Pathological gambling is a prevalent disorder that is gaining attention from patients, clinicians and policy makers. Aetiological factors that have been related to pathological gambling include: (i) abnormalities in the serotonergic, dopaminergic and noradrenergic systems; (ii) cognitive distortions; and (iii) a reinforcement of the gambling activity by either episodic gains or the excitement that accompanies gambling. Male gender, urban residence, lower income and the presence of a comorbid psychiatric disorder (particularly substance abuse) appear to constitute risk factors for the presence of the disorder.
A number of treatments have been suggested as potentially effective: Gamblers Anonymous, behavioural therapy, manualised cognitive therapy and several medications. At present, only manualised cognitive therapy and the selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitor fluvoxamine have shown efficacy in systematic (albeit small) studies. However, much research remains to be done to better understand the psychophysiology of pathological gambling, to firmly demonstrate the efficacy of the different proposed treatment approaches, and to establish criteria for treatment selection for individual patients.
Gambling is a popular and pleasurable activity for many people around the world. However, there is increased recognition by policy makers, professionals and the general public that certain individuals develop a pattern characterised by decreased control over their gambling and increased importance of gambling in their hierarchy of motivations. Named ‘compulsive gambling’, ‘excessive gambling’, ‘ludomania’ or ‘gambling addiction’ by different authors, pathological gambling was first formally recognised as a psychiatric disorder when it was included in the DSM-III.
Pathological gambling is associated not only with important money losses, but with a progressive disruption of the individual’s life and, in many instances, the lives of those emotionally close to him/ her. Many pathological gamblers lose their jobs or have increased emotional problems, general medical care needs and psychiatric comorbidity, as do their families. The rate of suicide attempts appears to be extremely high in patients with pathological gambling, with rates of 17 to 24% reported among pathological gamblers seeking treatment. When they seek help, access to treatment is frequently limited by the scarcity of clinicians with experience in the treatment of the disorder or a lack of third-party reimbursement.
All these factors result in important costs for the individual and society that are being insufficiently addressed at present. Increasingly, physicians and mental health professionals will come into contact with patients who have a diagnosis of pathological gambling. In this review, we provide an overview of the epidemiology and theories about the pathophysiology of the disorder, and offer some suggestions for the assessment and management of patients with pathological gambling.
Several studies have assessed the prevalence of pathological gambling, obtaining estimates ranging from 1.5 to 11.2% of the adult population. Although some of the differences are attributable to the instruments used, much of the variability in the results is better explained by the characteristics of the population sampled. Prevalence is higher in urban areas, particularly in poor areas or where there is a higher availability of gambling opportunities. A recent meta-analysis suggested that the 12-month and lifetime prevalences of pathological gambling in the adult population are 1.14 and 1.6%, respectively.
In the US, Volberg has noted that the prevalence of pathological gambling in states where gambling has been legalised for 10 years or less was 0.5%, compared with 1.5% in the states where gambling had been legalised for 20 years or more, raising the possibility that increased availability of gambling opportunities may lead to a higher prevalence of pathological gambling. Alternatively, it is possible that states that legalised gambling earlier may be inherently different to those with more recent legalisation. Such states may have a more positive view towards gambling or be less inclined to restrict the choice of activities by individuals.
Epidemiological studies suggest that males, adolescents, ethnic minorities and patients with psychiatric comorbidities are at a higher risk for experiencing the disorder. Other risk factors identified through the study of clinical samples include early exposure to gambling opportunities,[8,9] cognitive deficits and having parents with pathological gambling or alcohol dependence.[8–12]
There is little systematic information regarding the longitudinal course of the disorder. However, clinical impression suggests that the age of onset for most patients is adolescence or early adulthood, although the onset may be a little later for females. Number of exposures to gambling and time needed to develop the disorder is unknown, as well as the possible differential risk of different types of gambling opportunities such as horse racing, slot machines, roulette or cards. The course of the disorder is believed to be chronic, with periods of nongambling alternating with periods of gambling, in the general context of a progressive worsening of the disorder.
2. Aetiological Theories
2.1 Psychodynamic Theories
Dynamic theories were the first to offer an explanation for pathological gambling. Freud, and later Bergler, related pathological gambling to the oedipal complex. In essence, the pathological gambler would have a masochistic personality. The patient would experience conflict with authority figures, and use gambling as a means of achieving pleasure through self-punishment.
More recently, Rosenthal has suggested that pathological gambling is more related to pre-oedipal conflicts. Defence mechanisms such as denial and omnipotence would help explain the irrationality of the gambler who believes he/she can beat the odds. In Rosenthal’s view, narcissism would be one of the most characteristic traits of pathological gamblers.
2.2 Learning Theory
Learning theories try to explain pathological gambling as the result of a process of reinforcement. However, there is considerable disagreement regarding the identification of the reinforcer. Some authors suggest that occasional gains act as powerful intermittent reinforcers of the behaviour. Others believe that the excitement associated with the gambling situation is the true reinforcer. A third group emphasises the mechanism of behavioural completion. According to this latter theory, once a behaviour becomes habitual (e.g. gambling), any stimulus associated with that behaviour will arouse in the individual the wish to complete the behavioural sequence (in this case, gamble). Failure to complete the sequence results in intense discomfort for the patient. Thus, avoidance of this discomfort would act as a reinforcer of the behaviour.
2.3 Cognitive Theory
There is some evidence that pathological gamblers have distorted cognitive patterns that lead them to misassess the odds of their bets, and the meaning of the results. Winning bets are interpreted as a confirmation of their beliefs in their good luck, while losing bets are interpreted as a sign that the tide will turn and that they are on the verge of a winning streak. It has been shown that pathological gamblers have recall bias, and tend to remember and overestimate their wins, while they forget, underestimate or rationalise their losses. This recall bias may help explain the history of initial wins that many patients state happened in the initial stages of their gambling activity.
Several studies have suggested the involvement of different neurotransmitter systems in the pathophysiology of pathological gambling (table I).
2.4.1 Serotonergic Function
A dysfunction of the serotonin (5-hydroxytryptamine; 5-HT) system has been frequently described as playing an important role in impulsive behaviours, such as fire-setting, violent suicides and violent offenses. Moreno et al. administered intravenous clomipramine to 8 male and female pathological gamblers and 8 age- and gender-matched controls. Patients who were pathological gamblers demonstrated lower baseline prolactin levels and blunted prolactin responses to clomipramine 60 minutes after the infusion compared with controls, suggesting decreased serotonin transporter binding in those with pathological gambling.
Interestingly, genetic research has revealed that the serotonin transporter gene could be contributing to the pathogenesis of pathological gambling; the less functional allele variant was found to be significantly more represented in gamblers compared with controls.
In a subsequent study, DeCaria et al. showed an increased prolactin response to a single dose of m-chlorophenylpiperazine (m-CPP) in 10 male pathological gamblers compared with matched controls, suggesting hypersensitivity of postsynaptic serotonin receptors in pathological gamblers. More pronounced changes in prolactin response were associated with greater overall gambling severity.
In another study, we compared the activity of platelet monoamine oxidase (MAO) B (MAO-B), a peripheral marker of serotonergic function, in patients with pathological gambling and controls. Pathological gamblers had significantly lower MAO-B activity. A genetic study, also by our group, found no abnormalities in the gene for MAO-B, suggesting that low levels of MAO-B activity in pathological gamblers are not determined by the structural gene for MAO-B, although they may be mediated through genes that modulate the expression of the MAO-B structural gene. In contrast to findings with MAO-B, this study found an association between an allele variant of a polymorphism in the MAO-A gene and more severe cases of pathological gambling in the males in the sample. We are currently determining the possible functionality of the polymorphism.
2.4.2 Noradrenergic Function
Central noradrenaline (norepinephrine) is involved in the physiological functions associated with arousal and impulse control. A study by Roy et al.[25,26] suggested that levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) in the CSF and plasma, and levels of noradrenaline and vanillylmandelic acid in the urine are increased in pathological gamblers. This suggests that the noradrenergic system, via an effect on arousal, may play a role in the pathophysiology of pathological gambling.
The growth hormone response to clonidine, an α2-adrenergic agonist, has been used as a biological challenge to assess central noradrenergic function. A study found that a group of 5 pathological gamblers had an elevated growth hormone peak response to clonidine in comparison with a group of 8 healthy male volunteers. The severity of pathological gambling correlated with the magnitude of the clonidine-induced growth hormone response.
2.4.3 Dopaminergic Function
There is evidence suggesting that dopaminergic pathways are associated with reward mechanisms. Although Roy et al. did not find differences in plasma, urinary and CSF levels of dopamine in pathological gamblers compared with controls, in a recent study comparing 10 male pathological gamblers and 7 male controls, Bergh et al. found that the CSF levels of dopamine were decreased and of dopamine metabolites were increased in pathological gamblers, suggesting an increased release of dopamine in these individuals. Interestingly, our group has found that the variant allele of the dopamine D4 receptor gene, which leads to a poorer functioning of the receptor, is associated with pathological gambling.
There are a number of instruments that can be used as screening tools for pathological gambling. The most common instrument for assessing gambling problems is probably the self-administered South Oaks Gambling Screen (SOGS). Individuals endorsing 5 or more items are classified as probable pathological gamblers. The instrument is based on DSM-III-R criteria and has good reliability and validity in clinical samples. The main disadvantage of the SOGS is its length; a clinician is unlikely to ask a patient 20 questions as a routine screening for a disorder.
The recently developed Lie/Bet screen is a very promising alternative. In consists of 2 questions: ‘Have you ever felt the need to bet more and more money?’ and ‘Have you ever had to lie to people important to you about how much you gamble?’. Answering ‘yes’ to either of these questions yields a 0.99 sensitivity and 0.91 specificity in the identification of pathological gamblers using a checklist of DSM-IV criteria as the gold standard.
Once a diagnosis of pathological gambling is suspected on the basis of the screening questions or other clinical indications, it is necessary to confirm the diagnosis. There is at present no standardised way of doing this. Most clinicians appear to rely on clinical interview using DSM-IV (or ICD-10) criteria. An alternative is the use of the Diagnostic Interview Schedule (DIS) adapted for pathological gambling. New semistructured clinical interviews based on DSM-IV criteria are currently under development.
Finally, it is important to note that the presence of a manic episode is the only exclusionary criterion in DSM-IV for the diagnosis of pathological gambling.
One of the difficulties in the assessment of pathological gambling is that, in contrast with the assessment of substance abusers where urine drug screens can provide an objective estimate of recent use, the main source of information for gambling behaviour is self-report. Although collateral information from friends or relatives is frequently available, and should always be sought with the patient’s permission, pathological gamblers have an uncanny ability to deceive relatives and clinicians, at least in the short term. Therefore, patient-derived information may not always be accurate, but provides a lower bound for the magnitude of the problem.
An instrument that can be used to assess the severity of gambling is the Gambling Severity Index (GSI). This is a modified version of the Addiction Severity Index that adds items such as embezzlement, fraud and gambling offenses to the list of possible legal problems, and a set of questions regarding participation in gambling which focuses on frequency, financial problems related to gambling and other gambling-related problems. However, the GSI has been rarely used in clinical studies. Based on their conceptualisation of gambling as an obsessive-compulsive spectrum disorder, DeCaria et al. developed a modification of the Yale-Brown Obsessive-Compulsive Scale (YBOCS). This is a 10-question scale that assesses the interference with the individual’s life and distress caused by actual gambling behaviour or thoughts related to it. Preliminary data suggest that it has good reliability and validity, but further research is needed to confirm these initial results.
Severity has frequently been assessed by the number of SOGS criteria met by the patient. Alternatives measures include time spent or money lost gambling (in absolute terms, or relative to the individual’s income).
The relative merits of these methods have never been assessed and this assessment remains one of the most important challenges for the field as outcome evaluation and comparison of treatments become progressively important.
An essential part of the assessment of pathological gambling should be the ascertainment of possible comorbid disorders that may influence the course and severity of the disorder. Several studies have shown pathological gambling to be highly comorbid with other psychiatric disorders, especially substance abuse disorders, affective disorders and attention deficit hyperactivity disorder (ADHD).[37–39]
Epidemiological studies suggest that the lifetime prevalence of alcohol abuse/dependence in pathological gamblers is in the range of 40 to 60%,[40,41] with studies of clinical samples reporting similar estimates. Use of illicit drugs is also common, with estimates of lifetime prevalence ranging from 10 to 30%, whereas the prevalence of comorbid nicotine dependence may be as high as 85%.[37,42] There are some indications that substance abuse may precede the onset of pathological gambling.
Comorbidity with affective disorders is also high. Studies of inpatients have estimated that 75% of pathological gamblers have comorbid depression. However, a follow-up study of patients showed that only 18% of the gamblers remained depressed after abstinence. Community samples have yielded lifetime prevalence estimates of comorbid major depression of 10 to 20%.[40,41] It is unclear at present whether mood disorders are the cause or consequence of gambling, with data supporting both hypotheses (Ibáñez A, unpublished data).[38,44]
Based on the frequent association of pathological gambling with criminal behaviour, a number of studies have looked at antisocial features in pathological gamblers, and found positive results.[23,45] Epidemiological studies suggest that almost 40% of pathological gamblers may have comorbid antisocial personality disorders.[40,41] However, there are no studies that have looked at the stability of this diagnosis in gamblers who have achieved abstinence.
There are also some suggestions that pathological gambling is associated with high rates of ADHD; a recent study found that 20% of an outpatient sample of individuals who were pathological gamblers met criteria for ADHD. It is estimated that 3 to 5% of school-age children have ADHD, while data on the prevalence of ADHD in the adult population are limited. At present, there are no studies of the prevalence of pathological gambling among patients with ADHD.
Each of these comorbidities appears to occur with higher prevalence in pathological gamblers than in the general population, suggesting a relationship between the disorders. However, the directionality of this relationship remains unexplored. Studies that examine the temporal sequence of the disorders, or possible common aetiological mechanisms, may help clarify this relationship.
4.1 Gamblers Anonymous and Gam-Anon
Gamblers Anonymous (GA), a 12-step programme modeled after Alcoholic Anonymous, is probably the most popular intervention for pathological gambling. It emphasises the need for public confession to a peer group, and offers financial, legal and employment assistance. However, its efficacy as a stand-alone treatment has not been clearly established. Some reports indicate that retention rates of GA attendees are 10 to 30%. In addition, of those who continue, only 8% remain abstinent for 1 year and 7% for 2 years or more.
Two studies have looked at the outcome of patients whose significant other attended Gam-Anon, the spousal counterpart of GA. Both studies found that participation in Gam-Anon tended to improve outcome of the patients and reduce marital discord, but the differences were not statistically significant in either study.[47,48]
There is some evidence, from retrospective studies, that combining GA with professional help may improve the outcome of pathological gambling. Lesieur and Blume described the outcome of patients treated for pathological gambling in an inpatient programme. Of 124 patients admitted for treatment, 72 were contacted between 6 and 14 months after discharge (the remaining 52 patients could not be contacted or refused to be interviewed). Gambling behaviour had decreased significantly, and 64% of patients reported abstinence. Blackman and co-workers studied the outcome of 88 patients treated in a clinic specialising in the treatment of pathological gambling, and found significant decreases in indebtedness and gambling behaviour from pretreatment levels in patients who attended GA.
Two studies in veterans also support the notion that GA plus professional treatment may be an effective treatment for pathological gambling. Russo and colleagues surveyed 60 of 124 individuals treated in a inpatient programme (the mailed survey was not returned by 64 individuals). Patients were treated with individual and group psychotherapy, as well as attendance of GA. Abstinence was 55% by self-report. In a study by the same group, Taber et al. conducted a 6-month follow-up of 57 of 66 patients (9 patients were not located) consecutively admitted to the hospital. The self-reported rate of abstinence was almost identical to the previous study (56%), and improvements in associated psychiatric symptoms and psychosocial functioning were also documented.
4.2.1 Psychodynamic Psychotherapy
Bergler was one of the first to report the successful treatment of pathological gambling, using an ego-psychology psychoanalytic approach. 14 of 60 patients improved with treatment, but little information is provided about the other 46 patients. Others have also reported success in a number of single case studies. However, inadequate use of outcome measures as well as limited follow-up data make it difficult to assess the efficacy of this approach.
4.2.2 Cognitive-Behavioural Therapy
Early behavioural approaches to the treatment of pathological gambling included aversive conditioning using electric shocks, cue exposure with response prevention, and imaginal sensitisation.
More recently, approaches emphasising cognitive restructuring have become increasingly influential. Bujold and colleagues successfully used cognitive restructuring, problem solving, social skills training and relapse prevention to treat 3 individuals who had a diagnosis of pathological gambling. In a subsequent controlled trial by the same group, 29 patients were randomly assigned to a manualised treatment incorporating the 4 strategies used in the pilot work or a waiting list where patients were contacted monthly by a therapist. 12 of 14 patients who completed the treatment were considered responders, compared with 1 of 15 in the control group. At 12 months’ follow-up, 8 of the patients in the treatment group had maintained their gains.
A number of approaches to the psychopharmacological treatment of pathological gambling have been assessed and are summarised in table II.
4.3.1 Selective Serotonin Reuptake Inhibitors
Two different lines of reasoning have led to the use of selective serotonin reuptake inhibitors (SSRIs) in the treatment of pathological gambling. The first line is based on the conceptualisation of pathological gambling as an impulse control disorder and the abnormalities in the serotonergic system documented in several studies of pathological gamblers (see section 2.4.1). This advocates that the use of SSRIs may help to normalise serotonergic function and lead to improved impulse control. The second line is based on the inclusion of gambling in the obsessive-compulsive spectrum disorder, and the response of obsessive-compulsive disorder to serotonin reuptake inhibitors.
In a double-blind, single case study involving a 31-year-old woman with a 12-year history of pathological gambling, gambling behaviour decreased by 90% during the clomipramine treatment phase, but not during the placebo phase.
In a single-blind study of fluvoxamine, 16 patients entered an 8-week placebo washout phase, followed by an additional 8 weeks of fluvoxamine. Four patients were withdrawn from the study because of poor compliance and 2 withdrew because of a lack of improvement. Of the 10 patients who were able to finish the study, 6 were abstinent at the end of the study. A seventh patient who entered the fluvoxamine phase with no gambling behaviour or urges remained clinically unchanged at end-point. Two of the completers who failed to respond to fluvoxamine treatment had an additional diagnosis of cyclothymia, and higher dosages of fluvoxamine seemed to exacerbate their gambling and mood symptoms.
In addition, preliminary findings from a 16-week, double-blind placebo-controlled crossover trial in 15 patients indicate that fluvoxamine is superior to placebo in decreasing gambling urges and behaviour as measured by the Pathological Gambling Modification of the Yale-Brown Obsessive Compulsive Scale (PG-YBOCS) and Pathological Gambling Clinical Global Impression (PG-CGI) scale.
Additional placebo-controlled studies with other SSRIs are currently under way.
4.3.2 Mood Stabilisers
Moskowitz reported the successful treatment with lithium of 3 pathological gamblers who had comorbid bipolar disorder. Another case report has also documented the efficacy of lithium in pathological gamblers who had comorbid bipolar disorder. It is unclear how much of the improvement in these patients was specific to gambling behaviour and how much was the result of the successful treatment of their bipolar disorder.
Carbamazepine has also been documented to be effective in the treatment of gambling in a case report.
4.3.3 Opioid Antagonists
Naltrexone was found to be effective in reducing both gambling and shopping behaviour in a single case. The benefits were maintained over a 9-month follow-up period. A nonblind trial including 30 patients demonstrated that 16 patients were abstinent at the tenth month of follow-up.
The hypothesised mechanism of action of opioid antagonists is the inhibition of dopamine release in the nucleus accumbens, thus modulating the pathways that appear to be involved in the pathogenesis of addictive behaviours. Placebo-controlled studies with naltrexone for the treatment of pathological gambling are currently under way.
4.4 Choice of Treatment
There is evidence suggesting that a number of approaches may have efficacy in the treatment of pathological gambling. Professionally delivered cognitive-behavioural therapy is the psychotherapy with best documented efficacy for pathological gambling, and will probably prove to be an essential part of any treatment for the disorder in the future. The manuals used in the studies of this treatment approach have not yet been published, limiting the applicability of this therapy in the case of most individuals. However, some simple behavioural interventions can be easily implemented, if agreeable to the patient (see table III).
Fluvoxamine is the only medication that has been systematically studied to date. Although results appear modest at present, its safety and tolerability make it a reasonable option for patients agreeable to a trial of pharmacological treatment. Use in combination with cognitive-behavioural therapy is likely to improve compliance, similar to what has been found in the treatment of drug abuse, thus potentially increasing its therapeutic effect. Other SSRIs may be acceptable alternatives, although data regarding their efficacy are lacking. Use of other medications together or concomitantly in the presence of comorbidity may be considered, but there are no empirical data to support their efficacy at present.
There are currently no prospective studies of combined treatment for pathological gambling. However, based on our clinical experience and on the preceding review of the literature, we believe that it is unlikely that monotherapy (medication or psychotherapy) will be successful in the treatment of most patients. For that reason, in clinical practice, a multimodal approach, addressing both the symptoms and the psychosocial dysfunction of pathological gambling, may prove more fruitful. Attendance of GA, where available, should be encouraged as a complement to the treatment provided by professionals. Similarly, involvement of the family through Gam-Anon or through multifamily groups may be beneficial to both the patients and their relatives, and should be recommended. Given the frequent economic and criminal complications of pathological gambling, financial and legal counselling should also be an integral part of treatment.
5. Future Directions
Because Caucasian men are highly over-represented in treatment samples, much of what is known about pathological gambling is based on samples composed solely or mainly of Caucasian men. An important task for the future is to identify and eliminate barriers to treatment for women and minorities. As this happens, it will become increasingly important to confirm to what extent our current knowledge of the disorder is generalisable to these new subgroups.
It will also be important to obtain additional information regarding the longitudinal course of the disorder in the presence or absence of comorbidity. Closely related is the fact that much of the treatment research currently focuses on the short term outcome of the disorder. However, as pathological gambling appears to be a chronic condition, significant efforts will need to be devoted to relapse prevention and to determining the appropriate duration and characteristics of maintenance programmes.
Ongoing genetic and brain imaging studies will also help better delineate the biological basis of the disorder and inform potential therapeutic strategies. As our understanding of the epidemiology, pathophysiology and treatment response in pathological gambling increases, it will also be possible to decide whether pathological gambling is best understood as an addiction or an obsession.
After more than 10 000 years of the existence of the disorder, the field of pathological gambling research and treatment is still in its infancy. As the general population becomes aware of the symptoms and consequences of pathological gambling, increasing attention will be paid to gambling by policy makers, and an increasing number of consultations from patients is likely. We hope that this review will stimulate the interest of clinicians in this old ‘new disorder’ and provide some suggestions for its management.
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Blanco, C., Ibáñez, A., Sáiz-Ruiz, J. et al. Epidemiology, Pathophysiology and Treatment of Pathological Gambling. Mol Diag Ther 13, 397–407 (2000). https://doi.org/10.2165/00023210-200013060-00002
- Attention Deficit Hyperactivity Disorder
- Pathological Gambling