An international website dedicated to providing current information on news, reports, publications,and peer-reviewed research articles concerning alcoholism and alcohol-related problems throughout the world.
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Alcohol may affect dietary intake. However, little is known about diets on drinking days in the US population.
We determined whether the diets of drinkers differ on drinking compared with nondrinking days.
Data were from the 2003–2008 NHANES Mobile Examination Center interview. We identified 1864 current drinkers (1126 men and 738 women) who completed two 24-h dietary recalls, one of which was on a drinking day and the other of which was on a nondrinking day. Sex-specific repeated-measures analyses that were adjusted for dietary recall order and recall day of the week were used to compare within-individual differences in energy, nutrient, and food-group intakes. Analyses were weighted to produce representative estimates.
On their drinking (compared with nondrinking) days, men consumed an excess 168 nonalcohol kcal (P < 0.01), which was reflected in higher intakes of nutrients including total protein (P < 0.001), total fat (P < 0.01), saturated fat (P < 0.01), monounsaturated fat (P < 0.01), potassium (P < 0.001), and sodium (P < 0.05). Men also had higher intakes of food groups including meat (P < 0.001), white potatoes (P < 0.05), and discretionary oil and solid fat (P < 0.05) and lower intakes of total fruit (P < 0.05) and milk (P < 0.05). Women did not consume excess nonalcohol kilocalories but had higher intakes of total fat (P < 0.05), monounsaturated fat (P < 0.05), polyunsaturated fat (P < 0.05), potassium (P < 0.01), and discretionary oil and solid fat (P < 0.05) and lower intakes of milk (P < 0.01) and milk products (P < 0.01).
These mostly moderate drinkers had poorer diets on drinking days. Same-day associations between alcohol and diet could be useful targets for public health efforts to improve dietary intake.
A free 75-minute webinar, taking place on Wednesday, April 17, 2013, from 2:00 to 3:15 p.m. EDT, will focus on evidence-based strategies for preventing underage drinking that are age and culturally appropriate and address both individual and environmental factors. This webinar will be the third in the 2013 series of underage drinking prevention webinars sponsored by the Interagency Coordinating Committee on the Prevention of Underage Drinking (ICCPUD). The series features national leaders and experts discussing the extent and nature of the problem, lessons from recent research, and evidence-based strategies for addressing underage drinking. Presenters on April 17 will be:
Frances M. Harding, Director of the Center for Substance Abuse Prevention, Substance Abuse and Mental Health Services Administration (SAMHSA);
Kelli A. Komro, Ph.D., M.P.H., Professor in the Department of Health Outcomes and Policy within the College of Medicine and the Associate Director of the Institute for Child Health Policy at the University of Florida;
Robert F. Saltz, Ph.D., Senior Scientist for the Prevention Research Center in Berkeley, California; and
Richard Spoth, Ph.D., F. Wendell Miller Senior Prevention Scientist and Director of the Partnerships in Prevention Science Institute, Iowa State University.
This webinar is being presented by four ICCPUD members: the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Drug Abuse, the Office of National Drug Control Policy, and SAMHSA; SAMHSA is the lead agency for ICCPUD. Advance registration is now open.
Reports on the prevalence and nature of underage drinking and the national efforts and best practices to address the problem. Also reports on state policies, enforcement activities, and prevention programs underway to address underage drinking.
Underage drinking and associated problems have profound negative consequences for underage drinkers, their families, their communities, and society as a whole. Underage drinking contributes to a wide range of costly health and social problems, including motor vehicle crashes (the greatest single mortality risk for underage drinkers); suicide; interpersonal violence (e.g., homicides, assaults, rapes); unintentional injuries such as burns, falls, and drowning; brain impairment; alcohol dependence; risky sexual activity; academic problems; and alcohol and drug poisoning. On average, alcohol is a factor in the deaths of approximately 4,700 youths in the United States per year, shortening their lives by an average of 60 years (Centers for Disease Control and Prevention [CDC] Alcohol-Related Disease Impact [ARDI] software, 2011). Data show meaningful reductions in underage drinking, particularly among younger age groups. From 2004 to 2010, young people ages 12 to 20 showed statistically significant declines in both past-month alcohol use and binge alcohol use. These encouraging results were most significant in the 12- to 17-year-old age group, where past-month alcohol use declined by 22.7 percent and past-month binge drinking declined by 29.7 percent. But there is still cause for concern. For example, in 2010, 37 percent of 20-year-olds reported binge drinking (drinking at levels substantially increasing the risk of injury or death) in the past 30 days; about 14 percent of 20-year-olds had, in those 30 days, binged five or more times. Furthermore, although drinking levels are lower at younger ages, patterns of consumption across the age spectrum pose significant threats to health and well-being. Particularly troubling is the erosion of the traditional gap between underage males and females in binge drinking. This gap is disappearing as females’ drinking practices converge with those of males. Thus, females are at increasing risk of alcohol-related mortality and morbidity, including sexual violence. Still, there is reason for optimism and hope for continued progress. As discussed in Chapters 3 and 4 of this Report, States are increasingly adopting comprehensive policies and practices to alter the individual and environmental factors that contribute to underage drinking and its consequences; these can be expected to reduce alcohol-related death and disability and associated healthcare costs. These efforts can potentially reduce underage drinking and its consequences and change norms that support underage drinking in American communities.
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Prolonged ethanol (EtOH) intake may perturb function of the hypothalamic–pituitary–adrenal axis in a manner that promotes dependence and influences EtOH withdrawal severity. Prior in vivo and in vitro studies suggest that corticosteroids, in particular, may be elevated during EtOH intoxication and withdrawal, suggesting that intracellular glucocorticoid receptors (GRs) may promote the development of EtOH dependence.
Daily mean EtOH doses for D1 to D4 of the regimen were 14.4, 9.9, 7.1, and 8.6 g/kg, respectively. The EtOH gavage regimen produced mean BELs of 255 mg/dl at 0900 on D2 and 156.2 mg/dl at 0900 on D4 of the regimen. Withdrawal from the EtOH exposure regimen, beginning 10 hours after the last EtOH administration, produced significant elevations in BCL and behavioral abnormalities including tremors, stereotypy, and “wet dog shakes.” Mifepristone administration did not alter food intake or weight during the 4-day regimen, nor were there drug-dependent differences in BEL or BCL on withdrawal day. Although mifepristone produced no significant changes in behavior of EtOH-naïve animals, pretreatment with mifepristone (40 mg/kg) significantly reduced the severity of EtOH withdrawal.
Findings suggest that activation of GRs promotes neuroadaptation to binge-like EtOH exposure, contributing to the development of EtOH dependence. Further, GRs may represent therapeutic targets to be exploited in reducing the severity of EtOH withdrawal.
The mixing of alcohol and energy drinks (AMEDs) is a trend among college students associated with higher rates of heavy episodic drinking and negative alcohol-related consequences. The goals of this study were to take a person-centered approach to identify distinct risk profiles of college students based on AMED-specific constructs (expectancies, attitudes, and norms) and examine longitudinal associations between AMED use, drinking, and consequences.
A random sample of incoming freshmen (n =387, 59% female) completed measures of AMED use, AMED-specific expectancies, attitudes, and normative beliefs, and drinking quantity and alcohol-related consequences. Data were collected at 2 occasions: spring semester of freshmen year and fall semester of sophomore year.
Latent profile analysis identified 4 subgroups of individuals: occasional AMED, anti-AMED, pro-AMED, and strong peer influence. Individuals in the pro-AMED group reported the most AMED use, drinking, and consequences. There was a unique association between profile membership and AMED use, even after controlling for drinking.
Findings highlighted the importance of AMED-specific expectancies, attitudes, and norms. The unique association between AMED risk profiles and AMED use suggests AMED use is a distinct behavior that could be targeted by AMED-specific messages included in existing brief interventions for alcohol use.
Since its advent, alcohol has been utilized throughout history socially, for rituals, worship, and for its therapeutic, antibacterial, and analgesic properties. In moderation, alcohol consumption and its use are generally viewed as clinically beneficial. Excessive alcohol consumption on the other hand has been recognized as having several adverse implications. Excessive use increases the risk of liver and heart disease, metabolic disturbances, nutritional deficiencies, certain cancers, brain damage, dementia, neuropathy, as well as other facets of morbidity and mortality.
This review targets the sequelae of alcohol consumption on the heart, specifically on myocardial contractility, calcium channel signaling, and intracellular signaling pathways. With the incidence of alcohol-induced cardiac abnormalities being higher than previously thought, it is of increasing importance to elucidate the mechanisms behind them. Here, the cardiac effects of alcohol were not discussed in isolation but in conjunction with other important factors, such as high- and low-density lipoprotein levels and vascular dilatory influences. We explore these mechanisms, in particular, the oxidative stress as the major contributor, as well as pathways that may prove to be cardioprotective.
As such, we demonstrate the involvement of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2/NRF2) as well as AKT that act as regulators of oxidative balance during oxidative stress responses.
Thus, alcohol consumption may confer a cardioprotective effect when used in moderation through an AKT/NRF2-dependent mechanism.
Alcohol abuse is the second leading cause of dilated cardiomyopathy, a disorder specifically referred to as alcoholic cardiomyopathy (ACM). Rodent and human studies have revealed cardiac fibrosis to be a consequence of ACM, and prior studies by this laboratory have associated this occurrence with elevated transforming growth factor-beta (TGF-β) and activated fibroblasts (myofibroblasts). To date, there have been no other studies to investigate the direct effect of alcohol on the cardiac fibroblast.
Primary rat cardiac fibroblasts were cultured in the presence of ethanol (EtOH) and assayed for fibroblast activation by collagen gel contraction, alpha-smooth muscle actin (α-SMA) expression, migration, proliferation, apoptosis, collagen I and III, and TGF-β expression. The TGF-β receptor type 1 inhibitor compound SB 431542 and a soluble recombinant TGF-βII receptor (RbII) were used to assess the role of TGF-β in the response of cardiac fibroblasts to EtOH.
Treatment for cardiac fibroblasts with EtOH at concentrations of 100 mg/dl or higher resulted in fibroblast activation and fibrogenic activity after 24 hours including an increase in contraction, α-SMA expression, migration, and expression of collagen I and TGF-β. No changes in fibroblast proliferation or apoptosis were observed. Inhibition of TGF-β by SB 431542 and RbII attenuated the EtOH-induced fibroblast activation.
EtOH treatment directly promotes cardiac fibroblast activation by stimulating TGF-β release from fibroblasts. Inhibiting the action of TGF-β decreases the fibrogenic effect induced by EtOH treatment. The results of this study support TGF-β to be an important component in cardiac fibrosis induced by exposure to EtOH.
Alcohol consumption has been linked to increased tobacco use and craving in both dependent and nondaily smokers, yet the extent to which these relationships depend on interactions involving nicotine remains unclear. This study examined the acute effects of alcohol on the subjective and behavioral responses to nicotine-containing tobacco and denicotinized tobacco in 17 (10 male) dependent daily smokers (DDS) and 23 (11 male) nondependent nondaily smokers (NNS).
During 4 randomized double-blind sessions, participants assessed the effects of nicotine-containing tobacco or denicotinized tobacco following the administration of a moderately intoxicating dose of alcohol (mean blood alcohol concentration = 0.076 g/dl) or a placebo beverage. They could then self-administer additional puffs of the same type of cigarette sampled over a 60-minute period using a progressive ratio task.
In NNS, alcohol significantly increased the self-administration of both nicotine-containing and denicotinized cigarettes, and no differences in self-administration were observed between the 2 types of tobacco within either beverage condition. In contrast, in DDS, alcohol was associated with decreased denicotinized tobacco self-administration relative to the placebo beverage condition as well as with increased self-administration of nicotine-containing tobacco relative to denicotinized tobacco. DDS also exhibited relatively elevated craving following the administration of a nicotine-containing cigarette in the alcohol beverage condition.
Findings suggest that nicotine may be critical to the drinking–smoking relationship in DDS, but that nonnicotine smoking factors may be more important in NNS.
Animals that have chronically consumed alcohol and are subsequently deprived of it markedly increase their intake above basal levels when access to alcohol is reinstated. Such an effect, termed the alcohol deprivation effect (ADE), has been proposed to reflect (i) an obsessive–compulsive behavior, (ii) craving, or (iii) an increased reinforcing value of ethanol (EtOH). It has been reported that acetaldehyde, a highly reinforcing metabolite of EtOH, is generated in the brain by the action of catalase. Recent studies show that the administration of an anticatalase (shRNA)-encoding lentiviral vector into the brain ventral tegmental area (VTA) of naïve rats virtually abolishes (85 to 95%) their EtOH intake. It is hypothesized that the antireinforcing effect of the anticatalase vector will also inhibit the ADE.
Two-month-old Wistar-derived UChB alcohol drinker rats were offered free access to water and 10 and 20% EtOH for 67 days. Thereafter, the animals were deprived of EtOH for 15 days and were subsequently offered access to the EtOH solutions. At the start of the deprivation period, animals were microinjected a single dose of an anticatalase (or control) vector into the VTA. EtOH intake was measured on the first hour of EtOH re-exposure as well as on a 24-hour basis for 7 days.
A marked ADE was observed when EtOH intake was measured on the first hour or 24 hours following EtOH re-exposure, compared to the corresponding controls. The administration of the anticatalase vector reduced ADE by 60 to 80% (p < 0.001) on the first hour and by 63 to 80% (p < 0.001) on the initial 24 hours of EtOH re-exposure (first and second ADE, respectively) without changing the total fluid intake, indicating a specific effect on EtOH drinking.
Ethanol intake associated with ADE—a binge-like drinking behavior—is markedly inhibited by the administration of an anticatalase vector into the VTA, which blocks the conversion of EtOH into acetaldehyde, strongly suggesting that the marked increased EtOH intake that follows an alcohol deprivation period is mediated by acetaldehyde and its reinforcing metabolite.
The main theme of the three-day Conference is: Regional Health Priorities and Opportunities: Evidence for Action in the Changing Global Financial Situation.
”We and our members from all over the EAC think it is great that this conference takes place and that it is already the fourth time it is being held,” says Moses Waweru, Chairman
of the East African Alcohol Policy Alliance (EAAPA).”We need to come together anddiscuss obstacles to our development, and we need more research and evidence.”
”But we also need to make sure that these types of conferences manage to address a comprehensive approach to regional health priorities,” says Aimable Mwananawe, Chairpersonof RADAPA. ”In that sense I hope that this conference is not a missed opportunity to address alcohol harm and its impact in the EAC.” > > > > Read More
The α-Ca2+/calmodulin-dependent protein kinase II (αCaMKII) is a crucial enzyme controlling plasticity in the brain. The autophosphorylation of αCaMKII works as a ‘molecular memory’ for a transient calcium activation, thereby accelerating learning. We investigated the role of αCaMKII autophosphorylation in the establishment of alcohol drinking as an addiction-related behavior in mice.
We found that alcohol drinking was initially diminished in αCaMKII autophosphorylation-deficient αCaMKIIT286A mice, but could be established at wild-type level after repeated withdrawals. The locomotor activating effects of a low-dose alcohol (2g/kg) were absent in αCaMKIIT286A mice, whereas the sedating effects of high-dose (3.5g/kg) were preserved after acute and subchronic administration. The in vivo microdialysis revealed that αCaMKIIT286A mice showed no dopamine (DA) response in the nucleus accumbens to acute or subchronic alcohol administration, but enhanced serotonin (5-HT) responses in the prefrontal cortex. The attenuated DA response in αCaMKIIT286A mice was in line with altered c-Fos activation in the ventral tegmental area after acute and subchronic alcohol administration.
In order to compare findings in mice with the human condition, we tested 23 single-nucleotide polymorphisms (SNPs) in the CAMK2A gene for their association with alcohol dependence in a population of 1333 male patients with severe alcohol dependence and 939 controls. We found seven significant associations between CAMK2A SNPs and alcohol dependence, one of which in an autophosphorylation-related area of the gene.
Together, our data suggest αCaMKII autophosphorylation as a facilitating mechanism in the establishment of alcohol drinking behavior with changing the DA–5-HT balance as a putative mechanism.
The survey will provide the first ever national picture of the number and nature of the alcohol services in England’s hospitals and PHE will go on to develop guidance and materials to support the continued development and delivery of such services. Iain Armstrong of the NTA has indicated around half of the key Local Authority areas have completed the survey to date, with the survey remaining open to commissioners until 5th April 2013. > > > > Read More
This study examined whether parental drinking motives are associated with young adults' drinking motives, and their association with young adults' drinking behaviors.
The sample consisted of 290 18-year-old and 289 20-year-old drinking young adults and their parents.
For the younger group, stronger maternal coping motives were related to stronger social and enhancement motives, while stronger paternal coping motives were associated with stronger young adult coping motives. For the older group, stronger maternal coping motives were related to stronger social motives and stronger paternal enhancement motives were associated with stronger overall young adult drinking motives. For the younger group, both enhancement and conformity motives were predictive of their alcohol use. For the older group, only higher social motives were predictive of higher alcohol use. Both groups' higher coping and enhancement motives were associated with more drinking problems.
While, concerning content, there are some differences due to parent gender and adolescent age, stronger parental drinking motives are indeed associated with stronger adolescent drinking motives, which in turn are quite consistently related to more adolescent alcohol use and alcohol-related problems.
The aim of the study was to identify heavy drinking trajectories from age 16 to 42 years and to examine their associations with health, social, employment and economic disadvantage in mid-adulthood.
Finnish cohort study's participants who were 16 years old in 1983 were followed up at age 22, 32 and 42 (n = 1334). Heavy drinking was assessed at every study phase and based on these measurements trajectories of heavy drinking were identified. The trajectory groups were then examined as predictors of disadvantage at age 42.
Five distinct heavy drinking trajectories were identified: moderate (35%), steady low (22%), decreasing (9%), increasing (11%) and steady high (23%). Frequencies of the trajectory groups differed by gender. Using the moderate trajectory as a reference category, women in the steady high trajectory had an increased risk of experiencing almost all disadvantages at age 42. In men, increasing and steady high groups had an increased risk for experiencing health and economic disadvantage. Steady high female drinkers and steady high and increasing male drinkers had the highest risk for disadvantage in mid-adulthood. By identifying heavy drinking trajectories from adolescence to mid-adulthood we can better predict long-term consequences of heavy alcohol use and plan prevention and intervention programmes.
Forum Comments While any alcohol consumption during pregnancy is not encouraged, and heavy drinking is associated with an increase in risk of a number of adverse health outcomes in the fetus, there is controversy as to whether the occasional drink by the mother during pregnancy has any detectable effect on the child. The present study is based on cognitive and behavioral assessments in a large cohort of children at age 11 in relation to the mother’s reporting of alcohol intake during the first trimester. > > > > Read More
Clinical and epidemiologic evidence has documented the significant associations between medical illnesses and psychiatric disorders. However, extensive research has focused on the comorbidity of medical conditions and depression, and most were cross sectional, focused on clinical samples, and grounded in DSM-III or DSM-III-R diagnostic criteria.
The current prospective investigation examined associations among medical conditions at baseline and incident psychiatric disorders over a 3-year follow-up, using data from Waves 1 and 2 of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).
Overall, the 3-year incidence rates of DSM-IV substance use, mood and anxiety disorders ranged from 0.65% (bipolar II) to 5.2% (alcohol abuse). Multiple regression analysis was conducted to examine the prospective physical–mental associations, while controlling for sociodemographic characteristics, psychological stress and health-related risk factors, and comorbid physical and psychiatric disorders.
The present study represents, to our knowledge the largest population-based prospective study examining the physical–mental associations. Our results showed distinctly different patterns of comorbidity of medical illnesses with substance use, mood, and anxiety disorders. Stomach ulcer/gastritis, hypertension and arthritis emerged to be significant predictors of incident psychiatric disorders.
Although women occupy a central position in agriculture in many developing countries, they face numerous constraints to achieving their full potential including unequal access to assets and limited decision-making authority. We explore the intersection of agricultural livelihoods, food and economic security, and women’s sexual and reproductive health in Iringa Region, Tanzania. Our goal was to understand whether the benefits of supporting women in the agricultural sector might also extend to more distal outcomes, including sexual and reproductive health.
Using the Sustainable Livelihoods Framework to guide data collection, we conducted 13 focus group discussions (FGD) with female (n = 11) and male farmers (n = 2) and 20 in-depth interviews with agricultural extension officers (n = 10) and village agro-dealers (n = 10).
Despite providing the majority of agricultural labor, women have limited control over land and earned income and have little bargaining power. In response to these constraints, women adopt adaptive livelihood strategies, such as alcohol production, that allow them to retain control over income and support their households. However, women’s central role in alcohol production, in concert with the ubiquitous nature of alcohol consumption, places them at risk by enhancing their vulnerability to unsafe or transactional sex. This represents a dangerous confluence of risk for female farmers, in which alcohol plays an important role in income generation and also facilitates high-risk sexual behavior.
Alcohol production and consumption has the potential to both directly and indirectly place women at risk for undesirable sexual and reproductive health outcomes. Group formation, better access to finance, and engaging with agricultural extension officers were identified as potential interventions for supporting women farmers and challenging harmful gender norms. In addition, joint, multi-sectoral approaches from health and agriculture and alternative income-generating strategies for women might better address the complexities of achieving safe and sustainable livelihoods for women in this context.
The Nordic Page (Norway) - Women are Drinking
Norwegian women drink more and more and they are
about to take over the men’s drinking patterns, according to VG. Twenty years
ago, men drank four times as much as women, but now men drink twice as much as
women. General Secretary of Actis (Norwegian Policy Network on Alcohol and
Drugs), Anne Karin Kolstad says there are many factors that can explain the
growing trend among women.
MSN News (Norway) - Experts: Alcohol isn't a
cure-all, so hold off
"People have several motives for drinking
alcohol, but most evidence today indicates that health is not a valid argument,"
author Hans Olav Fekjaer, a psychiatrist in Oslo, Norway, told Reuters Health by
YLE.fi (Finland) - Rise in alcohol tax
sharply divides opinion
The Federation of the Brewing and Soft Drinks
Industry (FBSDI) is wondering why they are being punished with the new tax
hikes, while the Substance Abuse Prevention Association (EHYT ry) says that
fears of “booze tourism” to neighbouring countries are overstated.
Bangkok Post (Thailand) - Alcohol consumption
A new study claims that the average Thai aged 15
and older consumes 7.1 litres of pure alcohol per year. The study by the Centre
for Alcohol Studies says the number of retail shops selling alcohol has
increased by 120,000 in the past 10 years.
Huffington Post - Brain-Alcohol Study Reveals
How Drinking Disrupts Hand-Eye Coordination
Anyone who's failed a sobriety test will tell
you that making coordinated movements while drunk is hard, and a new study
explains why. Alcohol appears to disrupt connections between the brain's visual
and muscle control regions.
The Daily Telegraph - Energy drinks make
boozers more aggressive, as drinkers start boozing at home
MIXING energy drinks with alcohol and drugs may
lead to increased levels of violence, a new study suggests. They become more
intoxicated as the night progresses and fuel their partying with energy
Although alcoholism is a worldwide problem resulting in millions of deaths, only a small percentage of alcohol users become addicted. The specific neural substrates responsible for individual differences in vulnerability to alcohol addiction are not known.
In this study, we used rodent models to study behavioral and synaptic correlates related to individual differences in the development of ethanol locomotor sensitization, a form of drug-dependent behavioral plasticity associated with addiction vulnerability. Male Swiss Webster mice were treated daily with saline or 1.8 g/kg ethanol for 21 d. Locomotor activity tests were performed once a week for 15 min immediately after saline or ethanol injections. After at least 11 d of withdrawal, cohorts of saline- or ethanol-treated mice were used to characterize the relationships between locomotor sensitization, ethanol drinking, and glutamatergic synaptic transmission in the nucleus accumbens.
Ethanol-treated mice that expressed locomotor sensitization to ethanol drank significantly more ethanol than saline-treated subjects and ethanol-treated animals resilient to this form of behavioral plasticity. Moreover, ethanol-sensitized mice also had reduced accumbal NMDA receptor function and expression, as well as deficits in NMDA receptor-dependent long-term depression in the nucleus accumbens core after a protracted withdrawal.
These findings suggest that disruption of accumbal core NMDA receptor-dependent plasticity may represent a synaptic correlate associated with ethanol-induced locomotor sensitization and increased propensity to consume ethanol.
One alternative explanation for the observed impact of normative feedback interventions is that participants who receive normative information will just report reductions in their drinking rather than actually reducing the amount they drink. The current study tested the immediate impact of receiving normative information on self-reports of drinking.
A random half of participants (39 out of 80) were presented with normative information about college drinking and then asked information about their drinking. Participants in the control condition were not presented with the normative information before answering the questions about their drinking.
Risky drinking participants presented with the normative information reported significantly less drinking as compared to those in the control condition (p < .05).
This study examined types of internal and external motivations for seeking treatment and the predictive utility of different types of motivation among 180 women with an alcohol use disorder (AUD) participating in a two-armed trial testing different individual and couple therapies for AUDs. Reasons for seeking treatment were coded for type of internal or external motivation.
Most women (97%) cited internal reasons for seeking help, including: concern about progression of AUD (61.1%), health (43.3%), mental health (38.9%), and family (38.3%).
Occupational concerns, an internal motivator cited by 6% of women, were associated with better drinking outcomes; interpersonal-family concerns were associated with poorer outcomes.
Some motivators for seeking treatment may not be related to sustained changes in drinking, suggesting that understanding motivators for treatment may be inadequate to maintain change. Reasons for help-seeking may need to be addressed in treatment to produce long-lasting change.
Recent research findings suggest that heavy alcohol use is associated with alterations of the hypothalamic–pituitary–adrenal axis and autonomic nervous system function and that early abstinence is associated with blunted stress responsiveness.
This study investigated abstinent alcohol-dependent participants (AADs; n = 31), who had a drinking history of levels about 97 drinks per week (abstinence range: 2 weeks to 24 months), actively drinking problem drinkers (PRDs; n = 23), who reported drinking levels about 47 drinks per week and who were abstinent for at least 24 hours, and healthy control (HC) participants (n = 20). It was investigated how participants responded to a psychosocial stress task. All of them were exposed to a modified Trier Social Stress Test. Salivary cortisol, heart rate, skin conductance levels, and negative affect were assessed as stress indicators.
AADs showed stress reactions comparable to HC participants, whereas active PRDs showed increased heart rate and cortisol stress responses. In the AAD group, duration of abstinence was positively related to cortisol stress responses.
Active PRDs showed increased responses to psychosocial stress. Results indicate that duration of abstinence is a key factor when analyzing and interpreting stress responses in alcohol abuse and dependence.
During late prenatal and early postnatal life, the reproductive system in males undergoes an extensive series of physiological and morphological changes. Prenatal ethanol (EtOH) exposure has marked effects on the development of the reproductive system, with long-term effects on function in adulthood. The present study tested the hypothesis that prenatal EtOH exposure will delay the onset of spermatogenesis.
Development of the seminiferous tubules and the onset of spermatogenesis were examined utilizing a rat model of fetal alcohol spectrum disorder (FASD). Male offspring from ad libitum-fed control (C), pair-fed (PF), and EtOH-fed (prenatal alcohol exposure [PAE]) dams were terminated on postnatal (PN) days 5, 15, 18, 20, 25, 35, 45, and 55, to investigate morphological changes through morphometric analysis of the testes from early neonatal life through young adulthood.
PAE males had lower relative (adjusted for body weight) testis weights compared with PF and/or C males from PN15 through puberty (PN45). In addition, fewer gonocytes (primordial germ cells) were located on the basal lamina on PN5, while more of those touching the basal lamina were dividing in PAE compared with PF and C males, suggesting delayed cell division and migration processes. As well, the percentage of tubules with open lumena was lower in PAE compared with PF and C males on PN18 and 20, and PAE males had fewer primary spermatocytes per tubule on PN18 and round spermatids per tubule on PN25 compared with C males. Finally, the percentage of tubules at stages VII and VIII, when mature spermatids move to the apex of the epithelium and are released, was lower in PAE compared with PF and/or C males in young adulthood (PN55).
Maternal EtOH consumption appears to delay both reproductive development and the onset of spermatogenesis in male offspring, with effects persisting at least until young adulthood.
From studies using a diverse range of model organisms, we now acknowledge that epigenetic changes to chromatin structure provide a plausible link between environmental teratogens and alterations in gene expression leading to disease. Observations from a number of independent laboratories indicate that ethanol (EtOH) has the capacity to act as a powerful epigenetic disruptor and potentially derail the coordinated processes of cellular differentiation. In this study, we sought to examine whether primary neurospheres cultured under conditions maintaining stemness were susceptible to alcohol-induced alterations in the histone code. We focused our studies on trimethylated histone 3 lysine 4 and trimethylated histone 3 lysine 27, as these are 2 of the most prominent posttranslational histone modifications regulating stem cell maintenance and neural differentiation.
Primary neurosphere cultures were maintained under conditions promoting the stem cell state and treated with EtOH for 5 days. Control and EtOH-treated cellular extracts were examined using a combination of quantitative RT-PCR and chromatin immunoprecipitation techniques.
We find that the regulatory regions of genes controlling both neural precursor cell identity and processes of differentiation exhibited significant declines in the enrichment of the chromatin marks examined. Despite these widespread changes in chromatin structure, only a small subset of genes including Dlx2, Fabp7, Nestin, Olig2, and Pax6 displayed EtOH-induced alterations in transcription. Unexpectedly, the majority of chromatin-modifying enzymes examined including members of the Polycomb Repressive Complex displayed minimal changes in expression and localization. Only transcripts encoding Dnmt1, Uhrf1, Ehmt1, Ash2 l, Wdr5, and Kdm1b exhibited significant differences.
Our results indicate that primary neurospheres maintained as stem cells in vitro are susceptible to alcohol-induced perturbation of the histone code and errors in the epigenetic program. These observations indicate that alterations to chromatin structure may represent a crucial component of alcohol teratogenesis and progress toward a better understanding of the developmental origins of fetal alcohol spectrum disorders.
It has been argued that consuming alcohol mixed with energy drinks (AmED) causes a subjective underestimation of intoxication and an increased level of risk-taking behavior. To date, however, there is mixed support for AmED-induced reductions in perceived intoxication, and no objective assessment of risk-taking following AmED consumption. Consequently, the present study aimed to determine the effect of alcohol and energy drink (ED) consumption on subjective measures of intoxication and objective measures of risk-taking.
Using a placebo-controlled, single-blind, cross-over design, participants (n =28) attended 4 sessions in which they were administered, in counterbalanced order: 0.5 g/kg alcohol, 3.57 ml/kg ED, AmED, and a placebo beverage. Participants completed the Biphasic Alcohol Effects Scale and a Subjective Effects Scale at baseline and 30 and 125 minutes postbeverage administration; risk-taking was measured using the Balloon Analogue Risk Task (BART).
Participants reported greater subjective intoxication, impairment, and sedation after active relative to placebo alcohol consumption, with no interactive AmED effects. However, a significant moderate magnitude increase in stimulation ratings was observed in the AmED relative to alcohol, ED, and placebo conditions. There was no independent effect of alcohol, or interactive effect with ED, on the BART. A significant, yet small magnitude, increase in risk-taking was evident in active relative to placebo ED conditions.
The interactive effect of AmED appears restricted to perceived stimulation, with alcohol-induced increases in subjective intoxication occurring regardless of presence or absence of ED. Engagement in risk-taking behavior was only increased by ED consumption; however, this effect was only of small magnitude; at these doses, alcohol consumption, with or without EDs, did not affect risk-taking. Further research assessing the dose-dependent effects of AmED on objectively measured risk-taking behavior could clarify whether the ED effect increases with higher doses and whether an interactive effect is observed with higher alcohol doses.