23 September 2021 In Liver Disease
Background and Objective: There is no consensus regarding modest alcohol consumption in patients with non-alcoholic fatty liver disease (NAFLD) due to conflicting results. The aim of this meta-analysis was to examine the effects of modest alcohol consumption on histological severity, histological course, hepatocellular carcinoma, and long-term clinical outcomes in NAFLD patients. Methods: We searched MEDLINE and EMBASE databases from inception to October 2020 for studies evaluating the effects of modest alcohol consumption among patients with NAFLD. A random-effects meta-analysis using pooled odds ratio (OR) and hazard ratio (HR) was calculated with 95% confidence interval (CI). Study quality was assessed with the Newcastle-Ottawa Scale. Results: Fourteen cross-sectional or cohort studies with aggregate data on 14,435 patients were included in the analysis. Modest alcohol consumption resulted in lower risks for steatohepatitis (OR 0.59; 95% CI 0.45-0.78; I (2) = 12%) and advanced fibrosis (OR 0.59, 95% CI 0.36-0.95; I (2) = 75%). Histological follow-up data showed that modest alcohol use was associated significantly with less steatohepatitis resolution but not with fibrosis progression. The HR for developing hepatocellular carcinoma was 3.77 (95% CI 1.75-8.15; I (2) = 0%). NAFLD patients with modest alcohol intake had a lower mortality risk than lifelong abstainers (HR 0.85; 95% CI 0.75-0.95; I (2) = 64%). Conclusion: This meta-analysis suggests that medical advice for modest alcohol drinking should be made cautiously in caring for an individual patient based on the clinical context. Practically, patients with steatohepatitis or advanced fibrosis should avoid alcohol use, whereas patients with low fibrosis risk may be allowed for modest and safe drinking.
23 September 2021 In Cardiovascular System
The causal effects of alcohol-in-moderation on cardiometabolic health are continuously debated. Mendelian randomization (MR) is an established method to address causal questions in observational studies. We performed a systematic review of the current evidence from MR studies on the association between alcohol consumption and cardiometabolic diseases, all-cause mortality and cardiovascular risk factors. We performed a systematic search of the literature, including search terms on type of design and exposure. We assessed methodological quality based on key elements of the MR design: use of a full instrumental variable analysis and validation of the three key MR assumptions. We additionally looked at exploration of non-linearity. We reported the direction of the studied associations. Our search yielded 24 studies that were eligible for inclusion. A full instrumental variable analysis was performed in 17 studies (71%) and 13 out of 24 studies (54%) validated all three key assumptions. Five studies (21%) assessed potential non-linearity. In general, null associations were reported for genetically predicted alcohol consumption with the primary outcomes cardiovascular disease (67%) and diabetes (75%), while the only study on all-cause mortality reported a detrimental association. Considering the heterogeneity in methodological quality of the included MR studies, it is not yet possible to draw conclusions on the causal role of moderate alcohol consumption on cardiometabolic health. As MR is a rapidly evolving field, we expect that future MR studies, especially with recent developments regarding instrument selection and non-linearity methodology, will further substantiate this discussion.
23 September 2021 In Cardiovascular System
BACKGROUND: Light-to-moderate alcohol consumption has been reported to be cardio-protective among apparently healthy individuals; however, it is unclear whether this association is also present in those with disease. To examine the association between alcohol consumption and prognosis in individuals with pre-existing cardiovascular disease (CVD), we conducted a series of meta-analyses of new findings from three large-scale cohorts and existing published studies. METHODS: We assessed alcohol consumption in relation to all-cause mortality, cardiovascular mortality, and subsequent cardiovascular events via de novo analyses of 14,386 patients with a previous myocardial infarction, angina, or stroke in the UK Biobank Study (median follow-up 8.7 years, interquartile range [IQR] 8.0-9.5), involving 1640 deaths and 2950 subsequent events, and 2802 patients and 1257 deaths in 15 waves of the Health Survey for England 1994-2008 and three waves of the Scottish Health Survey 1995, 1998, and 2003 (median follow-up 9.5 years, IQR 5.7-13.0). This was augmented with findings from 12 published studies identified through a systematic review, providing data on 31,235 patients, 5095 deaths, and 1414 subsequent events. To determine the best-fitting dose-response association between alcohol and each outcome in the combined sample of 48,423 patients, models were constructed using fractional polynomial regression, adjusting at least for age, sex, and smoking status. RESULTS: Alcohol consumption was associated with all assessed outcomes in a J-shaped manner relative to current non-drinkers, with a risk reduction that peaked at 7 g/day (relative risk 0.79, 95% confidence interval 0.73-0.85) for all-cause mortality, 8 g/day (0.73, 0.64-0.83) for cardiovascular mortality and 6 g/day (0.50, 0.26-0.96) for cardiovascular events, and remained significant up to 62, 50, and 15 g/day, respectively. No statistically significant elevated risks were found at higher levels of drinking. In the few studies that excluded former drinkers from the non-drinking reference group, reductions in risk among light-to-moderate drinkers were attenuated. CONCLUSIONS: For secondary prevention of CVD, current drinkers may not need to stop drinking. However, they should be informed that the lowest risk of mortality and having another cardiovascular event is likely to be associated with lower levels of drinking, that is up to approximately 105g (or equivalent to 13 UK units, with one unit equal to half a pint of beer/lager/cider, half a glass of wine, or one measure of spirits) a week.
23 September 2021 In General Health
The aim of this study was to assess the association between alcohol intake and premature mortality (younger than 65 years) and to explore the effect of potential alcohol underreporting by heavy drinkers. We followed-up 20 272 university graduates. Four categories of alcohol intake were considered (abstainer, light, moderate and heavy consumption). Repeated measurements of alcohol intake and updated information on confounders were used in time-dependent Cox models. Potential underreporting of alcohol intake by some heavy drinkers (likely misclassified as light or moderate drinkers) was explicitly addressed in an attempt to correct potential underreporting by using indirect information. During 12.3 years of median follow-up (interquartile range: 6.8-15.0), 226 participants died before their 65th birthday. A higher risk of early mortality was found for the highest category of alcohol intake (>/=50 g/d) in comparison with abstention (multivariable-adjusted hazard ratio (HR) = 2.82, 95 % CI 1.38, 5.79). In analyses of alcohol as a continuous variable, the multivariable-adjusted HR was 1.17 (95 % CI 1.08, 1.26), for each 10 g/d of alcohol. This harmful linear association was present both in uncorrected models and in models corrected for potential underreporting. No significant inverse association between light or moderate alcohol intake and premature mortality was observed, even after correcting for potential misclassification. Alcohol intake exhibited a harmful linear dose-response association with premature mortality (
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