PURPOSE: To compare acute effects of moist snuff with or without nicotine and red wine with or without alcohol on prandial hormones and metabolism.
BASIC PROCEDURES AND METHODS: Two deciliters of wine, with or without alcohol, were taken together with a standardized supervised meal in 14 healthy women and men. All participants also combined the meal with usage of with moist snuff, with or without nicotine. The snuff was replaced hourly at each of the four settings, i.e. snuff with or without nicotine combined with red wine with or without alcohol, that started at 0800 o'clock and were finished at noon.
MAIN FINDINGS: We found ghrelin levels to be more efficiently suppressed when drinking red wine with alcohol compared to non-alcoholic wine by analyzing area under the curve (AUC). AUC for regular wine was 370 +/- 98 pg/ml x hours and 559 +/- 154 pg/ml x hours for de-alcoholized red wine, p < 0.0001 by general linear model. The postprandial metabolic rate was further elevated following alcohol containing red wine compared with non-alcoholic red wine (p = 0.022). Although glucose levels were not uniformly lower after alcoholic red wine, we found lowered glucose levels 3 h after the meal (mean glucose wine: 4.38 +/- 0.96 mmol/l, non-alcoholic wine: 4.81 +/- 0.77 mmol/l, p = 0.005). Nicotine-containing moist snuff (AUC: 1406 +/- 149 nmol/ml x hours) elevated the levels of serum cortisol compared with nicotine-free snuff (AUC: 1268 +/- 119 nmol/ml x hours, p = 0.005). We found no effects of nicotine or alcohol on feelings of satiety.
CONCLUSIONS: Alcohol in red wine augmented the postprandial suppression of ghrelin and it also lowered postprandial glucose 3 h post-meal. These effects are in line with observational trials linking regular intake of moderate amounts of red wine with lower risk for diabetes.
We examined whether the often-reported protective association of alcohol with cardiovascular disease (CVD) risk could arise from confounding. Our sample comprised 908 men (56-67 years), free of prevalent CVD. Participants were categorized into 6 groups: never drinkers, former drinkers, and very light (1-4 drinks in past 14 days), light (5-14 drinks), moderate (15-28 drinks), and at-risk (>28 drinks) drinkers.
Generalized linear mixed effect models examined the associations of alcohol use with three established CVD risk scores: The Framingham Risk Score (FRS); the atherosclerotic CVD (ASCVD) risk score; and the Metabolic Syndrome (MetS) Severity score, adjusting for group differences in demographics, body size, and health-related behaviors. In separate models we additionally adjusted for several groups of potentially explanatory factors including socioeconomic status, social support, physical and mental health status, childhood factors, and prior history of alcohol misuse.
Results showed lower CVD risk among light and moderate alcohol drinkers, relative to very light drinkers, for all CVD risk scores, independent of demographics, body size, and health-related behaviors. Alcohol-CVD risk associations were robust to further adjustment for several groups of potential explanatory factors.
Study limitations include the all-male sample with limited racial and ethnic diversity, and the inability to adjust for sugar consumption and for patterns of alcohol consumption.
Although this observational study does not address causation, results show that middle-aged men who consume alcohol in moderation have lower CVD risk and better cardiometabolic health than men who consume little or no alcohol, independent of a variety of health, behavioral, psychosocial, and earlier life factors.
AIMS: The association between low-to-moderate alcohol consumption and atrial fibrillation (AF) has yet to be fully elucidated. The main purpose of this meta-analysis was to estimate the risk of incident AF related to low-to-moderate alcohol consumption.
METHODS AND RESULTS: A meta-analysis was performed on 13 publications discussing the estimated risk for AF with habitual low-to-moderate alcohol intake in 10 266 315 participants. Graphical augmentations to the funnel plots were used to illustrate the potential impact of additional evidence on the current meta-analysis. Thirteen eligible studies were included in this meta-analysis. We found that moderate alcohol consumption was associated with an increased risk of incident AF in males [hazard ratio (HR) 1.09, 95% confidence interval (CI): 1.07-1.11, P < 0.00001], Europeans (HR 1.32, 95% CI: 1.23-1.42, P < 0.00001), and Asians (HR 1.09, 95% CI: 1.07-1.11, P < 0.00001). Moderate beer consumption was associated with an increased risk of developing AF (HR 1.11, 95% CI: 1.02-1.21, P = 0.01). Low alcohol consumption conferred an increased risk of AF in males (HR 1.14, 95% CI: 1.01-1.28, P = 0.04) and Europeans (HR 1.12, 95% CI: 1.07-1.17, P < 0.00001).
CONCLUSIONS: This analysis represents the increased risk of incident AF in males, Europeans, and Asians at moderate alcohol consumption levels and in males and Europeans at low alcohol consumption levels. Those who drink any preferred alcohol beverage at moderate levels should be cautious for incident AF. More studies are warranted to find those factors that influence alcohol's effect on predisposing AF.
Evidence from research studies reports that wine consumption is associated with lower cardiovascular disease risk, partly through the amelioration of oxidative stress. The aim of the present study was to examine the effect of regular light to moderate wine consumption from coronary heart disease (CHD) patients compared to the effect induced by alcohol intake without the presence of wine microconstituents, on oxidation-induced macromolecular damage as well as on endogenous antioxidant enzyme activity. A randomized, single-blind, controlled, three-arm parallel intervention was carried out, in which 64 CHD patients were allocated to three intervention groups. Group A consumed no alcohol, and Group B (wine) and Group C (ethanol) consumed 27 g of alcohol/day for 8 weeks. Blood and urine samples were collected at baseline and at 4 and 8 weeks. Urine oxidized guanine species levels, protein carbonyls, thiobarbituric acid substances (TBARS) levels, as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, were measured. Oxidized guanine species and protein carbonyl levels were significantly increased in the ethanol group during the intervention and were significantly decreased in the wine group. These results support the idea that wine's bioactive compounds may exert antioxidant actions that counteract the macromolecular oxidative damage induced by alcohol in CHD patients.