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      Alcohol Policies and Alcoholic Cirrhosis Mortality in the United States

      research-article
      , MD, MPH , , ScD, SM, , MPH, , PhD, , PhD, MPH, , MD, MPH
      Preventing Chronic Disease
      Centers for Disease Control and Prevention

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          Abstract

          Introduction

          Stronger alcohol policies predict decreased alcohol consumption and binge drinking in the United States. We examined the relationship between the strength of states’ alcohol policies and alcoholic cirrhosis mortality rates.

          Methods

          We used the Alcohol Policy Scale (APS), a validated assessment of policies of the 50 US states and Washington DC, to quantify the efficacy and implementation of 29 policies. State APS scores (theoretical range, 0–100) for each year from 1999 through 2008 were compared with age-adjusted alcoholic cirrhosis death rates that occurred 3 years later. We used Poisson regression accounting for state-level clustering and adjusting for race/ethnicity, college education, insurance status, household income, religiosity, policing rates, and urbanization.

          Results

          Age-adjusted alcoholic cirrhosis mortality rates varied significantly across states; they were highest among males, among residents in states in the West census region, and in states with a high proportion of American Indians/Alaska Natives (AI/ANs). Higher APS scores were associated with lower mortality rates among females (adjusted incidence rate ratio [IRR], 0.91 per 10-point increase in APS score; 95% confidence interval [95% CI], 0.84–0.99) but not among males (adjusted IRR, 0.97; 95% CI, 0.90–1.04). Among non-AI/AN decedents, higher APS scores were also associated with lower alcoholic cirrhosis mortality rates among both sexes combined (adjusted IRR, 0.89; 95% CI, 0.82–0.97). Policies were more strongly associated with lower mortality rates among those living in the Northeast and West census regions than in other regions.

          Conclusions

          Stronger alcohol policy environments are associated with lower alcoholic cirrhosis mortality rates. Future studies should identify underlying reasons for racial/ethnic and regional differences in this relationship.

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          Most cited references20

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          Global burden of alcoholic liver diseases.

          Liver diseases contribute markedly to the global burden of mortality and disease. This paper provides an overview from a global perspective of the contribution of alcohol to liver diseases. The Global Burden of Disease study methodology was used to estimate the burden of alcohol-attributable liver cirrhosis and alcohol-attributable liver cancer in 2010 as measured by deaths and disability adjusted life years (DALYs). This methodology estimates attributable fractions based on alcohol exposure distribution and relative risks associated with different levels of drinking. Globally, in 2010, alcohol-attributable liver cirrhosis was responsible for 493,300 deaths (156,900 female deaths and 336,400 male deaths) and 14,544,000 DALYs (4,112,000 DALYs for women and 10,432,000 DALYs for men), representing 0.9% (0.7% for women and 1.2% for men) of all global deaths and 0.6% (0.4% for women and 0.8% for men) of all global DALYs, and 47.9% of all liver cirrhosis deaths (46.5% for women and 48.5% for men) and 46.9% of all liver cirrhosis DALYs (44.5% for women and 47.9% for men). Alcohol-attributable liver cancer was responsible for 80,600 deaths (14,800 female deaths and 65,900 male deaths) and 2,142,000 DALYs (335,000 DALYs for women and 1,807,000 DALYs for men). The burden of alcohol-attributable liver cirrhosis and liver cancer is high and entirely preventable. Interventions to reduce alcohol consumption are recommended as a population health priority and may range from taxation increases for alcoholic beverages to increases in screening and treatment rates for alcohol use disorders. Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
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            Alcohol as a risk factor for liver cirrhosis: a systematic review and meta-analysis.

            Alcohol is an established risk factor for liver cirrhosis. It remains unclear, however, whether this relationship follows a continuous dose-response pattern or has a threshold. Also, the influences of sex and end-point (i.e. mortality vs. morbidity) on the association are not known. To address these questions and to provide a quantitative assessment of the association between alcohol intake and risk of liver cirrhosis, we conducted a systematic review and meta-analysis of cohort and case-control studies. Studies were identified by a literature search of Ovid MEDLINE, EMBASE, Web of Science, CINAHL, PsychINFO, ETOH and Google Scholar from January 1980 to January 2008 and by searching the references of retrieved articles. Studies were included if quantifiable information on risk and related confidence intervals with respect to at least three different levels of average alcohol intake were reported. Both categorical and continuous meta-analytic techniques were used to model the dose-response relationship. Seventeen studies met the inclusion criteria. We found some indications for threshold effects. Alcohol consumption had a significantly larger impact on mortality of liver cirrhosis compared with morbidity. Also, the same amount of average consumption was related to a higher risk of liver cirrhosis in women than in men. Overall, end-point was an important source of heterogeneity among study results. This result has important implications not only for studies in which the burden of disease attributable to alcohol consumption is estimated, but also for prevention.
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              Effects of minimum drinking age laws: review and analyses of the literature from 1960 to 2000.

              The goal of this article is to review critically the extant minimum legal drinking age (MLDA) research literature and summarize the current state of knowledge regarding the effectiveness of this policy. Comprehensive searches of four databases were conducted to identify empirical studies of the MLDA published from 1960 to 1999. Three variables were coded for each study regarding methodological quality: (1) sampling design, (2) study design and (3) presence or absence of comparison group. We identified 241 empirical analyses of the MLDA. Fifty-six percent of the analyses met our criteria for high methodological quality. Of the 33 higher quality studies of MLDA and alcohol consumption, 11 (33%) found an inverse relationship; only 1 found the opposite. Similarly, of the 79 higher quality analyses of MLDA and traffic crashes, 46 (58%) found a higher MLDA related to decreased traffic crashes; none found the opposite. Eight of the 23 analyses of other problems found a higher MLDA associated with reduced problems; none found the opposite. Only 6 of the 64 college-specific studies (9%) were of high quality; none found a significant relationship between the MLDA and outcome measures. The preponderance of evidence indicates there is an inverse relationship between the MLDA and two outcome measures: alcohol consumption and traffic crashes. The quality of the studies of specific populations such as college students is poor, preventing any conclusions that the effects of MLDA might differ for such special populations.
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                Author and article information

                Journal
                Prev Chronic Dis
                Prev Chronic Dis
                PCD
                Preventing Chronic Disease
                Centers for Disease Control and Prevention
                1545-1151
                2015
                15 October 2015
                : 12
                : E177
                Affiliations
                [1]Author Affiliations: Ziming Xuan, Jason G. Blanchette, Timothy C. Heeren, Boston University School of Public Health, Department of Community Health Sciences, Boston, Massachusetts; Monica H. Swahn, School of Public Health, Georgia State University, Atlanta, Georgia; Timothy S. Naimi, Boston University School of Public Health, Department of Community Health Sciences, and Boston Medical Center, Section of General Internal Medicine, Boston, Massachusetts. Dr Hadland is also affiliated with Harvard Medical School, Department of Pediatrics, Boston, Massachusetts.
                Author notes
                Corresponding Author: Scott E. Hadland, MD, MPH, Division of Adolescent/Young Adult Medicine, Boston Children’s Hospital, 300 Longwood Ave, Boston, MA, 02115. Telephone: 857-218-3236. Email: scott.hadland@ 123456childrens.harvard.edu .
                Article
                15_0200
                10.5888/pcd12.150200
                4611859
                26469950
                d51f53b7-31b3-493c-ba21-ed846a3990c9
                History
                Categories
                Original Research
                Peer Reviewed

                Health & Social care
                Health & Social care

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