Theoretical Concepts Used to Explain Addictive Behavior - Research Paper Example

Critical Analysis of Two Theories on the Origins of Addictive Behaviour: Orford’s Excessive Appetite Theory and the Disease Concept of Addiction INTRODUCTION The challenge of conceptualizing addiction has been a focus of research and discussion for decades (Griffiths, 2005). Among the behaviours common to addiction that have been described are salience, mood modification, tolerance, withdrawal, conflict and relapse (Griffiths, 2005). This diversity of behaviours associated with addiction has led to a new conceptual understanding of what constitutes addictive behaviour (Alexander, 2000). One such definition comes from the work of Marlatt (1985) who described addiction as “…a repetitive habit pattern that increases the risk of disease and/or associated personal or social problems” (P12). A key component to this concept of addiction involves the loss of control of one’s impulses or desires to modify or abstain from the addictive behaviour. The need for immediate gratification removes from consideration the longer term costs of the behaviour. Historically, definitions of addiction have focused on the concept of substance ingestion (Burglass & Schaffer, 1984; Heather, 1998). More recently, there is increasing consensus among researchers that addiction encompasses a far broader spectrum of behaviours with a compulsive manifestation that may be potentially addictive (Orford 2001a & b; Miller 1980). Developments in the conceptualisation of addiction have led to broader, more encompassing theories which are multi-disciplinary in nature incorporating psychological, biological and social explanations of addictive behaviours (West, 2006). Two prominent theories that attempt to explain the origins of addictive behaviour are reviewed in this paper: Orford’s Excessive Appetite Theory and the Disease Model based on the American Medical Association (AMA) assessment (Coombs, 2004). The underlying principles of each of these general theories of addiction will be presented in detail, along with empirical evidence that is relevant to each viewpoint. The theories chosen for analysis in this paper are differing in nature. A contemporary eclectic theory- Orford’s excessive appetite theory will be compared with the disease concept of addiction which is accepted by the American Medical Association in terms of how they explain the course of addictive behaviour (West, 2006). The theories will be discussed as to how they attempt to explain important characteristics and documented stages of addictive behaviour. These areas include the initiation to addiction, the maintenance of addictive behaviour and the processes involved in changing the course of addiction. This review will be followed by a critique of the strengths and limitations of each of these theories of addiction. The relevant theoretical issues that relate to the origins of addictive behaviour as well as the clinical and practical applications important to the treatment of addiction will be included as part of a critical analysis of each of these theoretical concepts. These two theories on the origins of addiction represent a small fraction of the total number of theories and models that have been developed by researchers to explain and ameliorate patterns of addictive behaviour. A review by West (2006) identified ninety-eight theories proposed to explain addictive behaviour. There are a number of important challenges that any relevant theory of addictive behaviour must address, including an explanation of the major identified stages of addiction as well as well as the behavioural parameters associated with the risk of developing addictions. Furthermore, a useful theory must have practical value in defining the applications for treatment and prevention based on its core concepts (West, 2006). It is the intention of this essay to explore these areas in the context of two important theories that seek to explain the origins of addictive behaviour and the implications of these theories to the treatment and prevention of addiction. A major focus of the essay will involve a discussion of how each of these theories fulfills the requirements of addressing these important components of addictive behaviour. Orford’s Excessive Appetite Theory Orford’s (2001a) definition of addiction encompasses a broader scope of addiction beyond the ingestion of addictive substances to propose that addiction is an attachment to an appetite activity that is so powerful that the individual cannot control the activity despite the harm associated with it. Orford’s theory encompasses “excessive appetites” that extend beyond the range of substances to include gambling and other non-substance addictions (Orford, 1985, 2001a). Orford’s theory is part of a synthetic theory of addictive behaviour whose conceptual premise involves a compulsive desire, inclination or “appetite” that is beyond the control of the individual such that it can be characterized as “excessive”. In this context, the constant craving for the desired object or activity constitutes an “excessive appetite” that becomes the basis for the observed addictive behaviour. The theory originated from Orford’s observations that seemingly diverse activities that are frequently associated with addictive behaviours such as drinking, gambling, drug use and even eating represented potential objects of addictive behaviours and processes that have a common behavioural origin. Orford’s theory places a strong emphasis on psychological foundations of addictive behaviours, including concepts of cognition and classical and operant conditioning (Orford, 1985). It stresses the concept that the uncontrolled behaviours associated with addiction involve acquired emotional regulation cycles and may reflect the consequences of unresolved conflict. Orford proposes a synthetic theory that incorporates psychological cognitive social and moral elements that may impact individual behaviour in ways that contribute to the development of “excessive appetites” but does not support a judgmental view of these behaviours. The theory rejects the notion that excessive appetite behaviours are linked to abnormal brain chemistry that constitutes a state of physiological disease. While he acknowledges that addictive behaviour and withdrawal from certain addictions may be associated with changes in neurotransmitter activity, Orford’s theory does not accept abnormal brain chemistry as an acceptable explanation for the complex origins of addictive behaviour (Orford, 1985, 2001a). In addition to the commonly recognized additions to alcohol and drugs, Orford’s definition of addictive behaviour encompasses eating disorders and sexually addictive behaviours. Excessive eating or “binge eating” as it is commonly termed, or “bulimarexia” ” (Coombs, 2004) may be classified as an addictive behaviour based on Orford’s theory. This type of eating disorder is characterized by an out-of-control craving for large amounts of food that are consumed over very short time frames. This behaviour is commonly followed by feelings of extreme guilt, shame and self-condemnation that may result in purging or the induced vomiting of the rapidly ingested food to mitigate its consequences. Other behaviours associated with binge eating include hoarding and hiding food, stealing food or the money to buy food and lying about food consumption or purging activities (Coombs, 2004; West, 2006). Likewise, excessive sexual behaviour may be defined as an addition based on Orford’s criteria. This excessive sexual hunger or craving has been termed “hetrosexualactivity by Goodman (1998). This form of addictive behaviour may be associated withan uncontrollable appetite for sex with multiple partners, minors and may include sex with the same gender or rape. This type of addictive behaviour may also be associated with addictions to drugs and/or alcohol. Based on Orford’s theory, the criteria for determination of addiction requires assessment of a given activity on a frequency scale, such that the craving or desire for a substance or activity is so great and the lack of personal control so high that the frequency of the behaviour is very high as compared to normal standards of behaviour. Moreover, cessation of the addictive behaviour is associated with significant mood changes that may be associated with depression or even violence. In addition the definition criteria for addictive behaviour require that the activity in excess is associated with significant physical, emotional, social and/or financial destruction, such that the behaviour has negative consequences. Thus, Orford’s theory defines the behaviour associated with addiction based not only on the frequency and loss-of-control issues that are commonly used to define addictive behaviours, but also the nature and the extent of the effects of the behaviour or the deprivation of the desired behaviour or activity on the individual and his/her surroundings. Orford’s theory provides explanations for each of the documented stages of addiction: from initiation to maintenance and even recovery that may be defined by a comprehensive psycho-social, cognitive and environmental synthetic model. Each of these stages of addiction is defined by appetite-based metaphors that define the components of addiction. These components of appetite include coping mechanisms, images and expectancies that develop in the earliest stages of addictive behaviour. The primary events are later supplemented by secondary effects associated with acquired emotional responses to the behaviour or its absence and the engagement of increasing levels of conflict in dealing with the effects of the addictive behaviour. Attempts at conflict resolution as an attempt to maintain the addictive behaviour frequently complicate the difficulties associated with addictive behaviours. This coping behaviour may involve secrecy, rationalisations, guilt, blame and the development of elaborate defense mechanisms. The resolution stage, at which the addictive behaviour may cease or decline, may be attributed to the resolution of these conflicts in ways that contribute to the abandonment of the addictive behaviour. Disease Model of Addiction The disease model of addiction was first articulated to describe the behaviour of alcoholics (Cappell & Herman,1972; Prochaska & DiClemente, 1982). The medical definition of disease is an abnormal medical condition that results in pain, bodily dysfunction or distress. The late 18th century Scottish physician Thomas Trotter was reportedly the first to define alcoholism as a disease (Abrams & Niaura, 1987). Jellinek’s book on the disease model to explain excessive alcohol consumption, published in 1960, rapidly became a model for understanding excessive behaviour and was subsequently endorsed by the American Medical Association (AMA) as a primary cause of alcoholism (Jellinek, 1960). The AMA set forth its major policy statement on alcoholism and drug addiction in 1987, describing both as medical conditions or diseases worthy of medical treatment. The American Psychiatric Association also defines alcoholism as a disease (Coombs, 2004). The World Health organization (WHO) has also embraced the concept that alcoholism and drug dependence are medical diseases requiring treatment (Coombs, 2004). This work cited the results of numerous research studies indicating that alcohol and drug use may lead to changes in brain chemistry that may engender further use and dependence on these substances (Coombs, 2004). Moreover, the document cited research evidence that addictive behaviour is the result of abnormal brain chemistry. The disease model proposes that addictions are the consequence of abnormal biological functions that may be impacted by the environment. Current thinking suggests that abnormal brain function represents the underlying patho-physiology responsible for many forms of addictive behaviour (West, 2006). Specifically, changes in the brain’s mesolimbic pathway have been implicated in addictive behaviour. The disease model does not rule out sociological, psychological or other factors that may contribute to the nature and extent of addictive behaviour; rather, the premise holds that the basic process is driven by an abnormal brain physiology. In this context, addiction is viewed as a primary disease that originates from abnormal neural function; it does not occur as a secondary response to other external or environmental factors (Coombs, 2004). Genetic studies have provided some supportive evidence that there may be a biochemical basis to at least some forms of addictive behaviour. Statistical data suggest that the children of alcoholics have a 3-5 fold increased risk of becoming alcoholics (Cappell & Greeley, 1987). In addition, identical twin studies have indicated that twins who are separated by birth display a concordant pattern of addicitive behaviour, especially as it relates to alcoholism. These studies indicate that there may be a genetic predisposition for some cases of alcoholism. Individuals who have a family history of alcoholism are considered to be at risk for addiction to alcohol, based on statistical assessments. Nevertheless, there are many alcoholics that lack a positive family history of alcoholism. Current statistics suggest that alcoholism may be associated with genetic factors comprising a 50% risk for developing this form of addiction (Coombs, 2004). McLellan et al (2001) conducted a retrospective study comparing the diagnostic criteria for drug dependence with type 2 diabetes, hypertension and asthma with respect to diagnosis, heritability, patho-physiology, genetic and environmental factors, and treatment responses. The results of this study suggested that similar parameters of genetically inherited risk factors, environmental factors and personal choice factors were similar for all the conditions evaluated. These results suggested that drug dependence displays many features in common with other chronic medical conditions of diverse aetiologies (Miller & Heather, 1998). Ohlms proposed (1983) that the metabolism of alcohol produces a highly addictive in alcoholics called THIQ. Additional studies suggested that the injection of THIQ into the brains of rats caused them to consume large amounts of alcohol. The THIQ remains in the brain for a very long period of time and may cause a pronounced additive behaviour toward alcohol consumption. The results of this study remain controversial. More recent research studies have provided evidence of low levels of serotonin and abnormalities in the dopamine receptor genes as possible physiological abnormalities that may contribute to addictive behaviour. Critique . Each of the theories presented above will now be analysed based on these critical parameters. According to McCurran, “…for any theoretical approach to fit the facts, it must describe the processes of initiation to, maintenance of, and dependence upon the use of any substance, and the processes involved in change.’ (McCurran 1994, P33). West (2006) has proposed that there are several critical parameters which must be used in the evaluation of the relative importance of diverse theories attempting to explain addictive behaviour. These areas that must be addressed in an inclusive theory of addiction include: Conceptualisation of the nature of addiction Explanation of the effects of addiction on the physiological and psychological state Basis of differences in susceptibility to addictive behaviours Environmental factors that may contribute to or prevent addiction Parameters of recovery from addiction and potential relapses Conceptualisation of the nature of addiction Among the many models proposed to explain addiction, there is a small group of basic core principles that serve as the foundations for theoretical expansion. These include moral, conditioning, social learning, environmental, public health, spiritual, disease and biological principles that comprise the basis for theories and models to explain the origins of addictive behaviour (Marlatt, 1985). Orford’s Theory of Excessive Appetite is rooted in psychological, conditioning, environmental, and social learning origins. His explanation of addictive behaviour is phenomenological, and synthetic as it attempts to draw together the many diverse elements and factors that may contribute to the multifaceted nature of addictive behaviour. In this context, Orford’s theory has a broad scope that encompasses many forms of addiction and attempts to explain the many stages of the addictive behavioural processes, along with the factors that may affect resolution and relapse. The essential premise of the theory, that the basic commonality of all addictive behaviours is an “excessive appetite” or craving for the desired object, addresses a central issue of addiction which involves a loss of control of volition, a centrally defined theme in the study of addiction. Although the concept of excessive appetite is phenomenological rather than strictly scientific, it embraces one of the most important characteristics of addictive behaviour, the loss of control of one’s actions (Marlatt, 1985). In this respect, it succeeds as an important conceptual view of addictive behaviour in regard to its origins. The strengths of this theory also comprise the basis for some of its important limitations. While providing an important conceptual basis for defining the origins of addictive behaviour, the theory of “excessive appetite” does not precisely define the mechanism by which this behavioural aberration originates. The theory addresses this question in its assessment of the initiation stage of the addictive process, but the argument is largely descriptive and correlational rather than defining a precise cause and effect mechanism. This absence may, however, reflect the nature of addiction more than revealing any intrinsic flaws in the theoretical basis of Orford’s model. Many researchers have cited the pleiotropic origins of addictive disorders and the fact that this complex behavioural manifestation has multifaceted causes. Overall, as a conceptual definition of the origins of addictive behaviour, Orford’s model succeeds as it addresses the most important characteristic of addiction, the loss of volitional behaviour, in a meaningful way that integrates many diverse theories of behaviour. Whilst the disease model concept of addiction had its origins in anecdotal, descriptive commentary, the theory has emerged over the past century to define a presumed biolog origin of addictive behaviour. In contrast to the “Excessive Appettite” model, the disease model is not a synthetic model but is drawn from a scientific perspective that seeks to define a cause and effect relationship between abnormal physiology and addictive behaviour. This conceptualisation has a more limited scope, which represents its primary theoretical defect. The definition of disease requires a physiological rationale, and despite the fact that there are some research studies that support genetic origins of addictive behaviour and physiological abnormalities that may be involved in its genesis, there has been no definitive scientific data to support the basic concept of the disease model of addiction. As it is not a synthetic model, but is driven by a central focus of origin, the narrow spectrum conceptualization of addiction represents a reductionist approach that fails to define addictive behaviour from a sound theoretical foundation. Nevertheless, its simplicity is attractive to clinicians anxious to understand better the complexities of addictive behaviour. Moreover, its scientific approach has removed some of the stigma associated with addictive behaviour, which was once largely attributed to moral laxity. Despite its conceptual limitations, the Disease Model of Addiction has attracted widespread attention to the problem and has produced many efforts to develop pharmacological treatment approaches. Explanation of the effects of addiction on the physiological and psychological state The greatest strength of the Disease Model is in delineating the effects of addiction on the physiological state in ways that may contribute directly to effects on the psychological behaviours that may contribute to addictive behaviour. Many research studies conducted over the past decade suggest that addictive behaviours either directly or indirectly contribute to changes in neurological functions and activities related to neurotransmitters that may cause temporary an/or long-lasting changes in thought patterns and emotional states that may contribute to acddictive compulsions Rohsenow et al, 200 . While failing to define a precise physiological basis of the origin of addiction, the Disease Model presents a compelling view of the effects of addiction at the physiological level as they contribute to the need to repeat the behaviour either to avoid the effects of physiological withdrawal or to re-experience the euphoria associated with the addictive behaviour (Heather & Robertson, 1997) Clearly, the Disease model cannot account for all aspects of increasing drug or alcohol dependency; insofar as it contributes to our understanding of the physiological changes that accompany addicitive behaviour and which may enhance addictive patterns of behaviour, the theory provides an important basis for understanding addictive behaviour as well as a therapeutic rationale for intervention (Khantzian, 1985). As a synthetic model, Orford’s theory does not discount the important physiologic effects of addiction, rather it stresses that the primary origin of addiction cannot be attributed singly to abnormal physiological dysfunction. As an inclusive theory, Orford’s model addresses the effects of addictive behaviour relating not only to substance abuse, but also to compulsive gambling and eating in regard to their physiological consequences that may contribute to this behaviour. These physiological effects, however, are viewed in a larger context to include behavioural conditioning, psychological withdrawal and the effects of environmental stressors and social behaviours which may affect the psychological state of the individual who displays addictive behavioural patterns (Ryle, 1982, 1990). The complex conceptual basis of Orford’s theory provide a broad-based paradigm through which to explore the multifaceted responses to addictive behaviour in the individual that may vary depending upon the nature of the addiction, the environmental circumstances in which it occurs, the physiological effects on brain activity, the psychological responses that contribute to further addiction and the social context of the individual which may contribute to attitudes and psychological effects that may either contribute to or thwart the addictive process (Davies, 1997). There are many important positive implications of eclectic models attempting to describe the origins of addictive behaviours, such as Orford’s Theory of Excessive Appetite. This type of theory represents a movement away from reductionism in attempting to define addictive behaviour based on more complex variables (Koski-Jännes, 1998). Although this approach may seem more complicated and more difficult to evaluate at first glance, the multiplicity of variables involved affords multiple measures of assessment which may make this theory more amenable to research assessment ( Miller & Carroll, 2006) . Another benefit of the eclectic approach is that the assessment involves a dynamic rather than a static process, which more typically represents the diverse spectrum of human behaviours (Peele, 1985). Most importantly, this approach lends itself to diverse modes of treatment and prevention strategies based upon its multifactorial theoretical premise on the origins and manifestations of addictive behaviours. Basis of differences in susceptibility to addictive behaviours One of the central questions at the core of understanding addiction involves the issue of why certain individuals display addictive behaviours while others do not (Niaura, 2000) . Its answer presumably defines the origins of addictive behaviour and could be very useful from a preventive and therapeutic standpoint (Sanchez-Craig, 1984). Any major theory of addiction must attempt to address this question in a meaningful way. Proponents of the Disease Model have sought for many years to define a genetic and/or physiological foundation for addictive behaviour that would provide a meaningful answer to this question (Goldberg, 1999). Certainly, family history studies and identical twin studies suggest that there may be an inherited predisposition to the development of some forms of addiction, particularly alcoholism (Berglas, 1987). The weakness in the data is that it has failed to define a specific genetic or physiological component that could provide a cause and effect basis for this relationship. Family histories are influenced by more than inherited genes and physiological similarities. Environmental, sociological, and psychological factors contribute to generate the familial culture which may either contribute to or diminish the likelihood that addictive behaviours will emerge among its members (Kallio, 2000). Nevertheless, it is entirely possible that certain physiological and neurological environments may play a role in addictive behaviour; the problem is that they are not sufficiently defined at the present time to support the disease model of addiction (Wise, 1990). Moreover, a plethora of research suggests that any physiological model of addition must be considered in the context of a broader conceptual view, given that even the most favourable genetic studies suggest no more than a 50% link between genetic background and addictive behaviour (Hull, 1987). Orford’s model attempts to explain individual differences in susceptibility to addictive behaviour by using a multi-disciplinary approach to evaluating the specific stage involved in the development of addiction):. To do so, he cites a broad spectrum of sociological and psychological evidence that distinguishes the stages of addiction and the primary characteristics of each in order to define characteristics that distinguish individuals who progress from casual experimenters from those who develop serious addictions. This is a very useful theoretical modality which relies heavily on empirical data from diverse disciplines to explore the essential parameters of behaviour that define addiction. The theory does not discount the role of genetic factors that may contribute to addictive behaviour, but integrates this data into a larger, more comprehensive view of the characteristics of the individual who may be at risk for addictive behaviour. The downside of this mode of inquiry is that it is not definitive; it is open-ended and does not generate a model with a high degree of prognostic accuracy (Newlin, 2002). Ultimately, this may reflect the nature of addiction, in that its occurrence may be probabilistic given a certain set of factors, but that human behaviour is ultimately based on choice and is not deterministic at the level of prediction (Bandura, 1977). Environmental factors that may contribute to or prevent addiction Orford’s Theory of Excessive Appetite presents a far superior theoretical foundation for exploring environmental factors that may contribute to or prevent addiction than that of the Disease Model. A consideration of the circumstances in which addiction is more likely to occur represents an essential component for exploring the nature of addictive behaviour (Tiffany, 1990). Orford’s model conceptualizes each stage of addiction and attempts to synthesize the psychological, demographic, developmental and sociological factors that may contribute to the occurrence of each stage of addiction (Copello & Orford, 2002). Beginning with the initiation stage, Orford defines the diverse elements that may contribute to the experimental use of substances or participation in activities that may ultimately develop into addictive behaviours in some individuals. The influence of age, socioeconomic factors, educational experiences, family circumstances, and psychological issues that may encourage an occasional experimental to become increasingly dependent on an addictive behaviour are systematically explored in his research (Miller & Rollnick, 1991). This inquiry does much to provide insight into the environmental circumstances that contribute to volitional behaviour that may at first be a matter of choice, but in some individuals develops into the obsessive, uncontrollable need that characterises addictive behaviour (Heather, 1994). As it divides the addictive process into a series of discrete stages, the model presents opportunity to evaluate environmental factors that may serve as deterrents for increasing patterns of addiction in individuals and in communities. Moreover, the theory explores later stages in the process associated with declining addictive behaviours that may occur as individuals grow older in order to assess these factors that may effect a decreased appetite for addictive behaviours (Baumeister, 1991). The Disease Model does little to address this important parameter. While it acknowledges that environmental factors may play an important role in addiction based on the fact that genetic factors have been estimated to account for 50% of addiction, the theory lacks the broad based foundation to address the specific nature of non-physiologic factors that may either contribute to or prevent addiction (Hester & Miller, 1995; McCusker, 2001). This represents a fundamental flaw in the Disease Model, since the identification of environmental factors is essential to the design of preventive and therapeutic strategies to combat addiction. If addictive behaviour is defined solely by genetic predisposition in association with ill-defined environmental factors, there is no theoretical foundation for preventive or therapeutics to address the problem of addiction, short of medical intervention (Beck, Wright, Newman, & Liese, 1993). The Disease Model is incomplete from the standpoint of realistic and meaningful application to the prevention and treatment of addiction as it proscribes a narrow view of its origins and an equally small window for intervention. Parameters of recovery from addiction and potential relapses The overall strengths and weaknesses of these two divergent models of addiction are apparent also in this last evaluation criterion. The potential strength of the Disease model in regard to parameters of recovery and relapse prevention lies in the identification of pharmacologic agents that may have therapeutic and preventive benefit in the treatment of addiction (Khantzian, 1997). There has been some success in this area; one example involves the treatment of heroin addiction with methadone, a medical practice that has met with mixed, but substantive results (Coombs, 2004). The greatest strength of the disease model is in this area, as the responses to addiction may have a significant physiological and neurological component, which is at least theoretically amenable to pharmacologic intervention (Heather & Stockwell, 2004). With the advent of new, molecular biology approaches to understanding the physiological effects of substance addictions, it is possible that new therapeutics to alleviate physical responses to addictive substances that may further drive addictive behaviour may become a useful therapeutic approach in the treatment of addiction and in the prevention of relapses (Annis & Davis, 1991). The Orford Model offers a multifaceted approach to the treatment of addiction and the prevention of relapse behaviours. While not discounting the potential efficacy of pharmacologics that may block the excessive cravings that may be elicited by the ingestion of addictive substances, it presents a broader view of the scope and nature of addiction along with its therapeutic and preventive possibilities (Coombs, 2004). By defining the myriad components that characterize the addictive process, the model exposes many possibilities for intervention and prevention (Griffiths, 2005). The model directly addresses these issues as part of its formulation, emphasizing the importance of family, community and mental health resources in intervention and preventive approaches to reduce the occurrence of addictive behaviours in the most susceptible at risk individuals and age groups (Khantzian, Halliday, & McAuliffe, 1990). Both models have much to offer in this area. Taken together, they afford an optimistic view that, by defining the problem of addition, one can articulate potential strategies to deal with this serious cultural problem. Conclusion The purpose of this essay was to explore two divergent models of addiction with respect to their theoretical components and their significance in regard to affording a better understanding of the nature of addiction, its origins, manifestations and potential relevance in providing a basis for treatment and prevention. The Orford Model was superior in its inclusiveness of the many documented diverse components of addiction and its origins. It presents the viewpoint that “excessive appetite” is not genetically hard-wired in the individual and may, therefore, be amenable to choice and change (Granfield & Cloud, 1999). The Disease Model, while reductionist and apparently insufficiently broad-based to explain the multifaceted nature of addictive behaviour, nonetheless, has resulted in a shift in focus from blaming the individual for addictive behaviour from a moralistic view to regarding addiction as a serious problem with documented clinical manifestations (Koski-Jännes, 1992). It has been argued that the best theory of addiction must be “biopsychosocial” to incorporate the many facets of behaviour that constitute addiction (Koski-Jännes, 2002; Lende & Smith, 2004). Taken together, these models generate a comprehensive view of many of the factors critical to an understanding of addictive behaviour. Moreover, from a therapeutic standpoint, each model offers the possibility of applying unique approaches to the problems of addiction that may serve to decrease the occurrence of this highly destructive and sometimes fatal behavioural manifestation. References Abrams, D. B. & Niaura, R. S. (1987). 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