Gambling: Risk Factors, Prevalence and Treatment Outcomes [illustrated] 1634857879, 9781634857871

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HEALTH PSYCHOLOGY RESEARCH FOCUS

GAMBLING RISK FACTORS, PREVALENCE AND TREATMENT OUTCOMES

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HEALTH PSYCHOLOGY RESEARCH FOCUS

GAMBLING RISK FACTORS, PREVALENCE AND TREATMENT OUTCOMES

YVONNE CARTER EDITOR

New York

Copyright © 2016 by Nova Science Publishers, Inc. All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. We have partnered with Copyright Clearance Center to make it easy for you to obtain permissions to reuse content from this publication. Simply navigate to this publication’s page on Nova’s website and locate the “Get Permission” button below the title description. This button is linked directly to the title’s permission page on copyright.com. Alternatively, you can visit copyright.com and search by title, ISBN, or ISSN. For further questions about using the service on copyright.com, please contact: Copyright Clearance Center Phone: +1-(978) 750-8400 Fax: +1-(978) 750-4470 E-mail: [email protected].

NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS. Additional color graphics may be available in the e-book version of this book.

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Published by Nova Science Publishers, Inc. † New York

CONTENTS Preface Chapter 1

vii Pathological Gambling: Risk Factors, Prevalence, Pathophysiology, and Treatment Outcomes Shannon Y. Chiu and Anhar Hassan

Chapter 2

Gambling: Taxes and Prevention Ingo Fiedler, Sylvia Kairouz and Chantal Robillard

Chapter 3

A Desire-Targeted Intervention Based on Naikan Counseling for Disordered Gamblers (DING) Yasunobu Komoto

Bibliography

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37 63

Related Nova Publications

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Index

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PREFACE Gambling is a public health problem characterized by persistent and recurrent maladaptive patterns of gambling. There is a social incentive to reduce current gambling problems and prevent future gambling addiction. In this book, Chapter One begins with an analysis of the risk factors, prevalence, pathophysiology and discusses treatment options for pathological gambling. Chapter Two provides a review on the idea that games should be taxed in accordance to the revenue they generate from addicts, and more effective multidimensional prevention measures should be implemented. Chapter Three focuses on a desire-targeted intervention based on Naikan counseling for disordered gamblers (DING). Chapter 1 – Pathological gambling (PG) is characterized by failure to resist the urge to gamble despite dire consequences on personal and family life. It is estimated to affect 0.4-2% of the general adult population in the US, and the prevalence varies with different cultures and countries. The etiology is multifactorial, involving biological, psychological and social factors. These include male gender, younger age, greater novelty-seeking personality, greater impulsivity, smoking history, family history of gambling, personal/family history of alcoholism or other psychiatric comorbidities. Certain medications may provoke PG: notably dopamine agonists, used for treatment of Parkinson’s disease and restless legs syndrome; and aripiprazole, an atypical antipsychotic. A genetic predisposition to PG is proposed, and PG has been associated with dopamine, serotonin, and glutamate gene polymorphisms. It is postulated that gene-environment interactions result in susceptibility to PG. In addition, dopamine agonists have selective affinity for the D3 receptor, which is primarily localized in the limbic system, and could explain medication modulation of reward and motivated behavior. Treatment of PG is challenging.

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Increased awareness in at-risk populations could help prevent PG. Behavioral interventions such as Gamblers Anonymous, support groups, computer firewalls, and limitation of credit cards, have been shown to limit PG. Cognitive behavioral therapy has been shown to be effective in a randomized control trial. Education of patients and their families prescribed dopamine agonists, and follow-up screening, can identify new emerging PG behavior. Reducing the dose or stopping dopamine agonists improves or eliminates PG. A black-box warning for dopamine agonists and aripiprazole has been suggested by the FDA. Additional approaches include off-label medication trials of mood stabilizers, anticonvulsants, or atypical antipsychotics. As PG causes significant psychosocial impact on affected individuals and their families, further research to prevent and treat this disorder is of significant importance. Chapter 2 – The gambling market is regulated because it involves costs to society. The standard approach to countering these is to tax gambling products. However, gambling taxes deter more recreational than pathological gamblers and are regressive, meaning that they increase social inequalities. Concurrently, health prevention measures reduce the social costs of gambling without reducing its benefits and are thus preferable to taxes. Currently, however, they are proportionally scarce and ineffective. The reason for this adverse political outcome is the fundamental conflict of interests between gambling revenues and prevention of addiction: social costs and market revenues both concentrate on addicted gamblers. On a societal level, this conflict of interest is projected onto the competing interests of stakeholders, where interests of politically not well organized parties remain unheard. To ensure a more effective regulatory intervention, the authors suggest a paradigmatic shift: games should be taxed in accordance to the revenue they generate from addicts, and more effective multidimensional prevention measures should be implemented. Chapter 3 – The author proposed a desire-targeted intervention based on Naikan counseling for disordered gamblers (DING) as a result of the limitations of abstinence-targeted interventions, which are based on the disease model of weakened self-control relative to craving for gambling. In contrast, in DING, the loss of gambling control is perceived as a failure of strategy, wherein it is assumed that gambling fulfills various desires (e.g., the desire for fame, money, and escapism). Therefore, the development of alternative behaviors to directly fulfill original desires constitutes the main therapeutic goal of DING. Naikan counseling is useful for uncovering original desires, and

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the principal question asked to disordered gamblers is “Who satisfied you when you were not satisfied?” Therefore, to reveal the efficiency of DING, the author introduced the six month-outcome study. Outpatients (n = 35) who were primarily diagnosed with gambling disorder using DSM-V were treated with DING. In principle, this intervention comprised six sessions that were conducted by psychiatrists and clinical psychologists. Participants were assessed for basic background characteristics such as gender and age; medical variables such as age of onset of problem gambling, duration of problem gambling, psychiatric complications, and motivation to quit gambling; assessments of the severity of gambling disorder based on DSM-5; and six-month outcomes after intervention (problem gambling/controlled gambling/abstinence). In results, at six months post-intervention, 40% of the participants were abstinent and 28.6% were controlled gamblers. Overall, 30.8% of the participants who initially reported low motivation to quit gambling were abstinent at six months post-intervention. History of suicide attempts was strongly associated with the outcomes. Thus, DING heightened the motivation for recovery without the individual feeling stigmatized or ashamed at being a gambler and without the individual feeling pressurized to quit gambling. Additionally, the abstinence rate for this intervention was nearly identical to the rates reported in previous literature.

In: Gambling Editor: Yvonne Carter

ISBN: 978-1-63485-787-1 © 2016 Nova Science Publishers, Inc.

Chapter 1

PATHOLOGICAL GAMBLING: RISK FACTORS, PREVALENCE, PATHOPHYSIOLOGY, AND TREATMENT OUTCOMES Shannon Y. Chiu and Anhar Hassan* Department of Neurology, Mayo Clinic, Rochester, MN, US

ABSTRACT Pathological gambling (PG) is characterized by failure to resist the urge to gamble despite dire consequences on personal and family life. It is estimated to affect 0.4-2% of the general adult population in the US, and the prevalence varies with different cultures and countries. The etiology is multifactorial, involving biological, psychological and social factors. These include male gender, younger age, greater novelty-seeking personality, greater impulsivity, smoking history, family history of gambling, personal/family history of alcoholism or other psychiatric comorbidities. Certain medications may provoke PG: notably dopamine agonists, used for treatment of Parkinson’s disease and restless legs syndrome; and aripiprazole, an atypical antipsychotic. A genetic predisposition to PG is proposed, and PG has been associated with dopamine, serotonin, and glutamate gene polymorphisms. It is postulated that gene-environment interactions result in susceptibility to PG. In *

Corresponding author: Anhar Hassan, [email protected].

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Shannon Y. Chiu and Anhar Hassan addition, dopamine agonists have selective affinity for the D3 receptor, which is primarily localized in the limbic system, and could explain medication modulation of reward and motivated behavior. Treatment of PG is challenging. Increased awareness in at-risk populations could help prevent PG. Behavioral interventions such as Gamblers Anonymous, support groups, computer firewalls, and limitation of credit cards, have been shown to limit PG. Cognitive behavioral therapy has been shown to be effective in a randomized control trial. Education of patients and their families prescribed dopamine agonists, and follow-up screening, can identify new emerging PG behavior. Reducing the dose or stopping dopamine agonists improves or eliminates PG. A black-box warning for dopamine agonists and aripiprazole has been suggested by the FDA. Additional approaches include off-label medication trials of mood stabilizers, anticonvulsants, or atypical antipsychotics. As PG causes significant psychosocial impact on affected individuals and their families, further research to prevent and treat this disorder is of significant importance.

INTRODUCTION Pathological (or problem) gambling (PG) is characterized by failure to resist gambling impulses despite dire consequences on personal, family or occupational life. There was a paradigm shift in the conceptualization of pathological gambling when the latest Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) was released in 2013. There was a change in terminology with “pathological gambling” replaced by “gambling disorder”. In addition, “gambling disorder” moved to the category of “Addiction and Related Disorders” in DSM-5, from the prior category of “Impulse Control Disorder” in DSM-4 (American Psychiatric Association, 2000 and 2013). The technical changes included a requirement for 4 rather than 5 criteria for diagnosis, and the omission of “illegal acts” criterion (Box 1). The key implication was recognizing similarities between gambling disorder and substance abuse disorders, as both are behavioral addictions with clinical and neurobiological bases (Clark, 2014; Potenza, 2006). Similarities include characteristic symptoms of craving, withdrawal, and tolerance; comorbidities; genetic heritability; and neural substrates.

Pathological Gambling

BOX 1. COMPARISON OF DSM-4 CRITERIA FOR “PATHOLOGICAL GAMBLING” AND DSM-5 CRITERIA FOR “GAMBLING DISORDER” DSM-4 diagnostic criteria for Pathological Gambling

DSM-5 diagnostic criteria for Gambling Disorder

Individual must meet 5 of 10 diagnostic criteria; all criteria are of equal weight 1. A preoccupation with gambling (e.g., preoccupation with reliving past gambling experiences, handicapping or thinking of ways to get money with which to gamble) 2. A need to gamble with increasing amounts of money in order to achieve the desired level of excitement 3. Repeated, unsuccessful efforts to control, cut back or stop gambling 4. Feels restless or irritable when attempting to cut down or stop gambling (withdrawal symptoms) 5. Uses gambling as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of hopelessness, guilt, anxiety and depression) 6. After losing money gambling, often returns another day to get even (“chasing” one’s losses) 7. Lies to family members, therapist or others to conceal the extent of one’s involvement with gambling 8. * Has committed illegal acts such as forgery, fraud, theft or embezzlement to finance gambling

A. Individual must meet 4 or more of 9 diagnostic criteria in a 12-month period 1. A preoccupation with gambling (e.g., preoccupation with reliving past gambling experiences, handicapping or thinking of ways to get money with which to gamble) 2. A need to gamble with increasing amounts of money in order to achieve the desired level of excitement 3. Repeated, unsuccessful efforts to control, cut back or stop gambling 4. Feels restless or irritable when attempting to cut down or stop gambling (withdrawal symptoms) 5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed)

6. After losing money gambling, often returns another day to get even (“chasing” one’s losses) 7. Lies to conceal extent of involvement with gambling 8. Has jeopardized or lost a significant relationship, job or educational or career opportunity because of gambling

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Shannon Y. Chiu and Anhar Hassan Box 1. (Continued) DSM-4 diagnostic criteria for Pathological Gambling

DSM-5 diagnostic criteria for Gambling Disorder

9. Has jeopardized or lost a significant relationship, job or educational or career opportunity because of gambling 10. Relies on others to provide money to relieve a desperate financial situation caused by gambling

9. Relies on others to provide money to relieve a desperate financial situation caused by gambling

B. **Gambling behavior is not better explained by a manic episode. Specify if: Episodic: meeting diagnostic criteria at more than one time point, with symptoms subsiding between periods of gambling disorder for at least several months Persistent: experiencing continuous symptoms, to meet diagnostic criteria for multiple years Specify if: In early remission: After full criteria for gambling disorder were previously met, none of the criteria for gambling disorder have been met for at least 3 months but for less than 12 months In sustained remission: after full criteria for gambling disorder were previously met, none of the criteria for gambling disorder have been met during a period of 12 months or more Specify current severity: Mild: 4-5 criteria met Moderate: 6-7 criteria met Severe 8-9 criteria met * “Illegal acts” criterion in DSM-4 is now omitted in DSM-5. ** Additional specifications clinician can apply to the diagnosis of gambling disorder Table is adapted from DSM-4 and DSM-5 (section 312.31).

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PREVALANCE The prevalence of gambling disorder in the general population varies worldwide. In North America, prevalence within the adult population has been reported to range from 0.4 to ~2% (Voon et al., 2006; Petry et al., 2005; Hodgins et al., 2011). In contrast, gambling rates are reported as low as 0.2% in Norway, and up to 5.3% in Hong Kong (Wardle et al., 2007). Epidemiological studies have further shown variable prevalence rates depending on accessibility of gambling opportunities. For example, Nevada is one of two states in the US where casino gambling is legal statewide. Prevalence surveys in 2000 indicated that prevalence of pathological gambling in Nevada was 3.5% compared to national rate of 1.9% (Volberg, 2002; Welte et al., 2001).

RISK FACTORS Demographic/Social In the general population, demographic features of male gender, younger age, and poor socioeconomic status are risks for gambling disorder. Individuals’ social settings can also influence gambling behavior. Those who are widowed, separated, or divorced, are at higher risk of developing gambling problems (Petry et al., 2005). Similarly, poor parental supervision, having deviant friends, and delinquency appear to be risk factors for younger individuals (Vitaro et al., 2001).

Psychiatric/Substance Abuse Smoking history, family history of gambling, and personal/family history of alcohol or substance abuse are other common factors associated with development of pathological gambling. (Kim et al., 2006; Shaffer and Martin, 2011; Santangelo et al., 2013). Personality risk factors include greater noveltyseeking and greater impulsivity traits, and psychiatric disorders (e.g., manic and depressive disorders). Studies have shown that pathologic gamblers are 5.5 times more likely to have substance abuse disorder, and 4 times more likely to have concurrent mood disorder, than non-pathologic gamblers

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(Kessler et al., 2008). One study surveyed a large population of household members age 18 years and over, and estimated that 75% of pathological gamblers had an alcohol disorder, 38% had drug use disorder, and 60% had nicotine dependency; within the same total cohort of pathological gamblers, 50% had a mood disorder, 41% had anxiety disorder, and 61% had personality disorder (Petry et al., 2005).

Gambling Type Types of gambling have been correlated with gambling behaviors. Studies have suggested that certain types of gambling are more likely to produce gambling addiction, as it relates to event frequency (i.e., time between gambling outcomes), immediate feedback, or gambling venue. Casino gambling, lottery, cards, and bingo have been cited as some of the major forms to predict gambling pathology (Welte et al., 2004; Griffiths, 1999). Pathological gamblers typically engage in a larger number of different gambling types than non-problem gamblers (Kessler et al., 2008).

Neurological Disorders and Medications People with Parkinson’s disease have a higher risk of developing pathological gambling. Lifetime prevalence of gambling disorder in Parkinson’s patients has been estimated to be between 3.4-8% (Djamshidian et al., 2011). This is strongly related to certain medications used to treat this condition, which can provoke pathological gambling as a side effect. Newly diagnosed Parkinson’s disease patients (not on treatment) do not differ from healthy controls in their baseline gambling rates (1.2 vs 0.7%). (Weintraub et al., 2013). However those treated with dopaminergic drugs, specifically dopamine agonists, are at risk of developing pathological gambling. The association between dopamine agonist therapy and gambling disorder was first reported in the early 2000s (Driver-Dunckley et al., 2003). Since then, the association has been increasingly recognized. The odds of developing pathological gambling is 2.15 times higher in Parkinson’s patients treated with dopamine agonist medications compared with patients not treated with them (Weintraub et al., 2010). In addition, dopamine agonists can provoke other pathological behaviors, alone or in combination with pathological gambling, including pathologic hypersexuality, compulsive shopping, binge eating, and

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compulsive hobbying, although these occur less frequently than pathological gambling (Dodd et al., 2005; Botswick et al., 2009; Hassan et al., 2011). The risk of these pathologic behaviors appears to be related to the medication dose. Studies have reported about 13 to 22% of Parkinson’s patients experience at least one pathologic behavior when taking dopamine agonists, and gambling was most common at about 5 to 6%. (Weintraub et al., 2010; Hassan et al., 2011) The risk correlates with higher dopamine agonist dose, and as many as one-quarter to one-third of Parkinson’s patients develop one or more behaviors at therapeutic or higher doses. Conversely, at subtherapeutic doses of dopamine agonists only about 3% of Parkinson’s patients develop compulsive behaviors. The pathologic behavior resolves after reducing or stopping the dopamine agonist in most patients (Hassan et al., 2011). These findings relating to dopamine agonist dose have been supported by other studies (Garcia-Ruiz et al., 2014; Voon et al., 2007a; Ahlskog, 2011). Concurrent levodopa therapy taken with dopamine agonists in Parkinson’s patients is also associated with pathological gambling and compulsive behaviors. (Bostwick et al., 2009; Hassan et al., 2011) Increased prevalence of pathological gambling related to the use of dopaminergic medications has been shown in other subgroup populations, such as patients with restless legs syndrome (Willis-Ekbom disease). Patients with restless legs syndrome not taking medication do not differ from age and gender-matched controls for baseline risk of impulsivity, impulse control disorders, or addictive behaviors (Bayard et al., 2010). However, the frequency of pathological gambling is significantly higher in restless legs patients taking dopamine agonists (5%) compared to controls with obstructive sleep apnea (0.4%). (Cornelius et al., 2010). There is also a significant dose effect found for dopamine agonists. (Cornelius et al., 2010). Aripiprazole is another medication recently linked to pathological gambling (Gaboriau et al., 2014; Smith et al., 2011; Grall-Bronnec et al., 2016). Aripiprazole is an atypical antipsychotic agent with dopamine receptor type-2 (D2) partial agonist properties, and is used to treat schizophrenia, bipolar disorder, and depression. One case report of 3 patients developed pathological gambling induced by aripiprazole, and the behavior was eliminated upon stopping aripiprazole. None had a prior history of pathological gambling. (Cohen et al., 2011) Another study reported aripiprazole-induced pathological gambling in 8 of 166 non-Parkinson’s patients, where symptoms abided with discontinuation of aripiprazole. (Gaboriau et al., 2014)

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Genetic There is growing literature on the role of molecular genetics on pathological gambling. Linkage analyses (i.e., identifying marker alleles in families with the disorder), and genome-wide association studies (i.e., comparing frequency of polymorphic allele between populations with and without the disease) constitute some of the major ways to examine the role of genetic predisposition in pathological gambling in the general population. Twin studies from the Vietnam Era Twin Registry showed that genetic factors, but not necessarily shared environmental factors, play a significant role in pathological gambling (Gyollai et al., 2014). Given the implicated roles of dopaminergic, serotonergic, and glutaminergic neurotransmission in pathological gambling, gene association studies have focused on identifying specific genes or single nucleotide polymorphisms (SNP) linked to these neurotransmitter systems. Genes linked to impulsivity and addiction include the dopamine D4 receptor (DRD4) and dopamine transporter (SLC6A3) (Kreek et al., 2005; Brewer and Potenza, 2008). Other studies have also found increased frequency of the A1 allele of DRD2 Taq 1A (D2 receptor) in pathological gamblers compared to controls; this same allele has similarly been linked to drug abuse, smoking, and compulsive eating (Blum et al., 1995; Comings et al., 1996). Serotonin transporter gene, 5-HTTLPR “S” allele, is associated with decreased transcriptional activity in pathological gambling in the general population, and appears to correlate with impulsivity (Perez de Castro et al., 2002). Studies in Parkinson’s patients have identified additional polymorphisms, some of which are not associated with pathological gambling in the general population. For example, homozygous variant Ser9Gly of DRD3 is hypothesized to lower dopamine binding affinity and increase risk of pathological gambling in Parkinson’s patients but not in the general population. Additional identified polymorphisms in Parkinson’s patients include CC genotype of the 2B subunit (GRIN2B) of the glutamate N-methyld-aspartate (NMDA) receptor, DRD2 Taq 1A of the dopamine D2 receptor, DRD3 p.S9G variant of the dopamine D2 receptor, DAT1 of dopamine transporter, COMT Val158Met of catechol-O-methyltransferase, and HTR2A of the serotonin 2A receptor (Lee et al., 2009; Santangelo et al., 2013).

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PATHOPHYSIOLOGY Within the general population, individuals with gambling disorder have been shown to exhibit different cognitive processes compared to control subjects. For example, they perform worse on measures of impulsivity, decision-making, cognitive flexibility and planning (Potenza, 2014). Interestingly, patients with restless legs also are more likely to have reduced decision-making performance under ambiguity than age- and gender-matched controls. This may place them at risk of developing pathologic gambling when exposed to dopamine agonists. (Bayard et al., 2010)

Neural Network Significant insight into the pathophysiology of gambling disorder stems from identifying the different brain activation patterns between individuals with and without pathological gambling – namely brain regions involved in reward, motivation, impulse control, decision processing, and memory. Functional magnetic resonance imaging (fMRI) and Positron Emission Tomography (PET) neuroimaging studies in pathological gamblers in the general population have mapped these traits to ventromedial prefrontal cortex, amygdala and ventral striatum. This network has been similarly implicated in Parkinson’s patients on dopamine agonists who develop pathological gambling (Cilia et al., 2008). While there appears to be a consensus on the overall mesocorticolimbic network of brain regions involved in pathological gambling, there is an ongoing debate on the exact pathophysiology in pathological gambling as it relates to brain perfusion and activation patterns. On the one hand, studies comparing individuals in the general population with and without gambling disorder have shown blunted activation of the aforementioned neural correlates in pathological gamblers compared to controls, during tasks that involve cognitive control (e.g., Stroop test), gambling urges, decision-making, processing of monetary losses and gains (Reuter et al., 2005; Leeman and Potenza, 2012). These data suggest a potential aberrant relationship between the reward system and response inhibition. In contrast, studies focusing on Parkinson’s patients (especially those initiated on dopaminergic therapy), have shown over-activity during resting state in these same critical brain areas in Parkinson’s patients on dopaminergic therapy with gambling disorder (Cilia et

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al., 2008). The hypothesis is that Parkinson’s patients on dopaminergic medication with pathological gambling may have resting state dysfunction of the mesocorticolimbic network due to drug-induced overstimulation of an otherwise normal reward-system. While the contradictory findings partly stem from differences in experimental designs, participant demographics, and situational cues, the conflicting data on under- vs. over-activation of the mesocorticolimbic network in pathological gambling within the general population have led to hypothetical models. One argument is that pathological gamblers have primary dysfunction in the lateral prefrontal cortex with downstream impairment of top-down impulse control, and another is based on increased lower level impulse drive (Potenza, 2014; Pirritano et al., 2014). It is also possible that the pathophysiology of pathological gambling amongst subpopulations such as Parkinson’s patients may differ slightly. Parkinson’s disease is characterized by loss of dopaminergic neurons in the substantia nigra, especially in the nigrostriatal pathway with decreased stimulation of striatal D1 and D2 receptors. As suggested previously, targeted dopamine stimulation of intact ventral striatal receptors in early Parkinson’s may lead to compensatory “overactivation” of the mesocorticolimbic network and increase the risk of developing pathological gambling (Cilia et al., 2008; Pirritano et al., 2014). There is ongoing research on the neural bases of gambling disorder and how it relates to potential targeted therapy.

Dopamine and the Brain Reward System Dopaminergic systems have been a central focus on identifying neurochemical bases of gambling disorder. Dopamine is a neurotransmitter involved in reward and reinforcement. That dopaminergic medications have been associated with gambling disorder suggests a potential role of dopamine transmission in promoting gambling urges or other executive dysfunction. The Dopamine Type 3 (D3) receptor within the limbic system has become a major focus, as dopamine agonists, especially pramipexole and ropinirole, have significantly higher affinity for the D3 receptor than D2 receptor. (Gerlach et al., 2003) The D3 receptors are mainly expressed within the ventral striatum, which has a major role in dopaminergic modulation of reward-seeking behavior. PET neuroimaging studies have evaluated D2/D3 receptors in relationship to gambling behaviors. One study compared Parkinson’s individuals with and without gambling disorder, using (11C)raclopride ligand, a D2-type receptor antagonist; and (11C)-(+)-PHNO ligand, a D3-type receptor agonist. (Boileau

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et al., 2013) There was binding of (11C)-(+)-PHNO in the substantia nigra, attributable to D3 receptors, which correlated with gambling severity and impulsiveness. A corollary study in non-Parkinson’s pathological gamblers showed that amphetamine administration led to increased dopamine release (based on increased (11C)-(+)-PHNO binding, i.e., D3 receptor level) in the substantia nigra of pathological gamblers compared to controls. (Boileau et al., 2014) This is in keeping with the incentive-sensitization model, whereby pathological gamblers are hypothesized to have more hypersensitive dopaminergic circuit toward anticipated rewards, thereby reinforcing gambling behaviors (Rømer Thomsen et al., 2014). Overall, the PET data suggest disruption of dopamine transmission in pathological gamblers, both in the general population and Parkinson’s patients, and highlight D3 receptors as a potential pharmacotherapy target in behavioral addictions.

Other Neurotransmitters of Interest In addition to dopamine, other neurotransmitters implicated in gambling disorder include serotonin, noradrenaline, opioid and glutamatergic systems (Labuzek et al., 2014). Serotonin influences motivated behaviors; and pathological gamblers show increased “high” sensation and increased prolactin levels after administration of serotonin agonist (Pallanti et al., 2006). Noradrenaline is a catecholamine that acts on the sympathetic nervous system. Pathological gamblers in the general population have higher noradrenaline levels in cerebral spinal fliud (CSF) and urine compared to controls, suggestive of hyperactivity of sympathetic outflow that influence mood and sensation-seeking behaviors (Roy et al., 1988). Amphetamine has been shown to increase dopamine synthesis, which may indirectly modulate gambling behavior in pathological gamblers (Sulzer et al., 2005; Boileau et al., 2014). Opioids influence the reward circuit by disrupting dopamine transmission in the nucleus accumbens (Kim, 1998). Similarly, glutamate plays a role in drug reward, reinforcement and relapse, as shown in animal studies (Labuzek et al., 2014). Together, these data have prompted continued research into other pharmacological targets in treatment of pathological gambling.

TREATMENT Studies have shown that pathological gambling can be successfully managed through various combinations of psychotherapy, pharmacology, education, and self-help interventions.

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Initial clinical assessment by a physician can help explore a patient’s history of gambling tendencies; the impact of gambling on self, interpersonal and social functioning; financial burdens; and patient’s readiness to change. This is also an opportunity to screen for patient’s present and past mental disorders, medication use, and relevant family history (Rizeanu 2015). Ultimately, this evaluation is critical in helping the patient formulate a treatment plan.

Psychotherapy Well-studied psychological therapies include referral to Gamblers Anonymous, cognitive-behavioral therapy (CBT), motivational interviewing therapy, integrative therapy, and other therapeutic techniques (e.g., anger management, relaxation training). A common goal in these treatments is to modify behavior by challenging erroneous beliefs of gamblers (e.g., misconception of randomness). CBT has been one of the most studied therapies, with positive outcomes in the general population (Petry et. al., 2006; Rizeanu, 2015). In a Cochrane review (Cowlishaw et al., 2012), 11 of 14 studies showed significant benefit of CBT, as well as motivational interviewing, at 0 to 3 months, in reducing gambling symptom severity (i.e., anxiety, depression) and financial loss from gambling. However, the long-term benefit of these therapies appears less clear, as few studies looked at outcomes beyond 12 months after therapy initiation. Regardless of the specific psychotherapy, the consensus is that effective outcome often requires a combination of treatment approaches. For example, Gamblers Anonymous is a self-help program that is thought to compliment other therapies and can help prevent relapse (Rizeanu, 2015). Likewise, CBT in conjunction with pharmacotherapy may be superior to either treatment alone (Ravindran et al., 2006).

Pharmacology Many pharmacological agents have been trialed for treatment of pathological gambling. Selective serotonin reuptake inhibitors (e.g., paroxetine, citalopram, sertraline, escitalopram) have shown mixed results in the general population (Kim et al., 2002; Grant et al., 2003); and no significant effect has been shown in Parkinson’s patients (Kurlan, 2004). Mood stabilizers

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(e.g., lithium, valproate) have shown some positive results in bipolar patients with pathological gambling (Hollander et al., 2005). Atypical antipsychotics (e.g., risperidone, quetiapine) may be effective in controlling gambling behaviors in Parkinson’s patients (Dodd et al., 2005; Sevincok et al., 2007), but not in the general population (McElroy et al., 2008). Opioid antagonists, such as naltrexone, were recently shown to have a positive effective in a double-blind placebo controlled trial amongst pathological gamblers in the general population, especially amongst those who had more severe gambling urges (Grant et al., 2008; Kim, 1998). However, there are mixed results of naltrexone on pathological gambling and other impulse control disorder in Parkinson’s patients. While a case report series of 3 Parkinson’s patients found naltrexone to be an effective treatment for pathological gambling (Bosco et al., 2012), a recent double-blind placebo-controlled study found no significant benefit for treatment of impulse control disorders based on clinician-based rating of global improvement (Papay et al., 2014). Nalmefene is another opioid antagonist that has shown promising results on pathological gambling in the general population (Grant et al., 2006). While there have been promising results in the literature on pharmacotherapy described above, data are limited by small sample sizes, conflicting results, lack of long-term follow-up, and questionable validity of results based on subjective scales and patient self-report of gambling behaviors. Several meta-analyses have attempted to compare the different classes of drugs against placebo, but no convincing data have shown superiority of one drug class over another (Pallesen et al., 2007; Bartley and Bloch, 2013). At this time, no medications are FDA-approved for treating gambling disorder specifically. (Rizeanu, 2015; Lubuzek et al., 2014; Pirritano et al., 2014) For patients treated with dopamine agonists who develop pathological gambling, significantly decreasing or cessation of dopamine agonist doses has been shown to reduce and/or eliminate pathological gambling symptoms. (Dodd et al., 2005; Botswick et al., 2009; Hassan et al., 2011) Therefore, attempts should be made to modify dopamine replacement therapy to its lowest effective daily dose.

CONCLUSION Pathological gambling is undoubtedly a debilitating disorder that frequently leads to dire personal and social consequences. A change in DSM

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classification of gambling disorder as a substance-related and addictive disorder provided a new framework in exploring pathophysiology, neural network and pharmacological strategies. The role of dopaminergic agents and aripiprazole in de novo pathological gambling has led to proposals of blackbox warning by the FDA. Prior to starting dopaminergic therapies, patients and families should be counseled on the risks of developing pathological gambling and other compulsive behaviors. Follow-up screening would help to identify new emerging pathological gambling symptoms. Management of gambling disorder is complex, involving psychobehavioral and psychopharmacological methods. Continued research is critical in preventing and treating this disorder.

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amphetamine-induced dopamine release in pathological gambling: a positron emission tomography study with (11C)-(+)-PHNO. Mol. Psychiatry., 19, 1305-1313. Bosco, D., Plastino, M., Colica, C., Bosco, F., Arianna, S., Vecchio, A., Galati, F., Cristiano, D., Consoli, A. & Consoli, D. (2012). Clin Neuropharmacol., 35(3), 118-120. Botswick, J. M., Hecksel, K. A., Stevens, S. R., Bower, J. H. & Ahlskog, J. E. (2009). Frequency of new-onset pathologic compulsive gambling or hypersexuality after drug treatment of idiopathic Parkinson disease. Mayo. Clin. Proc., 84(4), 310-316. Brewer, J. A. & Potenza., M. N. (2008). The neurobiology and genetics of impulse control disorders: Relationships to drug addictions. Biochem. Pharamcol., 75, 63-75. Cilia, R., Siri, C., Marotta, G., Isaias, I. U., De Gaspari, D., Canesi, M., Pezzoli, G. & Antonini, A. (2008). Functional abnormalities underlying pathological gambling in Parkinson disease. Arch. Neurol., 65(12), 16041611. Clark, L. (2014). Disordered gambling: the evolving concept of behavioral addiction. Ann. N. Y. Acad. Sci., 1327, 46-61. Cohen, J., Magalon, D., Boyer, L., Simon, N. & Christophe, L. (2011). Aripiprazole-induced pathological gambling: a report of 3 cases. Curr. Drug. Saf., 6(1), 51–53. Comings, D. E., Rosenthal, R. J., Lesieur, H. R., Rugle, L. J., Muhleman, D., Chiu, C., Dietz, G. & Gade, R. (1996). A study of the dopamine D2 receptor gene in pathological gambling. Pharmacogenetics., 6(3), 223234. Cornelius, J. R., Tippmann-Peikert, M., Slocumb, N. L., Frerichs, C. F. & Silber, M. H. (2010). Impulse control disorders with the use of dopaminergic agents in restless legs syndrome: a case-control study. Sleep., 33, 81-87. Cowlishaw, S., Merkouris, S., Dowling, N., Anderson, C., Jackson, A. & Thomas, S. (2012). Psychological therapies for pathological and problem gambling. Cochrane. Database. Syst. Rev., 11, CD008937. Davie, M. (2007). Pathological gambling associated with cabergoline therapy in a patient with a pituitary prolactinoma. J. Neuropsychiatry. Clin. Neurosci., 19(4), 473-474. Djamshidian, A., Averbeck, B. B., Lees, A. J. & O’Sullivan, S. S. (2011). Clinical aspects of impulsive-compulsive behaviours in Parkinson’s disease. J. Neurol. Sci., 310, 183-188.

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Dodd, M. L., Klos, K. J. & Bower, J. H. (2005). Pathological gambling caused by drugs used to treat Parkinson disease. Arch. Neurol., 62(9), 1377-1381. Driver-Dunckley, E., Samnta, J. & Stacy, M. (2003). Pathological gambling associated with dopamine agonist therapy in Parkinson’s disease. Neurology., 61(3), 422-423. Gaboriau, L., Victorri-Vigneau, C., Gerardin, M., Allain-Veyrac, G., JollietEvin, P., Grall-Bronnec, M., (2014). Aripiprazole: a new risk factor for pathological gambling? A report of 8 case reports. Addict. Behav., 39, 562-565. Garcia-Ruiz, P., Castrillo, J. C. M., Alonso-Canovas, A., Herranz Barcenas, A., Vela, L., Sanchez Alonso, P., Mata, M., Olmedilla Gonzalez, N. & Mahillo Fernandez, I. (2014). Impulse control disorder in patients with Parkinson’s disease under dopamine agonist therapy: a multicenter study. J. Neurol. Neurosurg. Psychiatry., 85, 841-845. Gerlach, M., Double, K., Arzberger, T., Leblhuber, F., Tatschner, T. & Riederer, P. (2003). Dopamine receptor agonists in current clinical use: comparative dopamine receptor binding profiles defined in the human striatum. J. Neural. Transm., 110(10), 1119-1127. Grall-Bronnec, M., Sauvaget, A., Perrouin, F., Leboucher, J., Etcheverrigaray, F., Challet-Bouju, G., Gaboriau, L., Derkinderen, P., Jolliet, P. & VictorriVigneau, C. (2016). Pathological gambling associated with aripiprazole or dopamine replacement therapy. Do patients share the same features? A review. J. Clin. Psychopharmacol., 36(1), 63-70. Grant, J. E., Kim, S. W., Potenza, M. N., Blanco, C., Ibanez, A., Stevens, L., Hektner, J. M. & Zaninelli, R. (2003). Paroxetine treatment of pathological gambling: a multi-centre randomized controlled trial. Int. Clin. Psychopharmacol., 18(4), 243-9. Grant, J. E., Potenza, M. N., Hollander, E., Cunningham-Williams, R., Nurminen, T., Smits, G. & Kallio, A. (2006). Multicenter investigation of the opioid antagonist nalmefene in the treatment of pathological gambling. Am. J. Psychiatry., 163(2), 303-312. Grant, J. E., Kim, S. W. & Hartman, B. K. (2008). A double-blind, placebocontrolled study of the opiate antagonist naltrexone in the treatment of pathological gambling urges. J. Clin. Psychiatry., 69(5), 783-789. Griffiths, M. (1999). Gambling technologies: prospects for problem gambling. J Gambl Stud., 15(3), 265-283. Gyollai, A., Griffiths, M. D., Barta, C., Vereczkei, A., Urbán, R., Kun, B., Kökönyei, G., Székely, A., Sasvári-Székely, M., Blum, K. &

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Demetrovics, Z. (2014). The genetics of problem and pathological gambling: a systematic review. Curr. Pharm. Des., 20(25), 3993-3999. Hassan, A., Bower, J. H., Kumar, N., Matsumoto, J. Y., Fealey, R. D., Josephs, K. A. & Ahlskog, J. E. (2011). Dopamine agonist-triggered pathological behaviors: Surveillance in the PD clinic reveals high frequencies. Parkinsonism. Relat. Disord., 17, 260-264. Hodgins, D. C., Stea J. N. & Grant, J. E. (2011). Gambling disorders. Lancet., 378, 1874-1884. Hollander, E., Pallanti, S., Allen, A., Sood, E. & Baldini Rossi, N. (2005). Does sustained-release lithium reduce impulsive gambling and affective instability versus placebo in pathological gamblers with bipolar spectrum disorders? Am. J. Psychiatry., 162(1), 137-145. Kessler, R. C., Hwang, I., LaBrie, R. A., Petukhova, M., Sampson, N., Winters, K. C. & Shaffer, H. J. (2008). DSM-IV pathological gambling in the National Comorbidity Survey Replication. Psychol. Med., 38, 13511360. Kim, S. W. (1998). Opioid antagonists in the treatment of impulse control disorders. J. Clin. Psych., 59(4), 159-164. Kim, S. W., Grant, J. E., Adson, D. E., Shin, Y. C. & Zaninelli, R. (2002). A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling. J. Clin. Psychiatry., 63(6), 501-507. Kim, S. W., Grant, J. E., Eckert, E. D., Faris, P. L. & Hartman, B. K. (2006). Pathological gambling and mood disorders: clinical associations and treatment implications. J. Affect. Disord., 92, 109-116. Kreek, M. J., Nielsen, D. A., Butelman, E. R. & LaForge, K. S. (2005). Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nat. Neurosci., 8(11), 14501457. Kurlan, R. (2004). Disabling repetitive behaviors in Parkinson's disease. Mov. Disord., 19(4), 433-437. Lee, J. Y., Lee, E. K., Park, S. S., Lim, J. Y., Kim, H. J., Kim, J. S. & Jeon, B. S. (2009). Association of DRD3 and GRIN2B with impulse control and related behaviors in Parkinson’s disease. Mov. Disord., 24, 1803-1810. Leeman, R. F. & Potenza, M. N. (2012). Similarities and differences between pathological gambling and substance use disorders: a focus on impulsivity and compulsivity. Psychopharm., 219, 469-490.

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Labuzek, K., Beil, S., Beil-Gawelczyk, J., Gabryel, B., Franik, G. & Okopień, B. (2014). The latest achievements in the pharmacotherapy of gambling disorder. Pharmacol. Rep., 66, 811-820. McElroy, S. L., Nelson, E. B., Welge, J. A., Kaehler, L. & Keck, P. E Jr. (2008). Olanzapine in the treatment of pathological gambling: a negative randomized placebo-controlled trial. J. Clin. Psychiatry., 69(3), 433-440. Pallanti, S., Bernardi, S., Quercioli, L., DeCaria, C. & Hollander, E. (2006). Serotonin dysfunction in pathological gamblers: increased prolactin response to oral m-CPP versus placebo. CNS. Spectr., 11(12), 956-964. Pallesen, S., Molde, H., Arnestad, H. M., Laberg, J. C., Skutle, A., Iversen, E., Støylen, I. J., Kvale, G. & Holsten, F. (2007). Outcome of pharmacological treatments of pathological gambling: a review and metaanalysis. J. Clin. Psychopharmacol., 27(4), 357-364. Papay, K., Xie, S. X., Stern, M., Hurtig, H., Siderowf, A., Duda, J. E., Minger, J. & Weintraub, D. (2014). Naltrexone for impulse control disorders in Parkinson disease: A placebo-controlled study. Neurology., 83(9), 826833. Pérez de Castro, I., Ibáñez, A., Saiz-Ruiz, J. & Fernández-Piqueras, J. (2002). Concurrent positive association between pathological gambling and functional DNA polymorphism in the MAO-A and the 5-HT transporter genes. Mol. Psychiatry., 7, 927-928. Petry, N. M., Stinson, F. S. & Grant, B. F. (2005). Comorbidity of DSM-IV pathological gambling and other psychiatric disorders: results from national epidemiologic survey on alcohol and related conditions. J. Clin. Psychiatry., 66(5), 564-574. Petry, N. M., Ammerman, Y., Bohl, J., Doersch, A., Gay, H., Kadden, R., Molina, C. & Steinberg, K. (2006). Cognitive-behavior therapy for pathological gamblers. J. Consult. Clin. Psychol., 74, 555-567. Pirritano, D., Plastino, M., Bosco, D., Gallelli, L., Siniscalchi, A. & De Sarro, G. (2014). Gambling disorder during dopamine replacement treatment in Parkinson’s disease: a comprehensive review. Biomed. Res. Int., 2014, 1-9. Potenza, M. N. (2006). Should addictive disorders include non-substancerelated conditions? Addiction., 101(Suppl), 142-151. Potenza, M. N. (2014). The neural bases of cognitive processes in gambling disorder. Trends. Cogn. Sci., 18(8), 429-438. Ravindran, A. V., Telner, J., Bhatla, R., Cameron, C., Horn, E. & Horder, D. (2006). Pathological gambling: treatment correlates. Eur. Neuropsychopharm., 16, S506.

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Raylu, N. & Oei, T. P. (2004). The Gambling Related Cognitions Scale (GRCS): Development, confirmatory factor validation and psychometric properties. Addiction., 99, 757-769. Reuter, J., Raedler, T., Rose, M., Hand, I., Gläscher, J. & Büchel, C. (2005). Pathological gambling is linked to reduced activation of the mesolimbic reward system. Nat. Neurosci., 8(2), 147-148. Rizeanu, S. (2015). Pathological gambling treatment – review. Procedia. Soc. Behav. Sci., 187, 613-618. Rømer Thomsen, K., Fjorback, L. O., Møller, A. & Lou, H. C. (2014). Applying incentive sensitization models to behavioral addiction. Neurosci. Biobehav. Rev., 45, 343-349. Roy, A., Adinoff, B., Roehrich, L., Lamparski, D., Custer, R., Lorenz, V., Barbaccia, M., Guidotti, A., Costa, E. & Linnoila, M. (1988). Pathological gambling: A psychobiological study. Arch. Gen. Psychiatry., 45(4), 369373. Santangelo, G., Barone, P., Trojano, L. & Vitale, C. (2013). Pathological gambling in Parkinson’s disease. A comprehensive review. Parkinsonism. Relat. Disord., 19, 645-653. Sevincok, L., Akoglu, A. & Akyol, A. (2007). Quetiapine in a case with Parkinson disease and pathological gambling. J. Clin. Psychopharmacol., 27(1), 107-108. Shaffer, H. J. & Martin, R. (2011). Disordered gambling: etiology, trajectory, and clinical considerations. Annu. Rev. Clin. Psychol., 7, 483-510. Smith, N., Kitchenham, N. & Bowden-Jones, H. (2011). Pathological gambling and the treatment of psychosis with aripiprazole: case reports. Br. J. Psychiatry., 199, 158-159. Sulzer, D., Sonders, M. S., Poulsen, N. W. & Galli, A. (2005). Mechanisms of neurotransmitter release by amphetamine: a review. Prog. Neurobiol., 75(6), 406-433. Vitaro, F., Brendgen, M., Ladouceur, R. & Tremblay, R. E. (2001). Gambling, delinquency, and drug use during adolescence: mutual influences and common risk factors. J. Gambl. Stud., 17, 171-190. Voon, V., Hassan, K., Zurowski, M., Duff-Canning, S., de Souza, M., Fox, S., Lang, A. E. & Miyasaki, J. (2006). Prospective prevalence of pathologic gambling and medication association in Parkinson disease. Neurology., 66(11), 1750-1752. Voon, V., Potenza, M. N. & Thomsen, T. (2007a). Medication-related impulse control and repetitive behaviors in Parkinson’s disease. Curr. Opin. Neurol., 4, 484-492.

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Voon, V., Thomsen, T., Miyasaki, J. M., de Souza, M., Shafro, A., Fox, S. H., Duff-Canning, S., Lang, A. E. & Zurowski, M. (2007b). Factors associated with dopaminergic drug-related pathological gambling in Parkinson disease. Arch. Neurol., 64(2), 212-216. Volberg, R. A. (2002). Gambling and Problem Gambling in Nevada. Report to the Nevada Department of Human Resources. Carson City, NV: Department of Human Resources. Wardle, H., Sproston, K., Orford, J., Erens, B., Griffiths, M., Constantine, R. & Pigott, S. (2007). British Gambling Prevalence Survey 2007. London: National Center for Social Research. Weintraub, D., Koester, J., Potenza, M. N., Siderowf, A. D., Stacy, M., Voon, V., Whetteckey, J., Wunderlich, G. R. & Lang, A. E. (2010). Impulse control disorders in Parkinson disease: cross-sectional study of 3090 patients. Arch. Neurol., 67, 589-595. Weintraub, D., Papay, K. & Siderowf, A., Parkinson's Progression Markers Initiative. (2013). Screening for impulse control symptoms in patients with de novo Parkinson disease: a case-control study. Neurology., Jan 8, 80(2), 176-80. Welte, J., Barnes, G., Wieczorek, W., Tidwell, M. C. & Parker, J. (2001). Alcohol and gambling pathology among U.S. adults: Prevalence, demographic patterns and comorbidity. J. Stud. Alcohol., 62, 706-712. Welte, J. W., Barnes, G. M., Wieczorek, W. F., Tidwell, M. C. & Parker, J. C.,(2004). Risk factors for pathological gambling. Addict Behav., 29(2), 323-335.

BIOGRAPHICAL SKETCH Anhar Hassan Department of Neurology, Mayo Clinic, Rochester, MN, US Education: Bachelor of Medicine and Bachelor of Surgery, Trinity College Dublin, Ireland (MBBCh), 2002. Fellow of the Royal Australasian College of Physicians (FRACP), 2010. Research and Professional Experience: Clinical and research experience in movement disorders, including Parkinson disease, atypical parkinsonian disorders, impulse control disorders, hyperkinetic movement disorders.

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Professional Appointments: Assistant Professor of Neurology, Mayo Clinic, Rochester, MN, USA Honors: Movement Disorders Society Leaders Program, 2016; Clinical Research Award, International Movement Disorder Society Congress, Stockholm, Sweden, 2014; Annual Fellow Scholar, American Academy of Neurology Institute, 2012. Publications Last 3 Years: Hassan A, Okun MS. Emerging Subspecialities in Neurology: Deep brain stimulation (DBS) and electrical neuro-network modulation (ENM). Neurology. 2013 Jan 29; 80(5): e47-50. Sriram A, Ward HE, Hassan A, Iyer S, Foote KD, Rodriguez RL, McFarland N, Okun MS. Valproate as a Treatment for Dopamine Dysregulation Syndrome (DDS) in Parkinson's Disease. J Neurol. 2013 Feb; 260(2): 5217. Hassan A, Leep-Hunderford A, Watson J, Boon AJ, Sorenson EJ. Median nerve ultrasound in diabetic peripheral neuropathy with and without carpal tunnel syndrome. Muscle Nerve. 2013 Mar; 47(3): 437-9. Hassan A, Wu S, Schmidt P, Daifung, Giladi N, Simuni T, Bloem B, Malaty IA, Okun MS, on behalf of NPF QII Investigators. High rates and the risk factors for Emergency Room Visits and Hospitalization in Parkinson’s disease. Parkinsonism Rel Disord. 2013 Nov; 19(11): 949-54. Roemmich RT, Nocera JR, Stegemöller EL, Hassan A, Okun MS, Hass CJ. Locomotor adaptation and adaptive learning in Parkinson's disease and normal aging. Clin Neurophysiol. 2014 Feb; 125(2): 313-9. Hassan A, Wijdicks EF. The Mayo Clinic experience. Pract Neurol. 2014 Feb; 14(1): 68-9. Hassan A, Vallabhajosula S, Zahodne LB, Bowers D, Okun MS, Zahodne L, Fernandez HH, Hass CJ. Correlations of Apathy and Depression with Postural Instability in Parkinson Disease. J Neurol Sci. 2014 Mar 15; 338(1-2): 162-5. International Parkinson and Movement Disorder Society Telemedicine Task Force “The Past, Present, and Future of Telemedicine for Parkinson Disease”. Mov Disord. 2014 Jun; 29(7): 871-83. GEO-PD Consortium. Global investigation and meta-analysis of the C9orf72 (G4C2)n repeat in Parkinson disease. Neurology. 2014 Nov 18; 83(21): 1906-13.

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Shannon Y. Chiu and Anhar Hassan

Morishita T, Foote KD, Archer DB, Coombes SA, Vaillancourt DE, Hassan A, Haq IU, Wolf J, Okun MS,. Smile Without Euphoria Induced by Deep Brain Stimulation: A Case Report. Neurocase. 2014 Oct 31: 1-5. Hassan A, Wu SS, Schmidt P, Simuni T, Giladi N, Miyasaki JM, Bloem BR, Malaty IA, Okun MS, on behalf of the NPF QII Investigators. The Profile of Long-term Parkinson’s Disease Survivors with 20 Years Disease Duration and Beyond. J Parkinsons Dis. 2015 Feb 26. Fujioka S, Strongosky AJ, Hassan A, Rademakers R, Dickson DW, Wszolek ZK. Clinical presentation of a patient with SLC20A2 and THAP1 deletions: Differential diagnosis of oromandibular dystonia. Parkinsonism Relat Disord. 2015 Jan 8. pii: S1353-8020(14)00498-2. Coon EA, Hassan A. Did the ‘woman in the attic’ in Jane Eyre have Huntington’s disease? Tremor Other Hyperkinet Mov (N Y). 2015 Jul 21; 5: 323. Smith RM, Hassan A, Robertson CE. Numb Chin Syndrome. Curr Pain Headache Rep. 2015 Sep; 19(9): 44 Labbe C, Ogaki K, Lorenzo-Betancor O, Ortolaza A, Walton RL, Rayaprolu S, Fujioka S, Murray ME, Heckman MG, McCarthy A, Lynch T, Siuda J, Opala G, Rudzinska M, Krygowska-Wajs A, Barcikowska M, Czyzewski K, Sanotsky Y, Rektorová I, McLean P, Rademakers R, Ertekin-Taner N, Hassan A, Ahlskog JE, Boeve BF, Petersen RC, Maraganore DM, Adler CH, Ferman TJ, Parisi PE, Graff-Radford NR, Uitti RJ, Wszolek ZK, Dickson DW, and Ross OA. Role for the microtubule-associated protein tau variant p. A152T in risk of alpha-synucleinopathies. Neurology. 2015 Nov 10; 85(19): 1680-6. Hassan A, Benarroch EE. Heterogeneity of the Midbrain Dopamine System: Implications for Parkinson Disease. Neurology. 2015 Nov 17; 85(20): 1795-805. Hassan A, Heckman MG, Serie DJ, Ahlskog JE, Wszolek ZK, Uitti RJ, van Gerpen JA, Okun MS, Rayaprolul S, Ross OA. Association of Parkinson disease age of onset with DRD2, DRD3 and GRIN2B polymorphisms. Parkinsonism Relat Disord. 2016 Jan; 22: 102-5. Arena JE, Weigand SD, Whitwell JL, Hassan A, Eggers SD, Hoglinger GU, Litvan I, Josephs KA. Progressive Supranuclear Palsy-Progression and Survival. J Neurol. 2015 Dec 24. [Epub ahead of print] Hassan A, Ahlskog JE, Matsumoto JY, Milber JM, Bower JH, Wilkinson JR. Orthostatic Tremor: Clinical, Electrophysiologic and Treatment Findings in184 Patients. Neurology. 2016 Feb 2; 86(5): 458-64

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Connect. Parkinson Investigators. National randomized controlled trial of virtual house calls for Parkinson disease: Interest and barriers. Telemed J E Health. 2016 Feb 17. [Epub ahead of print]

Shannon Chiu Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA Education: NYU School of Medicine, New York, NY M.D. in May 2014 University of Cambridge, Cambridge, England M.Sc. in Experimental Psychology, June 2010 Williams College, Williamstown, MA B.A. in Biology, magna cum laude, June 2008 Concentration in Neuroscience Address: Mayo Clinic Rochester Neurology, 200 1st Street SW, Rochester, MN 55902, US Research and Professional Experience: Dr. Thomas Wisniewski, Departments of Neurology, Pathology and Psychiatry, NYU School of Medicine, 2011-2014 Investigated in vivo detection of Alzheimer’s disease amyloid plaques by magnetic resonance imaging using bifunctional USPIO; also studied mechanisms of action of innate immunity stimulation with CpG-ODN on Alzheimer’s disease Professor Lorraine Tyler, Centre for Speech, Language and the Brain, University of Cambridge, Cambridge, UK, 2008-2010 Explored aging effects on the cognitive architecture and neural instantiation of phonological and semantic processing in language production Professor Lois Banta, Biology Department, Williams College, Williamstown, MA, 2005 Investigated the interaction between VirC1 and VirC2 in determining virulence in Agrobacterium tumefaciens

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Shannon Y. Chiu and Anhar Hassan

Honors: American Academy of Neurology Medical Student Prize for Excellence in Neurology, 2014 Gates Cambridge Scholarship, 2008 Publications Last 3 Years: Tyler L K, Chiu S, Zhuang J, Randall B, Devereux B J, Wright P, Clarke A, Taylor K I, (2013). Objects and categories: feature statistics and object processing in the ventral stream. J. Cogn. Neurosci. 25(10), 1723-1735. Chiu S, (2014). Primecuts – This Week In The Journals. Clinical Correlations: The NYU Langone Online Journal of Medicine. Published online November 10, 2014. http://www.clinicalcorrelations.org/?p=8145 Chiu S, (2015). Neurologic Complications In Infective Endocarditis: To Anticoagulate Or Not To Anticoagulate. Clinical Correlations: The NYU Langone Online Journal of Medicine. Published online July 10, 2015. http://www.clinicalcorrelations.org/?p=8612

In: Gambling Editor: Yvonne Carter

ISBN: 978-1-63485-787-1 © 2016 Nova Science Publishers, Inc.

Chapter 2

GAMBLING: TAXES AND PREVENTION Ingo Fiedler1,, Sylvia Kairouz2 and Chantal Robillard2 1

2

Division on Gambling, University of Hamburg, Hamburg, Germany Research Chair on Gambling Studies, Concordia University, Montreal, Canada

ABSTRACT The gambling market is regulated because it involves costs to society. The standard approach to countering these is to tax gambling products. However, gambling taxes deter more recreational than pathological gamblers and are regressive, meaning that they increase social inequalities. Concurrently, health prevention measures reduce the social costs of gambling without reducing its benefits and are thus preferable to taxes. Currently, however, they are proportionally scarce and ineffective. The reason for this adverse political outcome is the fundamental conflict of interests between gambling revenues and prevention of addiction: social costs and market revenues both concentrate on addicted gamblers. On a societal level, this conflict of interest is projected onto the competing interests of stakeholders, where interests of politically not well organized parties remain unheard. To ensure a more effective regulatory intervention, we suggest a paradigmatic shift: games should be taxed in 

Correspondence to Dr. Ingo Fiedler, University of Hamburg, Max-Brauer-Allee 60, 22765 Hamburg, Germany; email: [email protected]; phone: +49 42838-6454.

26

Ingo Fiedler, Sylvia Kairouz and Chantal Robillard accordance to the revenue they generate from addicts, and more effective multidimensional prevention measures should be implemented.

INTRODUCTION The objective of the state is to maximize welfare, which we define as the sum of the material and nonmaterial wellbeing of citizens. This translates into balancing the costs and benefits of gambling. The costs of gambling, which we define as the sum of all material and nonmaterial costs, are primarily induced by gambling addiction (see Table 1) and thus concentrate on addicted gamblers (the following studies focus on the different forms of social costs: Walker & Barnett 1999, Productivity Commission 1999, Köberl & Prettenthaler 2009, Fong 2011; Fiedler 2016;).1 Hence, there is a social incentive to reduce current gambling problems and prevent future gambling addiction. Benefits are analogously defined as the sum of all material and nonmaterial benefits, which can be summed up as market revenues (including taxes) and the joy of playing.2 Note that market revenues in the form of operators’ profits and paid taxes concentrate on addicts. The overall revenue share from problematic or pathological gamblers (SOGS 5+) is between 32% in Canada (CPGI 3+, Williams & Wood, 2004) and 33% in Australia (Productivity Commission, 1999, p. 7.46). These figures are strongly driven by lotteries, which account for a large proportion of gambling revenues in most jurisdictions but account for only a small portion of problem gamblers. For other games, the revenue share from addicts is much higher. For example, the revenue share of slot machine operators generated by problematic or pathological gamblers (CPGI 3+) is 61% in Australia (Productivity Commission 2010), as well as in Ontario, Canada (Williams & Wood 2004). Although the industry is unconcerned about addiction in and of itself, they are indirectly profiting from it because addicts are big spenders. Thus, operators have an indirect economic incentive to sustain their profits by not preventing addiction. The state also indirectly profits from addicts because their disproportionately high spending generates tax revenues. At the same time the state bears a part of the costs incurred by addicts, for example, in the form of treatment and redistribution costs. 1

In the literature, the only gambling costs unrelated to addiction are those associated with nonaddiction driven crime, mainly money laundering and match fixing. 2 As a social benefit of gambling, market revenues are well-known because of company and state reports; however, the benefits from the joy of playing have yet to be studied.

27

Gambling: Taxes and Prevention Table 1. Social Costs of Gambling

a

b

c

Cost of Gambling Addiction

Type of Costa

Monetaryb

Monetary losses Income losses caused by unemployment Self-borne costs of treatment Lost opportunities (costs of time) Loss of housing Criminal records for addiction-related crime Psychic costs/reduced quality of life Caused (substance) addictions Caused physical illnesses Changes in personality and brain structure Costs of cue managementb Unpaid debt Debt paid by thirds Increased social welfare Addiction-related crime Treatment costs Costs of debt consulting and private insolvency Administrative costs for increased social welfare Costs of prevention measures Costs of gambling research Debt collection measures Productivity losses from unemployment Productivity losses caused by lack of concentration Disruption of families and harm to dependents Increased risk of addiction for children of gambling addicts Addiction-induced loss of social capital

Private (pecuniaryb) Private (pecuniaryb) Private Private Private Private Private Private Private Private Private External (pecuniaryc) External (pecuniaryc) External (pecuniaryc) External (often pecuniaryc) External External External External External External External External

Yes Yes Yes No No No No No No No No Yes Yes Yes Often Yes Yes Yes Yes Yes Partially Partially Partially

External External

No No

External

No

private = costs borne by the gambler, external = costs borne by others. Private costs are not relevant to societal welfare, if people behave rationally, because there is then an equally large (or larger) self-benefit). Cue management is behavior to avoid cues in order to stay abstinent or consume less. In extreme cases, such as visiting a clinic, cue management is associated with serious constraints in the form of material and non-material costs for the addicted gambler. Monetary means that the costs can be expressed in dollar terms, whereas pecuniary is a technical term in economics that refers to a redistributive effect of money. It can be argued that pecuniary costs are not relevant to society because they are merely redistributed (e.g., between those who pay for social welfare and those who receive it), with no net loss.

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Figure 1. The addiction tradeoff: benefits, costs and corresponding incentives.

There is a strong tradeoff between market size and prevention of problem gambling; effective prevention reduces the market size considerably. Although the objective of the state is to find an optimal balance in this tradeoff, we argue in this paper that current regulatory efforts are suboptimal in two regards: (1) current regulation places too much emphasis on taxing gambling, and (2) there is insufficient prevention of gambling addiction. A more balanced approach would mean increasing prevention efforts, reducing the extra taxes on games with a low share of revenues from addicts, and increasing the taxes on games with a high share of revenues from addicts.

TAXES ON GAMBLING TO PREVENT ADDICTION Taxes reduce the demand for gambling. In this regard, taxes have a preventive effect on addiction. However, taxes come at the cost of mainly deterring recreational gamblers, who do not incur social costs but only create social benefits in the form of joy of playing, tax revenues and industry profits. In addition, taxes on gambling affect lower-income households more strongly and violate the principle of the modern welfare state. Demand for gambling is too high because of the negative externalities of gambling addiction. To reduce the negative externalities, the text book approach is to introduce an extra tax on these goods—a so-called “Pigovian tax”. The idea behind increasing taxes is that it causes prices to increase, which leads to a decrease in demand (Pindyck & Rubinfeld, 2012) and helps internalizing the externalities (Pigou 1932). Gambling taxes can be interpreted as Pigovian taxes: they lead to price increases and, correspondingly, to a decrease in demand. The effect of price changes on demand is measured by the

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price elasticity of a good. If, for example, the price elasticity is -1.5, a price increase of 1% will lead to a 1.5% decrease in demand. For gambling, the price elasticity varies between different forms of games and is largest for betting and lowest for lottery products (see Table 2).

Casino products Casino products

Price elasticity Lower bound -0.75 -0.9a

Upper bound -0.87 -1.5

UK lottery UK lottery Horseracing Horseracing

-0.66 -0.19 -1.64 -2.85

-1.03 -1.92 -1.64 -3.09

Horseracing Sports betting Toto betting

-1.59b -2.17 -1.3

-2.73 -2.17 -1.3

Product

a

Source Landers 2008 Thalheimer & Ali 2003 Forrest et al. 1999 Gulley & Scott 1991 Suits 1979 Thalheimer & Ali 1995 Suits 1979 Suits 1979 Morgan & Vasché 1982

Long-term elasticity. The most likely case, according to the author.

b

It is argued that the decreased demand caused by taxation reduces availability of gambling, thereby leading to reduced pathological gambling (Lester 1994, Welte et al. 2004, Abbott 2007, Adams & Fiedler 2014). Hence, gambling taxes have a preventive effect on addiction, but they come with two main problems: (1) the demand of addicts is less elastic and (2) gambling taxes are regressive. Increasing the price of gambling reduces the participation of all gamblers, not just pathological gamblers. Additionally, because pathological gamblers’ demand for gambling is less elastic than that of recreational players (Productivity Commission 1999, Clarke 2008), the impact of the price increase disproportionately drives recreational gamblers out of the market. This effect is contrary to the goal of maintaining recreational players while preventing addiction. In terms of regressive taxation, as long ago as 1975, Eadington argued that gambling and taxes on gambling are regressive (Eadington, 1975). The regressive effect of gambling and gambling taxes was particularly studied for lotteries and received strong empirical support (Clotfelter & Cook 1989, PirotGood & Miksell 1995, Abdel-Ghany & Sharpe 2001, Freund & Morris 2005, Blalock et al. 2007, Beckert & Lutter 2009, Ghent & Grant 2010). Regressive

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means leading to increased social inequalities, that is, the gap between the rich and the poor widens. Although richer households spend more on gambling in an absolute sense, lower-income households spend a larger proportion of their incomes on gambling (Williams et al. 2011). For instance, it was shown that Canadian households in the bottom income quintile spend 2.2% on gambling compared with 0.5% spent by the top income quintile (Marshall 1998). Even more relevant from the standpoint of addiction is that people with low incomes are overrepresented among the highest spending gamblers (MacDonald et al. 2004). To conclude, the shortcomings of taxation – targeting the wrong gamblers and being regressive – are the reasons why prevention is superior in terms of reducing the social costs of gambling without affecting its benefits. We now turn to the question why taxation still is a dominant tool for gambling regulators in most jusrisdictions.

STAKEHOLDERS’ INTERESTS AND THEIR INFLUENCE ON TAXES AND PREVENTION There are multiple stakeholders in the gambling field, and each one has a different agenda and different incentives in regard to the regulatory intervention in the market. The gambling industry can be described by its goal to maximize revenues and shareholder value. Its incentive to oppose anything that keeps its market size from prospering is clear. This opposition includes taxes, which generally reduce profits, as well as prevention efforts targeted at addicts, who are responsible for a large share of all revenues. Another major player in most jurisdictions is the Ministry of Finance, which collects taxes from gambling to pay for the state’s various duties. Its main interest is to maximize income from taxation. Hence, the Ministry of Finance favors a high tax rate. With a large share of gambling revenues (thus, taxes) coming from addicts, the Ministry of Finance lacks the incentive to implement effective prevention efforts. Other stakeholders include the Ministry of Health, treatment and public health professionals, gamblers, and the dependents of addicted gamblers. These stakeholders can be grouped by their mutual interest in effectively preventing addiction (with gamblers not wanting these preventions to interfere with their joy of play).

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Although health prevention efforts are in the best interest of many stakeholders, and taxes are inefficient in terms of reducing the social costs of gambling, the current outcomes of the political arena of gambling regulation are most often high taxes (compared with ordinary goods) on most gambling forms, particularly lotteries, while prevention efforts have still not proven to be effective. For example, measures that lead to “informed decision making” are often propagated. These measures include informational responsible gambling campaigns, educational programs, references to treatment around gambling offers, pop-up messages, and regulations on advertisements, such as prohibiting “misleading” advertisements. These and similar measures are often implemented to prevent gambling addiction, but they do not appear to be effective for the following reasons: it has been argued that responsible gambling campaigns necessarily have to fail because they compete with the operators’ better funded advertising campaigns (Lemarié & Chebat 2012); educational programs might lead to the exact opposite behavior (Productivity Commission 2010); pop-up messages have a positive but limited effect (Schellinck & Schrans, 2002) and are a nuisance to players; and the factors that comprise a “misleading” and, thus, forbidden advertisement must be debated on a case-by-case basis. At the same time, the effective tool of exclusion programs is often unenforced and not used proactively (Meyer & Hayer 2010). Another example is (self-)limitation systems, which help gamblers stay in control of their gambling behavior. These systems have high preventive power (Productivity Commission 2010), but they are often implemented as less effective opt-in rather than more effective opt-out systems (Fiedler & Krumma, 2013). The political outcome of high taxes and limited prevention efforts goes against the overall societal interest (which is the combined interest of all stakeholders). The reason for this gap between actual preferences and political outcomes is political power. All stakeholders preferring preventive efforts are politically rather weak. Particularly gamblers and the dependents of addicted gamblers, have little power over actual political decisions. They depend on what Vanberg and Buchanan (1989) call the dialogue notion: raising their voices in standardized procedures of regulation, such as passing changes in the law. However, these activities only occur infrequently, such as with classaction lawsuits. Thus, the groups in favor of strong and effective health prevention measures remain unheard, and their interests are not reflected in the political outcome.

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THE ROLE OF RESEARCH: INFORMING THE PUBLIC DEBATE Outcomes in the political arena are partially driven by evidence and partially driven by lobbyism. It is the role of research to objectively inform the public debate to foster evidence-driven regulation. In terms of gambling regulation, it is important to carve out the fundamental conflict of interest between revenues and preventing addiction, which is based on the fact that addicts account for most of the social costs of gambling and at the same time account for a large portion of gambling revenues. That means there is no method of preventing addiction and keeping revenues constant. Rather, effective prevention reduces the market size by the revenue share generated by addicts, which can be well above 50% for slot machines. Because of the different levels of stakeholder power in the gambling environment, we argue that current prevention efforts rely too heavily on taxation and that the overall prevention level is too low. Although it sounds promising to prevent addiction and increase the state budget with gambling taxes, this approach is problematic. Gambling taxes are regressive and increase social inequalities, and the corresponding price increases from the taxes deter more recreational than pathological gamblers. This result is particularly true when the tax structure does not factor in the addictive nature of the different gambling forms; for example, lotteries are taxed highest in most jurisdictions, although they have the lowest share of revenues from addicts. At the same time, other prevention efforts are not used effectively, which leads to an unhealthy low level of prevention. Thus, we propose a paradigmatic shift in gambling regulation. The main parameters of this shift include the following factors. (1) Change the tax structure to tax different gambling forms based on the share of revenues they generate from addicts. This structure reduces the negative effect of taxes that target mostly recreational players. (2) Implement effective measures to prevent addiction. The effectiveness of such prevention means that problem gambling is prevented while recreational gamblers are not deterred from enjoying themselves. We suggest that effective prevention efforts need to be implemented as a package rather than individual measures (Livingstone 2014). To start, we suggest (a) limiting exposure to the most addictive gambling form—slot machines—by not allowing them outside of casinos; (b) decreasing the speed of play for slot machines; (c) for all gambling forms, introducing exclusion programs that are enforced and that must be proactively used by

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operators if signs of potential addiction are imminent (this measure must be enforced by severe fines for noncompliance); and (d) introducing an opt-out self-limitation system across all gambling forms and operators. The authors do not have any conflict of interest in this publication.

REFERENCES Abbott M.W. (2007). Situational factors that affect gambling behavior. In: editors: Smith G, Hodgins D.C., Williams R.J., Research and Measurement Issues in Gambling Studies, Burlington, Academic Press. Abdel-Ghany, M. and Sharpe, D.L. (2001). Lottery expenditures in Canada: Regional analysis of probability of purchase, amount of purchase, and incidence. Family & Consumer Sciences Research Journal, 30(1): 64–78. Adams, M, and Fiedler, I. (2014). Glücksspiel regulieren: Was wirkt und warum?, in: Verhaltenssüchte, editor: Mann, K., heidelberg, Springer, 143-154. Beckert, J. and Lutter, M. (2009). The inequality of fair play: Lottery gambling and social stratification in Germany. European Sociological Review, 25(4): 475–488. Blalock, G., Just, D. R., and Simon, D. H. (2007). Hitting the jackpot or hitting the skids: Entertainment, poverty and the demand for state lotteries. American Journal of Economics & Sociology, 66(3): 545–570. Clarke, H. R. (2008). Taxing sin: some economics of smoking, gambling and alcohol. The Melbourne Review, 4: 30–36. Clotfelter, C. T. and Cook, P. J. (1989). Selling Hope. State Lotteries in America. Harvard University Press, Cambridge. Eadington, W. R. (1975). Economic implications of legalized casino gambling. Journal of Behavioral Economics, 4(1): 55–77. Fong, D. K., Fong, H. N., and Li, S. Z. (2011). The social cost of gambling in Macao: before and after the liberalisation of the gaming industry. International Gambling Studies, 11(1): 43–56. Fiedler, I. and Krumma, I. (2013), Das Selbstlimitierungssystem für Sportwetter nach dem neuen Glücksspielstaatsvertrag, Zeitschrift für Wettund Glücksspielrecht, 2: 82-87. Fiedler, I. (2014), Evaluierung des Sperrsystems in deutschen Spielbanken, research report prepared for the Ministry of Interior for the State of Hamburg, Germany.

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Fiedler, I. (2016), Glücksspiele: eine verhaltens- und gesundheitsökonomische Analyse mit rechtspolitischen Empfehlungen, editor: Adams, M., Bern, Peter Lang Verlag. Forrest, D., Gulley, O. D., and Simmons, R. (1999). Elasticity of demand for UK national lottery tickets. National Tax Journal, 53: 853–863. Freund, E. A. and Morris, I. L. (2005). The lottery and income inequality in the States. Social Science Quaterly, 86: 996–1012. Ghent, L. S. and Grant, A. P. (2010). The demand for lottery products and their distributional consequences. National Tax Journal, 253-268: 63(2). Gulley, O. D. and Scott, F. A. (1991). The demand for wagering on state operated lotto games. National Tax Journal, 45: 13–22. Landers, J. (2008). What‘s the potential impact of casino tax increases on wagering handle: estimates of the price elasticity of demand for casino gaming. Economics Bulletin, 8: 1–15. Lester, D. (1994) Access to gambling opportunities and compulsive gambling, International Journal of Addictions, 29: 1611–1616. Lemarié, L. and Chebat, J.-C. (2012). Resist or comply: Promoting responsible gambling among youth, Journal of Business Research, 66: 137-140. Livingstone C, Rintoul A and Francis, L. (2014). What is the evidence for harm minimisation measures in gambling venues?. Evidence Base, 2014;2:1-24. Loto Québec (2014). Rapport Annuel 2013, http://lotoquebec.com/cms/dms/ Corporatif/fr/la-societe/rapport-annuel/rapport_annuel_2013_fr.pdf. MacDonald, M., McMullan, J. L., and Perrier, D. C. (2004). Gaming households in Canada. Journal of Gambling Studies, 20(3): 187–236. Marshall, K. (1998). The gambling industry: Raising the stakes. Technical Report 75-001-XPE, Statistics Canada Catalogue. Meyer, G. and Hayer, T. (2010). Die Effektivität der Spielsperre als Maßnahme des Spielerschutzes – Eine empirische Untersuchung von gesperrten Spielern. Peter Lang, Frankfurt am Main. Morgan, W.D. and Vasché, J. D. (1982). A note on the elasticity of demand for wagering. Applied Economics, 14:469–474. Pigou, A.C. “II, Chapter IX: Divergences Between Marginal Social Net Product and Marginal Private Net Product” in: The Economics of Welfare (1932). Pindyck, R. and Rubinfeld. D. (2012). Microeconomics, 8th edition, Pearson. Pirot-Good, M. and Miksell, J. L. (1995). Longitudinal evidence of the changing socio-economic profile of a state lottery market. Policy Studies Journal, 23(3):451–465.

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Productivity Commission (1999). Australia’s gambling industries, report no. 10., Productivity Commission, Canberra. Productivity Commission (2010): Gambling – Productivity Commission Inquiry Report, Canberra. Schellinck, T. and Schrans, T. (2002). Video lottery responsible gaming feature research: Final report., Atlantic Lottery Corporation and Focal Research, New Brunswick. Suits, D.B. (2005). The elasticity of demand for gambling. The Quarterly Journal of Economics, 93: 155–162. Thalheimer, R. and Ali, M. M. (1995). The demand for pari mutual horse race wagering and attendance, Management Science, 41: 129–143. Thalheimer, R. and Ali, M. M. (2003). The demand for casino gaming. Applied Economics, 35: 907–918. Vanberg, V. and Buchanan, J. M. (1989) Interests and Theories in Constitutional Choice, Journal of Theoretical Politics, 1 (1): 49-62. Walker, D. M. and Barnett, A. H. (1999). The social costs of gambling: An economic perspective. Journal of Gambling Studies, 15 (3): 181–209. Welte, J.W., Wieczorek W.F. and Barnes G.M. (2004) The relationship of ecological and geographic factors to gambling behavior and pathology. Journal of Gambling Studies, 20: 405–423. Williams, R. J., Belanger, Y. D. and Arthur, J. N. (2011). Gambling in Alberta: History, current status and socioeconomic impacts. Technical report, Alberta Gaming Research Institute. Williams, R.J. and Wood, R.T. (2004). The proportion of gaming revenue derived from problem gamblers: Examining the issues in a Canadian context. Analyses of Social Issues and Public Policy, 4: 33–45.

In: Gambling Editor: Yvonne Carter

ISBN: 978-1-63485-787-1 © 2016 Nova Science Publishers, Inc.

Chapter 3

A DESIRE-TARGETED INTERVENTION BASED ON NAIKAN COUNSELING FOR DISORDERED GAMBLERS (DING) Yasunobu Komoto, MD Kurihama Medical and Addiction Center Yokosuka City, Japan

ABSTRACT I proposed a desire-targeted intervention based on Naikan counseling for disordered gamblers (DING) as a result of the limitations of abstinence-targeted interventions, which are based on the disease model of weakened self-control relative to craving for gambling. In contrast, in DING, the loss of gambling control is perceived as a failure of strategy, wherein it is assumed that gambling fulfills various desires (e.g., the desire for fame, money, and escapism). Therefore, the development of alternative behaviors to directly fulfill original desires constitutes the main therapeutic goal of DING. Naikan counseling is useful for uncovering original desires, and the principal question asked to disordered gamblers is “Who satisfied you when you were not satisfied?” Therefore, to reveal the efficiency of DING, I introduced the six month-outcome study. Outpatients (n = 35) who were primarily diagnosed with gambling disorder using DSM-V were treated with DING. In principle, this intervention comprised six sessions that were 

E-mail: [email protected].

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Yasunobu Komoto conducted by psychiatrists and clinical psychologists. Participants were assessed for basic background characteristics such as gender and age; medical variables such as age of onset of problem gambling, duration of problem gambling, psychiatric complications, and motivation to quit gambling; assessments of the severity of gambling disorder based on DSM-5; and six-month outcomes after intervention (problem gambling/controlled gambling/abstinence). In results, at six months post-intervention, 40% of the participants were abstinent and 28.6% were controlled gamblers. Overall, 30.8% of the participants who initially reported low motivation to quit gambling were abstinent at six months post-intervention. History of suicide attempts was strongly associated with the outcomes. Thus, DING heightened the motivation for recovery without the individual feeling stigmatized or ashamed at being a gambler and without the individual feeling pressurized to quit gambling. Additionally, the abstinence rate for this intervention was nearly identical to the rates reported in previous literature.

Keywords: gambling disorder, Naikan counseling, guilt, shame, desire model

INTRODUCTION Background Gambling disorder is a public health problem characterized by persistent and recurrent maladaptive patterns of gambling, with a worldwide prevalence rate of an estimated 0.4%–2.0%, which varies according to the parameters used for the disorder’s definition, and the availability and accessibility of gambling activities (Kessler et al., 2008; Petry, Stinson, & Grant, 2005; Welte, Barnes, Wieczorek, Tidwell, & Parker, 2001). In Japan, gambling is common. The prevalence rate of disordered gamblers (defined by a score of ≥5 on the South Oaks Gambling Screen; SOGS; Lesieur & Blume, 1987) is estimated to be 5.5% among adults (Higuchi, 2008), because the availability and accessibility of gambling is high. The major types of gambling in Japan are playing pachinko/pachi-slot. Pachinko/pachi-slot playing disorder accounts for close to about 90% of all gambling disorders (Komoto, 2014). Pachinko and pachi-slot are forms of gambling that are played individually using a device like a recreational arcade game. Further, there are many pachinko/pachi-slot parlors in the downtown of every city in Japan.

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Gambling disorder results in clinical and subclinical harmful consequences such as depression, suicidal behaviors, legal involvement, occupational/educational disruption, and financial and interpersonal difficulties. Generally, suicide attempts represent one of the most important indicators of the more extreme variants of gambling disorder. In Japan, the most harmful consequence of gambling disorder is suicidal attempts.

Suicidality, Family History, and Shame Evidence suggests that suicidal gamblers begin gambling at an earlier age, accrue larger debts, are more likely to experience marital difficulties, and have a first-degree relative or family member with gambling problems (Petry & Kiluk, 2002). Similarly, I reported that the most significant independent predictor of suicide attempts was a family history of addiction (Komoto, 2014). Therefore, a family history of addiction is one of the reliable predictors of the severity and progression of the addiction. An addictive family member is apt to engender maladaptive emotional coping skills, for example, refraining to seek help from others and not disclosing his/her problems, due to the belief that “Seeking help for others is shameful.” (Bijttebier & Goethals, 2006). This feeling of shame limits the person’s ability to seek help. As a result, avoidant coping skills such as nondisclosure become the addictive member’s main coping skills. The experience of shame and the use of avoidant coping strategies for the emotional crisis worsen the gambling problem (Yi et al., 2011). Therefore, psychotherapeutic strategies for disordered gamblers should carefully address feelings of shame, whose primary component is low self-esteem.

Limitations of Gambling-Frequency Targeted Interventions Historically, intervention strategies for gambling disorders have viewed legitimate and acceptable purposes in terms of gambling frequency (i.e., total abstinence or suppressed gambling) (Ladouceur, 2005). However, these strategies are often accompanied by distress, as they put moral and/or spiritual pressure on the individual, by forcing him/her to change his/her core self to one that does not need to gamble. This requires a fundamental change in the individual’s values, which is outside the realm of medical care. Therefore, I

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believe that the ‘removal of the root cause of suffering’ should be the first principle of medical care for gambling addicts. Indeed, short-term outcome studies of some psychological treatments indicate that active treatments are more beneficial than no-treatment or waitlist control conditions (Rash & Petry, 2014). Active treatments include the use of workbooks and peer support, and may be brief and motivational, cognitive and/or behavioral, or blended treatments. Similarly, a comprehensive metaanalysis of existing outcome studies by Pallesen and colleagues revealed medium to large effect sizes for cognitive-behavioral therapy (CBT), self-help interventions, aversive therapy, Gamblers Anonymous (GA) groups, imaginal desensitization, and imaginal relaxation (Pallesen, Mitsem, Kvale, Johnsen, & Molde, 2005). The accumulated evidence seems to suggest that interventions based on CBT produce the most favorable outcomes (Blaszczynski & Nower, 2014). Nevertheless, CBT is not yet recognized as a standard treatment for gambling disorder (Ladouceur, 2003; Leung & Cottler, 2009; Petry et al., 2006). The fundamental aim of CBT, especially cognitive therapy, for gambling disorder is to identify and correct irrational and unrealistic beliefs postulated to contribute to excessive gambling, such as an illusion of control. In other words, the addicted individual’s primary erroneous beliefs are that he/she has control over the outcome of gambling, and these beliefs fail to consider the random nature of gambling (Blaszczynski & Nower, 2014). However, although the majority of disordered gamblers already understand that this belief is theoretically irrational, they are unable to quit problem gambling (Larimer, 2012; Wulfert, Blanchard, Freidenberg, & Martell, 2006). Additionally, some gamblers continue to engage in problem gambling even if they recognize that they are likely to lose money; the craving for gambling continues and often becomes intense (Hodgins, Ching, & McEwen, 2009). Addicts have ambivalent thoughts toward their addictive behavior (Kennett et al., 2013). Contrary to the therapeutic aims, a therapist’s negativistic attitude toward gambling may increase cravings for gambling. On the other hand, a positivistic attitude may give gamblers a justification to gamble. Therefore, in order to prevent gamblers from recalling their ambivalent and shameful memories and to avoid unnecessarily reinforcing a craving for gambling, targeting the frequency and money-loss of gambling itself should not be targeted. In the treatment of gambling disorder, dealing with emotional distress such as conflict resulting from addiction-based family dynamics should take precedence over specialized treatment.

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DESIRE MODEL Desires and Recovery Recently, studies on the natural recovery process of gambling addiction have revealed important implications for treatment strategies. High recovery rates of natural recovery groups and relatively low recovery rates of treatmentseeking groups reveal the possibility that standard interventions, which usually target gambling frequency (abstinence or suppression), disturb the natural recovery process (Abbott, Williams, & Volberg, 2004; Hodgins et al., 1999; Slutske, 2006; Slutske, Piaseck, Blaszczynski, & Martin, 2010). These frequency-targeted strategies force disordered gamblers to make endless efforts to avoid engaging in the problematic behaviors. Therefore, if they experience gambling loss again, they feel shame and repeatedly put more money into gambling; this is because for them, winning is the outcome they hoped for, through which shameful memories triggered by gambling loss, which equals past unsatisfied experiences, may be rewritten. Natural recovery is usually achieved not through effort and patience but escape from suffering and through desire-satisfaction (Hodgins & el-Guebaly, 2000; Nathan, 2003). From a phenomenological viewpoint, a craving for gambling consists of multiple basic desires, such as the desire for fame (including winning), achievement, money, wasting time, relaxation, helping others, belonging, masochism/sadism, and escapism.

Gambling and Desire Generally, gambling starts with a single desire and brings satisfaction. When gamblers cease to become satisfied, they can easily stop gambling. This gambling pattern is called social (recreational) gambling. In many cases, the first single desire underlying gambling is relaxation or money. When an individual encounters stressful or sad events, he/she starts to try and fulfill other desires such as the desire to win or escape. Consequently, gamblers begin to try and fulfill multiple desires. This gambling with the purpose of fulfilling multiple desires involves an endless effort to satisfy all desires. An example of this is that some gamblers repeatedly try to get back lost money although they have already satisfied the desire to win or escape. As a result, gamblers lose sight of the original desire that triggered gambling, and continue to gamble with high levels of frustration. This is an explanation of the mechanism underlying gambling disorder according to the desire model (Figure 1).

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Figure 1. “Drive model” for gambling disorders.

A Desire-Targeted Intervention for Gambling Disorders My assumption is that disordered gamblers cannot quit or control gambling, because their original desires, which have been typically denied or minimized, have not been satisfied. Therefore, the most important erroneous beliefs that should be targeted are not those about gambling itself such as the random nature of gambling but those underlying the individuals’ original desires. Therefore, I designed and used a desire-targeted intervention for gambling disorders instead of an ordinary abstinence-targeted intervention. This intervention consists of three directive steps: 1) Identification of the individual’s original desires, which have been suppressed due to certain reasons, for example, the desire to earn more money There are two key-questions that need to be posed to disclose the individual’s original desires: “Does pouring money into gambling contradict the very idea that you are gambling to satisfy your desire for more money?” and “Is your desire for money strictly triggering calculations of self-interest?”

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2) Permission to gamble for satisfying only a single desire, if they hope to continue gambling If the individual’s only desire is money, he/she can gamble professionally. However, he/she cannot always stick to only professional gambling, because most disordered gamblers have multiple desires for gambling. In results, they fall in high impulsivity and low self-efficacy (Weinstock, 2013). 3) Facilitation of the individual’s search for and trying of alternative behaviors that directly satisfy original desires It is not easy to find alternative behaviors, as almost all disordered gamblers believe that alternative behaviors should be meaningful ones such as working or engaging in a useful hobby to compensate for past gambling loss. However, the first alternative behaviors/activities should be light and easy behaviors/activities that satisfy only a single desire, such as offline gaming, chatting, garbage collection, intensive singing (karaoke), video watching, and comic reading. After these useless behaviors/activities, productive behaviors/activities may also be engaged in, such as housework (dishwashing, grass picking, etc.), fishing, attending lectures, participation in various competitions, meditation (yoga, etc.), and physical activities. Through these steps, therapists must repeatedly reinforce two important messages. One message is that the aim of alternative behaviors is to primarily satisfy the individual’s original desires; for example, the aim of engaging in physical activity is not to improve the individual’s health but to fulfill his/her need to escape and/or to fulfill his/her desire for fame, and that the aim of engaging in housework is not housekeeping but to fulfill the individual’s need to escape. The other message the therapist needs to constantly clarify to the individual is that the cause of disordered gambling is not the loss of gambling ability including intuition but erroneous beliefs about one’s own desires. This message protects the individual’s sense of worth as a gambler, which is the most important component of his/her core self and the source of natural recovery. If this component is hurt or wounded, the individual is overwhelmed by feelings of shame, and recovery is hindered. I utilized a worksheet to track the progress of this intervention (Figure 2). Thus, this “desire model” focuses on the gamblers’ original desires on the basis of studies on the natural recovery process of gambling (Hodgins & el-Guebaly, 2000; Hodgins, Wynne, & Makarchuk, 1999; Nathan, 2003).

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Please answer the following questions. Q1: What was your initial motivation for gambling? 1. to waste time 2. to have a change of pace 3. to escape from a stressful situation 4. to have a sense of superiority and/or accomplishment 5: to have a sense of expectation and/or thrill 6. because of an attachment to items associated with gambling (e.g., a gaming animation character) 7. to have an allowance 8. to have money to live 9. to pay debts 10. other ( ) Q2: What is your current motivation for gambling? (same choices as above) Q3: What is the most important motivation (equal to your desire)? Q4: What kind of efforts or actions have you taken to satisfy your desires? Q5: Have your motivations been satisfied? If satisfied, congratulations! Please continue gambling if you wish. If not satisfied, please go to Q6. Q6: What is the reason why you could not satisfy your desires? A. Gambling became an inappropriate satisfaction method B. Gambling to satisfy multiple motivations (desires) at the same time caused me to lose sight of the original motivation. Which is more true, A or B? A: Please search for alternative behaviors to directly satisfy the identified desire. B: Please gamble to satisfy only a single desire if you wish, and search for alternative behaviors to directly satisfy other desires. Q7: What fascination has attracted you to gambling? (Fame/Winning/Achievement/Money/Relaxation/Masochism/Escapism/Other) Q8: In the past, have you had a similar fascination with behaviors other than gambling? Who or what did you satisfy when you were not bensatisfied? (What have others done for you?) Q9: Please list appealing behaviors to satisfy your original desire that come to mind (that are legally permissible). Q10: What will you do first? * Whether you quit gambling or not, please be persistent in searching for and trying alternative behaviors. Both abstinence and controlled gambling are not associated with your efforts. If you achieve these states, it is due to chance. Figure 2. Q & A Worksheet for identifying original desires and discovering alternative behaviors.

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NAIKAN THERAPY Naikan Therapy as a Method through Which Desires Are Discovered As mentioned earlier, in the recovery process from gambling disorder, it is most important to uncover (especially for the concerned individual’s family members), the individual’s hidden, original desires. There are many methods through which these original desires can be uncovered. Naikan therapy is a type of psychotherapy wherein an individual’s original desires are uncovered through the recalling of past memories concerning family members, especially one’s parents. Naikan therapy has developed as an insight-oriented psychotherapy in Japan (Maeshiro, 2009). In Naikan therapy, the individual is asked three fundamental questions, which reveal his/her unconscious desires: “What have others done for you?” (satisfied desires), “What have you done for others in return?” (desire to help), and “What troubles have you caused others?” (Overflowing of negativity as a result of unsatisfied desires). Patients are invited to consider their own behaviors toward a target person in relation to three questions that are posed to them in a chronological manner (i.e., the order in which they have been mentioned earlier). Usually, the main target person is the mother (or primary caregivers), and the process begins when the patient is seven years old, and is repeated every three years. Through this recalling process, disordered gamblers discover their original and unconscious desires. Similarly, in psychoanalysis, it is hypothesized that some people use gambling to cope with self-punitive feelings that arise due to their original desires including the Oedipus complex, and through the therapy, the therapist tries to uncover these original desires. However, psychoanalysis indirectly uncovers desires by means of the psychoanalytical methods of free association and metastasis analysis. Therefore, psychoanalytical treatment takes a long time. In contrast to psychoanalysis, in Naikan therapy, the dominant level at which therapist-patient interchanges take place is not that of unconsciousness but of consciousness; therefore, in Naikan therapy, patients express only facts and do so clearly.

Mechanism of Naikan Therapy In Naikan therapy, a therapist, who has also experienced Naikan, assists patients by asking the patient the three abovementioned questions, to discover

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his/her original desires. This technique has been shown to alter negative cognitions and make them positive and also to reduce inferiority complexes, which produce feelings of shame; this is done by asking the patient to recall an instance of parental (or caregiver) love. Through this process, the patient discovers the most important desire, namely, the desire to be loved (Komoto, 2015; Nagayama, 2013). This amelioration is brought about by two elements of the Naikan philosophy: (1) human beings are fundamentally selfish and guilt-prone however, (2) at the same time, they are shown/given incommensurate benevolence from other,s. In psychoanalytical terms, this would mean that the patient simultaneously becomes aware of his guilty self and his beloved (i.e., forgiven) self and the former is overpowered by the latter. (Chervenkova, 2014). Therefore, the first question (i.e., “What have others done for you?”) is the most important one in Naikan therapy (Figure 3).

Figure 3. Guilty Self and Be Loved Self.

Shame and Guilt in Naikan Therapy As mentioned above, in Naikan therapy, correcting distorted cognitions such as “I gamble to earn more money” is important in the recovery of gambling disorder. However, this distorted cognition is useful as a defense

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against shame, which is associated with the most terrible result, namely, having the thought, “I have lost my capacity to gamble.” In Naikan therapy, this feeling of shame is called pathological guilt, which is a feeling accompanied by a sense of being victimized, which results in the global devaluation of the self. Therefore, this is the greatest obstacle in the recovery process (defensive guilt) (Nagayama K., 2003). In Naikan therapy, egocentric cognitions are corrected by examining the concrete facts of the past from the perspective of other people. In other words, the facts of gambling problems are accepted, and defensive guilt is transformed into concrete and manageable guilt (relative guilt of daily life: i.e., guilt encountered in daily life) (Nagayama K., 2003). Based on this healthy and mutual guilt, abstinence and redemptive behaviors continue. This guilt is at a moderate level in the course of the process of Naikan therapy. If necessary, the Naikan therapist can bring about a deeper level of guilt in the individual.

Deepening of Guilt in Naikan Therapy While undergoing Naikan therapy, some people encounter a stone wall during the recovery process. Initially, the patient has an illusion, namely, “If I could quit gambling, everything would be alright,” which equips the person with resilience, but which sometimes reveals an inherent flaw of the self, namely, that “Gambling is a problem that is related to the core self.” There is only a slight deference between this deadlock that is reached, and inexcusable absolute guilt that results in deep introspection and suicidal impulses (painful guilt) (Nagayama K., 2003). This time, the desire to get help and/or to engage in excessive redemptive behavior arises; however, these are not always possible. Once again, defensive guilt, namely, shame, is rekindled. In this psychological crisis, by gambling again, the problem is limited to gambling and can be temporarily avoided to confront painful shame. In such instances, Naikan therapy suggests taking a paradoxical course, namely, deepening the sense of guilt under a protective frame (program or counseling, which are described later). The recovery mechanism involves the individual becoming aware of self-harm as a result of the gambling problem and involves making him/her realize that it is impossible to make amends through redemptive behavior. In other words, once redemptive behavior is devalued, painful guilt is intensified. Then, in the midst of despair, experiences wherein the individual has been satisfied are vividly recalled. In other words, the fact that the individual has already been satisfied stands out. Consequently,

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painful guilt will turn into guilt as a feeling of remorse, which is suggestive of a calm mind without a desire for immediate gratification and redemptive behaviors (guilt as penitence) (Nagayama K., 2003; Komoto, 2015). This process must take place through forgiveness granted by a symbolic and invisible, pure being (e.g., an idealized mother, higher power, etc.), because defensive guilt, namely, conflict with shame, may resurface when a real person such as a family member or therapist grants actual forgiveness. Therefore, in Naikan therapy, therapists keep asking the patient the three key questions. In conclusion, from the perspective of Naikan therapy, the ideal recovery from gambling disorder is considered to occur through the process of undergoing four levels of guilt (dependency-defensive guilt, relative guilt of daily life, painful guilt, and guilt as penitence). However, even if the therapist ensures that the individual only experiences relative guilt of daily life, it is enough to prevent him/her from engaging in problem gambling. Therefore, the most important key question in Naikan therapy is “What have others done for you?” Similarly, in the Q&A worksheet (Figure 2), Question 8 is the most important, because the answer to this question reveals who or what satisfied the individual and when he/she was not satisfied; in other words, this provides clear insight into the individual’s original desires.

The Two Types of Naikan Therapy There are two types of Naikan therapy: the first type involves the use of a programed method and the second type involves the use of a counseling method. The difference between the two types of Naikan therapy lies in how the three key questions are used. Programed Naikan therapy, whose most common sub-type is intensive Naikan therapy, usually requires the individual to be hospitalized for a week and involves the use of all three questions, and the target of the therapy is to make the individual feel a deeper sense of guilt such as penitence. In contrast, in Naikan counseling, which is used with outpatients, the first question is primarily posed to the patient and the counseling consists of only a few sessions. This approach aims to make the individual feel relative guilt of daily life and a sense of gratitude toward others by making the individual recall experiences during which he/she was satisfied. Therefore, Naikan counseling is useful for uncovering the individual’s original desires. Thus, I have proposed a desire-targeted intervention based on Naikan counseling for disordered gamblers (DING).

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INTERVENTION STUDY - EFFICIENCY OF DING Previously, I reported an outcome in treatment-seeking disordered gamblers (n = 19) three months after implementing DING, which revealed high abstinence rates (63.2%) and controlled gambling rates (21.1%) (Komoto & Sato, 2014). Therefore, to reveal the efficiency of DING more strongly, I introduce the six month-outcome study.

MATERIALS AND METHODS Participants Subjects were outpatients treated with DING between June 2013 and December 2014 at the Outpatient Unit for Gambling Disorders of Kurihama Medical and Addiction Center in Japan. In principal, the intervention consisted of six sessions, namely an initial psychiatric assessment, followed by two individual sessions with psychiatrists (30-60 miniutes/), and three group sessions with psychologists (60 miniutes/). The themes of group session were “total amounts of money lost,” “advantages and disadvantages of gambling,” and “alternative behaviors instead of gambling.” Patients with psychiatric comorbidities were treated with appropriate pharmacological regimens. All subjects were over 20 years of age and met Diagnostic and Statistical Manual of Mental Disorders 5th Edition (DSM-5) criteria for a diagnosis of gambling disorder (American Psychiatric Association, 2013). We excluded patients with acute psychotic symptoms, including manic symptoms or cognitive impairment, which could have compromised their ability to complete the research questionnaires. This investigation was approved by the ethical committee of Kurihama Medical and Addiction Center (I.D. 223), registered at ClinicalTrials.gov’s Protocol Registration and Results System (PRS; I.D. NCT02491996), and carried out in accordance with the Declaration of Helsinki. All participants provided written informed consent.

Procedure Participants were examined and the following were assessed at the first hospital visit:

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Yasunobu Komoto 1) Basic and medical background such as gender, age, marital status, years of education (more or less than 12), employment status, addiction-related family history (defined as a second-degree or closer family member with an addictive disorder), criminal history, suicide history, and current psychiatric complications; 2) Gambling-related variables such as age of gambling onset, age of problem gambling onset, time lag between gambling onset and onset of problem gambling, duration of problem gambling, predominant gambling activity (non-strategic or strategic; non-strategic means Pachinko and slot machines), total amount of debt, method of debt management (bankruptcy or not), attendance at self-help groups, and motivation to quit gambling; 3) Assessments of severity, such as the number of items present from the DSM-5 diagnostic criteria, scores on the South Oaks Gambling Screen (SOGS) (Lesieur & Blume, 1987), and the Gambling Symptom Assessment Scale (G-SAS) scores (Kim, Grant, Potenza, Blanco, & Hollander, 2009); and 4) Outcome concerning gambling behavior 6 months after DING.

Assessment of Severity Severity of gambling disorder was measured using the above three reliable and valid instruments. 1) DSM-5: The severity is assessed by the number of items in the DSM5, which are met: 4–5 is mild, 6–7 is moderate, and 8–9 is severe. 2) SOGS: 20-item self-report questionnaire providing a cut-off score for pathological gambling using DSM criteria. The accepted cut-off point for problem gambling is 5, with higher scores denoting more severe gambling problems. 3) G-SAS: 12-item self-report scale examining gambling urges, thoughts, and behaviors during the previous week.

Assessment of Outcomes We asked participants two questions concerning gambling behaviors 6 months after the intervention by mail or telephone, which were “Did you

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gamble in the past six months?” and “If you gambled, did you have trouble as a result of it in the past six months?” We tried calling or sending mail reminders two or more times. The outcome was divided into three levels through the above two questions: (continuous abstinence/continuing to gamble, but no problems/continuing to gamble and having problems). In this study, problem gambling was defined as “gambling accompanied by monetary, occupational/educational, familial, and legal problems such as debts, absence, marital crisis, and embezzlement.”

Statistical Analysis A Pearson correlation analysis was used to assess correlations between outcomes (abstinence/controlled gambling/problem gambling) and other variables in DING. To identify independent predictors of outcome, multiple stepwise backward linear regression analysis was used and an analysis of variance for the full regression model was performed. These analyses were repeated using all participants (intention-to-treat analysis: ITT). Therefore, cases that dropped out were set as cases that continued problem gambling (worst cases analysis). Statistical significance was set at p < 0.05.

RESULTS The resulting sample treated by DING included 35 subjects; all satisfied the inclusion and exclusion criteria. Seven individuals dropped out of the DING program (20.0%). Results after six months were obtained from all participants who completed all sessions (n=28). Clinical features of DING group Table 1 summarizes descriptive statistics of the participants and the efficacy of the DING. Twenty-four participants (68.6%) had been free from problem gambling for the past six months. The average G-SAS score significantly decreased after DING (from 31.3 to 14.0, p