To support the free and open dissemination of research findings and information on alcoholism and alcohol-related problems. To encourage open access to peer-reviewed articles free for all to view.

For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.


Saturday, January 26, 2013

Genetic and Environmental Predictors of Latent Trajectories of Alcohol Use from Adolescence to Adulthood: A Male Twin Study

Adolescence is characterized by higher levels of novelty-seeking and risk-taking behavior, including initiation of alcohol use. Also, there is considerable heterogeneity in the change and continuity of alcohol use over time, which emphasizes the need to examine factors predicting alcohol use and the patterns of use over time.

Retrospective data on average monthly alcohol use and risk and protective factors were obtained through interviews and questionnaires in 1,560 adult male twins. Latent class growth analysis in Mplus was performed on data of alcohol use over ages 15 to 36. Second, logistic regression analyses were used to associate risk and protective characteristics with membership in distinct latent trajectories of alcohol use.

Six trajectories of alcohol use were identified, varying in the level of alcohol use, the rate of change in use in early adolescence and the persistence of use into adulthood. Genetic risk of externalizing disorder and peer deviance showed the greatest risks for unfavorable alcohol trajectories with higher levels of use and higher rates of early increase in use. Parental monitoring and involvement in social activities showed protective effects. Involvement in religious activities was strongly associated with reduced persistence of high-level drinking in univariate but not multivariate regression analyses.

Risk and protective factors impacted differentially on level of alcohol use, rate of increase in use during adolescence, and persistence of heavy alcohol use over time. Insight into the different ways in which predictors impact on alcohol use is relevant for the development of new intervention strategies. For this purpose, causality of the associations should be further examined.

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The Persistent Effects of Minimum Legal Drinking Age Laws on Drinking Patterns Later in Life

Exposure to permissive minimum legal drinking age (MLDA) laws not only affects young adults in the short term, but also later in life; for example, individuals who could legally purchase alcohol before the age of 21 are more likely to suffer from drinking problems as older adults, long after the laws had been changed. However, it is not known how permissive MLDA exposure affects specific drinking behavior. This present study uses changes in MLDA laws during the 1970s and 1980s as a natural experiment to investigate the potential impact of permissive MLDA exposure on average alcohol consumption, frequency of drinking, and patterns of binging and more moderate, nonheavy drinking.

Policy exposure data were paired with alcohol use data from the 1991 to 1992 National Longitudinal Alcohol Epidemiologic Survey and the 2001 to 2002 National Epidemiologic Survey on Alcohol and Related Conditions. Past-year drinkers born between 1949 and 1972 (n = 24,088) were included. Average daily intake, overall drinking frequency, and frequency of both binge episodes (5+ drinks) and days without a binge episode (nonheavy drinking) for the previous year at the time of interview were tracked for each respondent.

Exposure to permissive MLDAs was associated with higher odds to report frequent binging and lower odds to report any moderate drinking; these associations were largely driven by men and those who did not attend college. Overall drinking frequency and average alcohol consumption were not affected by MLDA exposure.

The ability to legally purchase alcohol before the age of 21 does not seem to increase overall drinking frequency, but our findings suggest that it is associated with certain types of problematic drinking behaviors that persist into later adulthood: more frequent binge episodes and less frequent nonheavy drinking. We also propose that policymakers and critics should not focus on college drinking when evaluating the effectiveness of MLDAs.

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Assessment of a Modified DSM-5 Diagnosis of Alcohol Use Disorder in a Genetically Informative Population

Proposed changes to the upcoming DSM-5 include the following: (i) combining criteria for DSM-IV alcohol abuse (AA) and alcohol dependence (AD) into 1 diagnostic category (alcohol use disorder [AUD]); (ii) exclusion of the “legal problems” (LP) criterion; and (iii) addition of a “craving” criterion. Few published studies empirically assess the potential consequences of the proposed changes.

Using a population-based sample of twins assessed for lifetime AA/AD diagnoses, we explored phenotypic differences across DSM-IV and a modified DSM-5 diagnoses without craving because of its unavailability in the data set. We used factor analysis and item response theory (IRT) to evaluate the potential consequences of excluding the LP criterion from AUD and used twin modeling to examine genetic differences between DSM-IV and the modified DSM-5 diagnoses.

The prevalence of AUD was slightly higher than that of DSM-IV diagnoses. Individuals meeting DSM-IV or DSM-5 criteria, but not both, exhibit fewer comorbid diagnoses than those meeting both sets of criteria. Individuals meeting only DSM-5 criteria were slightly less severely affected than those meeting only DSM-IV criteria. Factor analysis indicated that the LP criterion loading is the lowest of all symptoms; IRT analysis suggested that this criterion has low discriminatory power. The genetic correlation between DSM-IV and DSM-5 diagnoses was slightly but significantly lower than unity.

The proposed DSM-5 AUD criteria are unlikely to result in significant changes in prevalence of diagnosed alcohol problems. However, it is unclear whether the new criteria represent a more valid diagnosis: new cases are no more severely affected than DSM-IV-only cases. Given the psychometric properties of LP, its exclusion should not negatively impact diagnostic validity. Similarly, the stable heritability across DSM-IV and DSM-5 diagnoses suggests that the proposed changes will not have substantial negative consequences in terms of familial influences, a key validator. These results provide equivocal empirical support for the proposed DSM-5 changes for AUDs.

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Binge Ethanol and Liver: New Molecular Developments

Binge consumption of alcohol is an alarming global health problem. Binge (acute) ethanol (EtOH) is implicated in the pathophysiology of alcoholic liver disease (ALD). New studies from experimental animals and from humans indicate that binge EtOH has profound effects on immunological, signaling, and epigenetic parameters of the liver. This is in addition to the known metabolic effects of acute EtOH. Binge EtOH alters the levels of several cellular components and dramatically amplifies liver injury in chronically EtOH exposed liver. 

These studies highlight the importance of molecular investigations into binge effects of EtOH for a better understanding of ALD and also to develop therapeutic strategies to control it. 

This review summarizes these recent developments.

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Determining the Threshold for Alcohol-Induced Brain Damage: New Evidence with Gliosis Markers

Chronic intake of ethanol (EtOH) has been linked to serious health consequences such as cardiac and liver problems, cognitive impairments, and brain damage. Alcohol's detrimental effects depend upon the dose, duration, and pattern of exposure with binge drinking as one of the most common, but most damaging, patterns of intake. Little is known about the threshold of the damaging effects of alcohol. Therefore, these experiments sought to determine a threshold for brain damage using various markers of neurodegeneration.

Adult male Sprague–Dawley rats were administered nutritionally complete liquid diet containing either EtOH (25% w/v) or isocaloric dextrose every 8 hours for either 1 (mean dose, 13.4 ± 0.3 g/kg/d; mean blood EtOH concentration (BEC), 336.2 ± 18.8 mg/dl) or 2 days (mean dose, 10.9 ± 0.3 g/kg/d; mean BEC, 369.8 ± 18.1 mg/dl). On the basis of a known time course of various neurodegeneration-associated events, rats were perfused transcardially immediately following, 2 days after, or 7 days post EtOH exposure. To label actively dividing cells, some animals were injected with BromodeoxyUridine (BrdU) 2 hours prior to perfusion. Tissue was then analyzed for the presence of BrdU (cell proliferation), FluoroJade B (degenerative neurons), and 
vimentin (reactive astrogliosis) immunoreactivity.

One or 2 days of EtOH exposure failed to alter cell proliferation at any of the time points analyzed. However, significant 2- to 9-fold increases in neuronal degeneration in limbic cortex and clear evidence of reactive gliosis as indicated by a 2- to 8-fold upregulation in vimentin immunoreactivity in the hippocampus were observed following as little as 1 day of binge EtOH exposure.

These results indicate that as little as 1 day (24 hours) of high BEC, binge-like EtOH exposure is enough to elicit signs of alcohol-induced brain damage in adult rats. Further, reactive gliosis may be a more sensitive marker of alcohol-induced damage in the hippocampus.

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Genotype modulates age-related alterations in sensitivity to the aversive effects of ethanol: an eight inbred strain analysis of conditioned taste aversion

Adolescent individuals display altered behavioral sensitivity to ethanol, which may contribute to the increased ethanol consumption seen in this age-group. However, genetics also exert considerable influence on both ethanol intake and sensitivity. Currently there is little research assessing the combined influence of developmental and genetic alcohol sensitivities. 

Sensitivity to the aversive effects of ethanol using a conditioned taste aversion (CTA) procedure was measured during both adolescence (P30) and adulthood (P75) in eight inbred mouse strains (C57BL/6J, DBA/2J, 129S1/SvImJ, A/J, BALB/cByJ, BTBR T+tf/J, C3H/HeJ and FVB/NJ). Adolescent and adult mice were water deprived, and subsequently provided with access to 0.9% (v/v) NaCl solution for 1 h. Immediately following access mice were administered ethanol (0, 1.5, 2.25 and 3 g/kg, ip). This procedure was repeated in 72 h intervals for a total of five CTA trials. 

Sensitivity to the aversive effects of ethanol was highly dependent upon both strain and age. Within an inbred strain, adolescent animals were consistently less sensitive to the aversive effects of ethanol than their adult counterparts. However, the dose of ethanol required to produce an aversion response differed as a function of both age and strain.

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Early Subjective Response and Acquired Tolerance as Predictors of Alcohol Use and Related Problems in a Clinical Sample

Previous studies have demonstrated that a low subjective response (SR) to alcohol is a risk factor for alcohol use disorders (AUDs), and a recent study suggests that acquired tolerance can be differentiated from initial SR and is also significantly associated with drinking problems. Because the prior study of SR and tolerance focused on a sample of moderate drinkers, the goal of the current study was to examine relations between early SR, acquired tolerance, alcohol use, and alcohol-related problems in a sample of young adults with clinically significant alcohol problems.\

The current study examined associations between early SR and acquired tolerance and both drinking behavior and alcohol-related problems within a sample of 113 heavy drinking young adults (66.1% male) volunteering for a clinical trial of naltrexone in combination with brief motivational counseling.

Consistent with the 1 prior study examining simultaneous effects of early SR and tolerance, both early SR and acquired tolerance were positively associated with typical drinking behavior, although tolerance was a much stronger predictor within this clinical sample. In contrast to the prior study, early SR was inversely associated with risk for alcohol-related problems, and tolerance was not a significant predictor of problems.

The results suggested that, controlling for weekly drinking, a low early SR protected against acute negative consequences within a sample of heavy drinkers who had acquired significant tolerance to alcohol effects. It is possible that this protective effect may eventually shift to a risk factor by allowing individuals with a low SR to persist in a pattern of hazardous drinking.

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Alcohol and Sleep I: Effects on Normal Sleep

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.

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Do alcohol use disorders destabilize the course of bipolar disorder?

To determine whether long-term data implicate a negative effect of alcohol-use disorders (AUDs) on time to remission, risk of mood episode recurrence, and risk of mood switch/cycling in patients with bipolar disorder (BD). The short-term temporal sequence between alcohol use and onset of mood episodes was also examined.

A MEDLINE literature search was conducted for measurement-based reports of alcohol and course of bipolar disorder.

Twenty-three original data publications were identified. Three out of 5 studies addressing the impact of AUDs on recovery from a mood episode demonstrated that alcohol did not prolong index mood episodes of any type. Six out of 11 reports evaluating the relationship between alcohol and the long term risk of mood episode recurrences suggested that high levels of alcohol intake increase the risk of a mood recurrence. Five out of 7 studies evaluating the short-term temporal sequence of AUDs and development of mood episodes among BD patients found that increased alcohol use preceded the development of new mood episodes. Four out of 5 studies examining the association between alcohol and rapid cycling indicated that AUDs were associated with higher rates of rapid-cycling.

We limited our review to studies that were large enough to perform statistical testing, which may have led us to overlook informative smaller studies.

Although alcohol does not seem to affect time to mood episode remission, alcohol use destabilizes the course of illness over the long run as evidenced by associations with more rapid cycling and mood episode recurrence.

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Friday, January 25, 2013

Reducing the alcohol and drug toll: Victoria's plan 2013 - 2017

The Minister for Mental Health, the Hon. Mary Wooldridge has released Reducing the alcohol and drug toll. Victoria’s plan 2013 – 2017. This is Victoria’s first whole of government strategy to reduce the impact of alcohol and drug abuse on the Victorian community.

The plan sets out how the Victorian Government will work with the community to bring down the alcohol and drug toll and deliver better health outcomes to thousands of Victorians who want to recover from the harm associated with alcohol misuse and drug use.

The Victorian Government is working to reduce the rates of risky drinking and drug use, and the toll of deaths, disease, injury, crime and other social costs from the misuse of alcohol and drugs.

Reducing the alcohol and drug toll sets out a 15-point plan that provides a comprehensive response to the three major drug types, alcohol, pharmaceutical drugs and illegal drugs. It also focuses on care, treatment and recovery as well as strengthening leadership and coordinated action in reducing the alcohol and drug toll.  > > > >  Read More

'Alcohol problems in the criminal justice system' WHO guidance released

The World Health Organization (WHO) have released a document outlining the scale of the link between alcohol and offending, and the missed opportunities to address alcohol misuse within the Criminal Justice System and prisons in particular.

Download 'Alcohol problems in the criminal justice system: an opportunity for
intervention' [pdf]

The document describes an integrated model of care for alcohol problems in prisoners, with elements for best practice. The model starts with assessment of prisoners’ alcohol problems, using a validated screening tool, the WHO Alcohol Use Disorders Identification Test (AUDIT), and calls for interventions tailored to prisoners’ specific needs.  > > > >  Read More

A spontaneous deletion of α-synuclein is associated with an increase in CB1 mRNA transcript and receptor expression in the hippocampus and amygdala: Effects on alcohol consumption

α-Synuclein (α-syn) protein and endocannabinoid CB1 receptors are primarily located in presynaptic terminals. An association between α-syn and CB1 receptors has recently been established in Parkinson's disease, but it is completely unknown whether there is an association between these two proteins in alcohol addiction

Therefore, we aimed to examine the α-syn mRNA transcript and protein expression levels in the prefrontal cortex, striatum, amygdala and hippocampus. These brain regions are the most frequently implicated in alcohol and other drug addiction.

In these studies, we used C57BL/6 mice carrying a spontaneous deletion of the α-syn gene (C57BL/6Snca-/-) and their respective controls (C57BL/6Snca+/+). These animals were monitored for spontaneous alcohol consumption (3-10%) and their response to a hypnotic-sedative dose of alcohol (3 g/kg) was also assessed. 

Compared with the C57BL/6Snca+/+ mice, we found that the C57BL/6Snca-/- mice exhibited a higher expression level of the CB1 mRNA transcript and CB1 receptor in the hippocampus and amygdala. 

Furthermore, C57BL/6
Snca-/- mice showed an increase in alcohol consumption when offered a 10% alcohol solution. There was no significant difference in sleep time after the injection of 3 g/kg alcohol. 

These results are the first to reveal an association between α-syn and the CB1 receptor in the brain regions that are most frequently implicated in alcohol and other drug addictions.

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Social Deprivation Enhances VTA Synaptic Plasticity and Drug-Induced Contextual Learning

Drug addiction
is driven, in part, by powerful drug-related memories. Deficits in social life, particularly during adolescence, increase addiction vulnerability. Social isolation in rodents has been used extensively to model the effects of deficient social experience, yet its impact on learning and memory processes underlying addiction remains elusive. 

Here, we show that social isolation of rats during a critical period of adolescence (postnatal days 2142) enhances long-term potentiation of NMDA receptor (NMDAR)-mediated glutamatergic transmission in the ventral tegmental area (VTA). This enhancement, which is caused by an increase in metabotropic glutamate receptor-dependent Ca2+ signaling, cannot be reversed by subsequent resocialization.

Notably, memories of amphetamine- and ethanol-paired contextual stimuli are acquired faster and, once acquired, amphetamine-associated contextual memory is more resistant to extinction in socially isolated rats. 

We propose that NMDAR plasticity in the VTA may represent a neural substrate by which early life deficits in social experience increase addiction vulnerability.

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Adjusting for unrecorded consumption in survey and per capita sales data: Quantification of impact on gender- and age-specific alcohol-attributable fractions for oral and pharyngeal cancers in Great Britain

Large discrepancies are typically found between per capita alcohol consumption estimated via survey data compared with sales, excise or production figures. This may lead to significant inaccuracies when calculating levels of alcohol-attributable harms. Using British data, we demonstrate an approach to adjusting survey data to give more accurate estimates of per capita alcohol consumption. 

First, sales and survey data are adjusted to account for potential biases (e.g. self-pouring, under-sampled populations) using evidence from external data sources. Secondly, survey and sales data are aligned using different implementations of Rehm et al.'s method [in (2010) Statistical modeling of volume of alcohol exposure for epidemiological studies of population health: the US example. Pop Health Metrics 8, 1–12]. Thirdly, the impact of our approaches is tested by using our revised survey dataset to calculate alcohol-attributable fractions (AAFs) for oral and pharyngeal cancers.

British sales data under-estimate per capita consumption by 8%, primarily due to illicit alcohol. Adjustments to survey data increase per capita consumption estimates by 35%, primarily due to under-sampling of dependent drinkers and under-estimation of home-poured spirits volumes. Before aligning sales and survey data, the revised survey estimate remains 22% lower than the revised sales estimate. Revised AAFs for oral and pharyngeal cancers are substantially larger with our preferred method for aligning data sources, yielding increases in an AAF from the original survey dataset of 0.47–0.60 (males) and 0.28–0.35 (females).

It is possible to use external data sources to adjust survey data to reduce the under-estimation of alcohol consumption and then account for residual under-estimation using a statistical calibration technique. These revisions lead to markedly higher estimated levels of alcohol-attributable harm.

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Global alcohol exposure estimates by country, territory and region for 2005 – a contribution to the Comparative Risk Assessment for the 2010 Global Burden of Disease Study

This study aimed to estimate the prevalence of lifetime abstainers, former drinkers and current drinkers, adult per capita consumption of alcohol, and pattern of drinking scores, by country and Global Burden of Disease region for 2005, and to forecast these indicators for 2010.

Statistical modelling based on survey data and routine statistics.

241 countries and territories.

Per capita consumption data were obtained with the help of the World Health Organization's Global Information System on Alcohol and Health. Drinking status data were obtained from Gender, alcohol and culture: an international study, the STEPwise approach to Surveillance study, the World Health Survey/Multi Country Study, and other surveys. Consumption and drinking status data were triangulated to estimate alcohol consumption across multiple categories.

Finding In 2005 adult per capita annual consumption of alcohol was 6.1 litres (l), with 28.8% stemming from unrecorded consumption. 17.1 l of alcohol were consumed per drinker, 45.8% of all adults were lifetime abstainers, 13.6% were former drinkers and 40.6% were current drinkers. Lifetime abstention was most prevalent in North Africa/ Middle East and South Asia. Eastern Europe and Southern Sub-Saharan Africa had the most detrimental pattern of drinking scores, while drinkers in Europe (Eastern and Central) and Sub-Saharan Africa (Southern and West) consumed the most alcohol.

Just over 40% of the world's adult population consumes alcohol and the average consumption per drinker is 17.1 litres per year. However, the prevalence of abstention, level of alcohol consumption and patterns of drinking vary widely across regions of the world.

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TIME 12:30 to 2 pm

To Participate online:
LINK and Spanish)

James F. Mosher, JD Alcohol Policy Specialist Alcohol Policy Consultations - FeltonCalifornia

Rebalancing the Public Good and Industry Profitability

According to the latest estimates of the global burden of disease study, alcohol is the leading risk factor in most countries of the Americas Region. Implementing effective alcohol policies that would reduce the burden of non communicable diseases, injuries, underage drinking, at the same time that they would make economic sense, remain both a challenge and a priority for PAHO/WHO and MemberStates. Such policies need also to counter balancing the influence of the alcohol industry, which is rapidly expanding in the Region.

Jim Mosher’s presentation will focus on preventing underage drinking: alcohol policies shown to be effective, the alcohol industry’s role and economic stake in the policy debate, and community-based implementation strategies.

James Mosher's pioneering work in alcohol policy has brought him international acclaim. His expertise spans numerous topics, including underage drinking prevention, alcohol marketing, community prevention strategies, alcohol law, dram shop liability, and social host liability. His services include consulting, keynote presentations, workshops and trainings, policy analysis, and advocacy in media and policy. He has also served as a WHO consultant on numerous occasions, an expert witness and consultant in alcohol litigation cases.

Maristela G. Monteiro, M.D., Ph.D.
Senior Advisor
Alcohol and Substance Abuse
Pan American Health Organization
525 23rd ST NWWashingtonDC 20037USA

The Assessment of Recovery Capital: Properties and psychometrics of a measure of addiction recovery strengths

Sociological work on social capital and its impact on health behaviours have been translated into the addiction field in the form of ‘recovery capital’ as the construct for assessing individual progress on a recovery journey.Yet there has been little attempt to quantify recovery capital.The aim of the project was to create a scale that assessed addiction recovery capital. 

Initial focus group work identified and tested candidate items and domains followed by data collection from multiple sources to enable psychometric assessment of a scale measuring recovery capital. 

The scale shows moderate test–retest reliability at 1 week and acceptable concurrent validity. Principal component analysis
determined single factor structure. 

The Assessment of Recovery Capital (ARC) is a brief
and easy to administer measurement of recovery capital that has acceptable psychometric properties and may be a useful
complement to deficit-based assessment and outcome monitoring instruments for substance dependent individuals in and out of treatment.

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Global Actions January 24, 2013

Key Recent Milestones:

· Worldwide: ICAP attended the International Chamber of Commerce (ICC) Commission on Marketing and Advertising meeting held in Paris on January 16 and 17, 2013. The meeting set forth a “digital economy” work plan for 2013 and agreed to develop a beverage alcohol framework to support the ICAP Guiding Principles.

Global Actions in Focus: ICAP Translated Materials

The recently announced commitments, “Reducing Harmful Use of Alcohol: Beer, Wine, and Spirits Producers Commitments” are now available in six languages: English, Chinese, French, Spanish, Japanese, and Russian. Most ICAP publications are available online, and many have been translated in part or in full into several languages.

spanish.jpgMany of ICAP’s policy tools were recently translated from English into other languages. You can now read the Toolkit for Working Together in French, German, and Spanish.

ICAP Issues Briefings address specific topics relevant to alcohol policy, providing a succinct overview of key evidence. ICAP recommends that the Issues Briefings be used in conjuction with ICAP's other Policy Tools, including the ICAP Blue Book and ICAP Policy Guides.

Taxation of Beverage Alcohol, for example, is now available to read in French, Russian, and Spanish. Alcohol Marketing and Young People has been translated into French, Portuguese, Russian, and Spanish. Determinants of Drinking is now available in French, Portuguese, Russian, and Spanish.

ICAP Issues Briefings are updated on an ongoing basis. Visit the website regularly as more translated materials become available.

What’s Happening Next:

· Thailand: Thailand’s Population and Community Development Association (PDA), the Thai Foundation for Responsible Drinking (TFRD), and ICAP will be reviewing activities from the community drink driving project and implementing training through January and February 2013. 

Alcohol: a key determinant for ill health and an obstacle to development

In 2000, world leaders promised to halve extreme poverty by 2015 with a global plan called the Millennium Development Goals (MDGs). The MDGs set clear targets for the development agenda, but 2015 is coming closer. Yet, 1.4 billion people still live in extreme poverty. New development targets are needed. Already there are formal and informal processes running in this process. A platform for consultation on the role of health in the post-2015 development agenda is co-convened by WHO and UNICEF, in collaboration with the Government of Sweden and the Government of Botswana. On the online consultation more than 100 papers were submitted from individuals, UN organizations, governments, research centers and civil society organizations.

In a paper contributed to the consultation the Global Alcohol Policy Alliance (GAPA) point out that alcohol is a risk factor for ill-health and should be included in the development agenda.The MDGs state that health is critical to the economic, political and social development of all countries. The health-related MDGs focus on reducing child mortality (no. 4), improving maternal health (no. 5), and combatting HIV/AIDS, malaria and other diseases (no. 6), but do not capture the increasing burden of non-communicable diseases (NCDs).  > > > >  Read More

Novel Oxytocin Gene Expression in the Hindbrain Is Induced by Alcohol Exposure: Transgenic Zebrafish Enable Visualization of Sensitive Neurons

Fetal Alcohol Spectrum Disorders (FASD) are a collection of disorders resulting from fetal ethanol exposure, which causes a wide range of physical, neurological and behavioral deficits including heightened susceptibility for alcoholism and addictive disorders. While a number of mechanisms have been proposed for how ethanol exposure disrupts brain development, with selective groups of neurons undergoing reduced proliferation, dysfunction and death, the induction of a new neurotransmitter phenotype by ethanol exposure has not yet been reported.

The effects of embryonic and larval ethanol exposure on brain development were visually monitored using transgenic zebrafish expressing cell-specific green fluorescent protein (GFP) marker genes. Specific subsets of GFP-expressing neurons were highly sensitive to ethanol exposure, but only during defined developmental windows. In the med12 mutant, which affects the Mediator co-activator complex component Med12, exposure to lower concentrations of ethanol was sufficient to reduce GFP expression in transgenic embryos. In transgenic embryos and larva containing GFP driven by an oxytocin-like (oxtl) promoter, ethanol exposure dramatically up-regulated GFP expression in a small group of hindbrain neurons, while having no effect on expression in the neuroendocrine preoptic area.

Alcohol exposure during limited embryonic periods impedes the development of specific, identifiable groups of neurons, and the med12 mutation sensitizes these neurons to the deleterious effects of ethanol. In contrast, ethanol exposure induces oxtl expression in the hindbrain, a finding with profound implications for understanding alcoholism and other addictive disorders.

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Thursday, January 24, 2013

Opposite social gradient for alcohol use and misuse among French adolescents

This study investigates the association of the family occupational category (F-OC) with adolescent alcohol use and its potential variation according to the frequency of use.

A national survey representative of adolescents aged 17 living in continental France conducted in 2005 (n = 29,393). Three outcomes were considered: overall use describes the drinking status (lifetime abstinence, use before the month prior the survey, use in the month prior the survey) without considering the frequency of use; last month use and binge drinking detail the frequency of use (1–5 uses, 6–9, 10–19 and 20+ uses) and of binge drinking (0, 1–2, 3–5, 6+ episodes of 5+ glasses in a single occasion) of the previous month users. F-OC was described in 7 categories based on the highest occupational category of the parents (from managers/professionals to unemployed). Analysis used generalised logistic regressions, controlling for gender, F-OC, parental separation, autonomy, other substance use, being out of school and sociability.

There was a double gradient: adolescents from high F-OC families were more often experimenters and drinkers during the previous month whereas those of low F-OC families were more often binge drinkers. Adolescents from farmers’ families were the most at risk for frequent use and binge drinking in the last month. Interactions tests show that the effect of F-OC was not significantly related to gender.

Except for gender, adolescents’ patterns of use reflect those observed in the adult population. Mechanisms that favour and hinder progression in alcohol use should be studied in various socioeconomic groups.

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Youth drinking cultures, social networking and alcohol marketing: implications for public health

Alcohol consumption and heavy drinking in young adults have been key concerns for public health. Alcohol marketing is an important factor in contributing to negative outcomes. 

The rapid growth in the use of new social networking technologies raises new issues regarding alcohol marketing, as well as potential impacts on alcohol cultures more generally. Young people, for example, routinely tell and re-tell drinking stories online, share images depicting drinking, and are exposed to often intensive and novel forms of alcohol marketing.

In this paper, we critically review the research literature on (a) social networking technologies and alcohol marketing and (b) online alcohol content on social networks, and then consider implications for public health knowledge and research. 

We conclude that social networking systems are positive and pleasurable for young people, but are likely to contribute to pro-alcohol environments and encourage drinking. 

However, currently research is preliminary and descriptive, and we need innovative methods and detailed in-depth studies to gain greater understanding of young people’s mediated drinking cultures and commercial alcohol promotion.

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Acute alcohol intoxication and suicide: a gender-stratified analysis of the National Violent Death Reporting System

Although it is well known that people with alcohol dependence are at a markedly elevated risk for suicide, much less is known about the role of acute alcohol use in suicidal behaviours. The primary aims of this epidemiological study were to assess the prevalence and factors associated with acute alcohol intoxication among 57 813 suicide decedents in 16 states.

Data from the restricted National Violent Death Reporting System 2003–2009 for male and female suicide decedents aged 18 years and older were analysed by multiple logistic regression to compare decedents with and without acute alcohol intoxication (defined as blood alcohol concentration (BAC) ≥0.08 g/dl).
Among men, those who were younger, American Indian/Alaska Native, Hispanic, veterans, of lower educational attainment, deceased from a self-inflicted firearm injury or hanging/suffocation and residing in rural areas were more likely to have been intoxicated at the time of death. Among women, the factors associated with a BAC ≥0.08 g/dl were younger age, being American Indian/Alaska Native, and using a firearm, hanging/suffocation or falling as method of death.

In both men and women, alcohol intoxication was associated with violent methods of suicide and declined markedly with age, suggesting that addressing risks associated with acute alcohol use may be of the greatest aid in the prevention of violent suicides among young and middle age adults.                           

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Moderate Prenatal Alcohol Exposure Reduces Plasticity and Alters NMDA Receptor Subunit Composition in the Dentate Gyrus

Although it is well documented that heavy consumption of alcohol during pregnancy impairs brain development, it remains controversial whether moderate consumption causes significant damage.

Using a limited access, voluntary consumption paradigm, we recently demonstrated that moderate prenatal alcohol exposure (MPAE) is associated with dentate gyrus-dependent learning and memory deficits that are manifested in adulthood.

Here, we identified a novel mechanism that may underlie this effect of MPAE. We found that MPAE mice exhibit deficits in NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) in the dentate gyrus. Further, using semiquantitative immunoblotting techniques, we found that the levels of GluN2B subunits were decreased in the synaptic membrane, while levels of C2′-containing GluN1 and GluN3A subunits were increased, in the dentate gyrus of MPAE mice. 

 These data suggest that MPAE alters the subunit composition of synaptic NMDARs, leading to impaired NMDAR-dependent LTP in the dentate gyrus.

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GluN2B subunit deletion reveals key role in acute and chronic ethanol sensitivity of glutamate synapses in bed nucleus of the stria terminalis

The bed nucleus of the stria terminalis (BNST) is a critical region for alcohol/drug-induced negative affect and stress-induced reinstatement. NMDA receptor (NMDAR)-dependent plasticity, such as long-term potentiation (LTP), has been postulated to play key roles in alcohol and drug addiction; yet, to date, little is understood regarding the mechanisms underlying LTP of the BNST, or its regulation by ethanol.

Acute and chronic exposure to ethanol modulates glutamate transmission via actions on NMDARs. Despite intense investigation, tests of subunit specificity of ethanol actions on NMDARs using pharmacological approaches have produced mixed results. Thus, we use a conditional GluN2B KO mouse line to assess both basal and ethanol-dependent function of this subunit at glutamate synapses in the BNST.

Deletion of GluN2B eliminated LTP, as well as actions of ethanol on NMDAR function. Further, we show that chronic ethanol exposure enhances LTP formation in the BNST. Using KO-validated pharmacological approaches with Ro25-6981 and memantine, we provide evidence suggesting that chronic ethanol exposure enhances LTP in the BNST via paradoxical extrasynaptic NMDAR involvement.

These findings demonstrate that GluN2B is a key point of regulation for ethanol's actions and suggest a unique role of extrasynaptic GluN2B-containing receptors in facilitating LTP.

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