Motivation theories for drug use and addiction - Research Paper Example

?Psychology: Human Motivation Motivation Theories for Drug/ Alcohol Use and Addiction Introduction The addicted individual uses drugs frequently and in great quantities; if drug use is interrupted it is highly possible that they will return to drug use. This occurs despite the negative health consequences, besides adverse outcomes in the social, economic and functional spheres. Although confronted with all the disadvantages caused by drug use, addicted individuals persist in taking addictive drugs. They take drugs to escape from reality or to avoid unpleasant states such as withdrawal or stress. “According to early models of drug motivation, negative reinforcement is a key motive for drug use” (Baker et al, 2004, p.33). These early views on the reasons for continued drug use have been replaced by recent research which have contrasting perspectives that suggest that negative reinforcement is not a strong influence on drug motivation. Thesis Statement: The purpose of this paper is to investigate the motivation theories for drug/ alcohol use and addiction. Motivations for Drug Use Contemporary theory of the motivation for drug addiction makes paradoxical claims about the psychological basis for seeking drugs. Drug-seeking is considered to result from subjective craving for the positive effects of the drug, which suggests that this behavior is intentional. On the other hand, a key factor in the clinical diagnosis of drug dependence is that drug-seeking is resistant to the intention to quit, which means that drug-seeking is habitual or automatic. This is paradoxical, because drug seeking cannot be concurrently intentional and automatic (Hogarth & Chase, 2011). There are several reasons for people to take drugs. These include “peer pressure, relief of stress, to have increased energy, to relax, to relieve pain, to escape reality, to feel more self-esteem, and for recreation” (Columbia Encyclopedia, 2009, p.14591). Individuals resort to taking stimulants to keep alert, or cocaine for the feeling of excitement it produces. Similarly, athletes and bodybuilders may take anabolic steroids to increase muscle mass. There are numerous stressors which increase the risk of alcohol use disorders in humans. In alcohol and other drug dependent (AOD) people, drug craving is increased by internal and external forms of stress, which can also trigger relapse (Wand, 2008). Stress is generally defined as “any stimulus that challenges physiological homeostasis – that is, which alters the balance or equilibrium of the normal physiological state of the organism” (Wand, 2008, p.119). However, various forms of stress have different physiological consequences, stimulating different combinations of signaling molecules. These molecules aid in cell-to-cell communication, such as neurohormones, and produce distinctive outcomes on physiological processes. Therefore, the type and duration of stress have to be specified, for planning the treatment. Further, individuals respond differently to a particular type of stress, “and physiological and behavioral responses tend to be associated with distinct coping styles” (Wand, 2008, p.120). An interaction of environmental and genetic factors play a part in both susceptibility to alcohol and other drugs (AOD) use disorders, and in people’s responses to stress. Prenatal and early life stress can have impacts on the body systems involved in the stress response, for the entire life span, thereby predisposing an individual to certain diseases. This early programming effect is partly affected by “epigenetic mechanisms that alter heritable traits without manifesting as changes in the DNA sequence, and which also can aid in the development of AOD disorders” (Wand, 2008, p.120). Motivation Theories for the Use and Addiction to Drugs and Alcohol An Affective Processing Model of Negative Reinforcement Baker, Piper and McCarthy (2004) reformulate the negative reinforcement model of drug addiction. They propose that the escape and avoidance of negative affect is the prepotent motive for addictive drug use. Further, Baker et al (2004: p.33) state that “negative affect is the motivational core of the withdrawal syndrome” and argue that, addicted individuals or organisms learn to identify and detect interoceptive cues of negative affect preconsciously. Hence, the motivational basis of much drug use is unclear, and reveals low cognitive control. Stressors or abstinence results in negative affect growing and entering consciousness, and increasing negative affect adversely impacts information processing in ways that promote renewed drug administration. “Among motivational accounts of addiction, negative reinforcement ranks as one of the earliest and most venerable” (Baker et al, 2004, p.33). Examples are theories of Wikler (1980) and Jellinek (1960) besides others. A negative reinforcement model which emphasizes the central role of negative affect in motivating drug use, has been reformulated in the context of contemporary basic science, in the areas of affect and information processing. This model of Baker et al (2004) can organize extant data in the literature, as well as produce new and specific hypothesis for future investigation. The authors try to combine traditional drug motivation theories with advances in basic research, to strengthen research on the key role of negative reinforcement in the continued maintenance of addiction. Negative affect is a motivationally prepotent element of the withdrawal syndrome. Although non-affective signs of withdrawal such as tremor are sometimes referred to by addicted individuals as causing drug use or relapse, affected individuals consider negative affect as a vital setting event for drug use or relapse (Baker et al, 2004). Abraham Wikler’s Withdrawal-Relief Theory of Opiate Addiction “Abraham Wikler developed a highly influential theory of opiate addiction based on research spanning several decades” (Lyvers, 1998, p.108). He emphasized physical dependence as the core feature of addiction. The main difference between psychic and physical dependence is that the former is a vaguely defined group of inferences obtained from the subjective reports of the subject of the study, while the latter is inferred from objective changes in his autonomic nervous system and behavior. According to Wikler (1980), distressing drug-withdrawal syndromes are promptly alleviated by renewed administration of the drug in question. It is considered that such need reduction has powerful and reinforcing effects. For opiates such as heroin or morphine, continuous administration for a few weeks will lead to withdrawal signs of autonomic hyperactivity, which begin several hours after the last dose and subside within a week. The most common symptoms include “diarrhea, tremor, rhinorrhea, lacrimation, mydriasis, chills, sweating, tachycardia, nausea, anorexia, and hyperthermia” (Lyvers, 1998, p.108). One of the withdrawal symptoms was self-reported craving, which emphasized the intense need of the individual to relieve himself of the distressing autonomic symptoms. Wikler noted two important problems in the withdrawal-relief theory of opiate addiction, and attempted to resolve them. One was that the model does not explain the reasons for an addict’s taking opiates so regularly and in such large quantities to become physically dependent in the first place. A commonly held perspective is that the pleasurable effects of a drug such as heroin provides the initial motivation for repeated, voluntary use. Only with the development of physical dependence is the user hooked. However, Wikler did not consider drug-induced euphoria to have a role in the acquisition of an opiate habit, noting that first-time use of heroin more frequently results in dysphoric effects such as nausea and dizziness than euphoria. In the United States, the vast majority of opioid addicts begin and continue to use drugs, usually heroin, to emulate their drug using peer group. Wikler’s hypothesis is that even a single injection of heroin induces physical dependence. Thus, after the first dose, repetition of drug-taking has a rewarding effect of alleviating hidden changes caused by abstinence. It is a subclinical withdrawal syndrome consisting of adverse, subtle symptoms (Lyvers, 1998). The second problem addressed by Wikler was the inability of the withdrawal-relief model to account for relapse after the withdrawal-syndrome subsided. The vast majority of opiate addicts in drug-treatment programs relapse within a year of detoxification, irrespective of the type of treatment used. Detoxified addicts being no longer physically dependent, the reason for their relapse to addiction had to be resolved, since they no longer required the withdrawal-relieving effects of opiates. Wikler proposed that “withdrawal symptoms become classically conditioned to the environment in which a junkie hustles for and self-administers opiates” (Lyvers, 1998, p.108). According to Wikler, addicts have been reported to experience flu-like symptoms when returned from in-patient detoxification to drug-associated home environments. Such conditioned responses cannot be eliminated merely by shifting the addict from the drug-associated home environment to jail or the hospital for detoxification. This is because, “when the detoxified addict is released and returns home, conditioned withdrawal symptoms are elicited, which demand relief” (Lyvers, 1998, p.108) through craving, thereby reinstating the cycle of addictive behavior. Theories of addiction based on physical-dependence regard compulsive drug-taking as the behavioral manifestation of a desperate need to relieve aversive autonomic withdrawal symptoms. Thus, the withdrawal-relief paradigm or opiate model of addiction is examined by Lyvers (1998) in the light of recent experimental and clinical evidence for various addictive drugs. Contrary to the opiate model, the set of pathological behaviors defining addiction such as compulsive drug use, craving, loss of control, and a persistent tendency to relapse, does not basically demonstrate a need to relieve actual or conditioned autonomic withdrawal symptoms. Recent theories of addiction “emphasize the positive reinforcing properties of drugs and sensitization of brain dopamine systems rather than negative reinforcement or drug-opposing neuroadaptations” (Lyvers, 1998, p.107). Despite the failure of the opiate model, recent evidence reveals that persistent drug-induced changes in the physical brain may underlie addictive behavior, in alignment with addiction as a physical disease. Jellinek’s Model of Alcoholism Jellinek (1960) applied the opiate model to alcoholism, with the approach of a disease concept to alcoholism only when physical dependence was present. In the medical of disease model of alcoholism, the critical symptom of alcohol addiction related to loss of control over alcohol intake, and not to excessive drinking. Loss of control referred to any drinking of alcohol that started a “chain reaction felt by the drinker as a physical demand for alcohol” (Lyvers, 1998, p.112). This state considered to be a conversion phenomenon, may take hours or weeks for its full development; it lasts until the drinker is unable to ingest more alcohol. The drinker loses the ability to control the quantity he consumes, but whether he drinks on any occasion is under his control. “The drinking pattern of the alcohol addict often takes the form of prolonged drunken binges or benders” (Lyvers, 1998, p.112). This is usually followed by several days or weeks of abstinence, during the ‘crucial phase’ of alcoholism, as termed by Jellinek. Hence, it was derived that physical dependence was not a defining feature of alcohol addiction as originally believed by Jellinek (1952), but rather loss of control was the essential symptom. Jellinek (1960) therefore changed his disease conception of alcoholism to align with the widely accepted withdrawal-relief theory of opiate addiction. According to Lyvers (1998, p.113), the “withdrawal syndrome that develops after chronic use of alcohol or other sedative drugs typically includes many of the autonomic symptoms of opiate withdrawal”, but they can be far more dangerous due to the additional possibility of delirium tremens and epileptiform seizures. In contrast to Wikler, however, Jellinek admitted that physical dependence could not account for the common phenomenon of relapse after the subsiding of the abstinence syndrome. Physical dependence also could not explain the years of heavy drinking that ultimately resulted in physical dependence in the first place. Compulsive drinking for several years in the absence of withdrawal symptoms, even under conditions of concurrent damage to “family, employment, socioeconomic status, brain, and liver” (Lyvers, 1998, p.113), was considered by Jellinek (1960) to be motivated fully by psychological factors, and therefore could not be denoted as actual addiction. The Theories of Incentive Sensitization and Hedonic Allostiasis Two of the models of motivation for drug and alcohol use and addiction are: incentive sensitization and hedonic allostiasis. These can be integrated to conceptualize the effect that various forms of stress have on the development of drug dependence (Vanderschuren & Everitt, 2005). According to the incentive sensitization theory, the effects of casual AOD use sensitize the mesocorticolimbic reward system, so that the drug user wishes to repeat these rewarding effects. This leads to the development of extremely high levels of motivation to use AOD again. This theory helps to explain the way in which “initial experimentation with AODs by an occasional user can escalate to repeated drug administration” (Wand, 2008, p.122). At this stage, the motivation is hedonic pleasure. However, with chronic AOD use, the motivation for drug use can change because of hedonic allostiasis. This leads to decreased activity or downregulation of positive reward circuits, which gives rise to a chronic stress situation. As a result of chronic stress, the body produces stress factors which produce a negative emotional state “characterized by withdrawal symptoms, sadness or dysphoria, and anxiety” (Wand, 2008, p.123). This negative effect develops into the main force that drives a craving for drug use. The individual at this stage seeks AODs for avoiding a negative-affect condition, rather than for achieving a pleasurable experience. Different types of stress can cause this change from incentive sensitization to hedonic allostiasis. The theory of motivation related to drug use and addiction by Koob and Le Moal (1997), explains the progression of drug addiction through three stages. These include the preoccupation/ anticipation stage; the binge/ intoxication stage; and the withdrawal/ negative affect stage. The first stage is characterized by a highly increased motivation for drug use associated with a sensitized mesocorticolimbic dopamine system. The model for this phase is the incentive sensitization theory, and is referred to as the acquisition phase in the study of animal models. In the second stage of binge/ intoxication, a down-regulation of positive reward pathways occurs, by which the drug levels required to trigger the brain reward system increase. This is similar to the maintenance phase in animal models. The final withdrawal/ negative affect stage during which the drug user transitions to drug addiction is “when the negative affect becomes dominant, further escalating craving and use of the addictive drug” (Wand, 2008, p.123). Experimental designs in animal models create the equivalent state by drug deprivation. According to Koob and Kreek’s (2007) model of allostatic transition from reward sensitization to negative-affect development, there is a harmful interaction between alcohol and other drugs (AODs) and the stress response. AODs can take over the stress and reward systems in three ways. First, AODs directly activate the stress response, and the glucocorticoids released can initially sensitize the reward pathways, resulting in further AOD use. During the preoccupation stage, this may contribute to reward sensitization. Second, with the AOD user’s transition to addiction, the dominant forces of negative affect and withdrawal symptoms take over, stimulating the release of anxiety-inducing or anxiogenic stress peptides such as CRE. At this stage, with the addict using AODs for eliminating stress rather than for pleasure, the use of AOD escalates. Third, environmental stress generally caused or increased by the chaotic lifestyle and negative consequences of AOD abuse, interacts with the negative-affect state produced by withdrawal or abstinence to amplify the anxiety and dysphoria induced by the stress peptides. “At each of these steps, allostatic mechanisms are initiated by the organism to try and maintain homeostasis in the presence of the AODs and the resulting stress” (Wand, 2008, p.123). Theory of Work-Stress Paradigm in Substance Use and Depression The research study conducted by Wiesner, Windle and Freeman (2005) on work stress, substance use, and depression among young adults, was based on the work-stress theory of motivation for drug/ alcohol use and addiction. According to this theory, “employee psychological problems and risky health-related behaviors occur in response to aversive conditions such as dangerous and noxious physical work environments, heavy workload, job insecurity, and unfair treatment regarding pay, benefits, and promotions” (Wiesner et al, 2005, p.83). Work-alienation factors that lead to unenriched jobs, for example work that demands only minimal skills, low job control, and lack of participation in decision-making, may also be included under this paradigm. There are numerous mechanisms that may explain the relationships between job stress and outcomes. If work stress arises from lack of self-direction in the work setting, it may activate cognitive vulnerability factors which then result in heightened levels of emotional distress or depressive symptoms (Mackie, Holahan & Gottlieb, 2001). Additionally, employees may consume alcohol for regulating negative affect and thoughts resulting from aversive work conditions, or drink for coping or escapist reasons. Employee drug use is also believed to function through a similar mechanism. Finally, “the work-stress paradigm recognizes the role of stable individual differences” (Wiesner et al, 2005, p.83), in the relationship between job stress and work, for example the psychological importance of work. According to Hogarth and Chase (2011), the data from their research was in agreement with the dual-process theories. They suggested that drug/ reward-seeking are mediated by goal-directed and habitual controllers under freely elected and cued conditions, respectively. Further, the “initial uptake of drug use is associated with hyper-valuation of the drug as an outcome of goal-directed drug-seeking rather than with accelerated habit formation” (Hogarth & Chase, 2011, p.1). Conclusion This paper has highlighted motivation for drug and alcohol use, and motivation theories related to their use and addiction. Various theories of motivation for addiction have been discussed including an affective processing model of negative reinforcement, Abraham Wikler’s withdrawal-relief theory of opiate addiction, Jellenik’s model of alcoholism, the theories of incentive sensitization and hedonic allostiasis, the theory of work-stress paradigm in substance use and depression, and dual-process theories. Among motivational accounts of addiction, negative reinforcement is considered to be one of the earliest theories, as exemplified by the models developed by Wikler (1980) and Jellinek (1960). 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