Journal: Alcoholism, clinical and experimental research
Attributes of alcohol sensitivity are present before alcohol use disorders (AUDs) develop, they predict those adverse alcohol outcomes, are familial in nature, and many are heritable. Whether measured by alcohol challenges or retrospective reports of numbers of drinks required for effects, alcohol sensitivity reflects multiple phenotypes, including low levels of alcohol response and alcohol-related stimulation. Identification of genes that contribute to alcohol sensitivity could help identify individuals carrying risks for AUDs through their alcohol responses for whom early intervention might mitigate their vulnerability. Such genes could also improve understanding of biological underpinnings of AUDs, which could lead to new treatment approaches. However, the existing literature points to a wide range of genetic mechanisms that might contribute to alcohol responses, and few such genetic findings have been widely replicated. This critical review describes the potential impact of the diverse methods used to study sensitivity on the diversity of genetic findings that have been reported, places the genetic variants mentioned in the literature into broader categories rather than isolated results, and offers suggestions regarding how to advance the field by interpreting findings in light of the methods used to select research subjects and to measure alcohol sensitivity. To date, the most promising results have been for GABA, glutamate, opioid, dopamine, serotonin, and cholinergic system genes. The more gene variants that can be identified as contributors to sensitivity the better future gene screening platforms or polygenic scores are likely to be.
Human adolescence is a crucial stage of neurological development during which ethanol (EtOH) consumption is often at its highest. Alcohol abuse during adolescence may render individuals at heightened risk for subsequent alcohol abuse disorders, cognitive dysfunction, or other neurological impairments by irreversibly altering long-term brain function. To test this possibility, we modeled adolescent alcohol abuse (i.e., intermittent EtOH exposure during adolescence [AIE]) in rats to determine whether adolescent exposure to alcohol leads to long-term structural and functional changes that are manifested in adult neuronal circuitry.
Alcohol consumption, alcohol-related emergency department visits, and hospitalizations have all increased in the last 2 decades, particularly among women and people middle-aged and older. The purpose of this study was to explore data from death certificates to assess whether parallel changes in alcohol-related mortality occurred in the United States in recent years.
The majority of U.S. older adults consume alcoholic beverages. The older population is projected to almost double by 2050. Substantially more drinkers are likely.
Alcohol hangover is a growing research area, but differences across the life span have not been assessed. Here, we test the hypothesis that the severity of hangovers depends on age.
Recently, Marczinski and colleagues (2013) showed that energy drinks combined with alcohol augment a person’s desire to drink more alcohol relative to drinking alcohol alone. The current study replicates the findings of Marczinski and colleagues (2013) using a robust measure of alcohol craving.
There has been a dramatic rise in the consumption of alcohol mixed with energy drinks (AmEDs) in social drinkers. It has been suggested that AmED beverages might lead individuals to drink greater quantities of alcohol. This experiment was designed to investigate whether the consumption of AmEDs would alter alcohol priming (i.e., increasing ratings of wanting another drink) compared with alcohol alone.
This review provides a qualitative assessment of all known scientific studies on the impact of alcohol ingestion on nocturnal sleep in healthy volunteer’s. At all dosages, alcohol causes a reduction in sleep onset latency, a more consolidated first half sleep and an increase in sleep disruption in the second half of sleep. The effects on rapid eye movement (REM) sleep in the first half of sleep appear to be dose related with low and moderate doses showing no clear trend on REM sleep in the first half of the night whereas at high doses, REM sleep reduction in the first part of sleep is significant. Total night REM sleep percentage is decreased in the majority of studies at moderate and high doses with no clear trend apparent at low doses. The onset of the first REM sleep period is significantly delayed at all doses and appears to be the most recognizable effect of alcohol on REM sleep followed by the reduction in total night REM sleep. The majority of studies, across dose, age and gender, confirm an increase in slow wave sleep (SWS) in the first half of the night relative to baseline values. The impact of alcohol on SWS in the first half of night appears to be more robust than the effect on REM sleep and does not appear to be an epiphenomenon REM sleep reduction. Total night SWS is increased at high alcohol doses across gender and age groups.
BACKGROUND: Previous studies have demonstrated that high alcohol consumption is a predictor of divorce. However, there is a lack of studies with prospective data from both spouses. The effects of drinking among husbands versus wives and of concordant versus discordant drinking in couples are therefore unknown. Concordant drinking may lead to increased divorce rates because the malignant effects of heavy drinking are experienced in double doses; alternatively it may lead to marital stability due to partner compatibility. METHODS: All inhabitants in a Norwegian county were invited to participate in a health study. We identified 19,977 married couples where both spouses participated. Respondents provided information on alcohol use and mental distress. Survival analysis was applied to study the risk of divorce over the next 15 years. Demographics and mental distress were used as covariates. RESULTS: Heavy drinking among men (hazard ratio [HR] = 1.39) and women (HR = 1.41) increased the risk of future marital dissolution, even after adjusting for demography (reference group “light drinkers”). The HR for divorce was 1.51 when only the husband was a heavy drinker, while it was 3.07 when only the wife was a heavy drinker. Moreover, there were strong interaction effects: concordant abstainers (HR = 0.40) and concordant heavy drinkers (HR = 0.35) had lower risks of divorce compared to the risk expected from combining the main effects. Nevertheless, couples with 2 heavy drinkers (HR = 1.63) had higher risk of divorce than couples with 2 light drinkers. CONCLUSIONS: This study demonstrated that both the level of alcohol use and compatibility in alcohol use are important predictors of marital dissolution.
Previous research has suggested that intrauterine alcohol exposure is associated with a variety of adverse outcomes in offspring. However, few studies have investigated its association with offspring internalizing disorders in late adolescence.