Campus: Support for Addiction Prevention and Treatment in Africa

Essay Title: The Disease and Learning Models of Addiction

Author: Albert Muraya

Supervisor: Catherine Ngarachu

Date: 24.02.2007

Introduction

Addiction is a condition in which individuals are unable to control their consumption or use of chemical compounds, or their engagement in processes that alter moods, and thus develop an unhealthy dependence on either the chemical or process. Addiction tends to be a progressive disorder characterised by increasing tolerance for the substance, severe symptoms of withdrawal upon cessation of use, and acute longing for the substance or activity when not using. This dependence is unhealthy, because it involves a preoccupation with the drug or activity, has deleterious effects on both mind and body, to the point of complete loss of control. Despite the harm that the dependency generates, the afflicted individuals find they are unable to the cease or moderate the activity without outside help. This essay will examine two of the theories put forward to explain this phenomenon, namely the Disease Model of Addiction, and the Learning Models of Addiction. The first states that chemical dependency is condition with genetic and biological underpinnings, and that it satisfies the accepted criteria for a condition to be termed a disease. I will examine the criteria and outline the rationale employed by those who put forward this argument. The Learning models are based on the idea that all behaviours are learned, and that in order to understand and moderate them, the environment in which they exist must be understood. These theories have been developed from what are known as the principles of social-learning. I will explain the different theories that fall under this category. Whilst the phenomenon of addiction encompasses process addictions such as sex addiction, compulsive gambling and eating disorders, I’ll limit myself to chemical addiction or dependency. Finally I will compare the two models for their implications on possibilities for addiction prevention and implications for treatment interventions and outcomes.

The Disease and Learning Models of Addiction

Addiction can be defined as a destructive, compulsive-obsessive relationship with any substance or process, that is characterised by an increasingly heightened need for a drug or process (tolerance), the painful suffering occasioned by its withdrawal or discontinued (withdrawal), and fixation with the drug or process either when not using/doing, or upon commencement (craving). Several models have been put forward to explain the phenomenon of addiction and the behaviours that they spawn, including the Disease Model and the Learning Models of addiction.

The disease model was first postulated in the late 18th century by philanthropist and social reformer Anthony Benezet, and later in 1784 by Dr. Benjamin Rush's “Inquiry into the Effects of Ardent Spirits on the Human Mind and Body”. Rush achieved five things with this highly influential pamphlet:

• He medically catalogued the signs of acute and chronic drunkenness. • He introduced a more medicalized language into the discussion of

intemperance by describing 'persons addicted to ardent spirits' and by declaring that chronic drunkenness was an 'odious disease' and a 'disease induced by a vice.'

• He medically confirmed Benezet's observation about the progressiveness of intemperance by noting that such episodes 'gradually increase in their frequency.'

• He offered medical speculation about the causes of this disease. • He provided the first recommended treatments for chronic drunkenness

based on a disease concept of addiction. Rush later used this embryonic disease concept to call for the creation of a special facility (a 'sober house') to care for the drunkard.

(“Addiction as a Disease”, By William L. White, MA, The Counsellor Magazine, October 2000, v.1, n.1, pp. 46-51, 73) Throughout the 19th and early 20th centuries, this concept was further developed and refined, culminating in the Dr. E.M.Jellinek's Disease Concept of Alcoholism (1960). The Disease Model or concept of addiction states that addiction to alcohol or other drugs is a primary, chronic, progressive disorder, characterised by loss of control over the drug(s) of choice, continued use of the drug and denial of the problem despite adverse consequences.

In order for a condition to be characterised as a disease, there are established criteria that need to be met, namely:

a) A clear biological basis; b) A set of unique identifiable symptoms; c) A predictable course and outcomes; d) A lack of internal causation.

(“Treating Patients with Alcohol and Other Drug Problems: An Integrated Approach”, By Robert D. Margolis and Jean E. Zweben, APA, 1998 Washington D.C.) The disease concept views addiction as having as a primary causative factor, an inherited or genetic component, with secondary environmental exposure elements. This fits the first criteria, a clear biological basis, the evidence for which is found in a considerable body of research evidence pointing to a biochemical or genetic basis for addictive behaviour. Numerous studies have been conducted that compare the effects of environment over genetic factors in alcoholics and addicts — adoption studies, twin studies, animal studies, and studies on the sons of alcoholic fathers. This research indicates that “alcoholism is a true medical disease rooted in abnormalities in brain chemistry biochemical aberrations that are inherited by the majority of alcoholics and, in some cases, acquired through intense and sustained exposure to alcohol and other drugs”. Further, research points to not just the development, but also the progression of the condition as being determined by heredity. As such, addiction is comparable to other chronic diseases such as asthma, diabetes, and cancer. Addictions, it has been noted, have common signs and symptoms which satisfy the second condition for identification as a disease. These include increased tolerance for the drug (normally followed by a precipitous drop in tolerance), loss of control over use of the drug, continued use despite the personal and social cost, and a pattern of relapsing. The third criterion is a predictable course and set of outcomes. Addiction follows a continuum of progression from early abuse to chronic, end-stage dependency. Left untreated, addiction is nearly always fatal either directly through damage to vital organs, or indirectly through consequential factors like suicide, car accidents (due to inebriation), drug–related violence and so on. The progressive nature of addiction is similar to other chronic disorders such as heart disease and gout. Since a constituent part of the ailment is loss of volition, the aetiology (cause) of the condition and its course are outside the control of the addict, thus chemical dependency satisfies the condition that a disease should not be intentionally caused. In summary, addiction qualifies as a disease because in its nature, it matches other chronic diseases in its biological causation, progression and identifiable symptoms.

The learning models postulate that addiction like all human behaviour is learned, and that “addictive behaviours represent a category of bad habits including problem drinking” (Marlatt G & Gordon J (1995) “Relapse Prevention: Maintenance Strategies in the Treatment of Addictive Behaviours”, New York, The Guilford Press – pg9). These models or theories are “derived from the principles of social-learning theory, cognitive psychology, and experimental social psychology” (ibid), and include classical conditioning, operant conditioning, and modelling theories. All these models are based on the notion that there is no behaviour that can be put down to genetic factors, and that conversely, all human behaviour is learned. Marlatt goes on to state that “Addictive behaviours are viewed as overlearned habits that can be analyzed and modified in the same manner as other habits” (ibid). Further, they perceive addictive behaviours as being on a range or continuum of behaviour from responsible or social use to addictive, compulsive use (Margolis & Zweben – pg55). Whilst acknowledging that addictive behaviour can bring about diseases, learning theorists place more weight on the role of personality and (ir)rational choice in the causation of addiction. Studies (Marlatt & Gordon 1980; Monti, Rohsenhow, Abrams & Brinkoff 1988) have shown that the mere expectation of the potency of a drug will produce the same effects from a placebo of the drug (tension reduction, euphoria) as the drug. This demonstrated the effect of expectations on learned behaviour. The first difference between the learning and disease models of addiction is therefore in the ways the different concepts view the initiation and maintenance of addiction and addictive behaviours. In the learning model, its adherents see addiction as a pattern of behaviour that stems from learning or adopting maladaptive habits and reinforcing them through conditioning (repetition). Any changes in the physiology of the addict including changes in brain chemistry are the result of this dysfunctional usage, and are essentially reversible by changing the behaviour pattern. With the disease model, addicts are seen as individuals with a genetic predisposition to addiction as evidenced from a genogram, and to the extent that they expose themselves to the addictive chemical, are almost invariably going to become addicts. This brings up the issues of prevention and treatment. Given the differences in the rationale for addiction that the two models hypothesize, they hold very different possibilities for either prevention or treatment. The disease model suggests that abstinence is the only possible remedy for the affliction. This follows on from the notion that addiction is a disease that is incurable, and that one can only arrest it; that whilst the addict is abstinent, the disease is merely dormant and should they try to resume usage of the chemical, the disease would be reactivated. The learning models on the other hand, whilst minimising the role of heredity in addiction aver, that whatever had been learned (addictive behaviours) can be

modified by the same processes that created them to begin with. They therefore focus on and seek to alter the addict’s cognitive (thinking and reasoning) processes, the environment in which they maintain their habit and their emotional responses to their environment. The differential approach on the significance and nature of the environment distinguishes one learning theory from another. In classical conditioning, cravings to use are set off by environmental triggers such as the sight or smell of the addict’s drug of choice. By attacking the association and questioning the rationale for the addict to expose themselves to such situations, this learning model suggests a viable, alternative solution. Operant conditioning on the other hand questions the addict’s response to the stimuli, and focuses on changing this response in the same situation. Cognitive–behaviour therapy, by enhancing the addict’s self-efficacy or self-assurance and questioning and bolstering the addict’s coping skills, would facilitate the addicts making a safe choice around any given situation. As such, cognitive–behavioural therapies seek to remove or modify irrational thinking and feelings, replacing them with more appropriate ones. The corollary is that they must avoid high-risk situations about which they are not strong or confident. Modelling behaviour seeks to change behaviour by having the addict copy the behaviour of a positive role model. It is particularly useful when dealing with adolescents, getting them to pattern their behaviour on that of someone positive and away from their destructive patterns. The real attractions of the learning models are their applicability in a treatment scenario. Whilst the disease model offers real options in treatment, the learning models, because they specifically deal with external factors and relationships and how to deal with high-risk situations are more practical and flexible than the pure disease model. The learning models also provide for greater scope in the prevention of the condition of addiction, because they can be applied to a broad spectrum of usage paradigms – social-users to serious abusers. They have available to them more treatment outcome possibilities than does the disease concept whose only potential outcome is abstinence, in addition to which the learning models have controlled using and harm reduction as a possible target for treatment, either as an end in itself, or as a stop-gap measure to eventually complete abstinence. Further, learning theories offer greater relapse prevention potential, and for the relapser a more achievable target than the disease model. In practice, both models have been combined in recent years, and the Bio-Psycho-Social model of addictions has emerged which explains the phenomena of addiction from both viewpoints – there is a variable genetic susceptibility with some addicts, as well as a psycho-social component in the development and sustainability of addictive disorders. Neither model on its own sufficiently explains addiction in its entirety, but when combined, goes some way in not just providing a viable and sustainable definition of addiction, but also a rich tapestry of treatment strategies and possibilities.