2015 April-June; 2(2): 36–47. ISSN: 2421-3349
Published online 2016 October 12.

Understanding and managing Gambling Disorder: an overview of recent evidence and current practices

Athanasios Alexandris,1 Neil Smith,2 and Henrietta Bowden-Jones2,3

1School of Medicine, Maurice Shock Medical Sciences Building, Leicester, UK
2National Problem Gambling Clinic, Soho Centre for Health and Care, London, UK
3Division of Brain Science, Department of Medicine, Imperial College London, South Kensington Campus, London, UK

Address for correspondence: Athanasios Alexandris, School of Medicine, Maurice Shock Medical Sciences, Building, University Road, LE1 9HN Leicester, UK, E-mail: aa612@le.ac.uk

Abstract

Gambling is a recreational activity observed across most cultures, yet for about 2% of the general population, and becomes significantly disordered and interferes with life functioning. This condition, long conceptualized as an impulse control disorder (DSM-IV, ICD-10) is increasingly recognized as a behavioral addiction akin to substance use disorders, a change reflected in DSM-5. Here we provide an overview of current ideas around GD from its phenomenology and aetiopathology to strategies towards its management. In particular this review summarizes the current status of understanding of the underlying neurobiology and the causes of gambling disorder (GD) while drawing parallels with neurophysiological models of addiction. Furthermore, we describe briefly services and treatments available for GD, potential pharmacological interventions as well as potential strategies for diagnosing and treating GD within and outside specialist services.

Keywords: pathological gambling, gambling disorder, neurobiology, neuroimaging, psychotherapy, interventions, screening, addiction

 

“At that point I ought to have gone away, but a strange sensation rose up in me, a sort of defiance of fate, a desire to challenge it, to put out my tongue at it. I laid down the largest stake allowed - four thousand gulden - and lost it. Then, getting hot, I pulled out all I had left, staked it on the same number, and lost again, after which I walked away from the table as though I were stunned. I could not even grasp what had happened to me”.

Fyodor Dostoevsky, The Gambler (1867)

Introduction

Gambling and gambling disorder: Historical Background
Gambling is one of the few social activities that have been observed across most cultures and throughout history (1, 2). Although its exact notion may depend every time on the related socio-historical context, in its wider sense refers to “risk-taking activities that can be found in almost every aspect of social life” (1). For the ancient Greeks a gambling match between Zeus, Poseidon and Hades shaped the very cosmos; while in the hindu sacred text, Mahabharata, a dice match among kings led to war and destruction (2). Herodotus (Histories 1.93.1–1.94.7) wrote that when the Lydians were plagued by decades of famine they resorted into inventing the dice and gambling in order to distract themselves from the hunger and eventually half of the population was expatriated by the draw of a lot. Gambling seems to be a universal activity whether used as a mythological explanation of the world or a coping mechanism against world’s unpredictability and problems. Of course, the most conventional definition of gambling in modern societies is in terms of “financial transactions – the staking of money, or an item of economic value, on the uncertain outcome of a future event” (1).

According to the 2010 British Gambling Prevalence Survey (2010 BGPS) (3) 73% of the general adult population had participated in some form of gambling in the previous year and a great proportion of them did so in a regular basis such as weekly. Similar rates have been described in national surveys in US and Australia (46). Nevertheless, the significance that an individual may assign to gambling should not be assumed to be that of any other financial transaction, especially when gambling ceases to be a recreational activity and becomes a maladaptive recurrent behaviour that causes significant distress and disruption to the person and their family. Such maladaptive behaviour has been termed as problem or pathological gambling and more recently as gambling disorder (GD).

A comprehensive review of about 200 prevalence studies revealed that the average prevalence of problem gambling across all countries examined was 2.3% of the general population, with standardised rates – given different methodologies, definitions and instruments used – varying from 0.5 to 7.6% (7).

Aim of this review is to provide a general overview of current knowledge and ideas on the nature of GD as well as explore current approaches on management.

Current definitions, controversies
Problem gambling has been for long recognized as a psychiatric disorder. Yet its actual name, definition and categorisation within the different families of psychiatric disorders has been controversial. Historically, it has been grouped under the name of ‘pathological gambling’ together with other impulse control disorders like kleptomania and pyromania (ICD 10, DSM-IV and ICD 11 draft). According to the ICD-11 draft definition (8) “impulse control disorders are characterized by the repeated failure to resist an impulse, drive, or urge to perform an act that is rewarding to the person, at least in the short-term, despite longer-term harm either to the individual or to others”. However, the new DSM-5 introduced several changes. First pathological gambling was renamed as ‘gambling disorder’ (GD) in order to avoid the label ‘pathological’ which can be appreciated as “a pejorative term that only reinforces the social stigma of being a problem gambler” (9) – this will be the preferred term for this review along with problem gambling. And second, GD was reclassified under Addiction and Related Disorders as a unique and prototypal ‘behavioural addiction’ i.e. a non-substance addiction. The rational for this decision has been based on several lines of evidence supporting shared underlying pathology between substance addictions and disordered gambling (e.g. vulnerability, neuropsychology), (8) and similar clinical features such as craving, tolerance, withdrawal and high rates of relapse (10, 11) – something reflected even by the diagnostic criteria (see Fig. 1 for comparison of current criteria for problem gambling and dependence syndrome). Nonetheless, although the ICD11 working group recognises the heuristic utility of such a reclassification in terms of public awareness, it considers it as rather premature based on current evidence (8).
Figure 1Figure 1
Current diagnostic criteria for ‘gambling disorder’ (DSM-5), ‘pathological gambling’ (ICD 10). For comparison abbreviated diagnostic criteria for the ‘dependence syndrome’ (ICD 10) are also presented. It is evident that several of the criteria for GD (more ...)

A diagnosis with health implications
Perhaps the most crucial difference between disordered gambling and substance addictions, is exactly the absence of a substance whose physical side effects or signs can be the only giveaway. Gambling causes no tar staining, no alcohol breath, no injection marks, no peripheral stigmata. Disordered gambling could remain well hidden from family and friends for years. It is usually when the financial consequences overwhelm the patient that he or she may start seeking help; but not necessarily for gambling. Overall GD is associated with poorer health measures (12) and higher prevalence of conditions like arthritis and angina compared to non-gamblers and recreational gamblers, while psychiatric comorbidities are also substantially higher (13). Rates of suicidal ideation among problem gamblers have been estimated to around 17–80% while up to 1 in 5 problem gamblers may eventually act on them (14). Yet, the patient that presents with anxiety, depression or substance dependence may not confide his gambling problems to the unsuspecting health care professional. Moreover, problem gambling does not affect just the gambler; GD is associated with family dysfunction, increased rates of divorce and separation, mental illness, drug abuse and suicide attempts in gamblers’ children, lost productivity and absences at workplace, debt, bankruptcy, and criminal activities (1518). Whether disordered gambling is an addiction or not, it remains a quite common condition whose implications are not limited to its semantics and its diagnosis is associated with significant social, psychological and health ramifications for both the individual and his/her environment.

Understanding the problem gambler

Common patterns in gambling
Being male, exposure at a young age, low income, delinquency, low education, poor academic achievements and being on social welfare are all risk factors for GD (19). Parental history is also very significant; in a study by Lesieur et al. (20) 50% of children of problem gamblers had GD. While a preliminary study showed that actually 11% of homeless people could be problem gamblers (21). Evermore, according to a recent systematic review and meta-analysis by Dowling et al. 75% of treatment seeking problem gamblers suffer from an Axis 1 disorder (22). In particular GD is associated with depression and mood disorders (~20%), anxiety (~20%), alcohol and substance use disorders (~30%), and nicotine dependence (~60%); but more interestingly, in population surveys the rates of comorbid mood, anxiety or addiction disorders are nearly two times higher (23) denoting either a large gap in service provision or reduced self-awarness from the point of the problem gambler. Yet, offering a comprehensive explanation about why in certain individuals, gambling – an otherwise common behaviour – becomes maladaptive, is impossible without considering the complex interplay of several biological, psychological and social factors.

Cognitive and emotional processes. Van Holst et al. (24) have identified four cognitive-emotional processes that are thought to be important in GD: behavioural conditioning, salience of gambling cues, impulsivity, and impaired executive functioning and decision making. It is believed that the first process leading to GD is classical and operant conditioning that increases involvement in gambling activities and leads to more gambling-related habitual patterns. This occurs as intermittent rewards are associated with arousal states similar to a ‘drug-induced-high’ and which are then associated with the gambling environment (24, 25). It has also been suggested that problem gamblers, like substance abusers, may experience dissociative states – altered states of consciousness or even depersonalization – compared to normal gamblers. Such dissociative states, may transiently reduce dysphoria and hence act as an additional negative reinforcer; although the literature is not very conclusive about dissociative states in gambling (26, 27). Consequently, problem gamblers become more sensitive to gambling cues which then result in stronger cravings for gambling. Increased impulsivity (difficulty inhibiting behaviours) is also a common observation that is thought to contribute towards GD (24). Vitaro et al. (28, 29) actually found that increased impulsivity in adolescence could predict risk of gambling in later life indicating that individuals with a difficulty in changing their behaviours despite negative consequences are more likely to suffer from GD. This is further compounded by increased frequency of irrational beliefs (e.g. talismanic superstitions or the gambler’s fallacy, i.e. the belief that series of losses increases the likelihood of a win), illusion of control (i.e. inability to distinguish chance from skill-determined events) and other cognitive biases (19).

Nevertheless one of the most interesting observations is that GD is associated with abnormal decision-making: although problem gamblers are addicted to gambling, they are bad at it. The Iowa Gambling Task (IGT) is a widely used tool that assesses complex decision-making. In the IGT subjects select cards from four different decks, which have different frequencies and magnitudes of wins. Two of them are disadvantageous in the long term but have high payouts and the other two are advantageous but with low penalties and also low payouts. After a number of trials, subjects are expected to infer which are the most advantageous decks and opt for them. However, GD and other substance addictions are associated with a persistent preference toward high payouts in the short term despite higher long-term losses (30). Yet, problem gamblers don’t seem to fail because of an inability to integrate information across time (i.e. an inherent inability to attend to the losses or determine risk and benefits over time); but because of a hypersensitivity (increased salience) to high rewards. In other words, this hypersensitivity to gambling cues is thought to ‘hijack’ the “cognitive and affective reflective processes necessary to choose on the basis of both short-term and long-term outcomes” (31). Interestingly, this effect seems to extend to their overall ability to recognize whether their decisions are poor or not, an impairment in insight which is not limited in gambling related activities (32) and as a result could have important implications in their management.

Neurobiology of addiction and gambling. Gambling does not entail the action of any exogenous physical substance, however it has been suggested that during gambling the reward processing neural systems may undergo neuroadaptive changes that are in principle similar to the changes occurring in substance addiction (31). Exogenous substances of abuse can have very diverse pharmacological actions and affect different neurotransmitter systems in various ways. Nonetheless most of them, if not all, seem to affect the mesocorticolimbic dopaminergic pathway, a pathway that is important for reward and motivated behavior (33). Other neurotransmitter systems that may directly or indirectly modulate the reward pathways and dopaminergic transmission have also been implicated and include, among others, the serotonergic, cholinergic glutamatergic, endocanabinoid systems (3437). However, their role still needs to be deeply investigated.

The domaninergic pathway arises in the ventral tegmental area (VTA) in the brainstem, which then projects to several areas like the nucleus accumbens (NAc) in the ventral striatum. NAc is involved in reinforcement learning and transient increases in dopamine levels in NAc after drug exposure mediate the rewarding/euphoric effects of the latter. The VTA projects also to other important areas like the amygdala, which links reward events with neutral stimuli and autonomic systems, and the prefrontal cortex (PFC), which is involved in stimulus evaluation and impulse control (33, 38).

Drugs of abuse are thought to hijack the mesocorticlimbic system that normally processes natural rewards like food and sex by direct or indirect modulation of dopamine release; this leads a shift in the balance of neurotransmitters and activity so that homeostasis can then be maintained only by exposure to the exogenous substance (33). For instance, several substances like alcohol, cocaine and methamphetamine seem to be associated with reduced levels of endogenous dopamine and dopamine receptors (D2/D3); the later being inversely associated with alcohol craving, consumption and years of abuse (39). On the other hand, it has been found that in humans addicted to cocaine, cocaine related cues can actually increase dopamine release in the dorsal but not in ventral striatum and these increases were associated with cocaine craving and severity of withdrawal symptoms (40). The dorsal striatum is involved in habitual learning and such findings have supported the hypothesis by Everrit and Robbins (38) that addiction is related with a neuroadaptive transition from ventral to dorsal striatal control over drug related behaviours; a process that reflects a transition from voluntary to more habitual drug-related behaviours.

At the same time it is thought that similar changes occur in the ‘reflective system’ of the frontal cortex, which is also associated with dopaminergic dysfunction (4144). This ‘reflective system’ includes the more conscious cognitive and emotional processes that control basic subcortical impulses and facilitate long-term goals. In doing so it depends on the balance between ‘cool’ and ‘hot’ executive functions (EFs) (45). ‘Cool’ EFs, associated mainly with the dorsolateral PFC, refer mostly to abstract reasoning of decontextualized problems, determination of risks and benefits, planning, evaluating outcomes and making necessary changes to attain goals. On the other hand, ‘hot’ EFs refer mostly to affective decision-making i.e. reasoning within motivationally and emotionally significant contexts, delaying gratification etc. and are associated with the ventral and ventromedial PFC which have strong interconnections with the limbic system (45, 46).

According to Goldstein and Volkow, in addiction there is an imbalance in the control that the ventral/ventromedial and dorsal PFC have on emotions, cognition and behaviour, in what they call impaired response inhibition and salience attribution (iRISA) syndrome (44). In the normal state, non-drug related emotions, cognitions and behaviours predominate while automatic responses from ventral/vetromedial PFC (‘hot’ functions) are suppressed by input from the dorsal PFC (cool functions); thus preventing drug use/abuse and allowing focus to other activities and goals. During addiction, however, drug-related ‘hot’ functions supress non-drug-related ‘cool’ functions: as a result attention is limited on drug-related cues, there is a strong emotional response and drug-seeking behaviour becomes automatic (43, 44). This imbalance between ventral-hot and dorsal-cool PFC executive functions is consistent with and explains the poor scores associated with either drug or gambling addiction on the Iowa Gambling Task previosly mentioned. This model has been further expanded to include the insula, which is thought to function as a separate gate between the reflective system of the PFC and the subcortical impulsive system by translating bottom-up signals into subjective experiences, like cravings (47). As such activation of the insula can hijack the ‘cool’ functions of the reflective system. All these long-term neuroadaptive changes are thought to be mediated by changes in synaptic plasticity and structure, as well as in the epigenome (48). The role of altered glutamatergic homeostasis in corticostriatal plasticity in addiction has also been highlighted (49).

The implication of the dopaminergic system in GD has been greatly exemplified by the finding that PD patients on dopamine replacement therapies are a particularly high-risk group for GD (50). In one of the largest cross-sectional studies on impulse control disorders in treated PD patients (n=3090) (51), the prevalence of problem gambling was 5% while impulse control disorders like compulsive sexual behavior and buying were also very common. Dopamine agonists are particularly implicated (51, 52). Similarly, it has been suggested that Huntington’s disease may also increase the risk of recreational gambling developing into GD (53) whereas aripiprazole, a partial dopamine agonist used as antipsychotic, has also been reported to adversely affect gambling (54), highlighting the role of dopaminergic dysfunction in the pathogenesis of GD. Current evidence suggests that there are several similarities and differences between GD and substance addictions (55). With regards to the involvement of dopaminergic systems, there is no evidence to support lower baseline dopamine levels (56) but it was shown very recently that GD is associated with an up to 60% increase of dopamine release in the dorsal striatum compared to controls (57) which is very similar to the cue-induced dopamine increases in cocaine users (40). Increased activity of the dorsal striatum in fMRI has also been observed together with decreased activity of the ventral striatum (58, 59) resonating the ventro-dorsal transition observed in substance addiction. Reduced activity of the ventral striatum in particular was associated with increased disease severity (59). Furthermore, GD is associated with both a dysfunction of the prefrontal cortex and abnormal connectivity of the PFC to the striatum (60, 61) leading so to loss of control over gambling-related activities and increased salience to gambling cues. It is not surprising therefore that administration of amphetamine in GD not only increases motivation to gamble and facilitates gambling–related activities (e.g. reading speed of gambing related words in a reading task) but also suppresses non-gambling related activities and cues (62); as predicted by the Goldstein and Volkow model of drug addiction. In contrast, amphetamine administration in controls does not have such a differential effect (i.e. results in an undifferentiated improvement in reading speed task) (62). Whether drugs of abuse have a synergistic effect on gambling needs to be further investigated, especially for those that act on the dopamine system. A trial on modafinil, an indirect DA agonist, revealed a bidirectional effect, as by increasing reward salience it seemed to deter loss chasing while reinforcing gambling in the case of increased wins (63). Finally, there is some evidence that GD is associated with increased insular activity in women when presented with gambling related cues (64), as well as self-reported cravings in men (65), but reduced activity with non-gambling rewards (66). All these findings point to interesting similarities in the changes occurring in GD and substance addictions (Fig. 2) and the possibility of a general model of addiction.

Figure 2Figure 2
Simplified model of neurocognitive changes in gambling disorder based on models of substance addiction (43, 44, 47). The reflective system refers to prefrontal cortical areas implicated in ‘cool’ executive functions (blue; mainly dorsolateral prefrontal (more ...)

Vulnerable brains: nature and nurture. The great majority of recreational gamblers do not develop GD and hence recognizing the factors that lead to it has been a major area of research. Based on twin studies the heritability of GD is estimated to be 50–60% while several studies have confirmed a shared genetic vulnerability with other psychiatric disorders including alcohol and other substance dependence, depression and antisocial behavior (67). Unfortunately, the only genome wide association study to this day did not identify any particular genes associated with GD (68). Nevertheless, previous candidate-gene approaches have highlighted several genes involved in the regulation of dopamine, serotonin and noradrenalin and which could hence affect reward pathways (67). More interestingly, a large study of 1675 male twins revealed that there is a significant association between GD and previous traumatic life-events like child abuse (relative risk [RR]=2.31), child neglect (RR=5.53), witnessing of violence or murder (RR=2.83), and physical attack (RR=3.39) (69); and this association was mediated to a great extent by genetic factors. Similarly, a significant relationship with early life adversities and self-reported illicit drug use has also been found (7- to 10-fold increase compared to people with no adversities) (70). Notably, a study on macaques revealed that social isolated or subordinate individuals had reduced levels of dopamine D2 receptor compared to dominant individuals; a difference that was associated with increased self-administration of cocaine (71). Life adversities may have similar and other effects in humans involving altered gene expression and brain maturation (72).

It is of interest to note that the development of executive functions in adolescence may also have important implications. It has been shown that healthy adolescents despite having normal ‘cool’ EFs, perform worse than adults and younger children in the IGT owing to a lag in the maturation of their affective ‘hot’ functions (inhibitory ventral PFC) and a relatively overactive striatum that promotes reward-driven responses (73). Hence, they are more emotionally driven by short-term losses/wins than known long-term outcomes. The way their immature ‘hot’ functions hijack their otherwise normal cognitive functions is in that sense similar to deficits observed in GD and substance dependence (see “cognitive and emotional processes” paragraph). Actually, in adolescence, success is predicted not by activation of the ventromedial-hot areas that occurs in adults, but depends on reduced activation of the (ventral) striatum (74). One could hypothesize then that adolescence presents an important window of vulnerability and actually rates of GD in adolescence are two times higher than in adults (3). As already mentioned, exposure to gambling at a young age is indeed associated with GD in later life (19) and moreover poor IGT scores in adolescents (due to affective deficits) further predict substance abuse behaviors like binge drinking (75). Reduced thickness of the (right) frontal cortex has been observed in both GD (76) and alcohol binge drinking (77) and although the causal relationship is still not clear, it would be tempting to consider potential neurodevelopmental vulnerabilities for both GD and substance addictions.

It would be misleading, however, to suggest that GD is a homogenous nosological entity. Current research indicates that GD could encompass several subtypes of patients that might have followed different pathways into GD. According to the pathways model proposed by Blaszczynski & Nower (25) there are three etiological subtypes of disordered gamblers: i) behaviorally conditioned gamblers who have no particular predispositions, ii) emotionally vulnerable gamblers with past trauma, depression, self-hatred and who use gambling as a coping mechanism against their emotional problems/life adversities; and iii) biologically-based gamblers (originally termed as anti-social impulsivist) who have a biological predisposition (25, 78). A Canadian factor analysis study in adolescents (n=109) identified these three subtypes as well as another two (a depression only subtype and a subtype with both internalizing and externalizing features, i.e. a combination of ii and iii) (78). The existence of different subtypes (along the co-existence of substance dependence) could explain several contradictions in current literature, and future research in the neurobiology of gambling will need to address these.

Managing gambling disorder

Overview of services available
GD has a rather variable course with some individuals having intermitted or chronic problems. Interestingly, based on the analysis of two US National Surveys (79) (along other observational studies) it seems that for the majority of people with GD, the course is that of a 1-year episode, with 1/3 of people probably achieving natural recovery without help. Yet, there is a substantial percentage of people with a more sever and long lasting course.

Historically, specialized care or support for people with GD has been provided predominately by foundations or non-profit organizations like Gamblers Anonymous (founded in US in 1950s), which now organize more than 1000 meetings internationally (80). Such services have been further supplied by helplines and other non-profit organizations or support groups for friends and relatives e.g. GamAnon. However, the evidence base for their effectiveness is lacking in both volume and quality with some initial studies highlighting high attrition rates (81, 82).

A 2004 report by Abbott et al. for the Responsibility in Gambling Trust, UK (83), revealed that there was significant variability in the provision, administration and access to services for problem gambling across and within different jurisdictions. Interestingly, even before the classification of GD as an addiction in DSM-5, most formal treatments were delivered as a specialised track within existing substance abuse programmes (83). This is the case, for instance, in the Netherlands where treatment of GD falls under the same insurance coverage as substance addictions and is provided in the same addiction treatment centres since 1991 (84). Levels of treatment generally range from inpatient programmes to brief and more informal interventions, but most commonly GD is treated in an outpatient basis following usually a multimodal approach. One such example is the National Problem Gambling Clinic (NPGC) in UK, founded just in 2008 and is currently the only specialized service for the treatment of GD within the British national health system (85). The NPGC, located in London, consists of a multidisciplinary team of doctors with a background in addictions psychiatry, nurses, therapists, psychologists and debt counsellors who offer brief interventions, cognitive behavioural therapy (CBT), family therapy and financial awareness sessions (85). In North America, service provision varies among states/provinces and follows a similar approach although it not usually reimbursed by health insurers (83) (in US state-funded treatment in 2013 was provided to only 0.18% of those in need) (86). However, given the lack of research on the evaluation of current services and the wide-range of treatments available, it is particularly difficult to comment on – and let alone, compare – the efficacy of the available treatment options.

Professionally delivered treatments and pharmacological agents
Currently there are no licensed pharmacological agents for the treatment of GD and unless there are other comorbid substance addictions, the main formal treatment option is individual or group psychotherapy including, cognitive and cognitive behavioural therapy (CBT), motivational interviewing (MI), mindfulness and others.

CBT is a common treatment modality for GD. In GD, CBT focuses on “identifying and managing triggers, conducting functional analysis of gambling episodes, increasing alternate activities, dealing with urges and cravings, building interpersonal conflict skills, recognizing and correcting cognitive biases, and preventing relapse” (82). According to a 2012 Cohrane review (87), there is variable and low quality evidence that at least in the short term, CBT can lead to significant reductions in frequency of gambling and diagnoses of GD, severity of gambling-related symptoms and those of depression and anxiety, and financial losses; although the long term outcomes are not clear. Nonetheless, a study by Echeburúa et al., (88) showed that just the addition of relapse prevention interventions could increase significantly the number of people with 1-year long benefits (in the particular study from 56 to 83%). Given the quite low number of people seeking treatment for their GD (7–12%) (79), single session interventions of motivational interviewing are also a particularly promising, low-cost option and have been shown to be effective in reducing gambling frequency to some extend as well (82, 87). [For a comprehensive review of psychological therapies see (82)].

Depending on the categorization of GD there have been different pharmacological treatment strategies (89). The conceptualization of GD as an impulse control disorder suggested antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs); as an addiction, opioid antagonists and glutamatergic agents; and as a mood disorder (due to similarities with mania), mood stabilizers. With regards, SSRIs and mood stabilizers, e.g. lithium and valproate, studies have shown very limited or no efficacy for treating GD and some benefit only if there is a concurrent anxiety or bipolar disorder respectively (8992). On the other hand, opioid antagonists like naltrexone and nalmefene, which modulate dopaminergic transmission in the mesolimbic pathway and are licensed for alcohol dependence, have been found to reduce significantly gambling urges and gambling behaviour compared to placebo and hence facilitate abstinence at least in the short term (RR:2–4) (91). Finally, although the evidence for agents targeting glutamatergic neurotransmission is limited so far, there are already some promising results for N-acetylcysteine and memantine (89, 93, 94); but of course more research is still needed.

It should be noted, however, that the pathways model of problem gambling may have significant implications with regards overall management of GD as different subtypes may respond differently to therapies. It has been suggested that the behaviourally conditioned gamblers (with no other underlying pathology) may respond very well to psychotherapy whereas the emotionally vulnerable gamblers and the biologically-based impulsive gamblers may need additional pharmacological interventions that target underlying functional/neurotransmitter imbalances (25). There is already some evidence, for instance, that a family history for alcoholism is predictive for a positive response to opiate antagonists (95) emphasising that a subgroup of people may be biologically predisposed and responsive to relevant treatments. There is also some very preliminary evidence that fMRI activation of ventral striatum and ventromedial PFC can be predictive of treatment outcomes in problem gamblers receiving CBT as is the case in substance dependence (96). The development of clinical tools that screen for the potentially different GD subtypes along the consideration of other psychiatric comorbidities will be pivotal in both individualizing therapy and assessing the efficacy of different therapies.

Screening for the ‘hidden addiction’ and interventions outside specialist care
As discussed above, there are several treatments available for GD, and several others with an increasing evidence base. Yet, one of the first and foremost challenges in helping disordered gamblers is that they are not recognised by healthcare services and even when they are recognised outside specialist services, little is usually offered. Nonetheless, there are several high-risk populations where a conscious effort in screening for GD could have high yields. According to a systematic review on the prevalence of gambling disorder in substance use treatment, 14% of patients can have comorbid GD; while in a more recent study up to half of patients on methadone maintenance met the DSM-5 criteria for GD (97). GD is also four times higher in patients with psychotic disorders (98, 99). Based on data from the US National Comorbidity Survey Replication, about 49% of individuals with disordered gambling had received treatment for emotional or substance use problems but none received any treatment for their gambling problems (100). Hence, although a significant number of people with GD are already in contact with psychiatric and addiction services, they remain largely undiagnosed and represent an important population for targeted screening. The same stands of course for those on dopamine agonist treatment who may not understand the possible link with their medication and rarely volunteer information about their gambling habits (52). Several instruments have been devised for screening for GD which can be used in clinical or research settings. Two common examples are the South Oaks Gambling Screen (SOGS), a 20-item paper-and-pencil questionnaire that is validated in many populations, and the National Opinion Research Center DSM-IV Screen for Gambling Problems (NODS), a 17-item structured interview (101).

However such instruments can be considered time consuming in the busy clinical setting (requiring approximately 20 minutes) and especially when gambling is not the presenting complain. For this reason several brief screening tools have also been devised that can identify individuals with GD on the basis of only 2 to 4 questions. Such tools like Lie/Bet, NODS-CLiP, NODS-PERC and BBGS (See table 1), are easy to administer within a couple of minutes, validated across different settings and could prompt further assessment (101, 102). Of those BBGS was shown most suitable within addiction services settings (102). Screening for GD is important not just because only a small number of disordered gamblers seek treatment (79) or are aware of available services (103), but also because very brief and uncostly interventions could have an impact on a larger population than formal treatments. Apart from single session interventions of MI, discussed above, even a 10-minute intervention during which the individual is presented with information regarding his levels of gambling, risk factors for gambling problems, and how he/she could prevent these (e.g. suggesting spending time doing other activities), may assist greatly in reducing gambling in GD and at-risk individuals compared to controls (104). Self-directed bibliotherapy (e.g., workbooks) and internet- or telephone-based interventions can also reduce gambling to some extend (82) and could be of great value outside specialist centres; although may not be as effective as formal CBT sessions (105). It is clear that just by increasing awareness and screening for GD within general addictions services – or other areas within increased prevalence of the condition (e.g. Parkinson’s disease clinics) – a large number of the “hiding” disordered gamblers could be identified and provided brief interventions without the need for extra resources or expertise. More research on screening and brief or self-directed interventions will show how effective this approach could be.

Table 1Table 1
Selection of brief screening tools for gambling disorder. [Based on (101, 102, 106109)].

Conclusion

Our understanding of how gambling, a common social activity, can develop into a disruptive disorder is still growing. GD has for long been discussed within academic contexts and nowadays its clinical significance is being recognised similar to other psychiatric conditions. Still GD, although not uncommon, remains ‘hidden’ and probably undertreated. It is very important that awareness is raised not only for patients but also for the non-specialist clinicians. Conceptualising GD as a form of an addiction along other substance addictions has played an important role in its increasing recognition and may guide further research and treatment avenues. Future research in gambling may shed more light on the underlying neurobiology of GD and inform not only medical definitions but also clinical practise and policies.

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