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, April 25, 2009

A Free Lunch
Journal of Drug Policy Analysis, Vol. 1 [2008], Iss. 1, Art. 2

Federal and state excise taxes on alcoholic beverages have declined sharply in real value over the last 50 years. The result is cheaper alcohol, more alcohol abuse, and more alcohol-related problems of all sorts than would otherwise have occurred.
Frequently voiced concerns that such taxes are regressive, or that they penalize the majority who drink moderately and safely, are off base. An increase in the federal alcohol taxes could provide almost everyone but the heaviest drinkers with a net financial gain even if there were no behavioral effects; the evidence that there are behavioral effects that improve health and safety is an important bonus.
In a sense, alcohol taxes are the proverbial free lunch.
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The TaqI A DRD2 polymorphism in type II alcohol dependence: a marker of age at onset or of a familial disease?
Alcohol Article in Press, 19 April 2009
Cloninger's type II is a severe, early-onset, male-limited, and genetically influenced, impulsive form of alcoholism. Significant association has been reported between the A1 allele of the D2 dopamine receptor (DRD2) gene, substance misuse and personality traits of impulsivity and novelty seeking.
We assessed the association between the TaqI A DRD2 gene polymorphism with Cloninger's typology and family history of alcohol abuse, which is thought to be more frequent in type II alcoholics.
Fifty-one male alcohol-dependent patients were discriminated between type I and type II according to age at onset of alcohol-related problems and interviewed about family history of alcoholism. The associations between DRD2 (A1 or A2 alleles), family history, and typology were assessed by Pearson's chi-square test.
Although typology was not associated with the studied polymorphism, a higher rate of general family history of alcohol abuse was still observed in type II patients (χ21 = 4.53; P = .033). Furthermore, the A1 allele of the DRD2 was significantly associated with paternal history of alcoholism (χ21 = 4.66; P = .031) and male, first-degree, collateral history of alcoholism (χ21 = 4.40; P = .036).
Age at onset of alcohol-related problems as main discriminator between type I and type II alcohol dependence does not seem to be associated by the TaqI A DRD2 polymorphism.

However, the A1 allele of the DRD2 may be a marker of male familial alcoholism, which has been associated with type II alcohol dependence.
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Friday, April 24, 2009

The role of alcoholic beverage preference in the severity of alcohol dependence and adherence to the treatment
Alcohol Volume 43, Issue 3, May 2009, Pages 185-195
The severity of dependence on alcohol and the efficacy of diverse types of treatments for alcoholism have been the subject of various researches.
This study focused on the types of beverages preferentially consumed by alcohol-dependent outpatients and their effects on the severity of dependence and therapeutic outcomes.
Our sample comprised 153 patients, 18–60 years of age, with an International Classification of Diseases (ICD-10) diagnosis of alcohol dependence, who were randomly divided into three different groups to receive topiramate (up to 300 mg/day), naltrexone (50 mg/day), or placebo during 12 weeks of follow-up.
Spirits and beer were the main beverages consumed. At the start of this research, the group of spirits drinkers showed higher severity of alcohol dependence, higher craving for alcohol, more frequent history of treatments for alcoholism, and lower income than the group of beer preference drinkers.
During the study, beer preference drinkers demonstrated higher adherence to the treatment, independently of the types of medications prescribed (P = .02, odds ratio, 2.46, 95% confidence interval, 1.17–5.19).
This study suggests that the severity of dependence and the adherence to the treatment can be factors that set apart beer drinkers from spirits drinkers. As the compliance with the treatment for alcoholism was lower among spirits preference drinkers, a more intensive model of treatment would be necessary.
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Dopamine D4 receptor gene exon III polymorphism associated with binge drinking attitudinal phenotype
Alcohol Volume 43, Issue 3, May 2009, Pages 179-184
Although binge drinking is a serious public health problem, relatively few studies have investigated the relationship between specific dopaminergic genes such as the dopamine D4 receptor (DRD4) and binge drinking attitudinal phenotypes.
This study used the DNA subsample (N = 233, mean age 19.8, standard deviation, 0.89) of the National Longitudinal Study of Adolescent Health to investigate the association between a 48 base-pair variable number of tandem repeats in the DRD4 gene and a measure of binge drinking.
Multivariate regression models indicated that the 7-repeat (7R) allele of the exon III polymorphism is significantly positively associated (β = 0.16, P < .05) with binge drinking while controlling for low self-control and demographic variables. Findings were sturdy across race and gender.
The present study provides unique evidence to the genetic underpinnings of binge drinking. Results suggest that the 7R allele may be an important contributor to the liability to binge drinking.
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Alcohol-impaired driving behavior and sensation-seeking disposition in a college population receiving routine care at campus health services centers
Accident Analysis & PreventionVolume 41, Issue 3, May 2009, Pages 380-386
Accidents stemming from alcohol-impaired driving are the leading cause of injury and death among college students. Research has implicated certain driver personality characteristics in the majority of these motor vehicle crashes. Sensation seeking in particular has been linked to risky driving, alcohol consumption, and driving while intoxicated.
This study investigated the effect of sensation seeking on self-reported alcohol-impaired driving behavior in a college student population while adjusting for demographics, residence and drinking locations.
A total of 1587 college students over the age of 18 completed a health screening survey while presenting for routine, non-urgent care at campus heath services centers. Student demographics, living situation, most common drinking location, heavy episodic drinking, sensation-seeking disposition and alcohol-impaired driving behavior were assessed.
Using a full-form logistic regression model to isolate sensation seeking after adjusting for covariates, sensation seeking remains a statistically significant independent predictor of alcohol-impaired driving behavior
Interventions should target sensation seekers and environmental factors that mediate the link between sensation seeking and alcohol-impaired driving behaviors.
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Alcohol, illicit and non-illicit psychoactive drug use and road traffic injury in Thailand: A case-control study
Accident Analysis & Prevention Volume 41, Issue 3, May 2009, Pages 651-657

The objective of this study was to determine the relationship between alcohol use, psychoactive drug use and road traffic injury (RTI).
A case-control study was conducted among drivers in Bangkok, Thailand. Two hundred cases and 849 controls were enrolled between February and November 2006. Cases who sustained a RTI were matched with four controls recruited from petrol stations within a 1-km radius of the reported crash site of the case.

A positive alcohol breath test (≥50 mg/dl), and positive tests for the presence of illicit (amphetamine, cocaine, marijuana) and non-illicit psychoactive drugs (antihistamine, benzodiazepine, antidepressants), using gas chromatography/mass spectrometry (GC/MS) were documented as primary measures.

There were significantly higher odds of an alcohol breath test ≥50 mg/dl (adjusted odds ratio (OR) 63.6 (95% CI: 25.5–158.9)), illicit psychoactive drugs (adjusted OR 3.4 (95% CI: 1.7–6.6)) and non-illicit psychoactive drug (adjusted OR 3.1 (95% CI: 1.5–6.3)) among cases than controls.

Even though driving under the influence of psychoactive drugs has been significantly linked to RTI, its contribution to road safety is much lower than driving under the influence of alcohol. With limited resources, the priority for RTI prevention should be given to control of driving under the influence of alcohol.

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Common genetic influences on the timing of first use for alcohol, cigarettes, and cannabis in young African-American women
Drug and Alcohol DependenceVolume 102, Issues 1-3, 1 June 2009, Pages 49-55

The risks associated with early age at initiation for alcohol, cigarette, and cannabis use are well documented, yet the timing of first use has rarely been studied in genetically informative frameworks, leaving the relative contributions of genetic and environmental factors to age at initiation largely unknown.

The current study assessed overlap in heritable and environmental influences on the timing of initiation across these three substances in African-American women, using a sample of 462 female twins (100 monozygotic and 131 dizygotic pairs) from the Missouri Adolescent Female Twin Study. Mean age at the time of interview was 25.1 years. Ages at first use of alcohol, cigarettes, and cannabis were gathered in diagnostic interviews administered over the telephone. Standard genetic analyses were conducted with substance use initiation variables categorized as never, late, and early onset.

Variance in the timing of first use was attributable in large part to genetic sources: 44% for alcohol, 62% for cigarettes, and 77% for cannabis. Genetic correlations across substances ranged from 0.25 to 0.70. Shared environmental influences were modest for alcohol (10%) and absent for cigarettes and cannabis.

Findings contrast with reports from earlier studies based on primarily Caucasian samples, which have suggested a substantial role for shared environment on substance use initiation when measured as lifetime use.

By characterizing onset as timing of first use, we may be tapping a separate construct. Differences in findings may also reflect a distinct etiological pathway for substance use initiation in African-American women that could not be detected in previous studies.

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Some Medical Inpatients With Unhealthy Alcohol Use May Benefit From Brief Intervention
J. Stud. Alcohol Drugs 70: 426-435, 2009

Studies of alcohol brief intervention for medical inpatients have mixed results. We explored potential moderators of the effectiveness of brief intervention for unhealthy alcohol use among medical inpatients.

This is a secondary analysis of a randomized controlled trial of brief motivational counseling among 341 urban-hospital medical inpatients (99 women) with unhealthy alcohol use. Self-reported main outcomes were receipt of alcohol treatment by 3 months in subjects with dependence and change in the mean number of drinks per day 3 and 12 months after enrollment in all subjects.

Among subjects with dependence, the effect of brief intervention on receipt of alcohol treatment differed significantly by gender and age (p = .02 for each interaction). In stratified analyses, brief intervention was associated with receipt of alcohol treatment in women (adjusted odds ratio [AOR] = 3.9, 95% confidence interval [CI]: 1.2-12.7), and younger (<44 aor =" 3.6," color="#cc0000">

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Thursday, April 23, 2009

Alcohol consumption and decreased risk of non-Hodgkin's lymphoma: role of mTOR dysfunction
Blood First Edition Paper, prepublished online March 17, 2009;

A number of epidemiologic studies to date support the emerging paradigm that current alcohol consumers have decreased risk of most types of non-Hodgkin's lymphoma. The observed lower risk among people who drank alcohol does not seem to vary with beverage type. The mechanisms accounting for alcohol-induced decrease in the incidence of lymphomas remain largely unknown.

We demonstrate that low dose chronic exposure to ethanol inhibits mTORC1 complex formation resulting in decreased phosphorylation events involved in mTOR pathway signaling in a lymphoid-tissue specific manner. These changes in mTOR signaling lead to a decrease in eIF4E associated with the translation initiation complex and a repression of global cap-dependent synthesis in both lymphoma cell lines and normal donor lymphocytes.

Significantly, we were able to show that chronic exposure of ethanol at physiologically relevant concentrations in a mouse xenograft model results in a striking inhibition of lymphoma growth.

Our data support a paradigm in which chronic ethanol exposure inhibits mTOR signaling in lymphocytes with a significant repression of cap-dependent translation, reducing the tumorigenic capacity of NHL in a human xenograft model.

The ethanol-mediated repression of mTOR signaling coupled with decreased in vivo lymphoma growth underscore the critical role of mTOR signaling and translation in lymphoma.

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Neuroscience: Pathways to Alcohol Dependence Part II — Overview of the Neuroadaptation, Risk, and Recovery
Alcohol Research & Health Volume 31, Number 4, 2009


Who Is at Risk? Population Characterization of Alcohol Selfadministration In Nonhuman Primates Helps Identify Pathways to Dependence
Alcohol abuse and dependence are uniquely human disorders. However, scientists sometimes use animal models to study different aspects of alcohol abuse and dependence, including aspects that cannot be easily or ethically studied in humans. For example, studies of nonhuman primates, who share many genetic, anatomical, physiological, and behavioral characteristics with humans, can help to uncover risk factors that may either predispose a person to alcoholism or accelerate the course of alcohol addiction; these models therefore can shed light on these processes in humans in a way that other animal models cannot. In this article, Dr. Kathleen A. Grant, Mr. James Stafford, Ms. Allison Thiede, Ms. Caitlin Kiley, Ms. Misa Odagiri, and Dr. Betsy Ferguson present findings of studies analyzing drinking behaviors in populations of nonhuman primates and the neurological factors that may underlie differences in alcohol intake levels. The authors also discuss how these findings can help scientists to prevent and treat alcoholism in humans. (pp. 289–297)

The Molecular Basis of Tolerance
Tolerance is the body’s diminished response to alcohol or other drugs over the course of time and repeated exposure. This article by Drs. Andrzej Z. Pietrzykowski and Steven N. Treistman discusses the various degrees of tolerance—acute, rapid, or chronic— and how changes in tolerance induced by alcohol may affect several processes at the molecular, cellular, or behavioral level that are related to the onset of acute, rapid, or chronic tolerance. (pp. 298–309)

How Adaptation of the Brain to Alcohol Leads to Dependence: A Pharmacological Perspective
Alcohol causes both short- and long-term changes in brain chemistry. Long-term changes in some of the brain’s signaling systems have been linked to the behavioral effects of alcoholism. If a heavy drinker stops drinking suddenly, these changes can lead to the syndrome of alcohol withdrawal; additionally, they can make an alcohol-dependent person who has stopped drinking more likely to relapse. As described by Drs. Peter Clapp, Sanjiv V. Bhave, and Paula L. Hoffman, many brain chemicals are affected by both chronic exposure to alcohol and sudden cessation of alcohol consumption. Both alcohol-induced and withdrawalinduced changes to these signaling systems may lead to behavioral effects such as reinforcement, enhanced anxiety, and increased sensitivity to stress. The authors also explain how certain brain chemicals can be targeted by drugs meant to treat alcohol dependence. (pp. 310–339)

From Actions to Habits: Neuroadaptations Leading to Dependence
Overlapping cerebral networks associated with behavioral control processes such as reward-guided Pavlovian conditional responses, goal-directed instrumental actions, and stimulus-driven habits can be altered by alcohol and other drug abuse and therefore are important to the study of substance abuse. In this article, Dr. Henry H. Yin describes these networks and the mechanisms underlying reward-guided action selection and discusses their implications for alcohol addiction. (pp. 340–344)

Alcohol Dependence, Withdrawal, and Relapse
Alcohol dependence is associated with the development of physical and psychological withdrawal symptoms when alcohol use is stopped or significantly reduced. According to Dr. Howard C. Becker, fear of these withdrawal symptoms can perpetuate alcohol abuse in many alcohol-dependent people; moreover, the presence of such symptoms can trigger relapse in those who have abstained from alcohol. As Dr. Becker reports, both clinical studies and basic research studies using animal and human models have demonstrated that alcohol-related (conditioned) cues and contexts as well as stressful stimuli and events can trigger relapse. Improved understanding of the processes contributing to withdrawal and relapse may aid in the development of medications to treat alcohol dependence more effectively. (pp. 348–361)

Magnetic Resonance Imaging of the Living Brain: Evidence for Brain Degeneration Among Alcoholics and Recovery With Abstinence
Magnetic resonance imaging, or MRI, is a safe and noninvasive technology that allows scientists to examine the brain’s structure and function in real time. MRI technologies can show how the brain changes when exposed to alcohol over the short and long term, as well as how long these changes persist after a person has stopped drinking. In this article Ms. Margaret J. Rosenbloom and Dr. Adolf Pfefferbaum discuss how MRI studies, including longitudinal studies of animal models of alcoholism, can help researchers to understand how alcoholism develops and how it affects the brain. Through these studies, scientists have been able to explore specific alcohol-related changes to the brain, their duration, their effects on behavior, and the mechanisms through which the brain compensates for these changes. These studies suggest that some changes are reversed with abstinence, while others endure long after a person has stopped drinking. (pp. 362–376)

Alcohol-Related Neurodegeneration and Recovery: Mechanisms From Animal Models
Animal studies have established that alcohol can cause damage to brain cells, resulting in the loss of structure and function as well as inhibiting the production of neurons (i.e., neurogenesis), which ultimately leads to cognitive impairment. This article by Dr. Fulton T. Crews describes models of binge alcohol consumption in rats that induce changes in cognition similar to those found in human alcoholics. Findings from these animal studies provide insight into when, where, and how alcohol abuse and abstinence recovery dynamically change braincell composition, which could lead to new potential therapies for neurodegeneration, mental diseases, and alcohol use disorders. (pp. 377–388)

The Role of Selected Factors in the Development and Consequences of Alcohol Dependence
Studying the risk for developing alcoholism and the negative consequences of alcohol dependence is a complex process that requires an understanding of the various factors that may determine the degree of that risk. In this article, Rebecca Gilbertson, Robert Prather, and Dr. Sara Jo Nixon examine how gender, family history, comorbid psychiatric and substance use disorders, and age interact to influence an individual’s risk for alcoholism as well as how they interact with alcoholism to influence neurocognitive functioning following detoxification. (pp. 389–399)

Treatment Implications: Using Neuroscience to Guide the Development of New Pharmacotherapies for Alcoholism
Developing new medications to treat alcohol dependence requires a better understanding of the neuroscience of alcohol-drinking behavior. Although there are currently three approved medications for treating alcohol dependence— disulfiram, naltrexone, and acamprosate—new medications that target different neurochemical systems and that could be used either as adjunctive treatments or to treat subpopulations of drinkers are needed. In this article, Drs. Suchitra Krishnan-Sarin, Stephanie O’Malley, and John H. Krystal discuss the complex neuropharmacology of alcohol and how it can affect many different brain neurotransmitter systems. (pp. 400–407)
Altered White Matter Integrity in Adolescent Binge Drinkers
Alcoholism: Clinical and Experimental Research
Published Online: 21 Apr 2009

White matter integrity has been found to be compromised in adult alcoholics, but it is unclear when in the course of alcohol exposure white matter abnormalities become apparent. This study assessed microstructural white matter integrity among adolescent binge drinkers with no history of an alcohol use disorder.

Binge drinkers had lower FA than controls in 18 white matter areas (clusters ≥27 contiguous voxels, each with p < 0.01) throughout the brain, including the corpus callosum, superior longitudinal fasciculus, corona radiata, internal and external capsules, and commissural, limbic, brainstem, and cortical projection fibers, while exhibiting no areas of higher FA. Among binge drinkers, lower FA in 6 of these regions was linked to significantly greater lifetime hangover symptoms and/or higher estimated peak blood alcohol concentrations.

Binge drinking adolescents demonstrated widespread reductions of FA in major white matter pathways. Although preliminary, these results could indicate that infrequent exposure to large doses of alcohol during youth may compromise white matter fiber coherence.

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Per capita alcohol consumption and sickness absence in Norway
The European Journal of Public Health Advance Access published online on April 15, 2009

There is only one previous study addressing the relationship between population drinking and sickness absence. That study, based on Swedish time-series data, showed a statistically significant relationship between per capita alcohol consumption and the male sickness absence rate. Estimates suggested that a 1-l increase in consumption was associated with a 13% increase in sickness absence among men. In the present study, we aim at replicating and expanding the Swedish study on the basis of data for Norway.

The results suggested that a 1-l increase in total consumption was associated with a 13% increase in sickness absence among men (P < 0.05). This corresponds to an elasticity coefficient equal to 0.62. The alcohol effect was not significant for women. Unemployment was negatively associated with the outcome for men as well as for women (P < 0.05). In the beverage-specific analyses, spirits were statistically significant for men (P < 0.05), but not beer and wine.

The present findings strengthen the conclusion from the Swedish study, that sickness absence may be added to the list of indicators of alcohol-related harm.

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Wednesday, April 22, 2009

Does binge drinking increase the risk of lung cancer: results from the Findrink study
The European Journal of Public Health Advance Access published online on April 15, 2009
There are controversies on the role of alcohol in lung cancer but no studies have examined the role of alcohol consumption patterns. We examined the association between binge drinking and lung cancer.
Prospective population based study of 2267 middle aged men from Finland without a history of lung cancer at baseline.
There were 65 cases of lung cancer during an average follow-up of 16.7 years. The relative risk (RR) of lung cancer for binge drinkers was 1.89 (95% CI 1.10–3.20) after adjusting for age, examination year, family history of cancer, smoking, socio-economic status (SES), leisure-time physical activity and body mass index (BMI). No increased risk was observed among non-smoking binge drinkers, RR 1.48 (95% CI 0.89–2.47). Binge drinking smokers had increased risks of lung cancer in all categories of daily smoking compared with non-binge drinking smokers. The RR were 2.70 (95% CI 1.61–4.53), 2.35 (95% CI 1.38–3.96) and 2.24 (95% CI 1.29–3.80) for those who smoked 1–19, 20–29 and 30/day, respectively.
Binge drinking is not associated with an increased risk of lung cancer among non-smokers but among smokers, it is associated with an increased risk irrespective of the number of cigarettes smoked daily. Even though the number of lung cancer cases among non-smokers was relatively small, the fact that the increased risk was limited to only smokers means that residual confounding by smoking may play a role. Larger studies are needed to clarify this association.
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Ethanol Teratogenesis in Five Inbred Strains of Mice
Alcoholism: Clinical and Experimental Research
Published Online: 21 Apr 2009

Previous studies have demonstrated individual differences in susceptibility to the detrimental effects of prenatal ethanol exposure. Many factors, including genetic differences, have been shown to play a role in susceptibility and resistance, but few studies have investigated the range of genetic variation in rodent models.

B6 mice exposed to ethanol in utero had fetal weight deficits and digit, kidney, brain ventricle, and vertebral malformations. In contrast, 129 mice showed no teratogenesis. The remaining strains showed varying degrees of teratogenesis.

Differences among inbred strains demonstrate genetic variation in the teratogenic effects of ethanol. Identifying susceptible and resistant strains allows future studies to elucidate the genetic architecture underlying prenatal alcohol phenotypes.

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Genetic variation in the CHRNA5 gene affects mRNA levels and is associated with risk for alcohol dependence
Molecular Psychiatry (2009) 14, 501–510

Alcohol dependence frequently co-occurs with cigarette smoking, another common addictive behavior. Evidence from genetic studies demonstrates that alcohol dependence and smoking cluster in families and have shared genetic vulnerability.

Recently a candidate gene study in nicotine dependent cases and nondependent smoking controls reported strong associations between a missense mutation (rs16969968) in exon 5 of the CHRNA5 gene and a variant in the 3'-UTR of the CHRNA3 gene and nicotine dependence.

In this study we performed a comprehensive association analysis of the CHRNA5–CHRNA3–CHRNB4 gene cluster in the Collaborative Study on the Genetics of Alcoholism (COGA) families to investigate the role of genetic variants in risk for alcohol dependence.

Using the family-based association test, we observed that a different group of polymorphisms, spanning CHRNA5-CHRNA3, demonstrate association with alcohol dependence defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edn (DSM-IV) criteria. Using logistic regression we replicated this finding in an independent case-control series from the family study of cocaine dependence.

These variants show low linkage disequilibrium with the SNPs previously reported to be associated with nicotine dependence and therefore represent an independent observation.

Functional studies in human brain reveal that the variants associated with alcohol dependence are also associated with altered steady-state levels of CHRNA5 mRNA.

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Tuesday, April 21, 2009

Improving public addiction treatment through performance contracting: The Delaware experiment
Health Policy Volume 87, Isue 3, pages 296-308 (September 2008

In fiscal 2002, Delaware replaced traditional cost-reimbursement contracts with performance-based contracts for all outpatient addiction treatment programs. Incentives included 90% capacity utilization and active patient participation in treatment.

One of the programs failed to meet requirements. Strategies adopted by successful programs included extended hours of operation, facility enhancements, salary incentives for counselors, and two evidence-based therapies (MI and CBT). Average capacity utilization from 2001 to 2006 went from 54% to 95%; and the average proportion of patients’ meeting participation requirements went from 53% to 70%—with no notable changes in the patient population.

We conclude that properly designed, program-based contract incentives are feasible to apply, welcomed by programs and may help set the financial conditions necessary to implement other evidence-based clinical efforts; toward the overall goal of improving addiction treatment.

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Monday, April 20, 2009

The Importance of Keeping Regular: Accurate Guidance to the Public on Low-Risk Drinking Levels
Alcohol and Alcoholism 2009 44(3):226-228

The aim of this study was to argue that recommendations to the general public on daily amounts for low-risk alcohol consumption must retain the word ‘regular’ in order to avoid being rejected.

Narrative review of the evidence-base for daily limits to alcohol consumption, the guidance the public actually receives in the UK and media reactions to this guidance.

Evidence for daily limits (not more than 3–4 units for men and 2–3 units for women) rests on epidemiological surveys that enquire about ‘average’ or ‘usual’ amounts of consumption and this is reflected by the use of ‘regular’ or ‘consistent’ in the UK Government's Sensible Drinking report in 1995 and in guidance currently issued by the English Department of Health. In contrast, guidance the public actually receives often omits the word ‘regular’ and implies that the limits in question are maximum daily amounts. Media reactions to this inaccurate information suggest that the general public is likely to find these recommendations incredible and to reject them.

If guidance to the public on daily drinking amounts is to stand any chance of being credible and effective, it must be accurate and must therefore retain the word ‘regular’.

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Explaining change and stasis in alcohol consumption
Addiction Research & Theory Published Online 10 March 2009

The term 'saturation' has often been used when alcohol consumption in a region stays the same despite there having been reason to expect an increase, e.g. after a decrease of taxation. However, the term 'saturation' has been used only descriptively, and in different ways.

We therefore propose a wider-ranging framework for understanding and explaining trends in alcohol consumption, illustrating the operation of the factors with historical or contemporary examples. In the framework, we include not only taxes and other alcohol controls, but also situational and other norms on drinking and intoxication, competing responsibilities and attractions that demand or favour sobriety, structural changes, external influences and the range of societal or cultural responses to alcohol problems.

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Should alcohol policies aim to reduce total alcohol consumption? New analyses of Canadian drinking patterns
Addiction Research & Theory, Volume 17, Issue 2 April 2009 , pages 135 - 151
We investigated whether high-risk drinking patterns are restricted to a few high-volume drinkers or are evenly distributed across the population to inform discussion regarding the optimal mix of targeted versus universal prevention strategies.
Drinking patterns reported in the 2004 Canadian Addiction Survey (CAS, n = 13,909) were assessed against various low-risk drinking guidelines. Under-reporting was assessed against known alcohol sales for 2004. Non-response bias due to the low response rate (47%) was investigated through comparisons with the 2002 Canadian Community Health Survey (CCHS).
Self-reported alcohol consumption for the past week and past year accounted for between 31.9% and 37.0%, respectively of official alcohol sales data. Comparisons with the 2002 CCHS suggested only limited non-response bias.
Many more respondents regularly placed themselves at risk of short-term harm (20.6%) than exceeded guidelines for avoiding long-term health problems (3.9%). Ten percent of respondents consumed more than 50% of total self-reported consumption. Most alcohol (73.4%) consumed by the sample in the previous week was drunk in excess of Canadian low-risk drinking guidelines - for 19 to 24 year olds this figure was 89.4%.
These data provide support both for universal prevention strategies (e.g. reducing economic and physical availability of alcohol) as well as targeted interventions for risky drinkers (e.g. screening and brief interventions in primary health care settings).
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Adolescent risk factors for excessive alcohol use at age 32 years. A 16-year prospective follow-up study
Social Psychiatry and Psychiatric Epidemiology 0933-7954 (Print) 1433-9285 (Online) April, 16, 2009

To examine which socioeconomic, family, personal and lifestyle risk factors in adolescence were the strongest independent predictors of excessive alcohol use in adulthood.

All the socioeconomic, family, personal, and lifestyle variables in adolescence, except parental social class in both genders and self-esteem among females, showed significant univariate associations with excessive alcohol use at age 32 years. Multivariate logistic regression analysis showed that among adolescent males, parental divorce, moderate and high level of depressive symptoms, leisure-time spent daily among friends and moderate and drunkenness-orientated drinking were the strongest predictors of excessive alcohol use in adulthood. Among females, the strongest adolescent predictors of excessive alcohol use in adulthood were drunkenness-orientated drinking and frequent smoking.

Early interventions for adolescent substance use and a set of specific psychosocial risk factors should be tailored and evaluated as methods for identifying those at high risk of and preventing excessive alcohol use in adulthood.

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Recovery: Linking Addiction Treatment and Communities of Recovery
Scottish Addiction Library 16 April 2009

William White and Ernest Kurtz primer for addiction professionals wanting to utilise the complementary power of mutual aid or self-help networks. Keywords: mutual aid, self-help, AA, NA, alcoholics anonymous, narcotics anonymous, recovery, recovery communities, abstinence.

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Population-based study of baseline ethanol consumption and risk of incident essential tremor
Journal of Neurology, Neurosurgery, and Psychiatry 2009;80:494-497

Recent postmortem studies have demonstrated pathological changes, including Purkinje cell loss, in the cerebellum in essential tremor (ET). Toxic exposures that compromise cerebellar tissue could lower the threshold for developing ET. Ethanol is a well-established cerebellar toxin, resulting in Purkinje cell loss.

To test whether higher baseline ethanol consumption is a risk factor for the subsequent development of incident ET.

Lifetime ethanol consumption was assessed at baseline (1994–1995) in a prospective, population-based study in central Spain of 3285 elderly participants, 76 of whom developed incident ET by follow-up (1997–1998).
In a Cox proportional hazards model adjusting for cigarette pack-years, depressive symptoms and community, the baseline number of drink-years was marginally associated with a higher risk of incident ET (relative risk, RR = 1.003, p = 0.059). In an adjusted Cox model, the highest baseline drink-year quartile doubled the risk of incident ET (RR = 2.29, p = 0.018), while other quartiles were associated with more modest elevations in risk (RR3rd quartile = 1.82 (p = 0.10), RR2nd quartile = 1.75 (p = 0.10), RR1st quartile = 1.43 (p = 0.34) vs non-drinkers (RR = 1.00)). With each higher drink-year quartile, the risk of incident ET increased an average of 23% (p = 0.01, test for trend).
Higher levels of chronic ethanol consumption increased the risk of developing ET. Ethanol is often used for symptomatic relief; studies should explore whether higher consumption levels are a continued source of underlying cerebellar neurotoxicity in patients who already manifest this disease.

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Ethanol- and cocaine-induced locomotion are genetically related to increases in accumbal dopamine
Genes, Brain and Behavior Volume 8 Issue 3, Pages 346 - 355
Neuroanatomical research suggests that interactions between dopamine and glutamate within the mesolimbic dopamine system are involved in both drug-induced locomotor stimulation and addiction. Therefore, genetically determined differences in the locomotor responses to ethanol and cocaine may be related to differences in the effects of these drugs on this system.
To test this, we measured drug-induced changes in dopamine and glutamate within the nucleus accumbens (NAcc), a major target of mesolimbic dopamine neurons, using in vivo microdialysis in selectively bred FAST and SLOW mouse lines, which were bred for extreme sensitivity (FAST) and insensitivity (SLOW) to the locomotor stimulant effects of ethanol. These mice also show a genetically correlated difference in stimulant response to cocaine (FAST > SLOW).
Single injections of ethanol (2 g/kg) or cocaine (40 mg/kg) resulted in larger increases in dopamine within the NAcc in FAST compared with SLOW mice. There was no effect of either drug on NAcc glutamate levels.
These experiments indicate that response of the mesolimbic dopamine system is genetically correlated with sensitivity to ethanol- and cocaine-induced locomotion.
Because increased sensitivity to the stimulating effects of ethanol appears to be associated with greater risk for alcohol abuse, genetically determined differences in the mesolimbic dopamine response to ethanol may represent a critical underlying mechanism for increased genetic risk for alcoholism.
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High-Risk Drinking Down as Result of Broad Initiative
News & Information April, 14, 2009

Fewer UC Davis students are engaging in high-risk drinking and the community is raising expectations for responsible behavior related to alcohol and parties, according to a report on a major local effort.

The Safe Party Initiative at UC Davis began as part of a $6.9 million research project at 14 UC and California State University campuses to help combat high-risk drinking among college students in California.

Over the last four years, the UC Davis initiative showed students how to reduce alcohol-related risks at parties, fostered better relationships among students and their neighbors, and increased the visibility of law enforcement related to alcohol use.
. . . . .

Assessing appetitive, aversive, and negative ethanol-mediated reinforcement through an immature rat model
Neuroscience & Biobehavioral Reviews Article in Press, 24 March 2009

The motivational effects of drugs play a key role during the transition from casual use to abuse and dependence. Ethanol reinforcement has been successfully studied through Pavlovian and operant conditioning in adult rats and mice genetically selected for their ready acceptance of ethanol. Another model for studying ethanol reinforcement is the immature (preweanling) rat, which consumes ethanol and exhibits the capacity to process tactile, odor and taste cues and transfer information between different sensorial modalities.

This review describes the motivational effects of ethanol in preweanling, heterogeneous non-selected rats. Preweanlings exhibit ethanol-mediated conditioned taste avoidance and conditioned place aversion. Ethanol's appetitive effects, however, are evident when using first- and second-order conditioning and operant procedures. Ethanol also devalues the motivational representation of aversive stimuli, suggesting early negative reinforcement. It seems that preweanlings are highly sensitive not only to the aversive motivational effects of ethanol but also to its positive and negative (anti-anxiety) reinforcement potential.

The review underscores the advantages of using a developing rat to evaluate alcohol's motivational effects.

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Policies for Reducing Problems Associated with Alcohol Availability

The 15th in a series of conferences on the avoidance of alcohol-related problems using public policy strategies

TBA during either the second half of 2010 or first half of 2011

Washington, DC (tentative)

Why now?
The new federal administration has signaled a renewed interest in science and public health. Meanwhile, states and localities are facing increased demand for public services in the face of declining revenues. Evidence-based alcohol policy can reduce alcohol problems and resultant social costs, simultaneously generating revenue (alcohol excise taxes and other user fees) to promote public health and safety.

Who should attend?
We welcome an anticipated attendance of up to 300 participants, including community-based practitioners, public officials, and researchers from across North America and beyond.

More information
Call for abstracts, scholarship availability, exhibit opportunities, and accommodations forthcoming via Reach Silver Gate Group staff by e-mail –

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Sunday, April 19, 2009

Influence of a Drinking Quantity and Frequency Measure on the Prevalence and Demographic Correlates of DSM-IV Alcohol Dependence
Alcoholism: Clinical and Experimental Research Volume 33 Issue 5, Pages 761 - 771

Recent research suggests that adding a quantity/frequency alcohol consumption measure to diagnoses of alcohol use disorders may improve construct validity of the diagnoses for Diagnostic and Statistical Manual of Mental and Behavior Disorders (DSM-V).

This study explores the epidemiological impact of including weekly at-risk drinking (WAD) in the DMS-IV diagnostic definition of alcohol dependence via 3 hypothetical reformulations of the current criteria.

The sample was the National Epidemiologic Survey on Alcohol and Related Conditions, a nationally representative sample with 43,093 adults aged >18 in the U.S interviewed with the Alcohol Use Disorder and Associated Disabilities Interview Schedule IV. The current (DSM-IV) definition of alcohol dependence was compared with 4 hypothetical alcohol dependence reformulations that included WAD: (1) WAD added as an eighth criteria; (2) WAD required for a diagnosis; (3) adding abuse and dependence criteria together, and including WAD with a 3 of 12 symptom threshold; (4) adding abuse and dependence criteria together, and including WAD with a 5 of 12 symptom threshold.

The inclusion of at-risk drinking as an eighth criterion of alcohol dependence has a minimal impact on the sociodemographic correlates of alcohol dependence but substantially increases the prevalence of dependence (from 3.8% to 5.0%). At-risk drinking as a required criterion or as part of a diagnosis that combines abuse with dependence criteria with a higher threshold (5+ criteria) decreases prevalence and has a larger impact on sociodemographic correlates. Blacks, Hispanics, and women are less likely to be included in diagnostic reformulations that include WAD, whereas individuals with low-income and education are more likely to remain diagnosed.

Including WAD as either a requirement of diagnosis or as an additional criterion would have a large impact on the prevalence of alcohol dependence in the general population. The inclusion of a quantity/frequency requirement may eliminate false positives from studies of alcohol disorder etiology and improve phenotype definition for genetic association studies by reducing heterogeneity in the diagnosis, but may also reduce eligibility for treatment services among women and racial/ethnic minorities compared

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Protective Effect of Vitamin E Against Ethanol-Induced Hyperhomocysteinemia, DNA Damage, and Atrophy in the Developing Male Rat Brain
Alcoholism: Clinical and Experimental Research Published Online: 9 Apr 2009
Chronic alcoholism leads to elevated plasma and brain homocysteine (Hcy) levels, as demonstrated by clinical investigations and animal experiments. It has been posited that elevated levels of Hcy mediate DNA damage, brain atrophy, and excitotoxicity. The current study sought to elucidate the effect of vitamin E on ethanol-induced hyperhomocysteinemia, DNA damage, and atrophy in the developing hippocampus and cerebellum of rats.

The results revealed that along with a significant decrease in brain, cerebellum, and hippocampus weights in animals that received alcohol, the levels of DNA damage and Hcy significantly increased. Significant amelioration of brain atrophy and DNA damage as well as restoration of the elevated level of Hcy to that of controls were found in vitamin E-treated rats.

These findings strongly support the idea that ethanol intake by dams during pregnancy and lactation induces Hcy-mediated oxidative stress in the developing hippocampus and cerebellum of offspring rats, and that these effects can be alleviated by vitamin E as an antioxidant.
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Sex Differences in Drug-Related Stress-System Changes: Implications for Treatment in Substance-Abusing Women
Harvard Review of Psychiatry, Volume 17, Issue 2 April 2009 , pages 103 - 119

Extensive research indicates that chronic substance abuse disrupts stress and reward systems of the brain. Gender variation within these stress-system alterations, including the impact of sex hormones on these changes, may influence sex-specific differences in both the development of, and recovery from, dependency.
As such, gender variations in stress-system function may also provide a viable explanation for why women are markedly more vulnerable than men to the negative consequences of drug use.
This article therefore initially reviews studies that have examined gender differences in emotional and biophysiological changes to the stress and reward system following the acute administration of drugs, including cocaine, alcohol, and nicotine.
The article then reviews studies that have examined gender differences in response to various types of stress in both healthy and drug-abusing populations. Studies examining the impact of sex hormones on these gender-related responses are also reported.
The implications of these sex-specific variations in stress and reward system function are discussed in terms of both comorbid psychopathology and treatment outcome.
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The affordability of alcoholic beverages in the European Union: Understanding the link between alcohol affordability,consumption and harms

The European Commission (EC) commissioned RAND Europe to conduct a study on theaffordability of alcohol products across the EU, and on the potential impacts ofaffordability on harmful use of alcohol. On this basis, the study is intende to provideevidence on whether alcohol affordability could be a useful policy lever to publicauthorities seeking to reduce harmful alcohol consumption in Europe.

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