{"title":"Using surveys to calculate disability-adjusted life-years.","authors":"Wolfgang Wiedermann, Ulrich Frick","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"128-33"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marta Varela-Rey, Ashwin Woodhoo, Maria-Luz Martinez-Chantar, José M Mato, Shelly C Lu
{"title":"Alcohol, DNA methylation, and cancer.","authors":"Marta Varela-Rey, Ashwin Woodhoo, Maria-Luz Martinez-Chantar, José M Mato, Shelly C Lu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cancer is one of the most significant diseases associated with chronic alcohol consumption, and chronic drinking is a strong risk factor for cancer, particularly of the upper aerodigestive tract, liver, colorectum, and breast. Several factors contribute to alcohol-induced cancer development (i.e., carcinogenesis), including the actions of acetaldehyde, the first and primary metabolite of ethanol, and oxidative stress. However, increasing evidence suggests that aberrant patterns of DNA methylation, an important epigenetic mechanism of transcriptional control, also could be part of the pathogenetic mechanisms that lead to alcohol-induced cancer development. The effects of alcohol on global and local DNA methylation patterns likely are mediated by its ability to interfere with the availability of the principal biological methyl donor, S-adenosylmethionine (SAMe), as well as pathways related to it. Several mechanisms may mediate the effects of alcohol on DNA methylation, including reduced folate levels and inhibition of key enzymes in one-carbon metabolism that ultimately lead to lower SAMe levels, as well as inhibition of activity and expression of enzymes involved in DNA methylation (i.e., DNA methyltransferases). Finally, variations (i.e., polymorphisms) of several genes involved in one-carbon metabolism also modulate the risk of alcohol-associated carcinogenesis.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"25-35"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic effects of ethanol on the liver and gastrointestinal system.","authors":"Shivendra D Shukla, Robert W Lim","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The widening web of epigenetic regulatory mechanisms also encompasses ethanol-induced changes in the gastrointestinal (GI)-hepatic system. In the past few years, increasing evidence has firmly established that alcohol modifies several epigenetic parameters in the GI tract and liver. The major pathways affected include DNA methylation, different site-specific modifications in histone proteins, and microRNAs. Ethanol metabolism, cell-signaling cascades, and oxidative stress have been implicated in these responses. Furthermore, ethanol-induced fatty liver (i.e., steatohepatitis) and progression of liver cancer (i.e., hepatic carcinoma) may be consequences of the altered epigenetics. Modification of gene and/or protein expression via epigenetic changes also may contribute to the cross-talk among the GI tract and the liver as well as to systemic changes involving other organs. Thus, epigenetic effects of ethanol may have a central role in the various pathophysiological responses induced by ethanol in multiple organs and mediated via the liver-GI axis.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"47-55"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Robin M Voigt, Christopher B Forsyth, Ali Keshavarzian
{"title":"Circadian disruption: potential implications in inflammatory and metabolic diseases associated with alcohol.","authors":"Robin M Voigt, Christopher B Forsyth, Ali Keshavarzian","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Circadian rhythms are a prominent and critical feature of cells, tissues, organs, and behavior that help an organism function most efficiently and anticipate things such as food availability. Therefore, it is not surprising that disrupted circadian rhythmicity, a prominent feature of modern-day society, promotes the development and/or progression of a wide variety of diseases, including inflammatory, metabolic, and alcohol-associated disorders. This article will discuss the influence of interplay between alcohol consumption and circadian rhythmicity and how circadian rhythm disruption affects immune function and metabolism as well as potential epigenetic mechanisms that may be contributing to this phenomenon.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"87-96"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The burden of alcohol use: excessive alcohol consumption and related consequences among college students.","authors":"Aaron White, Ralph Hingson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Research shows that multiple factors influence college drinking, from an individual's genetic susceptibility to the positive and negative effects of alcohol, alcohol use during high school, campus norms related to drinking, expectations regarding the benefits and detrimental effects of drinking, penalties for underage drinking, parental attitudes about drinking while at college, whether one is member of a Greek organization or involved in athletics, and conditions within the larger community that determine how accessible and affordable alcohol is. Consequences of college drinking include missed classes and lower grades, injuries, sexual assaults, overdoses, memory blackouts, changes in brain function, lingering cognitive deficits, and death. This article examines recent findings about the causes and consequences of excessive drinking among college students relative to their non-college peers and many of the strategies used to collect and analyze relevant data, as well as the inherent hurdles and limitations of such strategies.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"201-18"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41170365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The burden of alcohol use: focus on children and preadolescents.","authors":"John E Donovan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The study of alcohol use by children ages 12 and younger has been very limited. This article summarizes information from U.S. national and statewide surveys on the prevalence of alcohol use among children in grades 6 and lower, data on health conditions wholly attributable to alcohol, the prevalence of children's treatment admissions for alcohol abuse, and their rates of presentation at emergency departments for acute alcohol intoxication. Factors hampering the estimation of alcohol burden in this population include the lack of ongoing national surveys of alcohol use and problems in children, the hand-me-down nature of alcohol assessments in this population, and the lack of studies to establish whether there is a causal relationship between childhood-onset drinking and morbidity and mortality in adolescence and later in life that would permit determination of alcohol-attributable fractions. This article concludes that although the alcohol burden in childhood is low, it may be augmented by both referred alcohol burden through parental drinking and alcohol abuse and by deferred alcohol burden from longer-term consequences of early use.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"186-92"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vladimir Poznyak, Alexandra Fleischmann, Dag Rekve, Margaret Rylett, Jürgen Rehm, Gerhard Gmel
{"title":"The World Health Organization's global monitoring system on alcohol and health.","authors":"Vladimir Poznyak, Alexandra Fleischmann, Dag Rekve, Margaret Rylett, Jürgen Rehm, Gerhard Gmel","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"244-9"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41155981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"In utero alcohol exposure, epigenetic changes, and their consequences.","authors":"Michelle Ungerer, Jaysen Knezovich, Michele Ramsay","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Exposure to alcohol has serious consequences for the developing fetus, leading to a range of conditions collectively known as fetal alcohol spectrum disorders (FASD). Most importantly, alcohol exposure affects the development of the brain during critical periods of differentiation and growth, leading to cognitive and behavioral deficits. The molecular mechanisms and processes underlying the teratogenic effects of alcohol exposure remain poorly understood and are complex, because the specific effects depend on the timing, amount, and duration of exposure as well as genetic susceptibility. Accumulating evidence from studies on DNA methylation and histone modification that affect chromatin structure, as well as on the role of microRNAs in regulating mRNA levels supports the contribution of epigenetic mechanisms to the development of FASD. These epigenetic effects are difficult to study, however, because they often are cell-type specific and transient in nature. Rodent models play an important role in FASD research. Although recent studies using these models have yielded some insight into epigenetic mechanisms affecting brain development, they have generated more questions than they have provided definitive answers. Researchers are just beginning to explore the intertwined roles of different epigenetic mechanisms in neurogenesis and how this process is affected by exposure to alcohol, causing FASD.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"37-46"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic control of gene expression in the alcoholic brain.","authors":"Igor Ponomarev","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic alcohol exposure causes widespread changes in brain gene expression in humans and animal models. Many of these contribute to cellular adaptations that ultimately lead to behavioral tolerance and alcohol dependence. There is an emerging appreciation for the role of epigenetic processes in alcohol-induced changes in brain gene expression and behavior. For example, chronic alcohol exposure produces changes in DNA and histone methylation, histone acetylation, and microRNA expression that affect expression of multiple genes in various types of brain cells (i.e., neurons and glia) and contribute to brain pathology and brain plasticity associated with alcohol abuse and dependence. Drugs targeting the epigenetic \"master regulators\" are emerging as potential therapeutics for neurodegenerative disorders and drug addiction.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"69-76"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alcohol and mortality: Global alcohol-attributable deaths from cancer, liver cirrhosis, and injury in 2010.","authors":"Jürgen Rehm, Kevin D Shield","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alcohol consumption has long been recognized as a risk factor for mortality. By combining data on alcohol per capita consumption, alcohol-drinking status and alcohol-drinking patterns, risk relationships, and mortality, the Comparative Risk Assessment Study estimated alcohol-attributable mortality for 1990 and 2010. Alcohol-attributable cancer, liver cirrhosis, and injury were responsible for the majority of the burden of alcohol-attributable mortality in 1990 and 2010. In 2010, alcohol-attributable cancer, liver cirrhosis, and injury caused 1,500,000 deaths (319,500 deaths among women and 1,180,500 deaths among men) and 51,898,400 potential years of life lost (PYLL) (9,214,300 PYLL among women and 42,684,100 PYLL among men). This represents 2.8 percent (1.3 percent for women and 4.1 percent for men) of all deaths and 3.0 percent (1.3 percent for women and 4.3 percent for men) of all PYLL in 2010. The absolute mortality burden of alcohol-attributable cancer, liver cirrhosis, and injury increased from 1990 to 2010 for both genders. In addition, the rates of deaths and PYLL per 100,000 people from alcohol-attributable cancer, liver cirrhosis, and injury increased from 1990 to 2010 (with the exception of liver cirrhosis rates for women). Results of this paper indicate that alcohol is a significant and increasing risk factor for the global burden of mortality.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"174-83"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41153581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}