Alcohol-related Disease Research Articles

Contribution of excessive alcohol consumption to deaths and years of potential life lost in the United States.

IntroductionExcessive alcohol consumption is a leading cause of premature mortality in the United States. The objectives of this study were to update national estimates of alcohol-attributable deaths (AAD) and years of potential life lost (YPLL) in the United States, calculate age-adjusted rates of AAD and YPLL in states, assess the contribution of AAD and YPLL to total deaths and YPLL among working-age adults, and estimate the number of deaths and YPLL among those younger than 21 years.MethodsWe used the Centers for Disease Control and Prevention’s Alcohol-Related Disease Impact application for 2006–2010 to estimate total AAD and YPLL across 54 conditions for the United States, by sex and age. AAD and YPLL rates and the proportion of total deaths that were attributable to excessive alcohol consumption among working-age adults (20-64 y) were calculated for the United States and for individual states.ResultsFrom 2006 through 2010, an annual average of 87,798 (27.9/100,000 population) AAD and 2.5 million (831.6/100,000) YPLL occurred in the United States. Age-adjusted state AAD rates ranged from 51.2/100,000 in New Mexico to 19.1/100,000 in New Jersey. Among working-age adults, 9.8% of all deaths in the United States during this period were attributable to excessive drinking, and 69% of all AAD involved working-age adults.ConclusionsExcessive drinking was responsible for 1 in 10 deaths among working-age adults in the United States. AAD rates vary across states, but excessive drinking remains a leading cause of premature mortality nationwide. Strategies recommended by the Community Preventive Services Task Force can help reduce excessive drinking and harms related to it.

0111 Mortality study among Paris sewage workers

ObjectivesTo describe the mortality of sewage workers from Paris (France).MethodThe cohort of 1594 Paris sewage workers since 1970 was set up in 2010 and followed-up on mortality from 1970 to...

How inexpensive does an alcohol intervention in Kenya need to be in order to deliver favorable value by reducing HIV-related morbidity and mortality?

HIV remains a major cause of preventable morbidity and mortality with 100000 new infections and an estimated 62000 deaths in 2011. At the same time unhealthy alcohol consumption is an important risk factor for HIV acquisition and progression. Kenya has one of the highest rates of unhealthy alcohol use worldwide and as many as 13% of new HIV infections in Kenya may be attributable to unhealthy alcohol use. Randomized controlled trials (RCTs) of cognitive behavioral therapy (CBT)-based interventions addressing unhealthy alcohol consumption in Kenya show promising results increasing abstinence by 45% and decreasing risky sex. However alcohol remains conspicuously absent from programming in HIV and substance abuse. In low-resource settings the benefits of scaling up an effective intervention must be balanced against the opportunity costs of using those resources to scale up alternative interventions with potential benefit (for example increasingly eligibility for first-line antiretroviral therapy). Accordingly the researchers used a published validated computer simulation of the HIV epidemic in Kenya incorporating HIV transmission and disease progression to evaluate the cost-effectiveness of the alcohol intervention reported by Papas et al. Given the uncertainty surrounding costs of scale-up they varied costing assumption over a wide range to identify the threshold at which its incremental cost-effectiveness ratio (ICER) descended below those of alternative resource uses (e.g. when an alcohol intervention brought more “health” than alternative resource uses). [excerpt]

PTH-045 Integrated Alcohol And Hepatology Mdt: Reducing Alcohol-related Hospital Admission And Attendance

IntroductionIn 2010 a joint position paper on behalf of British Society of Gastroenterology, the Alcohol Health Alliance UK, and the British Association for Study of the Liver highlighted that the...

Acute pancreatitis in patients with type 2 diabetes mellitus treated with dipeptidyl peptidase-4 inhibitors: a population-based nested case-control study.

Concern about an increasing risk of acute pancreatitis associated with incretin-based drugs, including dipeptidyl peptidase-4 (DPP-4) inhibitors and glucagon-like peptide-1 analogs, has emerged recently. This nested case-control study examined the association between the use of DPP-4 inhibitors and acute pancreatitis using Taiwan's National Health Insurance Research Database. From a study cohort of patients with type 2 diabetes mellitus, we identified 1,957 acute pancreatitis cases (patients who had been admitted with a diagnosis of acute pancreatitis) and 7,828 age-, sex-, and cohort entry year-matched controls between 2000 and 2011. Multivariate conditional regression models were used to estimate the association between the use of DPP-4 inhibitors and acute pancreatitis. Sensitivity analyses were conducted by varying the definitions of timing of exposure to DPP-4 inhibitors. The risks of acute pancreatitis among current and past users of DPP-4 inhibitors were comparable with those of non-users (current users: adjusted odds ratio (aOR) 1.04; 95% CI [0.89-1.21]; past users: aOR 1.61 [0.93-2.77]). Similar results were found in sensitivity analyses with various definitions of "current users" of DPP-4 inhibitors. Nevertheless, the adjusted risk of acute pancreatitis was found to be increased significantly in patients with gallstone disease (aOR 5.89 [4.71-7.35]), alcohol-related disease (aOR 5.36 [4.05-7.08]), hypertriglyceridemia (aOR 1.80 [1.26-2.56]), pancreatic disease (aOR 17.29 [10.60-28.19]), and a higher Diabetes Complications Severity Index (DCSI) score (DCSI 3-4: aOR 1.49 [1.21-1.84]; DCSI≥5: aOR 1.32 [1.01-1.73]). This population-based study extends previous evidence by exploring the potential association between DPP-4 inhibitor use and the risk of acute pancreatitis in an ethnic Chinese type 2 diabetic cohort. We found that underlying diseases and severity of diabetes but not DPP-4 inhibitor use were associated with acute pancreatitis.

γ-Glutamyl Transferase as an Early and Sensitive Marker in Ethanol-Induced Liver Injury of Rats

γ-Glutamyl transferase (GGT) has been regarded as a biological marker of heavy alcohol consumption or hepatobiliary disease such as fatty liver. However, the role of GGT is unknown in the molecular pathway during alcohol-induced liver injury. To determine the role of GGT in alcohol-induced liver injury, Sprague-Dawley rats were administered 22% and 38% ethanol for 3 days as acute and 5 weeks as subchronic model. In serologic analysis, the level of GGT was significantly increased and the level of alanine aminotransferase, aspartate aminotransferase, and total bilirubin were not changed at 3 days and 5 weeks. In histologic analysis, ethanol exposure induced granular deposit formation and sinusoidal dilation in the acute model for 3 days. In the subchronic model for 5 weeks, ethanol exposure further increased the granular deposit formation, sinusoidal congestion, and mild fatty liver change. To determine whether ethanol-exposed liver is associated with changes of antioxidants levels, we performed reverse-transcriptase polymerase chain reaction (RT-PCR) analysis on ethanol-exposed livers of rats. In RT-PCR analysis, the mRNA levels of GPX1 and SOD1 were significantly increased as well as up-regulation of CYP2E1. In the glutathione assay, the level of glutathione was significantly reduced in response to ethanol in rats. Therefore, in this study, ethanol increased the level of serum GGT but depleted the level of glutathione. Moreover, the CYP2E1 was rapidly reflected to ethanol in rats. Taken together, our findings suggest that the elevated GGT is associated with cellular antioxidant defense system, and the CYP2E1 can be used for early diagnosis in alcohol-related diseases.

Alcohol Knowledge and Consumption among Medical Students in Lagos, Nigeria

Alcohol consumption has been linked to the risk of developing cancers and other Non communicable diseases. The knowledge, attitude and practices of alcohol use among the next generation of health care professionals will affect efforts to prevent alcohol related diseases. The aim of this study was to assess the knowledge, attitude and practices of medical students regarding alcohol consumption. It is a descriptive cross-sectional study conducted among a representative sample of 240 students using self administered questionnaires. Majority (83.3%) of the respondents had good knowledge about alcohol however less than half (46.6%) recognized that alcohol was a risk factor for cancer. About a third (33.3%) of the respondents drinks alcohol. The majority (73.8%) of the respondents who consumed alcohol did so “to have fun with friends”. Most (66.3%) of the respondents that did not consume alcohol did not do so because it is against their religion. The senior level students had better knowledge on alcohol than the junior students (p<0.05). However, this did not influence their practice. (p<0.05). Alcohol consumption was more prevalent among males than females (p<0.05). Education on alcohol needs to be given more emphasis to prepare them for work in alcohol control.

Cost-Effectiveness of Preventive Interventions to Reduce Alcohol Consumption in Denmark

IntroductionExcessive alcohol consumption increases the risk of many diseases and injuries, and the Global Burden of Disease 2010 study estimated that 6% of the burden of disease in Denmark is due to alcohol consumption. Alcohol consumption thus places a considerable economic burden on society.MethodsWe analysed the cost-effectiveness of six interventions aimed at preventing alcohol abuse in the adult Danish population: 30% increased taxation, increased minimum legal drinking age, advertisement bans, limited hours of retail sales, and brief and longer individual interventions. Potential health effects were evaluated as changes in incidence, prevalence and mortality of alcohol-related diseases and injuries. Net costs were calculated as the sum of intervention costs and cost offsets related to treatment of alcohol-related outcomes, based on health care costs from Danish national registers. Cost-effectiveness was evaluated by calculating incremental cost-effectiveness ratios (ICERs) for each intervention. We also created an intervention pathway to determine the optimal sequence of interventions and their combined effects.ResultsThree of the analysed interventions (advertising bans, limited hours of retail sales and taxation) were cost-saving, and the remaining three interventions were all cost-effective. Net costs varied from € -17 million per year for advertisement ban to € 8 million for longer individual intervention. Effectiveness varied from 115 disability-adjusted life years (DALY) per year for minimum legal drinking age to 2,900 DALY for advertisement ban. The total annual effect if all interventions were implemented would be 7,300 DALY, with a net cost of € -30 million.ConclusionOur results show that interventions targeting the whole population were more effective than individual-focused interventions. A ban on alcohol advertising, limited hours of retail sale and increased taxation had the highest probability of being cost-saving and should thus be first priority for implementation.

Price per unit: the cost of alcohol-related admissions to a regional ICU

A number of studies have demonstrated the significant and increasing morbidity and mortality associated with alcohol-related disease in the UK, and the corresponding impact this has on critical care services [1]. This study was designed to similarly evaluate the current burden of alcohol-related disease on admission rates to a regional ICU, but also to calculate the financial costs of such admissions.

Antioxidant properties of jujube honey and its protective effects against chronic alcohol-induced liver damage in mice

The antioxidant potential of jujube honey, one of the most widely consumed honeys in China, has never been determined fully. In this study, jujube honey from six geographical origins in China was analyzed for individual phenolic acid, total phenolic content, and the antioxidant effect in chronic alcohol-related hepatic disease in mice. The results showed that jujube honey from Linxian of Shanxi province contained higher phenol levels, exhibited DPPH antioxidant activity, ferric ion reducing antioxidant power (FRAP) and protective effects against DNA damage. Treatment with jujube honey (Shanxi Linxian) for 12 weeks significantly inhibited serum lipoprotein oxidation, reduced the impact of alcoholism on aspartate aminotransferase (AST) and alanine aminotransferase (ALT). It also inhibited the generation of 8-hydroxy-2-deoxyguanosine (8-OHdG), lowered the levels of malondialdehyde (MDA) and increased the activity of hepatic glutathione peroxidase (GSH-Px). The study indicates that jujube honey exerts potent antioxidant activity and significant protection in hepatic disorders associated with chronic alcoholism. The protective effect is attributed to its antioxidant mechanisms and inhibition of oxidative degradation of lipids.

Alcoholic disease: liver and beyond.

The harmful use of alcohol is a worldwide problem. It has been estimated that alcohol abuse represents the world's third largest risk factor for disease and disability; it is a causal factor of 60 types of diseases and injuries and a concurrent cause of at least 200 others. Liver is the main organ responsible for metabolizing ethanol, thus it has been considered for long time the major victim of the harmful use of alcohol. Ethanol and its bioactive products, acetaldehyde-acetate, fatty acid ethanol esters, ethanol-protein adducts, have been regarded as hepatotoxins that directly and indirectly exert their toxic effect on the liver. A similar mechanism has been postulated for the alcohol-related pancreatic damage. Alcohol and its metabolites directly injure acinar cells and elicit stellate cells to produce and deposit extracellular matrix thus triggering the "necrosis-fibrosis" sequence that finally leads to atrophy and fibrosis, morphological hallmarks of alcoholic chronic pancreatitis. Even if less attention has been paid to the upper and lower gastrointestinal tract, ethanol produces harmful effects by inducing: (1) direct damaging of the mucosa of the esophagus and stomach; (2) modification of the sphincterial pressure and impairment of motility; and (3) alteration of gastric acid output. In the intestine, ethanol can damage the intestinal mucosa directly or indirectly by altering the resident microflora and impairing the mucosal immune system. Notably, disruption of the intestinal mucosal barrier of the small and large intestine contribute to liver damage. This review summarizes the most clinically relevant alcohol-related diseases of the digestive tract focusing on the pathogenic mechanisms by which ethanol damages liver, pancreas and gastrointestinal tract.

Modulation of Inflammation by Alcohol Exposure

Modulation of Inflammation by Alcohol Exposure

Cost-effectiveness of changes in alcohol taxation in Denmark: a modelling study

IntroductionExcessive alcohol consumption is a public health problem in many countries including Denmark, where 6% of the burden of disease is due to alcohol consumption, according to the new estimates from the Global Burden of Disease 2010 study. Pricing policies, including tax increases, have been shown to effectively decrease the level of alcohol consumption.MethodsWe analysed the cost-effectiveness of three different scenarios of changed taxation of alcoholic beverages in Denmark (20% and 100% increase and 10% decrease). The lifetime health effects are estimated as the difference in disability-adjusted life years between a Danish population that continues to drink alcohol at current rates and an identical population that changes their alcohol consumption due to changes in taxation. Calculation of cost offsets related to treatment of alcohol-related diseases and injuries, was based on health care system costs from Danish national registers. Cost-effectiveness was evaluated by calculating cost-effectiveness ratios (CERs) compared to current practice.ResultsThe two scenarios of 20% and 100% increased taxation could avert 20,000 DALY and 95,500 DALY respectively, and yield cost savings of -€119 million and -€575 million, over the life time of the Danish population. Both scenarios are thus cost saving. The tax decrease scenario would lead to 10,100 added DALY and an added cost of €60 million. For all three interventions the health effects build up and reach their maximum around 15–20 years after implementation of the tax change.ConclusionOur results show that decreased taxation will lead to an increased burden of disease and related increases in health care costs, whereas both a doubling of the current level of alcohol taxation and a scenario where taxation is only increased by 20% can be cost-saving ways to reduce alcohol related morbidity and mortality. Our results support the growing evidence that population strategies are cost-effective and should be considered for policy making and prevention of alcohol abuse.

Human alcohol-related neuropathology

Alcohol-related diseases of the nervous system are caused by excessive exposures to alcohol, with or without co-existing nutritional or vitamin deficiencies. Toxic and metabolic effects of alcohol (ethanol) vary with brain region, age/developmental stage, dose, and duration of exposures. In the mature brain, heavy chronic or binge alcohol exposures can cause severe debilitating diseases of the central and peripheral nervous systems, and skeletal muscle. Most commonly, long-standing heavy alcohol abuse leads to disproportionate loss of cerebral white matter and impairments in executive function. The cerebellum (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degeneration. Although all cell types within the nervous system are vulnerable to the toxic, metabolic, and degenerative effects of alcohol, astrocytes, oligodendrocytes, and synaptic terminals are major targets, accounting for the white matter atrophy, neural inflammation and toxicity, and impairments in synaptogenesis. Besides chronic degenerative neuropathology, alcoholics are predisposed to develop severe potentially life-threatening acute or subacute symmetrical hemorrhagic injury in the diencephalon and brainstem due to thiamine deficiency, which exerts toxic/metabolic effects on glia, myelin, and the microvasculature. Alcohol also has devastating neurotoxic and teratogenic effects on the developing brain in association with fetal alcohol spectrum disorder/fetal alcohol syndrome. Alcohol impairs function of neurons and glia, disrupting a broad array of functions including neuronal survival, cell migration, and glial cell (astrocytes and oligodendrocytes) differentiation. Further progress is needed to better understand the pathophysiology of this exposure-related constellation of nervous system diseases and better correlate the underlying pathology with in vivo imaging and biochemical lesions.

Were James Bond’s drinks shaken because of alcohol induced tremor?

Objective To quantify James Bond’s consumption of alcohol as detailed in the series of novels by Ian Fleming.Design Retrospective literature review.Setting The study authors’ homes, in a comfy chair.Participants Commander...

Was Ethanolmetabolite als Biomarker über Alkoholkonsum aussagen

Alcohol and tobacco related disorders are the two leading and most expensive causes of illness in central Europe. In addition to self reports and questionnaires, biomarkers are of relevance in diagnosis and therapy of alcohol use disorders. Traditional biomarkers such as gamma glutamyl transpeptidase or mean corpuscular volume are indirect biomarkers and are subject to influence of age, gender and non alcohol related diseases, among others.Direct ethanol metabolites such as ethyl glucuronide (EtG), ethyl sulphate (EtS) and phosphatidylethanol (PEth) are direct metabolites of ethanol, that are positive after intake of ethyl alcohol. They represent useful diagnostic tools for identifying alcohol use even more accurately than traditional biomarkers. Each of these drinking indicators remains positive in serum and urine for a characteristic time spectrum after the cessation of ethanol intake--EtG and EtS in urine up to 7 days, EtG in hair for months after ethanol has left the body. Applications include clinical routine use, emergency room settings, proof of abstinence in alcohol rehabilitation programs, driving under influence offenders, workplace testing, assessment of alcohol intake in the context of liver transplantation and fetal alcohol syndrome.

Hepatitis C viral infection and the risk of dementia

Hepatitis C virus (HCV) infection may cause cognitive impairment, but no studies have focused specifically on cognitive impairment stemming from HCV. The purpose of this study was to investigate the potential increased risk for dementia in HCV-infected patients. A population-based cohort study based on the Taiwan National Health Insurance Research Database was conducted. From all potential participants aged 50 years or more, a total of 58,570 matched (1:1) pairs of HCV-infected patients and non-HCV-infected patients were included. Each subject was individually tracked from 1997 to 2009 to identify incident cases of dementia (onset in 1999 or later). Cox proportional hazards regressions were employed to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between HCV infection and dementia. There were 2989 dementia cases from the HCV-infected cohort during the follow-up period of 533,861.1 person-years; the overall incidence rates of dementia differed from the non-HCV cohort (56.0 vs. 47.7 cases per 10,000 person-years, P < 0.05). The adjusted HR for dementia was 1.36 (95% CI 1.27-1.42) for HCV-infected patients after adjusting for alcohol-related disease, liver cirrhosis, hepatic encephalopathy and hepatocellular carcinoma. HCV infection may increase the risk for dementia. Further mechanistic research is needed.

Alcohol and psoriasis: sobering thoughts

The association between psoriasis and alcohol consumption is complex. Epidemiological evidence suggests that patients with moderate to severe psoriasis have an increased incidence of alcohol-related diseases and mortality. This appears to be unique to psoriasis compared with other autoimmune diseases. Excessive alcohol consumption may contribute to systemic inflammation and the comorbidities associated with psoriasis, including cardiovascular disease and depression. Screening for hazardous alcohol consumption and appropriate interventions may be useful in patients with moderate to severe psoriasis.

Protective role of CYP2E1 inhibitor diallyl disulfide (DADS) on alcohol induced malondialdehyde-deoxyguanosine (M1dG) adduct formation

Background Alcohol use disorders are often associated with lung disease. Alcohol exposure leads to the production of reactive oxygen species, lipid peroxidation, and formation of malondialdehyde (MDA) as well as to induce the expression of cytochrome p450 2E1 (CYP2E1). Likewise, cigarette smoking can lead to lung lipid peroxidation and formation of MDA. MDA can bind to DNA forming MDA-deoxyguanosine (M1dG) adducts, which have been implicated in alcohol-related cancers and cardiovascular disease. Because CYP2E1 regulates MDA production, and our previous studies have shown that alcohol and cigarette smoke can lead to MDA formation, we hypothesized that CYP2E1 would modulate M1dG adduct formation and single-strand DNA damage in alcohol- and cigarette smoke-exposed lung cells and tissue. Methods Normal human bronchial epithelial cells (HBECs) were pretreated with 10 μM diallyl disulfide (DADS) for 1 hour and treated with 80 mM ethanol (EtOH) ± 5% cigarette smoke extract (CSE) for 3 hours for comet assay and 6 hours for CYP2E1, MDA, and M1dG adduct assays. C57BL/6 mice were administered 20% EtOH ad libitum in drinking water for 8 weeks and exposed to whole-body cigarette smoke for 5 weeks. Mice were also fed a CYP2E1 inhibitor, DADS, at 1 μM/g of feed in their daily diet for 7 weeks. Whole lung tissue homogenate was used for CYP2E1, MDA, and M1dG adduct assays. Results EtOH exposure significantly increased HBEC olive tail moment. DADS pretreatment of HBECs attenuated this EtOH effect. EtOH also induced MDA and M1dG adduct formation, which was also significantly reduced by DADS treatment. CSE ± EtOH did not enhance these effects. In lung tissue homogenate of 8-week alcohol-fed mice, MDA and M1dG adduct levels were significantly elevated in comparison with control mice and mice fed DADS while consuming alcohol. No increase in MDA and M1dG adduct formation was observed in 5-week cigarette smoke-exposed mice. Conclusions These findings suggest that CYP2E1 plays a pivotal role in alcohol-induced M1dG adducts, and the use of DADS as dietary supplement can reverse the effects of alcohol on M1dG formation.

The patient presenting with decompensated cirrhosis

The rates of liver disease in the UK are rising and hence more patients than ever are presenting to acute medical units with potentially life threatening sequelae. Early recognition and treatment of sepsis, kidney injury, bleeding and alcoholic hepatitis can significantly improve outcomes, but requires a comprehensive approach to assessment. This patient cohort often suffers from a perceived uniform poor prognosis, especially in alcohol related disease, but evidence for this is changing and reassessment of prognosis after 48 hours of organ support may be more accurate than that made ‘at the front door’. This article summarises the most important complications of decompensated cirrhosis, their early management, and presents a targeted system of care: ‘RING Liver’ – Renal failure, Infection, Nutrition, Gastrointestinal bleeding and transit, Liver dysfunction/transplantation. Factors favouring transfer to tertiary units are also explored.