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Pathological Gambling: Diagnosis & Treatment
Gambling continuing education addiction counselor CEUs

Section 13
Etiological Theories of Pathological Gambling

CEU Question 13 | CEU Answer Booklet | Table of Contents | Gambling
Psychologist CEs, Social Worker CEUs, Counselor CEUs, MFT CEUs

Epidemiology
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 legalized for 10 years or less was 0.5%, compared with 1.5% in the states where gambling had been legalized 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 legalized gambling earlier may be inherently different to those with more recent legalization. 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, cognitive deficits, and having parents with pathological gambling or alcohol dependence.

There is little systematic information regarding the longitudinal course of the disorder. However, clinical impression suggests that the age of onset foremost 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.

Etiological Theories
 Psychodynamic Theories: Dynamic theories were the first to offer an explanationfor pathological gambling. Freud, andlater Bergler, related pathological gambling tothe oedipal complex. In essence, the pathologicalgambler would have a masochistic personality. Thepatient would experience conflict with authorityfigures, and use gambling as a means of achievingpleasure through self-punishment.More recently, Rosenthal has suggested thatpathological gambling is more related to pre-oedipalconflicts. Defense mechanisms such as denialand omnipotence would help explain the irrationalityof the gambler who believes he/she can beat the odds.In Rosenthal’s view, narcissism would be one ofthe most characteristic traits of pathological gamblers.
Learning Theory: Learning theories try to explain pathological gamblingas the result of a process of reinforcement.However, there is considerable disagreement regardingthe identification of the reinforcer. Someauthors suggest that occasional gains act as powerfulintermittent reinforcers of the behavior. Othersbelieve that the excitement associated with the gamblingsituation is the true reinforcer. A third groupemphasizes the mechanism of behavioral completion. According to this latter theory, once a behaviorbecomes habitual (e.g. gambling), any stimulusassociated with that behavior will arousein the individual the wish to complete the behavioralsequence (in this case, gamble). Failure tocomplete the sequence results in intense discomfortfor the patient. Thus, avoidance of this discomfortwould act as a reinforcer of the behavior.
Cognitive Theory: There is some evidence that pathological gamblershave distorted cognitive patterns that lead themto misassess the odds of their bets, and the meaningof the results. Winning bets are interpreted as aconfirmation of their beliefs in their good luck, whilelosing bets are interpreted as a sign that the tidewill turn and that they are on the verge of a winningstreak. It has been shown that pathological gamblershave recall bias, and tend to remember andoverestimate their wins, while they forget, underestimateor rationalize their losses. This recallbias may help explain the history of initial wins thatmany patients state happened in the initial stages oftheir gambling activity.

Neurobiology: Several studies have suggested the involvementof different neurotransmitter systems in the pathophysiologyof pathological gambling.

Serotonergic Function: A dysfunction of the serotonin (5-hydroxytryptamine;5-HT) system has been frequently describedas playing an important role in impulsive behaviors, 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.

Noradrenergic Function: Central noradrenaline (norepinephrine) is involvedin the physiological functions associated with arousal and impulse control. A study by Roy et al. 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 2-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.

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 and7male 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.

- Blanco, C.; Ibáñez, A.; Sáiz-Ruiz, J.; Blanco-Jerez, C.; Nunes, E.V.; Epidemiology, Pathophysiology and Treatment of Pathological Gambling. CNS Drugs, 2000, Vol. 13 Issue 6, p397-407
The article above contains foundational information. Articles below contain optional updates.

Personal Reflection Exercise #6
The preceding section contained information regarding etiological theories of pathological gambling. Write three case study examples regarding how you might use the content of this section in your practice.

Online Continuing Education QUESTION 13
What are two factors in the cognitive theory of pathological gambling? Record the letter of the correct answer the CEU Answer Booklet

 
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