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Neurocognitive components of gambling disorder: Implications for assessment, treatment and policy



Gambling disorder (GD) is now recognized as a behavioral addiction. Evidence has shown that GD and substance use disorders (SUDs) have shared vulnerability factors, similar clinical characteristics, and neurobiological overlaps. However, these similarities have somewhat overshadowed the specificities that account for the differences between GD and SUDs, as well as the considerable heterogeneity of patients with gambling disorder (PGD). In this chapter, we aim to disentangle the key neurocognitive components involved in GD, as well as those underlying heterogeneity among PGD. Core components include the brain mechanisms for gambling reinforcement, and their association with incentive sensitization and craving. With regard to heterogeneity, we will focus on specific gambling-related rewards, and automatic (model-free) versus strategic (model-based) emotion regulation processes. These components are integrated into a psychobiologically-informed, multidimensional model for gamblers’ characterization. In such model, individual differences in sensitivity to gambling reinforcement, basic emotion regulation mechanisms, and strategic emotion regulation are used to explain heterogeneity within the GD population, and serve to re-conceptualize previous attempts to cluster GD phenotypes based on clinical observations and empirical research. The proposed model has a number of implications for policy, prevention, and treatment. First, the consideration of GD as an addiction provides ground for harm-reduction approaches. Second, the transdiagnostic nature of key vulnerability factors justifies profiling of high-risk individuals for secondary prevention of disordered gambling (along with other externalizing problems). Third, understanding individual differences within the population of disordered gamblers yields a practical avenue for health services to incorporate tailored treatment protocols.
Neurocognitive components of gambling disorder: Implications for assessment, treatment
and policy
Juan F. Navas1,2, Joël Billieux3,4, Antonio Verdejo-García5, José C. Perales1,2
1. Department of Experimental Psychology, University of Granada, Spain
2. Mind, Brain, and Behavior Research Center (CIMCYC), University of Granada, Spain
3. Addictive and Compulsive Behaviours Lab. Institute for Health and Behaviour, University of
Luxembourg, Esch-sur-Alzette, Luxembourg
4. Centre for Excessive Gambling, Lausanne University Hospital, Switzerland
5. Monash Institute of Cognitive and Clinical Neurosciences & School of Psychological
Sciences, Monash University, Melbourne, Australia
To be published as: Navas, J. F., Billieux, J., Verdejo-García, A., & Perales, J. C. (In press).
Neurocognitive components of gambling disorder: implications for policy, prevention, and
treatment. In H. Bowden-Jones, C. Dickson, C. Dunand, & O. Simon (Eds.), Harm Reduction
for Problem Gambling: A Public Health Approach. Routledge.
Aims and scope
The present chapter aims to describe the psychobiological bases of gambling disorder (GD), and
to identify how neuroscience research could inform better prevention and treatment strategies.
In the first section, we describe the characteristics shared by patients with gambling
disorder (PGD), and revisit the literature showing that GD is in essence a disorder of learning.
Among vulnerabilities, we highlight factors incrementing the allure of gambling, making it more
rewarding, or strengthening its negatively reinforcing properties.
Second, we pinpoint the variables contributing to individual differences within the PGD
population, with a particular focus on emotion regulation. Dysregulation of automatic (model-
free) emotion regulation is suggested to be a complicating factor of GD, and a transdiagnostic
vulnerability factor for psychopathology beyond GD. Dysregulation of controlled (model-based)
emotion regulation strategies, along with gambling-related cognitive distortions, are hypothesised
to contribute to self-deceptive thinking in some gamblers.
Lastly, all these variables are integrated into a dimensional model (the Gambling Space
Model), aimed at updating previous cluster-based proposals to subtype PGD, by incorporating
recent neurocognitive evidence. The implications of the model are discussed, and we address its
implications on policy and regulation. Additionally, we discuss whether or not other putative
behavioural addictions should be ascribed the same consideration. Eventually, we analyse how
better understanding individual differences could contribute to better treatment and prevention
Homogeneity in gambling disorder: Incentive sensitisation as the mechanism of gambling
Gambling research has flourished in recent years, and can be considered an example of integration
of knowledge from different disciplines. The recent reconceptualisation of GD as an addictive
disorder (American Psychiatric Association, 2013) and the ensuing translational advances would
have not occurred without such cross-talk.
In a joint attempt to define addictive disorders, animal and human research, behavioural
neuroscience and cognitive neuroscience have converged in stressing the importance of
progressive detachment of addictive behaviour from instrumental goals. According to some
etiological models, addictive behaviours are problematic because they become habit-driven or
compulsive (Everitt & Robbins, 2016). Other models stress that individuals with addictive
disorder cannot help craving their addictive substance or activity (Skinner & Aubin, 2010).
Beyond the subtleties of these two approaches, here we will stress their commonality; namely, the
fact that wanting (to gamble, to use the drug) and seeking behaviour, once a person meet criteria
for addictive disorder, have little to do with the hedonic properties of drug use/gambling
Craving is thus best defined as a multifaceted construct, manifested by the urge to engage
in the addictive behaviour, automatic hijacking of attention and cognitive resources by cues
reminding or signalling the availability of the object of desire, and imperative approach responses
to such cues. With regard to its proximal and distal causes, there is also convincing evidence that
craving is cue-driven, and acquired through exposure to the addictive agent (Sayette, 2016).
In keeping with the importance of craving in substance use disorders (SUDs; Kober &
Mell, 2015) considerable efforts have been made to prove the existence of gambling craving
(Ashrafioun & Rosenberg, 2012). Additionally, recent evidence suggests that craving may involve
a common brain circuitry, with an important hub in the insula, independently of the type of
addictive disorder (Garavan, 2010; Limbrick-Oldfield et al., 2017). The association between this
area and cravings accords with its status as an important node in interoceptive representation, and
the use of such information in decision-making (Garavan, 2010).
From a practical point of view, however, the key question is how gambling becomes
compulsive, and wanting detaches from hedonic value. A leading model in accounting for drug
craving acquisition is the incentive sensitisation (IS) hypothesis. The IS model posits that all
addictive drugs directly or indirectly sensitise dopamine release in the mesolimbic system, which
is responsible for attributing incentive salience to cues signalling the availability of reward
(Robinson & Berridge, 1993).
Incentive salience is hypothesised to be the inner engine of craving acquisition. In normal
circumstances, when an unexpected reward is encountered, a mismatch between predicted and
experienced utility generates error signals in the mesocorticolimbic system, and particularly in
the ventral striatum (VS; Humphrey & Richard, 2014). However, rewards become more
predictable as instrumental learning progresses, so the magnitude of error signals decreases, and
incentive salience reaches asymptote. Drugs of abuse alter this system by producing supra-
threshold stimulation and precluding habituation, and thus causing “irrationally strong motivation
urges that are not justified by any memories of previous reward values (and without distorting
associative predictions)(Berridge, 2012, p. 1124). In other words, substance use disorders
(SUDs) are normally accompanied by a subjective and behavioural dissociation between liking
and wanting the drug (Pool, Sennwald, Delplanque, Brosch, & Sander, 2016).
In view of the success of the IS hypothesis to account for some of the seemingly irrational
features of SUDs patients’ behaviour, the question arises whether the hypothesis can be also tested
in behavioural addictions (Rømer Thomsen, Fjorback, Møller, & Lou, 2014). That is, in the
absence of an external chemical agent, what misleads dopaminergic error signals?
This question can be addressed by revisiting the literature on reinforcement schedules.
According to recent analyses, most gambling behaviours are under random ratio (RR) schedules
(Haw, 2008). These are characterised by intermittent reward, such that the probability of reward
in any single trial does not depend on the previous density of rewards. Uncertainty in RR
schedules is irreducible, and the rates of responding they generate are particularly stable and free
of breaks after reward (Schoenfeld, Cumming, & Hearst, 1956).
Irreducible uncertainty in gambling scenarios can be regarded as a constant source of
prediction error for the mesocorticolimbic dopaminergic system to feed incentive salience.
Supporting that hypothesis, Anselme, Robinson, and Berridge (2013) have indeed shown that
increasing the uncertainty level in the relationship between a cue and a reward enhances incentive
salience of this cue, as measured by a sign-tracking response. Further evidence supports the
involvement of the incentive salience dopamine system in the effect of uncertainty on the ability
of contextual cues to behave as motivational magnets (Anselme & Robinson, 2013).
Sources of heterogeneity in gambling disorder
Differences in gambling disorder vulnerability
If IS resulting from RR schedules is the main learning mechanism underlying gambling
conditioning, any factors fuelling this mechanism will contribute to GD vulnerability. More
specifically, any factors increasing exposure to gambling or its rewarding properties will facilitate
transition from recreational to problematic gambling. Accordingly, research shows that early wins
have a particularly strong effect on behaviour under RR schedules and in gambling scenarios
(Haw, 2008).
Complementarily, people differ in the degree to which they are sensitive to the various
appetitive and aversive properties of different types of events. Gray’s (1994) psychobiological
model of personality proposes reward sensitivity (RS) and punishment sensitivity (PS; the overt
manifestations of two biological systems referred to as behavioural activation and behavioural
inhibitions systems) as the main foundation of motivation and personality. In the framework we
are starting to sketch here, RS and PS easily enter the equation as individual differences that
modulate IS. However, reinforcement-related sources of individual vulnerability could be less
general than PS and RS traits, and more circumscribed to the types of rewards that occur in
gambling scenarios.
There is evidence, for instance, that some gamblers experience gambling-triggered
arousal or uncertainty as intrinsically rewarding (Megias et al., 2017; Sharpe, Tarrier, Schotte, &
Spence, 1995), a result that converges with studies on the biological basis of individual differences
in risk proneness in animals (Fiorillo, 2011). Complementarily, individuals presenting high levels
of neuroticism and punishment sensitivity, or proneness toward negative mood, are more likely
to use gambling to cope with psychological distress (Balodis, Thomas, & Moore, 2014).
The role of basic emotion regulation mechanisms
A growing corpus of evidence suggests that craving management, that is, succeeding in keeping
IS below a given threshold, can be viewed as an instance of emotional regulation (Loewenstein,
1996) that can be implemented at different levels.
IS is subject to influences from same-level learning mechanisms (e.g. extinction, counter-
conditioning, cue-interaction; Kober et al., 2010). Etkin, Büchel, and Gross (2015) have recently
proposed that, at this level, emotion regulation proceeds in a model-free, automatic manner. This
could be the case for loss-related learning processes necessary to compensate IS. Supporting this
idea, a recent study has showed casino gamblers to underestimate how much money they spend
on gambling in the long run. And, that their gambling expenditures could be reduced just by
providing them with a player account with their personal spend (Wohl, Davis, & Hollingshead,
2017). Interestingly, behaviour changed with limited or no awareness. Accordingly, manipulations
that reduce loss awareness increase wagering, in a similar, mostly automatic way (Monaghan,
Etkin and colleagues (2015) have identified the ventromedial prefrontal cortex (vmPFC)
and the ventral anterior cingulate (vACC) as the main regions in the circuit for model-free emotion
regulation, although their review mostly focuses on fear regulation and it is unclear whether these
would also constitute the most important structures for craving regulation. A discussion on the
exact brain implementation of model-free emotion regulation goes beyond the scope of the present
chapter. Medial and ventral parts of the PFC, the insula, and their connections with the amygdala
and the VS are, however, the most frequently mentioned structures (Phillips, Ladouceur, &
Drevets, 2008).
With regard to the model-free regulation of craving in GD, the evidence to date remains
indirect. For example, Contreras-Rodríguez et al. (2016) found a common pattern of
hyperconnectivity in PGD and cocaine-dependent individuals, mostly between the orbitofrontal
cortex (OFC) and VS, and between the insula and the amygdala. Complementary evidence comes
from studies showing that PGD perform worse than controls on the Iowa Gambling Task, in which
successful performance is known to depend on balanced emotion-driven learning (Buelow &
Suhr, 2009).
Malfunctioning of basic, model-free emotion regulation will be subjectively experienced
as a pervasive influence of craving on behaviour, and if such malfunctioning is extensive enough,
as a disproportionate impact of emotions in other areas of decision and action. This resonates with
similar findings in the SUDs literature that craving correlates with negative urgency (NU), namely
the tendency to act rashly under the influence of strong negative emotions (Cyders et al., 2014;
Doran, Cook, McChargue, & Spring, 2009).
Higher-order emotion regulation mechanisms
Model-free emotion regulation is complemented by model-based emotion regulation strategies.
These form a category of learned goal-directed responses through which people act upon their
own emotional processes. Not surprisingly, then, specific cerebral areas involved in this type of
emotion regulation (lateral PFC, pre-supplementary and supplementary motor areas [pSMA,
SMA], and parts of the parietal cortex) overlap with those involved in model-based instrumental
behaviour (O’Doherty, Cockburn, & Pauli, 2017).
Emotion regulation strategies are varied. The emotion regulation questionnaire (ERQ;
Gross & John, 2003) distinguishes between expressive suppression (suppressing the external
manifestations of emotion), and reappraisal (reprocessing of the causes of the emotion), with use
of the latter being considered adaptive and the former maladaptive. The more comprehensive
cognitive emotion regulation questionnaire (CERQ, Garnefski & Kraaij, 2007) identifies nine
cognitive strategies to deal with negative affect (blaming oneself, blaming others, acceptance,
rumination, positive refocusing, refocus on planning, positive reappraisal, putting into
perspective, and catastrophising).
In psychobiological terms, reappraisal has been shown to downregulate the activity of the
VS and the amygdala, altering the balance in favour of either continuing or interrupting gambling
(Kober et al., 2010; Sokol-Hessner et al., 2009). Accordingly, studies on craving regulation have
focused on this cognitive strategy (Giuliani & Berkman, 2015), and have observed that successful
downregulation of craving is associated with increased activity of the lateral and dorsomedial
PFC, and dampened activity of the ventral striatum, subgenual cingulate, amygdala, and ventral
tegmental area (Kober et al., 2010).
GD can progress with malfunctioning of the basic mechanisms necessary to regulate
craving and other undesirable emotions, and this can have an influence on how model-based
strategies operate. In a recent study, we tested the hypothesis that regulation of negative emotions
in PGD imposes an extra burden on cognitive control mechanisms, relative to healthy controls
(Navas et al., 2017b). Downregulation of emotions triggered by negative pictorial stimuli
activated the control network in controls and PGD, but the latter showed further hyperactivation
of an area comprising parts of the premotor cortex and the dlPFC. Additionally, activation of
dlPFC correlated with NU. In a separate sample, NU significantly correlated with the proneness
to use expressive suppression as a (maladaptive) strategy to regulate negative affect.
The Gambling Space Model
So far, we have suggested a number of psychobiological processes (1) to account for the transition
from recreational to problem gambling, (2) to facilitate that transition and contribute to GD
vulnerability, and (3) to underlie individual differences in PGD. In the next section these
constructs are integrated into a coherent model (Table 1), and their contribution to the behavioural
manifestations and clinical implications of disordered gambling are explicated.
Table 1. The Gambling Space Model
Sensitivity to
properties of
Sensitivity to
properties of
elaboration and
Reward system,
systems of
escape and
system, cognitive
control structures
Positive motives
for gambling,
reward seeking
motives, poor
deficits in
decision making
biases, motivated
Vulnerability to
risk gambling,
low motivation to
quit gambling,
dropout risk
comorbidity, risk
of relapse
Low problem
dropout risk
preference for
games, low
Incentive sensitization driven by random ratio schedules
The first construct in the Gambling Space Model (sensitivity to appetitive properties of
gambling) is related to reward sensitivity. The relationship between RS and gambling has been
lingering in the literature for decades, yet it has been difficult to identify it as a strong and
independent predictor of disordered gambling behaviour (Goudriaan, van Holst, Veltman, & van
den Brink, 2013). More consistently, gamblers have been found to differ from non-gamblers in
how they respond to the different sources of reward present in gambling scenarios (Sescousse,
Barbalat, Domenech, & Dreher, 2013). Still, reward sensitivity can interact with gambling
features in shaping individual gambling preferences. In a recent article, Navas et al. (2017a) found
that recreational and disordered gamblers preferring card, skill and casino games show higher RS
scores than those preferring slot machines, lotteries, and bingo. These gamblers are more strongly
motivated by positive reinforcers, and also more sensitive to the positive features of the gambling
The second putative construct relies on the negatively reinforcing properties of gambling.
Negative trait emotions can interact with sensitivity to the mood-modifying properties of
gambling. In practical terms, gambling-to-cope has been observed to correlate with comorbid
depression and relapse risk (Ledgerwood & Petry, 2006; Lister, Milosevic, & Ledgerwood, 2015)
The third construct, generalised emotional dysregulation, captures deterioration of
model-free emotion regulation mechanisms. Weakness of low-level regulation mechanisms
necessary to limit gambling conditioning are hypothesised to characterise all disordered gamblers.
However, extensive malfunctioning of basic emotion regulation mechanisms is likely to be
responsible for differences among PGD. Unfortunately, to date, there is a dearth of reliable and
psychometrically sound neurobehavioural tasks that could be used as tools to assess the extent
and severity of this type of dysregulation. Provisionally, we propose NU as the most promising
available proxy to evaluate it across disorders (Berg, Latzman, Bliwise, & Lilienfeld, 2015).
Finally, the fourth construct has to do with the use of strategic, model-based emotion
regulation. Recent evidence shows the existence of a subgroup of PGD who effectively use
putatively adaptive forms of emotion regulation (Navas, Verdejo-García, López-Gómez,
Maldonado, & Perales, 2016). However, in these patients, such strategies correlate directly with
gambling severity and gambling-related cognitive distortions. In a similarly counterintuitive
fashion, gamblers with high dispositional optimism have been found to be more prone to maintain
positive expectations and remain motivated to gamble after negative outcomes (Gibson &
Sanbonmatsu, 2004). In our model, gamblersuse of model-based emotion regulation strategies
in combination with certain gambling-related cognitive distortions forms part of a self-deceptive
reasoning style. This ego-protective mechanism has been established as a factor contributing to
drug use perseverance, and to reluctance to treatment (Martínez-González, Vilar López, Becoña
Iglesias, & Verdejo-García, 2016). Here, we posit that self-deception has an emotional regulation
function, in line with models of motivated reasoning (Kunda, 1990).
According to the present model, certain types of cognitive distortions thus reflect spared
cognitive control, rather than cognitive dysfunction. Indeed, cognitive distortions are more
frequently encountered in young, educated, skill-game gamblers (Myrseth, Brunborg, & Eidem,
2010). Furthermore, and importantly, they are not systematically accompanied by signs of
cognitive/non-planning impulsivity or lack of conscientiousness (Navas et al., 2017a). This
relationship between elaborate distorted cognitions and planning abilities could partially account
for the inconsistency of findings regarding the link between GD and executive tasks (Goudriaan,
Yücel, & van Holst, 2014). In self-deceptive gamblers, preserved executive function would
contribute to false mastery, whereas in patients with less elaborated gambling beliefs weaker
executive functions would contribute to inflexible behaviour and unconscientious gambling.
Figure 1. A simplified depiction of the mapping of gamblers subtypes onto a dimensional model.
It is worth noting that there are important connections between our Gambling Space
Model and the Pathways Model (Blaszczynski & Nower, 2002). Figure 1 displays a simplified
depiction of the mapping of the Pathways Model onto the Gambling Space Model. In this space,
all PGD are conditioned gamblers, and subtypes would arise from the combination of
conditioning processes with sources of heterogeneity. In individuals with high levels of
neuroticism, poor mood or susceptibility to boredom, the negatively reinforcing properties of
gambling would give rise to the emotionally vulnerable gambler, whereas in cognitively spared
individuals, motivated reasoning and elaborated emotion regulation could give rise to self-
deceptive gamblers. The latter are not specifically considered in the Pathways Model, but are
easily identifiable in emerging profiles (Griffiths, Wardle, Orford, Sproston, & Erens, 2009).
With regard to the impulsive-antisocial gambler type, our model depicts a slightly more
complex scenario. Given the partial overlap between RS and impulsivity (Knezevic-Budisin,
Pedden, White, Miller, & Hoaken, 2015), reward-sensitive GD patients have remained partially
confounded with impulsive-antisocial ones. RS, however, reflects the hyper-reactivity of the
behavioural activation system to potential sources of, whereas other relevant aspects of emotion-
driven impulsivity reflect a more generalised regulatory dysfunction. Hence, it would be possible
to distinguish between predominantly reward- or sensation-seeking impulsive gamblers, and
gamblers with high levels of urgency, with the latter presenting a higher incidence of problematic
behaviours (Vachon & Bagby, 2009).
What has neuroscience ever done for us? Summary and implications
According to a recent opinion article by Markowitz (2016), there is such a thing as too much
neurosciencein psychopathology and psychotherapy research. In the context of GD research, it
is true that clear-cut biomarkers are still lacking, drug trials have yielded inconclusive, mixed or
unspecific results (Alexandris, Smith, & Bowden-Jones, 2015; Yip & Potenza, 2014), and other
manipulations of the brain (e.g. transcranial magnetic stimulation, neurofeedback) are still matters
of ongoing research (Goudriaan et al., 2014). Still, neuroscientific research has contributed to
change the way we conceptualise GD, and such a change is having consequences on the way we
deal with it.
Implications of conceptualising gambling disorder as an addictive disorder
Conceptualising GD as an addictive disorder implies endorsing the dissociation between wanting
to gamble and liking gambling, and thus the view of gambling as economically inconsistent.
Individuals with nicotine use disorder, for example, can invest considerable effort and money in
purchasing tobacco and trying to quit smoking (Reith, 2007). The liking/wanting dissociation thus
provides ethical ground for some degree of political paternalism. Given that likes also belong to
individuals, consideration of likes beyond and above wants actually sanctions what has been
called liberal paternalism (Camerer, 2006).
In other words, understanding the centrality of IS, its key role in the development of
craving, and how loss-based learning fails to compensate it, justifies product- and offer-centred
interventions regarding pervasiveness of gambling-triggering cues, and product design aimed at
reducing features that enhance their addictive potential (Parke, Parke, & Blaszczynski 2016). And
the other way round, if evidence does not support the consideration of a putative addictive
disorder as a genuine one, there would be less ethical ground to justify intervention. If we adopt
the same ‘addiction’ model for hypersexuality, dysregulated food intake or excessive video
gaming, there would be no reason not to implement similar rules in those markets. Previous
attempts to define addictive disorders based on the analogy between the excessive behaviour in
question and a previously accepted addictive disorder, based on the application of DSM diagnostic
criteria to the new putative ‘addictions’, has led to overdiagnosis and overtreatment. As stated by
Billieux, Schimmenti, Khazaal, Maurage, and Heeren (2015), behavioural addiction research
should shift “from a mere criteria-based approach toward an approach focusing on the
psychological processes involved(p. 119). As reviewed in this chapter, neuroscience definitely
has a role in defining such processes.
Implications of a psychobiological approach to heterogeneity among patients with gambling
Complementarily to the coexisting ways in which gamblersheterogeneity has been approached
to date, neuroscientific work can already provide a set of core dimensional constructs with
practical use.
Individual treatments are likely to benefit from the reviewed evidence. First, in
accordance with the Gambling Space Model, gambling motives should be assessed in order to
draw a profile of the reinforcement sources that patients find in gambling, which could become
targets of intervention. The identification of reinforcement sources linked to gambling could be
useful to implement individual and process-oriented psychological interventions aimed, for
instance, at developing skills to cope with high relapse-risk situations (anxiety, low mood, money-
related thoughts, or boredom; Ledgerwood & Petry, 2006).
Second, gamblers with deficits in basic emotional dysregulation have been found as
especially refractory to treatment attempts. For these cases, a better prospect is provided by
studies in which mindfulness-based training has shown promising results in comorbid addictive
and emotion disorders (Hoppes, 2006), and positive effects on decision-making
neuropsychological tasks linked with basic emotion regulation (Alfonso, Caracuel, Delgado-
Pastor, & Verdejo-García, 2011).
Third, intervening on planning executive functions is likely to benefit gamblers in the low
end of the elaboration-self deception continuum (as it has been shown with SUDs patients,
Verdejo-Garcia, 2016), whereas people in the high end would probably benefit more from
metacognitive training skills aimed at making them aware of the connection between their
dysfunctional beliefs and their motives to gamble (see Lindberg, Fernie, & Spada, 2011).
Complementarily, secondary prevention efforts in community populations could also be
enriched with this dimensional-psychobiological vision, through the implementation of screening
techniques aimed at identifying high-risk profiles (although we are aware that extra measures
must be taken to avoid stigmatisation and stereotyping; O’Leary-Barrett et al., 2013).
Neurobiologically-informed risk profiling has already gone a step further than traditional
personality profiling, in delineating a common vulnerability factor for externalising problems in
early adolescence, and dissociating it from other factors with differential loadings in separate
disorders (Castellanos-Ryan et al., 2014). Prevention programs could thus be directed to
individuals in general populations (not necessarily current gamblers) identified to have poorer
basic emotion regulation. These individuals could benefit from interventions aimed at improving
general emotional regulation and self-control, and thus see their risk of externalising problems,
including disordered gambling, reduced.
Final remarks
The sociodemographic and behavioural map of gambling is changing rapidly. New gambling
opportunities and media (e.g., mobile gambling) are generating new gambler profiles, so
understanding the mechanisms that generate the evolving variability of vulnerabilities, symptoms,
and outcomes is necessary to be proactive at providing the best possible clinical and political
response to eventually diminish the public health burden of disordered gambling.
As depicted in the current chapter, a combined psychobiological and behavioural-
cognitive framework has shown some capacity to capture at least some of these sources of
variability. The four proposed constructs are not necessarily exhaustive but are grounded in
sufficient evidence to have clear implications for policy, prevention and psychological
interventions. Still, further evidence should be gathered to help delineate or reconfigure this set
of dimensions and evaluate its predictive power.
In parallel, it is important to acknowledge that theories of psychopathology have
important, and potentially negative, consequences in real life. Biological approaches to
psychopathology are often accused of crystallising abnormal behaviours that would be better
understood as dynamically evolving and distributed in a continuum. As we have tried to illustrate
here, psychobiological models can be learning-based and dimensional and, simultaneously, able
to incorporate biological factors. At the same time, such models must be discriminative enough
to allow identifying genuine addictive disorders. So, the risk of overpathologisation and
psychiatrisation actually exists, in particular for many putative behavioural addictions. Probably,
misleading and overinclusive definitions are already creating more harm than good.
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... Recently, some authors attempted to conceptualize the role played by ER in GD (Navas, Billieux, Verdejo-García, & Perales, 2019;Rogier & Velotti, 2018a, 2018b. Conducting narrative reviews of existing literature, they argued that specific ER failures characterizing problem gambling account for distinct maladaptive patterns of gambling, such as the use of gambling as an escape strategy, chasing behavior, or hazardous decision making. ...
... Regarding cognitive reappraisal, however, the issue might be more complex. Indeed, recent results by Ruiz de Lara, Navas, and Perales (2019) showed that specific coping strategies, traditionally considered adaptive, such as positive refocusing and wishful thinking, appear to be overrepresented among the population of problematic gamblers. These authors provided an innovative interpretation of their results, arguing that proneness to positively reappraise negative triggers in order to reduce their emotional impact may be dysfunctional in gambling because it reduces the capacity to keep in touch with negative but functional emotional states that signal the need to change the behavioral strategy (i.e. to stop gambling after a loss). ...
The aim of this systematic review and meta-analysis was to provide a comprehensive evaluation of the role of emotion (dys)regulation in gambling disorder (GD). PsycINFO, PsycARTICLES, MEDLINE, Scopus, Web of Science, and PubMed were systematically searched for articles published until November 3, 2020. Forty-nine studies were considered for the systematic review; of these, 38 comprising 5242 participants met the inclusion criteria for the meta-analysis. Associations were found between GD and specific emotion regulation (ER) deficits, namely (1) nonacceptance of negative emotional states, (2) difficulties in maintaining goal-directed behaviors when faced with intense emotional contexts, (3) lack of clarity about emotional states (poor emotional awareness), (4) low impulse control in reaction to negative emotional states, and (5) difficulties in accessing adaptive ER strategies. We furthermore found that GD is associated with a tendency for emotional suppression, which is known as a maladaptive ER strategy and linked with reduced mindfulness abilities. Additional moderator analyses were conducted regarding age, gender, type of instrument used to measure GD, clinical status of the samples, and quality of the studies. Overall, the data demonstrated consistent and significant associations between GD and ER. This systematic review and meta-analysis mostly supports the conceptualization of GD as an addictive disorder characterized by ER deficits and stresses the need to develop interventions in ER deficits that are tailored to the specificities of GD.
... Al igual que en las adicciones a sustancias, las personas que padecen este trastorno muestran el impulso intenso de jugar pese al impacto evidentemente negativo que tiene a la larga en sus vidas. Sin embargo, en el caso de estos juegos no se trata de ninguna sustancia exógena con componentes psicoactivos la que promueve estas reacciones afectivas y las conductas asociadas a ellas 9 . ¿Qué convierte al juego de azar, entonces, en una actividad potencialmente adictiva? ...
... Over time, parts of the brain associated with reward processing-such as the mesocorticolimbic pathway-rewire in a predictable pattern. In functional magnetic resonance imaging (fMRI) studies, similar rewiring occurs in people with drug addictions and gambling disorder (Navas et al., 2019). The strengthening of reward pathways associated with gambling leads from the impulsion of unwinding at the casino monthly to the compulsion that damages lives. ...
... Using the DERS, Marchica, Mills [15] found in a linear regression that emotion regulation difficulties accounted for approximately 4% of the variance in problem gambling, in particular the impulsivity subscale. Individuals with GD represent a heterogeneous group and a sub-group might benefit more from a stricter focus on impulse control management and others from a more cognitive approach focusing on dysfunctional gambling cognitions and a self-deceptive cognitive style, such as that presented in the Gambling Space Model (GSM [55];). ...
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Background Despite the association of Gambling Disorder (GD) with poor mental health, treatment options generally lack components targeting emotional difficulties. This study investigated the feasibility and acceptability of adding strategies of emotion regulation to an eight-session weekly group treatment. Method This non-randomized pilot study recruited 21 treatment-seeking adults with GD, (mean age = 36.3, 19% females) from addiction care. In a mixed methods design, measures of within-group changes in self-reported symptoms of GD were complemented with thematic analysis of post-treatment interviews regarding the feasibility of the treatment. Results Within-group scores on the Gambling Symptoms Assessment Scale (G-SAS) showed a 47% decrease (β: -0.1599, 95% CI: − 0.2526 to − 0.0500) from pre-treatment to 12-month follow-up, with Hedges’ g = 1.07 (CI: 0.57–1.60). The number of GD-symptoms according to the Structured Clinical Interview for Gambling Disorder (SCI-GD) decreased from 7.0 (SD = 1.60) at pre-treatment to 2.1 (SD = 2.36) at 12-month follow-up. Participants completed an average of 6.3 sessions and rated the intervention high in satisfaction and acceptability. Feasibility interviews showed no noticeable negative effects or ethical issues. Furthermore, helpful components in the treatment were: increased awareness of emotional processes and strategies to deal with difficult emotions. Conclusions Adding emotion regulation strategies in the treatment of GD is feasible and acceptable and warrants further investigation in a controlled trial. Trial registration This study was registered with (Identifier NCT03725735).
... More specifically, recent works have proposed affect-driven impulsivity or urgency (the proneness to rash action when experiencing strong positive or negative emotions) as a proxy to this type of emotion dysregulation. Indeed, recent theoretical developments attribute a crucial etiological function to affect-driven impulsive action in the vulnerability and emergence of substance use disorders, antisocial/aggressive behavior, and gambling disorder [71,72]. ...
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Co-occurrence of drug misuse with other dysregulated behaviors is common. This study was aimed at exploring the associations between the risk of presenting a clinically relevant condition involving non-substance-related addictive or dysregulated behaviors (as measured by the MultiCAGE CAD-4 screening), and cannabis abuse/dependence (CAST/SDS) scores, and the role of gender therein. Participants were recruited using stratified probabilistic sampling at the University of Granada. Mann-Whitney's U tests were used to compare male and female students in SDS and CAST scores. Associations between gender and MultiCAGE scores were estimated using the γ ordinal correlation index, and tested with χ2. For each MultiCAGE dimension, a Poisson-family mixed-effects model was built with either SDS or CAST as the main input variable, while controlling for nicotine and alcohol dependence, and relevant sociodemographic variables. Incidence rate ratios (IRR) were computed for SDS/CAST effects, and the significance threshold was family-wise Bonferroni-corrected. Gender differences were significant for cannabis dependence/abuse and all MultiCAGE scores for non-substance-related conditions, with males showing higher risk scores for excessive gambling, excessive internet use, excessive video gaming, and hypersexuality, and females presenting higher scores in dysregulated eating and compulsive buying. Cannabis dependence and abuse were significantly associated with a higher risk of problematic video gaming. These associations were mostly driven by males. Importantly, although risk of problematic video gaming was specifically associated with cannabis abuse/dependence, there was only a weak non-significant association between problematic video gaming and alcohol use scores. Risk of alcohol use problems, in turn, was strongly associated with all other non-substance-related problems (problematic gambling, excessive Internet use, dysregulated eating, compulsive buying, and hypersexuality). These differential associations can cast light on the etiological similarities and dissimilarities between problematic substance use and putative addictive behaviors not involving drugs.
... Taken together, results fit well in the Gambling Space Model formulated by Navas et al. [45] (see also [42,46]). In this model, articulated as a development of the seminal Pathways Model [47], transition from recreational to disordered gambling is driven by the kind of reinforcement schedules that have been experimentally shown to also facilitate transition from goal-driven to compulsive behaviors. ...
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Background Decisions made by individuals with disordered gambling are markedly inflexible. However, whether anomalies in learning from feedback are gambling-specific, or extend beyond gambling contexts, remains an open question. More generally, addictive disorders—including gambling disorder—have been proposed to be facilitated by individual differences in feedback-driven decision-making inflexibility, which has been studied in the lab with the Probabilistic Reversal Learning Task (PRLT). In this task, participants are first asked to learn which of two choice options is more advantageous, on the basis of trial-by-trial feedback, but, once preferences are established, reward contingencies are reversed, so that the advantageous option becomes disadvantageous and vice versa. Inflexibility is revealed by a less effective reacquisition of preferences after reversal, which can be distinguished from more generalized learning deficits. Methods In the present study, we compared PRLT performance across two groups of 25 treatment-seeking patients diagnosed with an addictive disorder and who reported gambling problems, and 25 matched controls [18 Males/7 Females in both groups, Mage(SDage) = 25.24 (8.42) and 24.96 (7.90), for patients and controls, respectively]. Beyond testing for differences in the shape of PRLT learning curves across groups, the specific effect of problematic gambling symptoms’ severity was also assessed independently of group assignment. In order to surpass previous methodological problems, full acquisition and reacquisition curves were fitted using generalized mixed-effect models. Results Results showed that (1) controls did not significantly differ from patients in global PRLT performance nor showed specific signs of decision-making inflexibility; and (2) regardless of whether group affiliation was controlled for or not, gambling severity was specifically associated with more inefficient learning in phases with reversed contingencies. Conclusion Decision-making inflexibility, as revealed by difficulty to reacquire decisional preferences based on feedback after contingency reversals, seems to be associated with gambling problems, but not necessarily with a substance-use disorder diagnosis. This result aligns with gambling disorder models in which domain-general compulsivity is linked to vulnerability to develop gambling-specific problems with exposure to gambling opportunities.
Background and aims Emotion regulation (ER) and impulsivity impairments have been reported in patients with gambling disorder (GD). However, both constructs have not been studied in depth jointly in clinical samples. Therefore, the aim of this study was to analyze ER and impulsive tendencies/traits in a sample of n=321 treatment-seeking individuals with GD by differentiating them according to their gambling preference (n=100 strategic; n=221 non-strategic). Methods Our sample was assessed through the DERS (ER), the UPPS-P (impulsivity), and the DSM-5 (GD severity). Results The non-strategic group included a higher proportion of women and reported greater ER impairments, and more impulsive traits/tendencies compared to strategic gamblers. GD severity was associated with all DERS subscale (except for awareness) and with urgency dimensions of the UPPS-P. Discussion and Conclusions Our findings confirm that strategic and non-strategic gamblers differ in their ER processes and impulsive tendencies, showing the first clinical group a more adaptive profile. These results suggest the relevance of assessing these ER and impulsivity in order to tailor better treatment approaches.
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Background Distorted gambling-related cognitions are tightly related to gambling problems, and are one of the main targets of treatment for disordered gambling, but their etiology remains uncertain. Although folk wisdom and some theoretical approaches have linked them to lower domain-general reasoning abilities, evidence regarding that relationship remains unconvincing. Method In the present cross-sectional study, the relationship between probabilistic/abstract reasoning, as measured by the Berlin Numeracy Test (BNT), and the Matrices Test, respectively, and the five dimensions of the Gambling-Related Cognitions Scale (GRCS), was tested in a sample of 77 patients with gambling disorder and 58 individuals without gambling problems. Results and interpretation Neither BNT nor matrices scores were significantly related to gambling-related cognitions, according to frequentist (MANCOVA/ANCOVA) analyses, performed both considering and disregarding group (patients, non-patients) in the models. Correlation Bayesian analyses (bidirectional BF 10 ) largely supported the null hypothesis, i.e., the absence of relationships between the measures of interest. This pattern or results reinforces the idea that distorted cognitions do not originate in a general lack of understanding of probability or low fluid intelligence, but probably result from motivated reasoning.
Background Negative urgency –the tendency to lose control under the influence of strong negative emotions– has been proposed to be a sign of malfunctioning emotion regulation mechanisms, and to contribute to severity and complications of gambling disorder and other externalizing behaviors. Aims and method: This study is aimed at (1) testing whether negative urgency is linked to resistance to extinction in an emotional associative learning task in a sample of 70 community gamblers (with emotional pictures as unconditioned stimuli, and color patches as conditioned stimuli [CS]); and (b) exploring the link between these two variables (negative urgency and resistance to emotional extinction) and clinical manifestations of gambling (severity and craving). Mixed-effects generalized models were used to analyze trial-by-trial predictive responses during acquisition and extinction for erotic, disgusting, and gambling related pictures. Results and conclusions: Acquisition of CS-elicited responses remained unaffected by negative urgency, whereas extinction was hampered in individuals with high negative urgency, especially for CS associated with erotic and gambling-related pictures. Moreover, negative urgency predicted higher craving scores, and these predicted more severe gambling-related symptoms. This finding resonates with the well-known involvement of emotion regulation processes in craving control. However, extinction was not independently related to craving. This lacking effect suggests that negative urgency is a broad construct, and although some of its components are directly related to faulty extinction (and generalized emotion dysregulation), such components are not the same negative urgency shares with difficulties of craving control.
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Research has demonstrated that individuals suffering from Gambling Disorder (GD) are characterized by abnormal responses to pleasant stimuli and a proneness to act rashly in response to positive emotions. However, psychological impairments that may explain these results remain unexplored. This study tests the hypothesis that individuals with GD would show impairments in the capacity to appreciate positive emotions. The South Oaks Gambling Screen (SOGS), the Impulsive Behavior Scale Short Form (UPPS-P) and the Ways of Savoring Checklist (WOSC) were administered to clinical sample (n = 87) and to controls (n = 99). Scores of the clinical sample significantly differed from scores obtained by controls on some subscales of the WOSC (Comparing and Killjoy Thinking) and the UPPS-P. The proneness to act rashly in response to positive emotions and the capacity to appreciate positive emotional states emerged as predictors of GD’s severity. Findings support previous data showing a role played by the emotional facets of impulsivity in GD and suggest that individuals suffering from GD may experience dysfunctions in the capacity to appreciate positive emotions. This study suggests that individuals suffering from GD may fail to normally appreciate positive emotional states because of abnormalities in the savoring capacities.
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Putting money at stake produces anticipatory uncertainty, a process that has been linked to key features of gambling. Here we examined how learning and individual differences modulate the stimulus preceding negativity (SPN, an electroencephalographic signature of perceived uncertainty of valued outcomes) in gambling disorder patients (GDPs) and healthy controls (HCs), during a non-gambling contingency learning task. Twenty-four GDPs and 26 HCs performed a causal learning task under conditions of high and medium uncertainty (HU, MU; null and positive cue-outcome contingency, respectively). Participants were asked to predict the outcome trial-by-trial, and to regularly judge the strength of the cue-outcome contingency. A pre-outcome SPN was extracted from simultaneous electroencephalographic recordings for each participant, uncertainty level, and task block. The two groups similarly learnt to predict the occurrence of the outcome in the presence/absence of the cue. In HCs, SPN amplitude decreased as the outcome became predictable in the MU condition, a decrement that was absent in the HU condition, where the outcome remained unpredictable during the task. Most importantly, GDPs’ SPN remained high and insensitive to task type and block. In GDPs, the SPN amplitude was linked to gambling preferences. When both groups were considered together, SPN amplitude was also related to impulsivity. GDPs thus showed an abnormal electrophysiological response to outcome uncertainty, not attributable to faulty contingency learning. Differences with controls were larger in frequent players of passive games, and smaller in players of more active games. Potential psychological mechanisms underlying this set of effects are discussed.
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Impulsivity (and related traits reward/punishment sensitivity and tolerance to delayed rewards) and gambling cognitions have been linked to gambling. However, their independent associations with gambling preferences and clinical status have never been dissociated. The current study applied a data-driven strategy to identify gambling preferences, based on gambling frequency in several modalities. The two resulting factors were used to classify gambling disorder patients (GDPs) and non-problem recreational gamblers (RGs) into Type I (preferring cards, casino games and skill-based bets) and Type II (preferring slot machines, lotteries/pools and bingo). Participants were assessed in impulsivity, delay discounting, reward/punishment sensitivity, gambling-related cognitions, gambling severity, gambling frequency and average amount gambled per episode. GDPs scored higher than RGs in positive and negative urgency, delay discounting, reward sensitivity and intensity of gambling-related cognitions, but less in lack of perseverance. Additionally, Type II gamblers had greater difficulties delaying gratification, whereas Type I gamblers showed higher cognitive distortion and reward sensitivity levels. In practical terms, the finding that some characteristics are equally pervasive in disordered gamblers independently of their preferences (affect-driven impulsivity), whereas others (distorted cognitions, reward sensitivity, delay discounting) are more prominent in one type or the other, provides a basis to establish targets' priority in therapy.
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In the current research, we tested the utility of a responsible gambling tool that provides players with personalized behavioral feedback about their play. We hypothesized that when the player’s estimated monetary loss is less than their actual monetary loss, subsequent expenditures will be reduced. To this end, players (N=649) enrolled in a player-account rewards program were asked how much they have won or lost over a three-month period whilst using their loyalty card. They were then provided with their player-account data. Results indicated that players who under-estimated their losses (i.e., those who lost more money than they thought at Time 1) did not perceive that they had reduced their play in the 3-month follow-up period. However, data on actual play indicated that they significantly reduced the amount they wagered as well as the amount they lost during the follow-up period. Given that informed decision-making is the raison d'etre of responsible gambling tools, these results suggest that providing players with accurate information about how much they spend gambling can moderate gambling expenditures.
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Background and aims: Gambling disorder is characterized by poor regulation of negative emotions and impulsive behaviors. This study aimed to (1) compare gambling disorder patients (GDPs) and healthy controls (HCs) in self-report and brain activation measures of emotion regulation; and (2) establish its relationship with negative emotion-driven impulsivity. Design: Two cross-sectional case-control studies including GDPs and HCs. Setting and participants: GDPs and HCs were recruited from specialized gambling clinics in Andalusia (Spain), where they were following outpatient treatment, and from the community, respectively. Study 1 included 41 male GDPs and 45 HCs (Mage = 35.22, 33.22; SD = 11.16, 8.18; respectively). Study 2 included 17 GDPs and 21 HCs (16/20 males, Mage = 32.94, 31.00; SD = 7.77, 4.60). Measurements: In Study 1, we compared both groups on suppression and reappraisal emotion regulation strategies (Emotion Regulation Questionnaire [ERQ]). In Study 2, we compared GDPs with HCs on brain activation associated with downregulation of negative emotions in a Cognitive Reappraisal Task, measured with functional magnetic resonance imaging (fMRI). In both studies, we correlated the measures of emotion regulation with mood-related impulsivity indicated by negative urgency (UPPS-P scale). Findings: GDPs relative to HCs showed higher levels of emotional suppression [F = 4.525; p = 0.036; means difference MHCs-MGDPs = -2.433 (CI95% = -4.706, -0.159)] and higher activation of the premotor cortex and middle frontal gyrus during negative emotion regulation in the fMRI task (p ≤ 0.005, Cluster Size, CS > 50 voxels). Negative urgency positively correlated with emotional suppression [r = 0.399, (CI95% = 0.104, 0.629), one-tailed p = 0.005] and middle frontal gyrus activation during negative emotion regulation (p ≤ 0.005, CS > 50) in GDPs. Conclusions: Gambling disorder is associated with greater use of emotional suppression and stronger premotor cortex and middle frontal gyrus activation for regulating negative emotions, compared with healthy controls. Emotional suppression use and middle frontal gyrus activation during negative emotion regulation is linked with negative emotion-driven impulsivity in this disorder. This article is protected by copyright. All rights reserved.
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Cue reactivity is an established procedure in addictions research for examining the subjective experience and neural basis of craving. This experiment sought to quantify cue-related brain responses in gambling disorder using personally tailored cues in conjunction with subjective craving, as well as a comparison with appetitive non-gambling stimuli. Participants with gambling disorder (n=19) attending treatment and 19 controls viewed personally tailored blocks of gambling-related cues, as well as neutral cues and highly appetitive (food) images during a functional magnetic resonance imaging (fMRI) scan performed ~2–3 h after a usual meal. fMRI analysis examined cue-related brain activity, cue-related changes in connectivity and associations with block-by-block craving ratings. Craving ratings in the participants with gambling disorder increased following gambling cues compared with non-gambling cues. fMRI analysis revealed group differences in left insula and anterior cingulate cortex, with the gambling disorder group showing greater reactivity to the gambling cues, but no differences to the food cues. In participants with gambling disorder, craving to gamble correlated positively with gambling cue-related activity in the bilateral insula and ventral striatum, and negatively with functional connectivity between the ventral striatum and the medial prefrontal cortex. Gambling cues, but not food cues, elicit increased brain responses in reward-related circuitry in individuals with gambling disorder (compared with controls), providing support for the incentive sensitization theory of addiction. Activity in the insula co-varied with craving intensity, and may be a target for interventions.
Technical Report
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The aim of this report is to review evidence and theory regarding the gambling product through its structural characteristics (i.e., the ‘agent’ component of the epidemiological triangle). By providing a better understanding of structural characteristics, stakeholders should be better equipped to promote and evaluate responsible gambling and harm-minimisation strategies. Structural characteristics are essentially the building blocks of a gambling game. They are the basis for their differential appeal depending on how they satisfy different needs for different consumers. They combine with environmental and individual factors to determine both positive and negative outcomes of gambling participation. Structural characteristics vary considerably from game to game and evolve quickly in response to changes in technology; this renders associated policymaking challenging. The report is structured to consider categories of structural characteristics. Within each section we consider the theory and evidence concerning the possible links between characteristics and gambling problems, together with potential implications for specific interventions that may merit consideration by regulators and commercial gambling providers.
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In this review, we summarize findings supporting the existence of multiple behavioral strategies for controlling reward-related behavior, including a dichotomy between the goal-directed or model-based system and the habitual or model-free system in the domain of instrumental conditioning and a similar dichotomy in the realm of Pavlovian conditioning. We evaluate evidence from neuroscience supporting the existence of at least partly distinct neuronal substrates contributing to the key computations necessary for the function of these different control systems. We consider the nature of the interactions between these systems and show how these interactions can lead to either adaptive or maladaptive behavioral outcomes. We then review evidence that an additional system guides inference concerning the hidden states of other agents, such as their beliefs, preferences, and intentions, in a social context. We also describe emerging evidence for an arbitration mechanism between model-based and model-free reinforcement learning, placing such a mechanism within the broader context of the hierarchical control of behavior. Expected final online publication date for the Annual Review of Psychology Volume 68 is January 03, 2017. Please see for revised estimates.
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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 be-havioral addiction akin to substance use disorders, a change reflected in DSM-5. Here we provide an overview of current ideas around GD from its phe-nomenology 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.
Despite intensive research regarding dopamine (DA)'s role in addictive behavior, the precise mechanism of action for dopamine remains unclear. This chapter examines how schedules of reinforcement maintain gambling behavior. It discusses how dopamine works in the central nervous system with respect to schedules and learning. The chapter reviews genetic and neurological differences that contribute to maladaptive learning patterns in disordered gambling. It also discusses the effect of dopamine agonist therapies on individuals with a gambling disorder. Event-related potentials measure the activity in specific brain regions during a given activity using an electroencephalogram (EEG). The chapter focuses on two important questions: to what extent are the brains of disordered gamblers different from those of normal controls and how does gambling affect brain reward systems and foster disordered behavior?
In this chapter, behavioral gambling processes will be discussed in relation to the neurobiological processes underlying these behaviors, and their role in disordered gambling (DG) will be discussed. In discussing the neuroscience of disordered gambling, the question arises whether similar processes take place in the brain in gambling disorder as in substance use disorders (SUDs) or impulse control disorders. Therefore, in this chapter, results of SUDs studies will be compared to results of studies using disordered gamblers, to discuss similarities and differences. This chapter gives an overview of neurobehavioral research into motivational and cognitive brain-behavior processes in DG, and the overlap and differences between DG and SUDs. The neurocognitive studies on reward sensitivity, punishment sensitivity, and decision-making in DG show a consistent picture of preference for immediate rewards over delayed rewards in DG, disadvantageous decision-making associated with short-term rewards but long-term losses, and risky decision-making.