29 October 2018 In Phenolic compounds

There is a growing body of evidence implicating the gut 'microbiome' role in overall human health. Bacterial species belonging to the genera Lactobacillus and Bifidobacterium are generally considered to be beneficial and are commonly used in probiotic applications, whereas increases in some genera including Clostridum, Eubacterium and Bacteroides are implicated in negative health outcomes. Dietary polyphenols are bioactive compounds that have been found to increase the numbers of beneficial bacteria and antimicrobial actions against pathogenic bacteria, however most studies have been conducted in animal models or in-vitro colonic models. The aim of this systematic review was to provide an overview of recent trials on the effect of dietary grape and red wine polyphenols on the gut microbiota in humans. Following PRISMA guidelines, a systematic review was conducted of electronic databases (PubMed, CINAHL, Cochrane Library, Wed of Science and Scopus) to identify human intervention trials examining the effect of grape or wine polyphenols on gut microbiota. Seven trials met the inclusion criteria. One study looked at changes in gut microbiota following the ingestion of de-alcoholised red wine or red wine, and six studies referred to gut microbiota as intermediates in formation of phenolic metabolites. All studies confirmed that ingested polyphenols from grape and red wine, were modulated by gut microbiota, increasing numbers of polyphenolic metabolites which were found in blood, urine, ileal fluid and faeces. Intake of polyphenols derived from grape and red wine can modulate gut microbiota and contribute to beneficial microbial ecology that can enhance human health benefits. Additionally, grape and red wine polyphenols were modulated by the gut microbiota and there is a potential for a two-way relationship between the gut microbiota and polyphenolic compounds. Nevertheless, additional research is required to fully understand the complex relationship between gut microbiota and dietary polyphenols before any health claims can be made in relation to human health.

29 October 2018 In Drinking Patterns

OBJECTIVE: Labels indicating low/light versions of tobacco and foods are perceived as less harmful, which may encourage people to consume more. There is an absence of evidence concerning the impact on consumption of labeling alcohol products as lower in strength. The current study tests the hypothesis that labeling wine and beer as lower in alcohol increases their consumption.

METHOD: Weekly wine and beer drinkers (n = 264) sampled from a representative panel of the general population of England were randomized to one of three groups to taste test drinks in a bar-laboratory varying only in the label displayed; Group 1: verbal descriptor Super Low combined with 4% alcohol by volume (ABV) for wine/1% ABV for beer; Group 2: verbal descriptor Low combined with 8% ABV for wine/3% ABV for beer; Group 3: no verbal descriptors of strength (Regular). Primary outcome was total volume (ml) of drink consumed.

RESULTS: The results supported the study hypothesis: the total amount of drink consumed increased as the label on the drink denoted successively lower alcohol strength, BLin = .71, p = .015, 95% CI [0.13, 1.30]. Group contrasts showed significant differences between those offered drinks labeled as Super Low (M = 213.77) compared with Regular (M = 176.85), B = 1.43, p = .019, 95% CI [0.24, 2.61]. There was no significant difference in amount consumed between those offered drinks labeled as Low compared with Regular.

CONCLUSIONS: These results suggest that labeling drinks as lower in strength increases the amount consumed. Further studies are warranted to test for replication in non-laboratory settings and to estimate whether any effects are at a level with the potential to harm health.

TRIAL REGISTRATION: ISRCTN15530806. (PsycINFO Database Record)

27 July 2018 In Cancer

BACKGROUND: Individual participant data pooled analyses allow access to non-published data and statistical reanalyses based on more homogeneous criteria than meta-analyses based on systematic reviews. We quantified the impact of publication-related biases and heterogeneity in data analysis and presentation in summary estimates of the association between alcohol drinking and gastric cancer.

METHODS: We compared estimates obtained from conventional meta-analyses, using only data available in published reports from studies that take part in the Stomach Cancer Pooling (StoP) Project, with individual participant data pooled analyses including the same studies.

RESULTS: A total of 22 studies from the StoP Project assessed the relation between alcohol intake and gastric cancer, 19 had specific data for levels of consumption and 18 according to cancer location; published reports addressing these associations were available from 18, 5 and 5 studies, respectively. The summary odds ratios [OR, (95%CI)] estimate obtained with published data for drinkers vs. non-drinkers was 10% higher than the one obtained with individual StoP data [18 vs. 22 studies: 1.21 (1.07-1.36) vs. 1.10 (0.99-1.23)] and more heterogeneous (I(2): 63.6% vs 54.4%). In general, published data yielded less precise summary estimates (standard errors up to 2.6 times higher). Funnel plot analysis suggested publication bias.

CONCLUSION: Meta-analyses of the association between alcohol drinking and gastric cancer tended to overestimate the magnitude of the effects, possibly due to publication bias. Additionally, individual participant data pooled analyses yielded more precise estimates for different levels of exposure or cancer subtypes.

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.

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