23 February 2021 In Phenolic compounds
PURPOSE: Red wine polyphenols (RWP) are plant-based molecules that have been extensively studied in relation to their protective effects on vascular health in both animals and humans. The aim of this review was to quantify and compare the efficacy of RWP and pure resveratrol on outcomes measures of vascular health and function in both animals and humans. METHODS: Comprehensive database searches were carried out through PubMed, Web of Science and OVID for randomised, placebo-controlled studies in both animals and humans. Meta-analyses were carried out on acute and chronic studies of RWP in humans, alongside sub-group analysis where possible. Risk-of-bias assessment was carried out for all included studies based on randomisation, allocation, blinding, outcome data reporting, and other biases. RESULTS: 48 animal and 37 human studies were included in data extraction following screening. Significant improvements in measures of blood pressure and vascular function following RWP were seen in 84% and 100% of animal studies, respectively. Human studies indicated significant improvements in systolic blood pressure overall (- 2.6 mmHg, 95% CI: [- 4.8, - 0.4]), with a greater improvement in pure-resveratrol studies alone (- 3.7 mmHg, 95% CI: [- 7.3, - 0.0]). No significant effects of RWP were seen in diastolic blood pressure or flow-mediated dilation (FMD) of the brachial artery. CONCLUSION: RWP have the potential to improve vascular health in at risk human populations, particularly in regard to lowering systolic blood pressure; however, such benefits are not as prevalent as those observed in animal models.
23 February 2021 In Liver Disease
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. Whether moderate alcohol consumption plays a role for progression of NAFLD is disputed. Moreover, it is not known which tool is ideal for assessment of alcohol consumption in NAFLD. This study aimed to evaluate if moderate alcohol consumption assessed with different methods, including the biological marker phosphatidylethanol (PEth), is associated with advanced fibrosis in NAFLD. METHODS: We conducted a cross-sectional study of patients with biopsy-proven NAFLD. All participants were clinically evaluated with medical history, blood tests, and anthropometric measurements. Alcohol consumption was assessed using PEth in blood, the questionnaire AUDIT-C, and clinical interview. FINDINGS: 86 patients were included of which 17% had advanced fibrosis. All participants reported alcohol consumption /= 50ng/mL may be a biological marker indicating increased risk for advanced fibrosis in NAFLD. Patients with T2DM consuming moderate amounts of alcohol had the highest risk of advanced fibrosis, indicating a synergistic effect of insulin resistance and alcohol on the histopathological progression of NAFLD.
23 February 2021 In Liver Disease
OBJECTIVE: To study the interaction of alcohol consumption with body mass index (BMI) in the development of hepatic steatosis and mortality. PARTICIPANTS AND METHODS: We conducted a retrospective cohort study of 18,506 participants without fatty liver disease or cirrhosis at enrollment in the Mayo Clinic Biobank from April 9, 2009, through March 31, 2016. Participants were classified by self-reported alcohol consumption status (nondrinkers, moderate drinkers [0 to 2 drinks per day], and heavy drinkers [>2 drinks per day]). The primary outcome of interest was the incidence of hepatic steatosis, identified by International Classification of Diseases, Ninth Revision code and confirmed with imaging. The secondary outcome of interest was all-cause mortality. Multivariate Cox regression analysis determined the impact of alcohol consumption stratified by BMI on outcomes compared with nondrinkers. RESULTS: The cohort (mean +/- SD age, 55.8+/-16.9 years; 63.8% female; mean +/- SD BMI, 28.8+/-6.1 kg/m(2)) of 18,506 participants included 3657 (19.8%) nondrinkers, 14,236 (76.9%) moderate drinkers, and 613 (3.3%) heavy drinkers at enrollment. After a median follow-up of 5.8 years (interquartile range, 3.8 to 7.2 years), 684 participants had development of hepatic steatosis and 968 died. In moderate drinkers, the risk of hepatic steatosis development was high in the obese group (adjusted hazard ratio [AHR], 1.31; 95% CI, 1.03 to 1.67), insignificant in the overweight group (AHR, 0.86; 95% CI, 0.58 to 1.26), and decreased in the normal-BMI group (AHR, 0.48; 95% CI, 0.26 to 0.90). Heavy drinkers had an increased risk of hepatic steatosis irrespective of BMI. Moderate alcohol use was associated with decreased mortality in the normal-weight (AHR, 0.44; 95% CI, 0.34 to 0.58) and overweight (AHR, 0.70; 95% CI, 0.56 to 0.88) groups but not in the obese group (AHR, 0.80; 95% CI, 0.64 to 1.00). CONCLUSION: In obese individuals, even moderate alcohol use is associated with the development of hepatic steatosis. Moderate alcohol consumption is associated with lower mortality in normal-BMI and overweight individuals but not in those who are obese.
23 February 2021 In General Health
OBJECTIVE: Several, but not all studies, have shown a dose-dependent inverse association with alcohol consumption and rheumatoid arthritis (RA), whereas smoking is an established risk factor for RA. We aimed to study the association between alcohol consumption and RA incidence and investigate a potential interaction between alcohol and smoking habits, regarding RA incidence. METHODS: We used a prospective cohort study, based on 41 068 participants with detailed assessment of alcohol intake, smoking and potential confounders at baseline in 1997. We ascertained a total of 577 incident cases of RA during a mean of 17.7 years of follow-up through linkage to nationwide and essentially complete databases. Multivariate Cox proportional hazards models were used to estimate HR with 95% CI. Interaction on the additive scale between alcohol and smoking was estimated by calculating the attributable proportion due to interaction (AP). RESULTS: Overall, alcohol consumption was associated with a 30% reduced incidence of RA (HR 0.69, 95% CI 0.55 to 0.86) with a dose-response relationship (p value for trend
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