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)
BACKGROUND: Alcohol-induced cardiotoxicity is incompletely understood. Specifically, the long-term impact of alcohol use on ventricular remodeling or dysfunction, its modulators, and effect thresholds among young adults remain controversial.
OBJECTIVES: The authors sought to evaluate a potential relationship between alcohol intake and cardiac remodeling, assessed by echocardiography, over 20 years of follow-up.
METHODS: Among the CARDIA (Coronary Artery Risk Development in Young Adults) study cohort, the authors studied all subjects without baseline heart disorders who provided adequate information on their drinking habits and underwent echocardiographic evaluation at years 5 and 25 of the study. The echocardiographic outcomes were left ventricular (LV) ejection fraction, indexed LV end-diastolic volume and LV mass, and left atrial diameter. Participants were grouped according to their weighted-average weekly drinking habits. An additional analysis used the estimated cumulative alcohol consumption. Regression models and multivariable fractional polynomials were used to evaluate the association between alcohol consumption and the outcomes.
RESULTS: Among the 2,368 participants, alcohol consumption was an independent predictor of higher indexed LV mass (p = 0.014) and indexed LV end-diastolic volume (p = 0.037), regardless of sex. No significant relationship between alcohol intake and LV ejection fraction was found. Drinking predominantly wine was associated with less cardiac remodeling and there was a nonsignificant trend for a harmful effect of binge drinking.
CONCLUSIONS: After 20 years of follow-up, alcohol intake was associated with adverse cardiac remodeling, although it was not related with LV systolic dysfunction in this initially healthy young cohort. Our results also suggest that drinking predominantly wine associates with less deleterious findings in cardiac structure.
PURPOSE: To study the association between coffee and alcoholic beverage consumption and alcoholic liver disease mortality.
METHODS: In total, 219,279 men and women aged 30-67 years attended cardiovascular screening in Norway from 1994 to 2003. Linkage to the Cause of Death Registry identified 93 deaths from alcoholic liver disease. Coffee consumption was categorized into four levels: 0, 1-4, 5-8, and greater than or equal to 9 cups/d and alcohol consumption as 0, greater than 0 to less than 1.0, 1.0 to less than 2.0, and greater than or equal to 2.0 units/d, for beer, wine, liquor, and total alcohol consumption.
RESULTS: The hazard ratios per one category of consumption were 2.06 (95% confidence interval 1.62-2.61), 0.68 (0.46-1.00), and 2.54 (1.92-3.36) for beer, wine, and liquor, respectively. Stratification at 5 cups/d (the mean) revealed a stronger association between alcohol consumption and alcoholic liver disease at less than 5 versus 5 or more cups/d. With less than 5 cups/d, 0 alcohol units/d as reference, the hazard ratio reached to 25.5 (9.2-70.5) for greater than or equal to 2 units/d, whereas with greater than or equal to 5 cups/d, it reached 5.8 (1.9-17.9) for greater than or equal to 2 units/d. A test for interaction was significant (P = .01).
CONCLUSIONS: Coffee and wine consumption were inversely associated with alcoholic liver disease death. Total alcohol consumption was adversely associated with alcoholic liver disease mortality and the strength of the association varied with the level of coffee consumption.
OBJECTIVE: A systematic review and meta-analysis to estimate the magnitude of the association between alcohol consumption and the risk of community-acquired pneumonia (CAP) in adults was undertaken.
DESIGN: Systematic review and meta-analysis.
METHODS: Comprehensive searches of Medline, Embase and Web of Science were carried out to identify comparative studies of the association between alcohol intake and CAP between 1985 and 2017. Reference lists were also screened. A random-effects meta-analysis was used to estimate pooled effect sizes. A dose-response meta-analysis was also performed.
RESULTS: We found 17 papers eligible for inclusion in the review, of which 14 provided results which could be pooled. Meta-analysis of these 14 studies identified an 83% increased risk of CAP among people who consumed alcohol or in higher amounts, relative to those who consumed no or lower amounts of alcohol, respectively (relative risk=1.83, 95% CI 1.30 to 2.57). There was substantial between-study heterogeneity, which was attributable in part to differences in study continent, adjustment for confounders and pneumonia diagnosis (clinical vs death). Dose-response analysis found that for every 10-20 g higher alcohol intake per day, there was an 8% increase in the risk of CAP.
CONCLUSIONS: The findings suggest that alcohol consumption increases the risk of CAP. Therefore, strengthening policies to reduce alcohol intake would be likely to reduce the incidence of CAP.