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.
BACKGROUND: Recent trends in alcoholic liver disease, alcohol-related emergency room admissions, and alcohol use disorder prevalence as measured by general-population surveys have raised concerns about rising alcohol-related morbidity and mortality in the United States. In contrast, upward trends in per capita alcohol consumption have been comparatively modest.
METHODS: To resolve these discordant observations, we sought to examine trends in the prevalence of alcohol use and binge drinking from 6 regularly or periodically administered national surveys using a meta-analytic approach. Annual or periodic prevalence estimates for past-12-month or past-30-day alcohol use and binge drinking were estimated for available time points between the years 2000 and 2016. Estimates were combined in a random-effects regression model in which prevalence was modeled as a log-linear function of time to obtain meta-analytic trend estimates for the full population and by sex, race, age, and educational attainment.
RESULTS: Meta-analysis-derived estimates of average annual percentage increase in the prevalence of alcohol use and binge drinking were 0.30% per year (95% CI: 0.22%, 0.38%) and 0.72% per year (95% CI: 0.46%, 0.98%), respectively. There was substantial between-survey heterogeneity among trend estimates, although there was notable consistency in the degree to which trends have impacted various demographic groups. For example, most surveys found that the changes in prevalence for alcohol use and binge drinking were large and positive for ages 50 to 64 and 65 and up, and smaller, negative, or nonsignificant for ages 18 to 29.
CONCLUSIONS: Significant increases in the prevalence of alcohol use and of binge drinking over the past 10 to 15 years were observed, but not for all demographic groups. However, the increase in binge drinking among middle-aged and older adults is substantial and may be driving increasing rates of alcohol-related morbidity and mortality.
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.