Using Research Evidence, Compare And Contrast Two Theories Of Addiction Essay Example

Type of paper: Essay

Topic: Addiction, Drugs, Theory, Behavior, Brain, Alcoholism, Psychology, Study

Pages: 7

Words: 1925

Published: 2020/12/07

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Introduction

Addiction is a syndrome involving the reward-seeking behavior that can result in a significant harm to the person who is driven by an abnormal motivation process to regularly need or use something. It is often viewed as a psychological and physical compulsion of using habit forming substances, such as alcohol or drugs. Addiction is considered to be a complex disease affecting not only the individual’s health and well being, but also the people around the individual addict and the society at large. Hoffman and Froemke (2007) describe addiction as a chronic disease of the brain, as a disease, and as a national issue that needs to be addressed. Considering the magnitude of the impact of addiction to an individual addict, the addict’s family and society in general, it is essential to understand what can cause addiction.
There are a number of theories of addiction that seek to explain the possible causes why addiction behavior occurs. These consist of general principles that help to hypothesize the causes of addiction. Two of these theories of addiction, namely the neurobiological theory of addiction and the classical conditioning theory of addiction, will be the subject of this essay. Their comparison and contrasting principles about addiction will be presented and critically evaluated. Considering that addiction is a complex process, there is not a single theory of addiction that can accurately explain how this harmful habit forming behavior is formed. By analyzing these two theories of addiction, some aspects of addiction behavior will be understood, with supporting research studies as evidence that can support the hypothesis on why addiction occurs.

Discussion

Addiction is often referred to as substance abuse where the individual manifests dependency that is characterized by a compulsion of seeking certain habit forming substances, such as alcohol and drugs. The negative consequence when the individual is deprived an access to these substances include the manifestation of a negative emotional state, such as irritability, anxiety and dysphoria. The person who needs to take these substances in order to maintain a normal physiological functioning is an addict (West, 2006).
The concept of drug abuse is usually viewed as a progressive disorder that begins as an impulse that develops into one of compulsion (Koob, 2006). The neurobiological theory of addiction postulates that addiction primarily stems from genetic factors and metabolic imbalances. The genetic theory hypothesizes that a person’s predisposition to alcohol and drug addiction is influenced by heredity (Godlberg, 2014). Accordingly, the biological differences among every individual allows each person to have a distinct level of intoxication when consuming alcohol or drugs. The genetic epidemiology affecting alcohol and drug addiction has been the subject of a research study of Dick and Agrawal (2008). Their findings revealed that the heritability rate for both addictions estimates to about 50 percent or higher, while twin studies together with the electrophysiological characteristic study shows a high indication of a high risk of alcohol or drug (AOD) dependence. This comes with the risk of developing antisocial behavior due to shared genetic factor.
The neurobiological theory also indicates the role of molecular and cellular mechanisms involving the drug’s action to the brain and how it may impair control during the use of drugs. This is related to the chronic relapsing brain disease model presented by the National Institute of Drug Abuse. It provides that the self administration of drugs can produce enduring changes to the brain neurotransmitter system. This leaves an addict more vulnerable to relapse after withdrawal from substance abuse (Miller and Kavanagh, 2007). Current researches on neuroimaging studies reveal that chronic drug use can produce a significant effect of decreasing the activities of dopamine (Koob and Volkow, 2010). It results in the disruption of the normal function of the limbic and the prefrontal system of the brain that are responsible for recognizing the rewarding effects of natural reinforcers. Consequently, the disruptions in the normal activities of the prefrontal system results in the impairment of the impulse inhibition and decision making process of the addict. Moreover, by hijacking the normal reward circuit produced by the limbic system that is crucial to the survival of an individual, an addict finds drugs very appealing and becomes more inclined to abuse its use despite its aversive consequences. The disruption in the brain’s normal reward system circuit has also been associated by Lubman, Yucel and Pantelis (2004) to the development of compulsive and maladaptive behaviors through a study of the neuroimaging and neuropsychological evidence. They postulate that the inhibitory dysregulation explains why addicts lose control over their drug use and usually engage in self-destructive activities repeatedly.
The classical conditioning theory of addiction is also referred to as associative learning theory, where it provides that neural stimuli has the ability to produce or elicit a response. According to McCrady and Epstein (2013), the approach of classical conditioning redefined drug dependence as a habitual drug seeking and drug using behavior with emphasis on the pharmacological reinforcement and the role of cravings in relapse. A research study by Robinson and Berridge (1993) is consistent with this theory. Their findings describe the ability of addictive drugs to enhance the mesotelencephalic dopamine neurotransmission that may result in producing the psychological effects of salient rewarding effects of drugs. This makes them a highly attractive and wanted incentive stimuli. Thus, the sensitization of the dopamine system through the pharmacological effects of drugs enhances the development of drug cravings. The classical conditioning also postulates that addiction is a learned behavior through the process of pairing the pleasurable experience of using addictive substances with cues coming from the environment. Thus, the use of a syringe may be closely associated to the pleasurable experience of drug use. The mere seeing of the syringe needle increase one’s engagement to habitual drug seeking and drug using behavior.
The classical conditioning emphasizes the role of cues in stimulating the impulses to engage in a certain behavior (West and Brown, 2013). Consistent with the link between environmental cues and abusive use of drugs, the classical conditioning in addiction model explains that a stimulus can introduce a new meaning through association using alternative stimulus. As in drug addiction, the association of a particular smell, sound or sight related to substance use brings a new meaning to the person. Thus, the mere seeing of a syringe or rolling papers used in substance abuse, or the smell of the substance of choice, such as an alcohol, can induce a response to the individual. Over time, these cues will illicit some cravings for drugs or alcohol (Otto, Cleirigh, and Pollack, 2007).
Another study by Wikler (1948) associated with the classical conditioning theory showed the role of environmental cues associated with drug use in the past can act as a stimulus for the development of drug seeking behavior. Opiate addicts who were drug free for months are usually expected not to show any signs of withdrawal symptoms. However, they may actually develop withdrawal symptoms again whenever they talk about drugs during their group therapy sessions. This is coined as conditional withdrawal, which results from environmental stimuli where one acquires the ability to manifest the signs and symptoms of withdrawal syndrome from substance abuse through association.
While the neurobiological and classical conditioning theories of addiction seeks to explain the underlying cause of habitual drug seeking and drug using behavior in addiction, there are some points of differences between the approach of both theories. The neurobiological theory of addiction only accounts for the underlying cause of addiction and how the maladaptive behavior takes place. There are more rooms for further pre-clinical and clinical research studies that may be undertaken in order to fully account the possible long term treatment strategies that may help drug dependent individuals (Feltenstein and See, 2008). While it may explain the occurrences of relapse, only a few studies were taken in this direction and those that were already conducted seems unclear. The majority of literature studies and clinical research focuses on the neurobiological etiology of addiction without extending further on how the theory can help identify potential treatments for addiction. The classical conditioning theory of addiction is more comprehensive than the neurobiological theory. It focuses not only on emphasizing the possibility that addiction is a learned process, the research studies conducted based on the theory extend to the development of potential addiction treatment. The theory has been the source of several clinical therapies used for addiction, one of which is the cue exposure therapy. However, the theory also poses some limitations in its scope of study, as it does not account for the role of self conscious intention, beliefs or one’s desires (West, 2013).
The neurobiological theory of addiction directs its hypothesis in explaining why addiction can occur due to the neurological and biological causes. It postulates that genetic predisposition of an individual is a factor. This also includes changes in the molecular and cellular activities affecting major systems in the brain, such as the prefrontal and the limbic systems. The etiological cause of addiction is directed to the impairment in the reward circuits that disrupts one’s own decision making process (Platt, Watson, Hayden, Shepherd and Klein, 2010). As a result, failure to inhibit cravings enhances the development of harmful behavioral effects. The classical conditioning theory, on the other hand, directs the etiology of addictive behavior to association. While the neurobiological theory of addiction explains that addiction is a physiological consequence of an abnormal brain functioning, the classical conditioning theory of addiction explains that addiction is a learned behavior through association and conditioning.
Based on the classical conditioning theory, using environmental cues has been very helpful as a form of addiction treatment. It uses external cues or conditional stimuli without resorting to addictive behavior that can help an individual lose his inclination to cravings (Martin, 2008). The critical use of the neurobiological theory of addiction, on the other hand, can help an individual identify his genetic vulnerability that can predispose him to develop dependency on certain addictive substances like alcohol and drugs. Abstinence is considered to be an important and crucial factor in developing an aversion against addiction (National Institute on Alcohol Abuse and Alcoholism, 1974). Recognition of one’s risk factors of addiction, such as his genetic vulnerability and neurobiological traits, is helpful. In classical conditioning, avoiding the so-called reinforcers can help in the recovery against drug seeking and drug using behaviors.
It can be critically assumed that the neurobiological theory of addiction postulates that the introduction of prolonged use of drugs can alter the brain functions, causing some molecular and cellular responses that consequently enhances the development of addictive behavior (Koob and Le Moal, 2006). The classical conditioning theory of addiction postulates that the introduction of a stimulus can encourage an associative behavior that elicits cravings and addictive response to an individual. Considering these conditions, it can be critically hypothesized that addiction is an abnormal behavior that takes place when certain stimuli or substances are introduced to the brain that causes an alteration to its normal functioning and responses. Both the process of association through conditioning and the introduction of pharmacological substance use in the long term can produce similar consequences of malfunctioned brain activities. Only there is a difference in the mechanisms of producing such alteration in the brain function. With classical conditioning, the learning process of the individual is affected where cognition and decision making process are altered (Gould, 2010). The approach of altering the brain function under the neurobiological theory of addiction produces a magnitude of changes in the physiological aspect of brain functioning.
A significant relationship between these two theories involves the view point of Hyman and Malenka (2001), where the addictive behavior is considered to be influenced by the central mechanisms of drugs usurping the normal mechanisms of brain functions. The presence of environmental cues present during relapses is viewed to revive the molecular processes involved that disrupts the normal circuitry in the brain functions. Thus, there are more rooms for a further study showing the relationship between the study of neuroscience in addiction and the role of learning and memory. Patients are known to have a reduced risk of a relapse by avoiding cues that can reinforce their maladaptive behavior through aversion therapy (McMurran, 1994). The classical conditioning theory of addiction is being sought by clinical researchers in defining better treatment approaches to addiction, while the neurobiological theory of addiction is most likely used for preventing one’s predisposition or risks of developing addictive behavior.

Conclusion

In conclusion, the use of theories can significantly help in growing the knowledge of understanding about the various causes of addiction. Addiction is a complex process (Boone, 2004) that can be explained by various theories on its causes and the mechanisms involved that produce the maladaptive and compulsive behavior. With the emerging theories of addiction, it is easier to understand the complex process involved in the development of addictive behavior. The classical conditioning appears to be more effective in terms of helping an addict to recover from their maladaptive behavior. The therapeutic approach of addiction treatment using cue exposure therapy has been drawn out from the classical conditioning theory (Galanter and Kleber, 2011). It is consistently being used in addiction therapy and there are potential possibilities of exploring other treatments that may be effective for addiction recovery. Because craving is known to persist even through the recovery process, McLellan (2003) believes that classical conditioning theory is more consistent in helping an addict attain a full recovery. Classical conditioning theory, however, may not address the underlying neurological causes of addiction. This makes the neurobiological theory more helpful when underpinning the issues of addiction as a brain disease when developing the maladaptive behavior. But the theory may not suffice in addressing addiction when it is associated with learning behavior and association.

References:

Boone, S. (2004). The Role of Will in Addiction and Recovery. Bloomington, IN:AuthorHouse.
Dick, D.M. and Agrawal, A. (2008). The Genetics of Alcohol and Other Drug Dependence. Alcohol Research and Health. 31(2): 111-116.
Feltenstein, M.W. and See, R.E. (2008). The Neurocircuitry in Addiction: An Overview. British Journal of Pharmacology. 154(2): 261–274.
Galanter, M. and Kleber, H.D. (2011). Psychotherapy for the Treatment of Substance Abuse. Arlington, VA: American Psychiatric Publishing.
Godlberg, R. (2014). Drugs Across the Spectrum. Belmont, CA: Wadsworth Cengage Learning.
Gould, T.J. (2010). Addiction and Cognition. Addiction Science Clinical Practice. 5(2):4-14.
Hoffman, J. and Froemke, S. (2007). Addiction: Why Can’t They Just Stop? New York, NY: Rodale Books.
Hyman, S.E. and Malenka, R.C. (2001). Addiction and the Brain: The Neurobiology of Compulsion And Its Persistence. Neuroscience. 2:695-703.
Koob, G. F. (2006). The Neurobiology of Addiction: a Hedonic Calvinist View. In W.R. Miller & K.M. Carroll (eds.) Rethinking Substance Abuse. London: Guildford Press. Pp. 25-45.
Koob, G.F. and Le Moal, M. (2006). Neurobiology of Addiction. San Diego, California: Elsevier.
Koob, G.F. and Volkow, N.D. 2010. Neurocircuitry of Addiction. Neuropsychopharmacology. 35(1): 217-238.
Lubman, Dl., Yucel, M. and Pantelis, C. (2004). Addiction, a condition of compulsive behaviour? Neuroimaging and neuropsychological evidence of inhibitory dysregulation. Addiction. 99 (12): 1491-1502.
Martin, C.R. (2008). Identification and Treatment of Alcohol Dependency. UK: M&K Update Ltd.
McCrady, B.S. and Epstein, E.E. (2013). Addictions: A Comprehensive Guidebook. New York, NY: Oxford University Press.
McLellan, A.T. 2003. Relapse and Recovery: Behavioral Strategies for Change. New York: Caron Treatment Centers.
McMurran, M. (1994). The Psychology of Addiction. London: Taylor & Francis Ltd.
Miller, P.M. and Kavanagh, D. (2007). Translations to Addiction Science Into Practice. Oxford: Elsevier.
National Institute on Alcohol Abuse and Alcoholism (1974). Alcoholism. USA: National Clearinghouse for Alcohol Information.
Otto, M.W., Cleirigh, C.M. and Pollack, M.H. (2007). Attending to Emotional Cues for Drug Abuse: Bridging the Gap Between Clinic and Home Behaviors. Science Practice Perspective. 3(2): 48-55.
Platt, M.L., Watson, K.K., Hayden, B.Y., Shepherd, S.V., and Klein, J.T. (2010). Advances in the Neuroscience of Addiction. Atlanta, GA:  Taylor and Francis Group.
Robinson, T. E. & Berridge, K. C. (1993). The neural basis of drug craving.  Brain Research Reviews, 18, 247-291.
West, R. (2006). Theory of Addiction. Oxford: Blackwell Publishing.
West, R. (2013). Models of Addiction. Spain: Publications Office of the European Union.
West, R. and Brown, J. (2013). Theory of Addiction. Oxford: John Wiley and Sons.
Wikler, A. (1948). Research Progress In Research On The Neurophysiological Basis of Morphine Addiction. American Journal of Psychiatry. 105: 329-338.

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