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Background Heavy episodic (binge) drinking is common among young adults and can lead to injury and illness. Young adults who seek care in the Emergency Department (ED) may be disproportionately affected with binge drinking behavior, therefore provide an opportunity to reduce future risk through screening, brief intervention and referral to treatment (SBIRT). Mobile phone text messaging (SMS) is a common form of communication among young adults and has been shown to be effective at providing behavioral support to young adult drinkers after ED discharge. Efficacy of SMS programs to reduce binge drinking remains unknown. Methods/Design We will conduct a three parallel arm, randomized trial. A convenience sample of adults aged 18 to 25 years attending three EDs in Pittsburgh, PA and willing to participate in the study will be screened for hazardous alcohol consumption. Participants identified as hazardous drinkers will then be allocated to either 12 weeks of weekly SMS drinking assessments with feedback (SA+F), SMS drinking assessments without feedback (SA), or a control group. Randomization will be via an independent and remote computerized randomization and will be stratified by study site. The SA+F group will be asked to provide pre-weekend drinking intention as well as post-weekend consumption via SMS and will receive feedback messages focused on health consequences of alcohol consumption, personalized normative feedback, protective drinking strategies and goal setting. Follow-up data on alcohol use and injury related to alcohol will be collected through a password-protected website three, six and nine months later. The primary outcome for the study is binge drinking days (≥4 drinks for women; ≥5 drinks for men) during the previous month, and the main secondary outcome is the proportion of participants who report any injury related to alcohol in the prior three months. Discussion This study will test the hypothesis that a mobile phone text-messaging program will result in immediate and durable reductions in binge drinking among at-risk young adults. By testing an intervention group to an assessment-only and control group, we will be able to separate the effect of assessment reactivity. By collecting pre-weekend drinking intentions and post-weekend consumption data in the SA+F group, we will be able to better understand mechanism of change. Trial registration Clinicaltrials.gov NCT01688245

Background Internationally, studies show that similar levels of alcohol consumption in deprived communities (vs. more affluent) result in higher levels of alcohol-related ill health. Hypotheses to explain this alcohol harm paradox include deprived drinkers: suffering greater combined health challenges (e.g. smoking, obesity) which exacerbate effects of alcohol harms; exhibiting more harmful consumption patterns (e.g. bingeing); having a history of more harmful consumption; and disproportionately under-reporting consumption. We use a bespoke national survey to assess each of these hypotheses. Methods A national telephone survey designed to test this alcohol harm paradox was undertaken (May 2013 to April 2014) with English adults ( n  = 6015). Deprivation was assigned by area of residence. Questions examined factors including: current and historic drinking patterns; combined health challenges (smoking, diet, exercise and body mass); and under-reported consumption (enhanced questioning on atypical/special occasion drinking). For each factor, analyses examined differences between deprived and more affluent individuals controlled for total alcohol consumption. Results Independent of total consumption, deprived drinkers were more likely to smoke, be overweight and report poor diet and exercise. Consequently, deprived increased risk drinkers (male >168–400 g, female >112–280 g alcohol/week) were >10 times more likely than non-deprived counterparts to drink in a behavioural syndrome combining smoking, excess weight and poor diet/exercise. Differences by deprivation were significant but less marked in higher risk drinkers (male >400 g, female >280 g alcohol/week). Current binge drinking was associated with deprivation independently of total consumption and a history of bingeing was also associated with deprivation in lower and increased risk drinkers. Conclusions Deprived increased/higher drinkers are more likely than affluent counterparts to consume alcohol as part of a suite of health challenging behaviours including smoking, excess weight and poor diet/exercise. Together these can have multiplicative effects on risks of wholly (e.g. alcoholic liver disease) and partly (e.g. cancers) alcohol-related conditions. More binge drinking in deprived individuals will also increase risks of injury and heart disease despite total alcohol consumption not differing from affluent counterparts. Public health messages on how smoking, poor diet/exercise and bingeing escalate health risks associated with alcohol are needed, especially in deprived communities, as their absence will contribute to health inequalities.

Alcohol is a potent somnogen and one of the most commonly used “over the counter” sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol-induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep-promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired sleep homeostasis. In conclusion, we suggest that alcohol may disrupt sleep homeostasis to cause sleep disruptions.

Background Breast cancer (BC) rates have been increasing in young women in the U.S. Alcohol is an established risk factor for breast cancer and has been consistently associated with hormone receptor positive cancers, the type of breast cancer that has been increasing the fastest in young women. Given these trends, we conducted an ecological study to examine whether alcohol consumption, and specifically binge drinking trends, were correlated with female breast cancer diagnosed under 40 years of age using breast cancer data from the Surveillance, Epidemiology, and End Results (SEER) Cancer Registry. We accounted for a latent period before cancer diagnosis by using exposure 10 years before the outcome (lag model); we also conducted a separate cumulative analysis of 10-year aggregate exposure. Findings Moderate (Incidence Rate Ratio (IRR) = 1.05, 95% Confidence Interval (CI) = 1.02–1.07) and heavy (IRR = 1.05, 95% CI = 1.02–1.07)( ≥  1 and ≥  2 drinks/day, respectively) alcohol consumption were each associated with Luminal A breast cancer but not the other molecular subtypes. Binge drinking was associated with an increased rate of early-onset Luminal A BC in both the 10-year lag model (IRR = 1.06, 95% CI = 1.02 to 1.11) and the cumulative model (IRR = 1.05, 95% CI = 1.02–1.07). Binge drinking was also associated with early-onset Luminal B BC in the cumulative model (IRR = 1.04, 95% CI = 1.01–1.07), but not associated with ERBB2-enriched or triple negative early-onset BC in either model. Conclusion These trends support the hypothesis that one reason for the increase in early-onset breast cancer is from increased alcohol intake including binge drinking.

Background Epidemiological and biomedical evidence link adverse childhood experiences (ACEs) with health-harming behaviors and the development of non-communicable disease in adults. Investment in interventions to improve early life experiences requires empirical evidence on levels of childhood adversity and the proportion of HHBs potentially avoided should such adversity be addressed. Methods A nationally representative survey of English residents aged 18 to 69 (n = 3,885) was undertaken during the period April to July 2013. Individuals were categorized according to the number of ACEs experienced. Modeling identified the proportions of HHBs (early sexual initiation, unintended teenage pregnancy, smoking, binge drinking, drug use, violence victimization, violence perpetration, incarceration, poor diet, low levels of physical exercise) independently associated with ACEs at national population levels. Results Almost half (47%) of individuals experienced at least one of the nine ACEs. Prevalence of childhood sexual, physical, and verbal abuse was 6.3%, 14.8%, and 18.2% respectively (population-adjusted). After correcting for sociodemographics, ACE counts predicted all HHBs, e.g. (0 versus 4+ ACEs, adjusted odds ratios (95% confidence intervals)): smoking 3.29 (2.54 to 4.27); violence perpetration 7.71 (4.90 to 12.14); unintended teenage pregnancy 5.86 (3.93 to 8.74). Modeling suggested that 11.9% of binge drinking, 13.6% of poor diet, 22.7% of smoking, 52.0% of violence perpetration, 58.7% of heroin/crack cocaine use, and 37.6% of unintended teenage pregnancy prevalence nationally could be attributed to ACEs. Conclusions Stable and protective childhoods are critical factors in the development of resilience to health-harming behaviors in England. Interventions to reduce ACEs are available and sustainable, with nurturing childhoods supporting the adoption of health-benefiting behaviors and ultimately the provision of positive childhood environments for future generations.

Introduction According to a precautionary principle, it is recommended that pregnant women and women trying to conceive abstain from alcohol consumption. In this dose–response meta‐analysis, we aimed to examine the association between alcohol consumption and binge drinking and the risk of miscarriage in the first and second trimesters. Material and methods The literature search was conducted in MEDLINE, Embase and the Cochrane Library in May 2022, without any language, geographic or time limitations. Cohort or case–control studies reporting dose‐specific effects adjusting for maternal age and using separate risk assessments for first‐ and second‐trimester miscarriages were included. Study quality was assessed using the Newcastle–Ottawa Scale. This study is registered with PROSPERO, registration number CRD42020221070. Results A total of 2124 articles were identified. Five articles met the inclusion criteria. Adjusted data from 153 619 women were included in the first‐trimester analysis and data from 458 154 women in the second‐trimester analysis. In the first and second trimesters, the risk of miscarriage increased by 7% (odds ratio [OR] 1.07, 95% confidence interval [CI] 0.96–1.20) and 3% (OR 1.03, 95% CI 0.99–1.08) for each additional drink per week, respectively, but not to a statistically significant degree. One article regarding binge drinking and the risk of miscarriage was found, which revealed no association between the variables in either the first or second trimester (OR 0.84 [95% CI 0.62–1.14] and OR 1.04 [95% CI 0.78–1.38]). Conclusions This meta‐analysis revealed no dose‐dependent association between miscarriage risk and alcohol consumption, but further focused research is recommended. The research gap regarding miscarriage and binge drinking needs further investigation. No dose‐dependent association between miscarriage risk and alcohol consumption was found in this dose–response meta‐analysis.

The diversity of bacterial species in the oral cavity makes it a key site for research. The close proximity of the oral cavity to the brain and the blood brain barrier enhances the interest to study this site. Changes in the oral microbiome are linked to multiple systemic diseases. Alcohol is shown to cause a shift in the microbiome composition. This change, particularly in the oral cavity, may lead to neurological diseases. Alzheimer’s disease (AD) is a common neurodegenerative disorder that may cause irreversible memory loss. This study uses the meta-analysis method to establish the link between binge drinking, the oral microbiome and AD. The QIAGEN Ingenuity Pathway Analysis (IPA) shows that high levels of ethanol in binge drinkers cause a shift in the microbiome that leads to the development of AD through the activation of eIF2, regulation of eIF4 and p70S6K signaling, and mTOR signaling pathways. The pathways associated with both binge drinkers and AD are also analyzed. This study provides a foundation that shows how binge drinking and the oral microbiome dysbiosis lead to permeability changes in the blood brain barrier (BBB), which may eventually result in the pathogenesis of AD.

Both chronic and acute (binge) alcohol drinking are important health and economic concerns worldwide and prominent risk factors for the development of alcoholic liver disease (ALD). There are no FDA-approved medications to prevent or to treat any stage of ALD. Therefore, discovery of novel therapeutic strategies remains a critical need for patients with ALD. Relevant experimental animal models that simulate human drinking patterns and mimic the spectrum and severity of alcohol-induced liver pathology in humans are critical to our ability to identify new mechanisms and therapeutic targets. There are several animal models currently in use, including the most widely utilized chronic ad libitum ethanol (EtOH) feeding (Lieber–DeCarli liquid diet model), chronic intragastric EtOH administration (Tsukamoto–French model), and chronic-plus-binge EtOH challenge (Bin Gao—National Institute on Alcohol Abuse and Alcoholism (NIAAA) model). This review provides an overview of recent advances in rodent models of binge EtOH administration which help to recapitulate different features and etiologies of progressive ALD. These models include EtOH binge alone, and EtOH binge coupled with chronic EtOH intake, a high fat diet, or endotoxin challenge. We analyze the strengths, limitations, and translational relevance of these models, as well as summarize the liver injury outcomes and mechanistic insights. We further discuss the application(s) of binge EtOH models in examining alcohol-induced multi-organ pathology, sex- and age-related differences, as well as circadian rhythm disruption.

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.

Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a major public health concern, largely driven by the high‐fat, high‐sugar and low‐fibre Western diet. The Western diet is often accompanied by binge drinking, or the rapid consumption of alcohol in a short time leading to a blood alcohol concentration of ≥0.08%. Emerging evidence suggests that co‐consumption of a Western diet and binge drinking might converge on shared pathological mechanisms in males, but little is known about the role of sex in this interaction. Given these complex interactions between diet, alcohol, sex and liver health, we sought to investigate how the addition of binge drinking to a Western diet impacts MASLD progression in male and female mice. Young (6‐week‐old) male and female C57BL6/J mice (n = 9–11 per sex per group) were assigned to the following groups: Control, Control/Binge, Western, or Western/Binge. Following 12 weeks of treatment, Western diet, regardless of binge drinking, resulted in increased hepatic lipid accumulation and oxidative damage in both sexes, with males showing more evidence of disease than females. In general, male mice in the Western binge group had the most pronounced evidence of liver damage among males, whereas female mice in the Western diet group tended to have more evidence of disease than all other female groups as measured by histology, serum transaminases and immunohistochemistry. The collective results suggest that addition of binge drinking to a Western diet can result in a more progressive form of liver disease in males and that sex plays a key role in response to the combination of unhealthy diet and binge drinking. What is the central question of this study? Does addition of binge drinking to a Western diet result in a more progressive liver disease than either alone, and how is this modulated by sex? What is the main finding and its importance? In male mice, combining binge drinking and a Western diet resulted in more pronounced detriments in key liver measures than either factor alone, whereas females showed greater liver damage in response to a Western diet alone than to the combined exposure.