GSJP Volume 16 final Graduate Student Journal of Psychology 2015, Vol. 16 Copyright 2015 by the Department of Counseling and Clinical Psychology Teachers College, Columbia University 25 Expanding the Biopsychosocial Model: The Active Reinforcement Model of Addiction Annie Hunt University of Denver 7KH�FRQWHPSRUDU\�XQGHUVWDQGLQJ�RI �DGGLFWLRQ�LV�H[SDQGLQJ�UDSLGO\�DV�UHVHDUFK�DFURVV�VSHFLDO�ÀHOGV�LQIRUPV�WUHDW- ment and intervention techniques. Current prevention efforts work from the well-accepted biopsychosocial model and are aimed at identifying the underlying causes of addiction and attempting to block them from manifesting, primarily through educational methods. However, once an addiction has already emerged, intervention and treat- ment efforts should operate from a more comprehensive conceptualization of addiction that takes into account more than just underlying factors – these efforts must address how these factors are currently operating and rein- forcing one another. The active reinforcement model proposed in this paper addresses the mechanisms of action that govern the relationships among three primary elements of addiction: a) impaired neurological mechanisms; b) unmet psychological needs; and c) dysfunctional behavior. This model serves as a more comprehensive conceptu- alization of addiction as it accounts for each of the present factors and places them in an interdependent context. Thus, while the biopsychosocial model effectively addresses the underlying causes of addiction, the proposed active reinforcement model addresses the mechanisms of existing addictions in a more comprehensive manner. A better description of the relationship between each element provides a deeper understanding of the full phenomenon of addiction, and may therefore be more effective in generating successful treatment outcomes than previous models. Introduction to Addiction Medical, psychological, and social understandings of addiction have evolved rapidly over the past century, and contemporary addiction research and treatment is becoming increasingly interdisciplinary. Addiction VWXGLHV�� LQLWLDOO\�EDVHG�LQ�WKH�ÀHOG�RI �SKDUPDFRORJ\�� now incorporate psychological, neurobiological, ge- netic, environmental, social, and spiritual consider- ations. Furthermore, addiction is being studied in schools of social work, public health, medicine, and psychology. Addiction has thus become a multi-dis- ciplinary construct that necessitates a wide range of understanding from contemporary practitioners, and as this understanding expands, the professional obli- gation to maintain a consistent and regulated standard RI � SUDFWLFH� EHFRPHV� VLJQLÀFDQWO\�PRUH� FKDOOHQJLQJ��� � 6WDQGDUGL]HG� FOLQLFDO� SUDFWLFHV� LQ� WKH� ÀHOG� RI � addiction are developed, tested, and disseminated through clinical research, and the myriad factors in- ÁXHQFLQJ�WKLV�ÀHOG�SUHVHQW�DQ�LQWHUHVWLQJ�FKDOOHQJH�IRU� researchers who must take them into consideration when designing and implementing studies. These studies are the mechanism for generating empirically EDVHG�ÀQGLQJV��ZKLFK�DUH� WKH�QHFHVVDU\�SUHUHTXLVLWH� in allowing new considerations to be incorporated into standardized treatment options. In order to in- crease evidence-based treatment options in response to the expanding conceptualization of addiction, RQH�PXVW� ÀUVW� EHJLQ�ZLWK� D� FOHDU� XQGHUVWDQGLQJ� RI � WKH�FXUUHQW� VWDWH�RI � WKH�ÀHOG�� DQG� WKHQ�SURSRVH�DU- eas for further academic consideration and research. The starting point for this process is the Diagnostic and Statistical Manual of Mental Disorders (DSM), RULJLQDOO\�SXEOLVKHG�LQ�������ZKLFK�VLJQLÀFDQWO\�LQÁX- ences treatment options, research, insurance policies, public opinion, and social stigma. While the DSM DFNQRZOHGJHV� WKDW� WKH� GLDJQRVWLF� FODVVLÀFDWLRQ� SUR- cess is a challenging one, and that there are no strict boundaries dividing one disorder from the others or from no mental disorder at all, it does offer a profes- sional consensus about the categorization and iden- WLÀFDWLRQ�RI �PHQWDO�GLVRUGHUV�DW�WKH�WLPH�RI �LWV�SXE- lication (DSM-5; American Psychiatric Association, 2013). Thus, it provides a reliable tool for establish- ing standards of diagnoses, terminology, and criteria IRU�FODVVLÀFDWLRQ�ZKLOH�DW�WKH�VDPH�WLPH�HPSKDVL]LQJ� WKH� LPSRUWDQFH� RI � ÁH[LELOLW\�� DSSURSULDWH� WUDLQLQJ�� and cultural sensitivity during clinical application. Addiction terminology. Chemical and behav- ioral addictions have long been recognized as serious and prevalent psychological problems throughout history, so it is interesting that the most recent version RI � WKH�'60³WKH� )LIWK�(GLWLRQ�� SXEOLVKHG� LQ�0D\� ����³GRHV�QRW�DFWXDOO\�LQFOXGH�WKH�WHUP�́ DGGLFWLRQµ� (APA, 2013). The category used in the DSM-5 to de- Annie Hunt is doctoral student at the University of Denver. Cor- respondence concerning this article should be addressed to: an- niehunt1@gmail.com 26 scribe the phenomenon colloquially referred to as chemical or substance addiction is titled “Substance Use Disorder,” and it combines the former catego- ries of substance abuse and substance dependence (from the DSM-IV) into a single disorder that is to be measured on a scale from mild to severe (APA, 2013). Neither did the previous edition, the Fourth Edition, Text Revision, published in 2000 by the American Psy- chological Association, include the term “addiction,” as the term ‘dependence’ won out over ‘addiction’ by one vote during the last revision process (DSM- IV-TR, APA, 2000; O’Brien, Volkow, & Li, 2006). � 6SHFLÀF� DQG� DFFXUDWH� WHUPLQRORJ\� SOD\V� DQ� LP- portant role in the conceptualization of this phenom- enon. According to the National Institute on Drug Abuse (NIDA), the term “dependence” indicates a physiological need or dependency on a substance. This is evidenced by a biological adaptation to the substance in which the body requires more of it to achieve an effect (the phenomenon of tolerance) and also manifests physical indicators if use is sudden- ly stopped (the phenomenon of withdrawal; NIDA, 2012). Physical dependence, however, can occur with continued use of many different substances, includ- ing those taken as prescribed, and does not necessarily include the psychological or behavioral consequenc- es that characterize an “addiction” or “disorder.” The term “disorder,” according to the APA (2012), includes the following: 1. A behavioral or psychological syndrome or pattern that occurs in an individual ��� 7KDW�UHÁHFWV�DQ�XQGHUO\LQJ�SV\FKRELRORJLFDO� dysfunction 3. The consequences of which are clinically VLJQLÀFDQW�GLVWUHVV�RU�GLVDELOLW\ 4. Must not be merely an expectable response to common stressors and losses or a culturally sanctioned response to a particular event 5. That is not primarily a result of social devi- DQFH�RU�FRQÁLFWV�ZLWK�VRFLHW\� Thus, “disorder” indicates the presence of behavioral and psychological symptoms, but fails to clearly ar- ticulate the aspect of compulsory repetition that the terms “dependence” or “addiction” include in their GHÀQLWLRQV� Finally, the term “addiction,” according to the National Institute on Drug Abuse, indicates com- pulsive use of a substance despite harmful con- VHTXHQFHV�� VXFK� DV� IDLOXUH� WR� IXOÀOO� VRFLDO�� ZRUN�� RU� family responsibilities, and an inability to stop using the substance of one’s own accord (2013). Addition- ally, according to the APA website, addiction falls under the category of “Mental Health Disorders/ ,VVXHV�µ� DQG� LV� GHÀQHG� DV� ´D� FKURQLF� EUDLQ� GLVHDVH� that causes compulsive substance use despite harm- ful consequences” (APA, 2012). Arguably, the most FRPSUHKHQVLYH� DQG� VSHFLÀF� GHÀQLWLRQ� RI � DGGLFWLRQ� comes from the American Society of Addiction 0HGLFLQH��$6$0���������ZKR�GHÀQH�DQ�DGGLFWLRQ�DV� a primary, chronic disease of brain reward, moti- vation, memory and related circuitry . . . [which] LV�UHÁHFWHG�LQ�DQ�LQGLYLGXDO�SDWKRORJLFDOO\�SXUVX- ing reward and/or relief by substance use and other behaviors. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recogni- WLRQ� RI � VLJQLÀFDQW� SUREOHPV� ZLWK� RQH·V� EHKDY- iors and interpersonal relationships, and a dys- functional emotional response (ASAM, 2010). It is interesting to compare the terms to identify dif- ferences as well as overlaps. According to the above GHÀQLWLRQV�� GHSHQGHQFH� RQ� D� VXEVWDQFH� GRHV� QRW� necessarily constitute an addiction, and an addiction does not necessarily involve physiological depen- dence (NIDA, 2012). Furthermore, a disorder does not necessarily constitute an addiction. These terms therefore cannot be used interchangeably, as they each indicate the presence of different symptoms. It should be noted, however, that the DSM-5 does use the category of “Addictive Disorders” to describe pathological gambling as a behavioral addic- tion (APA, 2013). This is the only condition listed in this category, despite general clinical recognition of other non-chemical, behavioral addictions such as sex addiction, internet addiction, compulsive tan- ning, and compulsive shoplifting (e.g., Grant, Po- tenza, Weinstein, & Gorelick, 2010). Neither the 1,'$� GHÀQLWLRQ� RI � GLVRUGHU� QRU� WKH� $3$� GHÀQL- HUNT 27 tion of addiction include non-chemical addictions, despite the widespread social, medical, and cultural call for recognition and treatment of these partic- XODU� SUREOHPV� �*ULIÀWKV�� ������ :DQJ� HW� DO��� ������ This paper argues that one of the most critical aspects of active addiction treatment is addressing the phenomenon of being unable to stop certain substance use or behaviors solely of one’s own vo- lition – namely, the compulsive aspect of the condi- tion regardless of known negative consequences. As of the most current edition, the DSM still does not FRPSUHKHQVLYHO\�DUWLFXODWH� WKH�SUHVHQFH�DQG�VLJQLÀ- cance of this symptom. The continued exclusion of this component indicates that at this point in time, FRQWHPSRUDU\�UHVHDUFK�KDV�VWLOO�QRW�VXIÀFLHQWO\�SLQ- pointed what exactly this phenomenon is, what it involves, how it operates, and how to address it. It is this phenomenon that the proposed active rein- forcement model attempts to describe, validate, and address by drawing together parts of prior concep- tualizations and constructing a more comprehensive model. This paper argues that once an addiction is manifest, it is actively reinforced by the relationships between three essential factors: a) impaired neuro- logical mechanisms; b) unmet psychological needs; and c) dysfunctional behavior, the combination of which results in the compulsive aspect of the phe- nomenon. Understanding the relationship between these factors and how they actively reinforce addic- tion would offer a starting point for developing in- terventions aimed at disrupting these relationships. Previous conceptualizations of addiction. Addiction has previously been conceptualized using different models, with the most historically prom- inent being the “adaptive” and the “disease” mod- els. The adaptive model preceded the disease model, DQG�VXJJHVWHG�WKDW�DGGLFWLRQV�GHYHORS�ZKHQ�VSHFLÀF� psychological needs – such as acceptance, autonomy, FRPSHWHQFH�� RU� FRQÀGHQFH�²� DUH� QRW�PHW�� WKLV�ZDV� also termed “integration failure” (Alexander, 1990). The adaptive model argues that addictions develop WR�PHHW�WKHVH�VSHFLÀF�SV\FKRORJLFDO�QHHGV��DQG�WKDW� the addictive behavior provides a sense of support, reassurance, or meaning that individuals feel is miss- ing in their lives. The disease model, also sometimes called the medical model, posited that addiction is neither an issue of failed willpower nor the result of conscious repeated habitual behavior, but is rather a chronic, progressive medical illness characterized by abnormalities or defects in brain functioning (Shee- han & Owen, 1999). Silkworth (1939) was one of the pioneers of this model, originally applying it to alcohol dependence. In the primary text of the Al- coholics Anonymous program, he described alcohol- ism as an unusual or distorted behavioral response to alcohol consumption, and described problematic chronic drinking as a manifestation of a “physical allergy” to alcohol (Alcoholics Anonymous, 2001). Sheehan and Owen (1999) argue that the disease model represents a more comprehensive explanation of addiction through its depiction of neurological GHÀFLWV� DQG� DEQRUPDO� EHKDYLRUDO� UHVSRQVHV�� �7KHVH� models offered initial foundations for the develop- ment of addiction studies and treatment, and they remained prominent until the emergence of George Engel’s “biopsychosocial model” (Engel, 1978). Current conceptualization of addiction. The biopsychosocial model, which is used to describe many different mental disorders, is arguably the most prominent construct used to conceptualize addiction today (Alonso, 2004). This model built upon the dis- ease model by accepting that addiction involves ab- normalities in brain functioning, but then expanded that model by integrating the subjective psychological experiences of individuals into the conceptualization of illness. It suggests that an understanding of the patient’s subjective experience is critical in devel- oping accurate diagnoses and successful treatment options (Borrel-Carrio, Suchman, & Epstein, 2004). The biopsychosocial model thus seeks to explain suf- fering, disease, and illness as generated by multiple causes, including social, biological, and psychological factors. This inclusion of subjective psychological components into the disease model expands the con- cept of addiction to include individual experiences, perceptions, stressors, and perspectives as mediat- ing factors in the expression of clinical illnesses and medical problems. Thus, this model helps to bridge WKH�JDS�EHWZHHQ�WKH�PHGLFDO�DQG�SV\FKRORJLFDO�ÀHOGV�� DQG� LV� H[WHQVLYHO\� DFFHSWHG� LQ� WKH� ÀHOG� RI � DGGLF- ACTIVE REINFORCEMENT MODEL OF ADDICTION 28 tion studies and psychology today (Alonso, 2004). Drawing from the above-mentioned previous DQG� FRQWHPSRUDU\� GHÀQLWLRQV� RI � DGGLFWLRQ�� WKUHH� FRUH�HOHPHQWV�RI �DGGLFWLRQ�FDQ�EH�LGHQWLÀHG�²�XQPHW� psychological needs, impaired neurological mech- anisms, and problematic behaviors. However, the DGDSWLYH� DQG�GLVHDVH�PRGHOV�GR�QRW� VXIÀFLHQWO\�GH- scribe the relationships involved in the phenomenon of addiction because they suggest simple linear cau- sality between either coping and problematic behav- iors or disease and problematic behaviors. This paper argues that the previous conceptualizations of addic- tion, including the biopsychosocial model, do identify WKH�FRUH�HOHPHQWV�RI �DGGLFWLRQ��EXW�IDLO�WR�VXIÀFLHQWO\� demonstrate the reciprocal relationships among them. Emerging research reveals evidence that unmet psy- chological needs, impaired neurological mechanisms, and problematic behaviors can act as both causes and effects in the construct of addiction (Castel- lani, Wedgeworth, Wootton, & Rugle, 1997; Grant, Brewer, & Potenza, 2006; Hyman & Malenka, 2001). While the biopsychosocial model offers a more substantive argument for acknowledging the presence of combined psychological and biological/pharma- cological factors in the development of addiction, and SDUWLDOO\�LGHQWLÀHV�VRPH�RI �WKH�UHODWLRQVKLSV�LQYROYHG� among these factors, it does not offer a comprehen- sive conceptualization of all of the relationships be- tween these factors that contribute to active addiction and compulsive behaviors. It states that these differ- ent factors play a role in impacting outcomes, and that there is a relationship between biological/psycholog- ical elements and external functioning, but it makes XVH�RI �DQ�HFOHFWLF�DSSURDFK�WKDW�GRHV�QRW�VSHFLÀFDOO\� or explicitly describe how that relationship functions and impacts addiction (Ghaemi, 2009). Furthermore, it fails to establish the impact that psychological fac- tors have on neurobiological factors, the impact that neurobiological factors have on psychological fac- tors, and the reverse impact that dysfunctional be- haviors may have upon psychological and biological IXQFWLRQLQJ³DQ�LPSRUWDQW�QHZ�UHODWLRQVKLS�WKDW�KDV� been demonstrated in emerging research (Hyman & Malenka, 2001). This paper will propose a new model that includes the critical elements of addic- tion and places them in an interdependent context that offers a more comprehensive understanding of how addictions function. It will also defend each RI �WKHVH�UHODWLRQVKLSV�ZLWK�UHFHQW�UHVHDUFK�ÀQGLQJV� Proposed “Active Reinforcement Model of Addiction.” Current research consistently indicates the presence of neurological, psychological, and ex- ternal/behavioral components in the overall concep- tualization of addiction, though each element may have varying degrees of intensity and causality (i.e., one element may be more powerful or have more LQÁXHQFH� WKDQ� RWKHUV�� GHSHQGLQJ� RQ� WKH� LQGLYLGXDO�� Grant, Brewer, & Potenza, 2006). This paper argues that there is a cause-effect relationship between all three elements, meaning that each element both in- ÁXHQFHV�DQG�LV�UHLQIRUFHG�E\�WKH�RWKHU�WZR�HOHPHQWV��� In light of this knowledge, a new model, entitled the “Active Reinforcement Model of Addiction” (Fig- ure 1), is proposed. From this conceptualization, the critical principle that emerges is not the impor- WDQFH� RI � GHWHUPLQLQJ�ZKLFK� HOHPHQW� FDPH� ÀUVW�� RU� ÀQGLQJ� DQ�XQGHUO\LQJ� UHDVRQ� IRU�ZK\� WKH� DGGLFWLRQ� emerged. Rather, the focus is shifted to the impor- tance of acknowledging how all three coexist and reinforce one another in an interdependent context once an addiction has become active. From there, an altered focus for treatment and interventions can be proposed, again shifting the focus of treatment techniques from why to how addictions function. Prevention efforts generally focus on the ques- tion of why addictions develop and use education, risk protection techniques, and resilience training based on the proposed answers to this question, though there still is no consensus on exactly what FDXVHV�DGGLFWLRQ��6$0+6$����������7KH�ÀHOG�LV�IXOO� of varying hypotheses and theories that attempt to explain addiction’s underlying causes in order to cre- ate successful prevention efforts and education pro- grams aimed at stopping addiction before it starts. This paper, however, is not focused on prevention efforts, but rather proposes use of a different model to guide treatment of active addictions. Prevention efforts are distinctive from treatment efforts, ac- cording to the American Society of Addiction Med- icine, though they may both be used concurrently in certain circumstances (ASAM, 2005). Treatment, according to ASAM, is aimed at helping individ- HUNT 29 ACTIVE REINFORCEMENT MODEL OF ADDICTION 11 � Treatment, according to ASAM, is aimed at helping individuals currently suffering from an addiction. Once addiction symptoms (according to either the DSM or APA criteria) are manifest, prevention models should be substituted for a working understanding of how the addiction is actively functioning. While research on preventive measures is valuable and will continue to hold its place in the field, this paper argues that addiction treatment and intervention should be based on a more comprehensive conceptual model of how addictions are actively sustained. Figure 1: Active Reinforcement Model of Addiction. This figure illustrates the critical relationships that reinforce active addiction. As demonstrated by the figure above, the phenomenon of addiction is sustained by the presence of and relationship among three elements: a) impaired neurological mechanisms; b) � � ���������������� �� ��� � � ������������ �� ��� ���� ������� ��!����� ������ � ���� ��� � ���������� �� ���� ����� uals currently suffering from an addiction. Once addiction symptoms (according to either the DSM or APA criteria) are manifest, prevention models should be substituted for a working understanding of how the addiction is actively functioning. While research on preventive measures is valuable and ZLOO� FRQWLQXH� WR� KROG� LWV� SODFH� LQ� WKH� ÀHOG�� WKLV� SD- per argues that addiction treatment and intervention should be based on a more comprehensive concep- tual model of how addictions are actively sustained. � $V�LOOXVWUDWHG�E\�WKH�ÀJXUH�DERYH��WKH�SKHQRPH- non of addiction is sustained by the presence of and relationship among three elements: a) impaired neu- rological mechanisms; b) unmet psychological needs; and c) dysfunctional behavior. This model serves as a comprehensive conceptualization of addiction that incorporates the main elements of addiction and places them in an interdependent context. It helps to organize the concept of active addiction into a struc- WXUHG�PHFKDQLVP�GHÀQHG�E\�UHLQIRUFLQJ�UHODWLRQVKLSV�� which may allow studies and interventions to specif- ically focus on particular sections or relationships in the model. At the same time, it also offers a full de- piction of the phenomenon, which may help to re- mind practitioners that each element and relationship must be attended to in treatment. This paper will de- scribe how many existing theories and interventions ÀW�GLUHFWO\�LQWR�WKH�DFWLYH�UHLQIRUFHPHQW�PRGHO��DQG� will explain how each encompasses one or some of the six relationships described: a ȹ (causing) b, a ȹ c, b ȹ a, b ȹ c, c ȹ�b, and c ȹ�a. Any element, standing alone or impacting only one of the other elements, does not necessarily lead to the emergence of an addiction. This model theorizes that all rela- tionships must be present to some degree in order to constitute an active addiction. This paper will begin to justify this theory by examining the current work- LQJ�GHÀQLWLRQ�RI �ZKDW� WKH� WHUP�´DGGLFWLRQµ�PHDQV� 'HÀQLWLRQ�RI �$GGLFWLRQ��D��E� �F� All people engage in self-regulatory behaviors in re- sponse to their biological, psychological, social, and spiritual wants and needs (Bandura, Adams, & Bey- er, 1977). Many people use substances or engage in risky behaviors to meet these needs, and these do not always develop into disruptive or chronic patterns of use. The crossover from substance use or occasional dysfunctional behavior to the full manifestation of DGGLFWLRQ�LV�DPELJXRXV�DQG�GLIÀFXOW�WR�GHÀQH���2QH� must consider the motivations for, frequency and intensity of, and consequences of the substance use or dysfunctional behavior in order to deter- mine whether it can be considered problematic (c). As noted previously, the DSM acknowledges that there are no absolute boundaries in diagnoses, and the VDPH�ÁH[LELOLW\�PXVW�EH�XWLOL]HG�ZKHQ�DWWHPSWLQJ�WR� GHÀQH�DGGLFWLRQ��$3$����������'HVSLWH�WKH�FKDOOHQJH� the phenomenon of addiction poses, it is still critical WR�GHYHORS�D�JHQHUDOO\�DFFHSWHG�ZRUNLQJ�GHÀQLWLRQ�VR� that researchers and clinicians can work toward stan- GDUGL]LQJ�WKH�ÀHOG��GHYHORSLQJ�EHVW�SUDFWLFHV��DQG�UHJ- ulating the associated treatment options for addiction. The American Society of Addiction Medicine’s GHÀQLWLRQ� RI � DGGLFWLRQ�� SUHYLRXVO\� TXRWHG� LQ� WKLV� paper, clearly supports the concept of a biological element in the reinforcement model of addiction, suggesting that neurological dysfunction (a) directly causes problematic psychological (b) and behavioral (c) manifestations (a ȹ b, a ȹ�c). It also indicates that the behavior (c) in turn can affect psychological and emotional components (b) of the individual’s life (c ȹ�E����,Q�WKH�ORQJHU�GHÀQLWLRQ��$6$0�JRHV�RQ�WR�H[- plain that brain “morphology, connectivity, and func- tioning are still in the process of maturation during development and young adulthood, and early expo- VXUH�WR�VXEVWDQFH�XVH�LV�DQRWKHU�VLJQLÀFDQW�IDFWRU�LQ� the development of addiction” (ASAM, 2011). This suggests that dysfunctional behaviors such as chem- Figure 1: $FWLYH�5HLQIRUFHPHQW�0RGHO�RI �$GGLFWLRQ���7KLV�ÀJXUH� illustrates the critical relationships that reinforce active addiction. ACTIVE REINFORCEMENT MODEL OF ADDICTION 30 ical abuse (c) also impact brain development (a) in a phenomenon known as “neuroadaptation” (c ȹ a; $6$0����������,W�LV�ZRUWKZKLOH�WR�QRWH�WKDW�WKLV�GHÀ- nition includes both “substance use and other behav- LRUVµ�LQ�LWV�GHÀQLWLRQ��DQG�WKDW�WKH�LQFOXVLRQ�RI �ERWK� chemical and non-chemical addictions is a critical ele- ment to the reinforcement model, as will be discussed ODWHU���7KXV��$6$0·V�GHÀQLWLRQ�RI �DGGLFWLRQ�ÀWV�LQWR� the proposed model, and supports some of the rela- tionships it describes (a ȹ b, aȹ c, c ȹ a, c ȹ b). � $QRWKHU� ZLGHO\�UHFRJQL]HG� GHÀQLWLRQ� of addiction came from the former pres- ident of the American Society of Addic- tion Medicine, Dr. Michael Miller, who stated: At its core, addiction isn’t just a social problem or a moral problem or a criminal problem. It’s a brain problem whose behaviors manifest in all these other areas . . . [the] disease is about brains, not drugs. It is about underlying neurol- ogy, not outward actions. (Smith, 2011, p. 901) This statement also directly supports the reinforce- PHQW�PRGHO��DQG�GHPRQVWUDWHV�WKH�VLJQLÀFDQFH�RI �QHX- rophysiology in affecting the full conceptualization of addiction (a ȹ�b, a ȹ c). Goodman (1990) proposed D� VLPLODUO\� ZHOO�DFFHSWHG� GHÀQLWLRQ� RI � DGGLFWLRQ� $GGLFWLRQ�PD\�EH�GHÀQHG�DV�D�SURFHVV�ZKHUHE\� a behavior that can function to produce pleasure and provide relief from internal discomfort, [and] is employed as a pattern characterized by (1) re- current failure to control the behavior (powerless- ness) and (2) continuation of the behavior despite severe negative consequences (unmanageability). 7KLV� GHÀQLWLRQ� KLJKOLJKWV� WKH� EHKDYLRUDO� HOHPHQW� LQFOXGHG� LQ� WKH� UHLQIRUFHPHQW� PRGHO�� DQG� GHÀQHV� what is meant by “dysfunctional” behavior (c) and psychological causes and consequences (b). While LW� GRHV� QRW� VSHFLÀFDOO\� PHQWLRQ� QRQ�FKHPLFDO� EH- haviors, it does not explicitly exclude them, and as such they too can be incorporated into this con- FHSWXDOL]DWLRQ�� � )XUWKHUPRUH�� WKLV� GHÀQLWLRQ� DG- dresses the impact that these behaviors have on SV\FKRORJLFDO� IXQFWLRQLQJ�� DQG� VXSSRUWV� DQG� ÀWV� into the reinforcement model (b ȹ c, c ȹ b). Smith and Seymour (2004) included the additional ele- ment of “compulsive use or engagement in the behav- LRUµ�WR�WKLV�GHÀQLWLRQ��ZKLFK�VXJJHVWV�DQ�XQGHUO\LQJ� biological urge (a ȹ c). Moreover, they suggested that addictive behaviors (c) are used to gain either psychic (mood-related), recreational (social or activity-relat- ed), or instrumental achievement (performance-relat- ed) rewards (b). This also directly ties into the rein- forcement model in that it explains the relationship that dysfunctional behaviors can have on psychologi- cal functioning and the attainment of needs (c ȹ b). Application of the term “addiction” to both chemical and behavioral disorders. One critical theoretical consideration that supports the reinforce- ment model is the inclusion of non-chemical or be- havioral dependencies (c) in the broader conceptual- ization of addiction. Chemical dependencies alone are not necessarily considered dysfunctional, as many medical patients develop dependencies even when they take their medications as prescribed. These de- pendencies do not necessarily result in a compulsive or disruptive pursuit of chronic use. Dependencies become dysfunctional only once they develop causal relationships with psychological and biological pro- cesses (c ȹ b, c ȹ a). Additionally, certain behaviors, such as gambling, hand-washing, or exercising, are QRW� FRQVLGHUHG� G\VIXQFWLRQDO� RQ� WKHLU� RZQ³WKHVH� behaviors only become dysfunctional when they dis- rupt psychological and biological processes (c ȹ b, c ȹ a), resulting in a non-chemical addiction. For example, hand-washing is a normal human behavior, but if it becomes a psychological obsession and an individual feels compelled to do it repetitively, then it has developed into an addiction (c ȹ a, c ȹ b). Traditionally, the clinical terms “addiction” and “addictive behavior” have been applied exclusive- ly to substance abuse and dependency, but there is growing empirical evidence of a related category of “non-chemical” addictive behaviors, “including gam- bling, eating disorders, and sexual behavior,” that have recently been included in the conceptualization of addiction (Donovan & Marlatt, 2005, p. 4). There are easily recognizable external patterns that are sim- ilar between chemical and behavioral addictions, in- cluding tolerance, withdrawal, repeated unsuccessful DWWHPSWV�WR�VWRS��DQG�VLJQLÀFDQW�LPSDLUPHQW�LQ�DUHDV� of life functioning. However, the emerging recog- QLWLRQ� RI � ELRORJ\·V� LQÁXHQFH� RQ� DGGLFWLRQ� KDV� HQ- HUNT 31 couraged researchers to explore whether behavioral addictions and substance addictions recruit similar biological processes (a ȹ c, c ȹ a; Grant, Brewer, & Potenza, 2006). Brain science and neural imag- ing have begun to validate food and sex addictions, compulsive shopping and gambling, and eating dis- orders, among others, as “process,” “non-chemical,” or “behavioral” addictions that can be included in the new, broader category of addiction disorders. Emerging research indicates that dysfunctional behaviors can be powerful determinants of psycho- logical functioning (c ȹ b) and can also cause neuro- adaptation (c ȹ�a; Lubman, Yucel, & Pantelis, 2004; Hyman & Malenka, 2001). It has also been demon- strated that dysfunctional behavior can be the direct UHVXOW�RI �EUDLQ�GHÀFLWV�RU�PDODGDSWLYH�SV\FKRORJLFDO� states (a ȹ�c, b ȹ�F���*UDQW�HW�DO�����������7KHVH�ÀQG- ings support the incorporation of non-chemical ad- dictions into the reinforcement model, as they follow the same relationship patterns of chemical addictions. This recognition greatly enhances the argument for the reinforcement model of addiction, as it helps to il- luminate the interconnectedness of both internal and external factors involved in this phenomenon, regard- less of the involvement of substances and chemicals. � 7KH������'60�UHYLVLRQV� UHÁHFW� WKLV� LQFUHDVLQJ� awareness of the role of non-chemical dysfunctional behaviors in the construct of addictions through their inclusion of “Gambling Disorder” (APA, 2012). This movement to include a non-chemical addictive disor- der demonstrates that researchers and practitioners are migrating toward the general understanding that both chemicals as well as behaviors can impact neuro- adaptation within the brain’s reward system (c ȹ a). Smith (2012) reinforced this by stating that addiction disrupts the areas of the brain responsible for regu- lating cognitive, emotional, and social behaviors, and Marks suggested that “syndromes of behavioral ad- diction share [similar neurological] features with those of substance abuse . . . [including] obsessive-com- pulsive disorder, compulsive spending (including gambling), overeating, hypersexuality, kleptomania, and perhaps trichotillomania, tics, and the Tourette syndrome” (c ȹ a, c ȹ b; Marks, 1990, p. 1389). � $V� VXSSRUWHG� E\� WKHVH� ÀQGLQJV�� ERWK� FKHPLFDO� and behavioral dependencies can be included in the reinforcement conceptualization of addiction. The emerging understanding of the ability of external be- KDYLRUV�WR�LQÁXHQFH�EUDLQ�FKHPLVWU\��DV�ZHOO�DV�WKH�UHF- ognition that brain chemistry affects external behav- iors, demonstrates that these two factors are mutually LQÁXHQWLDO��Dȹ c, c ȹ a). Thus, including problematic and dysfunctional behaviors that do not include chem- icals greatly supports the active reinforcement model, and further illuminates the extent to which external IDFWRUV� LQÁXHQFH� LQWHUQDO� SURFHVVHV� DQG� YLFH� YHUVD� Three Core Components and Six Core Relationships The psychological and behavioral components of addiction have been well established in contemporary research, so an extensive discussion of these elements is not necessary in this paper and they will be only EULHÁ\�PHQWLRQHG�EHORZ���5HVHDUFK�RQ�WKH�QHXURELR- logical components, however, is the more recent and emerging area that will be discussed in more detail. 3V\FKRORJLFDO�&RPSRQHQWV�RI �$GGLFWLRQ��E�ȹ a, bȹF� The active reinforcement model indicates a dis- tinct relationship between psychological components (b), such as stressors, the effects of environmental LQÁXHQFHV�� WKRXJKWV�� DQG� HPRWLRQV�� XSRQ� ERWK� WKH� brain as well as behavior (b ȹ a, b ȹ c). There are numerous studies that support the causal relationship between unmet psychological needs and dysfunction- al behaviors, as well as the impact of psychological stress on brain chemistry and neurological function- ing (b ȹ c, b ȹ a) (Castellani et al., 1997; Whang, Lee, & Chang, 2003; Young, Boyd, & Hubbel, 2000; Sinha, 2001). These two relationships in the rein- forcement model of addiction are well established, and a detailed discussion of these two mechanisms can be easily found in contemporary literature and is thus beyond the scope of this paper. One particularly good explanation of these relationships can be found in Franken (2003), who explains the relationship between psychological urges and their impact upon neurological functioning and addictive behaviors. ACTIVE REINFORCEMENT MODEL OF ADDICTION 32 %HKDYLRUDO�&RPSRQHQWV�RI �$GGLFWLRQ��F�ȹ a, c ȹ�E� As previously mentioned, dysfunctional or risky behaviors alone do not comprise addiction. Dys- functional behavioral or chemical dependencies only become addictions when they develop relationships with the psychological and neurobiological elements of the active reinforcement model. This means that when a behavior or chemical use becomes a method of psychological coping to deal with stress, or when the individual feels compelled to engage in this be- havior due to pressing internal impulses, the full rela- tionship of these factors manifests as an active addic- tion (c ȹ a, c ȹ b). There are numerous studies that demonstrate the wide range of addictive behaviors, including both non-chemical and chemical depen- dencies, and a discussion of all of the behavioral ele- ments associated with addiction is beyond the scope of this paper. For a more detailed discussion of these relationships, see Smith (2012), Smith and Seymour (2004), Marks (1990), or Hyman and Malenka (2001). 1HXURELRORJLFDO�&RPSRQHQWV�RI �$GGLFWLRQ��D� ȹ b, a ȹ�F� � :KLOH�WKH�FXUUHQW�GHÀQLWLRQV�RI �DGGLFWLRQ�H[SODLQ� VRPH�RI �WKH�QHXURORJLFDO�DQG�SV\FKRORJLFDO�LQÁXHQF- es on behavior (aȹ c, bȹ c), it is critical to also incor- porate recent research that indicates that behaviors LQÁXHQFH�QHXURORJLFDO�DQG�SV\FKRORJLFDO�IXQFWLRQLQJ� (c ȹ a, c ȹ b). This research indicates that behav- iors can contribute to neuroadaptation and psycho- logical problems (Lubman, Yucel & Pantelis, 2004). An individual may not necessarily have an underlying QHXURORJLFDO�GHÀFLW�WR�EHJLQ�ZLWK��EXW�FRXOG�GHYHORS� one as a result of engaging in dysfunctional behavior or encountering psychological stressors (Lubman et al. 2004). Thus, neurobiology is not necessarily the primary causative factor of this phenomenon. The active reinforcement model effectively demonstrates ERWK�WKH�VLJQLÀFDQFH�DV�ZHOO�DV�WKH�UHODWLRQVKLS�RI �QHX- robiology to the overall conceptualization of addic- tion, instead of placing it as the primary causal factor. The active reinforcement model indicates that QHXURELRORJ\� ERWK� LQÁXHQFHV� DQG�PHGLDWHV� WKH� UH- lationship between dysfunctional behaviors and psy- chological issues, and in combination with these fac- tors it can generate chemical or behavioral addictions. Neuroimaging and neuropsychological studies have revealed clear differences in brain function between chronically addicted and non-addicted individuals, suggesting that addiction is indeed associated with al- terations in brain functioning and neuropsychological changes (Lubman, Yucel, & Patelis, 2004; a ȹ c, c ȹ a). The research they describe has been primari- ly focused on the brain’s reward pathways, which in- volve dopamine and serotonin receptors. Dopamine and serotonin are neurotransmitters released by the brain as a result of certain actions and behaviors, and they are associated with the experience of pleasure and reinforcement and can function as ‘rewards’ in the brain. Hyman and Malenka (2001) report that the chemicals released as a direct result of engage- ment in addictive behaviors are both rewarding, or interpreted as intrinsically positive by the brain, as well as reinforcing, meaning that the behaviors in- volved with these rewards tend to be repeated (c ȹ a, a ȹ c). Thus, substances and behaviors that produce these neurotransmitters can become very SRZHUIXO� UHLQIRUFHUV� WKDW� LQÁXHQFH� IXWXUH� EHKDYLRU� and can result in inhibitory dysregulation (Hyman & Malenka, 2001). This means that individuals either develop lowered inhibitions against risky behavior or experience urges so strong that they overwhelm typical inhibitions (c ȹ a; Lubman et al., 2004). Tolerance. Neurochemical changes in response to addiction often manifest in the development of tol- HUDQFH��GHÀQHG�DV�D�GHFUHDVH�LQ�WKH�HIIHFW�RI �DQ�DG- dictive substance that often results in more frequent or intense engagement in addictive behavior (a ȹ c). Individuals who develop these altered brain states PD\�GHPRQVWUDWH�WROHUDQFH�DV�́ UHZDUG�GHÀFLHQF\�V\Q- drome, a hypothesized hypo-dopaminergenic state involving multiple genes and environmental stimuli that puts an individual at high risk for multiple addic- tive, impulsive, and compulsive behaviors” (a ȹ c; Grant et al., 2006, p. 925). This hypo-dopaminergen- ic state is one of the proposed mechanisms of brain chemistry in addiction. Lower levels of dopamine (or decreased activation of dopamine circuits and receptors) may result in an individual’s increased at- HUNT 33 WHPSWV�WR�FRPSHQVDWH�IRU�WKHVH�GHÀFLWV�WKURXJK�SDU- ticular chemicals or behaviors (a ȹ c). Higher lev- els of tolerance can promote increased and frequent use, which may then result in dependence (c ȹ a). Sensitization. Another result of chronic addiction is sensitization. This occurs through enhanced reward responses in the brain resulting from repeated ad- ministration of a substance or engagement in an ad- dictive behavior (c ȹ�a; Hyman & Malenka, 2001). Individuals who develop more sensitive brain states may experience a higher level of euphoria after en- gaging in behaviors that release dopamine or sero- tonin. Due to the experience of more substantial ´UHZDUGV�µ� WKH\�PD\� KDYH� JUHDWHU� GLIÀFXOW\� LQ� FRQ- trolling impulses to engage in and continue addictive behavior (c ȹ a, a ȹ c). With chronic use of or engagement in these behaviors, adaptations at genet- ic, molecular, and cellular levels occur within distinct brain regions that counter acute drug effects in an attempt to maintain internal homeostasis (c ȹ a). When intake of the substance ceases, these neuroad- aptations initially persist and act unopposed, result- ing in a characteristic rebound syndrome, or “with- drawal” (Lubman et al., 2004). Hyman and Malenka (2001) note that this response can develop beyond just a physical or psychological liking of one’s addic- tive behavior into the experience of intense urges or “wanting.” It is at that point that physical depen- dence can cross over to compulsive desire and pur- suit as neurological systems become hypersensitive, ZKLFK�VLJQLÀFDQWO\�LQFUHDVHV�WKH�LQFHQWLYH�WR�VHHN�RXW� these stimuli (a ȹ c, c ȹ a; Hyman & Malenka, 2001). Disrupting the Relationships between the Ac- tive Elements of Addiction As discussed, the active reinforcement model of addiction demonstrates six relationships between WKUHH�SULPDU\�HOHPHQWV�RI �DGGLFWLRQ��ELRORJLFDO�GHÀ- cits (a), unmet psychological needs (b), and dysfunc- tional behaviors (c); these relationships are described as a ȹ b, a ȹ c, b ȹ a, b ȹ c, c ȹ a, and c ȹ b. Any of these elements in isolation do not nec- essarily indicate an addiction, and as such cannot be considered primary causal factors of this phenome- non. For example, an individual can engage in dys- functional or risky behavior without it affecting their psychological or biological functioning. Similarly, one may experience stress from unmet psychological needs but never turn to dysfunctional behavior as a coping mechanism, or may suffer from neurological GHÀFLWV�ZLWKRXW� WKH�DGGLWLRQDO�H[SHULHQFH�RI �XQPHW� psychological needs or attempting to compensate for WKHVH�GHÀFLWV�EHKDYLRUDOO\���5DWKHU��LW�LV�WKH�UHODWLRQ- ships among these factors – not the factors them- selves – that indicate an active addiction. Therefore, this model suggests that addiction treatment research should be devoted to disrupting these mechanisms and developing interventions to block the relation- ships between the factors that combine to sustain ad- diction (indicated by the sign X). A comprehensive treatment plan must therefore involve interventions to disrupt these relationships (a X b, a X c, b X a, b X c, c X a, c X b). Addressing and resolving one element can reduce the severity of the addictive behavior, but this paper argues that attention to all three factors and their respective relationships with one another is vi- tal to successful, comprehensive addiction treatment. 7UHDWPHQW�RI �%LRORJLFDO�)DFWRUV��D�;�E��D�;�F� Emergency care.�7KH�YHU\�ÀUVW� VWHS� LQ�DGGLF- tion treatment is to focus on the most urgent needs of the client (Wallace, 2005). This typically involves meeting essential physiological requirements and en- suring that basic physical functioning is supported and maintained, as many clients cannot take action LQ�DGGUHVVLQJ�SUREOHP�EHKDYLRUV�LI �WKH\�DUH�QRW�ÀUVW� stabilized (Wallace, 2005). Regardless of whether cli- ents enter addiction treatment voluntarily or not, they can initially present in a state of shock, trauma, se- vere emotional disturbance, despair, depression, and other varying states of instability, and at that stage they may not be capable of identifying or attend- ing to their basic needs. Thus, prior to any psycho- logical interventions, the client must be placed in a safe, calm environment without easy access to their addictive drug or behavior, and they must be thor- oughly screened for any pressing physiological prob- lems that can be immediately addressed (a X b, a X c). This includes any kind of treatment of overdose symptoms, medicine for management of withdrawal V\PSWRPV� GXULQJ� GHWR[LÀFDWLRQ�� DGPLQLVWUDWLRQ� RI � essential nutrients or electrolytes for severe cases of ACTIVE REINFORCEMENT MODEL OF ADDICTION 34 eating disorders, and other related medical treatment. Pharmacological treatment. The use of pre- VFULSWLRQ�GUXJV� WR� WUHDW� QHXURELRORJLFDO� GHÀFLWV� LV� D� critical component of addiction treatment. This has become the subject of extensive research as the conceptualization of addiction as a brain disease be- comes more prevalent. While a full discussion of the pharmacological component of addiction treatment is beyond the scope of this paper, it is worth noting that the emerging trends of successful prescription drug use in the treatment of addiction often involve drugs associated with supporting or enhancing the serotonin or dopamine pathways of the brain (Grant HW� DO��� ������� �$OOHYLDWLQJ� WKHVH� QHXURORJLFDO� GHÀFLWV� can directly promote psychological health and re- duce engagement in dysfunctional behaviors as cop- ing mechanisms (a X b, a X c; Grant et al., 2006). 7UHDWPHQW�RI �3V\FKRORJLFDO�)DFWRUV��E�;�D��E�;� F� Interdisciplinary approaches to addiction studies have allowed for more comprehensive incorporation of the psychological aspects of addiction. There have been several widely recognized movements WKDW� KDYH� GHÀQHG� DQG� LQÁXHQFHG� WKH� ÀHOG� DV� LW� UH- lates to addiction treatment, and while there are many different orientations to psychological counseling, one of the primary approaches – cognitive behav- ioral therapy – will be discussed here as an exam- ple of a psychological treatment that can be directly incorporated into the active reinforcement model. The cognitive-behavioral orientation is one of the main approaches used in addiction treatment to- day, and it purports that that human thoughts and behavior are driven by the conditioning and rein- forcement that people experience throughout their lives (b ȹ c). Dysfunctional thoughts and behav- ior, such as behavioral and chemical addictions, are considered to be the result of the development of inaccurate and unhealthy life schemas, which are the mental framework used to organize informa- tion about the self and the external world (b ȹ c) (Alford & Beck, 1997). The goals of cognitive-be- havioral therapy are therefore to focus on individual problematic behaviors and thoughts, identify their or- LJLQV�DQG�LQÁXHQFHV��DQG�FKDOOHQJH�DQG�FKDQJH�WKHP� as needed to promote healthier psychological func- tioning and recovery (b X c). Cognitive-behavioral therapy, or CBT, developed out of this psychological orientation and is prominent in addiction treatment programs today. It is a highly standardized therapeu- tic process that utilizes such techniques as identify- ing individual goals, focusing on present problems, exposure therapy, cognitive restructuring, behavior change, and psychoeducation (b X c). Thus, while there are many approaches to the treatment of the psychological factors of addiction, CBT is one exam- ple of a well-established practice that is compatible with and supports the active reinforcement model. 7UHDWPHQW�RI �%HKDYLRUDO�)DFWRUV��F�;�D��F�;�E� � $� ÀQDO� FULWLFDO� FRPSRQHQW� RI � WKH� DFWLYH� UHLQ- forcement model is the existence and relationship of dysfunctional behaviors and their impact on both psychological functioning and neurology. The most prominent treatment approach is the promotion and facilitation of abstinence or sobriety from dysfunc- tional behaviors or chemical dependencies as a way WR�GLVUXSW� WKH�ÀQDO� UHODWLRQVKLSV� LQ� WKLV�PRGHO� �F�;� a, c X b). Other approaches, such as the harm-re- duction model, emphasize the importance of mod- eration, self-regulation, honest and open self-report- ing of engagement in problematic behaviors, and RWKHU� PHDVXUHV� WR� VLJQLÀFDQWO\� UHGXFH� HQJDJHPHQW� in disordered behavior (Marlatt & Tapert, 1993). One critical aspect of intervention efforts aimed at treatment of behavioral factors is the consideration of replacement behaviors that may be utilized in the absence of the typical addictive behavior, and the importance of providing the client with adaptive rather than harmful substitutes for these behaviors (Shaffer et al., 2004). Treatment of behavioral fac- tors also involves a combination of the techniques used to treat the neurological and psychological as- pects of addiction, and each of the interventions described above also work to disrupt the relation- ships between dysfunctional behaviors and psycho- logical or neurological mechanisms (c X a, c X b). Conclusion The working conceptualization of addiction HUNT 35 continues to develop as emerging research across PXOWLGLVFLSOLQDU\� ÀHOGV� LQIRUPV� WUHDWPHQW� DQG� LQ- tervention techniques. While prevention efforts are often aimed at identifying the underlying causes of addiction, intervention and treatment should oper- ate from a more comprehensive conceptualization of addiction that is focused on the mechanisms of action among three primary elements: a) impaired neurological mechanisms; b) unmet psychological needs; and c) dysfunctional behavior. This paper ar- gues that all three must be present and involved in an active relationship with one another for an active addiction to be manifest. Thus, the proposed active reinforcement model serves as a more comprehen- sive conceptualization of addiction that accounts for and incorporates all of the elements of addiction and places them in an interdependent context that may be more effective in generating successful ad- diction treatment outcomes than previous models. The next steps in validating the proposed model are to evaluate it using research studies and psycho- metric evaluations. One of the most critical aspects of this model is its comprehensive incorporation of multiple concepts of addiction, and demonstrating its effectiveness empirically could start with an evalu- ation of each of these elements and the six relation- ships described by the active reinforcement model. Demonstrating the validity of these individual rela- tionships empirically and introducing intervention efforts intended to disrupt them would support the relevance of this model and demonstrate the need for continued exploration of this conceptualization of addiction. Once the individual relationships have been empirically validated, a treatment approach that addresses all components should be implemented, evaluated, and compared to models that operate from a less comprehensive conceptualization of addiction. In conclusion, the active reinforcement model serves as a more comprehensive conceptualization of addiction as it accounts for multiple interrelated factors. While the currently accepted biopsychoso- cial model effectively addresses the underlying caus- es of addiction, the proposed active reinforcement model addresses the mechanisms of existing addic- tions in a more comprehensive manner. A better de- scription of the relationship between each element provides a deeper understanding of the full phenom- enon of addiction, and may therefore be more ef- fective in generating successful treatment outcomes. References Alcoholics Anonymous. (2001). Alcoholics anony- mous (4th ed.). New York: A.A. World Services. Alexander, B. K. (1990). The empirical and theoret- ical bases for an adaptive model of addiction. Journal of Drug Issues, 20, 37-65. Alford, B. A., & Beck, A. T. (1997). The relation of psychotherapy integration to the established sys- tems of psychotherapy. Journal of Psychother- apy Integration, 7, 275-289. doi:10.1023/B:JO- PI.0000010884.36432.0b. Alonso, Yolanda. (2004). The biopsychosocial mod- el in medical research: the evolution of the health concept over the last two decades. Pa- tient Education and Counseling, 53(2), 239-244. doi:10.1016/S0738-3991(03)00146-0. American Psychiatric Association. (2000). Introduc- tion. In Diagnostic and statistical manual of mental disorders (4th ed., text rev.). doi:10.1176/ appi.books.9780890423349.7443. American Psychiatric Association. (2012). Substance use and addictive disorders. In DSM-5 Devel- opment. Retrieved from http://www.dsm5.org/ proposedrevision/Pages/SubstanceUseandAd- dictiveDisorders.aspx American Psychiatric Association. (2013). Sub- stance-related and addictive disorders. In DSM- 5 Development. Retrieved from http://www. dsm5.org/Documents/Substance%20Use%20 Disorder%20Fact%20Sheet.pdf American Society of Addiction Medicine. (2011). 3XEOLF� SROLF\� VWDWHPHQW�� GHÀQLWLRQ� RI � DGGLF- tion. Retrieved from http://www.asam.org/re- VHDUFK�WUHDWPHQW�GHÀQLWLRQ�RI�DGGLFWLRQ� Bandura, A., Adams, N. E., & Beyer, J. (1977). Cog- nitive processes mediating behavioral change. Journal of Personality and Social Psychology, 35, 125-139. Borrell-Carrio, F., Suchman, A. L, & Epstein, R. M. (2004). The biopsychosocial model 25 years lat- ACTIVE REINFORCEMENT MODEL OF ADDICTION 36 HU��3ULQFLSOHV��SUDFWLFH��DQG�VFLHQWLÀF�LQTXLU\���$Q- nals of Family Medicine, 2(6), 576-582. Brauser, D. (2001, Aug 31). Addiction a brain disease, ASAM says. Medscape. Retrieved from http:// www.medscape.com/viewarticle/748867. Buhler, C. (1971). Basic theoretical concepts of hu- manistic psychology. American Psychologist, 26(4), 378-386. doi:10.1037/h0032049. Castellani, B., Wedgeworth, R., Wootton, E., & Rugle, L. (1997). A bi-directional theory of addiction: Examining coping and the factors related to sub- stance relapse. Addictive Behaviors, 22, 139-144. Donovan, D. M., & Marlett, G. A. (Eds.) (2005). As- sessment of Addictive Behaviors (2nd ed.). New York: Guilford Press. Engel, G. (1978). The biopsychosocial model and the education of health professionals. Annals of New York Academy of Sciences, 310, 169-181. doi:10.1111/j.1749-6632.1978.tb22070. Frager, R. (1979, Fall). What is transpersonal psy- FKRORJ\"� � $VVRFLDWLRQ� IRU� 7UDQVSHUVRQDO� 3V\- chology Newsletter, 6. Franken, I. H. A. (2003). Drug craving and addiction: integrating psychological and neuropsychophar- macological approaches. Progress in Neuro-Psy- chopharmacology and Biological Psychiatry, 27(4), 563-579. Ghaemi, S. (2009). The rise and fall of the biopsy- chosocial model. The British Journal of Psychia- try, 195, 3-4. doi:10.1192/bjp.bp.109.063859. *RRGPDQ��$�� ��������$GGLFWLRQ��GHÀQLWLRQ�DQG� LP- plications. British Journal of Addiction, 85, 1403-1408. Grant, J. E., Brewer, J. A., & Potenza, M. N. (2006). The neurobiology of substance and behavioral addictions. CNS Spectrums, 11, 924-930. Grant, J. E., Potenza, M.N., Weinstein, A., & Gore- lick, D. A. (2010). Introduction to behavioral ad- dictions. American Journal of Drug and Alcohol Abuse, 36, 233-241. *ULIÀWKV��0�����������,QWHUQHW�DGGLFWLRQ�²�WLPH�WR�EH� WDNHQ�VHULRXVO\"��$GGLFWLRQ�5HVHDUFK�DQG�7KHRU\�� 8, 413-418. Hall, A. (2001). Internet addiction: college student case study using best practices in cognitive be- havior therapy. Journal of Mental Health Coun- seling, 23, 312. Hastings, A. (1999). Transpersonal psychology: The fourth force. In D. Moss (Ed.), Humanistic and transpersonal psychology: A historical and bi- ographical sourcebook (pp. 192-208). Westport, CT, US: Greenwood Press/Greenwood Publish- ing Group. Hyman, S. E., & Malenka, R. C. (2001). Addiction and the brain: The neurobiology of compulsion and its persistence. Nature Reviews Neurosci- ence, 2, 695-703. Keutzer, C. S. (1984). Transpersonal psychotherapy: 5HÁHFWLRQV�RQ�WKH�JHQUH��3URIHVVLRQDO�3V\FKROR- gy: Research and Practice, 15, 868-883. Lubman, D. I., Yucel, M., & Pantelis, C. (2004). Ad- GLFWLRQ�� D� FRQGLWLRQ� RI � FRPSXOVLYH� EHKDYLRU"� Neuroimaging and neuropsychological evidence of inhibitory dysregulation. Addiction, 99, 1491- 1502. Marlatt, G. A., & Tapert, S. F. (1993) Harm reduc- tion: Reducing the risks of addictive behaviors. Addictive Behaviors across the Lifespan: Pre- vention, Treatment, and Policy Issues. Newbury Park, CA: Sage. Marks, I. (1990). Behavioural (non-chemical) addic- tions. British Journal of Addictions, 85, 1389– 1394. Maslow, A. H. (1968). Toward a Psychology of Being. New York: Van Nostrand. May, R. (1983). The discovery of being. New York: W.W. Norton.National Institute on Drug Abuse. (2012). Principles of Drug Addiction Treatment: A Research-Based Guide (Third Edition). NIH Publication Number: 12-4180. Retrieved from: KWWS���ZZZ�GUXJDEXVH�JRY�VLWHV�GHIDXOW�ÀOHV� podat_1.pdf O’Brien, C. P., Volkow, N., & Li, T. K. (2006). What’s LQ� D� ZRUG"� $GGLFWLRQ� YHUVXV� GHSHQGHQFH� LQ� DSM-V. American Journal of Psychiatry, 163, 764-765. Shaffer, H. J., LaPlante, D. A., LaBrie, R. A., Kidman, R. C., Donato A. N., & Stanton, M. V. (2004). Toward a syndrome model of addiction: multiple expressions, common etiology. Harvard Review of Psychiatry, 12, 367–374. Sheehan, T., & Owen, P. (1999). The disease model. HUNT 37 In B. S. McCrady & E. E. Epstein (Eds.), Ad- dictions: A comprehensive guidebook (pp. 268– 286). New York: Oxford University Press. Sinha, R. (2001). How does stress increase risk of GUXJ� DEXVH� DQG� UHODSVH"� 3V\FKRSKDUPDFROR- gy,158, 343–359. Slife, B. D., & Barnard, S. (1988). Existential and cognitive psychology: Contrasting views of con- sciousness. Journal of Humanistic Psychology, 28, 119-136. doi:10.1177/0022167888283008. Smith, D. E., & Seymour, R. B. (2004). The nature of addiction. In R. H. Coombs (Ed.), Handbook of addictive disorders: A practical guide to diagnosis and treatment (pp. 3–30). New Jersey: John Wiley & Sons, Inc. Smith, D. E. (2011). The evolution of addiction medicine as a medical specialty. American Med- ical Association Journal of Ethics, 13, 900-905. Smith, D. E. (2012). Editor’s note: The process addic- WLRQV�DQG�WKH�QHZ�$6$0�GHÀQLWLRQ�RI �DGGLFWLRQ��� Journal of Psychoactive Drugs, 44, 1-4. Substance Abuse and Mental Health Services As- sociation. (2011). Leading change: A plan for SAMHSA’s roles and actions, strategic initiative #1: Prevention of substance abuse and mental illness. SAMHSA Pub ID: SMA11-4666. Ac- cessed from: http://store.samhsa.gov/shin/con- tent/SMA11-4629/03-Prevention.pdf Wallace, B. C. (2005). Making mandated addiction treatment work. Lanham, MD: Rowman & Lit- WOHÀHOG�3XEOLVKHUV��,QF� Wang, L., Luo, J., Bai, Y., Kong, J., Luo, J., Gao, W., & Sun, X. (2013). Internet addiction of adolescents in China: Prevalence, predictors, and association with well-being. Addiction Research and Theory, 21, 62-69. Whang, L., Lee, S., & Chang, G. (2003). Internet RYHU�XVHUV·� SV\FKRORJLFDO� SURÀOHV�� $� EHKDYLRU� sampling analysis on internet addiction. Cy- berpsychology and Behavior, 6, 143-150. Yalom, I. D. (1980). Existential psychotherapy. New York: Basic Books. Young, A. M., Boyd, C., & Hubbell, A. (2000). Pros- titution, drug use, and coping with psychological distress. Journal of Drug Issues, 3, 789–800. ACTIVE REINFORCEMENT MODEL OF ADDICTION