Pathological gambling

Clinical Psychology Review 22 (2002) 1009 – 1061

Pathological gambling A comprehensive review Namrata Raylu, Tian P.S. Oei* School of Psychology, University of Queensland, Brisbane, Queensland, 4072, Australia Received 19 March 2001; received in revised form 28 June 2001; accepted 21 November 2001

Abstract Due to recent changes of gambling laws, accessibility to gambling has become more widespread and thus, there has also been an increase in the prevalence of pathological gambling (PG). The wide range of social, economic, and psychological problems associated with PG are well known. There is a need for better understanding of PG and this review attempts to do so. Literature searches using the Medline and PsycINFO databases were used. Critical examining of the literature showed that familial/genetic, sociological, and individual factors (e.g., an individual’s personality, biochemistry, psychological states, and cognitions) are implicated in the development and maintenance of PG, yet at present, the evidences are not solid. Similarly, there have been a lot of theories for PG but again, none of them are solid enough to provide a clear understanding of PG. Recent psychological-based theories seem to provide some solid ground for further research. We highlight four areas for future consideration for research. (1) Most studies have generalized findings from one form of gambling to another. It is suggested that it is now not tenable to consider gambling as a single phenomenon that can explain all forms of gambling. (2) Almost all of the studies in the gambling literature are Western-based and the results are often generalized to other ethnic and cultural groups. There is now an urgent need to close this gap. (3) Future studies need to address methodological problems in the current gambling/PG literature. (4) Almost all of the gambling literature has focused on the issue of why people start gambling. It is suggested that looking at variables as to why people stop gambling in a single episode may be a more fruitful area of research then why people start gambling. This is because what motivates one to continue gambling, despite losses in a session and across sessions, is a characteristic that distinguishes

* Corresponding author. E-mail address: [email protected] (T.P.S. Oei). 0272-7358/02/$ – see front matter D 2002 Elsevier Science Ltd. All rights reserved. PII: S 0 2 7 2 - 7 3 5 8 ( 0 2 ) 0 0 1 0 1 - 0

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nonproblem gamblers from problem gamblers and pathological gamblers (PGs). D 2002 Elsevier Science Ltd. All rights reserved. Keywords: Pathological gambling; Gaming machines; Gambling; Addiction; Psychopathology; Review

1. Introduction Gambling has been defined as placing value upon a game/event or a bet of any type that has an unpredictable outcome, and in which the result to some magnitude is determined by chance (Bolen & Boyd, 1968). Pathological gambling (PG) is a progressive and chronic disorder that encompasses an unrelenting failure to resist impulses to gamble and where this ‘‘maladaptive behavior disrupts, or damages personal, family, or vocational pursuits’’ (American Psychiatric Association [APA], 1994, p. 615). There is a lack of systematic research about the course of the disorder. However, age of onset is usually during adolescence or early adulthood, and slightly later for females than for males (APA, 1994). In the gambling literature, three main terms: ‘‘problem gambling,’’ ‘‘compulsive gambling,’’ and ‘‘PG’’ have been used, and often interchangeably, to describe the above condition. The term ‘‘compulsive’’ is more often used by laypersons such as Gamblers Anonymous (GA) members, while the term ‘‘pathological’’ is more often used by clinicians. Presently, the term ‘‘problem’’ is preferred as it avoids the medical and pejorative implications of ‘‘pathological’’ (Walker & Dickerson, 1996). However, in some studies, the term ‘problem gambler’ is used to define someone whose gambling is at an earlier stage and to a lesser degree than required by the diagnostic criteria (clinical definition of gambling as a Diagnostic Statistical Manual (DSM) disorder of impulse control), while in others, it is used more to refer to both the pathological gamblers (PGs) and to those who do not meet the criteria (Rosenthal, 1989). Currently, most researches have assumed that the term ‘‘problem gambling’’ includes a wide range of difficulties with gambling, not merely the most severe as often represented by the term ‘‘PG.’’ Thus, in this paper, the term PG would be used to define gambling behavior that meets the diagnostic criteria, while the term ‘‘problem gambling’’ would be used in a broader sense to also include those individuals that may be experiencing gambling problems but do not meet the criteria. Some of the common social costs of PG include its negative impact on gamblers’ physical and mental health and performance in vocational situations (Productivity Commission, 1999). Financial hardship (via debts and asset losses) may lead to legal consequences, such as bankruptcy, loans, or criminal acts to gain money (Ladouceur, Boisvert, Pe`pin, Loranger, & Sylvain, 1994). Costs imposed by PG on the society include the cost of crimes committed by some gamblers and costs related to their treatment (Productivity Commission, 1999). Interpersonal problems between gamblers and their significant others include domestic violence, relationship breakdown, neglect of family, and the negative impacts on the physical and mental health of family members (Lorenz & Yaffee, 1986, 1988, 1989). Serious psychosocial problems in the children of PGs, such as substance abuse, delinquency,

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depression, suicide, and other behavioral and psychological problems are also common (Lorenz & Shuttlesworth, 1983; Lorenz & Yaffee, 1988). It was not till 1980 that PG was officially included in the DSM as a disorder of impulse control not otherwise specified (APA, 1994). Since then, the disorder has sparked much speculation and research regarding its nature, etiology, and treatment. In the present time, it is still gaining interest due to the liberalization of gambling and to the recent research that has suggested a possible link between increased rates of PG and increased accessibility to gambling (Campbell & Lester, 1999; Ladouceur, Jacques, Ferland, & Giroux, 1999; Productivity Commission, 1999). Liberalization of gambling not only impacts on the growth of the gambling industry by increasing the variety, availability, and accessibility of games; it also increases acceptance and support from societies and governments (Becona, Labrador, Echeburua, Ochoa, & Vallejo, 1995). Many researchers agree that this stimulates participation, which eventually leads to gambling problems (Moran, 1970; Productivity Commission, 1999). Studies from different countries have provided evidence that legalization of gambling and increased accessibility to gambling have led to an increase in the number of regular gamblers and problem gamblers (Campbell & Lester, 1999; Emerson & Laundergan, 1996; Jacques, Ladouceur, & Ferland, 2000). The total number of legal gambling opportunities has also been found to correlate positively with number of GA groups (Lester, 1994). While it is difficult to establish causation beyond any doubt, there is sufficient evidence to suggest an association between increased availability/accessibility to gambling and increased PG prevalence rates (Productivity Commission, 1999). The PG literature discusses many different forms of gambling, such as casino gambling (e.g., roulette, black jack), pari-mutuels (e.g., horse races), gaming machines, and lotteries. These different forms of gambling have been shown to have the potential of becoming problematic to varying degrees, but recent research suggests that gaming machines, especially modern video gambling machines, are now the leading form of gambling by PGs treated in several countries (Fisher & Griffiths, 1995). More recently with computer technology advances, gambling has developed on the Internet. Internet gambling (similar to gaming machines) also has the potential to become problematic due to its easy accessibility, rapid event frequency, and short payout intervals. Gambling on the Internet also allows anonymity as it enables one to play in the privacy of one’s own home (King & Barack, 1999). Several authors have reviewed the gambling and PG literature in the past (Allcock, 1986; Lesieur & Rosenthal, 1991; Murray, 1993). However, since then many studies have been completed that have provided new information regarding the nature, etiology, and treatment of PG. Although a recent review (Zuckerman, 1999) discussed a wide range of factors using a diathesis–stress model to explain the development and maintenance of PG, it did not comprehensively address certain factors (e.g., the cognitive and sociological factors). It also did not discuss theoretical models that have attempted to explain the development and maintenance of this disorder. Thus, there is currently a need for a comprehensive review of the research in this area. The present paper aims to provide such a review by examining the literature on gambling, problem gambling, and PG indexed within PsycINFO and Medline databases (all years up to the year 2001), using the search keyword ‘gambling’. From the

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resulting 1639 searches, articles focusing on economic-based and decision-making theories were discarded. The remaining articles were considered in preparing this review.

2. Prevalence Various studies have shown that 70–90% of adults gamble sometime in their lives (Ladouceur, 1991; Productivity Commission, 1999). Similar rates have been found for adolescents (Gupta & Derevensky, 1997; Shaffer & Hall, 1996). Current prevalence rates of PGs among community sample in a range of countries have been found to be around 1– 2% (Walker & Dickerson, 1996), while lifetime prevalence rates have ranged from 0.1% to 5.1% (Petry & Armentano, 1999). In contrast to the abundant prevalence rates that exist in the gambling/PG literature, there are very limited studies that explore incidences (number of new cases occurring over a specified period of time) of PG, and these studies have contradictory results. Some studies suggest no significant increase, in that rates of PG after introduction of a new gambling institution, such as opening a new casino (Govoni, Frisch, Rupcich, & Getty, 1998) or after the introduction of a new form of gambling such as introducing a new lottery (Shepherd, Ghodse, & London, 1998), while others have shown a link (Ladouceur et al., 1999; Shaffer, Hall, & Vanderbilt, 1997). Prevalence rates among general psychiatry patients also tend to be high—6.7–12% (Lesieur & Blume, 1990; Miller & Westermeyer, 1996). Among substance abusers, prevalence rates of PG have been found to be between 7% and 39% (Spunt, Dupont, Lesieur, Liberty, & Hunt, 1998). Comorbidity between substance abuse and PG has been linked to a history of childhood experiences of gambling among family members (Daghestani, Elenz, & Crayton, 1996) and high rates of stress-related diseases and serious psychiatric problems, including suicide attempts (Ciarrocchi, 1987). Slutske et al.’s (2000) study of 6744 adult male twins provided evidence to the possibility of a common genetic vulnerability for PG and alcohol dependence among men. More research is required to evaluate the differences and similarities between the risk factors for the two disorders as well as the risk factors of the comorbidity. Shaffer and Hall (1996) reviewed published and unpublished studies that estimated prevalence of adolescent gambling problems in the US and found that current prevalence rates of PG adolescents appear to be slightly higher (compared to community samples), around 4.4–7.4%, with another 10–14% at risk of developing severe gambling problems. More recent studies have confirmed these high rates of PG among adolescents (Gupta & Derevensky, 1998a; Westphal, Rush, Stevens, & Johnson, 2000; Wood & Griffiths, 1998) including studies undertaken in other countries such as Britain (Fisher, 1999), Canada (Poulin, 2000), and New Zealand (Clarke & Rossen, 2000). Lifetime prevalence rates and incidence rates of PG among adolescents have been less researched. High risk-taking, delinquency, impulsivity, and depression have all been shown to act as predisposing factors for developing PG among adolescents (Gupta, 2000). The methodologies of these prevalence studies have often been criticized. The first criticism refers to the definition of PG. Walker and Dickerson (1996) emphasized that

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although current prevalence of PG relates to ‘‘the percentage of cases of PG occurring in the community at a given time’’ (p. 236), most of the prevalence studies have not adhered to this definition. Most studies have tried to identify current prevalence by questioning whether gambling problems have ever happened, rather than if they are presently happening. This can lead to an overestimation of the current prevalence of PG in the given community. The second criticism refers to the reliability and validity of the South Oaks Gambling Screen (SOGS; Lesieur & Blume, 1987), the measure that is most often used in research studies to identify PGs (Walker & Dickerson, 1996). The SOGS was developed in a clinical setting, but is often used in general population studies. It was not till recently that Ferris, Wynne, and Single (1999) presented a measure (the Canadian Problem Gambling Index [CPGI]) to assess PG among the general public. In addition to the criteria and items of current measures of PG, which include gambling involvement, behavioral signs of gambling problems, and consequences of gambling problems, the CPGI includes items measuring cognitive and emotional factors related to PG as well as environmental factors and correlates. Several studies have raised the issue of obtaining high false-positives in general population surveys when using the SOGS to identify PGs (Abbott & Volberg, 1992; Dickerson, 1993). Abbott and Volberg (1992) also reported that individuals in New Zealand were more likely to respond positively to particular items than individuals in America. Such differences could be due to cross-cultural issues (Lesieur, 1994). Ladouceur et al.’s (2000) study that attempted to explore subjects’ (children, adolescents, and adults) understanding of the SOGS items, found that participants did not understand some items and a clarification of items reduced the number of subjects identified as PGs or probable PGs. Also, those studies that have used translated versions of the instrument have generally not reported the instruments’ reliabilities or validities (Ladouceur, 1991). It is important that future cross-cultural studies address this issue. Furthermore, assessment tools that have been used to measure PG such as the SOGS, Massachusetts Gambling Screen (MAGS; Shaffer, LaBrie, Scanlan, & Cummings, 1994), GA 20 questions, and the Lie/Bet screen (Johnson, Hamer, Nora, & Tan, 1997) have not been validated against one another (Yaffee & Brodsky, 1997). The third criticism involves the characteristics of the participants used in PG studies and whether they are the best representation of the population being assessed. Dickerson and Walker (1996) pointed out that prevalence studies do not properly define the community that they are sampling. These studies have been performed in a range of countries, most of which have a vast number of cultural groups and appropriate methods are not usually used to make sure that all of the cultural groups in a given community are fairly sampled. Exclusion of certain groups could also occur due to the method of sampling. Most telephone surveys would automatically exclude military living in barracks, those that are overseas, the homeless, youth (especially school dropouts and institutions such as college or university residences), and individuals in penal and mental health facilities (Lesieur, 1994). As gambling problems have been found at higher rates in these groups, exclusion of these groups can lead to an underestimation of PG rates found in the general population. There are other problems related to telephone surveying. Unlisted numbers may be a source of bias in that only households with high incomes can afford to pay a fee for that service.

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Also, those that do not have a phone are often low-income earners, unemployed, and younger adults. Those with serious gambling problems may not answer their telephones because they fear it may be a bill collector calling. Some individuals, especially immigrants, may not be able to talk in English, the language most researches are performed in. The other problem of using telephone surveys is the high nonresponse and refusal rates (Reilly & Guida, 1990), which also applies to field studies. Gamblers could be out of the home gambling or trying to find money to gamble with (Lesieur, 1994). Also, PGs may be tempted to deny or minimize their problems during telephone surveys, especially if there are other people around them.

3. Demographics PGs generally appear to be a heterogeneous group. However, several groups have been reported more likely to gamble and/or develop PG. Several factors including low socioeconomic status, lack of employment, low education levels, and low income have been linked to greater rates of PG (Hraba & Lee, 1995; Ladouceur, 1991; Shepherd et al., 1998; Volberg & Steadman, 1988). Some studies have shown that more males than females are identified as PGs (Volberg, 1994; Volberg & Steadman, 1988; Wood & Griffiths, 1998), although others have not (Hing & Breen, 2001; Ohtsuka, Bruton, DeLuca, & Borg, 1997). Research has documented that there are gender differences in gambling attitudes (Abbott & Cramer, 1993), betting behaviors (Bruce & Johnson, 1994), forms of gambling preferred (Hing & Breen, 2001), extent of gambling (Hraba & Lee, 1996), and differences in problems presented for treatment as well as treatment outcomes (Crisp et al., 2000). Researchers have suggested that there might also be some gender differences in the motivations towards gambling. Several studies indicate that females use gambling to escape personal (e.g., loneliness, isolation, and depression) or familial problems, whereas males gamble more for excitement and to win money (Brown & Coventry, 1997; Lesieur & Blume, 1991b). The exact nature of gender differences in the motivations towards gambling is still unclear. It must be noted, however, that the majority of research studies on PGs have focused only on male participants. Many studies in the gambling literature have a total or predominately male sample and have tried to generalize the findings to females. Some researchers have tried to identify groups of gamblers based on male samples, and then tried to fit females into these categories (Mark & Lesieur, 1992). Currently, there are no clear guidelines for health professionals to deal with female PGs (Spunt et al., 1998). Although some surveys have reported that PGs tend to be disproportionately young (Sommers, 1988; Volberg, 1993), others have not supported these findings (Legarda, Babio, & Abreu, 1992; Volberg & Steadman, 1989). While the state of research in youth and adolescent gambling is on the rise, there is still however, a lack of research on gambling behaviors in the elderly. Reasons for such a lack of research among the elderly are unclear. There is some suggestion that this group is vulnerable to begin gambling and consequently develop PG (McNeilly & Burke, 2000, 2001; Stewart & Oslin, 2001). This is especially

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significant as many elderly are on rigid incomes and even small losses can have significant financial and legal consequences (Stewart & Oslin, 2001). There is also a lack of awareness of the disorder among this group and they are more likely to hide or deny their gambling due to religious beliefs and age-related perceptions of how older adults should morally and ethically behave (Bazargan, Bazargan, & Akanda, 2001). The above discussion demonstrates variability in the results of studies investigating whether certain demographic groups are more likely to experience PG. Such variability could be related to the differences in methodologies used (e.g., variances in instruments and differences in sampling procedures used). A more consistent finding in this area of research involves high rates of gambling and PG among ethnic minorities (Cuadrado, 1999; Lesieur & Rosenthal, 1991; Productivity Commission, 1999; Zane & Huh-Kim, 1998; ) and among indigenous cultures in several countries (Volberg & Abbott, 1997; Zitzow, 1996a, 1996b). Several articles have reported significant gambling among certain ethnic groups such as the Chinese (Blaszczynski, Huynh, Dumlao, & Farrell, 1998; Chen, Wong, Lee, Chan-Ho, & Lau, 1993) and the Jewish (Ciarrocchi & Richardson, 1989; Lorenz & Shuttlesworth, 1983). Despite such findings, very little is known about the gambling and PG patterns among different cultural groups (Raylu & Oei, 2001). Psychological literature has shown that cultural variables such as cultural values and beliefs, effects of acculturation and culturally related help-seeking behaviors are often associated with increased rates of psychological problems among certain cultural groups (Raylu & Oei, 2001). Currently, there is a major gap in the gambling literature on cultural factors that may play a role in the development and maintenance of problem gambling. There are also differences between people who pursue different types of gambling. Smart and Ferris (1996) found that lottery players, compared with other gamblers, were more likely to be female, poorer, and older. Kroeber (1992) found that gamblers who played gaming machines excessively began to play at an earlier age (average age of 19 vs. 30 years), and were more likely to be of lower socioeconomic status compared with excessive roulette gamblers. It was also found that excessive roulette gamblers had significantly more disturbed personalities and often had a more psychosocially disturbed lifestyle (e.g., loneliness, social decline, large debts, and criminal lifestyle) compared with machine gamblers. Currently, very little research exists that explores why different groups of individuals choose different forms of gambling and the processes that are involved in determining which forms of gambling are chosen.

4. Factors implicated in the development and maintenance of PG No motive for gambling has been consistently identified among social gamblers and PGs (Murray, 1993). The exact reason why one starts gambling is still unknown. Several motivations are implicated in literature. These include demonstrating one’s worth, getting approval and social acceptance from others, rebelling, relieving negative and painful events/ emotions (e.g., anger, depression, frustration, and anxiety), hoping to win, participating due to social reasons, trying to beat the odds, participating in a favorable activity, and participating

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to experience the excitement (e.g., to reduce boredom), passing time, and having fun (Blaszczynski, 1995; Cotte, 1997; Dumont & Ladouceur, 1990; Griffiths, 1991a, 1993a; Productivity Commission, 1999). Chantal, Vallerand, and Vallieres (1995) identified two categories of motivational profile for gamblers: self-determined motivational profile (SDMP) and non-self-determined motivational profile (nSDMP). The SDMP included intrinsic motivation (e.g., gambling for excitement, a sense of accomplishment, or an opportunity to broaden knowledge) or identified regulation (e.g., gambling to reach a goal such as socializing with friends). The nSDMP included external regulation (e.g., gambling to gain external rewards such as to win money). They measured motivation among 186 male and 59 female gamblers who bet on horses and found that those with high-SDMP were more involved in gambling and more likely to continue gambling than low-SDMP gamblers, who gambled for external reasons (e.g., to win money). Chantal and Vallerand (1996) found that subjects with SDMP were more involved in skill games (e.g., horse racing) possibly because they encourage fun and self-involvement and are challenging. Individuals with nSDMP were more involved in games of luck (e.g., lottery) possibly because they prohibit self-involvement and orient gamblers towards material gains. Motivations appear to vary in different geographical locations. Zimmer (1985) stated that during her fieldwork among the Gende people in Madang Province in the early 1980s, she discovered that villagers used card games as a means of minimizing income variations and the negative social effects resulting from the unbalanced distribution of money among village households. The game network provided the villagers opportunities to display their kindness for others and create an environment where less privileged individuals were given the opportunity to obtain money and to enjoy the friendly and relaxed social atmosphere of the game. Brenner and Lipeb (1993) studied attitudes toward gambling in the two cities of Cameroon and found that lottery playing in Cameroon was strongly associated with the economic crisis that has been occurring in the country for a number of years. However, caution must be taken with such results as this was a correlational study between those groups most affected by the economic crisis (e.g., those with lower income or young age) and lottery playing. Such correlation does not necessarily indicate causation. Research continues to determine factors that encourage individuals to begin gambling or continue gambling despite continuous losses and, thus, increase their chances of developing PG. At present, there are several variables that have been identified in the gambling literature as playing a role in the development and maintenance of PG. These include familial factors (social learning and genetics), sociological factors (social factors), and individual factors (personality, biological/biochemistry, cognition, and psychological states). 4.1. Familial factors—social learning and the role of genetics The role familial influences play in the cause, development, or maintenance of PG can be viewed from two perspectives, that is, the genetics and the social learning perspective. Social learning theory suggests that individuals learn, model, and maintain behaviors that are observable and are reinforced. Thus, family members as well as friends can often act as

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significant models for gambling. Children who gamble tend to gamble with friends and family members (Daghestani et al., 1996; Gupta & Derevensky, 1997). Although there is a lack of systematic family prevalence studies for PG, several studies have included questions about parental or family gambling and their coincidences with gambling problems. However, none of these studies interviewed the parents of gamblers or used the standard PG diagnostic measures (Zuckerman, 1999). In Lesieur et al.’s (1991) study of 1771 university students, among the subjects who said either of their parents had gambling problems, 19% were PGs themselves, compared to 5% of the remaining sample that did not report gambling problems in their parents. Jacobs et al. (1989) surveyed 844 children and found that those who had parents that gamble reported more gambling-related problems (29%) compared to peers (14%). Retrospective studies conducted among adult PGs reveal that 25– 40% of their parents had a gambling problem (Custer, 1982; Jacobs, Marston, & Singer, 1985). Lesieur and Rothschild (1989) surveyed 105 children of GA members and PGs in treatment concerning behavioral, psychological, and emotional problems. They compared results to Jacobs et al.’s (1989) study and found that children of PGs were less likely to gamble, contradicting the results found in Jacobs et al.’s study. However, children from multiple-problem families (i.e., where PG parents were also experiencing other problems including substance abuse and overeating) appeared to be experiencing at least as many, and sometimes more, problems than children in Jacobs et al.’s study. Several reasons were provided for these contrary results. Firstly, children of PGs in Lesieur and Rothschild’s study could have come from ‘disrupted but fairly stable families’ (e.g., two-parent households), considering most were GA members. Volberg and Steadman (1987), as cited by Lesieur and Rothschild, reported that PGs who attend GA are less likely to be divorced than PGs in the general population. Children whose parents do not attend GA may be at a greater risk for psychological, behavioral, emotional, and other problems. Secondly, attendance at GA may help minimize escalation of problems in only the families of pure gamblers. Thirdly, the discrepancy could be due to the differences in the sampling procedures used in the two studies. Finally, differences could also be attributed to the fact that Jacobs et al.’s study did not control for multiple problems on families. PGs that are in substance abuse treatment programs tend to have a much greater prevalence of PG among their family members, especially their fathers (Lesieur & Heineman, 1988). Gambino, Fitzgerald, Shaffer, Renner, and Courtnage (1993) explored rates of PG among 93 veterans attending clinics for substance-related problems and other mental disorders. They found a link between parental (and grandparental) problem gambling and PG. Lesieur, Blume, and Zoppa (1986) studied parental gambling among inpatients in an alcoholic and drug treatment center and found that 38% of the children of PGs were PGs themselves. However, this was determined by interviews with significant others and a predominately male sample. In a substance abuse hospital, Daghestani et al. (1996) found that 49% of PGs had family members with gambling problems. Zuckerman (1999) stated that this greater prevalence of PG among family members of dual addicts could be attributed to either the retrospective bias of these individuals or the high comorbidity of PG among substance abusers. The discussion above at least suggests that familial factors can increase the risk of gambling and PG. Linden, Pope, and Jonas (1986), however, found that only 1% of the first-

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degree relatives of a group of members of GA were PGs. Eisen et al. (1998) investigated the familial contributions (i.e., inherited factors and/or experiences shared by male twin siblings during childhood) to PG symptoms and the disorder. Using 3359 twin pairs, they showed that heavy gambling without PG symptoms had a heritability of 0.35 and was increased to 0.54 when there were at least two symptoms of PG from the DSM-III (APA, 1980). In addition, familial factors explained 56% of the variability when there were three or more symptoms of PG and they explained 62% of the variability given the diagnosis of PG. A similar study with females may be beneficial in understanding gender differences in relation to familial contributions and the development of PG. Winters and Rich (1998) tried to determine the extent of genetic influences on gambling behavior among 155 young adult twin pairs. They found that kinship had a nonsignificant relationship with overall gambling involvement, onset of gambling, and for most forms of gambling. However, for only the ‘‘high-action’’ games (heavy player promotion and high payoffs), male monozygotic twins were similar in their frequency of gambling. For females, the association between gambling frequency and kinship was only found for gaming machines. Although this study points to the importance of genes in the development of PG, generalization of the results is difficult as the study did not consider environmental or personality factors. Further exploration of gender differences is required. A molecular genetic study of PG provided strong evidence of a shared genetic component for PG (Comings et al., 1996). The Taq A1 variant of the human DRD2 (dopamine 2 [D2] receptor) gene that has already been linked with drug addiction and alcoholism has been suggested to be associated with PGs. Of 171 PGs, 51% had the D2A1 allele compared to 26% of controls. Frequency of the allele also varied with the severity of the gambling problem. It was also found that although comorbidity with alcohol or drug abuse increased the frequency of the allele, depression was associated with a reduced frequency of the allele especially for females. Although depression is often associated with PG (especially for females), it may represent ‘‘an alternative nongenetic association’’ with PG (Zuckerman, 1999, p. 309). 4.1.1. Summary There is evidence for the role of genetics as well as social learning in the development and maintenance of PG. Systematic family prevalence studies for PG, as well as twin and adoption studies which could distinguish between genetic and shared environmental effects, would be useful (Zuckerman, 1999). Winters and Rich’s (1998) study showed an association between genetics and excessive gambling only for some forms of gambling. Further investigation is required in order to explore this. Furthermore, the role familial factors play in determining the form of gambling an individual chooses, also needs investigation. Gender and cultural differences in this area also require some research. 4.2. Sociological factors A sociological perspective assumes that PG may be a response to an inability to cope with the larger society. Gambling helps create a more controllable subculture where life is less complex and more rewarding. Sociological research attributes social structures (i.e., facilities

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and social relationships) within a gambling environment as playing a role in the development and maintenance of PG. Sociological explanations suggest that gambling lies on a spectrum with social gambling at one end and PG on the other. Sociological research has mainly been done in gambling settings, through intensive interviews and observations with gamblers of all types rather than focusing on PGs in treatment (Lesieur, 1987). By observing gamblers in a cardroom, Hayano (1982) reported that besides providing its regular gamblers with a range of goods and services, the contact between the gamblers and employees of the cardroom encouraged social interaction. It is this self-enclosed system that reinforces gambling and generates further pressures for the individual to continue gambling despite losses. Martinez (1983) stated that within a gambling environment, formal and informal norms help reduce the tension and pressure while gambling. If a player violates these norms, it has a significant impact on their acceptance in the system/environment and subsequently has an impact on their gambling. Rosecrance (1986, 1988) reported that inveterate horse race gamblers continued gambling despite losses, as the rewards of gambling were greater than the costs. These rewards include ‘‘social interaction, sensory stimulation, economic gain, decision-making opportunities, and demonstration of character’’ (Ocean & Smith, 1993, p. 322). Ocean and Smith (1993) examined the relationships between regular gamblers, the gambling institution (casino), and the outside society through a range of methods including surveys, participant observations, and in-depth interviews. They found that the social rewards available in the casino (e.g., group membership, emotional and moral support, self-esteem, and social status) and the gamblers’ problems with the outside society (e.g., loss of outside social networks and value conflicts) played a role in encouraging regular gamblers to continue gambling despite losses. A ‘double reinforcement’ process occurs, where social rewards operate as positive reinforcers, while the gambler’s problems with the outside society operate as negative reinforcers. Variables such as age, gender, immigration status, ethnicity, marital status, income, education, employment status, and social status can further influence an individual’s gambling patterns. For example, for gamblers that belong to lower status and minority groups (e.g., immigrants, ethnic minorities, and the poor), social rewards may be more appealing and thus, these individuals may be more attracted and committed to the gambling institution. This could increase their chances of developing PG. Treatments based on the sociological approach try to take gamblers out of a gambling subculture that is rewarding their behavior and place them back into mainstream society by teaching them how to stop or control their gambling (Ocean & Smith, 1993). These goals can be achieved by teaching gamblers relevant coping skills, guiding them to develop alternative reward systems, and helping them reestablish or strengthen ties with family, friends, and the community (Peele & Brodsky, 1992). The major strength of the sociological perspective is its focus on environmental and cultural factors, which is a limitation of other approaches. There are, however, some doubts as to the sociological explanations of PG. Individuals who gamble on gaming machines usually play alone and generally are not involved in conversation with other gamblers. Caldwell (1974) highlighted the social rules, which exist in relation to playing gaming machines. It was suggested that stringent rules of access to machines appear to be maintained via social

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agreement. If gamblers used the machines only to gain social interaction, these regulations would not be so thoroughly practiced and players would not need to protect their machines against each other (Walker, 1992a). Griffiths and Minton (1997) carried out an observational study of machine gamblers in two amusement arcades in England. It was found that mostly adolescent males visited the arcades and they played the machines alone, even when they came to the arcades as a group. It is possible that the social interaction and other comforts found in the gambling environment provide the motivation to begin gambling and encourage continued gambling, only for some gamblers. The sociological theory has also been criticized for its lack of clinical focus (Lesieur & Rosenthal, 1991). 4.2.1. Summary Although sociological explanations take into account environmental and cultural factors, they have limited clinical utility and may not apply to all forms of gambling. It is possible that sociological factors are relevant for some gamblers (e.g., card gamblers) and not for others (e.g., machine gamblers). 4.3. Individual factors Several individual factors have been implicated in the development and maintenance of PG. These include personality, biology/biochemistry, cognitions, and psychological states. Each are discussed below. 4.3.1. Personality Numerous researchers have tried to identify core personality traits of PGs, who appear to be a heterogeneous group. However, there is a consensus among researchers that certain personality traits may act as a risk for gambling or developing PG. These include sensationseeking and impulsivity. Some other related traits mentioned in the literature include psychoticism and neuroticism. Antisocial personality disorder, narcissistic personality disorder, and attention-deficit hyperactive disorder (ADHD), all of which are associated with the above traits, have also been linked to PG. Each of these is discussed below. 4.3.1.1. Sensation-seeking. Sensation-seeking is a dispositional characteristic that involves a desire for diverse, new, and complex feelings and experiences and taking risks in order to achieve this. High sensation-seekers are likely to participate in risky activities such as gambling (Coventry & Brown, 1993). Sensation-seeking is also related to the arousal hypothesis of gambling which suggests that rather than the money, it is the excitement of playing which acts as a reward for PGs (Anderson & Brown, 1984). Dickerson (1984) suggested that there is a range of stimuli in gambling situations (including the spinning wheel, the croupier’s calls, placing bets, and other activities at roulette) that act as reinforcers by producing excitement and arousal. Through observations of last-second wagers at off-course betting shops, Dickerson (1979) found that high-frequency gamblers were more likely to place their bets in the last 2 min allowed than were low-frequency betters. This has a reinforcing effect by producing excitement and

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arousal in the players. Also, using higher wagers and increasing the possibility of winning greater amounts of money produce greater excitement and arousal. PGs continue gambling despite losses, which may ultimately lead to deprivation, which further gambling helps relieve (Dickerson, 1984). Early laboratory investigations of heart rate as a measure of arousal found no significant changes in heart rates for regular gamblers (Rule & Fischer, 1970; Rule, Nutler, & Fischer, 1971). However, Anderson and Brown (1984) found that heart rates of regular gamblers did not increase in laboratory conditions but did in field conditions (e.g., the casino), emphasizing the issue of ecological validity. Currently, there is vast amount of empirical evidence that regular gamblers become aroused during gambling regardless of whether arousal was assessed via heart rate measurements (Anderson & Brown, 1984; Griffiths, 1993a; Leary & Dickerson, 1985), self-reports (Griffiths, 1991b; Wray & Dickerson, 1981), or psychometric questionnaires (Dickerson & Adcock, 1987; Dickerson, Hinchy, & Fabre, 1987). This has been found for a range of games, including blackjack (Anderson & Brown, 1984), gambling machines (Coulombe, Ladouceur, Desharnais, & Jobin, 1992; Griffiths, 1993a; Leary & Dickerson, 1985), and horse race gambling (Blaszczynski, Winters, & McConaghy, 1986). Although there are some suggestions that high-frequency gamblers get more aroused during gambling than low-frequency gamblers, the evidence for this hypothesis is controversial. Leary and Dickerson (1985) found significantly greater heart rate increase during machine gambling in high-frequency compared to low-frequency players. Some studies have not replicated these findings (Coulombe et al., 1992; Griffiths, 1993a). However, Griffiths (1993c) did report preliminary evidence for the tolerance phenomenon (when individuals need increasing levels of experience in order to achieve the same levels of excitement/ pleasure). He investigated the psychophysiology using heart rate measures in 15 frequent and 15 nonfrequent male and female gamblers and found no differences in heart rates between the two groups. However, during gambling, heart rates increased for both groups. The heart rate of frequent gamblers reduced after play, whereas those of nonfrequent gamblers did not. It must be noted that there are methodological problems in using heart rates as a measure of arousal, as the heart rate oscillates greatly in relation to motor activity, relaxation, and adaptation to experimental conditions (Coventry & Norman, 1997). Coventry and Norman (1997) controlled for the confounding effects of movement on heart rates present in earlier studies and investigated arousal in 32 male off-course horse racing gamblers before, during, and after the gambling process, together with sensation-seeking and gambling behavior/patterns. No differences were found when comparing high- and lowfrequency gamblers or gamblers that chase (persisted effort and using increased money to try and regain the money they have lost) with those that do not. They suggested that during gambling activity, arousal is likely to be a by-product of an interaction between cognitive strategies the gambler employs and the information from the gambling setting itself. Therefore, arousal can increase for two different reasons. Firstly, the more exciting the game, the greater the arousal experienced by the gambler (e.g., when the gambler is winning the game). Secondly, it is likely that cognitions of a gambler help determine the amount of arousal experienced. The role of cognitions in the development and maintenance of PG is explored in later sections of this article.

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The levels of arousal that people prefer appear to be related to the type of gambling chosen. Cocco, Sharpe, and Blaszczynski (1995) assessed levels of anxiety, preferred state of arousal, and motivations to gamble among 12 problem machine gamblers and 13 problem horse race gamblers. They found that problem horse race gamblers preferred heightened levels of arousal and appeared to gamble to achieve these desired levels of arousal, whereas machine gamblers were more anxious and tended to avoid arousal. Several studies have found higher sensation-seeking among problem gamblers (Breen & Zuckerman, 1999; Kuley & Jacobs, 1988). Blaszczynski, Wilson, and McConaghy (1986) contradicted this, demonstrating that male PGs in their sample did not have elevated sensationseeking scores compared with controls. They suggested that such individuals were not necessarily seeking sensation but rather, were trying to avoid or reduce negative states (e.g., loneliness or boredom). Further support for this notion comes from studies reporting that PGs have elevated boredom proneness (Blaszczynski, McConaghy, & Frankova, 1990) and that PGs report gambling to reduce boredom and loneliness (Coman, Burrows, & Evans, 1997). Kuley and Jacobs’ and Breen and Zuckermans’ studies had a totally male sample. Other studies assessing sensation-seeking among problem gamblers have found some evidence that sensation-seeking is associated with excessive gambling with samples of both genders. Moore and Ohtsuka (1997) found venturesomeness (a trait similar to sensation-seeking) was associated with gambling frequency in youths of both sexes. However, high venturesomeness did not predict problem gambling. High sensation-seekers were probably trying out a range of gambling activities but not necessarily getting hooked. Powell, Hardoon, Derevensky, and Gupta (1999) studied whether risk-taking and/or sensation-seeking helped in distinguishing PGs from nonproblem gamblers using 63 gamblers. Results indicated that risk-taking and sensation-seeking scales distinguished between probable/PGs and nonproblem gamblers, with probable/PGs scoring the highest on each measure. Risk-taking was the only measure able to distinguish probable/PGs from gamblers experiencing some problems relating to their gambling behavior. Also, females encountering some problems resulting from their gambling behavior consistently reported higher risk-taking and sensation-seeking scores than males with no gambling problems. These studies are of gamblers in the community (i.e., not in treatment). PGs seeking or those that are in treatment have either shown no difference or lower sensation-seeking scores than non-PGs or controls (Allcock & Grace, 1988; Blanco, Orensanz-Munoz, Blanco-Jerez, & Saiz-Ruiz, 1996; Blaszczynski et al., 1990; Blaszczynski, Wilson, et al., 1986). Zuckerman (1999) provided two suggestions as to why sensation-seeking might be low among the sample in treatment or posttreatment compared to those that are not. It is possible that only those PGs that are low sensation-seekers pursue treatment. Alternately, treatment itself may influence sensation-seeking inclinations among PGs. It is difficult to determine whether sensation-seeking leads to gambling or gambling increases an individual’s tendency to be a sensation-seeker. Being a sensation-seeker may predispose an individual to gamble but gambling may also change the personality of the individual (e.g., heavy financial losses due to excessive gambling may lead to depression which may lead to a decrease in sensation-seeking). It may also be possible that sensationseeking is more relevant for some types of gambling but not others due to differences in

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forms of gambling. For example, sensation-seeking could be relevant for casino gamblers and for people who participate in illegal gambling (Dickerson, 1993). Coventry and Brown (1993) found that those who only bet in the off-course betting offices, scored lower on sensation-seeking than nongamblers and individuals in the general population. However, those who bet on several forms of gambling and/or in the casino, scored higher on sensationseeking than the general population and nongamblers. Also, Coventry and Brown found that sensation-seeking in off-course gamblers correlated with subjective arousal, bet size, gambling expenditure, and loss of control, supporting Anderson and Brown’s (1984) and Dickerson et al.’s (1987) findings that sensation-seeking may influence the loss of control in a gambler. Other researchers have also found such differences in personality traits associated with different forms of gambling. Adkins, Kruedelbach, Toohig, and Rugle (1988) found that gamblers who played games that required low skill (e.g., machine gambling) scored significantly higher on social extroversion and lower on hypomania than gamblers who played games that required high skill (e.g., horse race gambling). 4.3.1.2. Impulsivity. Impulsivity, a core dimension of human personality, can be defined as spontaneous or unintentional behavior where one acts without thought or self-control. It has been seen as an important factor in a number of clinical problems (APA, 1994). Steel and Blaszczynski (1996) pointed out that even a couple of decades ago, studies were demonstrating that impulsivity might be an important component in PG (Allcock & Grace, 1988; Moran, 1970). However, most of those studies did not use psychometrically validated measures of impulsivity. Allcock and Grace’s (1988) study was the only published study that had employed a psychometrically validated measure of impulsivity with PGs. This study compared 10 PGs, 10 alcoholics, and 10 drug addicts with 25 control subjects drawn from a population of hospital or associated staff. It was found that PGs did not differ from controls on sensation-seeking or impulsivity. However, until recently, results remained inconclusive given the relatively small sample size in this study. Research over the past couple of years has provided increasing evidence that impulsivity is a major characteristic of PG. Several recent studies found that PGs score higher on impulsivity compared to nongamblers, recreational gamblers, and low-frequency gamblers (Carlton & Manowitz, 1994; Steel & Blaszczynski, 1998). Vitaro, Ferland, Jacques, and Ladouceur (1998) investigated whether problem gambling and substance use are related and linked to impulsivity using a community sample of 765 adolescents. They found that comorbid participants were more impulsive than those that either had problems only with gambling or only with substance use. They proposed the possibility that PG and substance use problems develop at the same time during adolescence and are related to a deficit in impulse control. Impulsivity is a major characteristic of ADHD. There is evidence that links PG with ADHD. On self-report measures, PGs characterized themselves as having had greater than normal numbers of ADHD symptoms when they were children (Carlton & Goldstein, 1987; Carlton & Manowitz, 1992; Carlton et al., 1987; Goldstein, Manowitz, Nora, Swartzburg, & Carlton, 1985; Rugle & Melamed, 1993). Specker, Carlson, Christenson, and Marcotte (1995) investigated occurrence of attention-deficit disorders (ADD) and impulse control disorders in 40 PGs in treatment for gambling problems and 60 controls. ADD was seen in

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20% of the gamblers. An impulse control disorder, other than PG, was seen in 35% of the gamblers, compared to 3% of the controls. Rugle and Melamed (1993) found that PGs compared to nongamblers scored lower on all measures of attention, including all measures of frontally mediated attention processes. Although these studies are retrospective and have small sample sizes, the findings support the notion that attention deficit may act as a risk factor for the development of impulse control disorders such as PG. Aspects of impulsivity such as the inability to delay gratification and concentrate on the long-term consequences of the behavior, as well as the absence of an internalized value system that regulates action, have been reported to be frequent issues in therapy with PGs (McCormick, Taber, Kruedelbach, & Russo, 1987). McCormick et al.’s (1987) study of the personality of 70 PGs in treatment compared to 70 medical/surgical controls also found that gamblers and alcoholics differed significantly from hospitalized controls on measures of socialization, ego control, and flexibility. This was supported by Livingston (1974) and Taber, Russo, Adkins, and McCormick (1986) who reported low ego strength and possibly high incidence of narcissistic personality disorder among PGs. Rosenthal (1986) suggested that PGs use defensive strategies to deceive themselves and others. Gamblers seeking treatment have been shown to score higher than norms on impulsivity (Blaszczynski, Steel, & McConaghy, 1997; Castellani & Rugle, 1995). Steel and Blaszczynski (1998) demonstrated increased impulsivity among clinic samples of PGs compared to normative data. They also showed that impulsivity is related to the severity of gambling behavior. These studies used gamblers in treatment and found differences in impulsivity but not differences or even lower scores on sensation-seeking. It is possible those gamblers in treatment are ready to control their impulsivity but not their desire for excitement and diversity (Zuckerman, 1999). Breen and Zuckerman’s (1999) study of 248 male college students found that impulsivity discriminated chasers from nonchasers. It is likely that impulsivity compared to sensation-seeking may be more fundamental in relation to PG as the chasing component is more distinctive of PGs compared to nongamblers or nonproblem gamblers (Zuckerman, 1999). It is possible that sensation-seeking and impulsivity operate at two separate stages of PG. Sensation-seeking may motivate some gamblers (especially young ones) to participate in different forms of gambling, whereas impulsivity may drive them to continue gambling despite heavy or continuous losses (Zuckerman, 1999). 4.3.1.3. Other related traits—neuroticism, psychoticism, and extraversion. Since sensationseeking and impulsivity have both been related to the trait of psychoticism, and the neurotic aspects of PG have often been linked with depression, it may be predicted that PGs score high on both psychoticism and neuroticism. Also, according to Gray’s (1981) theory of introversion and extraversion, extraverts should demonstrate stronger reactions to stimuli of reward than stimuli of punishment. Thus, it may be predicted that PGs would be more extraverted than non-PGs. There is, however, mixed evidence regarding these traits among PGs. Blaszczynski, Wilson, et al. (1986) reported that PGs compared to the general population have elevated psychoticism and neuroticism scores. High psychoticism scores have also been found in older PGs (Blaszczynski, Buhrich, & McConaghy, 1985). Carroll and Huxley (1994) found only elevated psychoticism scores (but no difference in neuroticism or extraversion

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scores) in young slot machine players. Barnes and Parwani (1987) measured depression and personality of 20 PGs and 20 nongambling blue-collar workers, and found that PGs showed significantly higher mean scores on neuroticism and depression. In regard to extraversion, although Bartussek, Diedrich, Naumann, and Collett (1993) found evidence for this, other studies have failed to show that regular problem gamblers are more extroverted than social gamblers or nongamblers (Barnes & Parwani, 1987; Malkin & Syme, 1986). It must be noted that gamblers who had completed a treatment program with success, showed a noticeable decrease in neuroticism and anxiety scores compared to those that were still gambling (Blaszczynski, McConaghy, & Frankova, 1991). It is possible that treatment helps gamblers cope with stresses their gambling problems produce and this is reflected in reduced anxiety and neuroticism at posttreatment (Zuckerman, 1999). Psychoticism and neuroticism have often been linked with antisocial personality disorder (ASPD). Roy, Custer, Lorenz, and Linnoila (1989) investigated whether 19 male PGs demonstrated significant differences on personality scores compared with 18 male normal controls. Besides having significantly higher neuroticism and psychoticism scores than controls, PGs also had significantly higher hostility scores than controls. Bolen, Caldwell, and Boyd (1975) and Lowenfeld (1979) presented evidence that PGs scored highly on psychopathic deviate subscale of the Minnesota Multiphasic Personality Inventory (MMPI). In a group of PGs in a treatment agency, the average T score on the psychopathic deviance scale was about three times greater than that of the norm. Also, the most common profile on the MMPI for these PGs was similar to the characteristic profile of individuals with ASPD (Graham & Lowenfeld, 1986). Evidence supports the contention that PGs are at high risk for committing criminal offenses in order to maintain their gambling behavior. Several studies have shown that between 21% and 85% of PGs commit gambling-related crimes (Blaszczynski, 1994; Blaszczynski & McConaghy, 1994a; Meyer & Fabian, 1992; Templer, Kaiser, & Siscoe, 1993). Those that resort to crime are more likely to experience severe gambling-related problems, multiple forms of gambling, excessive gambling, debts, suicidal ideation, excessive drug and alcohol use, mental health treatment, and more psychosocial problems (Meyer & Fabian, 1992; Potenza et al., 2000). Those PGs that resort to crime are often engaged in offenses such as larceny, embezzlement, and the direct theft of money for gambling, mostly nonviolent crimes against property (Blaszczynski & McConaghy, 1994b). Most of these conclusions are based on male PGs. One study that explored gambling-related crime among females reported that female PGs also get involved in crime to support their gambling. Females, however, were more likely than males to pass bad checks and less likely than males to get involved in frauds, larceny, burglary, selling drugs, and dealing with stolen items (Lesieur & Blume, 1991b). Meyer and Stadler (1999) investigated the impact of gambling problems on criminal behavior among 300 PGs in treatment and 274 high- and low-frequency gamblers from the general population and the army. Although a causal analysis suggested that the gambling problem was an important variable in explaining criminal behavior among PGs, this variable alone could not explain criminal behavior among PGs. Personality variables were found to directly affect the intensity of criminal behavior.

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Blaszczynski and McConaghy (1994b) found that among PGs that resorted to crime as a consequence of their gambling problems, approximately 15% met the criteria for ASPD compared with 4.5% among the general adult male population. The authors concluded that while antisocial personality traits may act as a risk factor in increasing the probability of offending, there is no evidence to suggest that the majority of offending PGs suffer from ASPD. Other authors have suggested that antisocial features in the majority of cases emerge as a consequence of PG (Blaszczynski et al., 1997). A twin study by Slutske et al. (2000) provided a possible shared common genetic vulnerability between PG and antisocial behaviors such as ASPD, conduct disorder, and adult antisocial behavior. 4.3.1.4. Personality disorders. There is also evidence of high rates of some personality disorders among PGs. Black and Moyer (1998) found that 87% of 30 PGs had at least one personality disorder, the most common being obsessive – compulsive disorder (OCD), avoidant, schizotypal, and paranoid personality disorders. PGs in this study also had a relatively high rate of ASPD, supporting the above discussion. Blaszczynski and Steel (1998) investigated prevalence of personality disorders in 82 PGs in a treatment program for gambling problems. They found that 93% of the subjects met diagnostic criteria for at least one personality disorder and there was a mean of 4.6 personality disorders per gambler. Most of these personality disorders belonged to the Cluster b personality disorders (i.e., personality disorders that appear to be dramatic, emotional, and erratic such as borderline, histrionic, and narcissistic personality disorder), and were linked to high impulsivity and affective instability. It was also reported that ASPD and narcissistic personality disorder may be associated with the severity of the gambling problem. The high level of personality disorder found in this study contradicted those found in Specker, Carlson, Edmonson, Johnson, and Marcotte’s (1996) study, which reported that only a quarter of their 40 volunteer problem gamblers (representing 60% of gamblers receiving treatment in an outpatient treatment program) had a personality disorder. They also failed to find high rates of Cluster b personality disorders. Such variability could be due to differences in assessment procedures used to identify personality disorders, differences in the onset of problem gambling, and differences between volunteer and nonvolunteer samples (Blaszczynski & Steel, 1998). 4.3.1.5. Summary. The above discussion on the role of personality in the development and maintenance of PG suggests that PGs differ from nongamblers or other gamblers in some personality traits. Strongest evidence exists for impulsivity. In regard to sensation-seeking, it appears to be more significant for younger individuals, for only some forms of gambling, and less in those individuals who are in treatment. As Zuckerman (1999) highlighted, it is possible that sensation-seeking and impulsivity operate at two separate stages of PG. Sensation-seeking may encourage some gamblers (especially young ones) to participate in different forms of gambling, whereas impulsivity may encourage them to continue gambling despite losses. Impulsivity compared to sensation-seeking may be more fundamental in relation to PG as the chasing component is more distinctive of PGs compared to nongamblers or nonproblem gamblers (Zuckerman, 1999). It is also possible those gamblers in treatment are ready to control their impulsivity but not their desire for excitement and diversity (Zuckerman, 1999).

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Although there is evidence of other related personality traits among PGs (e.g., extraversion, neuroticism, psychoticism, and narcissistic and antisocial characteristics), the evidence for them is weaker and less consistent. Further research might be necessary to understand the role of these traits in PG. The one strength of the personality theories that attempt to explain the development and maintenance of PG is that they allow some agreement in terms of the personality traits that underlie PGs (Ferris et al., 1999). Categorization can guide therapists in treatment. However, there is little consistency in personality theory. There appear to be several types of gamblers, and the personality profiles of these types of gamblers are quite different, making it impossible to generalize to the profile of PG. Also, existing personality studies in the PG literature contain several methodological weaknesses. Most of these studies have not distinguished the forms of gambling and other gambling factors such as the amount of time and money spent on gambling (Zuckerman, 1999). It is possible that certain personality types are more susceptible to certain forms of gambling and not others. The existing research has predominately looked at Caucasian male samples and thus, it is hard to generalize results to female PGs or PGs from other cultural groups. Research is also required to investigate how these personality factors affect treatment outcomes. 4.3.2. Biological/biochemistry Different approaches have been taken to illustrate a biological role among PG, including examination of endorphin and plasma uric acid levels, EEG waves, and brain chemical imbalances (e.g., noradrenaline, serotonin, and dopamine). Biologically based theories suggest that there is some physiological condition, or tendency, which results in PG. Although research in this area is still in its infancy, several biological factors have been linked to PG, including hemispheric dysregulation, chemical imbalances/dysfunctional neurotransmitter systems, and physiological arousal. 4.3.2.1. Hemispheric dysregulation. Hare and McPherson (1984) hypothesized that in psychopaths, the left hemisphere is not as specialized for linguistic processing as in normals, and this lack of mature lateralization could be responsible for the dissociation between cognitive and emotional functioning. This suggests that there might be a hemispheric dysregulation among impulse control disorders. Since PG is classified under impulse control disorder, such an explanation may also be true for PG. Goldstein et al. (1985) compared EEG patterns of eight recovered PGs to controls matched on income and education. Subjects viewed two tasks (verbal and spatial tasks) under two conditions, eyes open and eyes closed. PGs showed less differential hemispheric activation than non-PGs as well as a reversal of normal hemispheric differentiation. This was similar to the EEG patterns noticed in children with ADHD (Carlton & Goldstein, 1987). Gamblers performed worse than controls on higher-order attention measures, and were more likely to report childhood behaviors consistent with attention deficits. Neurophysiological tests have also demonstrated frontal lobe lesions with a profile of hypometabolism (Carlton & Goldstein, 1987) similar to that found in children with ADHD. This suggests that PGs may be distinguished by dysfunctional attentional mechanisms similar to those suggested for

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alcoholism and ADHD and supports studies that have reported increased rates of ADHD symptoms among PGs (Rugle & Melamed, 1993). 4.3.2.2. Neurotransmitter systems. Several studies have suggested that there are disturbances in neurotransmitter systems among PGs. Blanco, Ibanez, Saiz-Ruiz, Blanco-Jerez, and Nunes (2000) provided a summary of these studies. Most of these are summarized below. Serotonergic system. The enzyme monoamine oxidase (MAO) is one of the most dependable biological markers of sensation-seeking and impulsivity traits (Weyler, Hsu, & Breakefield, 1990). A dysfunction of the serotonin (5-hydroxytryptamine [5HT]) system has been often described as playing a role in psychiatric syndromes that are characterized by impaired impulse control, including PG (Blanco et al., 1996). Low levels of MAO activity has been found among PGs compared to controls suggesting that low platelet MAO activity may be a biological predisposition for impulsivity in PGs compared to normals (Blanco et al., 1996; Carrasco, Saiz-Ruiz, Monero, Hollander, & Lopez-Ibor, 1994). Treatments with serotonin reuptake inhibitors, such as clomipramine and fluvoxamine, have also been effective in reducing PG symptoms (Hollander et al., 1998; Hollander, Frenkel, DeCaria, Trungold, & Stein, 1992). However, well-defined and controlled clinical trials with large samples of PGs are needed. Also, no significant relationship has yet been established between platelet MAO activity and psychological measures (e.g., sensation-seeking), suggesting that these factors may be independently related to PG (Carrasco et al., 1994). Measurement of cerebrospinal fluid (CSF) metabolites is one way of assessing serotonergic function in PGs. Reduced CSF 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin, has been associated with impulse control disorders (Blanco et al., 2000; DeCaria et al., 1996). However, Bergh, Eklund, Soedersten, and Nordin (1997) and Roy et al. (1988) failed to find such differences between PGs compared to controls. There is clear evidence that deficient impulse control is associated with serotonin (Mehlman et al., 1994). It is possible that ‘‘risk-taking does not have a unitary neurochemical correlate. If risk-taking is a form of loss of control over impulse, it follows that impulse control is not merely a simple function of the neural serotonin systems’’ (Bergh et al., 1997, p. 475). Other procedures that have been used to test serotonergic function in PGs involve pharmacological challenges. Intravenous clomipramine (CMI) was administered to eight pathological male and female gamblers and eight matched controls to measure the degree of activity of the serotonin system (Moreno, Saiz-Ruiz, & Lopez-Ibor, 1991). Prolactin, growth hormone, and cortisol levels were also measured. Compared with controls, PGs showed lower baseline prolactin levels and blunted prolactin response to CMI, suggesting a reduced sensitivity of serotonergic receptors and reduced serotonin transporter binding in PGs. Perez de Castro, Ibanez, Saiz-Ruiz, and Fernandez-Piqueras (1999) found that there was a significantly less functional deoxyribonucleic acid (DNA) polymorphism at the serotonin transporter gene in PG males compared to controls, suggesting that this gene could be related to the development of PG. DeCaria et al. (1996) reported a study that showed increased prolactin responses to m-chlorophenylpiperazine (m-CPP) among 10 male PGs suggesting possible postsynaptic hypersensitivity of serotonin receptors. A correlation between prolactin

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levels and the severity of PG suggested the severity of the disorder is related to the severity of the serotonin dysregulation. Impulsivity has been associated with a primary genetic defect coding for the MAO-A gene (Brunner et al., 1993). Ibanez, Perez de Castro, Fernandez-Piqueras, Blanco, and Saiz-Ruiz (2000) found a link between an allele variant of a polymorphism in the MAO-A gene and severity of PG in males. In contrast, low levels of MAO-B activity in PGs might not be influenced by the structural gene for MAO-B as no irregularities in the gene were found. It is possible that these levels are influenced via genes that accentuate expression of MAO-B structural gene instead. Further explorations are being done to determine the possible functions of this polymorphism (Blanco et al., 2000). Thus, the above studies demonstrate that there is some evidence of reduced serotonergic activity with possible postsynaptive hypersensitivity of serotonin receptors among PGs (Blanco et al., 2000). Serotonin dysfunction is linked to behavioral initiation, disinhibition and poor impulse control in PG, which is related to the onset of the vicious gambling cycle and difficulty in stopping gambling. Noradrenergic system. Noradrenaline has been linked with arousal and impulse control (Siever, 1987). Evidence suggests that PGs may have a disturbance of their central noradrenergic system. PGs tend to have lower plasma noradrenaline metabolite 3-methoxy4-hydroxyphenylglycol (MHPG) but higher CSF MHPG and urinary noradrenaline compared to controls (Bergh et al., 1997; Roy et al., 1988). The low levels of plasma MHPG support Zuckerman’s hypothesis that sensation-seeking may underlie PG and suggest under arousal in gamblers as presumed for high sensation-seekers, while the high levels of CSF MHPG and urinary noradrenaline may play a role in mediating arousal displayed by PGs (Zuckerman, 1999). Roy, de-Jong, and Linnoila (1989) also reported a positive correlation between noradrenergic function in CSF, plasma, and urine and extraversion scores for 17 male PGs. DeCaria et al. (1997) found that their sample of five PGs had an elevated growth hormone peak response to an a2-adrenergic agonist, clonidine (used to assess central noradrenergic function), compared with a group of eight healthy male controls. There was a correlation between the severity of PG and the magnitude of the clonidine-induced growth hormone response. Such evidence suggests that the noradrenergic system plays a possible role in moderating selective attention among PGs and is related to heightened arousal (perhaps related to sensation-seeking), ‘readiness for gambling’ or risk-taking among these individuals (Blanco et al., 2000). Dopaminergic system. The dopaminergic system has often been implicated in reward mechanisms in the brain (Blum, Wood, Sheridan, Chen, & Comings, 1995). Individuals whose genetic or environmental situation creates insufficient dopamine in the reward system (i.e., deficiency in dopamine neurotransmission) are prone to anxiety, cravings, and not being well. In order to replace these feelings, they may engage in activities that momentarily compensate for this scarcity (Sunderwirth & Milkman, 1991). Similar predictions can be made for PGs. Evidence for this was provided by a study that compared 10 male PGs with 7 male controls and found that CSF levels of dopamine were reduced and dopamine

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metabolites were increased in PGs, suggesting an increased release of dopamine in these individuals (Bergh et al., 1997). Increased activity of the dopaminergic pathways could be related to positive reinforcement (e.g., increased arousal) that the gambler receives for gambling. Increased activity of the dopaminergic pathways may also be related to negative rewards as increased gambling may produce a withdrawal state that is reflected in increases in brain stimulation reward thresholds, similar for opiate withdrawals (Bergh et al., 1997). This may produce the behavioral (e.g., anxiety) and cognitive symptoms (e.g., irrational thinking) of withdrawal from gambling in PGs. The role of the D2 receptor gene has been implicated in a range of addictive, impulsive and compulsive disorders including drug abuse, smoking, ADHD, and conduct disorder (Blum et al., 1995). As discussed earlier, the Taq A1 variant of the D2 receptor gene has been linked to PGs (Comings et al., 1996). In a recent study, Perez de Castro, Ibanez, Torres, Saiz-Ruiz, and Fernandez-Piqueras (1997) reported finding a variant allele of the dopamine D4 receptor gene that leads to a poorer functioning of the receptor gene, that is also related to PG. This supports studies that have found the D4 receptor gene to be associated with novelty-seeking behaviors (Benjamin, Li, Patterson, & Greenberg, 1996; Ebstein et al., 1996). Evidence regarding dopamine suggests that PGs may have a hyperactivity of the dopaminergic pathways, which are associated with both positive and negative rewards (Blanco et al., 2000). 4.3.2.3. Increased arousal/stimulation. Physiological studies that have looked at heart rate measures have already suggested increased arousal among PGs (Anderson & Brown, 1984; Dickerson & Leary, 1985). There is also biological evidence that supports the role of increased arousal among PGs. PG has been theorized to be a defense against mood disturbance, such as depression and anxiety. Plasma endorphins (a group of peptides found in the brain and pituitary) have been implicated in ‘‘mood disturbances associated with psychological states and in addictive processes, the latter through their reward transmitting properties in accordance with operant and classical conditioning principles’’ (Blaszczynski, Wilson, et al., 1986, p. 3). Thus, it may be predicted that development and maintenance of gambling is related to endorphin activity. Using radioimmunoassay techniques, Blaszczynski, Winters, et al. (1986) measured plasma endorphin levels among 39 gamblers seeking treatment compared to 35 nongamblers and did not find any significant differences between the two. However, endorphin levels of horse PGs was significantly lower than those of machine gamblers demonstrating a chronic state of underarousal among horse race gamblers but not among machine gamblers. This indicates that distinct subgroups of gamblers exist and, thus, different causal factors may characterize each group. Excitement and arousal may serve a different purpose in horse gamblers than in machine gamblers. There have been several correlative studies that indicate an increase in uric acid is associated with psychological activation (arousal or activity level). For example, there has been a range of studies attempting to link uric acid and achievement behavior (Kasl, 1974; Rahe, Ryman, & Biersner, 1976). Manowitz, Amorosa, Goldstein, and Carlton (1993)

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investigated the effect of gambling on plasma levels of uric acid. Blood samples were obtained from three men while they gambled for money or while they played checkers without betting. Uric acid levels increased over time during gambling. This indicates that an increase in uric acid levels may be related to psychological activation that occurs during gambling. 4.3.2.4. Summary. Together, these studies seem to support some biological connection between ‘‘action seeking,’’ impulsivity, and PG, which supports findings from psychological studies. However, caution is warranted in drawing conclusions from these biological studies as most of them have an exclusively male sample, small sample sizes, and the subjects usually have comorbid disorders and/or are usually engaged in therapy. Thus, more biological/psychopharmacological research is needed, with improved methodologies compared to the existing studies in this area (e.g., controlled studies using double-blind methods) and with those that are not in treatment, in order to make this biological evidence more convincing. Furthermore, evidence such as that presented by Blaszczynski, Winters, et al. (1986) demonstrates that there may be different causal factors of PG for different types of gambling and, thus, future biological studies need to take this into consideration when trying to investigate biological factors associated with PG. There are several advantages of biological theories. Biological markers of gambling problems can assist in separating PGs from non-PGs. Biological dysfunctions can be detected and thus, be prevented or treated (Ferris et al., 1999). However, one disadvantage of biological models is that it is difficult to conclude whether biological markers act as the cause or are the effect of PG. Biological models also tend to be wordy and have a narrow focus as they concentrate on physiological factors that are not restricted to those with gambling problems, or those at risk for gambling problems (Ferris et al., 1999). 4.3.3. Cognitions Evidence suggests that irrational thinking plays a significant role in the development and maintenance of PG. That is, gamblers hold a set of false and erroneous beliefs about gambling that helps to maintain their gambling despite heavy/continuous losses. Gamblers typically have two types of biases: believing that they can directly or indirectly influence the outcome of a game or believing that they can correctly predict the outcome. The more a chance situation contains factors of choice (e.g., having the opportunity to choose own ticket), familiarity (e.g., having a favorite gambling machine), and involvement (e.g., being able to throw own dice in game of craps), the more it creates an illusion of control. Also, the more it is perceived as a skill situation, the more the individual tries to control their environment and overestimate their chances of winning (Langer, 1975; Reid, 1986). It has also been found that regular machine gamblers are more likely to believe that skill is as important as chance in determining outcomes and that they possess above-average skill at playing gaming machines than do nonregular players (Griffiths, 1996). Toneatto, BlitzMiller, Calderwood, Dragonetti, and Tsanos (1997) investigated the nature and prevalence of cognitive distortions in 38 heavy or problem gamblers and found that a larger number of cognitive distortions were associated with playing games which required skill (e.g., cards or sports gambling) than ones that did not (e.g., lotteries). Walker (1992a) reported that

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machine gamblers have higher levels of irrational thinking compared to gamblers that play other games. Several variables have been found to influence psychological processes that are responsible for self-control over gambling and act as significant determinants of impaired control for PGs. These include alcohol (Baron & Dickerson, 1999; Kyngdon & Dickerson, 1999), stress (Friedland, Keinan, & Regev, 1992), and negative emotions such as frustration and depression (Corless & Dickerson, 1989; Dickerson, 1993). Griffiths (1993b) outlined the importance of structural characteristics in machine gambling designed to reinforce beliefs of winning and control at gaming machines. Some of these include: the payout interval (time elapsed before gamblers receive winnings payment), probability of winning, bettor involvement (extent to which gamblers are or perceive themselves as taking an active part in the gambling activity), payout ratio (ratio of potential wins to gamblers’ stake), and suspension of judgment (structural characteristics that temporarily disrupt the gamblers financial value system, e.g., thinking that by using 5¢ coin machines they would loose little on each gamble). Even environmental properties, such as light, color, and sound effects, may have the capability of producing psychologically rewarding experiences even when the gambler is losing. These structural characteristics of gambling machines can induce excessive gambling regardless of individuals’ biological and psychological make-up (Griffiths, 1993b). Dickerson (1993) suggested that there might be different psychological processes causing impaired control in different forms of gambling. He suggests this to be due to the fact that different forms of gambling vary across dimensions. Some forms of gambling are continuous in nature (inconsiderable time between stake and result) such as gaming machines, while others are discontinuous in nature (considerable time between stake and result) such as lotteries. Games that are continuous in nature are more likely to produce impaired control, and thus, have significant impact on the maintenance of controlled gambling. Furthermore, games that have high frequency and immediacy of payout (e.g., gambling machines) would be more appealing for gamblers as the instant gratification and excitement/arousal experienced would be greater than for games that have low frequency and delayed payment (e.g., lotteries). Games that require or are perceived to require skill (e.g., horse racing) are more likely to produce impaired control and encourage continued gambling despite losses, than those that require luck such as lotteries (Dickerson, 1993). Levenson (1974, 1981) argued that different perceptions of the control external factors have over their lives are associated with differences in thinking and behavior. Thus, those who believe that the outcome of an event is entirely contingent upon their own behavior tend to develop an internal locus of control, and those who believe it is dependent on others, chance, or luck tend to develop an external locus of control. Theoretically, it can be predicted from Levenson’s suggestion that an internal locus of control would protect against the development of PG, whereas PGs would have a high external locus of control (Kweitel & Allen, 1998). Literature indicates that only a few studies have explored the associations of perceptions of control people have over their lives (locus of control) with gambling behaviors. Some studies (e.g., Hong & Chiu, 1988; Kweitel & Allen, 1998; Lester, 1980) tend to support a role for locus of control in PG, but others do not (e.g., Kusyszyn & Rutter, 1985; Malkin & Syme, 1986).

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The thinking-aloud method is a technique where gamblers are asked to provide commentary (i.e., verbalizations—everything that is going on in their minds including intentions, urges, ideas, and images) on their play as the game is proceeding. Using the thinking-aloud method with 30 subjects on both roulette and slot, Gaboury and Ladouceur (1989) showed that 70% of gamblers’ verbalizations are erroneous during gambling. This result has been replicated under different conditions: frequent or infrequent wins, limited or unlimited stakes, regular or occasional gamblers and in a variety of games such as black jack, slot machine, videopoker, and roulette (Coulombe et al., 1992; Gaboury & Ladouceur, 1989; Ladouceur, Gaboury, Bujold, Lanchance, & Tremblay, 1991; Walker, 1992a). Ladouceur and Dube (1997) also found that the percentage of erroneous perceptions was not influenced by monetary incentives. The correction of erroneous perceptions using cognitive therapy has also been found to reduce monetary risk, frequency of gambling, and urges to gamble as well as to increase perceptions of control (Coulombe et al., 1992; Gaboury & Ladouceur, 1989; Ladouceur, Sylvain, Duval, Gaboury, & Dumont, 1989; Sylvain & Ladouceur, 1992; Sylvain, Ladouceur, & Boisvert, 1997) adding support to the idea that erroneous perceptions might be playing a role in the development and maintenance of PG (Coulombe et al., 1992). By evaluating the available research literature on the erroneous thinking present during gambling, Toneatto (1999) presented a list of gamblingrelevant cognitive distortions (Table 1). Studies have also suggested that a gambler’s cognitions may work together with physiological factors such as arousal to help explain the maintenance of PG (Griffiths, 1991b). When a gambler wins or nearly wins, he or she gets physiologically aroused and gamblers’ cognitions suggest that they are not constantly losing but constantly ‘‘nearly winning’’ and, thus, this stimulates further play (Griffiths, 1991b). Most of the support for this is, however, based on self-report studies. Frequency of irrational verbalizations during some forms of gambling, especially gambling on gaming machines, has also been found to correlate significantly with autonomic arousal as measured by heart rate, which indicates that arousal in problem gambling may be cognitively mediated (Coulombe et al., 1992; Sharpe, Tarrier, Schotte, & Spence, 1995). However, Coventry and Norman (1998), in a study that attempted to examine the relationship between arousal, erroneous verbalizations, and the illusion of control, found: (a) no significant relationships between types of verbalizations and arousal; (b) no relationships between illusion of control measures and either arousal level or type of verbalizations; (c) a lack of differences between chasers and nonchasers. Thus, it was suggested that rather than being due to any differences in gambler’s arousal levels, personality, or reasoning abilities that are brought to the gambling context, a gambler’s continued gambling despite losses may be a function of only what they experience during the game. 4.3.3.1. Summary. Currently, there is a lot of support for the role of dysfunctional cognitions in the development and maintenance of PG. Research in this area needs further refining due to some limitations of the theory. Wagenaar (1988) pointed out that there are no specified rules on which heuristics or biases will be used in which situation. Also, even though similar heuristics may be chosen in similar situations, they may consequently lead to different behaviors

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Table 1 Gambling-relevant cognitive distortions (Toneatto, 1999) Type of cognitive distortion

Definition/example

Magnification of gambling skills and minimization of other gambler’s skills Superstitious beliefs (a) Talismanic (b) Behavioral (c) Cognitive Interpretive biases (a) Internal attributions, external attributions (b) Gambler’s fallacy (c) Chasing

Overestimation of one’s own ability to win and underestimating other’s ability to win

(d) Reframed losses (e) Hindsight bias

Temporal telescoping Selective memory Predictive skill Illusion of control over luck (a) luck as an uncontrollable variable (b) luck as a controllable variable (c) luck as a trait variable (d) luck as a contagion

Illusory correlation

Obtaining ways to manipulate gambling outcomes - Possession of certain objects such as rabbit’s foot - Specific action and rituals - Certain mental states such as prayer or having a positive attitude - Attributing successes to one’s own skill and failures to other’s influences or luck - Expecting that series of losses will be corrected by series of wins - Believing that engaging in more frequent involvement, increased persistence and elevated monetary risk might recoup lost money - Reframing repeated losses as a learning experience, which may finally help lead to repeated wins - Appraising gambling decisions as correct or incorrect based on whether they result in wins or losses (i.e., deciding that a gambling choice was correct since they actually did win, thus, strengthening their beliefs that they are skilled gamblers and have the ability to predict wins). Losses may be reframed in hindsight as an outcome which the gambler could have predicted and, thus, avoided (e.g., concluding that they knew they should have bet on another horse) Believing that wins are actually nearer—may lead them to sit at one machine for hours, believing that they are going to eventually win Recalling wins more easily than losses and thus, expecting to win at games where they have lost previously Believing that they have the skill of making accurate predictions regarding gambling based on salient cues (e.g., the weather) - Believing that luck fluctuates between periods of good and bad and cannot be manipulated directly so they wait for periods of good luck - Believing luck can be manipulated by superstitious behaviors - Believing that they are good at only some games (they may deduce trait luck from a series of prominent wins at an unfamiliar game) - Interpreting good luck or success in other areas of life as signs that they will also succeed at gambling. They may also believe other gamblers affect their luck and, thus, avoid gamblers that are losing Perceiving illusory correlations and assigning causality to salient features of environment that they feel correlate with gambling outcomes (e.g., gamble only when they think they are likely to win)

(Rachlin, 1990). Thus, research still needs to explore the irrational cognitions predominant in each form of gambling and how they influence behaviors. Cognitive explanations also indicate that PGs are irrational (more affected by biases and heuristics) in relation to their gambling.

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However, there is no evidence that PGs/gamblers are less rational in their judgments about chance events than are nongamblers (Rachlin, 1990). Further explorations of any gender or cultural variations in cognitions among PGs might also be beneficial. 4.3.4. Psychological states Mood states such as anxiety and depression have been frequently linked to PG (Blaszczynski & McConaghy, 1989a). Dickerson, Cunnigham, England, and Hinchy (1991) reported that for high-frequency gamblers, prior mood and cognitions significantly accounted for continuation of gambling despite successive losses. People who are anxious or depressed may gamble to relieve these negative psychological states, which may be reinforcing in the short term but may make PGs more anxious and depressed in the long term. Raghunathan and Pham (1999) investigated whether sad and anxious affective mood states have particular effects on decision-making processes. They demonstrated that in decisions related to gambling, individuals who are sad have a bias towards high-risk/high-reward choices, whereas those who are anxious have a bias towards low-risk/low-reward choices. They suggested that these differences appear to be due to the fact that anxiety and sadness communicate different types of information to the individual who is making the decision and thus, influence the production of goals. Anxiety leads to a goal involving the reduction of uncertainty, whereas sadness leads to a goal involving the replacement of rewards. Fundamentally, anxious or sad individuals are attempting to make a decision regarding what would make them feel better. In relation to depression, although some studies have reported no significant relationship between gambling/PG and depression (Becona, Del-Carmen-Lorenz, & Fuentes, 1996; Thorson, Powell, & Hilt, 1994), others have reported high rates of depression among PGs (Blaszczynski & McConaghy, 1988, 1989a; Graham & Lowenfeld, 1986; Griffiths, 1995). Studies have reported comorbidity of depression among PGs ranging from 21% to 75% (Bergh & Kuhlhorn, 1994; Linden et al., 1986). However, it is still not known whether depression is a result or cause of PG. Suicide attempts are also very common among PGs, especially those who are depressed (Blaszczynski & Farrell, 1998). Suicide attempts have consistently been reported in populations of PGs and range from 12% to 24% (Ciarrocchi & Richardson, 1989; Frank, Lester, & Wexler, 1991; Ladouceur et al., 1994; McCormick, Russo, Ramirez, & Taber, 1984). Other risk factors that have been identified for suicide among PGs include large financial debts and relationship difficulties (Blaszczynski & Farrell, 1998). In relation to anxiety, there is support for the role of anxiety in the development of PG. Henry (1996) tested a theory that the development of PG is associated with unresolved trauma-related anxiety. There was a reduction in PG behavior with reduced anxiety following treatment for those with reported trauma history. In another study, Blaszczynski et al. (1991) showed that gamblers who had successfully completed treatment showed a noticeable decrease in anxiety compared to those who were still gambling. However, similar to depression, it is unclear whether anxiety is the cause or result of PG. Not only does stress appear to play a role in the cause and maintenance of PG (Coman et al., 1997; Friedland et al., 1992; Toerne & Konstanty, 1992), it has also been found to

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precipitate relapse, and block both change and the maintenance of change (McCartney, 1995). There is currently very limited research regarding the role of traumatic events in a PGs’ life. Taber, McCormick, and Ramirez (1987) evaluated the role of traumatic events among gamblers admitted to an inpatient gambling program for veterans. About a quarter of the group reported severe traumatic events, 16% reported moderately heavy trauma, 30% less severe trauma, and 32% reported no severe life trauma. However, nearly two thirds of the group did not report severe trauma, thus casting doubts on the significance of stress from traumatic events in PG. Although the authors reported that 90% of cases reported severe life trauma, and that the traumatic experiences occurred before gambling became pathological, this does not prove the etiological role of stress in PG. Also, due to a small sample size (N = 10), it is hard to confidently make conclusions. Thus, there is a need for longitudinal studies to investigate the role of stress/traumatic events in PGs. There is also evidence that suggests different moods might lead to different games. Coman, Evans, and Burrows (1996) found that gamblers who focus their attention on low-skill gambling such as gaming machines are more likely to be suffering from stress and anxiety. Depressed gamblers utilize more skilled games to lift their depressed mood, with daydreams of winning. They may also engage in more social forms of gambling, such as card games, to enhance social interaction. Alexithymia, a disorder that includes affective deficits as well as concrete, externalized cognitions, has often been linked to addictive and compulsive disorders. Lumley and Roby (1995) investigated the rate of alexithymia among PGs and found that among 1147 adolescent PGs, 31.4% had alexithymia compared to only 11% of the controls. However, it is unknown whether alexithymia is a cause or consequence of PG. Several studies have looked at the comorbidity of PG with other psychological disorders suggesting that such comorbidity may either increase the chances of an individual developing PG or aid in the maintenance of PG. Specker et al. (1996) investigated psychiatric comorbidity among 25 male and 15 female PGs seeking outpatient treatment for gambling, and 41 male and 23 female controls, using structured clinical interviews. High-lifetime rates of Axis I (92%), but not Axis II (25%), psychopathology were found in PGs compared to controls. No differences between male and female gamblers were found in rates of affective, substance use, or personality disorders. Females had higher rates of anxiety disorders and histories of physical/sexual abuse. Other Axis I disorders reported to be comorbid with PG include hypomanic disorder (McCormick et al., 1984), schizoaffective disorder, paranoid schizophrenia, substance use disorders (Gambino et al., 1993; Lesieur & Blume, 1990), and panic disorder (Linden et al., 1986). Black and Moyer (1998) also investigated psychiatric comorbidity of 30 subjects reporting PG behavior using structured and semistructured assessments. It was found that 60% of participants had a lifetime mood disorder, 64% had a lifetime substance use disorder, and 40% had a lifetime anxiety disorder. Impulse control disorders were common, especially compulsive buying and compulsive sexual behavior. Several studies have included PG among the compulsive disorders, implying a relationship with OCD. DeCaria et al. (1996) suggest a number of reasons for this relationship, including increased rates of OCD or OCD symptoms among PGs (Linden et al., 1986), increased harm avoidance subscale scores (Carrasco et al., 1994), problems in resisting thoughts and urges to

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gamble, and increased distress before gambling and satisfaction after gambling (APA, 1980). However, it must be noted that PGs differ from individuals with OCD. PGs are preoccupied with the positive aspects of gambling such as the rewards that they gain from the gambling activity (i.e., reducing negative mood states or winning money), the action of gambling, or with finding money to gamble with, not with the negative aspects of gambling such as the fear of negative outcomes or with some feared result of failure to perform a ritual. Data on the presence of OCD or compulsivity in PG remain inconclusive with most studies tangentially reporting a weak (Hollander & Cohen, 1994; Linden et al., 1986) or absent relationship (Black, Goldstein, Noyes, & Blum, 1994; Specker et al., 1996). To date, only one study has specifically explored presence of OC traits among PGs using 40 PGs and 40 normal control subjects. Blaszczynski’s (1999) study found that PGs have elevated traits of ‘‘impulsivity’’ as well as ‘‘obsessionality’’ providing preliminary evidence for the possibility of classifying PG as an OC spectrum disorder. 4.3.4.1. Summary. There is strong support for the role of mood states, especially anxiety and depression, in the development and maintenance of PG. Affective disorders, particularly depressive disorders, are often comorbid to PG. Crockford and el-Guebaly (1998) reviewed the current literature on PG as regards the significant psychiatric comorbidities associated with it. In relation to mood disorders, they suggested that although there is evidence of comorbidity between mood disorders and PG, it is difficult to make firm conclusions regarding these factors due to methodological concerns and inconsistencies within the data. Also, most research studies in psychiatric comorbidity have used predominantly male samples. While there is sufficient evidence to suggest that some psychological states may make an individual more susceptible to begin gambling and subsequently develop PG, it is difficult to determine the cause-and-effect relationship (e.g., depression, anxiety, loneliness, alexithymia, etc.). Different psychological states may lead to different forms of gambling. Skill gamblers are more likely to fit the profile of the bored gamblers identified by Blaszczynski et al. (1990), while luck gamblers are more likely to fit with the profile of the depressed/anxious gambler outlined by Blaszczynski and McConaghy (1989a). Since different forms of gambling vary across dimensions (e.g., continuity vs. discontinuity, skill vs. luck, frequency and immediacy of payout), different psychological processes may operate in the development and maintenance of PG for different forms of gambling (Dickerson, 1993). Thus, it is important that future studies aim to differentiate the roles played by psychological states in different forms of gambling.

5. Main theories and treatment of PG Several researchers have attempted to produce theoretical models to explain the development and maintenance of PG. Although in the past, psychodynamic explanations were predominant (Bergler, 1957; Freud, 1928), several theoretical orientations have since been put forward, including the medical model (Blume, 1987), behavioral models (Brown, 1987a;

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McConaghy, 1980), psychologically based models (e.g., Jacobs, 1986), and more recently, cognitive–behavioral (CB) models (e.g., Sharpe & Tarrier, 1993). Other theoretical orientations (already discussed earlier) include the sociological (Ocean & Smith, 1993), biological/ physiological (e.g., Blanco et al., 2000; Roy et al., 1988), and personality-based explanations (e.g., Zuckerman, 1999). Some of these models of PG and their relation to treatment are reviewed below. 5.1. Psychodynamic model The first attempts to conceptualize PG were in the early 1900s by psychoanalysts. They emphasized that gambling was the expression of an underlying neurosis that was connected to the pregenital psychosexual stages (Greenson, 1947; Hattinger, 1914). Simmel (1920) stated that PGs feel denied the love and attention of parents and long for erotic satisfaction. This creates a void of pleasure, excitement, and promise of gain which gambling appears to fill. Psychoanalysts (Fenichel, 1946; Freud, 1928) explained gambling as an unconscious substitute for unresolved sexual conflicts. According to Freud (1928), gamblers do not play for money but rather for the action of gambling itself. They also gamble to lose, as losing is a means of self-inflicted punishment to atone for guilt over the compulsion to masturbate, which in time is related to unresolved Oedipal conflicts. Although a few authors have reported that the sexual drive of PGs appears to disappear during gambling episodes (Bolen & Boyd, 1968), few today accept this view (Greenberg, 1980). Bergler (1957, 1967) agreed with Freud’s idea that a gambler has an unconscious desire to lose, resembling masochism. He, however, offered a different explanation. He stated that PGs unconsciously resent authority figures that in their childhoods forced them to consider the reality principle over the pleasure principle. As a consequence, PGs attempt to rebel against the reality principle and those who encourage it. The unconscious willingness to self-punish is considered to result from the guilt of having unconscious aggression. With regard to the role of masochism, Lesieur and Custer (1984) have observed that some gamblers who initially have a period of winning can continue gambling for a long period of time, whereas a masochist would not be expected to do this. Rosenthal (1987), however, argued that masochists do substantially well in many activities and only start destroying them once they become important to them. They use defense mechanisms such as denial and omnipotence as well as splitting, projection, idealization, and devaluation to delude themselves and others (Rosenthal, 1986). Many PGs fit the criteria for narcissistic personality disorder or show noticeable narcissistic characteristics (Blaszczynski & Steel, 1998; Rosenthal, 1986). Other psychodynamic orientated authors such as Livingston (1974) and Taber et al. (1986) support Rosenthal’s view that PG is related to narcissistic personality and related defense mechanisms. Thus, in consideration of the psychoanalytic explanations put forward so far, there appear to be three major aspects of the psychoanalytic theory of PG. These include gambling being ‘‘an unconscious substitute for pregenital libidinal and aggressive outlets associated with Oedipal conflicts,’’ a desire ‘‘for punishment in reaction to the guilt,’’ and a means for recurrent ‘‘reenactments, but not resolutions, of the conflict’’ (Allcock, 1986, p. 262). The

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main strength of psychodynamic models is their in-depth focus on the internal processes, which may lead to problem gambling. In addition, the case study-based literature is useful for describing and detailing the progress of problem gambling and its treatment. However, the psychoanalytic rationalizations tend to overlook social factors as they mainly deal with unconscious impulses of the gamblers (Graham & Lowenfeld, 1986). Much of the ‘‘evidence’’ put forward is based on single case histories and elaborate speculation and thus, tends to be descriptive and wordy. They also do not sufficiently explain why the individuals gamble in the first place, or how PG is developed or maintained (Allcock, 1986). Psychodynamic hypotheses are also very difficult to test (Allcock, 1986). Psychoanalytic treatments concentrate on dealing with narcissistic personality characteristics and related defense mechanisms. Several individual case studies have reported use of psychoanalysis in the formulation and treatment of PGs (Galdston, 1960; Greenson, 1948; Harris, 1964; Lindner, 1950). Effectiveness rates of gamblers treated psychoanalytically have ranked from poor to guarded optimism (Greenberg, 1980). Bergler’s (1957) study showed an effectiveness rate of 75%. However, this rate was based on only 30% of the total group seeking treatment (disregarding dropouts). Several authors have pointed out that PGs tend to have poor motivation for therapy as indicated by high dropout rates and high relapse rates (Bolen & Boyd, 1968; Greenberg, 1980). Furthermore, methodological flaws in treatment studies such as selection bias, absence of acceptable outcome criteria, and limited follow-up data, negatively influence the importance of these findings (Allcock, 1986). Most of the studies that have assessed psychoanalytic treatment are case studies, did not include control groups, and have small sample sizes. 5.2. Medical model The medical model (Blume, 1987) sees PG in ‘‘black and white’’ or ‘‘all or nothing’’ terms, with the gambler being either pathological or not. It assumes that gambling problems are caused by a physiological predisposition. The model supports that the disease follows a course, which is similar to the course that occurs for others with the same problem, and is manifested through characteristic signs, symptoms, and stages of development (Blume, 1987), and is outside of the individual’s conscious control. As the biological systems underlying the problem are thought to be irreversible, the disease model includes the idea of a progressive worsening of the habit, which requires treatment in order to arrest the condition. GA favors the medical model of PG and believes that recovery from the condition requires lifetime abstinence, suggesting that there is no true recovery. In the present times, the medical model is only loosely utilized and has been used as a stepping stone to other explanations. The current biological/biochemical explanations (discussed in prior sections) of the development and maintenance of PG agree with the medical model in that gambling problems are caused by some biological predisposition. However, there are distinct differences between the two explanations. The biological/ biochemical explanations assume that correction of some biological abnormalities can help treat PG. In contrast, the traditional medical model assumes that the underlying addiction is irreversible, and only total abstinence can control the problems. Also, most of the researchers

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who take a biological approach to gambling problems do not see gambling problems as a disease or illness but rather as a phenomenon that is acquired (Ferris et al., 1999). More recently, the view that some individuals may have physiological weaknesses (e.g., inability to plan ahead or recognize long term consequences of actions) that manifest themselves into gambling problems has been adopted (Rugle, 1993). Similar to the biological models, the medical model of PG helps reduce the burden of guilt from gamblers and their significant others by avoiding responsibility for the behavior, as it enables one to be defined as ‘‘sick’’ (Blume, 1987). Presence or absence of the disease can be measured, which is useful in the medical/health/psychiatric system. It also assists in the organization and delivery of treatment to gamblers and their significant others (Blume, 1987). The medical model has come under many criticisms. The first criticism is related to the labeling of the gambler as ‘‘sick.’’ A sick label may lead to a state of mind where a single slip may result in a sense of despair or hopelessness, and this would increase the likelihood that the recovering gambler would have a full-blown relapse (Rosecrance, 1986). The labeling can result in a shifting of individual responsibility for behavior to a disease process (Blaszczynski & McConaghy, 1989b) clearing gamblers from any responsibility for their own recovery. Blume (1987) addressed this criticism, suggesting that while the model does not hold an individual responsible for contracting the disease, the individual is responsible for doing everything possible to recover. Secondly, since the medical model emphasizes that the disease is something that happens to an individual (Brown, 1987a), there is less emphasis on preventive measures, and more on treatment. Thirdly, the medical model does not clearly distinguish between the gambling behavior patterns of those who have a gambling problem compared to those who do not. Many factors have been implicated and it has not yet been determined which factor(s) are more important than others (Blaszczynski & McConaghy, 1989b). Fourthly, the model does not adequately account for the continuum of gambling behavior that is seen across the population as a whole as it focuses only on gamblers who seek treatment (Blaszczynski & McConaghy, 1989b). Although the disease model requires abstinence as the treatment goal, clinical evidence suggests that it is possible to start gambling in a controlled way with treatment (Blaszczynski et al., 1991). The model does not account for those who have episodes of problem gambling interspersed with periods of controlled gambling, or for those who experience spontaneous remissions of serious gambling problems (Brown, 1987a). If PG is a disease, some individuals should display a distinct addiction syndrome. Yet population studies (as opposed to treatment studies) of PGs regularly reveal that different people display different types of problems, and that the number and severity of these problems occur across a continuum rather than forming distinct profiles. In gamblers, there are significant changes and variability in severity of problems over time (Shaffer et al., 1997). Finally, there is evidence that PGs do not fit the medical model. Wedgeworth (1998) studied 12 PGs admitted to a private inpatient treatment center via interviews and autobiographies to evaluate whether PGs fit the medical model. The author concluded that rather than a medical diagnosis, PG is a socially constructed phenomenon (i.e., patients were diagnosed for practical purposes, in order to fulfill insurer criteria while allowing them to repair their personal relationships).

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5.3. Recent psychologically based theories Recent psychological based theories seem to provide some solid ground for further research. These include addiction-based, social learning (behavioral), and CB models. 5.3.1. Addiction-based theories Some of the premises for psychologically based theories are taken from the understanding that PGs are similar in many ways to individuals with other addictions, such as substance disorders (Lesieur & Rosenthal, 1991). Jacobs (1986) presents a general theory of addictions, including PG, where he proposes a common dissociative phenomenon that helps addicts escape from psychological distress. He defines addiction as a dependent state acquired over time (by a person who is predisposed) to relieve stress. Furthermore, he suggests the importance of two interrelated predisposing factors to addictions including an inherited abnormal unipolar physiological resting state (in which an individual is chronically over, or under, stimulated) and childhood experiences that result in feelings of inadequacy, rejection, and/or guilt (Jacobs, 1986). There is some support for this, in treatment samples (Jacobs, 1988), community samples (Kuley & Jacobs, 1988), and among adolescents (Gupta & Derevensky, 1998b). Brown (1987b) modified Apter’s (1982) reversal theory that accounts for addiction and relapse to develop an arousal and reversal theory that can be applied to normal and PGs (Anderson & Brown, 1987b). Arousal and reversal states take place in two states, telic (goaloriented) and paratelic (playful) states. PGs switch from one metamotivational state to another (e.g., highly aroused to highly anxious states) during gambling and when they stop gambling. They are concerned with monetary gain and loss (the telic) as well as excitement (the paratelic). Anderson and Brown suggested that to have a proper understanding of PG, it is vital to consider both physiological (paratelic) and cognitive (telic) processes (Lesieur & Rosenthal, 1991). Many authors have identified similarities between PG and other addictions and, thus, consider PG as an addiction rather than an impulse control disorder. Lopez Viets (1998) outlined several ways in which PG is similar to other addictions. PG and other addictions have a high state of arousal, both being activities that enable one to escape life’s problems, both have similar symptoms such as cravings, tolerance, and withdrawal, and addicts have similar psychological profiles. Furthermore, there is high comorbidity between gambling and other addictions (Lesieur & Rosenthal, 1991; Lopez Viets, 1998). However, she also emphasized that there are clinically important differences between the two. PG involves psychological dependence, whereas substance addiction involves physiological dependence (Walker, 1989). Lesieur (1994) suggested other major differences including the phenomenon of chasing, which is unique to PGs, and the fact that gamblers can hide their problems more easily due to fewer physical signs (Lopez Viets, 1998). There are also differences in the content and format of the 12-step program GA (created based on AA). GA focuses on peer support and individual counseling and views PG as a progressive illness which cannot be cured but can be stopped (Allcock, 1986). Currently, there is a lack of studies testing GA’s efficacy. However, despite high dropout rates (70%–90%) among GA members, and

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low abstinence rates (7 – 8%), it appears to be really beneficial for some gamblers (Rosecrance, 1988). 5.3.2. Learning theories (cognitive social learning and behavioral theories) From the early 1950s, behavioral explanations of PG emerged. Learning theorists view gambling as a learned behavior that is a result of a combination of classical and operant conditioning, where gambling behavior is reinforced through intermittent schedules of reinforcement (Anderson & Brown, 1984; Dickerson, 1979). Researchers in this field, however, have emphasized different reinforcers including intermittent gains such as the money won (Moran, 1970), the excitement related to the gambling situations (Brown, 1986), or the mechanisms of behavior completion (McConaghy, Armstrong, Blaszczynski, & Allcock, 1988). Negative reinforcement may operate through reduction of aversive stress states by escaping from life problems and distress as they narrow their attention during play (Blaszczynski & McConaghy, 1989a; Diskin & Hodgins, 1997). The models assume that there may be underlying physiological or psychological mechanisms which predispose individuals toward gambling as a response to specific stimuli or situations. Behavioral theories of PG have also been criticized. Sharpe and Tarrier (1993) have criticized behavioral explanations for not being ‘‘clinically oriented’’ and for not acknowledging how complicated gambling behaviors are, as they concentrate on only one mechanism and ignore other crucial ecological and cognitive influences. For example, McConaghy’s (1980) behavioral model, ‘‘behavior completion mechanism,’’ suggests that a particular behavior (gambling) is established in the gambler’s central nervous system when it becomes habitual. Thus, the behavior has to be completed to reduce aversive sensations of arousal, thus encouraging the gambler to continue gambling despite losses. Learning models, such as the cognitive social learning model postulated by Brown (1987a), also tend to be entirely descriptive (Sharpe & Tarrier, 1993). They do not make explicit the relationships between the variables they present and the mechanisms through which an individual acquires these behavioral patterns (Sharpe & Tarrier, 1993). Behavioral models also fail to acknowledge importance of internal events, as they tend to underestimate the power of individual motivation, emotions, and perceptions to influence outcomes and overestimate the effects of external social factors (Brown, 1988). They also fail to account for the role of punishment (e.g., the costs of gambling) in encouraging the termination of gambling (Blaszczynski & Silove, 1995). Behavioral treatment studies have, however, provided some of the most comprehensive treatment literature on PG. Treatments based on learning principles (i.e., behavior modification) have involved aversion therapy using physical or imaginal stimuli (Barker & Miller, 1966, 1968; Goorney, 1968), controlled gambling/behavioral counseling (Dickerson & Weeks, 1979), positive reinforcement of gambling abstinence, paradoxical intention (Victor & Krug, 1967), covert sensitization (Bannister, 1977; Cotler, 1971), and imaginal desensitization (McConaghy, Armstrong, Blaszczynski, & Allcock, 1983). These have been administered singularly or in combination. However, due to methodological shortcomings in such studies, it is difficult to assess how effective these treatments are. Most of these treatment studies have small sample sizes and limited follow-up periods. They have

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unspecified or poorly operationalized dependent variables/criteria for successful outcome or treatment objectives (Allcock, 1986). Also, there is usually a lack of controlled comparisons of one treatment with another or with a placebo procedure, or combinations of several techniques are used concurrently so that identification of the active component is impossible (Blaszczynski & Silove, 1995). 5.3.3. CB models Harris (1988) presented a comprehensive formulation of a theoretical CB model for gambling based on the CB model of addiction and Marlatt’s (1985) model of addiction relapse. It highlighted that dysfunctional cognitions, perceptions, and motivations for gambling, and poor coping skills were important factors in the development and maintenance of gambling problems. However, Blaszczynski and Silove (1995) criticized Harris’s model for being too broadly descriptive and not supporting a specific theoretical cognitive model. They also stated that it failed to outline the nature and source of dysfunctional cognitions. Sharpe and Tarrier’s (1993) heuristic model is one of the most comprehensive CB models that exist to explain development and maintenance of PG. The model takes account of a range of variables (discussed in earlier sections of this paper) as playing a role in the development and maintenance of PG. It supports Anderson and Brown’s (1987a) view that gambling is achieved via the principles of operant and classical conditioning. They assume that physiological arousal during gambling is initially reinforced by monetary reward and later becomes conditioned to the gambling situation. The complicated interactions between the physiological (e.g., increased autonomic arousal such as increased heart rate), cognitive (cognitive distortions), and behavioral correlates associated with PG operate at the initial stages of gambling. Reinforcement contingencies increase the likelihood that the gambler continues to gamble and, consequently, connections form between these variables. Development of gambling problems is mainly mediated by poor coping skills (e.g., control over autonomic arousal, ability to challenge cognitions and delay reinforcement, and problemsolving skills), which encourage the gambler to continue gambling. This excessive gambling is maintained by the consequences of gambling (e.g., social pressures, substance dependence, low self-esteem, and stress), which act by reducing the availability of coping resources. Although CB models appear to be more refined than the previous behavioral ones, and have been found to be effective in formulating and dealing with problem gambling, they have not yet been rigorously tested using control groups or in comparison with other treatments. Four multimodal outcome studies, with a CB component (Lesieur & Blume, 1991a; Russo, Taber, McCormick, & Ramirez, 1984; Schwarz & Lindner, 1992; Taber et al., 1987) have reported high success rates in regard to treatment of PG. However, due to the inclusion of other treatment components, it is difficult to assess the efficacy of the CB component. Outcomes of two case studies (Bannister, 1977; Toneatto & Sobell, 1990) and recently, several controlled studies (Echeburua, Baez, & Fernandez Montalvo, 1996; Ladouceur & Sylvain, 1999; Sylvain et al., 1997) have shown cognitive behavior therapy (CBT) to be an effective treatment for gambling problems. Several studies have also shown that the cognitive restructuring aspect of CBT can significantly reduce PG symptoms (Gaboury & Ladouceur, 1990; Ladouceur et al., 1989, Ladouceur, Sylvain, Letarte, & Giroux, 1998).

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5.4. Discussion of existing models and available treatments Although theoretical models of problem gambling all have strengths and weaknesses, they do provide valuable insights into development of PG and the characteristics of problem gamblers. There are more points of agreement than disagreement on the causes of gambling problems across the approaches. Most theoretical approaches agree, at least partially, that PG may be a consequence of physiological or psychological predispositions, and that there are triggers for the behavior such as negative emotions or stressful events (Ferris et al., 1999). These triggers create an unpleasant state for PGs, either emotionally or physiologically, which gambling helps normalize to preferred states. Disagreements among researchers seem to be related to the emphasis placed on each of these factors. Those outside the clinical field tend to regard social and environmental factors as the vital factors in conceptualizing PG, while psychologists and psychiatrists tend to emphasize that the gambling problems are related to internal factors (Ferris et al., 1999). Thus, treatment for the latter focuses on changing the behavior or addressing the biological predisposition of the individual in order to address the gambling problem. Most of these theoretical perspectives tend to focus on characteristics of the most seriously affected problem gamblers, while the profile of the less affected or episodic gambler remains less well understood. The theoretical models that try to explain the development and maintenance of PG tend to be restricted in their conceptualization (Blaszczynski & Silove, 1995). They either concentrate on single biological or individual psychological variables or a few simple mechanisms to explain the development or maintenance of PG, without considering the heterogeneity that exists among PGs. It is likely that the processes contributing to PG involve a complex and dynamic interaction between intrapsychic, biological, social, ecological, psychophysiological, developmental, cognitive, and behavioral components. Thus, all these factors need to be assessed and, if necessary, targeted within a treatment plan in order to get the best possible success rate. There is currently no theoretical model comprehensive enough to account for the complex interaction of these factors, nor to illustrate the ‘‘pathogenic process leading to the transition from controlled PG, its persistence and maintenance over time, and why relapse occurs after periods of control/ abstinence’’ (Blaszczynski & Silove, 1995, p. 196). Thus, in recent times, most professionals are taking the eclectic view that these factors play an interactive role in the development and maintenance of PG (Shaffer et al., 1997). Despite a range of theoretical models, no one single treatment approach currently exists to treat PG. The ultimate goals for treatment (abstinence or controlled gambling) have also differed depending on the theoretical model adopted. Lopez Viets and Miller (1997) provided a comprehensive literature review of the treatments available for PGs and found that the main treatment approaches include cognitive, behavioral, CB, psychodynamic, multimodal, pharmacotherapeutic, and 12-step approaches. However, they pointed out the need for further research in several areas. Effectiveness of GA as a treatment modality has not been adequately tested. There is not only a need for better-controlled research for the 12-step program, but also to test the psychodynamic approaches (Lopez Viets, 1998). Multimodal approaches have been assessed most often in inpatient and outpatient settings,

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however, due to the wide variety of treatment components used in combination, it is hard to determine how effective each specific treatment components is. Studies in the pharmacological area need to be replicated with larger sample sizes and with both genders. Research also needs to address the issue of lack of follow-up data in treatment studies and the lack of representation of certain groups in these treatment studies (e.g., ethnic minorities, females, etc.). Further clinical research needs to be performed to compare CBT with other treatment modalities. In general, the PG literature indicates that PG can be treated successfully. Presently, behavioral, cognitive, and combined CB therapies have the most outcome research and appear to be most effective at treating gambling problems. Pharmacological approaches also look promising. However, it must be pointed out that no particular treatment could be seen as the treatment for PG as different gamblers have responded well to different approaches. Behavioral and CB therapy appear to have several advantages, such as being cost-effective and allowing for booster sessions. For a recent and comprehensive analysis of the PG treatment literature, refer to Lopez Viets and Miller’s (1997) review.

6. General discussion and conclusion PG continues to gain much attention due to the adverse social consequences it has on gamblers, their significant others, and society in general, as well as the emerging evidence of a link between greater accessibility to gambling (e.g., as a result of legalization of gambling) and PG (especially in relation to gaming machines). The gambling literature indicates that PGs are a heterogeneous group and that higher rates of gambling occur among some groups, such as adolescents, substance abusers, psychiatric patients, certain cultural groups, and perhaps the elderly. Although no single motivation has consistently been identified among gamblers or PGs, a range of variables has been implicated in playing a role in development and maintenance of PG including individual variables (i.e., personality, biological, psychological states, and cognitive factors), familial/genetic factors, and sociological factors. The role of familial factors (both social learning and genetics) is apparent, but more systematic family prevalence studies, as well as twin and adoption studies, are needed to determine the strength and nature of this role. Sociological explanations appear to have some relevance, however, since there appear to be some inconsistencies in these justifications. It is possible that social amenities that gambling provides may be important only for some gamblers. Personality, cognitions, psychological states, and biology/biochemistry all appear to contribute to the development and maintenance of PG. In regard to personality traits, the strongest evidence exists for impulsivity and possibly sensation-seeking for only certain forms of gambling. Evidence for other traits such as psychoticism, neuroticism, and extraversion has been less consistent. Personality disorders (e.g., ASPD and narcissistic personality disorder) and attentional disorders (e.g., ADD) (related to the personality traits mentioned above) are also linked to PG. There also is strong evidence for the role of irrational thinking and psychological mood states such as anxiety and depression in the

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development and maintenance of PG. Although this area is still in its infancy, biological and biochemical influences such as hemispheric dysregulation, chemical imbalances, dysfunctional neurotransmitters (e.g., serotonergic, dopaminergic, and noradrenergic systems), and physiological arousal have been implicated as playing a role in the development and maintenance of PG. Obviously, research in this area will continue to find other variables that may play a role in development and maintenance of PG including life event stresses, social support, cultural variables, and many more. Other gaps in the current gambling/PG literature also need to be addressed. Despite findings regarding motivations for gambling, we still do not have a clear picture of the true motivators of gambling. Longitudinal studies are required to find out which motivational factors play a role in the continuation of gambling as well as the motivational factors that may act as a buffer against the development of PG. Knowledge is also required on the gambling patterns of specific subgroups so far neglected in the gambling literature, such as females, adolescents, and children. Research that is emerging in this area suggests that prevalence rates for children are significantly high and possibly on the rise. Thus, prevalence of gambling problems among adolescents and children requires thorough investigation and ongoing monitoring. Furthermore, recent evidence indicates high rates of problem gambling among the elderly, which also warrants further investigation. Despite the steady increase in literature addressing gambling, problem gambling, and its associated problems, there is a noticeable lack of new research on the treatment of gambling problems. Current research supports psychotherapy, especially CB therapy, as a treatment modality. However, outcome results have to be seen as equivocal as most of them have design problems, small sample sizes, and problems with generalizability. Four very important issues are apparent in this review. The first issue relates to the generalizability of findings from one form of gambling to another. Gambling cannot be viewed as a simple phenomenon or a single entity and researchers must now consider different forms of gambling in their own right, especially those that appear to be more problematic (such as gaming machines) compared to other forms of gambling (e.g., lottery). There is emerging evidence that different forms of gambling can have different etiologies and thus, have a distinct impact on research. For example, it has already been demonstrated that there are differences between profiles of gamblers who engage in different types of gambling. As discussed above, there are differences in people who pursue different forms of gambling not only in relation to demographics (Kroeber, 1992; Smart & Ferris, 1996), but also in their moods (Coman et al., 1996), their motivations towards gambling (Chantal & Vallerand, 1996; Dickerson, Fabre, & Baylis, 1985), the number of cognitive distortions they have (Toneatto et al., 1997; Walker, 1992a), and their personalities (Adkins et al., 1988). Even biological studies on endorphins have suggested the possibility of different causal factors related to the choice of different forms of gambling (Blaszczynski, Winters, et al., 1986). One study showed that heritability of the frequency of gambling occurs only for some games such as games that have heavy player promotion and high pay-offs (Winters & Rich, 1998). It has also been shown that certain personality traits (e.g., sensation-seeking) are associated with PG only for some forms of gambling (e.g., games that are illegal and casino gambling compared to those played in off-course betting offices). Such differences highlight the need for research

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to be done separately for different forms of gambling. This is significant, as there are some forms of gambling (e.g., casino gambling, gaming machines, and Internet gambling) that appear more likely to be linked with gambling problems than other forms (e.g., lottery gambling). These forms of gambling are all very highly available and accessible and have a short payout interval. Different forms of gambling vary across dimensions (e.g., continuity vs. discontinuity, skill vs. luck, frequency and immediacy of payout). This suggests that distinct processes may operate for different forms of gambling (Dickerson, 1993) and, thus, there might be a need for different theories to explain such differences as well as different treatment approaches for each form of gambling. This is not a new concept and what we suggest is consistent with other DSM-IV disorders. For example, substance-related disorders in the DSM are divided into subcategories. That is, heroin addiction is treated differently than alcohol addiction. Such subcategories also exist for mood and anxiety disorders. Thus, future studies need to determine whether the variables found to be associated with one form of gambling can be applied to all forms. Secondly, most of the research in the gambling literature is based on Western samples, but results are often generalized to other ethnic and cultural groups. There are vast differences in individuals from different cultural groups, and generalizing the current literature to all cultural groups is inappropriate. Thus, studies are needed to test whether the variables that have been implicated in playing a role in the development and maintenance of PG (findings come from studies with predominantly nonethnic minority samples) can also be applied to other cultural groups. Furthermore, our current review (Raylu & Oei, 2001) indicated a major gap in the gambling literature on the cultural differences in gambling and PG. Few studies have looked at cultural variables that might affect gambling patterns (i.e., gambling behaviors such as the frequency and modes of gambling, urges, and the likelihood of encountering gambling problems). This is significant as those factors identified in the current gambling literature as playing a role in the development and maintenance of PG (e.g., individual, sociological, and familial variables) cannot fully account for the higher rates of gambling among some cultural groups. Many different aspects of culture can play a role in the development and maintenance of PG. Values and beliefs can influence gambling behaviors. For example, they can encourage or discourage involvement in available forms of gambling. The laws and regulations of the culture can determine the kinds of gambling that would be punished and the ones that would be reinforced (Walker, 1992b). The addiction literature has already shown that cultural variables such as cultural values and beliefs, effect of acculturation, and culturally related help-seeking behaviors appear to play a very prominent part in the cause, maintenance, and treatment of addictive disorders among certain cultural groups (Raylu & Oei, 2001). There are several questions that need to be researched: (1) Do certain cultural groups gamble more than other groups?, (2) Are certain groups more likely to develop gambling problems?, and (3) What cultural variables play a role in the cause, development and maintenance of PG? Thirdly, the methodology used in studies in this area needs to be examined with caution. As pointed out earlier, certain areas of research need to be replicated with larger sample sizes and with both genders (e.g., studies investigating the biological evidence of PG) to increase the

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generalizability and validity of results. There are also methodological issues related to the definitions of PG, the efficiency of instruments used to measure PG and sampling procedures. As highlighted earlier, terms PG, problem gambling, and compulsive gambling have been used in the literature interchangeably despite the fact that they do not have the same meaning. Furthermore, substance-related problems have distinguished between dependence and abuse. Although PG symptoms can be distinguished in a similar way, this approach has not been taken for PG. Thus, there is a need for language to be standardized. Shaffer and Hall (1996) introduced the term ‘‘disordered gambling,’’ and offered a four-level classification system, which allows for more precise communication about distinct levels of gambling problems. The four levels included nongamblers (Level 0), nonproblematic gamblers (Level 1), gamblers with subclinical levels of gambling problems (e.g., individuals that other studies have identified as ‘‘problem,’’ ‘‘at-risk,’’ ‘‘in transition,’’ and ‘‘potential pathological’’ gamblers—Level 2), those who have the most severe level of gambling problems (those that meet the established clinical diagnostic criteria for PG—Level 3), and gamblers who are a subset of Level 3 gamblers and have presented themselves for treatment (Level 4) (Shaffer et al., 1997). By conceptualizing gambling behavior and gambling problems along a continuum not only allows movement between categories (e.g., those that do not gamble and those without gambling problems) but also along continuum (e.g., from less severe gambling problems to more severe ones). It might be useful if future studies adopt a similar scheme of conceptualizing problem gambling to maintain consistency in the gambling/PG literature. Lastly, research studies in PG have been similar to most alcohol studies, in that they try and identify what motivates one to gamble and what encourages them to continue gambling despite losses. However, why one stops gambling (rather than why one begins gambling) after starting a single episode may be more important, as that is a characteristic that distinguishes gamblers who gamble socially and those who develop PG. PGs do not know when to stop after starting gambling in a session, whereas social gamblers can stop at will. The importance of understanding episodic cessation is not new in the literature; it has been suggested for problematic drinking (Oei, Sweeton, Dingle, & Chalmers, 1999). There is currently a lack of research in this area for both PG and substance abuse disorders. Pursuing this path of investigation might shed some new light on the variables that distinguish nongamblers, social gamblers, and PGs. Past efforts to theorize and develop theoretical models to explain problem gambling all have strengths and weaknesses but they have resulted in rich insights into the etiology of problem gambling and the characteristics of problem gamblers. Since there is currently no theoretical model adequate and comprehensive enough to account for the complex interaction of these factors, or to adequately explain the development and maintenance of PG, most professionals today are taking the eclectic view that the factors play an interactive role in the cause, development, and maintenance of PG. References Abbott, D. A., & Cramer, S. L. (1993). Gambling attitudes and participation: a Midwestern survey. Journal of Gambling Studies, 9 (3), 247 – 263.

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