Understanding Gambling Disorder

Within the context of recent debate around regulation of the (arguably profligate) technology-enabled gambling industry, this article aims to summarise the current evidence-base informing therapeutic gambling interventions.

Warning: although this article includes no gambling-related images likely to amplify incentive salience^(Appendix), the information contained herein may evoke some distress for those affected by disordered gambling.

Introduction

Gambling in its various forms is on the rise as a popular pastime within mainstream Australian culture, with around 40% of adults engaging in some form of gambling activity within a typical month (AIHW). Australia leads the world in per capita gambling expenditure (more than $20 billion annually):

We are the biggest losers in the world when it comes to gambling.

“Game bet match”. (June 2023).‘Four Corners’. S2023 E20

While for the majority, gambling may be a harmless and enjoyable activity, a minority of gamblers experience significant harms as a result^(1.).

Indeed, with its around-the-clock availability and omnipresence of cues (‘positive stimuli’, or things which attract us to gambling), the evolving landscape of gambling and betting raises important public health questions^(2.).

‘Crossing the line’: what is unhealthy gambling?

There are many harsh lessons to be learned from the gambling experience, but the harshest one of all is the difference between having Fun and being Smart.

Hunter S. Thompson (1937-2005).

Gambling has been defined by researchers as “an activity where something of value is risked on the outcome of an event when the probability of winning or losing is less than certain”^(3.).

It is when engagement in this activity becomes a persistent and recurrent behaviour pattern, and negative consequences emerge (within a continuum of outcome-based ‘severity’) in relation to individuals and their significant others’ in important life domains such as finances, physical & psychological wellbeing, and relationships, that ‘the line’ is crossed.

It is important to note that “high involvement” is not necessarily associated with negative consequences or disordered gambling symptoms. Indeed, past research has shown that it is possible to distinguish harmonious passion (i.e., a strong inclination to engage in the activity willingly and with a sense of volition) from obsessive passion (i.e., an uncontrollable urge to engage in the activity)^(2.).

Presaging current research trajectories as exemplified above, individual gambling narratives furnish an apposite preface to this review.

Sociology Professor and author Lesieur’s 1977 ‘confessional’ book The Chase^(7.), provides both a comprehensive archive of lived experiences of disordered gambling that is still relevant today, and an early behavioural model underpinning (in his words) the subculture of gambling (p.181):

Everybody gambles, and that is socially acceptable. People don’t get twelve grand in the hole. That ain’t socially acceptable. If I told the story that I just told you to certain people that I know, they’d just, they’d want me in the nuthouse. They’d really think I’m crazy; maybe I am, but they couldn’t appreciate the fact that you cannot, under any conditions, stop. They can’t appreciate that. I would never admit to anybody that I was a failure. Ego. The image.

The Chase, p. 196.

In grappling over time with reconciling healthcare modelling with these complex individual narratives, gambling typology, which has evolved descriptors including ‘excessive’, at-risk’, ‘problem’, ‘pathological’,  ‘compulsive’, ‘type 2’, and ‘disordered’, somewhat recapitulates medical taxonomy: the latest (Fifth) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), in renaming ‘Pathological Gambling’ Gambling Disorder (GD), also changed its classification from an ‘Impulse-Control Disorder’ to a ‘Substance-Related and Addictive Disorder’.

Thus, more consonant with clinical experience, unhealthy gambling is now considered, for the purposes of treatment selection, a behavioural addiction (BA), with much in common with disorders related to food, sex, gaming, internet usage, social media etc.

How is disordered gambling identified?

Staying with the medical model, statistically validated gambling assessment instruments (most involving questionnaires), feature in diagnostic protocols^(8.,9.), however a consensus on diagnostic/screening criteria is lacking.

For example, despite a growing body of knowledge on the relevant role of craving in gambling behaviour, it has not yet been proposed as a diagnostic GD criterion in the DSM, nor does it explicitly appear in the most common GD screening instruments^(10.).

More generally, the researcher asserts:

Further studies are needed to reach a consensus on the diagnostic criteria for GD^(10.).

One scale in the public domain may be self-administered- the 2001 Problem Gambling Severity Index (PGSI)- however it is not a replacement for professional advice, there exists ambiguities in the questions, and the scale does not accommodate advances in research since the early 2000s:

Notably, all but question 4 are subsumed in Lesieur’s ‘twenty questions’ (pp.260-261) formulated 25 years earlier, with those remaining worthy of enumeration:

• 6. Does gambling cause a decrease in your ambition or efficiency?
• 8. After a win do you have a strong urge to return and win more?
• 9. Do you often gamble until your last dollar is gone?
• 13. Does gambling make you careless of the welfare of your family?
• 15. Do you ever gamble to escape worry or trouble?
• 16. Have you ever committed, or considered committing, an illegal act to finance gambling?
• 18. Do arguments, disappointments or frustrations create within you an urge to gamble?
• 19. Do you have an urge to celebrate any good fortune by a few hours of gambling?
• 20. Have you ever considered self-destruction as a result of your gambling?

So, for the record, what medically defines GD?

According to the DSM-5 (the ICD-11 is more inclusive of trait impulsivity), GD is characterised by recurrent maladaptive gambling behaviour (which leads to negative consequences in one or more areas of life functioning) including:

• the need to gamble with increasing amounts of money (i.e., tolerance)
• the tendency to chase losses; irritability when attempting to stop the behaviour (i.e., abstinence)
• the presence of unsuccessful efforts to control gambling behaviour (i.e. relapse)
• a predominance of thoughts focused on the gambling behaviour
• the presence of lies or the loss of a significant relationship or job/educational opportunities
• the propensity to gamble when feeling distressed or to rely on others to provide relief money

Put simply: it’s complicated! A step-wise approach to understanding is presented below:

What differences have been found between ‘normal’ and ‘disordered’ gamblers?

Early laboratory animal studies revealed addicted brains differ in terms of brain anatomy, physiology, and electroencephalography (EEG) profile, as well as executive and cognitive efficiency^(11.).

More recent human neuro-imaging studies have concluded that ‘normal’ and ‘disordered’ gamblers differ in insula, orbital frontal cortex, and frontal lobe activity, with skewed patterns linked to both winning/losing state (frontoparietal activation) and cognitive interpretation/assessment (insula) of, for example, ‘near-miss’ experiences and overall success rate.

On the whole, data indicates that, relative to non-gamblers and non-disordered gamblers, at-risk and ‘problem’ gamblers showed higher levels of impulsivity, steeper delay discounting, shorter time horizon (i.e. less forward-thinking), and reported experiencing significantly higher levels of depression, anxiety, and stress^(12.).

Understanding cue reactivity (see appendix also).

Some expectation of consequences must in every case like this be aroused; and this expectation, according as it is, that of something desired or of something disliked, must necessarily either reinforce or inhibit the mere impulse.

William James, The Principles of Psychology. Dover Publications; New York: 1918 p. 390.

Cue-reactivity has frequently been investigated in functional neuroimaging studies to identify the neural substrates of craving in alcohol, drug and behavioural addictions^(13.).

Increased reactivity to gambling-related cues results from the activation of specific associative pathways in long-term memory. These associations are built and strengthened gradually through classical conditioning processes, that is, by the learning history of temporal or spatial coactivation between external (e.g., environmental) or internal (e.g. mood state) cues and reward consumption effects.

In line with this account, the incentive sensitisation theory (Berridge, 1993) predicts that the repeated pairing of environmental cues with gambling consumption leads these cues to acquire increased motivational salience (see appendix) and to capture attention, over and above primary natural rewards (e.g., food, sex).

At the cerebral level, a wealth of fMRI studies has shown that the incentive salience of gambling-related cues (triggering so-called “wanting”) is generated by a large and distributed brain system involving the ventral and dorsal striatum, amygdala, hippocampus, insula, anterior cingulate cortex, orbitofrontal cortex, and dorsolateral prefrontal cortex, as well as sensory, visual and motor cortices.

In other words, this extended brain pathway likely reflects the complex nature of interactions between the so-called bottom-up “impulsive” and top-down “reflective” systems inherent in the human brain.

Specifically, the fMRI literature on cue reactivity suggests that the motivational salience carried by gambling-related cues may:

(i) sensitise or exacerbate the activity of the amygdala-striatal “impulsive” system, which generates positive affective (‘outward’ mood/disposition) associations and fast approach behaviour towards gambling-related stimuli; and

(ii) subvert attention, reasoning, planning, and decision-making resources of the prefrontal “reflective” system to seek and reach rewards.

Importantly, cue reactivity does not necessarily lead to weaker or hypoactive cognitive (thinking) control (as commonly described by dual-process models of behavioural addiction), but instead redirects attention and executive control resources towards goals related to gambling.

In line with this account, triadic models of addiction (see the ‘3 stage model’ below) advance that, under certain circumstances (e.g., homeostatic imbalance, reward deprivation, stress, sleep deprivation etc), the insular cortex plays a pivotal role in promoting the drive and motivation to get a reward by “hijacking” goal-oriented processes toward addiction-related cues at the expense of inhibitory control resources.

Theories and models.

The public health debate around gambling is predicated in the main on biopsychosocial modelling (Engels 1977), a trans-disciplinary systems theory approach which focuses on the interconnection of biological, psychological, and socio-environmental factors.

Importantly, this public health approach looks at the impact of gambling harm at a population level, and as such views harm in terms of a continuum (e.g., from mild to severe harm) as opposed to whether or not an individual within the population meets diagnostic criteria for Gambling Disorder^(1.).

On the other hand, clinically-oriented modelling, which relies on measuring disordered gambling behavioural components stemming from addiction symptomatology, possess more utility at the individual targeting of treatment interventions level.

Based on the premise that substance use disorders (SUDs) and behavioural addictions are characterised by neuroplastic changes mirroring a shift from impulsive to compulsive behaviours primarily revolving around the avoidance of negative consequences, and the overlapping diagnostic criteria for the two, multiple syndrome models (where addiction resides in the relationship and not in the object^(14.)) have emerged including the 3-stage GD model^(15.):

The schematic illustrates a shift in motivational state as initial positively reinforcing effects are augmented by negatively reinforcing relief from a negative emotional state. Neuroadaptations that encompass the recruitment of extrahypothalamic corticotropin-releasing factor (CRF) and dynorphin brain stress systems are key to this shift.

Additionally, through ontogenic (developmental) processes, trait impulsivity (more on this later) interacts with various environmental risk factors to alter neurodevelopment of the prefrontal cortex (PFC), canalise externalising behaviour, and pull many impulsive individuals along the developmental trajectory described above.

Most researchers agree that diverse neural systems participate in the pathophysiology of GD^(11.):

• Initial gambling is characterised by activation of the hypothalamic-pituitary-adrenal axis to drive the binge/intoxication stage.
• Impulsive gambling is characterised by prefrontal cortex dysfunction with activation of CRF, y-aminobutyric acid (GABA), and dynorphin in the prefrontal cortex and subsequent disinhibition of the nucleus accumbens and extended amygdala that in turn drive increases in dynorphin in the nucleus accumbens and CRF in the extended amygdala.
• Compulsive gambling involves a pronounced activation of CRF in the extended amygdala, dynorphin-induced decreases in dopamine in the nucleus accumbens, and a pronounced loss of executive control in the prefrontal cortex.
• The withdrawal/negative affect stage involves changes such as emotional dysregulation, whereby chronic activation of the reward system recruits dysregulated neurotransmitters and hormones that are not found in the fronto-striatal reward pathway. The hypothalamic-pituitary adrenal axis becomes dysregulated though chronically-raised CRF, resulting in elevated adrenaline and dynorphin levels and contributing towards the development of negative emotional states and “blunting” of the reward circuitry during protracted abstinence. Blockade of the κ opioid system can also block anxiety-like and reward deficits associated with withdrawal^(5.).
• Craving is a key factor in promoting relapse. The prefrontal cortex is a key regulator of incentive salience (see appendix) and conditioned behaviour in the presence of salient cues. Common in both drug and non-drug addictions, similar activatory pathways have been noted, including the PFC, anterior cingulate gyrus, dorsolateral PFC, and medial orbitofrontal cortex. Disruptions in frontal cortical activity are correlated to disruptions in GABAergic activity, affecting decision making, self-regulation, inhibitory control and working memory. Disruptions to the insula’s interoceptive functions, which allow subjects to integrate autonomic and visceral information with emotion and awareness, inhibits conscious recognition of craving urges.

All of the above contribute to the spiralling distress and loss of control associated with full­blown dependence.

Finally, the Basic Psychological Needs Theory (BPNT), a mini theory that was developed within the self-determination theory, has also been applied to GD.

According to the BPNT, when their psychological needs are chronically thwarted, people are likely to develop various coping strategies, including need substitutes and maladaptive compensatory behaviours. Previous literature has associated need frustration with problematic gambling, but it is still unclear how need frustration fully affects gambling behaviour.

It is feasible that need frustration works in conjunction with certain gambling motives and accelerates the development of problem gambling. Thus, thwarted intrinsic needs may drive toward more extrinsic rewards and motivate gambling behaviour as a means of compensation.

In contrast, motives to escape, to win money, and to compete, along with need frustration, predicted problem gambling over time in the full model. In addition, money motive and need frustration had an interaction effect so that higher need frustration combined with money motive predicted more severe gambling problems^(16.).

More on the addiction connection.

From an aetiological (origins & causes) perspective, neuroimaging, genetic, and biochemical studies have suggested shared vulnerability factors between GDs and SUDs. One researcher^(4.) has proposed the term “Dual Disorder” as an apt descriptor of this clinical entity.

Neuropsychological features linked to addiction-related executive function disorders include not only impaired response inhibition, self-regulation, decision-making, and cognitive flexibility and planning, but also working memory disorders (hippocampal networks have been shown to be triggered by gambling-related cues).

Importantly however, attention and working memory deficits are more common in SUD than PG, which could be due to the neurotoxicity of the substances involved.

Furthermore, difficulties in emotion regulation and poorer psychological states have been linked to GD, particularly in women, older individuals and others exhibiting a preference for non-strategic gambling (i.e. lotteries, ‘scratchies’) or manifestations of co-morbid neuropsychological impairments.

The above vulnerabilities statistically predict poorer GD intervention outcomes and a higher frequency of treatment dropout and disordered gambling relapse.

Finally, it should be noted that acute and even binge gambling does not necessarily constitute a behavioural addiction^(5.).

• In GD, anticipation of monetary gain proportionally correlates with activation in the ventral striatum, potentially promoting irrational decision-making. Risk aversion has been associated with activation of the anterior insula, and a balance between these two circuits may be required for optimal decision making. It is important to note that the representation of interoceptive information through the insula might drive an intense motivation not only to seek reward but also to avoid punishment.
• Another similarity between GDs and SUDs are the dysfunctional dopaminergic responses to respective cues. In GD, we see significantly higher dopamine release in the ventral striatum compared to healthy controls during the Iowa Gambling Task.
• A higher level of dopamine, noradrenaline, and 5-HT in the hippocampus predicts for exploratory and risky behaviours in gambling.
• In general, it seems that the PFC (including medial and ventromedial area) is relevant in the dynamics of GD, with its disruption impairing decision making, especially if lower network action and sustained activity of the amygdala are present.
• Several studies have found neural signatures associated with reward prediction error and fictive error (how much a person gains versus how much they could have gained if they had bet more). Fictive error was associated with activation in the ventral caudate, ventral putamen, and posterior parietal cortex as well as with behavioural changes. The higher the fictive error, the more likely a person was to change their next bet^(17.).
• Several endocrine factors have been implicated in brain responses to rewards and gratification including gut hormones (e.g., ghrelin) and adipocytokines (e.g., leptin and adiponectin), classically associated with food intake regulation and energy balance^(18.). An antagonist of ghrelin named liver enriched antimicrobial peptide 2 (LEAP2) has been recently described. It has been related to impulsivity and cognitive functioning and may contribute to addictions due to its interplay with ghrelin. Furthermore, genetic alterations related to the ghrelin system, such as receptor polymorphisms, have been associated with reward-seeking behaviours and consumption. Similar to other addiction-related disorders, these endocrine substrates represent potential candidates involved in the pathogenesis of GD.

The stress factor.

Increasing levels of stress have been shown to decrease PFC function and increase striatal activity, perpetuating low cognitive control.

Psychological and neurobiological aspects of stress play a significant role in the starting, prolongation, and relapse of BAs including disordered gambling. Moreover, the mechanisms include interactions between biological mediators of the stress-response, stimulus-reward, and other neural-hormonal systems.

Key neurotransmitter systems with circumscribed neurocircuitry that mediate behavioural responses to stressors are involved, including glucocorticoids, corticotropin-releasing factor (CRF), noradrenaline, and dynorphin, as well as key neurotransmitter systems that act in opposition to the brain stress systems include neuropeptide Y, nociceptin, and endocannabinoids^(5.).

Adverse life experiences (stressful events) may be considered as contributing to in-the-moment allostatic load. The concept underpins other psychotherapeutic approaches including trauma and polyvagal-informed therapies.

Personality traits (Endophenotypes).

Beyond neuropsychological factors, other psychological and clinical features have been implicated in the development of addictive disorders. Certain personality traits such as extraversion and high levels of reward and novelty-seeking (related to impulsivity) and harm avoidance, especially in women, together with low self-directedness have been linked to both GD and SUDs.

Gambling disorder, one researcher asserts, is an ontogenic process whereby a common, multi-factorially inherited trait interacts with endogenous and exogenous influences to yield increasingly intractable externalising behaviours across development^(15.).

The same source postulates a specific trait impulsivity SUD/GD nexus of expression within this context:

Often termed “myopia for the future^(15.)”, trait impulsivity is a bottom-up, subcortically mediated vulnerability to all externalising disorders including gambling. This vulnerability arises from deficient mesolimbic dopamine responding, which imbues psychological states (e.g. irritability, discontentment) that motivate excessive approach behaviour (e.g. hyperactivity, impulsivity).

At its extremes, trait impulsivity is expressed as a preference for immediate rewards over larger delayed rewards, as actions taken without forethought, as failures to plan ahead, and as deficiencies in self-control.

Through complex interactions with (a) aversive motivational states that arise from largely independent subcortical systems, (b) emotion regulatory mechanisms that arise from top-down cortical modulation of subcortical neural function, and (c) environmental risk factors that shape and maintain emotion dysregulation, trait impulsivity confers vulnerability to increasingly severe externalising behaviours across development.

Choice impulsivity, or, more specifically, delay discounting- where more immediate rewards are chosen over those in the future (a hallmark sign in BAs and SUDs)- is elevated in GD.

Notably also, trait anxiety is an individual difference that moderates the expression of trait impulsivity. Depending on how an individual scores for trait anxiety, their impulsivity may be amplified, resulting in progression to more severe externalising outcomes, or mollified.

Indeed, cortical regulation of anxiety has moderating effects on trait impulsivity. Thus, those individuals who possess both traits are less likely to succumb to GD as co-morbid trait anxiety facilitates slower neural processes, allowing them to more effectively evaluate potential impulse outcomes toward choosing less risky or less dangerous options. Even a cursory review of the literature supports this notion, with evidence coming from both behavioural and neurobiological levels of analysis.

For more information regarding trait impulsiveness, please see this previous article.

Further to impulsivity, sufferers of GD show many similarities to addicts in the domain of compulsiveness, (or, ‘compulsivity’) where there is a tendency to repeat an action leading to undesirable consequences.

Response perseveration, a measure of compulsivity where a person is likely to repeat an action despite a stimulus being stopped, (demonstrated in PG but only some SUDs) leads to negative alterations in risk/reward decision making.

Genetic & epigenetic factors.

From a genetic perspective, several studies have shown that inherited factors account for approximately 50% of the risk for GD.

However, there exists an overall notable paucity of genetic/epigenetic studies (and corresponding omics-related repositories) which comprehensively explore the multitude of relationships between different neurobiological features (i.e., endocrine, and neuropsychological factors) and psychological and clinical variables^(19.).

With some genetic markers already identified, genetic variants associated with the severity of GD, especially in the era of genomics, could be interesting from a clinical perspective to improve treatment approaches based on personalised medicine^(20.).

Considerable research has addressed the mechanisms of experience dependence, including epigenesis, maternal programming effects, allostasis, and other forms of neuroplasticity. Of note, these mechanisms are often overlapping.

The literature regarding genetic vulnerability to GD being too voluminous to review here, numerous studies implicate links associated with genes that affect dopamine turnover, availability, metabolism, or a combination of these.

Neuroplasticity—which refers to experience-dependent changes in the efficiency, sensitivity, and time course of responding within and across neural networks—can also be effected epigenetically. Epigenesis occurs when DNA structure is altered (primarily via methylation) by environmental experience, leading to changes to gene expression (timing and extent of protein synthesis) which may have implications for behaviour.

For example, expression of brain-derived neurotrophic factor, which is implicated in differentiation of dopamine neurons in maturing mesolimbic structures, is susceptible to environmentally induced epigenetic regulation.

Studies indicate a statistically significant association between gambling symptoms and lifetime major depression, and marginally significant links with lifetime panic disorder, specific phobia, major depression, and generalised anxiety disorder^(21.).

Additionally, cycles of addiction have been shown to be additive and co-reinforcing, with use of substances exacerbating GD by further disrupting top-down regulation of mesolimbic structures.

The two have a high co-occurrence as 57.7% of problem gamblers also have a SUD^(22.).

Although level of neurotoxicity is an amplifying factor, even casual use of, for example, alcohol whilst gambling elicits additive dopamine release in the nucleus accumbens.

That is, once initiated, use of certain substances- particularly strong stimulants, including cocaine and methamphetamine (powerful dopamine releasers)- can alter both subcortical and cortical structure and function in ways that amplify trait impulsivity and potentiate emotion dysregulation.

Stimulants can be especially appealing to those who are trait impulsive because increased neural firing in the nucleus accumbens and other mesolimbic structures provides temporary relief from the chronically aversive mood state that heritable deficiencies in dopamine activity and reactivity imbue^(15.).

Only around 10% of pathological and problem gamblers ever seek help for gambling difficulties^(21.).

From various support group sources:

Individuals suffering from GD rarely admit that there’s anything wrong. Therefore, their friends, family, or co-workers are often the first to notice a problem. If a loved one has expressed their concerns about your gambling behaviours, it is best to listen to them. Denial is often a characteristic of GD.

If you’re concerned that a close friend may have a gambling problem, you should try and talk to them. Try to be supportive, and understanding, and express your concerns calmly. Try to avoid judging or blaming them, as it might make them defensive.

If you have a close one who is in remission, you should consider avoiding triggers that may result in a relapse of GD. For example, consider activities that do not involve gambling or bidding of any sort — even games or ‘play’. It’s also best to avoid visiting places such as casinos, racetracks, or similar establishments.

Many sources^(9.) promote self-help strategies including:

• Keep money and cards out of easy reach.
• If you have arranged an exclusion, you know you ‘can’t’ gamble so there’s no point trying.
• Do something to distract yourself – it could involve a friend who doesn’t gamble.
• Go for a walk or run (keeping away from gambling vectors).
• Do relaxation exercises or have a shower/bath to relax you.
• Try deep breathing, mindfulness, or meditation to change your thoughts or focus.
• Phone a supportive friend, your counsellor, or the Gambling Helpline to express your thoughts and get support and suggestions.
• Use self-talk, for example, ‘I don’t need to go now, I’ll wait a while and see how I feel’ and then do something else.
• Think of a holiday or something you would like that you need to keep your money for.
• Think of how good you’ll feel after you have resisted the urge.
• Think of how proud your family and friends will be of you for resisting.
• Think of being able to pay all your bills and save money if you overcome the urges.
• Write down feelings and urges and how you overcame them – this is good reference for future urges.

Gambling Intervention Apps.

These may include the monitoring of gambling activity, urges, and triggers, the promotion of gambling behaviour self-awareness through data collection, and the provision of some psychoeducation and therapeutic tools.

In short, the evidence-base behind apps for disordered gambling is very limited^(23.), with no randomised clinical trial (RCT) findings yet available.

For those considering them, a previous article offers some general Health App assessment guidelines.

Similarly, recent forays into virtual reality gambling interventions have so far proven no more effective than the standard (in this case, CBT- see below) protocols^(10.)

How can counselling for disordered gambling help?

Currently, evidenced-based treatments for GD utilise proven approaches including cognitive behavioural therapy (CBT), psychodynamic psychotherapy, motivational interviewing, exposure therapy (including eye movement desensitisation and reprocessing (EMDR)) and Mindfulness, alone or in combination (e.g. Mindfulness-based cognitive therapy (MBCT)), delivered face-to-face or via telehealth^(8.), and may involve psychoeducation and technology-based interactive strategies.

A robust relationship has been shown between gambling-related cognitive distortions and GD, with disordered gamblers consistently being found to hold more cognitive distortions about gambling than non-disordered gamblers.

Adept at individually-tailored treatment planning, a highly trained and experienced counsellor will utilise multiple roadmaps/pathways:

Notably, addiction-focused EMDR has a particularly cogent evidence-base:

..in accordance with preliminary findings about AF-EMDR therapy in general and findings about AF-EMDR for GD in particular, the present study shows that AF-EMDR seems to be of value for patients with GD^(13.).

and,

EMDR has been shown to be effective in overcoming accumulated psychological, cognitive, and behavioural problems and psychosocial dysfunction. Given the efficiency of the EMDR treatment, it demands further controlled studies to confirm the effects of the desensitization of triggers and urge reprocessing (DeTUR) on pathological gambling^(24.).

One researcher elaborates:

The addiction memory may hold positive- or negative-valanced memory representations of the past (autobiographical memories, e.g., of an event whereby a high amount of money was won in a casino), present (e.g., an image of a current, often repeating trigger situation, such as feeling alone or feeling worthless), or future (e.g., imagining all problems being solved after winning the jackpot).

In PTSD as well as in gambling, pathogenic memories are associated with high levels of emotional intensity, intrusiveness, and vividness. Similarities between addiction and emotional memory networks implicated in PTSD suggest that the addiction memory may also be influenced by EMDR.

Eye (or other bilateral) movements lead to a desensitisation of the original memory, with the reprocessed memory then able to be reconsolidated into long-term storage, generating less distress on subsequent retrieval, or—in case of GD—may induce less urge and addictive behaviour^(25.).

Additionally, couples/family approaches may address the effects of disordered gambling on ‘significant others’ or interrogate ‘family of origin’ issues, with 12-step programs available as therapeutic adjuncts (Gamblers Anonymous (GA) and GAM ANON for family/friends).

When I think back now, at the time I was really hopin’ that Gamblers Anonymous would show me a place to get money. That’s what I really went there for. I figured they would show me where to get money, how to pay these bills, and I’ll be back in gamblin’ again. Just keep it down this time where I don’t get hurt, you know. So I went home, you know; Gamblers Anonymous, they don’t tell you where to get money^{(7. p.207)}.

An interesting endnote: loot boxes & sports betting as ‘gateways to gambling’.

Sports Betting

One striking development in online sports gambling is the advent of in-play betting that allows bets to be placed during the game (e.g., on particular events or combinations of events during a game).

Moreover, in contrast to other types of gambling activities, sports betting is not negatively connoted in our society. Specifically, one key aspect of sports betting is that it binds gambling to watching sport, that is, a popular, enjoyable, and valorised activity.

Recent research findings^{(2., 12.)} have highlighted that despite having never gambled, some young sports fans displayed technical knowledge of sports betting, including being able to discuss and describe “odds”, different gambling markets, and how to place bets.

This betting-related knowledge can be predominantly traced back to the abiding marketing, for example, ‘pop-up’ messages occurring during live sports events that feature dynamic betting ratios have been found to induce increased recall and awareness of sports betting brands and specific promotions. As such, these and other cues might increase the incentive salience of sports betting in young individuals long before they reach the minimum legal age for gambling.

Loot boxes (game monetisation)

A key empirical finding that underscores the link between loot boxes and gambling is evidence of a positive correlation in cross-sectional surveys between measures of loot box engagement (e.g., spending) and problem gambling symptoms. A 2022 survey observed that about 1 in 5 participants retrospectively believed their loot box use influenced subsequent gambling.

Rarer, more desirable, loot box rewards have been seen to elicit behavioural markers of reward reactivity (post reinforcement pauses), and increased physiological arousal (skin conductance level) has been detected prior to loot box outcomes.

Numerous researchers refer to this pathway, from loot boxes to gambling, as ‘migration’:

Uncertain rewards can recruit the dopamine system and a process of incentive sensitisation that is implicated in addictions^(26.).

Epidemiological data indicate that earlier age of onset of gambling (typically during adolescence) is a risk factor for adult gambling problems, implying that youth, for whom conventional gambling is an age-restricted activity, may be introduced to gambling via the variable-ratio rewards of loot boxes.

The same researchers have also noted that the risks of overspending with loot boxes are separate from any debates about their legal classification as gambling, and regulatory action could mitigate both gaming and gambling-related financial harms.

Conclusion

This article, written for educational purposes only, is not intended to replace professional advice and in no way reflects the views of Brisbane Counselling Centre. Notwithstanding this, readers are welcome to contact us for more information regarding gambling counselling.

If you have immediate concerns about your gambling (or someone else’s) please consider phoning the Qld Gambling Helpline on 1800 858 858 for free and confidential counselling and crisis support (24 hours, 7 days). They also offer referrals to the closest Gambling Help service for face-to-face counselling.

Appendix: GD key concepts

Motivational salience

A cognitive process and a form of attention that motivates or propels an individual’s behaviour towards or away from a particular object (attraction or aversion), perceived event or outcome. Motivational salience regulates the intensity of behaviours that facilitate the attainment of a particular goal, the amount of time and energy that an individual is willing to expend to attain a particular goal, and the amount of risk that an individual is willing to accept while working to attain a particular goal.

Incentive salience: the attractive form of motivational salience that causes approach behaviour, and is associated with operant reinforcement, desirable outcomes, and pleasurable stimuli.

Aversive salience: the aversive form of motivational salience that causes avoidance behaviour, and is associated with operant punishment, undesirable outcomes, and unpleasant stimuli.

Behavioural considerations: the assignment of incentive salience to stimuli is dysregulated in addiction. Addictive drugs are intrinsically rewarding (not to be confused with pleasure), whilst addictive behaviours (such as gambling) are extrinsically pleasurable; both function as primary positive reinforcers of continued use.

During the development of an addiction, the repeated association of otherwise neutral and even non-rewarding stimuli with addictive stimulation triggers an associative learning process that causes these previously neutral stimuli to act as conditioned positive reinforcers of addictive behaviour. i.e., these stimuli start to function as cues. As conditioned positive reinforcers, these previously neutral stimuli are assigned incentive salience (which manifests as a craving)– sometimes at pathologically high levels due to reward sensitisation– which can transfer to the primary reinforcer (e.g., the use itself) with which it was originally paired.

Primary rewards

Primary rewards are a class of rewarding stimuli which facilitate the survival of one’s self and offspring, and they include homeostatic (e.g., palatable food) and reproductive (e.g., sexual contact and parental investment) rewards.

Intrinsic rewards are unconditioned rewards that are attractive and motivate behaviour because they are inherently pleasurable, whilst extrinsic rewards (e.g., money or seeing one’s favourite sports team winning a game) are conditioned rewards that are attractive and motivate behaviour but are not inherently pleasurable.

Extrinsic rewards derive their motivational value as a result of a learned association (i.e., conditioning) with intrinsic rewards. Extrinsic rewards may also elicit pleasure (e.g., euphoria from winning a lot of money in a lottery) after being classically conditioned with intrinsic rewards.

Regarding behavioural addiction: due to the effect of reward cues and Pavlovian-instrumental transfer on the amplification of incentive salience for rewarding stimuli, “cue-triggered wanting”, or craving may occur even after long periods of abstinence.

References

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