is associated with increased risk of type 2 diabetes in individuals with nonalcoholic fatty liver disease: a nine-year cohort study. Am J Gastroenterol 2020;115:876-884.
crossref pmid
40. Blomdahl J, Nasr P, Ekstedt M, Kechagias S. Moderate alcohol consumption is associated with advanced fibrosis in nonalcoholic fatty liver disease and shows a synergistic effect with type 2 diabetes mellitus. Metabolism 2021;115:154439.
crossref pmid
41. Ajmera V, Belt P, Wilson LA, Gill RM, Loomba R, Kleiner DE, et al.; Nonalcoholic Steatohepatitis Clinical Research Network. Among patients with nonalcoholic fatty liver disease, modest alcohol use is associated with less improvement in histologic steatosis and steatohepatitis. Clin Gastroenterol Hepatol 2018;16:1511-1520.e5.
crossref pmid pmc
42. Taniai M. Alcohol and hepatocarcinogenesis. Clin Mol Hepatol 2020;26:736-741.
crossref pmid pmc pdf
43. Huang DQ, Tan DJH, Ng CH, Amangurbanova M, Sutter N, Lin Tay PW, et al. Hepatocellular carcinoma incidence in alcohol-associated cirrhosis: systematic review and metaanalysis. Clin Gastroenterol Hepatol 2022 Aug 5;doi: 10.1016/j.cgh.2022.06.032.
44. Turati F, Galeone C, Rota M, Pelucchi C, Negri E, Bagnardi V, et al. Alcohol and liver cancer: a systematic review and meta-analysis of prospective studies. Ann Oncol 2014;25:1526-1535.
crossref pmid
45. Heckley GA, Jarl J, Asamoah BO, G-Gerdtham U. How the risk of liver cancer changes after alcohol cessation: a review and metaanalysis of the current literature. BMC Cancer 2011;11:446.
crossref pmid pmc pdf
46. Savitz DA, Wellenius GA. Can Cross-Sectional Studies Contribute to Causal Inference? It Depends. Am J Epidemiol 2022 Mar 1;doi: 10.1093/aje/kwac037.
crossref pdf
47. Livingston M, Callinan S. Underreporting in alcohol surveys: whose drinking is underestimated? J Stud Alcohol Drugs 2015;76:158-164.
crossref pmid
48. Rosoff DB, Charlet K, Jung J, Lee J, Muench C, Luo A, et al. Association of high-intensity binge drinking with lipid and liver function enzyme levels. JAMA Netw Open 2019;2:e195844.
crossref pmid pmc
49. Mitchell T, Jeffrey GP, de Boer B, MacQuillan G, Garas G, Ching H, et al. Type and pattern of alcohol consumption is associated with liver fibrosis in patients with non-alcoholic fatty liver disease. Am J Gastroenterol 2018;113:1484-1493.
crossref pmid pdf
50. Liu YT, Lee JH, Tsai MK, Wei JC, Wen CP. The effects of modest drinking on life expectancy and mortality risks: a populationbased cohort study. Sci Rep 2022;12:7476.
crossref pmid pmc pdf
51. Kim BY, Nam H, Yoo JJ, Cho YY, Choi DH, Jung CH, et al. Association between alcohol consumption status and obesity-related comorbidities in men: data from the 2016 Korean community health survey. BMC Public Health 2021;21:733.
crossref pmid pmc pdf
52. Zhu L, Baker SS, Gill C, Liu W, Alkhouri R, Baker RD, et al. Characterization of gut microbiomes in nonalcoholic steatohepatitis (NASH) patients: a connection between endogenous alcohol and NASH. Hepatology 2013;57:601-609.
crossref pmid
53. Engstler AJ, Aumiller T, Degen C, Dürr M, Weiss E, Maier IB, et al. Insulin resistance alters hepatic ethanol metabolism: studies in mice and children with non-alcoholic fatty liver disease. Gut 2016;65:1564-1571.
crossref pmid
54. Yuan J, Chen C, Cui J, Lu J, Yan C, Wei X, et al. Fatty liver disease caused by high-alcohol-producing Klebsiella pneumoniae. Cell Metab 2019;30:675-688.e7 Erratum in: Cell Metab 2019;30:1172.
crossref pmid
55. Li NN, Li W, Feng JX, Zhang WW, Zhang R, Du SH, et al. High alcohol-producing Klebsiella pneumoniae causes fatty liver disease through 2,3-butanediol fermentation pathway in vivo. Gut Microbes 2021;13:1979883.
crossref pmid pmc
56. Centers for Disease Control and Prevention (CDC). Alcohol and Public Health. CDC web site, <>. Accessed 31 Oct 2022.

57. Dunn W, Xu R, Schwimmer JB. Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease. Hepatology 2008;47:1947-1954.
crossref pmid
58. Rosenzweig T, Skalka N, Rozenberg K, Elyasiyan U, Pinkus A, Green B, et al. Red wine and wine pomace reduced the development of insulin resistance and liver steatosis in HFD-fed mice. J Funct Foods 2017;34:379-389.
59. Marques C, Dinis L, Barreiros Mota I, Morais J, Ismael S, PereiraLeal JB, et al. Impact of beer and nonalcoholic beer consumption on the gut microbiota: a randomized, double-blind, controlled trial. J Agric Food Chem 2022;70:13062-13070.
crossref pmid pmc pdf
60. Hernández-Quiroz F, Nirmalkar K, Villalobos-Flores LE, Murugesan S, Cruz-Narváez Y, Rico-Arzate E, et al. Influence of moderate beer consumption on human gut microbiota and its impact on fasting glucose and β-cell function. Alcohol 2020;85:77-94.
crossref pmid

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