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Friday, September 21, 2012
Alcohol Industry Influence on Public Policy: A Case Study of Pricing and Promotions Policy in the UK
In the field of health policy, much attention has been paid to attempts by Transnational Tobacco Corporations (TTCs) to stymie regulation of their industry (Holden and Lee 2009). Relatively little research has been conducted on alcohol industry actors and their attempts to influence policies to reduce alcohol related harm. This is surprising given the rising burden of disease in many countries associated with harmful and hazardous levels of alcohol consumption. In the UK, increasing levels of alcohol consumption – and the associated harms – over recent decades have coincided with the increased availability and affordability of alcohol. There has been a trend away from consuming alcohol in licensed premises towards the purchase of cheaper alcohol from the off-sales sector for consumption at home (Foster and Ferguson 2012). In particular, significant volumes of alcohol are now sold through the ‘big four’ supermarkets, which wield significant political power (Seth and Randall 1999). On the production side, the UK alcohol market has become increasingly dominated by a small number of large, multi-national corporations (Jernigan 2009).
Alcohol policy under New Labour followed an agenda closely aligned with that advocated by alcohol industry actors (Cabinet Office 2004; Department of Health 2007). Policies targeted interventions on those sections of the public seen to be at greatest risk of harm, placing education, public information, health and treatment services, crime and disorder at the centre of the strategy. Particular emphasis was given to the role of the alcohol industry as a key partner in achieving policy goals through a system of voluntary self-regulation (see Portman Group 1996; Advertising Standards Agency et al. 2005).The thrust of this policy stands in stark contrast to the policy prescriptions advocated by public health researchers and campaigners , who favoured ‘whole population’ measures to restrict the availability and price of alcohol, which were supported by a significant evidence base (Babor et al. 2010).
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Key Recent Milestones:
Global Actions in Focus: Nigeria Alcohol Marketing Summit
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Alcoholic liver disease (ALD) is a major cause of acute and chronic liver disease worldwide. The progressive nature of ALD is well described; however, the complex interactions under which these pathologies evolve remain to be fully elucidated.
Clinically there are no clear biomarkers or universally accepted, effective treatment strategies for ALD. Experimental models of ALD are an important component in identifying underlying mechanisms of alcohol-induced injury to develop better diagnostic markers, predictors of disease progression, and therapeutic targets to manage, halt, or reverse disease progression. Rodents remain the most accessible model for studying ALD pathology.
Effective rodent models must mimic the natural history of ALD while allowing examination of complex interactions between multiple hepatic, and non-hepatic, cell types in the setting of altered metabolic or oxidative/nitrosative stress, inflammatory responses, and sensitivity to cytotoxic stress.
Additionally, mode and duration of alcohol delivery influence hepatic response and present unique challenges in understanding disease pathology.
This review provides an overview of rodent models of ALD, their strengths and weaknesses relative to human disease states, and provides insight of the potential to develop novel rodent models to simulate the course of human ALD.
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In the present study, we sought to determine whether the interoceptive effects of alcohol (1 g/kg, IG) could be assessed using a Pavlovian discrimination method, in which the alcohol drug state sets the occasion for which an environmental stimulus (e.g., light) will be followed by a sucrose reward.
This procedure takes advantage of a naturally occurring behavior (i.e., food-seeking) which can be trained rapidly prior to the initiation of discrimination training. Given that the interoceptive effects of alcohol are routinely assessed using operant drug discrimination methods, another group of rats was trained using standard two-lever operant drug discrimination procedures in an effort to compare the Pavlovian procedure to a known behavioral benchmark.
The results from this work show that, in addition to operant discrimination procedures, a Pavlovian discrimination task can be used to evaluate the interoceptive effects of alcohol. In addition to the brief behavioral sucrose access training (3 days) required prior to the initiation of the Pavlovian discrimination, the alcohol discrimination was acquired relatively rapidly (i.e., 8 training sessions), shortening the overall duration of the experiment.
These features of the Pavlovian procedure make it a valuable method by which to assess the interoceptive effects of alcohol if a short experimental time frame is required, such as assessing the interoceptive effects of alcohol during a brief developmental window (e.g., adolescence) or determining the effects of a pretreatment (i.e., chronic stress, chronic drug pretreatment) on the acquisition of the alcohol discrimination. As such, this initial characterization confirms the feasibility of using this Pavlovian discrimination training method as an additional tool by which to assess the interoceptive effects of alcohol, as there may be experimental situations that necessitate short term discrimination training.
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This forum focuses on two globally important themes:
‘Alcohol Education, what works?’
The development of lower alcohol beverages, with a spotlight on successful markets and innovations.
Thursday, 18th October 2012
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Thursday, September 20, 2012
Sensitivity and Specificity of a Brief Personality Screening Instrument in Predicting Future Substance Use, Emotional, and Behavioral Problems: 18-Month Predictive Validity of the Substance Use Risk Profile Scale
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Wednesday, September 19, 2012
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The Effects of Prenatal Alcohol Exposure and Attention-Deficit/Hyperactivity Disorder on Psychopathology and Behavior
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Studies of the adverse neurobehavioral effects of maternal alcohol consumption on the fetus have been largely confined to the postnatal period, after exposure to alcohol has finished. This
Five groups of fetuses, defined by maternal alcohol consumption patterns, were examined: control (no alcohol); moderate (5 to 10 units/wk either drunk evenly across the week or as a binge, in 2 to 3 days); heavy (20+ units/wk drunk evenly or as a binge). Fetal habituation performance was examined on 3 occasions, separated by 7 days, beginning at 35 weeks of gestation. The number of trials required to habituate on each test session and the difference in performance across test sessions were recorded.
Fetuses exposed to heavy binge drinking required significantly more trials to habituate and exhibited a greater variability in performance across all test sessions than the other groups. Maternal drinking, either heavily but evenly or moderately as a binge, resulted in poorer habituation, and moderate binge drinking resulted in greater variability compared with no, or even, drinking.
Decreased information processing, reflected by poorer habituation, and increased variability in performance may reflect the initial manifestations of structural damage caused by alcohol to the brain. These results will lead to a greater understanding of the effects of alcohol on the fetus's brain, enable the antenatal identification of fetal alcohol spectrum disorders, and lead to the early implementation of better
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Reduced bone mineral density (BMD) is commonly found in alcohol-dependent patients. Many risk factors have been reported, yet the course of markers of bone formation and resorption in abstinent alcoholic patients have not received much attention.
In a prospective longitudinal study, we investigated BMD in male abstinent inpatients of an alcohol rehabilitation clinic aged 21 to 50 years at baseline and after 8 weeks of treatment. At baseline and at week 8, all patients had blood drawn for the analysis of liver function tests, calcium, phosphate, parathormone, 25-hydroxyvitamin D, osteocalcin (OC), serum crosslaps, sex hormones, and prolactin. BMD was determined by dual X-ray absorptiometry in the lumbar spine and the proximal right femur. We also determined the amount of physical activity prior to inpatient treatment by using the International Physical Activity Questionnaire (IPAQ).
Low BMD was found in 15.1% of the patients for the lumbar spine, in 5.7% for the femoral neck, and in 1.9% for the total hip. BMD differed significantly from normal values, in the lumbar spine and in the femoral neck. At baseline, crosslaps were elevated in 34% of the patients, while OC levels were lowered in 17%. Over the course of the 8 weeks, we found a significant increase in OC plasma levels, indicating a higher rate of bone formation during continuous abstinence. There were also positive correlations between IPAQ scores and BMD as reflected by Z-scores in all regions, pointing to a protective effect of physical activity.
In summary, this report confirms earlier cross-sectional studies of lowered BMD in alcoholic noncirrhotic men. We could also demonstrate that the initial imbalance between bone formation and resorption seems to adjust toward a balance between the two during abstinence.
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Genome-wide association (GWA) studies have led to a paradigm shift in how researchers study the genetics underlying disease. Many GWA studies are now publicly available and can be used to examine whether or not previously proposed candidate genes are supported by GWA data. This approach is particularly important for the field of alcoholism because the contribution of many candidate genes remains controversial.
Using the Human Genome Epidemiology (HuGE) Navigator, we selected candidate genes for alcoholism that have been frequently examined in scientific articles in the past decade. Specific candidate loci as well as all the reported single nucleotide polymorphisms (SNPs) in candidate genes were examined in the Study of Addiction: Genetics and Environment (SAGE), a GWA study comparing alcohol-dependent and nondependent subjects.
Several commonly reported candidate loci, including rs1800497 in DRD2, rs698 in ADH1C, rs1799971 in OPRM1, and rs4680 in COMT, are not replicated in SAGE (p > 0.05). Among candidate loci available for analysis, only rs279858 in GABRA2 (p = 0.0052, OR = 1.16) demonstrated a modest association. Examination of all SNPs reported in SAGE in over 50 candidate genes revealed no SNPs with large frequency differences between cases and controls, and the lowest p-value of any SNP was 0.0006.
We provide evidence that several extensively studied candidate loci do not have a strong contribution to risk of developing alcohol dependence in European and African ancestry populations. Owing to the lack of coverage, we were unable to rule out the contribution of other variants, and these genes and particular loci warrant further investigation. Our analysis demonstrates that publicly available GWA results can be used to better understand which if any of previously proposed candidate genes contribute to disease. Furthermore, we illustrate how examining the convergence of candidate gene and GWA studies can help elucidate the genetic architecture of alcoholism and more generally complex diseases.
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Alcohol use disorders (AUDs) are clinically heterogeneous and strongly influenced by familial/genetic factors. Can we identify specific clinical features of AUDs that index familial liability to illness?
In twins from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders meeting DSM-IV criteria for lifetime AUDs, we examined whether clinical features of AUDs, including individual DSM-IV criteria for alcohol dependence (AD) and alcohol abuse (AA), predicted risk for AUDs in cotwins and/or parents. Analyses of individual criterion were repeated controlling for the total number of endorsed criteria.
Across these analyses, examining narrowly and broadly defined AUDs, risk of AUDs in relatives was more consistently predicted by abuse criteria than by dependence criteria, and by criteria reflecting negative psychosocial consequences rather than pharmacologic/biological criteria. Age at onset (AAO) poorly predicted risk in relatives. AUD associated legal problems, the one criterion slated for removal in DSM-5, was the most consistent single predictor of familial risk. Associations observed between individual criteria and risks of illness in relatives were generally stronger in monozygotic than dizygotic twin pairs, suggesting that these symptoms reflect a genetic risk for AUDs.
Individual DSM-IV criteria for AA and AD differ meaningfully in the degree to which they reflect the familial/genetic liability to AUDs. Contrary to expectation, the familial/genetic risk to AUDs was better reflected by
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State Panel Estimates of the Effects of the Minimum Legal Drinking Age on Alcohol Consumption for 1950 to 2002
Despite strong evidence supporting the effectiveness of the minimum legal drinking age (MLDA), recent movements have attempted to evoke policy changes that will allow 18- to 20-year-olds to buy and drink alcohol legally. The primary aim of this study was to evaluate the effects of both raising and lowering the MLDA on per capita ethanol (EtOH) consumption in longer and more accurate time series panel than any previous study.
Generalized least squares model specifications controlling for income, unemployment rates, and population characteristics were implemented using MLDA and aggregate EtOH consumption data from U.S. states from 1950 to 2002.
Results from the full 1950 to 2002 period, which include both the lowering and raising of the MLDA, show that an increase in the MLDA by 3 years was associated with decreases in per capita total EtOH consumption (1.51% reduction), as well as in beer (2.31% reduction) and spirits consumption (1.86% reduction).
Lowering the MLDA would likely induce increased rates of drinking and subsequent alcohol-related consequences. If increased consumption is of concern, policymakers should resist movements to lower the MLDA.
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To investigate prosipping beliefs about alcohol among parents and the relations among these beliefs, parents' alcohol-specific attitudes and practices, and children's reports of initiation of alcohol use.
Telephone interview study of parent-child dyads. Data for the present study are from the baseline interviews of a 4-year intervention trial.
Southeastern United States.
One thousand fifty pairs of mothers or mother surrogates and their third-grade children who were recruited for the 4-year intervention trial.
Key measures from parents included prosipping beliefs (ie, beliefs that sipping alcohol has protective consequences for children), attitudes about children's sipping, and parenting practices that affect children's opportunity to try alcohol. The key measure from children was experience sipping beer, wine, or other types of alcohol.
The belief among mothers that allowing children to sip alcohol can have protective consequences for children, including making children less likely to drink as adolescents and making them better at resisting peer influence to drink, ranged from approximately 15% to almost 40%. Alcohol use was reported by 32.8% of children. A strong, significant association was found between parental prosipping beliefs and children's reported alcohol use.
The notion that early exposure to alcohol can be beneficial has a strong foothold among some parents of elementary school–aged children. More research is needed to understand how parents acquire prosipping beliefs and to test messages that effectively modify such beliefs and associated prosipping attitudes and practices among parents.
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α-Synuclein has recently been implicated in the pathophysiology of alcohol abuse due to its role in dopaminergic neurotransmission.
In these studies, genetic variability in the α-synuclein gene influences its expression which may contribute to susceptibility to chronic alcohol abuse. Real-time PCR was used to quantify α-synuclein mRNA expression in autopsy samples of human dorsolateral prefrontal cortex. Because of the association between length of the α-synuclein-repeat 1 microsatellite marker and expression levels of the gene, this marker was genotyped in a Caucasian sample of 126 controls and 117 alcoholics using capillary gel electrophoresis.
The allele and genotype frequencies of α-synuclein-repeat 1 marker differed significantly between alcoholics and controls. Alcoholics had greater frequencies of the shortest allele found (267 bp). The shortest allele of the α-synuclein-repeat 1 marker was associated with decreased expression of α-synuclein in prefrontal cortex. Individuals with at least one copy of the 267 bp allele were more likely to exhibit an alcohol abuse phenotype.
These results suggest that individuals with the 267 bp allele may be at increased risk of developing alcoholism and that genetic variation at the α-synuclein-repeat 1 locus may influence α-synuclein expression in the prefrontal cortex.
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Tuesday, September 18, 2012
In 1990, Blum and colleagues first reported an association between DRD2 and alcoholism. While there have been subsequent replications of this genetic association, there have also been numerous studies that failed to detect an association between DRD2 and alcohol dependence.
We propose that one aspect contributing to this inconsistency is the variation in alcohol phenotype used across studies. Within the population-based Finnish twin sample, FinnTwin16, we previously performed multivariate twin analyses to extract latent genetic factors, which account for the variation across seven measures of alcohol consumption (frequency of drinking, frequency × quantity, frequency of heavy drinking, frequency of intoxication and maximum drinks in a 24-hour period) and problems (the Rutgers Alcohol Problem Index—RAPI and the Mälmö-modified Michigan Alcohol Screen Test—MmMAST) in 3065 twins.
In the present study, we examined the association between 31 DRD2/ANKK1 single-nucleotide polymorphisms (SNPs) and the genetic factor scores generated by twin analyses in a subset of FinnTwin16 (n = 602). We focus on two of the genetic factors: a general alcohol consumption and problems factor score, which represents shared genetic variance across alcohol measures, and a alcohol problems genetic factor score, which loads onto the two indices of problematic drinking (MAST and RAPI).
After correction for multiple testing across SNPs and phenotypes, of the 31 SNPs genotyped across DRD2/ANKK1, one SNP (rs10891549) showed significant association with the general alcohol consumption and problems factor score (P = 0.004), and four SNPs (rs10891549, rs1554929, rs6275, rs6279), representing two independent signals after accounting for linkage disequilibrium, showed significant association with the alcohol problems genetic factor score (P = 0.005, P = 0.005, P = 0.003, P = 0.003).
In this study, we provide additional positive evidence for the association between DRD2/ANKK1 and alcohol outcomes, including frequency of drinking and drinking problems.
Additionally, post hoc analyses indicate stronger association signals using genetic factor scores than individual measures, which suggest that accounting for the genetic architecture of the alcohol measures reduces genetic heterogeneity in alcohol dependence outcomes in this sample and enhances the ability to detect association.
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