Alcohol consumption and leukocyte telomere length.

The relationship between alcohol consumption and mortality generally exhibits a U-shaped curve. The longevity observed with moderate alcohol consumption may be explained by other confounding factors, and, if such a relationship is present, the mechanism is not well understood. Indeed, the optimal amount of alcohol consumption for health has yet to be determined. Leukocyte telomere length is an emerging quantifiable marker of biological age and health, and a shorter telomere length is a predictor of increased mortality. Because leukocyte telomere length is a quantifiable and objectively measurable biomarker of aging, we sought to identify the amount of alcohol consumption associated with the longest telomere length and least telomere length attrition. Among over 2,000 participants from two distinct cohort studies, we found no pattern of alcohol consumption that was associated with longer telomere length or less telomere length attrition over time. Binge drinking may reduce telomere length. Using telomere length as a marker of age and health, these data fail to demonstrate any benefits of alcohol consumption, even when consumed in moderation.

Binge alcohol consumption 18 h after induction of sepsis in a mouse model causes rapid overgrowth of bacteria, a cytokine storm, and decreased survival.

Alcohol abuse increases vulnerability to infections and infection-related mortality. In previous studies, we found that acute alcohol abuse in a binge-drinking model in mice decreased resistance to bacterial sepsis when alcohol was administered near the time of bacterial challenge. In the present study, we investigated the effects of alcohol administered later in the course of sepsis (18 h after injection of Escherichia coli). Our working hypothesis was that decreased production of cytokines caused by alcohol at this time would actually improve survival, because overproduction of pro-inflammatory mediators is thought to be the proximate cause of mortality in sepsis. Unexpectedly, administration of alcohol late in the course of sepsis led to a rapid increase in the number of viable bacteria in the peritoneal cavity. Significant increases in the concentrations of several cytokines and chemokines coincided with the increased number of bacteria in alcohol-treated mice and decreased survival time. These results demonstrated our working hypothesis to be incorrect, and reiterated the complexity of sepsis. Hypothermia is a consistent feature in this model of sepsis. In control mice (E. coli only), body temperature was near normal by 18 h or 21 h after administration of E. coli, but in mice treated with alcohol 18 h after E. coli, hypothermia was significant 3 h later and ultimately mortality was significantly increased. However, counteracting the hypothermic effect of alcohol by external warming of mice led to earlier mortality, demonstrating that hypothermia was not the major cause of mortality. These results, along with previous results from studies in which alcohol was given before initiation of sepsis, suggest that decreased cytokine and chemokine production may not be the key effect of alcohol that decreases resistance to sepsis. It seems more likely that suppression of mechanisms by which macrophages and neutrophils kill bacteria is critical, and this can occur even in the presence of high levels of cytokines and chemokines.

Evaluation of Acute Alcohol Intoxication as the Primary Cause of Death: A Diagnostic Challenge for Forensic Pathologists.

Deaths caused by acute alcohol intoxication (AAI) remain a major public health issue. This study is retrospective and descriptive: an 8-year case analysis of deaths due to AAI in Maryland. Study showed that of 150 AAI deaths, the death rate among Hispanics (10.41/100,000 population) was significantly higher than all the non-Hispanics combined (1.88/100,000 population). The majority of individuals were young adults, overweight, and binge drinkers. The obese group showed significantly lower mean heart and peripheral blood alcohol concentration (BAC) (0.36%, 0.37%) than the normal weight group (0.45%, 0.42%). Based on the PBAC and urine AC ratio, 49.6% deaths likely occurred close to peak phase, followed by postabsorptive phase (31.6%) and absorptive phase (18.8%). Our results indicate that forensic pathologists should evaluate postmortem BAC in the light of individual's age, drinking history, body weight, possible phase of alcohol intoxication, and other autopsy findings when certifying AAI as primary cause of death.

Alcohol, drinking pattern and all-cause, cardiovascular and alcohol-related mortality in Eastern Europe.

Alcohol has been implicated in the high mortality in Central and Eastern Europe but the magnitude of its effect, and whether it is due to regular high intake or episodic binge drinking remain unclear. The aim of this paper was to estimate the contribution of alcohol to mortality in four Central and Eastern European countries. We used data from the Health, Alcohol and Psychosocial factors in Eastern Europe is a prospective multi-centre cohort study in Novosibirsk (Russia), Krakow (Poland), Kaunas (Lithuania) and six Czech towns. Random population samples of 34,304 men and women aged 45-69 years in 2002-2005 were followed up for a median 7 years. Drinking volume, frequency and pattern were estimated from the graduated frequency questionnaire. Deaths were ascertained using mortality registers. In 230,246 person-years of follow-up, 2895 participants died from all causes, 1222 from cardiovascular diseases (CVD), 672 from coronary heart disease (CHD) and 489 from pre-defined alcohol-related causes (ARD). In fully-adjusted models, abstainers had 30-50% increased mortality risk compared to light-to-moderate drinkers. Adjusted hazard ratios (HR) in men drinking on average ≥60 g of ethanol/day (3% of men) were 1.23 (95% CI 0.95-1.59) for all-cause, 1.38 (0.95-2.02) for CVD, 1.64 (1.02-2.64) for CHD and 2.03 (1.28-3.23) for ARD mortality. Corresponding HRs in women drinking on average ≥20 g/day (2% of women) were 1.92 (1.25-2.93), 1.74 (0.76-3.99), 1.39 (0.34-5.76) and 3.00 (1.26-7.10). Binge drinking increased ARD mortality in men only. Mortality was associated with high average alcohol intake but not binge drinking, except for ARD in men.

Impaired respiratory function and heightened pulmonary inflammation in episodic binge ethanol intoxication and burn injury.

Clinical data indicate that cutaneous burn injuries covering greater than 10% of the total body surface area are associated with significant morbidity and mortality, in which pulmonary complications, including acute respiratory distress syndrome (ARDS), contribute to nearly half of all patient deaths. Approximately 50% of burn patients are intoxicated at the time of hospital admission, which increases days on ventilators by 3-fold, and doubles the length of hospitalization, compared to non-intoxicated burn patients. The most common drinking pattern in the United States is binge drinking, where an individual rapidly consumes alcoholic beverages (4 for women, 5 for men) in 2 h. An estimated 38 million Americans binge drink, often several times per month. Experimental data demonstrate that a single binge-ethanol exposure, prior to scald injury, impairs innate and adaptive immune responses, thereby enhancing infection susceptibility and amplifying pulmonary inflammation, neutrophil infiltration, and edema, and is associated with increased mortality. Since these characteristics are similar to those observed in ARDS burn patients, our study objective was to determine whether ethanol intoxication and burn injury and the subsequent pulmonary congestion affect physiological parameters of lung function, using non-invasive and unrestrained plethysmography in a murine model system. Furthermore, to mirror young adult binge-drinking patterns, and to determine the effect of multiple ethanol exposures on pulmonary inflammation, we utilized an episodic binge-ethanol exposure regimen, where mice were exposed to ethanol for a total of 6 days (3 days ethanol, 4 days rest, 3 days ethanol) prior to burn injury. Our analyses demonstrate mice exposed to episodic binge ethanol and burn injury have higher mortality, increased pulmonary congestion and neutrophil infiltration, elevated neutrophil chemoattractants, and respiratory dysfunction, compared to burn or ethanol intoxication alone. Overall, our study identifies plethysmography as a useful tool for characterizing respiratory function in a murine burn model and for future identification of therapeutic compounds capable of restoring pulmonary functionality.

Vital signs: alcohol poisoning deaths - United States, 2010-2012.

BACKGROUND: Alcohol poisoning is typically caused by binge drinking at high intensity (i.e., consuming a very large amount of alcohol during an episode of binge drinking). Approximately 38 million U.S. adults report binge drinking an average of four times per month and consuming an average of eight drinks per episode. METHODS: CDC analyzed data for 2010­2012 from the National Vital Statistics System to assess average annual alcohol poisoning deaths and death rates (ICD-10 codes X45 and Y15; underlying cause of death) in the United States among persons aged ≥15 years, by sex, age group, race/ethnicity, and state. RESULTS: During 2010­2012, an annual average of 2,221 alcohol poisoning deaths (8.8 deaths per 1 million population) occurred among persons aged ≥15 years in the United States. Of those deaths, 1,681 (75.7%) involved adults aged 35­64 years, and 1,696 (76.4%) involved men. Although non-Hispanic whites accounted for the majority of alcohol poisoning deaths (67.5%; 1,500 deaths), the highest age-adjusted death rate was among American Indians/Alaska Natives (49.1 per 1 million). The age-adjusted rate of alcohol poisoning deaths in states ranged from 5.3 per 1 million in Alabama to 46.5 per 1 million in Alaska. CONCLUSIONS: On average, six persons, mostly adult men, die from alcohol poisoning each day in the United States. Alcohol poisoning death rates vary substantially by state. IMPLICATIONS FOR PUBLIC HEALTH PRACTICE: Evidence-based strategies for preventing excessive drinking (e.g., regulating alcohol outlet density and preventing illegal alcohol sales in retail settings) could reduce alcohol poisoning deaths by reducing the prevalence, frequency, and intensity of binge drinking.

Acute alcohol exposure has an independent impact on C-reactive protein levels, neutrophil CD64 expression, and subsets of circulating white blood cells differentiated by flow cytometry in nontrauma patients.

Acute and massive alcohol exposure (blood alcohol concentration of ≥1 g/L) is a common way to consume alcohol. In a prospective study performed in critically ill nontrauma patients, we compared C-reactive protein (CRP) values, circulating subsets of white blood cells, and neutrophil CD64 indexes recorded at admission to the intensive care unit between abstinent or moderate drinkers (n = 173), patients with acute or chronic alcohol exposure (n = 32), and patients with acute exposure but not chronically exposed to alcohol (n = 27). Values for CRP (P < 0.001), circulating neutrophils (P < 0.001), and neutrophil CD64 indexes (P < 0.001) were significantly lower in patients acutely exposed compared with the other patients, whereas values for B lymphocytes (P < 0.001) and cytotoxic (P < 0.001) and noncytotoxic T lymphocytes (P < 0.001) were significantly higher. After multiple regression analysis, alcohol exposure remained independently associated with values of CRP, neutrophils CD4 indexes, cytotoxic and noncytotoxic T lymphocytes, and CD16-negative and -positive monocytes. These results were not affected by the presence or absence of infection at admission. Our results suggest that in nontrauma critically ill patients, acute alcohol exposure diminishes inflammation and increases numbers of circulating B and T lymphocytes.

Mortality risks associated with average drinking level and episodic heavy drinking.

Data from the 1997 to 2004 National Health Interview Survey Sample Adult questionnaires were linked to the National Death Index (N = 242,397) to examine mortality risks associated with average and episodic heavy drinking. Cox proportional hazard models (Stata 12.0) revealed that (average) heavier drinkers and episodic heavy drinkers (5+ in a day) had increased mortality risks but when examined together, episodic heavy drinking added only modestly to the mortality risks of light and moderate drinkers. Limitations and implications of results for survey measurement of potentially harmful levels of alcohol use are noted. This was a Federal study that received no outside funding.

Episodic heavy drinking and 20-year total mortality among late-life moderate drinkers.

BACKGROUND: Analyses of moderate drinking have focused overwhelmingly on average consumption, which masks diverse underlying drinking patterns. This study examined the association between episodic heavy drinking and total mortality among moderate-drinking older adults. METHODS: At baseline, the sample was comprised of 446 adults aged 55 to 65; 74 moderate drinkers who engaged in episodic heavy drinking and 372 regular moderate drinkers. The database at baseline also included a broad set of sociodemographic, behavioral, and health status covariates. Death across a 20-year follow-up period was confirmed primarily by death certificate. RESULTS: In multiple logistic regression analyses, after adjusting for all covariates, as well as overall alcohol consumption, moderate drinkers who engaged in episodic heavy drinking had more than 2 times higher odds of 20-year mortality in comparison with regular moderate drinkers. CONCLUSIONS: Among older moderate drinkers, those who engage in episodic heavy drinking show significantly increased total mortality risk compared to regular moderate drinkers. Episodic heavy drinking-even when average consumption remains moderate-is a significant public health concern.

Alcohol-attributable mortality and years of potential life lost in Chile in 2009.

AIMS: The aim of the study was to estimate mortality and years of potential life lost (YPLL) attributable to alcohol consumption in 2009 in Chile. METHODS: The population considered for this study included those 15 years and over. Exposure to alcohol in the population was estimated by triangulating the records of alcohol per capita consumption in Chile with information from the Eighth National Study of Drugs in the General Population (2008). The effect of alcohol consumption on each cause of death (relative risk) was extracted from previously published meta-analyses. With this information we estimated the alcohol-attributable fraction (AAF) and deaths and YPLL due to alcohol consumption. The confidence intervals for the AAF were estimated with Monte Carlo sampling using the estimated variances of the exposure prevalence and relative effect. RESULTS: The estimated total number of deaths attributable to alcohol consumption was 8753 (95% CI: 6257, 11,584) corresponding to 9.8% (95% CI: 7.01%, 12.98%) of all deaths in Chile in 2009. The total estimated YPLL attributable to alcohol were 195,475 (95% CI: 164,287, 227,726), corresponding to 21.5% (95% CI: 18.1%, 25.0%) of total YPLL for that year in Chile. CONCLUSION: Alcohol consumption is a major risk factor and accounts for nearly one of ten deaths in Chile. These results may be used to guide the design of public health policies and evaluations.

Religion and selected health behaviors among Latinos in Texas.

Though research has shown that religion provides a protective influence with respect to a number of health-related outcomes, little work has examined its influence on patterns of alcohol (especially binge drinking) and tobacco consumption among Latinos in Texas. Thus, we used a probability sample of Texas adults to test this relationship via logistic regression. Our results revealed that clear distinctions emerge on the basis of both denomination and frequency of attendance. Specifically, Protestants who regularly attend religious services are significantly more likely to be abstainers and to have never smoked, while those with no religious affiliation exhibit relatively unfavorable risk profiles. These findings persist despite a range of socio-demographic controls. Our study supports the assertion that religion may serve as an important protective influence on risky health behaviors.

Divergent associations of drinking frequency and binge consumption of alcohol with mortality within the same cohort.

BACKGROUND: Observational studies show beneficial effects of moderate alcohol drinking on all-cause and cardiovascular disease (CVD) mortality, while binge drinking has been linked with increased mortality. The aim of this study was to assess the associations of alcohol use with mortality in a population with a hybrid of drinking patterns. METHOD: Participants in a population based cardiovascular health survey in Finnmark county in 1987-1988, aged 20-62 years, constituted the study cohort. Alcohol use was self-reported by use of questions on frequency of beer, wine and liquor intake, and one question on intake of around five drinks or more per occasion (binge drinking). Information on education, income and use of alcohol in an earlier and in a later survey was linked to the file. Mortality was assessed throughout 2009 by Cox regression, with adjustment for potential confounding factors. In the analysis of mortality by frequency of any alcohol use, we adjusted for binge consumption and vice versa. RESULTS: Two opposite trends appeared: a higher all-cause mortality in both sexes, and higher CVD mortality in men, with increasing frequency of binge drinking, compared with non-bingers. Second, in both sexes low-frequent use of any alcohol was associated with lower all-cause and CVD mortality, compared with abstention. The combination of any use of alcohol at least weekly and binge consumption at least monthly was common, particularly in men. CONCLUSIONS: Questions on drinking frequency and a specific question on binge drinking capture different effects of alcohol use on all-cause and CVD mortality.

All-cause mortality and fatal alcohol poisoning in Belarus, 1970-2005.

INTRODUCTION AND AIMS: Although alcohol appears to be an important contributor to the burden of disease in the countries of eastern Europe, little systematic research has been undertaken on its impact on mortality in the former Soviet republic of Belarus. There may be a number of factors underlying the particularly negative effect of alcohol on mortality in Belarus, including the pattern of drinking and use of surrogates. A solid body of research and empirical evidence suggests that hazardous patterns of alcohol consumption (binge drinking) lead to quicker and deeper intoxication, increasing the propensity for alcohol-related mortality. DESIGN AND METHOD: To estimate the aggregate level effect of binge drinking on the all-cause mortality rate, trends in the all-cause mortality and fatal alcohol poisoning rates (as a proxy for binge drinking) in Belarus from 1970 to 2005 were analysed employing AutoRegressive Integrated Moving Average (ARIMA) time-series analysis in order to assess a bivariate relationship between the two time-series. RESULTS: The results of time-series analysis suggest a close relationship between all-cause mortality and fatal alcohol poisoning rates at the population level. CONCLUSIONS: This study supports the hypothesis that alcohol and all-cause mortality are connected closely in countries where the drinking culture is characterised by heavy drinking episodes and adds to the growing body of evidence that a substantial proportion of total mortality in Belarus is due to acute effects of binge drinking.