Compulsive features in behavioural addictions: the case of pathological gambling

Aims To describe, in the context of DSM‐V, how a focus on addiction and compulsion is emerging in the consideration of pathological gambling (PG). Methods A systematic literature review of evidence for the proposed re‐classification of PG as an addiction. Results Findings include: (i) phenomenological models of addiction highlighting a motivational shift from impulsivity to compulsivity associated with a protracted withdrawal syndrome and blurring of the ego‐syntonic/ego‐dystonic dichotomy; (ii) common neurotransmitter (dopamine, serotonin) contributions to PG and substance use disorders (SUDs); (iii) neuroimaging support for shared neurocircuitries between ‘behavioural’ and substance addictions and differences between obsessive–compulsive disorder (OCD), impulse control disorders (ICDs) and SUDs; (iv) genetic findings more closely related to endophenotypic constructs such as compulsivity and impulsivity than to psychiatric disorders; (v) psychological measures such as harm avoidance identifying a closer association between SUDs and PG than with OCD; (vi) community and pharmacotherapeutic trials data supporting a closer association between SUDs and PG than with OCD. Adapted behavioural therapies, such as exposure therapy, appear applicable to OCD, PG or SUDs, suggesting some commonalities across disorders. Conclusions PG shares more similarities with SUDs than with OCD. Similar to the investigation of impulsivity, studies of compulsivity hold promising insights concerning the course, differential diagnosis and treatment of PG, SUDs, and OCD.     

A pathways model of problem and pathological gambling

At the moment, there is no single conceptual theoretical model of gambling that adequately accounts for the multiple biological, psychological and ecological variables contributing to the development of pathological gambling. Advances in this area are hampered by imprecise definitions of pathological gambling, failure to distinguish between gambling problems and problem gamblers and a tendency to assume that pathological gamblers form one, homogeneous population with similar psychological principles applying equally to all members of the class. The purpose of this paper is to advance a pathways model that integrates the complex array of biological, personality, developmental, cognitive, learning theory and ecological determinants of problem and pathological gambling. It is proposed that three distinct subgroups of gamblers manifesting impaired control over their behaviour can be identified. These groups include (a) behaviourally conditioned problem gamblers, (b) emotionally vulnerable problem gamblers and (c) antisocial, impulsivist problem gamblers. The implications for clinical management are discussed.     

Pathological Gambling and Substance Use Disorders

Background: Pathological gambling (CPG) has been considered as a behavioral addiction having similarities with substance use disorders (SUDs). Objectives and Methods: Current conceptualizations of addiction, as well as experimental studies of PG and SUDs, are reviewed in order to provide a perspective on tbe areas of convergence between addictive behaviors in PG and SUDs. Results: Shared features exist in diagnostic, clinical, physiological, and behavioral domains. Conclusions and Scielltific Significance: Similarities between PG and SUDs have important implicatiol1s for categorizing, assessing, preventing and treating both PO and SUDs.     

Problem gamblers share deficits in impulsive decision-making with alcohol-dependent individuals

Aims   Problem gambling has been proposed to represent a 'behavioural addiction' that may provide key insights into vulnerability mechanisms underlying addiction in brains that are not affected by the damaging effects of drugs. Our aim was to investigate the neurocognitive profile of problem gambling in comparison with alcohol dependence. We reasoned that shared deficits across the two conditions may reflect underlying vulnerability mechanisms, whereas impairments specific to alcohol dependence may reflect cumulative effects of alcohol consumption.
Design   Cross-sectional study.
Setting   Out-patient addiction treatment centres and university behavioural testing facilities.
Participants   A naturalistic sample of 21 male problem and pathological gamblers, 21 male alcohol-dependent out-patients and 21 healthy male control participants.
Measurements   Neurocognitive battery assessing decision-making, impulsivity and working memory.
Findings   The problem gamblers and alcohol-dependent groups displayed impairments in risky decision-making and cognitive impulsivity relative to controls. Working memory deficits and slowed deliberation times were specific to the alcohol-dependent group.
Conclusions   Gambling and alcohol-dependent groups shared deficits in tasks linked to ventral prefrontal cortical dysfunction. Tasks loading on dorsolateral prefrontal cortex were selectively impaired in the alcohol-dependent group, presumably as a consequence of long-term alcohol use.     

Genetic aspects of pathological gambling: a complex disorder with shared genetic vulnerabilities

Aims   To summarize and discuss findings from genetic studies conducted on pathological gambling (PG).
Methods   Searches were conducted on PubMed and PsychInfo databases using the keywords: 'gambling and genes', 'gambling and family' and 'gambling and genetics', yielding 18 original research articles investigating the genetics of PG.
Results   Twin studies using the Vietnam Era Twin Registry have found that: (i) the heritability of PG is estimated to be 50–60%; (ii) PG and subclinical PG are a continuum of the same disorder; (iii) PG shares genetic vulnerability factors with antisocial behaviours, alcohol dependence and major depressive disorder; (iv) genetic factors underlie the association between exposure to traumatic life-events and PG. Molecular genetic investigations on PG are at an early stage and published studies have reported associations with genes involved in the brain's reward and impulse control systems.
Conclusions   Despite the paucity of studies in this area, published studies have provided considerable evidence of the influence of genetic factors on PG and its complex interaction with other psychiatric disorders and environmental factors. The next step would be to investigate the association and interaction of these variables in larger molecular genetic studies with subphenotypes that underlie PG. Results from family and genetic investigations corroborate further the importance of understanding the biological underpinnings of PG in the development of more specific treatment and prevention strategies.     

A response to commentaries: the effects of self–selection

A major criticism of the hypothesis which states that non–drinkers are mainly a selected group of ex–drinkers who have given up for reasons of ill health, particularly cardiovascular disease, is that such a high selective migration seems unlikely. It is emphasized that ex–drinking status is related to a wide range of disorders although it is particularly marked for cardiovascular disorders. In addition, mortality in middle–aged men is affected most strongly by cardiovascular disease. Virtually all previous prospective studies have not paid sufficient attention to the reasons for people changing their drinking behaviour, or to the burden of disease in non–drinkers. The increase in HDL–cholesterol associated with light drinking (the ‘narrow window’ of protective effect) is small and unlikely to account for significantly reduced coronary heart disease mortality. Studies claiming a protective effect for alcohol are entreated to examine closely the burden of disease in their alcohol intake groups, particularly the non– and occasional drinkers.