BACKGROUND: In cross-sectional studies and short-term clinical trials, it has been suggested that there is a positive dose-response relation between alcohol consumption and HDL concentrations. However, prospective data have been limited.
OBJECTIVE: We sought to determine the association between total alcohol intake, the type of alcohol-containing beverage, and the 6-y (2006-2012) longitudinal change in HDL-cholesterol concentrations in a community-based cohort.
DESIGN: A total of 71,379 Chinese adults (mean age: 50 y) who were free of cardiovascular diseases and cancer and did not use cholesterol-lowering agents during follow-up were included in the study. Alcohol intake was assessed via a questionnaire in 2006 (baseline), and participants were classified into the following categories of alcohol consumption: never, past, light (women: 0-0.4 servings/d; men: 0-0.9 servings/d), moderate (women: 0.5-1.0 servings/d; men: 1-2 servings/d), and heavy (women: >1.0 servings/d; men: >2 servings/d). HDL-cholesterol concentrations were measured in 2006, 2008, 2010, and 2012. We used generalized estimating equation models to examine the associations between baseline alcohol intake and the change in HDL-cholesterol concentrations with adjustment for age, sex, smoking, physical activity, obesity, hypertension, diabetes, liver function, and C-reactive protein concentrations.
RESULTS: An umbrella-shaped association was observed between total alcohol consumption and changes in HDL-cholesterol concentrations. Compared with never drinkers, past, light, moderate, and heavy drinkers experienced slower decreases in HDL cholesterol of 0.012 mmol . L-1 . y-1 (95% CI: 0.008, 0.016 mmol . L-1 . y-1), 0.013 mmol . L-1 . y-1 (95% CI: 0.010, 0.016 mmol . L-1 . y-1), 0.017 mmol . L-1 . y-1 (95% CI: 0.009, 0.025 mmol . L-1 . y-1), and 0.008 mmol . L-1 . y-1 (95% CI: 0.005, 0.011 mmol . L-1 . y-1), respectively (P < 0.0001 for all), after adjustment for potential confounders. Moderate alcohol consumption was associated with the slowest increase in total-cholesterol:HDL-cholesterol and triglyceride: HDL-cholesterol ratios. We observed a similar association between hard-liquor consumption and the HDL-cholesterol change. In contrast, greater beer consumption was associated with slower HDL-cholesterol decreases in a dose-response manner.
CONCLUSION: Moderate alcohol consumption was associated with slower HDL-cholesterol decreases; however, the type of alcoholic beverage had differential effects on the change in the HDL-cholesterol concentration.
There has been little focus on the effects of alcohol on the elderly. Although the cardiovascular benefits of moderate alcohol consumption could be of the greatest benefit in this group, so might be the detrimental effects of abuse. In this article, we review available data on the effects of alcohol consumption on cardiovascular disease, cardiomyopathy, arrhythmias, hypertension, and vascular function in older adults. Alcohol consumption has increased in the US population age 65 years and older in the last decade, as has monthly heavy episodic drinking in older alcohol consumers. Studies of alcohol consumption in older subjects suggest that consumption in moderation does not increase the risk of heart failure, hypertension, or atrial arrhythmias, and may in fact improve vascular function and reduce cardiovascular disease events. As in younger subjects, heavy consumption, or abuse of alcohol, negates any potential protective cardiovascular effects, increasing the incidence of heart failure and hypertension. Although alcohol consumed in moderation does not appear harmful in the elderly population, heavier consumption exacerbates hypertension and increases the incidence of heart failure.
AIMS: Alcohol intoxication is a source of significant illness and injury commonly resulting in emergency department (ED) visits. We characterize recent trends in alcohol-related visits to US EDs using nationally representative data.
METHODS: We conducted a retrospective review of data on national ED visits among patients aged 18 years or older with alcohol intoxication between 2001 and 2011 using the National Hospital Ambulatory Medical Care Survey (NHAMCS). Demographic and resource utilization trends in alcohol-related visits were examined. We also assessed ED length of stay (LOS) across the study period, as well as the total hours spent on ED care for alcohol-related complaints.
RESULTS: Between 2001-2002 and 2010-2011, alcohol-related visits increased from 2,459,748 to 3,856,346 (P = 0.049). Utilization of resources such as laboratory tests, medications and radiography increased, with the use of advanced imaging (i.e. computed tomography and magnetic resonance imaging) increasing 232.2% (P < 0.001) from 2001-2002 to 2010-2011. Overall LOS increased 16.1% (P = 0.028), while LOS among patients admitted to the hospital increased 24.9% (P = 0.076). Total alcohol-related hours spent in EDs nationwide increased from 5.6 million in 2001 to 11.6 million in 2011, an increase of 108.5% (P < 0.001) compared with an increase in overall ED hours of 54.0% (P < 0.001).
CONCLUSION: Alcohol-related ED visits are increasing at a greater rate than overall ED visits and represent a growing burden on hospital resources.
Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76x10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1x10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3x10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.