BACKGROUND: Some of the previously reported health benefits of low-to-moderate alcohol consumption may derive from health status influencing alcohol consumption rather than the opposite. We examined whether health status changes influence changes in alcohol consumption, cessation included.
METHODS: Data came from 571 current drinkers aged >/=60 years participating in the Seniors-ENRICA cohort in Spain. Participants were recruited in 2008-2010 and followed-up for 8.2 years, with four waves of data collection. We assessed health status using a 52-item deficit accumulation (DA) index with four domains: functional, self-rated health and vitality, mental health, and morbidity and health services use. To minimise reverse causation, we examined how changes in health status over a 3-year period (wave 0-wave 1) influenced changes in alcohol consumption over the subsequent 5 years (waves 1-3) using linear/logistic regression, as appropriate.
RESULTS: Compared with participants in the lowest tertile of DA change (mean absolute 4.3% health improvement), those in the highest tertile (7.8% worsening) showed a reduction in alcohol intake (beta: -4.32 g/day; 95% CI -7.00 to -1.62; p trend=0.002) and were more likely to quit alcohol (OR: 2.80; 95% CI 1.54 to 5.08; p trend=0.001). The main contributors to decreasing drinking were increased functional impairment and poorer self-rated health, whereas worsening self-rated health, onset of diabetes or stroke and increased prevalence of hospitalisation influenced cessation.
CONCLUSIONS: Health deterioration is related to a subsequent reduction and cessation of alcohol consumption contributing to the growing evidence challenging the protective health effect previously attributed to low-to-moderate alcohol consumption.
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: To assess sex-specific associations between risk-based alcohol drinking levels and the 10-year cardiovascular disease (CVD) risk scores and cardiovascular (CV) risk factors.
Methods: Data from 9,995 Koreans (4,249 men, 5,746 women), aged 40 to 79 years who did not have CVD and participated in the 2011 to 2013 Korea National Health and Nutrition Examination Survey, were used to assess risk-based alcohol drinking levels in the past year (no drinking, drinking at low risk, and drinking at risk) categorized by the National Institute on Alcohol Abuse and Alcoholism, components of the 10-year CVD risk scores using the Adult Treatment Panel III risk score and the 10-year hard atherosclerotic CVD risk score, CV risk factors, and confounding factors (age, smoking status, body mass index, educational attainment, income level, and physical activity).
Results: Drinking levels had positive associations with blood pressure and levels of glucose, triglycerides, and high-density lipoprotein cholesterol (HDL-C) and inverse associations with levels of low-density lipoprotein cholesterol and non-HDL-C and ratio of total cholesterol (TC) to HDL-C in men, while higher drinking levels were associated with higher HDL-C levels and lower ratio of TC to HDL-C in women after adjusting for confounding factors (p for trend < 0.001). With respect to the 10-year CVD risk scores, higher drinking levels were associated with lower scores in both sexes (p for trend < 0.001).
Conclusions: Risk-based drinking levels were more likely to have dose-dependent associations with CV risk factors in men than in women and had inverse relationships with 10-year CVD risk in both men and women.
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.