18 May 2018 In General Health

BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease.

METHODS: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies.

FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1.14, 95% CI, 1.10-1.17), coronary disease excluding myocardial infarction (1.06, 1.00-1.11), heart failure (1.09, 1.03-1.15), fatal hypertensive disease (1.24, 1.15-1.33); and fatal aortic aneurysm (1.15, 1.03-1.28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0.94, 0.91-0.97). In comparison to those who reported drinking >0-100-200-350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively.

INTERPRETATION: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines.

FUNDING: UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

Binge drinking (BD) is a public health concern with serious implications for brain development. This review is the first in which neuropsychological studies of healthy young BDs are synthesized following PRISMA guidelines. We conducted a literature search in PsycINFO, Web of Science, and PubMed. Articles were screened using strict inclusion criteria. Two authors independently assessed the methodological quality. Of the 27 studies included, 14 (52%) were of intermediate quality, 7 (26%) of poor quality and 6 (22%) of high quality. BD is associated with deficits in verbal memory and executive functions, principally poor inhibitory control. Tentatively, BD may be related to deficits in cognitive flexibility and monitoring of information in working memory. Further studies are needed to determine potential impairments in prospective memory and decision-making. BDs do not seem to show difficulties in planning, short-term memory, attention, processing speed or visuospatial construction. The evidence does not seem to support greater vulnerability in females. Future longitudinal studies should identify the characteristics of extreme trajectories, explore recovery deficits and design intervention programs.

03 May 2018 In Liver Disease
To what extent could alcohol consumption affects female fertility is still unclear. The aim of this study was to quantitatively summarize the dose-response relation between total and specific types of alcohol beverage (beer, wine, and spirits) consumption in female and the fecundability. Four electronic databases were searched. Observational studies (cohort and case-control) that provided female alcohol consumption and fecundity were eligible. Nineteen studies, involving 98657 women, were included in this study. Compared to non-drinkers, the combined estimate (with relative risk, RR) of alcohol consumers on fecundability was 0.87 (95% CI 0.78-0.95) for overall 19 studies. Compared to non-drinkers, the pooled estimates were 0.89 (95% CI 0.82-0.97) for light drinkers (=12.5 g/day of ethanol) and 0.77 (95% CI 0.61-0.94) for moderate-heavy drinkers (>12.5 g/day of ethanol). Moreover, compared to non-drinkers, the corresponding estimates on fecundability were 0.98 (95% CI 0.85-1.11), 1.02 (95% CI 0.99-1.05), and 0.92 (95% CI 0.83-1.01) for studies focused on wine, beer and spirits, respectively. Dose-response meta-analysis suggested a linear association between decreased fecundability and every 12.5 g/d increasing in alcohol consumption with a RR 0.98 (95% CI 0.97-0.99). This first systematic review and meta-analysis suggested that female alcohol consumption was associated with a reduced fecundability
03 May 2018 In General Health
BACKGROUND: Alcohol and in particular red wine have both immunomodulatory and neuroprotective properties, and may exert an effect on the disease course of multiple sclerosis (MS). OBJECTIVE: To assess the association between alcohol and red wine consumption and MS course. METHODS: MS patients enrolled in the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital (CLIMB) who completed a self-administered questionnaire about their past year drinking habits at a single time point were included in the study. Alcohol and red wine consumption were measured as servings/week. The primary outcome was the Expanded Disability Status Scale (EDSS) at the time of the questionnaire. Secondary clinical outcomes were the Multiple Sclerosis Severity Score (MSSS) and number of relapses in the year before the questionnaire. Secondary MRI outcomes included brain parenchymal fraction and T2 hyperintense lesion volume (T2LV). Appropriate regression models were used to test the association of alcohol and red wine intake on clinical and MRI outcomes. All analyses were controlled for sex, age, body mass index, disease phenotype (relapsing vs. progressive), the proportion of time on disease modifying therapy during the previous year, smoking exposure, and disease duration. In the models for the MRI outcomes, analyses were also adjusted for acquisition protocol. RESULTS: 923 patients (74% females, mean age 47 +/- 11 years, mean disease duration 14 +/- 9 years) were included in the analysis. Compared to abstainers, patients drinking more than 4 drinks per week had a higher likelihood of a lower EDSS score (OR, 0.41; p = 0.0001) and lower MSSS (mean difference, - 1.753; p = 0.002) at the time of the questionnaire. Similarly, patients drinking more than 3 glasses of red wine per week had greater odds of a lower EDSS (OR, 0.49; p = 0.0005) and lower MSSS (mean difference, - 0.705; p = 0.0007) compared to nondrinkers. However, a faster increase in T2LV was observed in patients consuming 1-3 glasses of red wine per week compared to nondrinkers. CONCLUSIONS: Higher total alcohol and red wine intake were associated with a lower cross-sectional level of neurologic disability in MS patients but increased T2LV accumulation. Further studies should explore a potential cause-effect neuroprotective relationship, as well as the underlying biological mechanisms
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