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Alcohol consumption has been shown to have complex, and sometimes paradoxical, associations with cardiovascular diseases (CVDs). Several hundred epidemiological studies on this topic have been published in recent decades. In this narrative review, the epidemiological evidence will be examined for the associations between alcohol consumption, including average alcohol consumption, drinking patterns, and alcohol use disorders, and CVDs, including ischaemic heart disease, stroke, hypertension, atrial fibrillation, cardiomyopathy, and heart failure. Methodological shortcomings, such as exposure classification and measurement, reference groups, and confounding variables (measured or unmeasured) are discussed. Based on systematic reviews and meta-analyses, the evidence seems to indicate non-linear relationships with many CVDs. Large-scale longitudinal epidemiological studies with multiple detailed exposure and outcome measurements, and the extensive assessment of genetic and confounding variables, are necessary to elucidate these associations further. Conflicting associations depending on the exposure measurement and CVD outcome are hard to reconcile, and make clinical and public health recommendations difficult. Furthermore, the impact of alcohol on other health outcomes needs to be taken into account. For people who drink alcohol, the less alcohol consumed the better.

To systematically summarize the risk relationship between different levels of alcohol consumption and incidence of liver cirrhosis. MEDLINE and Embase were searched up to March 6, 2019, to identify case-control and cohort studies with sex-specific results and more than 2 categories of drinking in relation to the incidence of liver cirrhosis. Study characteristics were extracted and random-effects meta-analyses and meta-regressions were conducted. A total of 7 cohort studies and 2 case-control studies met the inclusion criteria, providing data from 2,629,272 participants with 5,505 cases of liver cirrhosis. There was no increased risk for occasional drinkers. Consumption of one drink per day in comparison to long-term abstainers showed an increased risk for liver cirrhosis in women, but not in men. The risk for women was consistently higher compared to men. Drinking ≥5 drinks per day was associated with a substantially increased risk in both women (relative risk [RR] = 12.44, 95% confidence interval [CI]: 6.65-23.27 for 5-6 drinks, and RR = 24.58, 95% CI: 14.77-40.90 for ≥7 drinks) and men (RR = 3.80, 95% CI: 0.85-17.02, and RR = 6.93, 95% CI: 1.07-44.99, respectively). Heterogeneity across studies indicated an additional impact of other risk factors. Alcohol is a major risk factor for liver cirrhosis with risk increasing exponentially. Women may be at higher risk compared to men even with little alcohol consumption. More high-quality research is necessary to elucidate the role of other risk factors, such as genetic vulnerability, body weight, metabolic risk factors, and drinking patterns over the life course. High alcohol consumption should be avoided, and people drinking at high levels should receive interventions to reduce their intake.

BackgroundWe summarise the evidence for an association between screening scores from the Alcohol Use Disorders Identification Test (AUDIT) and all-cause mortality.MethodsUsing the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, prospective cohort studies reporting all-cause mortality risk by AUDIT scores (complete AUDIT-10 or AUDIT-C) were identified through MEDLINE, Embase, PubMed and Web of Science up to September 2016. Risk estimates were pooled using random effects meta-analyses.ResultsSeven observational studies with 18 920 observed deaths among 309 991 participants were identified. At-risk drinking (ie, hazardous/harmful consumption, AUDIT-10 ≥8 and AUDIT-C ≥4) was associated with elevated mortality risk after 2–10 years of follow-up (pooled relative risk (RR)=1.24, 95% CI 1.12 to 1.37) compared with moderate drinking (AUDIT-10=1–7, AUDIT-C=1–3). Compared to past year abstainers (AUDIT=0), moderate drinkers had a lower mortality risk (RR=0.75, 95% CI 0.71 to 0.79) in US Veterans and a similar mortality risk (RR=0.99, 95% CI 0.72 to 1.38) in population-based studies. Most data came from studies among Veterans using the short AUDIT-C in men and showed a dose–response relationship (RR=1.04, 95% CI 1.04 to 1.05 for each AUDIT-C score among drinkers). Data for women and young adults were scarce.ConclusionAUDIT screening scores were associated with mortality risk. The association was differential depending on the population examined, which may be related to prevalence of former drinkers among current abstainers. Due to heterogeneity between studies and the small number of populations examined, generalisability may be limited.

Background Observational studies have suggested a complex relationship between alcohol consumption and stroke, dependent on sex, type of stroke and outcome (morbidity vs. mortality). We undertook a systematic review and a meta-analysis of studies assessing the association between levels of average alcohol consumption and relative risks of ischemic and hemorrhagic strokes separately by sex and outcome. This meta-analysis is the first to explicitly separate morbidity and mortality of alcohol-attributable stroke and thus has implications for public health and prevention. Methods Using Medical Subject Headings (alcohol drinking, ethanol, cerebrovascular accident, cerebrovascular disorders, and intracranial embolism and thrombosis and the key word stroke), a literature search of MEDLINE, EMBASE, CINAHL, CABS, WHOlist, SIGLE, ETOH, and Web of Science databases between 1980 to June 2009 was performed followed by manual searches of bibliographies of key retrieved articles. From twenty-six observational studies (cohort or case-control) with ischemic or hemorrhagic strokes the relative risk or odds ratios or hazard ratios of stroke associated with alcohol consumption were reported; alcohol consumption was quantified; and life time abstention (manually estimated where data for current abstainers were given) was used as the reference group. Two reviewers independently extracted the information on study design, participant characteristics, level of alcohol consumption, stroke outcome, control for potential confounding factors, risk estimates and key criteria of study quality using a standardized protocol. Results The dose-response relationship for hemorrhagic stroke had monotonically increasing risk for increasing consumption, whereas ischemic stroke showed a curvilinear relationship, with a protective effect of alcohol for low to moderate consumption, and increased risk for higher exposure. For more than 3 drinks on average/day, in general women had higher risks than men, and the risks for mortality were higher compared to the risks for morbidity. Conclusions These results indicate that heavy alcohol consumption increases the relative risk of any stroke while light or moderate alcohol consumption may be protective against ischemic stroke. Preventive measures that should be initiated are discussed.

Background Although alcohol consumption has long been considered as a risk factor for chronic disease, the relationship to cardiovascular disease (CVD) is complex and involves at least two dimensions: average volume of alcohol consumption and patterns of drinking. The objective of this contribution was to estimate the burden of CVD mortality caused by alcohol consumption. Methods Risk assessment modelling with alcohol-attributable CVD mortality as primary outcome. The mortality burden of ischaemic heart disease (IHD) and ischaemic stroke (IS) attributable to alcohol consumption was estimated using attributable-fraction methodology. Relative Risk (RR) data for IHD and IS were obtained from the most comprehensive meta-analyses (except for Russia and surrounding countries where alcohol RR data were obtained from a large cohort study). Age-group specific RRs were calculated, based on large studies. Data on mortality were obtained from the World Health Organization’s Global Health Estimates and alcohol consumption data were obtained from the Global Information System on Alcohol and Health. Risk of former drinkers was modelled taking into account global differences in the prevalence of sick quitters among former drinkers. Alcohol-attributable mortality estimates for all other CVD causes except IHD and IS were obtained from the 2014 Global Status Report on Alcohol and Health. Results An estimated 780,381 CVD deaths (441,893 and 338,490 CVD deaths among men and women respectively) were attributable to alcohol consumption globally in 2012, accounting for 1.4 % of all deaths and 26.6 % of all alcohol-attributable deaths. This is in contrast to the previously estimated 1,128,273 CVD deaths attributable to alcohol consumption globally, and represents a decrease of 30.8 % in alcohol-attributable CVD mortality and of 10.6 % in the global burden of all alcohol-attributable deaths. Conclusions When the most comprehensive and recent systematic reviews and meta-analyses are taken as bases, the net impact of alcohol consumption on CVD is lower than previously estimated.

Previous meta-analyses have reported either a protective, neutral or detrimental association from chronic heavy drinking in relation to ischaemic heart disease (IHD). We investigated the potential for systematic error because of study design. Using MOOSE guidelines, studies were identified through MEDLINE, EMBASE and Web of Science up to end of March, 2014. Epidemiological studies reporting on chronic heavy drinking and IHD risk in population studies and samples of people with alcohol use disorder (AUD) were included. Random-effects meta-analysis was used to pool eligible studies. The I2 statistic was used to assess heterogeneity across studies. In total, 34 observational studies with 110 570 chronic heavy drinkers and 3086 IHD events were identified. In population studies among men, the pooled risk for IHD incidence (fatal+non-fatal events) among chronic heavy drinkers (on average ≥60 g pure alcohol/day) in comparison to lifetime abstainers (n=11 studies) was relative risk (RR)=1.04 (95% CI 0.83 to 1.31, I2=54%). Few studies were available for women. In patients with AUD, the risk of IHD mortality in comparison to the general population was elevated with a RR=1.62 (95% CI 1.34 to 1.95, I2=81%) in men and RR=2.09 (95% CI 1.28 to 3.41, I2=67%) in women. There was a general lack of adjustment other than sex and age in studies among patients with AUD. There is no systematic evidence for a protective association from any type of chronic heavy drinking on IHD risk. Patients with AUD were at higher risk for IHD mortality, but better quality evidence is needed with regard to potential confounding.

Background Alcohol use is an important risk factor for suicidal behavior, with a heightened risk found among women. The objective of this study is to determine the gender-specific risk of suicidal behaviors (suicide attempt and death by suicide) for different levels and dimensions of alcohol use—i.e., for (1) average alcohol volume consumed, (2) binge drinking, and (3) individuals with an alcohol use disorder. Methods We will systematically search the available literature for primary studies on the risk relationships specified above. Using a predetermined set of keywords, a comprehensive systematic literature search will be conducted in the following electronic databases: Embase, PsycINFO, PubMed, and Web of Science. The basic inclusion criteria will be (1) an original, quantitative (cohort, case–control or cross-sectional) study; with (2) a measure of risk of at least one dimension of our alcohol exposures in relation to at least one of our outcomes of interest (suicide attempt or death by suicide), and its corresponding measure of variability is reported (or sufficient data to calculate these); and (3) estimates of risk stratified by gender. Studies (1) that use only qualitative labels of alcohol use, and (2) where suicide attempt and non-suicidal self-harm cannot be disaggregated will be excluded. There will be no restrictions on language, geographical region, or year of publication. Two reviewers will independently perform the search and systematic assessment of each identified study and subsequent extraction of data. Categorical random-effects meta-analyses will be conducted to obtain gender-specific pooled risk estimates. Risk of bias will be assessed using the Risk of Bias In Non-randomised Studies—of Interventions tool and the Grading of Recommendations Assessment, Development and Evaluation approach will be used to rate the quality of evidence. Discussion This study will synthesize all available data on the gender-specific relationship between various dimensions of alcohol use and suicidal behavior simultaneously in a coherent framework. We will provide risk estimates with the detail needed to better understand the respective risk relationships and appreciate the burden of alcohol-attributable suicide. Systematic review registration PROSPERO CRD42022320918.

To refine estimates of the burden of alcohol-related oesophageal cancer in Japan. We searched PubMed for published reviews and original studies on alcohol intake, aldehyde dehydrogenase polymorphisms, and risk for oesophageal cancer in Japan, published before 2014. We conducted random-effects meta-analyses, including subgroup analyses by aldehyde dehydrogenase variants. We estimated deaths and loss of disability-adjusted life years (DALYs) from oesophageal cancer using exposure distributions for alcohol based on age, sex and relative risks per unit of exposure. We identified 14 relevant studies. Three cohort studies and four case-control studies had dose-response data. Evidence from cohort studies showed that people who consumed the equivalent of 100 g/day of pure alcohol had an 11.71 fold, (95% confidence interval, CI: 2.67-51.32) risk of oesophageal cancer compared to those who never consumed alcohol. Evidence from case-control studies showed that the increase in risk was 33.11 fold (95% CI: 8.15-134.43) in the population at large. The difference by study design is explained by the 159 fold (95% CI: 27.2-938.2) risk among those with an inactive aldehyde dehydrogenase enzyme variant. Applying these dose-response estimates to the national profile of alcohol intake yielded 5279 oesophageal cancer deaths and 102,988 DALYs lost - almost double the estimates produced by the most recent global burden of disease exercise. Use of global dose-response data results in an underestimate of the burden of disease from oesophageal cancer in Japan. Where possible, national burden of disease studies should use results from the population concerned.

Background Alcohol consumption is a major global risk factor for mortality and morbidity. Much discussion has revolved around the diverse findings on the complex relationship between alcohol consumption and the leading cause of death and disability, ischemic heart disease (IHD). Methods We conducted a systematic search of the literature up to August 2014 using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to identify meta-analyses and observational studies examining the relationship between alcohol drinking, drinking patterns, and IHD risk, in comparison to lifetime abstainers. In a narrative review we have summarized the many meta-analyses published in the last 10 years, discussing the role of confounding and experimental evidence. We also conducted meta-analyses examining episodic heavy drinking among on average moderate drinkers. Results The narrative review showed that the use of current abstainers as the reference group leads to systematic bias. With regard to average alcohol consumption in relation to lifetime abstainers, the relationship is clearly J-shaped, supported by short-term experimental evidence and similar associations within strata of potential confounders, except among smokers. Women experience slightly stronger beneficial associations and also a quicker upturn to a detrimental effect at lower levels of average alcohol consumption compared to men. There was no evidence that chronic or episodic heavy drinking confers a beneficial effect on IHD risk. People with alcohol use disorder have an elevated risk of IHD (1.5- to 2-fold). Results from our quantitative meta-analysis showed that drinkers with average intake of <30 g/day and no episodic heavy drinking had the lowest IHD risk (relative risk = 0.64, 95% confidence interval 0.53 to 0.71). Drinkers with episodic heavy drinking occasions had a risk similar to lifetime abstainers (relative risk = 1.12, 95% confidence interval 0.91 to 1.37). Conclusions Epidemiological evidence for a beneficial effect of low alcohol consumption without heavy drinking episodes is strong, corroborated by experimental evidence. However, episodic and chronic heavy drinking do not provide any beneficial effect on IHD. Thus, average alcohol consumption is not sufficient to describe the risk relation between alcohol consumption and IHD. Alcohol policy should try to reduce heavy drinking patterns.

Purpose The prevalence of postoperative emergence delirium in paediatric patients (pedED) following desflurane anaesthesia is considerably high at 50–80%. Although several pharmacological prophylactic strategies have been introduced to reduce the risk of pedED, conclusive evidence about the superiority of these individual regimens is lacking. The aim of the current study was to assess the potential prophylactic effect and safety of individual pharmacotherapies in the prevention of pedED following desflurane anaesthesia. Methods This frequentist model network meta-analysis (NMA) of randomized controlled trials (RCTs) included peer-reviewed RCTs of either placebo-controlled or active-controlled design in paediatric patients under desflurane anaesthesia. Results Seven studies comprising 573 participants were included. Overall, the ketamine + propofol administration [odds ratio (OR) = 0.05, 95% confidence intervals (95%CIs) 0.01–0.33], dexmedetomidine alone (OR = 0.13, 95%CIs 0.05–0.31), and propofol administration (OR = 0.30, 95%CIs 0.10–0.91) were associated with a significantly lower incidence of pedED than the placebo/control groups. In addition, only gabapentin and dexmedetomidine were associated with a significantly higher improvement in the severity of emergence delirium than the placebo/control groups. Finally, the ketamine + propofol administration was associated with the lowest incidence of pedED, whereas gabapentin was associated with the lowest severity of pedED among all of the pharmacologic interventions studied. Conclusions The current NMA showed that ketamine + propofol administration was associated with the lowest incidence of pedED among all of the pharmacologic interventions studied. Future large-scale trials to more fully elucidate the comparative benefits of different combination regimens are warranted. Trial registration PROSPERO CRD42021285200.