Research and Measurement Issues in Gambling ...

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CHAPTER 13

Research and Measurement Issues in Gambling Studies: Etiological Models Alex Blaszczynski

Lia Nower

School of Psychology Department of Medical Psychology University of Sydney Sydney, New South Wales, Australia

Center for Gambling Studies Rutgers University New Brunswick, New Jersey

Introduction Overview Etiological Models Psychoanalytic and Psychodynamic Public Health Social Reward Image Social Validation Behavioral Models Cognitive Conceptualizations Neurobiological, Genetic, and Biobehavioral Integrated Models General Theory of Addictions Biopsychosocial Pathways Summary

INTRODUCTION A primary function of research in gambling is to identify the risk and protective factors that predispose some individuals to continue gambling despite serious adverse consequences. It is well accepted that statistical principles of probability applied to gambling indicate that payout rates and overall advantage always favor the house. The cost of each gamble is a combination of the proportion of each bet retained for taxes and the “house edge,” with the remainder allocated to 323

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a prize pool for distribution to winners.This means that the longer one gambles, the greater the likelihood of losing. Under these conditions, an economically prudent person would minimize risk by limiting exposure to gambling. Yet a minority of the adult population manifest patterns of recurrent excessive gambling behavior that cause significant functional impairment across a range of domains (Walker 1992a). This chapter will provide a brief outline of early psychological explanatory accounts of the origins of problem gambling, followed by a description of more recent unitary and multifactorial etiological models.

OVERVIEW Etiological models attempt to describe the causal processes contributing to a condition or phenomenon. In the field of gambling, researchers have identified specific internal and external predictive risk factors associated with the development of pathological gambling: age, gender, impulsivity, family history, genetic vulnerabilities, and ecological variables (for a comprehensive review, see National Research Council 1999 and the chapters by Toneatto and Nguyen and Abbott in this volume). Setting these individual variables aside, it is evident that there is no single empirically validated theoretical model of gambling that effectively integrates the multivariate biological, psychological, sociopolitical, and environmental factors and processes into a cohesive conceptual framework sufficient to explain the critical pathways leading to the development of problem or pathological gambling. Indeed, debate continues as to whether the condition represents a unidimensional construct with arbitrary boundaries delineating levels of gambling according to intensity of expenditure of time and/or money, or a categorically discrete syndrome differentiated by biological and/or personality factors causing impaired control (Shaffer, LaBrie, and LaPlante 2004;Walker 1992a). Adherents of both the public health (Korn and Shaffer 1999; Shaffer et al. 2004) and dimensional models (Dickerson 1991; Walker 1992a) set aside individual psychological elements in favor of a need to attend to aggregated population, environmental, and social variables that expose community members to risk of excessive gambling. The development of problem and pathological gambling is considered the inevitable outcome of the interactive influences of the degree and duration of exposure to gambling, “addictive” or toxic structural characteristics of the nature of the gambling activity, and vigor of commercial promotions. Public health initiatives designed to promote responsible gambling, therefore, take into consideration elements of accessibility, availability, and acceptability, then attempt to modify these through government policy initiatives and legislated regulatory strategies that restrict access, limit venues and opportunities, and educate and inform participants of the risks associated with gambling.

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The categorical or “disease” model (American Psychiatric Association 2000; Blaszczynski and Nower 2002; Oldham, Hollander, and Skodol 1996) maintains that there is an underlying pathogenesis at the individual level that produces an inherent biological or intrapsychic vulnerability or predisposition that under specific circumstances results in impaired control over behavior. Pathological gambling is conceptualized as the behavioral outcome of intrapsychic conflicts, affective dysregulation coupled with poor problem-solving and coping skills, obsessive-compulsive spectrum features, addiction linked to neurotransmitter dysregulation in brain reward centers, behavioral disturbances resulting from schedules of reinforcement and/or irrational and erroneous belief schemas regarding probabilities and estimates of winning, and adverse personality traits (Blaszczynski and Nower 2002). It is important to appreciate that theoretical models explaining the etiology of gambling are not mutually exclusive but share many common overlapping elements. For example, principles of learning and contingencies of reinforcement fundamental to conditioning theories are relevant to the addiction, affective dysregulation, cognitive, and biological reward deficiency models. Essentially, all conceptual models acknowledge the interaction of key biopsychosocial variables in the etiology process. However, they assume that pathological gamblers form a homogeneous population, and these models are therefore limited by a set of fundamental principles in their search for a single, narrow, theoretically oriented explanatory cause or set of processes to account for the motivation to participate initially through to the transition to impairment in control and consequent persistence over time. There is increasing evidence that although sharing common attributes, pathological gamblers differ among themselves psychologically and demographically in many important respects, which precludes application of the same etiological processes to all members of the gambling population. Converging lines of emerging research suggest the existence of distinct subgroups of pathological gamblers. Although the clinical manifestations and presentations may appear superficially similar, there are significant differences in their causal pathways that offer important distinctions with a major influence on management, course, and prognosis. The following sections will describe the predominant etiological models.

ETIOLOGICAL MODELS PSYCHOANALYTIC

AND

PSYCHODYNAMIC

The primary focus of early concerns with gambling rested with social and political agencies attempting to curtail moral corruption, crime, and public and social disorder associated with gambling, or to protect vulnerable gamblers

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from exploitation and cheating by unscrupulous operators. The moral weakness view of gambling, prevalent until the twentieth century, failed to distinguish social from immoderate and excessive gambling and accepted all forms of the behavior as sinful and a regression to primitive instincts (France 1902). Heralding contemporary explanations of the motives underlying excessive gambling and its perception as an addiction, early formulations emphasized avarice and the pursuit of wealth or held the premise that “the true temptation [underlying gambling] is the desire which prompts most men to drink hard,” that is, excitement, escape from boredom, and “a desire to forget self ” (France 1902, p. 383). In contrast, sociological accounts showed a tendency to emphasize broader ecological aspects of industrial capitalism, in which gambling represented an escape from regimentation, poor quality of life, and a concomitant sense of alienation and anomie (Bloch 1951; Goffman 1969; Herman 1976). Commencing with von Hattinger’s (1914) case study, the earliest formal etiological theories were psychoanalytic and psychodynamic in orientation. Freud (1945) equated gambling to a compulsive neurotic state which was conceptualized as an addiction in the same context as alcoholism and substance abuse (Galdston 1951; Rosenthal and Rugle 1994). Gambling was seen as the manifestation of an addiction with masturbation, which was considered the “primal addiction for which all later addictions are substitutes” (Herman 1976, p. 94). Freud (1945) contended that as a result of unfulfilled desires for his mother and wishes for his father’s death, the gambler remained stationary in a compulsive neurotic state engaging in self-punishment as in the form of masturbatory obsession played out in the arousal and stimulation of gambling. Although there is no detailed account of his direct involvement in the treatment of a case of pathological gambling, Freud (1945) provided a fascinating psychoanalytic analysis of the Russian novelist and pathological gambler Fyodor Dostoevsky founded on the content of the novelist’s letters and writings. Freud hypothesized that gambling provides a substitute for unresolved sexual conflict. Fueled by guilt and depression, the gambler bets, not for the money, but for excitement generated by ambivalence.The gambler commits moral masochism to punish himself by losing, while, alternately, continuing the activity in hopes of receiving the “love” of the symbolic parent while winning. McCormick and Taber (1987) hypothesized that this ambivalence is generated by “the early presence in the patient’s life of a parent figure who was perceived as punishing and demanding, yet evocative of respect and fear” (McCormick and Taber 1987, p. 10); for example, Dostoevsky’s father, who died suddenly when the novelist was 18 (Herman 1976). Gambling becomes an unconscious reenactment of childhood rebellion against parental figures and propels the gambler toward life situations of rejection that need to be overcome (Bergler 1957). These situations result in an ever-present balancing of a pleasure–pain tension level fueling the gambling. The gambler masks that tension with narcissistic charm that actually belies hostile

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and aggressive personality features that are postulated to underlie the addiction (Lindner 1950). Freud’s analysis laid the foundation for the myriad of subsequent psychodynamic explanations, emphasizing a range of intrapsychic processes and conflicts: sexualization of gambling, the presence of underlying psychoneuroses related to regressions to pregenital psychosexual phases of development, regressive infantile conduct and attempts to obtain longed-for erotic satisfaction, fulfillment of primitive superego demands, and challenges and provocations to destiny and fate (Fenichel 1945; Kris 1938; Laforgue 1930; Reik 1942; von Hattinger 1914). Fenichel (1945) observed that gamblers present as narcissists, feeling entitled to privilege and exempt from negative consequences and fate’s dire circumstances. In contrast, Galdston (1951) suggested that the weak ego state of the gambler caused him to reach out to a surrogate parent—Lady Luck—in a symbolic attempt to garner favor and approval. This effort, of course, meets with continual frustration. Harris (1964) summarized the varying psychoanalytic positions by concluding that all possess three characteristic conceptions of gambling, as: (a) an unconscious substitute for pregenital libidinal and aggressive outlets associated with unresolved Oedipal conflicts, (b) the wish for punishment emerging as a reaction to guilt associated with indulgences in forbidden impulses, and (c) a medium for repeated reenactments—but not resolution—of these conflicts. It is important to note that psychoanalytic reports prior to the 1980s described clinical observations of single cases or small samples of patients whose primary diagnoses or referrals were not specifically gambling related, conducted before diagnostic criteria for the disorder were established. In addition, treatment goals and levels of gambling severity were left unspecified. Only Rosenthal and Rugle (1994) have postulated a clear rationale for the effectiveness of integrated insight-oriented supportive therapies, though their argument is largely theoretical. In general, psychoanalytic explanations are impossible to empirically validate and are therefore of limited utility in explaining the pathogenesis of pathological gambling (Cornish 1978; Rosecrance 1985). As a result, the scientific standing of psychoanalytic and psychodynamic frameworks as empirically supported models for pathological gambling has failed to advance significantly over the last 20 years, as public health, behavioral, cognitive-behavioral, biological, and addiction models have assumed greater importance.

PUBLIC HEALTH Gambling occurs within a social context in which availability, accessibility, and acceptability are influenced by a myriad of socioeconomic and political influences. Government legislation dictates the nature and range of legalized gaming

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products, their distribution and location within communities, age restrictions, and enforcement procedures to ensure that commercial advertising and promotional activities comply with appropriate codes of conduct and legislative requirements. In addition, the structural characteristics of gaming products and environmental contingencies in the venues have implications for their toxic or “addictive” quality and likelihood of creating problems (Dowling, Smith, and Thomas 2005; Griffiths 1993;Walker and Dickerson 1996). The public health model of gambling, therefore, adopts a critical position in pursuing a population-based prevention orientation. Accordingly, this model shifts the focus of attention away from micro-level individual intrapsychic and personality variables to aggregated data describing elements at a macro level. It is important to stress that the model does not ignore micro (psychological) factors. Rather, it focuses on mapping global risk and protective factors that contribute to the transition from recreational to problem gambling and the distribution of gambling within the community to identify vulnerable ethnic and other subcommunities (Shaffer et al. 2004). The public health model, derived from an epidemiological framework, is geared toward assessing and monitoring harm caused by gambling and shaping government policies designed to reduce harm and guarantee equitable and timely access to treatment. Korn and Shaffer (1999) and Korn (2001) were the first to formally apply the communicable disease control paradigm to gambling in describing the complex interrelationship between the host (gambler), agent (gambling opportunity), and vector (money) operating within a specific environment (family, sociopolitico-economic, and cultural). The central tenet of this model, as eloquently described in a 2004 article by Shaffer et al., is that exposure to gambling (by analogy, equivalent to exposure to germs) is a necessary but not sufficient factor that “infects” individuals insofar as it influences patterns of gambling behavior and problem gambling; increased risk for problem gambling is functionally related to duration of exposure and toxicity of the product. Social, cultural, religious, and ethnic attitudes toward gambling may serve as protective factors—for example, contributing to low prevalence rates among Islamic and some fundamentalist Christian communities (Seventh-Day Adventists, Mormons). Evidence supporting the public health model is sourced from epidemiological studies suggesting a link between gambling availability and higher prevalence rates (see Abbott, this volume; Petry 2005), although Shaffer et al. (2004) assert that there is minimal scientific data to demonstrate a definitive causal relationship between the two. These authors point to studies that produce conflicting data on this topic. Nevertheless, there is evidence that the introduction of opportunities into a virginal gambling environment is associated with increased participation rates with diminishing marginal increases after the market reaches saturation (Abbott, this volume).

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Shaffer et al. (2004) also advanced the concept of social adaptation to gambling.This social adaptation model is based on the notion that individuals and communities learn to adapt to changes within their environment in such a way that a cohort follows a progression, beginning with escalating involvement in the early, introductory phase of gambling in a community, which levels to a plateau as the market matures, which in turn is followed by environmental adaptation. The next cohort generation fails to experience novelty or “honeymoon” effects of gambling and/or may be exposed to or experience gambling-related harm within the family or society; thus, they become more cognizant of the negative aspects of gambling. This theory is supported by longitudinal data, suggesting lower rates of problem gambling among Nevada adolescents and the reduction in prevalence rates in Canada (Wynne, Smith, and Jacobs 1996) and Minnesota (Stinchfield 2001). The public health model is predominantly concerned with the external societal determinants of gambling, suggesting that strategies designed to ameliorate gambling-related harms are best pursued through public policy decision-making initiatives. The model does not address concerns at the individual psychological and biological level that explain why only some individuals develop problem gambling behaviors.

SOCIAL REWARD A few theorists have provided etiological conceptualizations based on social reward. There is little empirical validation for these theories; however, two of the more creative hypotheses derived from these theories provide constructs that could yield interesting and important information on the role of the social system in pathological gambling. Image Holtgraves (1988) asserted that the urge to gamble is rooted in a need to present a desired image to others. He theorized that that desire, labeled “selfpresentation,” would encompass other explanations for gambling, like the gambler’s desire to be punished (Bergler 1957), to affirm his existence (Kusyszyn 1977), and to escape boredom (Herman 1976). Self-presentation theory holds that actions carry messages about the image of the social actor. As a result, the actors attempt, consciously or unconsciously, to use their actions to control their image. The image of the gambler is multifaceted. Gambling involves risk taking and is usually conducted in a social setting (e.g., casino, racetrack) that promotes extravagance and a “carefree, reckless, freewheeling image” that bestows prestige (Holtgraves 1988, p. 81). Holtgraves (1988) added that “fateful” activities like

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gambling allow for an expression of character: Even when losing, the gambler can display “courage, gameness, integrity and composure” (p. 82). In two preliminary studies, Holtgraves (1988) found that four ego ideals similar to those suggested by Goffman (1969) emerged as motivations for gambling behavior: 1. 2. 3. 4.

competence (perceptive, skilled responsive, observant), confidence (venturesome, positive outlook), control (deliberate, consistent, composed), and sociability (personable, sportsmanlike).

In addition, despite the fact that all gambling outcomes are determined by chance, gamblers rated their peers who won as more competent (i.e., perceptive, skilled, responsible) than those who lost. Betting style also affected perceptions of confidence and control. Gamblers who continued to increase their wagers were perceived as more confident but less controlled than those who bet the same amount each time. Holtgraves (1988) claimed that these findings suggest that “riskiness” can result in the “imputation of both positive qualities (venturesome, confident, competitive, positive outlook) and negative qualities (impulsive, inconsistent, and excitable)” (p. 86). Social Validation Ocean and Smith (1993) broadened the concept of social reward by positing a theoretical model to explain how the gambling venue as an institution perpetuates the need for social validation, which ultimately may result in pathological behavior. These authors hypothesized that a casino environment offers social rewards which include “group affiliation, emotional and moral support, selfesteem, social status and salient identity” (p. 334). At the same time, “outside society” fosters stigmatization, disculturation, and value conflicts, particularly for members like disenfranchised minority groups and those who are unwilling or unable to conform to societal norms. Gambling provides double reinforcement: Social rewards (positive reinforcers) increase the gambler’s commitment to the casino, while the negative reinforcers from society are removed when the gambler enters the casino. As the gambler increases play, her problems with the outside world increase and thus she is more likely to seek escape in the casino. Most research on pathological gambling has focused on the personality and family of the gambler or on the gambler’s physiological or psychological state (Ocean and Smith 1993).The theory advanced by Holtgraves (1988) suggests that it would be wise to devote research to examining the seductive power of gambling institutions and to devising new ways of decreasing the alienation gamblers feel from society. Future study of minority-group and senior-citizen gamblers should provide valuable information in this area. As with the public health model, the social reward model focuses on (a) macro-level factors, with an implicit two-tiered

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assumption of homogeneity, (b) variables influencing gambling that apply equally to all gamblers, and (c) the underlying psychological dynamics as being similar for all problem gamblers.

BEHAVIORAL MODELS The underlying assumption in behavioral models is that gambling is a learned maladaptive behavior governed by principles of Skinnerian operant and Pavlovian classical conditioning. As noted by Petry (2005), variable ratio and random contingencies of immediate reinforcement where the intertrial interval (placing a bet and learning of its outcome) is short are instrumental in maintaining high-frequency repetitive behaviors that are resistant to extinction. Dickerson (1979) extended Skinner’s operant conditioning model to postulate the presence of two available reinforcers: (a) money won, reinforced on a random reinforcement schedule, and (b) excitement associated with cognitions and environmental stimuli reinforced on a fixed interval schedule to account for observed betting shop behaviors such as delayed placement of bets. Anderson and Brown (1984) further suggested a two-factor neo-Pavlovian model to account for the maintenance of pathological gambling patterns, emphasizing the classical conditioning of environmental cues and autonomic/cortical arousal, together with the negative reinforcement associated with a reduction in aversive emotional states produced by the narrowing of attention and distraction from awareness of life problems. Within these behavioral models, positive and negative reinforcement are crucial determinants.Winning money (reward) coupled with its concomitant physical and subjective arousal represents a positive reinforcement that increases the probability that a behavior (gambling) will be repeated. The unpredictability of receiving a reward delivered on a random or variable ratio schedule maintains gambling behavior, since the gambler anticipates that the next bet will result in a positive outcome. In addition, as suggested by Anderson and Brown (1984) and Jacobs (1986), a proportion of gamblers experience dissociative states that enable them to emotionally escape from stresses resulting in negative reinforcement, that is, the removal of an aversive (stress or affective) state or stimulus. Negative reinforcements similarly increase the likelihood that future behaviors will increase in frequency. Through classical conditioning, the association of gambling-related environmental stimuli with excitement through repeated pairings of conditional (gambling cues) and unconditional (winning money) stimuli becomes such that, over time, conditional stimuli are sufficient to elicit the unconditional stimuli. Accordingly, subsequent exposure to any environmental gambling cue will elicit a state of excitement that is interpreted as an urge, drive, or craving to gamble or will

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provoke a reaction that is interpreted as a withdrawal state.Any positive (wins) and negative reinforcement (elimination of the urge, drive, or craving and withdrawal state) will consolidate the operant and classical conditioning processes. McConaghy (1980) advanced the behavior completion mechanism model, which suggests that habitual gambling results from a process of cortical excitation in which repeated occurrences of complex sets of behaviors establish a neuronal representation of those habits in the cortex.With each repetition, the set of behaviors becomes increasingly consolidated to form a habitual pattern of behavior. Consistent with Sokolov’s orienting reflex model, formulated in 1963, incoming stimuli are compared against cortical representations of habitual behavior patterns, and if matching occurs, the drive to complete the habit is inhibited. If mismatching occurs, the behavior completion neuronal model initiates a drive for the individual to continue engaging in the sequence of behaviors until the habit is carried out to its completion. Consequently, interruption of the habit results in a state of aversive physical arousal or tension that is experienced as a persistent drive to carry out the habit. Once the habit is successfully completed, the drive is satisfied and the aversive state of arousal dissipates. This model is consistent with the principles underlying operant conditioning in that positive reinforcement associated with the gambling behavior and negative reinforcement produced by the removal of the aversive arousal strengthen the neuronal model of behavior. These learning models have led to the application of a variety of operant or classical conditioning–based aversive techniques to countercondition the arousal/ excitement associated with gambling.The most frequent forms are electric shocks or nausea-producing pharmacological agents (Barker and Miller 1968; Koller 1972; McConaghy et al. 1983; Salzmann 1982; Seager 1970), covert sensitization (Bannister, 1977; Cotler 1971), and stimulus control and exposure (Greenberg and Rankin 1982). The behavior completion mechanism model led to the innovative application of imaginal desensitisation as a successful intervention (McConaghy et al. 1983). Although behavioral treatments can be effective (see Hodgins, this voume), the behavioral etiological models fail to explain (a) the reason that fewer than 5% of gamblers persist in excessive gambling or (b) the transition from an extended period of recreational gambling to excessive habitual patterns. These behavioral models also fail to explain the effects of punishment (accumulating losses) on human behavior. In animal paradigms, pigeons or rats persist in pressing levers for food even to the point of exhaustion under conditions of variable reinforcement. However, persistence does not result in other concomitant costs to the animal. In contrast, persistence in gambling is associated with significant direct response costs to the individual: emotional distress, remorse, lack of finances, and anticipated marital conflicts and legal/social consequences during or toward the end of sessions as funds are depleted and the gambler realizes the consequences of his/her action. Unlike alcohol abuse, where there is a delay in the negative effects (a hangover)

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following excessive consumption, negative emotions are experienced during or immediately after completion of gambling. Behavioral models have all but neglected the role of punishment, focusing instead on the role of positive and negative reinforcement. Though valuable in explaining persistence in gambling and underpinning addiction paradigms, pure behavioral etiological models are of limited utility as a conceptual framework explaining problem and pathological gambling. In contrast, cognitive-behavioral models acknowledge limitations by combining learning principles with additional elements.

COGNITIVE CONCEPTUALIZATIONS Without doubt, the cognitive model is most frequently utilized to guide treatment interventions for problem gambling. A number of studies have found that gamblers who receive cognitive restructuring treatment (Echeburua, Baez, and Fernandez-Montalvo 1996) in conjunction with social skills training, problem solving, and relapse prevention (Sylvain, Ladouceur, and Boisvert 1997) report decreased levels of problem gambling. (For reviews, see Hodgins in this volume, and Petry 2005.) The cognitive model is predicated on the assumption that erroneous and irrational belief structures, misunderstanding of probabilities and concepts related to randomness and mutual independence, and the drawing of causal associations between independent chance events form the basis for persistence in gambling despite accumulating losses (Ladouceur and Walker 1996; Toneatto et al. 1997; Walker 1992a).Toneatto et al. (1997) and Ladouceur and his colleagues (Gaboury and Ladouceur 1989; Ladouceur and Gaboury 1988; Ladouceur et al. 1988) have consistently found that up to 80% of the verbalizations made by a sample of problem gamblers seeking treatment were irrational or contained cognitive distortions, with a mean number of 3.5 cognitive distortions per participant. Experiences of social learning, such as vicarious exposure to parental gambling, participation in family and peer-related gambling activities, and positive parental attitudes, engender in children and adolescents positive acceptance of gambling as a legitimate recreational pastime. Experientially, early wins are instrumental in shaping beliefs that winning is possible and that gambling represents a convenient and easy source of supplementary income. Increased frequency and intensity of gambling invariably lead to a progressive, downward spiral of accumulating losses (Lesieur 1984), which in turn produces cognitive dissonance, as the gambler justifies behaviors and overestimates the probabilities of winning. There is clear evidence that irrational and erroneous beliefs are prevalent among not only problem but also recreational gamblers. Studies have identified a myriad of erroneous and irrational perceptions and cognitive distortions, identified

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by psychometric measures, experimental manipulations, and audiotaped verbalizations elicited using the “thinking aloud” technique, whereby uncensored thoughts are recorded during play. Toneatto (2002) and Ladouceur et al. (2002) provide a detailed account of the common types of cognitive distortions. These can be broadly categorized into those related to personal skill and judgment (illusions of control: Langer 1975), ability to influence outcomes (superstitious rituals and beliefs: Joukhador, Maccallum, and Blaszczynski 2003; Joukhador, Blaszczynski, and Maccallum 2004), selective recall and biased evaluation of outcomes (Gilovich 1983; Gilovich and Douglas 1986), and erroneous perceptions regarding randomness and the independence of events (Coulombe et al. 1992; Gaboury and Ladouceur 1989;Walker 1992b).Toneatto et al. (1997) reduced 13 such identified cognitive distortions into five classifications under three similar higher-order categories: control, reframing, and prediction. Other studies have also identified a positive relationship between gambling severity and erroneous cognitions related to illusions of control and expectancy of winning (see e.g., Felscher, Derevensky, and Gupta 2004; Ladouceur 2004). Overall, problem gamblers exhibit greater levels of irrational beliefs compared with recreational gamblers, although the direction of causality is yet to be established. By some mechanism, possibly cognitive dissonance, the problem gambler maintains an “illusion of control”—a belief that he has a degree of skill or mastery over the outcome of a game of chance—despite mounting losses and other adverse consequences. In addition, he discounts losses through biased evaluations in which failure is attributed to external factors rather than deficits in personal skills (Gilovich 1983). The illusion of control is supplemented by overvalued beliefs in luck as a personal attribute, unrealistic optimism, and superstitious ideations that coalesce to reinforce the concept that winning is possible. Selective recall of past wins over losses and patterns of intermittent wins reinforce this optimism, as does the gambler’s fallacy (Cowan 1969), which maintains that a win is “due” following a series of losses. Structural characteristics of electronic gaming machines foster the gambler’s fallacy and other related erroneous perceptions. In particular, the phenomenon of the “near miss”—in which a gambler perceives that he or she almost won based on the visual presentation of slot machine symbols—has been found to correlate with increased persistence in gambling (Dixon and Schreiber 2004; Kassinove and Schare 2001). Gamblers misinterpret the randomly generated sequences of symbols displayed on the screen, nearly matching a paying combination, to suggest that the machine is about to pay out. In reality, symbols on the “virtual reel”—the visual representation of outcome on the screen—bear little relation to the “real reel,” a random computer generator of numbers with infinite combinations, housed within the machine. Erroneous perceptions related to near misses increase levels of arousal, which in turn reinforce the belief that winning is imminent (Griffiths 1991).

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Evidence from cognitive studies consistently demonstrates that irrational and erroneous belief schemas are prevalent among problem gamblers (Ladouceur and Walker 1996). However, cognitive theories have yet to adequately explain the functional interaction between arousal and cognitive activity as a causative factor in the onset and maintenance of problem gambling.

NEUROBIOLOGICAL, GENETIC, AND BIOBEHAVIORAL Pathological gambling is frequently described as an “addiction without the drug” (Potenza et al. 2001), the assertion being that with the exception of chasing losses, all diagnostic criteria “have their counterpart in alcohol, heroin, cocaine, and other forms of substance drug dependence.” Evidence for this assertion is based, in part, on the repetitive nature of gambling, persistence despite adverse consequences, preoccupation, impaired control, and features of tolerance and withdrawal. An increasing number of investigations have implicated abnormalities in brain regions associated with decision-making processes, biobehavioral functioning, specifically dysregulation in noradrenergic, serotonergic, dopaminergic, and opioidergic neurotransmitters, and genetic mechanisms, notably twin concordance data and dopamine D2 receptor genes, which may contribute to the development or maintenance of gambling disorder (for comprehensive reviews, see Goudriaan et al. 2004 and Potenza, this volume). Neurobiological and genetic models maintain a common thread in adopting sensitivity to reward and the reward deficiency concept in explaining correlates of problem gambling: craving, relapse, decision making, impulsivity, delayed discounting, and failure to learn. Neuropsychological studies (Carlton and Manowitz 1992; Rugle and Melamed 1993) and performance on tasks such as the Iowa Gambling Test (Bechara et al. 1994; Petry 2001) suggest that pathological gamblers display deficits in higher executive functioning, delay discounting, fluency, and interference control, as well as higher levels of impulsivity and disinhibition often seen in patients suffering attention deficit and ventromedial prefrontal cortex disorders. Using functional magnetic resonance imaging (fMRI), Reuter et al. (2005) found that reduced ventral striatal and ventromedial prefrontal activation on a guessing game were negatively correlated with gambling severity in a sample of pathological gamblers.This pattern of decreased activation, similar to findings in drug addiction, led these authors to conclude that pathological gambling was a non–substance related addiction. Several studies have investigated the role of heritability in gambling disorder (Black, Moyer, and Schlosser 2003; Daghestani, Elenz, and Crayton 1996; Gambino et al. 1993). A meta-analysis by Walters (2001) found wide variation, 16 to 46%, in the proportion of family members of gamblers who also reported disordered

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gambling, substantially less than the predisposition for alcohol or crime. Findings indicated a stronger effect for higher-severity cases in support of a continuum model of gambling, at least for males, suggesting that learning variables and genetics fostered observed gender differences in familial transmission. Likewise, twin studies have reported similarities in the gambling behaviors of male monozygotic twins (Winters and Rich 1998) and identified an association between genetic predispositions to both alcohol dependence and gambling disorder (Slutske et al. 2000). Genetic studies have reported associations between dopamine-related gene sequences and pathological gambling (Comings et al. 1996, 1997, 2001). Gambling acts to release dopamine, a chemical that mediates pleasure responses in the brain. As further evidence, some patients suffering from Parkinson’s disease, which depletes the brain of dopamine, begin gambling pathologically when prescribed medication to increase dopamine production (Seedat et al. 2000). In addition to dopamine, dysregulation in two other brain chemicals largely responsible for mood—serotonin and norepinephrine—have been implicated in the dysphoric mood states that are often cited as predisposing factors for problem gambling (DeCaria et al. 1996; Moreno, Saiz-Ruiz, and Lopez-Ibor 1991; Roy, DeJong, and Linnoila 1989). These studies suggested that genetic variants implicating dopaminergic systems set the foundation for sensitivity to certain types of rewards, such as the excitement associated with winning and risk taking inherent in gambling.Through cortical excitatory processes (winning and environmental stimuli), which involve the meso-limbic reward circuit structures, ventral tegmental area, amygdala, and nucleus accumbens, the reinforcing effects of gambling are consolidated in hippocampal memory. Conditioned responses (amygdala) to relevant cues and/or withdrawal in response to the absence of cues subsequently triggers feelings of craving to resume gambling. Deficits in response inhibition caused by the action of neurotransmitters on the prefrontal cortex result in the decreased capacity of higher frontal lobe executive functioning to inhibit urges, which, when combined with (a) erroneous cognitive belief schemas, (b) cravings generated by reward memories, and (c) anticipatory reinforcement, inevitably leads to continued gambling. Withdrawal and tolerance phenomena also play central roles in the maintenance of the addictive cycle (Bozarth 1994). Initially, the euphoric effects of gambling are highly reinforcing and lead to a shift in incentive-salience that is described variously as “wanting,” “craving,” or “toxic motivation” (Bozarth 1990; Koob and Moal 1997). With repetition, greater incentive salience to gamblingrelated stimuli occurs in line with the increasing sensitization of the dopamine system (Robinson and Berridge 1993). Concomitantly, the strength of the appetitive effects of drugs is sufficient to supplant those elicited by other reinforcers, precipitating a downward spiral whereby the gambler focuses on gambling to the exclusion of all other social, personal, and familial inclinations and obligations.

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Over time, the need to reduce or avoid aversive gambling-withdrawal symptoms, fostered by neuroadaptational changes and motivational shifts, emerge as the predominant reason for continued behavior and relapse episodes (Baker et al. 2004).Withdrawal-induced negative affective states become potent motivators for relapse (Baker et al. 2004), and the drive to reduce withdrawal fosters dependence in negative reinforcement models of addiction (Cappell and Le Blanc 1981; Hershon 1977; Robinson and Berridge 1993). As Goudriaan (2005) notes, methodological difficulties and inconsistent findings in the limited number of neurobiological and genetic studies conducted to date preclude a conclusive interpretation of the causative role these factors play in pathological gambling. It yet remains to be demonstrated that observed neurotransmitter dysregulation and neuropsychological deficits are the causes or the effects of pathological gambling. Nevertheless, the concepts of reward deficiency (Blum et al. 2000) and impaired response inhibition and salience attribution (see Heidbreder 2005 for a review) propose addiction models that may be productively applied to gambling. Data from neurobiological models suggest commonalities between gambling and substance abuse disorders, a fruitful area for further research but one fraught with many unchallenged assumptions (see Potenza, this volume).

INTEGRATED MODELS The complex and multifactorial nature of biopsychosocial findings in research suggest that problem gambling results from the interplay of a variety of factors that coalesce to result in disorder. In response, the general-theory-ofaddictions (Jacobs 1986), biopsychosocial (Sharpe 2002; Sharpe and Tarrier 1993) and pathways models (Blaszczynski and Nower 2002) attempt to explain and integrate salient factors.

GENERAL THEORY

OF

ADDICTIONS

The general theory of addictions was the first attempt to account variously for physiological and psychological factors in the etiology of pathological gambling and other addictive behaviors (Jacobs 1986). Jacobs proposed that pathological gamblers possess two interrelated sets of predisposing factors: (a) a physiological resting state of arousal that is either hypotensive/depressed or hypertensive/anxious and (b) a psychological predisposition toward feelings of inadequacy, low selfesteem, and low self-efficacy, influenced by early rejection from caregivers and peers, which fosters a need for recognition and approval (Jacobs 1986). The theory maintains that predisposing factors combine with a need for wish fulfillment and escape and cause the gambler to seek chance encounters with

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substances, behaviors, or both that foster dissociation from reality and a feeling of being “alive” and “normal.” Gambling maintains the fantasy in which anxiety becomes excitement, depression transforms into relaxation, and the gambler feels successful and accepted. In keeping with learning theory, such an experience establishes a “reciprocal relationship between positive and negative reinforcement” (Jacobs 1986, p. 28).The gambler continues in this pattern in order to avoid returning to the prior aversive resting state and resists attempts to discontinue the behavior. Ultimately, mounting adverse consequences propel the desperate gambler into a “state of physical and psychological exhaustion” (p. 28) that may, in the best circumstances, lead to treatment. Gupta and Derevensky (1998) reported empirical support for the model in a cohort of adolescents; however, the study was limited by use of a convenience sample and existing survey instruments to test the constructs.

BIOPSYCHOSOCIAL Based on research findings, Sharpe and Tarrier (1993) proposed a heuristic cognitive-behavioral model to account for the development and maintenance of problem gambling. The model, figuratively depicted as a systemic feedback loop, suggests that gambling behavior initiates from a trigger, usually an early monetary win that causes a physiological reaction in the form of autonomic arousal. The gambling is then reinforced by the desire for increased arousal amplified by gambling, by a partial reinforcement schedule of wins, and by arousal-generating cues in the gambling environment. The model further postulates that problem-solving and stress-coping skills serve as mediators for problem gambling behavior, such that individuals with poor problem-solving and coping skills, particularly those exposed to environmental factors that reduce the efficacy of those skills, are more likely than others to develop gambling problems. A reformulation of the model by Sharpe (2002) adopted a diathesis-stress perspective on predisposing factors, maintaining that adverse experiences in the early psychosocial environment, combined with genetic vulnerabilities such as deficits in the dopaminergic and serotonergic systems, result in psychological and/or biological vulnerabilities that trigger a loss of control in gambling situations.

PATHWAYS In response to etiological conceptualizations that perceive pathological gambling either as a categorical or as a spectrum disorder and assume that problem gamblers are a homogeneous population, Blaszczynski and Nower (2002) proposed the pathways model, a conceptual framework that identifies three primary subgroups/clusters of gamblers: behaviorally conditioned, emotionally vulnerable,

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and biologically based impulsive pathological gamblers. All three groups have common exposure to related ecological factors (e.g., availability, accessibility, acceptability), cognitive processes and distortions, and contingencies of reinforcement. However, according to the proposed model, predisposing emotional stressors and affective disturbances for some individuals and biological impulsivity for others represent significant additive risk factors. The differential pathways model has significant implications for treating adults and adolescent pathological gamblers (Blaszczynski and Nower 2002; Nower and Blaszczynski 2004). Based on the research literature, the model proposes three different etiological pathways. Pathway 1 gamblers are characterized by an absence of specific premorbid features of psychopathology, and their gambling results largely from the effects of conditioning, distorted cognitions surrounding probability of winning and disregard for the notion of independence of events, and/or a series of bad judgments/poor decision making rather than because of impaired control. Cognitive therapy and brief interventions are treatments of choice.The Pathway 2 gamblers share similar ecological determinants, conditioning processes, and cognitive schemas; however, these individuals also present with premorbid drug abuse, anxiety, and/or depression, a history of poor coping and problem-solving skills, problematic family background experiences, and major traumatic life events that fuel gambling participation motivated by a desire to modulate affective states and/or meet specific psychological needs. For this group, cognitive-behavioral interventions require the addition of stress management, problem-solving, and other appropriate adjunctive therapies designed to address premorbid psychopathology. Finally, Pathway 3 gamblers possess psychosocial and biologically based vulnerabilities similar to Pathway 2 gamblers but are distinguished by a high degree of impulsivity, antisocial personality disorders, and attention deficit, manifesting in severe multiple maladaptive behaviors. Given the putative role of biological factors linked to neurotransmitter dysregulation and traits of impulsivity, psychopharmacological interventions should be considered as an important supplementary treatment. While these pathways purport to account for differences among problem gamblers, it is important to note that empirical testing is needed to validate, refute, or supplement proposed variables within the model and to further elucidate differences among subgroups of problem gamblers with regard to age, gender, ethnicity, and other relevant factors.

SUMMARY Problem gambling is a complex disorder with a variety of biopsychosocial risk factors. Theoretical conceptualizations ranging from Freudian and neurobiological explanations to cognitive-behavioral theories attempt to explain persistence

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in behavior despite unfavorable odds and mounting adverse consequences. Due to variants in individual differences, family history, psychobiology, and cognitive interpretations, no single theory can fully account for the etiology of disorder in all problem gamblers. Future research is needed to further identify salient risk and resiliency factors and to refine methods of identification and treatment that are tailored to individual differences among problem gamblers. It is imperative to pursue efforts to develop an integrated conceptual model of gambling and pathological gambling that acknowledges the heterogeneity of the gambling condition.

GLOSSARY Etiology factors and processes contributing to the development of pathological gambling. Pathways model a model based on the notion of three subgroups of pathological gamblers each having similar phenomenological features but different factors contributing to its development. Theoretical models conceptual models explaining how pathological gambling develops and factors that may contribute to its maintanence. Explanatory models derived from specific theoretical orientations of psychology include sychodynamic, behavioral, cognitive, biobehavioral, and public health.

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