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
Washington Marriott Wardman Park
Washington, DC, USA
The US 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.
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This review summarises the different motivational frameworks that are commonly applied to the study of substance misuse and explores the potential of a comprehensive conceptualisation of motivation based on the self-determination theory (SDT).
The most prominent conceptualisations of motivation to change amongst substance misusing patients are identified. Defining and measuring the concept of motivation within a sound theoretical framework has been a challenge. The literature lends little support to the conceptualisation of motivation as internal and external types. Promising work employs a dynamic model of motivation, but empirical research based on such a framework is still in its infancy.
There is empirical support to the conceptual distinction between motivation and treatment readiness and it appears that such a distinction can be particularly useful to treatment services.
Clients’ motivation has significant implications for initiating and sustaining recovery, and future conceptual and methodological improvements are needed that can improve our understanding of how people change addictive behaviours and what can be done better to assist them in their attempts to recover from addiction.
Several studies have found protective effects of low/moderate (hereafter ‘light’) alcohol consumption compared with ‘abstinence’ on mortality, health and wage. Some of these studies have been criticised because former drinkers have been included among the abstainers, which may overstate the protective effect of light alcohol consumption.
It has also been proposed, but not shown, that the commonly pooled group of light drinkers and former heavy drinkers would understate the protective effect of light drinking. We also suggest that former abstainers might cause the same effect when pooled with light drinkers.
The aim of this article is to study whether the pooling of consumption groups creates bias in the form of misclassification and confounding. The analysis focuses on: ‘former drinker error’ (pooling of lifelong abstainers and former drinkers); ‘former abstainer error’ (pooling of former abstainers and lifelong light drinkers) and ‘former heavy drinker error’ (pooling of light drinkers with and without a history of heavy drinking).
Swedish panel data were used in a multinomial logit model, presenting odds ratios when comparing the subgroups.
The results demonstrate that commonly pooled groups are heterogeneous with respect to a number of variables, which may implicate confounding. Given appropriate controls, misclassification bias is likely in the pooled group of light drinkers.
The direction of the misclassification bias, however, is to underestimate the beneficial effect of light alcohol consumption on wage and therefore cannot explain the wage penalty of abstinence compared to light drinking.
Request Reprint E-Mail: johan.
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This review article discusses the importance of identifying gene-environment interactions for understanding the etiology and course of alcohol use disorders and related conditions.
A number of critical challenges are discussed, including the fact that there is no organizing typology for classifying different types of environmental exposures, many key human environmental risk factors for alcohol dependence have no clear equivalents in other species, much of the genetic variance of alcohol dependence in human is not 'alcohol specific', and the potential range of gene-environment interactions that could be considered is so vast that maintaining statistical control of Type 1 errors is a daunting task.
Despite these and other challenges, there appears to be a number of promising approaches that could be taken in order to achieve consilience and ecologically valid translation between human alcohol dependence and animal models.
Foremost among these is to distinguish environmental exposures that are thought to have enduring effects on alcohol use motivation (and self-regulation) from situational environmental exposures that facilitate the expression of such motivations but do not, by themselves, have enduring effects. In order to enhance consilience, various domains of human approach motivation should be considered so that relevant environmental exposures can be sampled, as well as the appropriate species to study them in (i.e. where such motivations are ecologically relevant).
Foremost among these are social environments, which are central to the initiation and escalation of human alcohol consumption.
The value of twin studies, human laboratory studies and pharmacogenetic studies is also highlighted.
Request Reprint E-Mail: sherk@missouri.edu
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Reward is a concept fundamental to discussions of drug abuse and addiction.
The idea that altered sensitivity to either drug–reward, or to rewards in general, contributes to, or results from, drug-taking is a common theme in several theories of addiction. However, the concept of reward is problematic in that it is used to refer to apparently different behavioural phenomena, and even to diverse neurobiological processes (reward pathways).
Whether these different phenomena are different behavioural expressions of a common underlying process is not established, and much research suggests that there may be only loose relationships among different aspects of reward.
Measures of rewarding effects of drugs in humans often depend upon subjective reports. In animal studies, such insights are not available, and behavioural measures must be relied upon to infer rewarding effects of drugs or other events. In such animal studies, but also in many human methods established to objectify measures of reward, many other factors contribute to the behaviour being studied. For that reason, studying the biological (including genetic) bases of performance of tasks that ostensibly measure reward cannot provide unequivocal answers.
The current overview outlines the strengths and weaknesses of current approaches that hinder the conciliation of cross-species studies of the genetics of reward sensitivity and the dysregulation of reward processes by drugs of abuse.
Some suggestions are made as to how human and animal studies may be made to address more closely homologous behaviours, even if those processes are only partly able to isolate 'reward' from other factors contributing to behavioural output.
Request Reprint E-Mail: d.stephens@sussex.ac.uk
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The study showed a significant association of -141C Ins allele and a trend of association of TaqI A1 allele of DRD2 with alcohol dependence. Haplotype with the predisposing -141C Ins and TaqI A1 alleles (-141C Ins-A-A1) seems to confer [almost equal to] 2.5 times more risk to develop alcohol dependence.
The study provides preliminary insight into genetic risk to alcohol dependence in Indian males. Two polymorphisms namely, -141C Ins/Del and TaqI A in DRD2 gene may have clinical implications among Indian alcoholic subjects.
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