Pathological Gambling and Alcohol Use Disorder

Jon E. Grant, M.D., Matt G. Kushner, Ph.D., and Suck Won Kim, M.D.

Problematic gambling is more common among people with alcohol use disorders (AUDs) (i.e., either alcohol abuse or dependence) compared with those without AUDs. This association holds true for people in the general population and is even more pronounced among people receiving treatment. No broadly accepted explanation for the link between problematic gambling and AUD currently exists. The available literature suggests that common factors may increase the risk for both conditions. For example, a defect of functioning in a particular brain system may underlie both conditions. This hypothesis should be further developed using brain imaging and psychopharmacological studies. Effective treatment and prevention will require additional research into relevant associations on both the event level (e.g., the effects of drinking on gambling behavior and vice versa) and the syndrome level (e.g., the relative onset and course of each condition among those who have either one or both disorders). A prudent interpretation of the available data suggests careful screening and treatment when necessary for problematic gambling among people with alcohol abuse and for alcohol abuse among people with gambling problems. KEY WORDS: pathological gambling; AODD (alcohol and other drug dependence); comorbidity; etiology; diagnostic criteria; disinhibition; impulsive behavior; ventral tegmental area; encephalopathy; naltrexone; genetic linkage; causal path analysis; treatment outcome

athological gambling (PG) is both community and clinical samples. problem compared with PG. Rather, characterized by a persistent mal­ The article then reviews the processes this term is used to distinguish between Padaptive pattern of gambling and mechanisms that might account problem gambling formally shown to behavior. PG was first formally included for the frequent co-occurrence of these meet the DSM criteria (PG) and all in the Diagnostic and Statistical Manual disorders. Finally, it examines what the other cases of problematic gambling of Mental Disorders, Third Edition (DSM– co-occurrence of these disorders implies behavior (disordered gambling behavior). III) in 1980 (American Psychiatric for treatment and highlights promising Association [APA] 1980). Currently, areas for future research. PG is classified under the category Many terms have been used to describe JON E. GRANT, M.D., is a psychiatry resi­ “disorders of impulse control not else- people with problematic gambling dent, MATT G. KUSHNER, PH.D. is an where classified” (APA Committee on behavior (see Cunningham-Williams associate professor, and SUCK WON KIM, Nomenclature and Statistics 2000). and Cottler 2001). In this article, PG M.D., is an associate professor, all in the This article explores the association refers to pathological gambling as diag­ Department of Psychiatry, University of between pathological gambling and nosed using DSM diagnostic criteria. Minnesota Medical School, Minneapolis, alcohol use disorders (AUDs) (i.e., the The term “disordered gambling behavior” Minnesota. general name for either alcohol abuse is used to refer to problematic gambling or alcohol dependence). It first examines behavior that is not defined by DSM This research was supported, in part, by the separate and overlapping preva­ diagnostic criteria. Note, however, that a grant from the National Institute on lences of PG and AUD as estimated by this term is not used as a means of Alcohol Abuse and Alcoholism (AA–12426) epidemiological surveys conducted in identifying a less serious gambling awarded to the second author.

Vol. 26, No. 2, 2002 143 Epidemiology findings from the National Comorbidity with disordered gambling behavior also Survey (NCS) (Kessler et al. 1994), the report a lifetime history of AUD estimated lifetime prevalence is 14.2 (Cunningham-Williams et al. 1998), Pathological Gambling percent for alcohol dependence and 9.4 a rate that greatly exceeds general preva­ percent for alcohol abuse, based on cri­ lence estimates for AUD (see above). In During the 1990s, changes in State and teria in the DSM–III–R (APA 1987). fact, these studies reported that as gam­ local legislation encouraged the expan­ The National Longitudinal Alcohol bling severity increased, so did the risk sion of all types of wagering (e.g., casino Epidemiologic Survey (NLAES) found for AUD, even when sociodemographic gambling, lotteries, Internet gambling). that over the 12 months preceding the variables were controlled. Similarly, As an apparent consequence, gambling survey, 4.4 percent of adults age 18 or Feigelman and colleagues (1998) found and gambling-related problems are on older met the criteria for alcohol depen­ that 26 percent of U.S. community-based the rise in the United States and Canada. dence and 3.0 percent met the criteria respondents with disordered gambling A recent meta-analysis of 120 published for alcohol abuse (Grant et al. 1994). behavior reported having experienced studies estimated that 1.6 percent of In sum, between 7 percent and 14 per- AUD or some other substance use disor­ adults in the United States and Canada cent of adults in the United States der at some point during their lifetime. meet the DSM criteria for pathological experience an AUD at some point in These survey findings, considered gambling at some point in their lives their lives. against findings from the ECA survey (Shaffer et al. 1999). Among people The NCS found that the median age showing that approximately 14 percent younger than 18 years of age, the cur- of onset was 19 years for alcohol abuse of U.S. adults experience AUD (above), rent prevalence of PG is estimated to and 18 years for alcohol dependence indicate that, in the general population, be 3.9 percent, with past-year rates for (Kessler et al. 1997). The NLAES found the risk for AUD is two to four times adults and adolescents estimated at 1.1 that the risk for developing an AUD higher for people with PG compared percent and 5.8 percent, respectively was substantially increased among those with those without PG. However, a (Shaffer and Hall 1996). who started drinking before age 17 more recent study found a substantially Slightly lower prevalence rates of (24.5 percent lifetime prevalence) com­ greater association between AUD and PG were found by a national study pared with those who started drinking PG (Welte et al. 2001). This study conducted by the National Opinion at age 21 or 22 (10 percent lifetime reported an odds ratio for current alcohol Research Center (NORC). This study prevalence) or at age 25 years or older dependence with current PG of 23.1 found the lifetime prevalence of adult (less than 4 percent lifetime prevalence) (Welte et al. 2001). That is, the odds of pathological gambling to be 0.9 per- (Grant and Dawson 1997). In fact, the having a current alcohol dependence cent, with past-year rates of 0.6 percent prevalence of alcohol abuse detected in diagnosis were 23 times greater among (NORC 1999). that study declined with each increas­ those in the survey who had a PG diag­ Although studies using historical ing year of age of onset of drinking. nosis than for those with no PG diag­ review (i.e., retrospective methodologies) nosis. It should be noted that this study have tended to point to a young age of Comorbid AUD and PG focused on having a current (vs. lifetime) onset of PG (Cunningham-Williams diagnosis and on alcohol dependence, and Cottler 2001), more definitive Given the relative frequency of both rather than abuse. Similar to the study studies that follow participants over PG and AUD, these conditions would reported by Cunningham-Williams time (i.e., prospective studies) to deter- be expected to co-occur in some cases and colleagues (1998), Welte and col­ mine the natural course of PG have yet by chance alone. However, there is evi­ leagues (2001) also found that the to be conducted. Studies looking at dence that disordered gambling behav­ prevalence of current PG increased with cross sections of different age groups ior and AUD co-occur in U.S. and increasing alcohol consumption. Among have shown that PG prevalence rates Canadian residents at a rate exceeding those people with higher socioeconomic appear higher for adolescents and that expected by chance. As described status, alcohol dependence and PG were young adults than for middle-aged and below, studies of treatment populations even more strongly correlated (Welte et older adults (Shaffer and Hall 1996). found an increased risk of PG in alco­ al. 2001). Long-term studies are necessary, how- holism treatment patients and an ever, to clarify these findings. increased risk for AUD in PG treat­ Treatment Populations. Consistent ment patients. with observations pertaining to comor­ AUD bidities involving a variety of disorders Community Populations. A large epi­ (e.g., Kushner et al. 1990), comorbid Based on DSM–III criteria, the demiological survey in Canada esti­ PG and AUD tend to be more prevalent Epidemiologic Catchment Area (ECA) mated that the relative risk for AUD is in treatment (vs. community) samples. survey estimated that 13.8 percent of 3.8 times higher when disordered gam­ One early study suggested that 17 per- adults in the United States meet the cri­ bling behavior is present (Bland et al. cent of alcoholism treatment patients teria for AUD at some time during their 1993). A study conducted in the United reported disordered gambling behavior lives (Robins et al. 1991). According to States found that 44 percent of those (Haberman 1969). A later study of 100

144 Alcohol Research & Health Pathological Gambling and Alcohol Use Disorder

inpatients with alcohol dependence to develop an AUD (e.g., Helzer et al. on comorbidity without also consider­ found that 14 percent met the criteria 1991). Because men are more likely than ing a wide range of variables that often for PG, and that an additional 14 per- women to experience both AUD and correlate strongly with race/ethnic des­ cent suffered from subclinical gambling PG, the co-occurrence of these disorders ignations (e.g., social, economic, cul­ problems (Lesieur and Heineman 1988). by chance alone should be more com­ tural, and geographic variables). Studies In a study of 79 patients with alcohol mon among men. In one of the few showing different base rates of AUD dependence, 7 (8.9 percent) met the studies to examine gender differences and PG across racial/ethnic groups sug­ criteria for PG (Lejoyeux et al. 1999). in comorbidity rates, men with disor­ gest the potential importance of further Other researchers have estimated that dered gambling behavior were more study in this area. 20 percent of patients undergoing sub- likely to report drinking problems than As reported above, AUD and PG stance abuse treatment have problems were women with disordered gambling co-occur at a rate significantly exceed­ with gambling (Lesieur et al. 1986; behavior (20 percent vs. 15 percent); ing that expected by chance in both Giacopassi et al. 1998). In a study of however, this difference was not general community and treatment 276 patients consecutively admitted to deemed statistically significant (Potenza samples. No explanation or cause for a Veterans’ Administration Hospital for et al. 2001). the association between AUD and PG substance abuse, 33 percent met the Additional comorbidities involving is apparent or implied in the epidemio­ DSM–III–R criteria for comorbid sub- other psychiatric disorders may further logical studies reviewed thus far. The stance abuse and PG (Daghestani et al. complicate understanding of the rela­ next section addresses this question. 1996). Given that the lifetime prevalence tionship between AUD and PG. For of PG in the general population has example, recent studies have shown been estimated to be anywhere from 1 that people with attention deficit hyper- Temporal and Causal percent to 6 percent (see above), these activity disorder (ADHD) are at increased Relationships findings indicate a dramatic increase in risk for developing a substance use dis­ risk for PG among alcoholism treat­ order (Mannuzza et al. 1993; Biederman When attempting to understand ment patients. et al.1995). In addition, studies show comorbidity, establishing the temporal Elevated rates of alcohol dependence that pathological gamblers have an relationship of the two disorders is in people receiving treatment for PG increased prevalence rate of comorbid intuitively appealing (i.e., which disorder further support the importance of the ADHD (Carlton et al. 1987; Specker started first?). However, clearly estab­ association between PG and AUD. A et al. 1996). Although little relevant lishing and interpreting such relationships recent study found that 23.2 percent of research has been conducted, a reason- as a means of better understanding the PG patients suffered from current AUD, able hypothesis for further study is that nature of comorbid associations has and that 34.8 percent reported lifetime some psychiatric conditions may mark proven challenging (e.g., Kushner et al. AUD (Ibanez et al. 2001). Similarly, a those who are more likely to develop 2000). One disorder consistently pre- relatively large study of PG patients both AUD and PG. Such a finding might ceding the other would be consistent found that 27 percent suffered from also point toward factors (e.g., impulsiv­ with, but not proof of, a direct causal lifetime AUD (Grant and Kim 2001). ity associated with ADHD) common relationship. Heterogeneity in the order Earlier studies have reported that any- to the etiology of both AUD and PG. of onset, on the other hand, would be where from 19 percent to 48 percent of Studies have also examined whether consistent with (but again, not proof PG patients have a lifetime or current rates of PG differ among racial or ethnic of) the existence of a third variable alcohol problem (Roy et al. 1988; Linden groups (Cunningham-Williams and (e.g., shared genetic factors or patho­ et al. 1986; McCormick et al. 1984; Cottler 2001). For example, research physiology) serving as a common cause Ramirez et al. 1984). Contrasted with has shown higher rates of PG among for both conditions. Further complicat­ risk estimates reviewed above, these Native Americans in alcoholism treat­ ing the picture, causal associations may findings support an approximate dou­ ment compared with Caucasians (5.9 manifest on an event level (e.g., alcohol bling to quadrupling of risk for AUD to 22 percent versus 0.8 to 7.3 percent) use may disinhibit a wide range of among PG treatment patients relative (Volberg and Abbott 1997; Elia and inappropriate behaviors including to the risk for people in the general Jacobs 1993). The St. Louis site for the problematic gambling [e.g., Smart and community with no PG. ECA study found a higher proportion Ferris 1996]) or on a syndrome level of African-Americans represented among (e.g., a new onset of PG occurring, Moderating Variables. The data reviewed problem gamblers (31 percent) than ostensibly as a substitute for drinking, above lack detail concerning the poten­ among nonproblem gamblers (15 per- following alcoholism treatment [e.g., tial influence of various sociodemographic cent) (Cunningham-Williams et al. Ingram-Smith 1967; Lesieur and variables on risk for comorbidity. Surveys 1998). Importantly, however, a variety Heineman 1988]). estimate that approximately two-thirds of of characteristics (e.g., socioeconomic In one of the few studies to examine pathological gamblers are men (Volberg status) are correlated with race and eth­ the temporal pattern of disorder onset 1994). It is also well known that men nicity. That is, it is hard to interpret in comorbid PG and AUD, Cunningham- are substantially more likely than women findings comparing racial/ethnic groups Williams and Cottler (2001) reported

Vol. 26, No. 2, 2002 145 that PG began after comorbid nicotine, the substance despite significant substance- tegmental area (VTA)/nucleus accum­ alcohol, and cannabis dependence in related problems” (APA 1994, p. 176). bens/orbital frontal cortex circuit. The 56 percent to 68 percent of the cases. More so than other impulse control VTA is a brain region containing cells However, confidence in this finding is disorders, the criteria for PG share (neurons) that release the brain chemi­ limited by the absence of similar studies striking similarities with those for sub- cal (neurotransmitter) dopamine, with against which to evaluate its reliability. stance dependence (Lesieur and Rosenthal target molecules (receptors) in the brain Further, because information was col­ 1991). Reflecting the fact that the DSM– areas known as the nucleus accumbens lected in this study by asking partici­ IV criteria include the concepts of pre- and the orbital frontal cortex (Koob pants to recall significant historical occupation, loss of control, tolerance, and Bloom 1988; Mogenson et al. events (i.e., a retrospective design), con­ and withdrawal, PG has been described 1980; Berridge 1996; Hyman 1993). fidence in its findings is further quali­ as an “addiction without the drug” This circuit is thought to influence fied. The ideal study design to assess (Potenza et al. 2001). People with PG, behavior by modulating motivation patterns of onset for comorbid disor­ like many people with AUD, experi­ that, at the level of subjective experi­ ders would entail assessing people with ence an intense wish to engage in the ence, is perceived as urges or cravings. neither, one, or both of the comorbid behavior (Castellani and Rugle 1995). Dopamine may also play a major role disorders at numerous time points (i.e., In fact, those with PG may even undergo in the regulation of this region’s func­ a prospective design). Ideally, such a withdrawal symptoms such as irritabil­ tioning (Kuhar et al. 1991; Self et al. study would follow participants through ity and agitation (Wray et al. 1981) 1996). In fact, researchers have theo­ the ages of greatest risk for the onset of and experience the equivalent of toler­ rized that dysregulation in the systems these disorders, and the assessment peri­ ance (i.e., the need to gamble with supporting the activities of dopamine ods would be spaced closely enough to larger amounts of money to attain the and the neurotransmitter serotonin capture changes in relevant behaviors same “high”) (Wray et al. 1981; Blanco may be central in both AUD and PG in near real time. et al. 2001). Additionally, as can be the (Comings et al. 1996; Blum et al. 1995). Until such studies are conducted in case for addictions involving a substance, Further, evidence suggests that specific this area, researchers cannot confidently pathological gamblers’ preoccupation genetic variations in the gene for the identify a typical pattern of comorbid with gambling can lead to the abandon­ dopamine D2 receptor (a specific bind­ disorder onset. However, based on ment of other interests and negative ing molecule with which dopamine the one relevant study identified social and occupational consequences interacts) and the serotonin transporter (Cunningham-Williams and Cottler (Lesieur 1979; Wray and Dickerson gene may mediate, to some extent, 2001), it would appear that neither PG 1986). Although defining nondrug use individual differences in reward motiva­ nor AUD routinely precedes the other behaviors such as PG as an addiction is tion and responsiveness (Potenza 2001; in cases of comorbidity. As noted, this not without controversy, a recent criti­ Ibanez et al. 2001). Therefore, common pattern is most consistent with a common cal review of this topic concluded that etiologic factors underlying AUD and cause for both conditions. Potential mounting evidence supports such a PG may be partially genetic and mediated common causes are described below. conceptualization (Holden 2001). through nervous system functioning. Because the fact that they are addictive behaviors is fundamental to both AUD Processes and Features and PG, physical and psychological Genetic and Environmental Factors Common to PG and AUD processes that drive addictive behaviors are likely candidates in the search for a Researchers can estimate the extent of common cause of these comorbid dis­ genetic versus environmental contribu­ Common Diagnostic Criteria orders (e.g., Holden 2001). The next tions to specific behaviors and condi­ section considers such processes. tions by contrasting their concordance Addictive behaviors are broadly charac­ between identical (i.e., monozygotic) terized by a number of features. These and fraternal (i.e., dizygotic) twin pairs. general characteristics include an intense Common Neurobiological Processes In the only twin study that specifically desire to satisfy a need, a loss of control Underlying Urges and Rewards examined these associations for PG and over the substance or behavior, com­ The repetitive use of alcohol or engage­ AUD, Slutske and colleagues (2000) pulsive thoughts about the substance or ment in gambling following an urge reported that in a large male twin sam­ behavior, and engaging in the behavior may reflect a unitary process. That is, ple, 12 to 20 percent of the genetic despite negative consequences (World both behaviors may stem from the same variation in risk for PG and 3 percent Health Organization [WHO] 1993). underlying mechanism. Preclinical and to 8 percent of the nonshared environ­ In fact, the DSM–IV defines the essen­ clinical studies suggest that an underlying mental variation in the risk for PG was tial features of substance dependence as biological mechanism for urge-based accounted for by risk for AUD. being “a cluster of cognitive, behavioral, disorders involves the processing of Additionally, 64 percent of the co­ and physiological symptoms, indicat­ incoming reward inputs by a specific occurrence between PG and AUD ing that the individual continues to use brain system. This system is the ventral appears to be attributable to genes that

146 Alcohol Research & Health Pathological Gambling and Alcohol Use Disorder

simultaneously influence both disor­ PG have also demonstrated its benefit with the hypothesis, one study found ders. Similarly, family studies have also in reducing gambling urges (Crockford that alcohol intake was associated with found that study participants with PG and el-Guebaly 1998; Kim et al. in press; greater spending on gambling activities tended to have first-degree relatives Kim and Grant 2001). One pharmaco­ and with gambling problems (Smart with AUDs (McElroy et al. 1992; logical action of naltrexone is to inhibit and Ferris 1996). Another study found Slutske et al. 2000). Although these the release of dopamine in the nucleus a significant increase in the willingness findings have not been replicated, they accumbens by restoring the neurotrans­ to gamble when alcohol was consumed, suggest some overlap in the genetically mitter gamma-aminobutyric acid’s but only when the amount consumed transmitted underpinnings of both of (GABA’s) inhibition of dopamine cells was limited to about two drinks. The these conditions. Notably, however, these in the VTA (Broekkamp and Phillips effect disappeared at higher doses findings also point to significant genetic 1979; Matthews and German 1984; (Breslin et al. 1999). Several studies do and environmental risks for PG and Spanagel et al. 1992). As mentioned not support the notion that alcohol use AUD that are unique to each disorder. above, it has been postulated that symp­ affects willingness to gamble (Cutter et toms of AUD and PG are modulated, al. 1973; Meier et al. 1996). One study in part, by the neural systems (that reg­ also showed that risk-taking while gam­ Responsiveness to Treatment ulate pleasure) affected by naltrexone. bling is not increased by alcohol con­ Based on the view that PG and AUD Thus, the positive naltrexone treatment sumption (Breslin et al. 1999). These share common causal/maintaining fac­ outcome found in AUD and PG pro­ data appear to call into question the tors, one could predict that these disorders vides evidence that systems affected by intuitively appealing hypothesis that would respond positively to the same this drug play roles in both conditions. problem gambling follows from problem treatments. In fact, various nonmedical drinking when intoxication promotes treatment modalities that are effective excessive or highly risky gambling behav­ in treating AUD are also useful in Alcohol Use Disinhibits ior. Further study in this area is necessary. treating PG (e.g., 12-step approaches Gambling Behavior and cognitive behavioral therapies; Petry and Roll 2001). In addition, several As described above, a number of pro­ Gambling Promotes influential psychosocial interventions cesses might serve as common underly­ Alcohol Use for both conditions rely on a relapse ing mechanisms for PG and AUD, prevention model. This model encour­ thereby promoting comorbidity. An Another possible association between ages abstinence by identifying patterns alternative explanation for the frequent pathological gambling and alcohol use of abuse, avoiding or coping with high- association of these disorders is that disorders is that PG may promote AUDs. risk situations, and making lifestyle repetitive or problematic alcohol use For example, if people are more likely changes that reinforce activities not might, itself, serve to increase the risk to drink while gambling, then it might related to substance use. for PG. In fact, engaging in gambling follow that the risk for alcohol prob­ Researchers have only recently started while drinking is common (Lesieur et lems increases when frequent gamblers to explore pharmacologic treatment al. 1986). Further, evidence suggests that are regularly exposed to alcohol. Very approaches for PG. Several studies have alcohol use can adversely affect cogni­ little empirical work has addressed this shown promising results for the efficacy tive processes, leading to poor judg­ question. One exception is a recent of selective serotonin reuptake inhibitors ment and increased risk-taking. For study by Stewart and colleagues (in (SSRIs) (medications that affect the example, studies have shown that alco­ press). They found that frequent gam­ production and/or absorption of sero­ hol intake is associated with impaired blers self-administered more alcohol in a tonin) in the treatment of PG (Hollander decisionmaking (Baron and Dickerson simulated gambling situation than did et al. 2000; Kim et al. in press; Zim­ 1999) and reduced self-reflection (e.g., matched study participants engaged in merman and Breen 2000; Blanco-Jerez considering the consequences of behav­ a control activity. These findings are 1999; de la Gandara 1999). The use of ior) associated with risk-related judgments provocative and invite more research to SSRIs in the treatment of AUD, however, (Breslin et al. 1999). Alcohol might also determine the extent to which gambling has been less impressive (Kranzler et al. increase risk-taking by restricting attention behavior promotes alcohol consumption. 1995; Kabel and Petty 1996; Angelone to only the most salient and immediate et al. 1998; Cornelius et al. 1997). cues (Steele and Josephs 1988), leading Naltrexone, which blocks the action to less regard for the actual odds of a Treatment Implications of opioids (i.e., it is an opioid antago­ gamble and past gambling losses. nist), has been effective in reducing the In spite of the prima facia evidence Regardless of the specific causal associa­ frequency and amount of drinking in for an association between drinking and tion linking PG and AUD, the fact that patients with AUD (Volpicelli et al. gambling behavior, studies to date are they frequently co-occur raises important 1992; O’Malley et al. 1992; Anton et mixed in their support of the hypothesis treatment issues. Treatment of either al. 1999). Studies evaluating the effi­ that alcohol frequently causes problem­ AUD or PG could be complicated or cacy of naltrexone in the treatment of atic behavior leading to PG. Consistent even compromised by the presence of

Vol. 26, No. 2, 2002 147 the other untreated condition (e.g., PG (Kim et al. 2001). It may be that influence this relationship (e.g., gender, Kranzler and Liebowitz 1988). Treating this subgroup, more than others with dose of alcohol, type of gambling one disorder alone may not be effective PG, are likely to develop comorbid decision/behavior, degree of urge driving if the second disorder is exerting a substance use disorders. That is, some the gambling behavior, stakes). Although causal or maintaining influence on the disorder subtypes may be associated naturalistic study of such factors might treated condition. Even in the more with neurobiological processes that over- not be practical, experimental studies likely event that AUD and PG are asso­ lap for both PG and AUD, whereas have the potential to produce results ciated via the influence of a third vari­ other subtypes of these disorders may that bear directly on processes related able that can promote both disorders, have a different etiology that is unrelated to comorbidity. treating one but not the other condition to the comorbid condition. Research would be potentially problematic. For findings from genetic and brain imaging example, the circumstances and envi­ studies will further help identify key Conclusions ronments associated with either public subgroup variables and serve as a drinking or gambling are likely to increase methodology for identifying common PG frequently co-occurs with AUD. a person’s risk for engaging in the other biological substrates associated with The preponderance of the available activity. Further, more intense treatment both PG and AUD. data suggests that overlapping brain may be required for comorbid patients In addition to studies aimed at unrav­ systems may leave people vulnerable to because they are likely to have more eling the shared and unique etiologies both disorders. However, some researchers functional impairment and a poorer of these conditions, research must also have speculated that the causal influ­ prognosis than are those with either seek to develop and test treatment and ences in PG and AUD may be hetero­ condition alone (Bukstein et al. 1989). prevention strategies. For example, it is geneous. That is, some common causal currently unknown whether parallel, influences shared by AUD and some serial, or integrated treatment approaches subtypes of PG may promote comor­ Future Research would best serve the comorbid popula­ bidity, but the causes and maintaining tion. Given that the bulk of systematic influences of other subtypes of PG and Prospective studies of the temporal research into the psychosocial and AUD may not overlap. From a clinical association of AUD and PG are virtually pharmacological treatment of PG has perspective, findings reviewed here absent from the literature but would be been ongoing for less than 10 years, highlight how important it is for AUD best suited to the important goal of however, it is not surprising that a lot treatment programs to provide careful clarifying the natural history and tem­ of work still needs to be done in this screening and treatment planning that poral relationship of these disorders. It area (Kim and Grant 2001). is capable of recognizing and reacting would be important for such studies to Yet another area of potential inquiry to the presence of comorbid PG. From capture people early in the window of is that of commonalities in personality a scientific standpoint, understanding risk for both disorders (e.g., early ado­ dimensions between people with PG comorbidity will necessarily refine views lescence; see above). Also, because one’s and those with AUD. PG and AUD on the psychopathology and taxonomy drinking or gambling status can change share features of impulsivity and behav­ of the two conditions. Hopefully, reviews rapidly, the prospective assessments nec­ ioral excess. Whether these disorders such as this will encourage both gam­ essary to document important interac­ share some common personality traits bling and alcohol use researchers and tions between these conditions should or a categorical personality disorder is clinicians, where possible, to expand be appropriately frequent (e.g., at 6- currently unknown. Future research is their scientific and clinical enterprises month intervals). Although prospective needed to assess the personality dimen­ to explicitly include comorbid cases. studies like these are difficult and expen­ sions of those who engage in these sive to conduct, reliable information addictive behaviors and determine concerning key interactions between whether shared personality traits may References gambling and drinking behavior may have possible treatment implications. American Psychiatric Association (APA). Diagnostic not be otherwise obtainable. Finally, additional experimental and Statistical Manual of Mental Disorders, Third Another question that has not yet studies may be needed to map more Edition. Washington, DC: APA, 1980. been adequately addressed through precisely the impact of drinking on American Psychiatric Association (APA). Diagnostic research is whether different subtypes gambling behavior and vice versa (e.g., and Statistical Manual of Mental Disorders, Third of PG and AUD are more likely than see Stewart et al. 2000). As reviewed, Edition, Revised. Washington, DC: APA, 1987. others to manifest as a comorbid disor­ only a very small number of such stud­ American Psychiatric Association (APA). Diagnostic der. For example, some evidence indi­ ies have been conducted and these have and Statistical Manual of Mental Disorders, Fourth cates that strong subjective urges of the produced mixed findings. Clearer trends Edition. Washington, DC: APA, 1994. type linked to specific brain regions (as would be expected to emerge from a American Psychiatric Association (APA) Committee described above) are an important larger number of studies. These studies on Nomenclature and Statistics. Diagnostic and dynamic in the motivation to gamble have the capacity to systematically Statistical Manual of Mental Disorders, Fourth among some, but not all, people with manipulate myriad variables that may Edition, Revised. Washington, DC: APA, 2000.

148 Alcohol Research & Health Pathological Gambling and Alcohol Use Disorder

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