Changing landscape of alcohol-associated liver disease in younger individuals, women, and ethnic minorities.

Alcohol use is the most important determinant of the development of alcohol-associated liver disease (ALD) and of predicting long-term outcomes in those with established liver disease. Worldwide, the amount, type, and pattern of use of alcohol vary. Alcohol use and consequent liver disease have been increasing in certain ethnic groups especially Hispanics and Native Americans, likely due to variations in genetics, cultural background, socio-economic status, and access to health care. Furthermore, the magnitude and burden of ALD have been increasing especially in the last few years among females and young adults who are at the prime of their productivity. It is critical to recognize the problem and care for these patients integrating cultural aspects in liver clinics. At the federal level, a societal approach is needed with the implementation of public health policies aiming to reduce alcohol consumption in the community. By addressing these challenges and promoting awareness, we can strive to reduce the burden of ALD, especially in high-risk demographic groups to improve their long-term health outcomes. Finally, we need studies and quality research examining these changing landscapes of demographics in ALD as a basis for developing therapeutic targets and interventions to reduce harmful drinking behaviours in these high-risk demographic groups.

Racial and ethnic disparities in the natural history of alcohol-associated liver disease in the United States.

BACKGROUND: Outcomes in alcohol-associated liver disease (ALD) are influenced by several race and ethnic factors, yet its natural history across the continuum of patients in different stages of the disease is unknown. METHODS: We conducted a retrospective cohort study of U.S. adults from 2011 to 2018, using three nationally representative databases to examine potential disparities in relevant outcomes among racial and ethnic groups. Our analysis included logistic and linear regressions, along with competing risk analysis. RESULTS: Black individuals had the highest daily alcohol consumption (12.6 g/day) while Hispanic participants had the largest prevalence of heavy episodic drinking (33.5%). In a multivariable-adjusted model, Hispanic and Asian participants were independently associated with a higher ALD prevalence compared to Non-Hispanic White interviewees (OR: 1.4, 95% CI: 1.1-1.8 and OR: 1.5 95% CI:1.1-2.0, respectively), while Blacks participants had a lower ALD prevalence (OR: .7 95% CI: .6-.9), and a lower risk of mortality during hospitalization due to ALD (OR: .83 95% CI: .73-.94). Finally, a multivariate competing-risk analysis showed that Hispanic ethnicity had a decreased probability of liver transplantation if waitlisted for ALD (SHR: .7, 95% CI: .6-.8) along with female Asian population (HR: .40, 95% CI: .26-.62). CONCLUSIONS: After accounting for key social and biological health determinants, the Hispanic population showed an increased risk of ALD prevalence, even with lower alcohol consumption. Additionally, Hispanic and Asian female patients had reduced access to liver transplantation compared to other enlisted patients.

Changing Trends in Etiology-Based Annual Mortality From Chronic Liver Disease, From 2007 Through 2016.

BACKGROUND & AIMS: Although treatment of hepatitis C virus (HCV) infection has improved, the prevalence of alcoholic liver disease (ALD) has been increasing, so we need an updated estimate of the burden and etiology-specific mortality of chronic liver diseases. We studied trends in age-standardized mortality of chronic liver diseases in adults at least 20 years old in the United States from 2007 through 2016. METHODS: We collected data from the US Census and National Center for Health Statistics mortality records and identified individuals with HCV infection, ALD, nonalcoholic fatty liver disease, or hepatitis B virus infection using ICD-10 codes. We obtained temporal mortality rate patterns using joinpoint trend analysis with estimates of annual percentage change (APC). RESULTS: Age-standardized HCV-related mortality increased from 7.17 per 100,000 persons in 2007 to 8.14 per 100,000 persons in 2013, followed by a marked decrease in the time period at which patients began receiving treatment with direct-acting antiviral agents (from 8.09 per 100,000 persons in 2014 to 7.15 per 100,000 persons in 2016). The APC in HCV mortality increased 2.0%/year from 2007 through 2014 but decreased 6.4%/year from 2014 through 2016. In contrast, age-standardized mortality increased for ALD (APC 2.3% from 2007 through 2013 and APC 5.5% from 2013 through 2016) and nonalcoholic fatty liver disease (APC 6.1% from 2007 through 2013 and APC 11.3% from 2013 through 2016). Mortality related to hepatitis B virus decreased steadily from 2007 through 2016, with an average APC of -2.1% (95% CI -3.0 to -1.2). Etiology-based mortality in minority populations was higher. HCV-related mortality (per 100,000 persons) was highest in non-Hispanic blacks (10.28) and whites (6.92), followed by Hispanics (5.94), and lowest in non-Hispanic Asians (2.33). Non-Hispanic Asians had higher mortality for hepatitis B virus infection (2.82 per 100,000 vs 1.02 for non-Hispanic blacks and 0.47 for non-Hispanic whites). CONCLUSION: In our population-based analysis of chronic liver disease mortality in the United States, the decrease in HCV-related mortality coincided with the introduction of direct-acting antiviral therapies, whereas mortality from ALD and nonalcoholic fatty liver disease increased during the same period. Minorities in the United States have disproportionately higher mortality related to chronic liver disease.

Ethnic Variations in Liver- and Alcohol-Related Disease Hospitalisations and Mortality: The Scottish Health and Ethnicity Linkage Study.

AIMS: Preventing alcohol-related harms, including those causing liver disease, is a public health priority in the UK, especially in Scotland, but the effects of ethnicity are not known. We assessed liver- and alcohol-related events (hospitalisations and deaths) in Scotland using self-reported measures of ethnicity. METHODS: Linking Scottish NHS hospital admissions and mortality to the Scottish Census 2001, we explored ethnic differences in hospitalisations and mortality (2001-2010) of all liver diseases, alcoholic liver disease (ALD) and specific alcohol-related diseases (ARD). Risk ratios (RR) were calculated using Poisson regression with robust variance, by sex, adjusted for age, country of birth and the Scottish Index of Multiple Deprivation (SIMD) presented below. The White Scottish population was the standard reference population with 95% confidence intervals (CI) calculated to enable comparison (multiplied by 100 for results). RESULTS: For all liver diseases, Chinese had around 50% higher risks for men (RR 162; 95% CI 127-207) and women (141; 109-184), as did Other South Asian men (144; 104-201) and Pakistani women (140; 116-168). Lower risks for all liver diseases occurred in African origin men (42; 24-74), other White British men (72; 63-82) and women (80; 70-90) and other White women (80; 67-94). For ALD, White Irish had a 75% higher risk for men (175; 107-287). Other White British men had about a third lower risk of ALD (63; 50-78), as did Pakistani men (65; 42-99). For ARD, almost 2-fold higher risks existed for White Irish men (182; 161-206) and Any Mixed Background women (199; 152-261). Lower risks of ARD existed in Pakistani men (67; 55-80) and women (48; 33-70), and Chinese men (55; 41-73) and women (54; 32-90). CONCLUSIONS: Substantial variations by ethnicity exist for both alcohol-related and liver disease hospitalisations and deaths in Scotland: these exist in subgroups of both White and non-White populations and practical actions are required to ameliorate these differences.

Ethnic differences in presentation and severity of alcoholic liver disease.

BACKGROUND: The frequency of alcoholic liver disease (ALD), including alcoholic steatosis, hepatitis, and cirrhosis, varies significantly by ethnicity. METHODS: With the goal to assess the role of ethnicity in determining the age of onset and severity of ALD and to compare the risk factors for its progression among ethnic groups, we conducted a retrospective chart review of all patients with ALD who were admitted or were followed as outpatients at University of California Davis Medical Center between 2002 and 2010. After excluding HBsAg- and HIV-positive subjects, we reviewed the charts of 791 patients with ALD including 130 with alcoholic fatty liver, 154 with alcoholic hepatitis, and 507 with alcoholic cirrhosis. RESULTS: When controlling for all variables in the model, Hispanic patients presented at significantly 4 to 10 years younger ages than White/Caucasian patients, in each of the 3 disease severity categories, and the results were confirmed after excluding HCV Ab-/RNA-positive subjects. There were more obese Hispanic patients than White/Caucasian patients, whereas the proportion of patients with hepatitis C was significantly greater in African American subjects with alcoholic hepatitis, and the proportion of patients with diabetes mellitus was significantly lower in White/Caucasian subjects than in Hispanic subjects with cirrhosis. The proportion of subjects with severe alcoholic hepatitis was similar in Hispanic and White/Caucasian patients, but lower in African American subjects. CONCLUSIONS: Ethnicity is a major factor affecting the age and severity of presentation of different subtypes of ALD.

Predictors of chronic liver disease in individuals with human immunodeficiency virus infection.

INTRODUCTION. Chronic liver disease (CLD) is becoming a major cause of mortality in patients who are positive with human immunodeficiency virus (HIV). Our aim was to assess the prevalence of CLD in HIV+ individuals. MATERIAL AND METHODS. We utilized the National Health and Nutrition Examination Survey (1999-2008) to assess the association of CLD with HIV infection. In eligible participants (18-49 years), HIV infection was defined as positive anti-HIV by enzyme immunoassay further confirmed by Western blot. The diagnosis of CLD included chronic hepatitis C (CH-C), alcohol-related liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Clinic-demographic and laboratory parameters were used to assess differences between those with and without HIV infection. RESULTS. 14,685 adults were included. Of those, 0.43 ± 0.08% were HIV-positive and 13.8% had evidence of CLD, including 26.3% in HIV-positive individuals and 13.7% in HIV-negative controls (p = 0.0341). In the U.S. population, independent predictors of CLD included HIV positivity [OR = 1.96 (1.02-3.77), p = 0.04], older age [OR = 1.03 (1.02-1.03), p < 0.0001], male gender [OR = 2.15 (1.89-2.44), p < 0.0001] and obesity [OR = 2.10 (1.82-2.43), p < 0.0001], while African American race/ethnicity was associated with lower risk for CLD [OR = 0.68 (0.58-0.80), p < 0.0001]. CONCLUSIONS. CLD is common in HIV positive individuals. With successful long term treatment of HIV, management of CLD will continue to remain very important in these patients.

Liver disease in Viet Nam: screening, surveillance, management and education: a 5-year plan and call to action.

Despite a high prevalence of liver disease in Viet Nam, there has been no nationwide approach to the disease and no systematic screening of at-risk individuals. Risk factors include chronic hepatitis B (estimated prevalence of 12%), chronic hepatitis C (at least 2% prevalence), and heavy consumption of alcohol among men. This combination of factors has resulted in liver cancer being the most common cause of cancer death in Viet Nam. There is a general lack of understanding by both the general public and health-care providers about the major risk to health that liver disease represents. We report here the initial steps taken as part of a comprehensive approach to liver disease that will ultimately include nationwide education for health-care providers, health educators, and the public; expansion of nationwide screening for hepatitis B and C followed by hepatitis B virus vaccination or treatment of chronic hepatitis B and/or hepatitis C; education about alcoholic liver disease; long-term surveillance for liver cancer; reduction of infection transmission related to medical, commercial, and personal re-use of contaminated needles, syringes, sharp instruments, razors, and inadequately sterilized medical equipment; and ongoing collection and analysis of data about the prevalence of all forms of liver disease and the results of the expanded screening, vaccination, and treatment programs. We report the beginning results of our pilot hepatitis B screening program. We believe that this comprehensive nationwide approach could substantially reduce the morbidity and mortality from liver disease and greatly lessen the burden in terms of both lives lost and health-care costs.

Genetic polymorphism of two enzymes with alcoholic liver disease in Northeast China.

BACKGROUND/AIMS: Alcohol abuse is becoming an increasingly severe problem among the Han, Mongol and Chaoxian nationalities in the northeast of China. The study aimed to investigate the relationship between alcoholic liver disease (ALD) and the genetic polymorphism of two enzymes, cytochrome P450IIE1 (CYPIIE1) and glutathione S-transferase P1 (GSTP1) in patients of three nationalities. METHODOLOGY: Peripheral blood was collected from 353 Chinese patients with ALD, 300 alcohol-dependent patients without liver disease (alcoholic) and 360 healthy controls. Each group included patients from the Han, Mongol and Chaoxian nationalities. PCR-restriction fragment length polymorphism (PCR-RFLP) was used in this research. RESULTS: Regardless of nationality patients who carried the rare CYPIIE1 C2 and GSTP1 Val allele were at higher risk of ALD. The frequency of C2 and Val in patients with ALD was 50.00% and 26.98% in the Han, 31.36% and 22.87% in the Mongol and 45.87% and 22.02% in the Chaoxian, respectively. No significant differences were seen in the frequency of either the C2 or Val alleles in ALD, among the three nationalities. In each nationality, the frequency of both the C2 and Val alleles was significantly higher in ALD compared to alcoholic and healthy controls. CONCLUSIONS: In this group of Chinese patients, we found that regardless of nationality, patients with ALD tended to carry the C2 allele and the Val allele. This may indicate a causal relationship between these polymorphic alleles that lead to the development of ALD.

Alcoholic liver disease-related mortality in the United States: 1980-2003.

OBJECTIVES: Data on temporal changes in alcoholic liver disease (ALD)-related mortality in the United States are lacking. This longitudinal assessment is important, given the divergent data on trends in worldwide ALD-related mortality, concerns for underestimation of mortality attributed to ALD in previous investigations, and shifting attention to hepatitis C virus (HCV)-related mortality. METHODS: We analyzed mortality data compiled in the multiple cause-of-death public-use data file from the National Vital Statistics System from 1980 to 2003 using categorization by both International Classification of Diseases (ICD)-9 and ICD-10 systems. The main outcome measure was age- and sex-adjusted death rates attributable to ALD, HCV, or both (ALD/HCV) listed as immediate or underlying cause of death. RESULTS: A total of 287,365 deaths were observed over the 24-year period. Age- and sex- adjusted incidence rates of ALD-related deaths decreased from 6.9/100,000 persons in 1980 to 4.4/100,000 persons by 2003. After introduction of HCV diagnostic testing, HCV-related liver mortality increased to 2.9/100,000 persons by 2003. Death rates for subjects with concomitant ALD/HCV rose to 0.2/100,000 persons by 1999 and then remained unchanged through 2003. Age-specific mortality related to ALD was highest in the ages of 45-64 years. Between 1980 and 2003, the age- and sex-adjusted ALD-related mortality (per 100,000 persons) decreased from 6.3 to 4.5 among Caucasians, 11.6 to 4.1 among African Americans, and 8.0 to 3.7 among the "other" race group. CONCLUSIONS: Despite a decline in ALD-related mortality, the proportion of alcohol-related liver deaths is still considerably large and comparable in scope to that of HCV.

Genetic polymorphism and mRNA levels of cytochrome P450IIE1 and glutathione S-transferase P1 in patients with alcoholic liver disease in different nationalities.

BACKGROUND: Alcohol abuse and dependence are major factors in the pathogenesis of alcoholic liver disease (ALD). Alcohol abuse is becoming an increasingly severe problem among the Han, Mongol, and Korean nationalities in northeast China. This study aimed to investigate the relationship between ALD and the genetic polymorphism and expression levels of two enzymes, cytochrome P450IIE1 (CYPIIE1) and glutathione S-transferase P1 (GSTP1) in patients of three nationalities. METHODS: Peripheral blood was collected from 353 Chinese patients with ALD, 300 alcohol dependent patients without liver disease (alcoholic), and 360 healthy controls. Each group included patients from the Han, Mongol and Korean nationalities. Real-time polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) were used. RESULTS: Regardless of nationality, patients who carried the rare CYPIIE1 C2 and GSTP1 Val alleles were at higher risk of ALD. The frequency of C2 and Val in patients with ALD was respectively 50.00% and 26.98% in the Han, 31.36% and 22.87% in the Mongol, and 45.87% and 22.02% in the Korean nationality. No significant differences were seen in the frequency of either C2 or Val alleles in ALD patients among the three nationalities. In each nationality, the frequency of both C2 and Val alleles was significantly higher in ALD compared to alcoholic and healthy controls. Except for nationality, the average mRNA levels of CYPIIE1 in ALD patients and healthy controls were 10.05% and 2.21%, respectively. The average mRNA levels of GSTP1 in ALD patients and healthy controls were 0.53% and 2.12%, respectively. The mRNA level of CYPIIE1 was higher, and that of GSTP1 was lower in patients with ALD compared to the controls. CONCLUSIONS: Except for nationality, patients with ALD in this series tended to have a higher mRNA expression of CYPIIE1 and to carry the C2 allele, and tended to have a lower mRNA expression of GSTP1 and to carry the Val allele. There is a causal relationship between the polymorphic alleles, which leads to different mRNA levels and the development of ALD.

Alcohol-attributable deaths and years of potential life lost among American Indians and Alaska Natives--United States, 2001--2005.

Excessive alcohol consumption is a leading preventable cause of death in the United States and has substantial public health impact on American Indian and Alaska Native (AI/AN) populations. To estimate the average annual number of alcohol-attributable deaths (AADs) and years of potential life lost (YPLLs) among AI/ANs in the United States, CDC analyzed 2001-2005 data (the most recent data available), using death certificate data and CDC Alcohol-Related Disease Impact (ARDI) software. This report summarizes the results of that analysis, which indicated that AADs accounted for 11.7% of all AI/AN deaths, that the age-adjusted AAD rate for AI/ANs was approximately twice that of the U.S. general population, and that AI/ANs lose 6.4 more years of potential life per AAD compared with persons in the U.S. general population (36.3 versus 29.9 years). These findings underscore the importance of implementing effective population-based interventions to prevent excessive alcohol consumption and to reduce alcohol-attributable morbidity and mortality among AI/ANs.

Single-nucleotide rs738409 polymorphisms in the PNPLA3 gene are strongly associated with alcoholic liver disease in Han Chinese males.

OBJECTIVE: Alcoholic liver disease (ALD) is a chronic liver disorder caused by the consumption of large amounts of alcohol. Genome-wide association studies have recently confirmed that polymorphisms in PNPLA3 predispose individuals to ALD and have identified risk loci of MBOAT7 and TM6SF2 in persons of European descent. However, the association with alcoholic liver damage has not been evaluated thus far in a Han Chinese population. METHODS: We performed a large case-control multicenter study of 507 ALD patients and 645 ethnically matched healthy controls. Five SNPs were genotyped using matrix-assisted laser desorption/ionization time of flight mass spectrometry, and association analysis was performed using PLINK 1.07 software. RESULTS: The rs738409 in the PNPLA3 gene was found to be significantly associated with ALD in allele and genotype frequencies (p = 6.25 × 10-14 and p = 9.05 × 10-13). The frequencies of the risk allele G in rs738409 were notably higher in ALD compared to controls (odds ratio = 1.93, 95% confidence interval = 1.63-2.28). The current study showed that the genotype frequencies of three genetic models were also statistically significant (p = 1.07 × 10-13, p = 9.3 × 10-8, and p = 1.57 × 10-12). Additionally, the G-allele of rs738409 was associated with a variety of clinical manifestations such as elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transpeptidase (GGT), and mean corpuscular volume (MCV) in the patients with ALD. CONCLUSION: In a Han Chinese population, the present study confirmed that PNPLA3 polymorphism rs738409 was more likely to influence the susceptibility to ALD. However, no statistically significant differences for the allele and genotype frequencies of rs626283, rs641738 in MBOAT7, rs10401969 in SUGP1 and rs58542926 in TM6SF2 were found between ALD patients and healthy controls.

Frequency of primary iron overload and HFE gene mutations (C282Y, H63D and S65C) in chronic liver disease patients in north India.

AIM: To identify the frequency of iron overload and study the three mutations in the HFE gene (C282Y, H63D, and S65C) in patients with chronic liver disorders (CLD) and controls. METHODS: To identify patients with iron overload (transferrin saturation > 45% in females and > 50% in males and serum ferritin > 1000 ng/mL) we evaluated 236 patients with CLD, including 59 with non-alcoholic steatohepatitis (NASH), 22 with alcoholic liver disease (ALD), 19 of cirrhosis due to viruses (HBV, HCV), and 136 with cryptogenic cirrhosis. Mutations of the HFE gene were analyzed by PCR-RE. hundred controls were screened for iron status and the mutations. RESULTS: Seventeen patients with CLD showed evidence of iron overload. Fifteen cases of iron overload had cryptogenic cirrhosis and two had ALD. None of the controls showed iron overload. We did not find any individual with 282Y or 65C either in the cases or in the controls. The prevalence of H63D heterozygosity was 12% in normal individuals, 14.8% in 236 patients (16.9% in NASH, 13.6% in ALD, 26.3% in viral and 12.5% in cryptogenic cirrhosis) and the overall prevalence was 13.98%. Only two of the 17 patients with primary iron overload were heterozygous for H63D. One patient with NASH and one normal individual who were homozygous for H63D showed no iron overload. CONCLUSION: Primary iron overload in Indians is non-HFE type, which is different from that in Europeans and further molecular studies are required to determine the defect in various iron regulatory genes.

Ethnicity, alcohol drinking and changes in transaminase activity among heavy drinkers.

BACKGROUND: Liver cirrhosis mortality differs by ethnicity in the United States. Some studies suggest alcohol sensitivity may contribute to this finding. This analysis evaluated if alcohol-associated changes in aspartate aminotransferase (AST) and alanine transaminase (ALT) differed by ethnicity among heavy drinkers. METHODS: Subjects included 1691 subjects from Project MATCH, a multicenter alcohol use disorders treatment trial. Changes in AST and ALT over 15 months were modeled as functions of ethnicity, age, gender, time, study site and alcohol use. The main focus was on ethnic differences in changes in transaminase activity occurring with changes in alcohol use. RESULTS: At all levels of alcohol consumption AST was lower in non-Hispanic whites relative to African Americans and Mexican Americans. Changes in AST associated with changes in alcohol use did not vary by ethnicity. ALT significantly differed only between Mexican Americans and non-Hispanic whites. Similar to AST, alcohol-associated ALT change did not differ by ethnicity. CONCLUSIONS: Among individuals with alcohol use disorders participating in a treatment trial, the effect of alcohol drinking on transaminase activity did not vary by ethnicity. However, in the general population, alcohol may still interact with other factors in mediating ethnic differences in cirrhosis mortality.

Elevated fasting glucose and albuminuria may be a marker for all-cause mortality in Indigenous adults in North Queensland - a follow up study, 1998-2006.

AIMS: To document risk factors of all-cause mortality in a cohort of indigenous Australians from 23 communities of North Queensland during 1998-2006. METHODS: Among 2787 indigenous adults, baseline weight, waist circumference, blood pressure, fasting glucose, lipids, gamma-glutamyl transferase, urine albumin creatinine ratio, smoking, alcohol intake and physical activity were measured in 1998-2000. Deaths were ascertained from State Registry of Deaths, hospitalization and clinical records till 2006. Mortality risk factors were assessed using a Cox proportional-hazards model. RESULTS: The standardized all-cause mortality rate was 23.2/1000 person-years (95% CI 20.3-26.3/1000 pys). After adjusting for age, sex, and ethnicity, baseline plasm fasting glucose >=5.5mmol/L was associated with a 50% increased risk of death (HR 1.5, 95% CI 1.2-2.0). Albuminuria was associated with all-cause mortality with a hazards ratio of 1.4 for microalbuminuria (95% CI 1.0-1.9) and 2.6 (95% CI 1.8-3.7) for macroalbuminuria. Gamma-glutamyl transferase >=50IU was associated with an increased risk of all-cause mortality by 40% (95% CI 1.04-1.8). CONCLUSIONS: Fasting glycaemia, albuminuria, and gamma-glutamyl transferase, may be a marker for all-cause mortality within this cohort.

Racial and ethnic differences in alcohol-associated aspartate aminotransferase and gamma-glutamyltransferase elevation.

BACKGROUND: Recent analyses have confirmed that Hispanic and black non-Hispanic Americans are at an increased risk for death from liver cirrhosis. The reasons for this are unknown. As a common cause of cirrhosis, differing sensitivities to alcohol-related hepatocellular injury may play a role. This study compared racial and ethnic aspartate aminotransferase and gamma-glutamyltransferase level elevations within alcohol-drinking categories. METHODS: A cross-sectional analysis of adult subjects from the Third National Health and Nutrition Examination Survey. Logistic regression models were used to estimate the risk for elevation of aspartate aminotransferase and gamma-glutamyltransferase levels among Mexican American and black non-Hispanic subjects compared with white non-Hispanic subjects within categories of alcohol use. Adjustment was made for age, sex, exposure to hepatitis C and B, and body mass index. RESULTS: Among current drinkers, black non-Hispanic and Mexican Americans were more likely to have a 2-fold elevation in aspartate aminotransferase levels when compared with white non-Hispanic Americans. This was most pronounced in the highest-frequency drinkers (Mexican Americans: odds ratio, 9.1 [95% confidence interval, 3.9-21.0]; and black non-Hispanic Americans: odds ratio, 3.1 [95% confidence interval, 1.4-6.8]). No racial and ethnic differences were apparent among current abstainers. A similar pattern was found for 2-fold gamma-glutamyltransferase level elevations. CONCLUSIONS: Among current drinkers, Mexican and black non-Hispanic Americans may have an increased risk for hepatocellular injury. These results require confirmation in other study populations for whom validated measures of quantity and pattern of drinking exist.

'White liquor hits black livers': meanings of excessive liquor consumption in South Africa in the second half of the twentieth century.

Four years into South Africa's first democracy, the African National Congress Youth League, with the help of the liquor industry's Social Aspects of Alcohol Committee drafted a policy to prevent substance abuse in black communities. They declared that alcohol was 'often not used in a socially acceptable way'. Concerned not so much with post-apartheid policy as with making sense of what socially acceptable alcohol usage might mean, this article explores narratives of alcohol use and abuse in South Africa in the second half of the twentieth century. It demonstrates that while multiple understandings of excess in alcohol consumption were articulated, those notions tied to particular constructions of racial difference prevailed. Ideas pairing drinking habits with race were given effect by state institutions. By tying drinking habits to 'race' and by locating 'race' in a social hierarchy, state institutions determined access to liquor and welfare services. By naturalising Africans as heavy drinkers, the state justified its sale of liquor to African men while denying the need for rehabilitation in the event of alcoholic dependence. By placing 'coloured' closer to 'white' in its racial order, the apartheid state found cause to extend limited rehabilitation services to those designated 'coloured'. By tying liquor revenues to apartheid administration, the ruling regime exonerated its policy of excluding blacks from the retail liquor trade even after lifting prohibition in 1962. This policy encouraged rampant illicit liquor dealing, created a social environment in which alcoholic excess, particularly after 1976, reached new proportions and generated new and dangerous meanings of socially acceptable drinking. Against the grain of these dominant discourses of racially designated meanings of drinking, African people forged a more complex set of practices and meanings not rendered any clearer by the ANC Youth League's discourse of acceptable and unacceptable usage.