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.
Nonalcoholic fatty liver disease (NAFLD) comprises more than two thirds of patients with chronic liver disease in the United States. The effect of alcohol consumption on survival in patients with NAFLD is not clear. We gathered data on National Health and Nutrition Examination Survey participants from 1988 to 2010, and linked them to the National Death Index for follow-up of their survival. We diagnosed NAFLD based on a previously validated biochemical model (Hepatic Steatosis Index). We built multivariate Cox proportional hazards models to evaluate the effect of alcohol consumption on survival of patients with NAFLD. After excluding participants with significant alcohol use, viral hepatitis, or increased transferrin saturation, 4,568 participants with NAFLD were included in the analysis. In a Cox model adjusted for age, sex, and smoking history, drinking 0.5-1.5 drinks per day decreased the risk of overall mortality by 41% (hazard ratio [HR] = 0.59, 95% confidence interval [CI] 0.40-0.85, P = 0.005) compared with not drinking. Drinking >/=1.5 drinks per day showed a trend toward harm (HR = 1.16, 95% CI 0.99-1.36, P = 0.119). After further adjustment for race, physical activity, education level, diabetes, and fiber and polyunsaturated fatty acid intake, drinking 0.5-1.5 drinks per day continued to show a significant protective effect (HR = 0.64, 95% CI 0.42-0.97, P = 0.035), and drinking >/=1.5 drinks per day showed a significant harmful effect on mortality (HR = 1.45, 95% CI 1.01-2.10, P = 0.047). Among patients with NAFLD, modest alcohol consumption is associated with a significant decrease in all-cause mortality, whereas drinking >/=1.5 drinks per day is associated with an increase in mortality. These results help to inform the discussion of potential risks and benefits of alcohol use in patients with NAFLD.
BACKGROUND/OBJECTIVES: Low/moderate alcohol consumption seems to be protective against cardiovascular disease (CVD). This study aimed to investigate the association of wine/beer consumption with the 10-year CVD incidence.
SUBJECTS/METHODS: During 2001-2002, 3042 CVD-free adults consented to participate in the ATTICA study; of them 2583 completed the 10-year follow-up (85% participation rate), but precise information about fatal/nonfatal CVD incidence (myocardial infarction, angina pectoris, cardiac ischemia, heart failure, chronic arrhythmias, and stroke) was available in 2020 participants (overall retention rate 66%). Alcohol/ethanol intake and the alcoholic beverages consumed were assessed; participants were categorized into three groups (no use; 1 glass/week).
RESULTS: Alcohol drinking was reported by 56% of the participants who did not develop a CVD event and 49% of those who had (p = 0.04); whereas ethanol intake was 14 +/- 16 g among those who did not had an event vs. 21 +/- 18 g among those who had a CVD event (p < 0.001). A strong inverse and similar association between low wine/beer intake (20 g/day had CVD-risk HRs (95% CI) of 0.60 (0.40-0.98), 1.22 (0.60-1.14), and 1.81 (0.70-4.61), respectively.
CONCLUSIONS: This study revealed similar results of low wine/beer consumption against CVD incidence, mainly due to its implication on low-grade chronic inflammation.