US Mortality from Liver Cirrhosis and Alcoholic Liver Disease in 1999–2004: Regional and State Variation in Relation to Per Capita Alcohol Consumption

Apparent per-capita alcohol consumption in 2001 in four US regions (West, Northeast, South, and Midwest), and in 50 states was examined in relation to mortality rates (1999–2004) from liver cirrhosis and for the subcategory alcoholic liver disease. Alcohol consumption and mortality rates were highest in the west. The alcoholic liver disease mortality rate by state was strongly correlated with alcohol consumption, but several outlier or mismatch states were identified. Per-capita alcohol consumption should be useful for US public health policy, as suggested for Europe and Canada, but outlier states require further study.     

The direct and indirect relationships between alcohol prevention measures and alcoholic liver cirrhosis mortality

OBJECTIVE: The objective of this article is to investigate direct and indirect relationships between prevention measures and alcoholic liver cirrhosis mortality in Canadian provinces from 1968 to 1986. METHOD: The data base that was assembled included alcoholic cirrhosis mortality rates, alcohol availability measures (rate of licensed premises, year in which the legal drinking age was reduced), per capita consumption of alcohol, rates of AA members and groups, and economic and demographic measures. This article develops a two-equation analytic model based on the availability theory of alcohol problems and prevention (Single, 1988). The distinction between direct and indirect effects of prevention measures can be made explicitly with this model. RESULTS: Alcohol availability measures, but not AA measures, had a significant direct potential impact on alcohol consumption. AA measures had a significant direct relationship to cirrhosis mortality rates. Alcohol consumption also had a significant direct relationship to cirrhosis mortality, and alcohol availability measures had an important indirect relationship through their influence on per capita alcohol consumption. CONCLUSIONS: While these observations need to be interpreted cautiously, the two-equation model shows promise as an approach to understanding direct and indirect influences on alcohol problems. As expected, AA measures and per capita alcohol consumption demonstrated significant direct relationship to cirrhosis mortality. In addition, important indirect influences of drinking-age changes and rates of licensed premises on cirrhosis mortality were observed through their relationships to per capita alcohol consumption.     

Review article: alcoholic liver disease--pathophysiological aspects and risk factors

BACKGROUND: Alcoholic liver disease has a known aetiology but a complex and incompletely known pathogenesis. It is an extremely common disease with significant morbidity and mortality, but the reason why only a relatively small proportion of heavy drinkers progress to advanced disease remains elusive. AIM: To recognize the factors responsible for the development and progression of alcoholic liver disease, in the light of current knowledge on this matter. METHODS: We performed a structured literature review identifying studies focusing on the complex pathogenetic pathway and risk factors of alcoholic liver disease. Results In addition to the cumulative amount of alcohol intake and alcohol consumption patterns, factors such as gender and ethnicity, genetic background, nutritional factors, energy metabolism abnormalities, oxidative stress, immunological mechanisms and hepatic co-morbid conditions play a key role in the genesis and progression of alcoholic liver injury. CONCLUSIONS: Understanding the pathogenesis and risk factors of alcoholic liver disease should provide insight into the development of therapeutic strategies.     

Chronic ethanol abuse and membrane fluidity changes in liver disease.

The long-term effect of ethanol on human red cell membrane fluidity was studied, by fluorescence polarization with 1,6-diphenyl-1,3,5-hexatriene as a probe, in 11 healthy subjects, 9 chronic alcoholics without evidence of liver disease, 12 chronic alcoholics with biopsy-proven alcoholic liver disease and 9 abstemious patients with chronic active liver disease, most of them cirrhosis of the liver. Fluorescence polarization values were not significantly different in the two groups without liver disease. Patients with alcoholic and non-alcoholic liver disease showed higher fluorescence polarization values than patients without liver disease. These changes correlated with the severity of liver dysfunction and were not related to alcohol consumption. In conclusion, the decrease in fluidity of the erythrocyte membrane in alcoholic patients with chronic liver disease, is related to liver dysfunction but not to chronic ethanol ingestion. Changes in membrane fluidity in chronic alcoholics are found only in the presence of liver disease.     

Effects of Alcoholic Beverage Control Policies and Contextual Factors on Alcohol Consumption and its Related Harms in France From 1960 to 2000

Important social changes such as urbanization, increases in female education and employment, and increased incomes have occurred in France from 1960 to 2000 along with a major decrease in alcoholic beverage consumption (from 25 L pure alcohol per inhabitant 15 years and old to 13 L); especially due to wine consumption decrease. These changes in drinking patterns are associated with significant decreases in alcohol consumption-related harms (liver disease mortality and transport accident mortality). Several alcoholic beverage consumption control policy measures were also created during this period. This study explores the impact of these policies measure on alcohol consumption and alcohol consumption-related harms, adjusted with selected social changes. France's control policy has been associated, partially, with regressive effects on alcohol consumption but not on alcohol consumption-related harms. Study limitations are noted.     

Alcohol dehydrogenase: an autoantibody target in patients with alcoholic liver disease

The link between alcohol consumption and liver disease is not direct and several factors including autoimmunity to hepatocyte components have been implicated. We have previously identified alcohol dehydrogenase (ADH) as an autoantigen in autoimmune liver disease and in a proportion of patients with alcoholic liver disease. The aim of the present study is to investigate the association between the presence of anti-ADH antibodies, alcohol consumption and severity of liver damage in alcoholic patients. The presence of antibodies to human ADH beta2 and horse ADH was investigated in 108 patients with documented history of alcohol consumption and alcohol related liver disease, 86 being active alcohol abusers and 22 on sustained alcohol withdrawal, 39 with non-alcohol related disease and 22 normal subjects. Antibodies to either ADH form were more frequently detected in active alcohol abusers (55/86, 64%) than in patients on sustained alcohol withdrawal longer than 6 months (1/8, 13 %, P < 0.005), HBV infection (2/8, 25 %, P=0.03), non-alcohol related disease (9/29, 23 %, P < 0.0001) and in normal controls (3/22, 14 %, P < 0.0001); were more frequent in patients with cirrhosis than in those with steatosis (26/34, 76 % vs 34/64, 53 %, P=0.02); and were associated with elevated levels of ALT (anti-ADH beta2, P < 0.05), immunoglobulin A (P < 0.05) and gamma-glutamyl transpeptidase (P=0.01). Anti-ADH antibody positive serum samples were able to inhibit the enzymatic activity of ADH. These findings suggest that anti-ADH antibodies may be triggered by alcohol consumption and act as a disease activity marker in alcoholic liver disease.     

Alcoholic liver diseases and hepatitis virus C in Japan]

Recently incidence of alcoholic liver disease (ALD) has been increasing in Japan associated with an increase in alcoholic beverage consumption. There have been a large number of reports about the relationship between alcohol and hepatocarcinogenesis, but it remains controversial. In the present study, we addressed the recent trend in incidence of ALD including liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in heavy drinkers in Japan. We carried out nation-wide survey by asking for the hospitals that are approved by the Japanese Society of Gastroenterology for recent aspects of in-patients with ALD. Except for HCC, percentage of ALD without viral hepatitis is more than 70%, which is increased when compared to the national survey carried out in 1992. In alcoholic LC patients, those who did not have viral hepatitis were 81%. However, the percentage of HCC without viral hepatitis was 34% of all of the heavy drinkers with HCC. Regarding the case in our university hospital, 138 cases (32%) of 432 patients with HCC were heavy drinkers. However, regarding in our general hospital, 15 cases of 23 patients with HCC (61%) were heavy drinkers. In conclusion, since the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers.     

Review article: Nutritional therapy in alcoholic liver disease

Chronic alcohol consumption may lead to primary and secondary malnutrition. In particular, protein energy malnutrition not only aggravates alcoholic liver disease but also correlates with impaired liver function and increased mortality. Therefore, in these patients, adequate nutritional support should be implemented in order to improve their prognosis. Clinical trials addressing this issue have shown that nutritional therapy either enterally or parenterally improves various aspects of malnutrition, and there is increasing evidence that it may also improve survival. Therefore, malnourished alcoholics should be administered a diet rich in carbohydrate- and protein-derived calories preferentially via the oral or enteral route. Micronutrient deficiencies typically encountered in alcoholics, such as for thiamine and folate, require specific supplementation. Patients with hepatic encephalopathy may be treated with branched-chain amino acids in order to achieve a positive nitrogen balance. Fatty liver represents the early stage of alcoholic liver disease, which is usually reversible with abstinence. Metadoxine appears to improve fatty liver but confirmatory studies are necessary. S-adenosyl-L-methionine may be helpful for patients with severe alcoholic liver damage, since various mechanisms of alcohol-related hepatotoxicity are counteracted with this essential methyl group donor, while a recent large trial showed that the use of polyenylphosphatidylcholine is of limited efficacy.     

酒精性脂肪肝脂质代谢研究进展

酒精性脂肪肝(AFL)是长期大量饮用酒精引发的肝脏损害性病变,可逆转也可进一步发展为肝纤维化和肝硬化。众多的脂肪细胞因子如瘦素(Leptin)、抵抗素(Resistin)和肿瘤坏死因子-α(TNF-α)在脂肪肝的发病中起到一定的促进作用,脂联素(Adiponectin)能改善脂质代谢,延缓脂肪肝的发生;脂联素通过腺苷酸活化蛋白激酶(AMPK)调节糖脂代谢、改善胰岛素敏感性。脂联素/AMPK信号通路是酒精在肝脏的作用靶点、也是调节PPARγ作用的重要信号通路;脂肪分化相关蛋白(ADRP)调节脂质代谢、促进酒精性脂肪肝的形成;过氧化物酶增殖体激活受体γ(PPARγ)参与机体脂质稳态的调节,脂肪肝时PPARγ表达增高,肝纤维化时PPARγ表达减少。对酒精性脂肪肝脂质代谢的深入研究,有助于阐明酒精性脂肪肝发病机制并为临床防治ALD及脂质代谢相关疾病提供新策略。     

Increasing socioeconomic inequalities in male cirrhosis of the liver mortality: Australia 1981-2002

Liver cirrhosis mortality is an indicator of harms associated with high levels of alcohol consumption. There is good evidence that changes in political and economic systems can lead to changing patterns of liver cirrhosis mortality. Socioeconomic inequalities in liver cirrhosis mortality have been periodically reported but there are few studies of changes in socioeconomic inequalities in liver cirrhosis mortality over time. This paper examines changes in socioeconomic inequalities in liver cirrhosis mortality in Australia for the period 1981 - 2002. Age standardised, liver cirrhosis mortality rates were calculated for occupational groupings for Australia 1981 - 2002. Occupations were grouped into non-manual and manual categories, and there was imputation for missing data. Despite decreasing overall liver cirrhosis mortality rates over time, liver cirrhosis mortality continues to account for about 3% of all deaths. Manual workers have consistently experienced liver cirrhosis mortality rates which are twice or more the rate experienced by non-manual workers. These inequalities appear to have increased in recent years and currently appear to be at historic highs (manual workers have mortality rates of about 2.5 times those of non-manual workers). Increasing socioeconomic inequalities in liver cirrhosis mortality in Australia suggest that lower SES groups have, over time, increased their level of harmful alcohol consumption relative to middle and higher SES groups. It is suggested that this might be attributed to a relative improvement in the affordability of alcohol over time. [Najman JM, Williams GM, Room R. Increasing socioeconomic inequalities in male cirrhosis of the liver mortality: Australia 1981 - 2002. Drug Alcohol Rev 2007;26:]     

酒精性骨质疏松症和酒精性肝病的相关性研究

目的　探讨酒精性骨质疏松和酒精性肝病的关系及其发病机制。方法　回顾性研究2016年3月至2020年12月内蒙古科技大学包头医学院第二附属医院及第一附属医院收治的122例饮酒超过5年，折合乙醇量男性≥40 g/d，女性≥20 g/d的患者为研究对象，男82例，女40例，年龄（40.0±14.6）岁。所有患者测量骨密度，检测肝功能、骨钙素、25-羟基维生素D［25（OH）D3］、肿瘤坏死因子α（TNF-α）及肝脏彩超检查。根据骨密度检查结果、肝功能检测结果及腹部彩超分为3组，酒精性骨质疏松症组35例、酒精性肝病组45例、酒精性肝病合并骨质疏松症组42例。选择同期性别及年龄相匹配的体检健康者45例纳入健康对照组。采用SPSS 24.0进行数据分析，计量资料行t检验。结果　酒精性骨质疏松组、酒精性肝病组、酒精性肝病伴骨质疏松组的骨钙素分别为（24.73±3.66）μg/L、（27.34±2.94）μg/L、（17.44±3.09）μg/L，25（OH）D3分别为（22.47±2.82）μg/L、（25.63±3.84）μg/L、（16.87±4.33）μg/L，均不同程度地低于健康对照组［分别为（32.65±3.27）μg/L、（30.21±4.22）μg/L］，酒精性肝病伴骨质疏松组骨钙素、25（OH）D3均低于酒精性骨质疏松组和酒精性肝病组，差异均有统计学意义（均P<0.05），酒精性骨质疏松组骨钙素、25（OH）D3低于酒精性肝病组，但是差异均无统计学意义（均P>0.05）。酒精性骨质疏松组、酒精性肝病组、酒精性肝病伴骨质疏松组TNF-α分别为（10.33±3.41）pg/ml、（13.23±4.02）pg/ml、（16.94±3.92）pg/ml，均不同程度地高于健康对照组［（5.54±2.39）pg/ml］，酒精性肝病伴骨质疏松组高于酒精性骨质疏松组和酒精性肝病组，酒精性骨质疏松组低于酒精性肝病组，差异均统计学意义（均P<0.05）。结论　我们考虑酒精性肝病、酒精性骨质疏松在发病过程中呈相辅相成作用。骨钙素、25（OH）D3、TNF-α可能为其共同的发病机理，其既是发病的始动因素，又是其导致的结果。     

Alcoholic liver diseases in Japan and modification by hepatitis virus]

Recently incidence of alcoholic liver disease (ALD) has been increasing in Japan associated with an increase in alcoholic beverage consumption. There have been a large number of reports about the relationship between alcohol and hepatocarcinogenesis, but it remains controversial. In this review, we addressed 1) the recent trend in incidence of ALD including severe alcoholic hepatitis (SAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in heavy drinkers in Japan, and 2) the characteristics of HCC in heavy drinkers with negative serum markers for viral hepatitis. We carried out nation-wide survey by asking for the hospitals that are approved by the Japanese Society of Gastroenterology for recent aspects of in-patients with ALD. Except for HCC, percentage of ALD without viral hepatitis is more than 70%, which is increased when compared to the national survey carried out in 1992. Percentage of alcoholic LC without positive markers for viral hepatitis was 61% and alcohol plus virus group was 39%. Furthermore, in alcoholic LC patients without HCC, those who did not have viral hepatitis were 80%. However, the percentage of HCC without viral hepatitis was 27% of all of the heavy drinkers with HCC. Regarding our own cases, subjects were 432 HCC patients who were admitted to our hospital since 1995. There were 296 cases (68.5%) of HCV-positive, 70 cases (16.2%) of HBV-positive, 27 cases (6.3%) of both HCV- and HBV-positive. Thirty-nine cases (6.7%) were negative for serum markers for viral hepatitis. Among them, 13 cases (3.0%) were not heavy drinkers (non-B, non-C, non-alcohol) and 26 cases (6.0%) were heavy drinkers (non-B, non-C, heavy drinkers). Twenty-five of these 26 (96.2%) cases had cirrhosis. In conclusion, since the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers. Radiographic examinations at an appropriate interval for HCC are recommended, even in cases with alcoholic liver cirrhosis who are negative for serum markers of viral hepatitis, to ensure the early diagnosis of HCC.     

The impact of alcohol taxation on liver cirrhosis mortality

OBJECTIVE: The objective of this study is to investigate the impact of distilled spirits, wine, and beer taxes on cirrhosis mortality using a large-panel data set and statistical models that control for various other factors that may affect that mortality. METHOD: The analyses were performed on a panel of 30 U.S. license states during the period 1971-1998 (N = 840 state-by-year observations). Exogenous measures included current and lagged versions of beverage taxes and income, as well as controls for states' age distribution, religion, race, health care availability, urbanity, tourism, and local bans on alcohol sales. Regression analyses were performed using random-effects models with corrections for serial autocorrelation and heteroscedasticity among states. RESULTS: Cirrhosis rates were found to be significantly related to taxes on distilled spirits but not to taxation of wine and beer. Consistent results were found using different statistical models and model specifications. CONCLUSIONS: Consistent with prior research, cirrhosis mortality in the United States appears more closely linked to consumption of distilled spirits than to that of other alcoholic beverages.     

Disposition of bupropion in healthy volunteers and subjects with alcoholic liver disease

Bupropion hydrochloride is a new monocyclic antidepressant. In humans, its disposition results in the formation of three major metabolites: the morpholinol metabolite, the erythroamino alcohol, and the threoamino alcohol metabolite. Bupropion's disposition was monitored following a single oral 200 mg dose in eight healthy volunteers and eight age- (44.5 +/- 8.4 years) and weight- (77.4 +/- 6.7 kg) matched volunteers with alcoholic liver disease. This latter group is of interest because the incidence of depression is more frequent in alcoholics than in the general population, and the liver is the major route of elimination for cyclic antidepressants. The mean elimination half-life of the morpholinol metabolite was significantly prolonged in subjects with alcoholic liver disease (32.2 +/- 13.5 vs. 21.1 +/- 4.9 hours (p less than 0.05), while the differences in bupropion (17.3 +/- 8.6 hours vs. 16.5 +/- 10.4 hours for healthy subjects and subjects with alcoholic liver disease, respectively), erythroamino alcohol (26.1 +/- 13.3 hours vs. 29.8 +/- 6.9 hours for healthy subjects and subjects with alcoholic liver disease, respectively), and threoamino alcohol (25.5 +/- 8.6 hours vs. 23.4 +/- 10.7 hours for healthy subjects and subjects with alcoholic liver disease, respectively) were minimal. Mean area under the plasma concentration time curves for bupropion and metabolites were increased in subjects with alcoholic liver disease; however, clear differences between means of these small groups did not emerge, probably due to the increased variability of bupropion pharmacokinetics in these subjects. As a therapeutic agent for the treatment of depression in chronic alcoholics who may consume alcohol in combination with their antidepressant therapy, the lack of sedation with bupropion could be advantageous.(ABSTRACT TRUNCATED AT 250 WORDS)     

Berberine protects liver from ethanol-induced oxidative stress and steatosis in mice

Alcohol consumption is customary in many cultures and it is a common human behavior worldwide. Binge ethanol and chronic alcohol consumption, two usual drinking patterns of human beings, produce a state of oxidative stress in liver and disturb the liver function. However, a safe and effective therapy for alcoholic liver disease in humans is still elusive. This study identified the natural product berberine as a potential agent for treating or preventing ethanol-induced liver injury. We demonstrated that berberine attenuated oxidative stress resulted from binge drinking in liver by reducing hepatic lipid peroxidation, glutathione exhaust and mitochondrial oxidative damage. Furthermore, berberine also prevented the oxidative stress and macrosteatosis in response to chronic ethanol exposure in mice. Either the total cytochrome P450 2E1 or the mitochondria-located cytochrome P450 2E1, which is implicated in ethanol-mediated oxidative stress, was suppressed by berberine. On the other hand, berberine significantly blunted the lipid accumulation in liver due to chronic alcohol consumption, at least partially, through restoring peroxisome proliferator-activated receptor α/peroxisome proliferator-activated receptor-gamma Co-activator-1α and hepatocyte nuclear factor 4α/microsomal triglyceride transfer protein pathways. These findings suggested that berberine could serve as a potential agent for preventing or treating human alcoholic liver disease.     

Relationship Between Morbidity and Mortality Due to Alcoholic Cardiomyopathy and Alcohol Consumption in Australia

The study was undertaken to determine whether morbidity and mortality rates for alcoholic cardiomyopathy vary with community alcohol consumption levels. The cardiomyopathy mortality comparisons for Australia from 1968 to 1978 showed a positive relationship for both males and females aged 30 to 59 years, and 60 years and over. From 1979 to 1986 a decrease in consumption was associated with a decrease in alcoholic cardiomyopathy mortality for females, and to a lesser extent males, aged 30 to 59 years. The morbidity comparisons for Western Australia from 1971 to 1984 gave similar results to the Australian mortality findings for the males aged 30 to 59. It appears that the prevention of alcoholic cardiomyopathy will be facilitated by lowering the overal level of alcohol consumption in the community.     

Liver cirrhosis mortality in Argentina: its relationship to alcohol intake

In Argentina, rates of liver cirrhosis mortality increased significantly in both sexes (men 81.3% and women 79.8%) between 1962 and 1970. A tendency towards a decrease in mortality rates for liver cirrhosis was observed in all groups, except for men aged 35-44 years, between 1970 and 1978, but the age-adjusted mortality rate persisted in 1978 at a level significantly higher than in 1962. The high mortality rate caused by liver cirrhosis may be the consequence of high alcohol intake in Argentina. In 1975, the average per capita consumption of alcoholic beverages, per year was 80 l of wine, 16.75 l of beer and 7.5 l of distilled liquors. These results indicate that important educational and legislative measures should be undertaken to try to correct life styles in an attempt to decrease the incidence of alcohol-related diseases and accidents in Argentina.     

Tailored dose baclofen in patients with alcoholic liver disease: A case series with 2-year follow-up of hospitalisation

Introduction: Alcohol addiction is a major health burden with its consequences including liver disease and frequent hospitalisations. We used tailored-dose baclofen in patients with alcoholic liver disease and investigated hospital re-admissions before and after baclofen dose was initiated as well as tolerability and patient-reported alcohol consumption. Methods: Fifty-three hospitalised patients with alcoholic liver disease started tailored dose baclofen (median: 5.05 months, median highest dose before tapering down: 60?mg). Patients were followed-up for hospitalisation data from the health board database (mean hospitalisation follow up: 31 months) and patients were sent standardized questionnaires. Results: Baclofen was generally well tolerated with dose reductions in four patients. In the 2 years after initiation of the treatment, patients spent on an average of 19.1?d in the hospital per year compared to 25.48?d before the treatment initiation (p?=?0.59). Respondents (19 patients) reported a reduction in alcohol consumption by an average of 58.7% (240.1?g to 144.09?g). Conclusions: After initiation of the baclofen treatment, there was a trend towards decrease in hospitalisations and in patients who answered the questionnaire, alcohol consumption decreased.     

Polymorphisms of alcohol-metabolizing enzymes and the risk for alcoholism and alcoholic liver disease in Caucasian Spanish women

BACKGROUND: The relationship of polymorphisms of the genes that encode for alcohol-metabolizing enzymes and individual vulnerability to alcoholism and alcoholic liver disease (ALD) in women is unclear. We determined the genotypes of ADH1B, ADH1C, CYP2E1 (Dra-I and Pst-I) and ALDH2 in a group of Caucasian Spanish women. METHODS: We performed a cross-sectional case-control study. The study group was made of 220 women. Of these, 85 were alcoholic (27 without liver disease and 58 with alcoholic liver disease) and 135 were non-alcoholic (42 healthy controls and 93 with liver disease unrelated to alcohol). Genotyping of alcohol-metabolizing enzymes was performed using PCR-RFLP methods. RESULTS: The distribution of the allelic variants (alleles 1 and 2) in the whole subjects analyzed was: ADH1B 91.6% and 8.4%; ADH1C 58.4% and 41.6%; CYP2E1 Dra-I 15% and 85%; CYP2E1 Pst-I 96.8% and 3.2%; and ALDH2 100% and 0%, respectively. Carriage of genotypes containing the ADH1B*2 mutant allele significantly protected against alcoholism [odds-ratio (OR)=0.00; 95% confidence interval (95% CI): 0.00-0.94; p=0.02] but was associated with an increased risk for alcoholic liver disease among alcohol-dependent women [OR=0.43; 95% CI: 0.18-0.41; p=0.004]. Analysis of the remaining loci showed no significant associations. CONCLUSIONS: In Caucasian Spanish women the ADH1B*2 allele modulates the risk for alcohol dependence and for alcoholic liver disease. Given the small number of alcoholic women analyzed here, these data need further validation in larger cohorts.     

Alcohol consumption appears to protect against non-alcoholic fatty liver disease

Aliment Pharmacol Ther 2011; 33: 378–388

Summary

Background Moderate alcohol consumption may have certain beneficial effects against non‐alcoholic fatty liver disease, which is associated with metabolic syndrome. Aim To determine the association between drinking pattern and fatty liver in Japanese men and women. Methods A cross‐sectional study was performed with health checkup data including information concerning alcohol consumption and ultrasonographic assessment of fatty liver. Results We analysed 4957 men and 2155 women without reported liver diseases (median age, 49 years). In men, 40% of nondrinkers and 28% of drinkers had fatty liver. Alcohol consumption was inversely associated with fatty liver (adjusted odds ratio, 0.54; 95% confidence interval, 0.46–0.63). The prevalence of fatty liver in each category of drinking frequency was 38% (1–3 days/week), 29% (4–6 days/week), and 24% (daily drinking); there was a significant inverse correlation between drinking frequency and the prevalence of fatty liver (P < 0.001). In women, 16% of nondrinkers and 10% of drinkers had fatty liver. Drinking less than 20 g on 1–3 days/week was associated with low prevalence of fatty liver (adjusted odds ratio, 0.47; 95% confidence interval, 0.23–0.96). Conclusions Alcohol consumption appears to protect against non‐alcoholic fatty liver disease.