Disease model of addiction: Difference between revisions
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==Criticism== |
==Criticism== |
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Critics of the disease model, particularly those who subscribe to the [[life-process model of addiction]] argue that labeling people as ''addicts'' keeps them from developing self-control and [[social stigma|stigmatizes]] them. As noted by the [[harm reduction]] specialist [[Andrew Tatarsky]]: |
Critics of the disease model, particularly those who subscribe to the [[life-process model of addiction]] argue that labeling people as ''addicts'' keeps them from developing self-control and [[social stigma|stigmatizes]] them. As noted by the [[harm reduction]] specialist [[Andrew Tatarsky]]: |
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{{cquote|The essence of this model is the pragmatic recognition that treatment must meet active substance users ‘‘where they are’’ in terms of their needs and personal goals. Thus, harm reduction approaches embrace the full range of harm-reducing goals including, but not limited to, abstinence.<ref>{{cite journal|last=Tatarsky|first=Andrew|title=Harm reduction psychotherapy: Extending the reach of traditional substance use treatment|journal=Journal of Substance Abuse Treatment|date=24 April 2003|volume=25|pages=249–256|url=http://www.harmreduction.org/downloads/Harm%20Reduction%20Psychotherapy:%20Extending%20the%20Reach%20of%20Traditional%20Substance%20Use%20Treatment.pdf|accessdate=11 July 2011|doi=10.1016/s0740-5472(03)00085-0}}</ref>}} |
{{cquote|The essence of this model is the pragmatic recognition that treatment must meet active substance users ‘‘where they are’’ in terms of their needs and personal goals. Thus, harm reduction approaches embrace the full range of harm-reducing goals including, but not limited to, abstinence.<ref>{{cite journal|last=Tatarsky|first=Andrew|title=Harm reduction psychotherapy: Extending the reach of traditional substance use treatment|journal=Journal of Substance Abuse Treatment|date=24 April 2003|volume=25|pages=249–256|url=http://www.harmreduction.org/downloads/Harm%20Reduction%20Psychotherapy:%20Extending%20the%20Reach%20of%20Traditional%20Substance%20Use%20Treatment.pdf|accessdate=11 July 2011|doi=10.1016/s0740-5472(03)00085-0|deadurl=yes|archiveurl=https://web.archive.org/web/20110927122219/http://www.harmreduction.org/downloads/Harm%20Reduction%20Psychotherapy%3A%20Extending%20the%20Reach%20of%20Traditional%20Substance%20Use%20Treatment.pdf|archivedate=27 September 2011|df=dmy-all}}</ref>}} |
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==See also== |
==See also== |
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Revision as of 09:22, 11 September 2017
The disease model of addiction describes an addiction as a disease with biological, neurological, genetic, and environmental sources of origin.[1] The traditional medical model of disease requires only that an abnormal condition be present that causes discomfort, dysfunction, or distress to the individual afflicted. The contemporary medical model attributes addiction, in part, to changes in the brain's mesolimbic pathway.[2] The medical model also takes into consideration that such disease may be the result of other biological, psychological or sociological entities despite an incomplete understanding of the mechanisms of these entities.
The common biomolecular mechanisms underlying all forms of addiction – CREB and ΔFosB – were reviewed by Eric J. Nestler in a 2013 review.[3]
Genetic factors and mental disorders can contribute to the severity of drug addiction. Approximately fifty percent of the chance a person will develop an addiction can be attributed to genetic factors.[4]
Alcoholics Anonymous contributed to the growth in popularity of the disease model of addiction through their publication of The Big Book (Alcoholics Anonymous) and press campaigns.[5]
Criticism
Critics of the disease model, particularly those who subscribe to the life-process model of addiction argue that labeling people as addicts keeps them from developing self-control and stigmatizes them. As noted by the harm reduction specialist Andrew Tatarsky:
The essence of this model is the pragmatic recognition that treatment must meet active substance users ‘‘where they are’’ in terms of their needs and personal goals. Thus, harm reduction approaches embrace the full range of harm-reducing goals including, but not limited to, abstinence.[6]
See also
References
- ^ McLellan et al., Addiction is a Chronic Brain Disease (2000). Archived at the National Institute on Drug Abuse website.
- ^ Leshner, Alan I., Addiction Is a Brain Disease, and It Matters, Science 3 October 1997: Vol. 278. no. 5335, pp. 45 - 47
- ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin Neurosci. 15 (4): 431–43. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. Here, we review the types of molecular and cellular adaptations that occur in specific brain regions to mediate addiction-associated behavioral abnormalities. These include alterations in gene expression achieved in part via epigenetic mechanisms, plasticity in the neurophysiological functioning of neurons and synapses, and associated plasticity in neuronal and synaptic morphology mediated in part by altered neurotrophic factor signaling. [emphasis in original]
- ^ "Addiction as a Disease." The National Center on Addiction and Substance Abuse. The National Center on Addiction and Substance Abuse, 23 August 2016. Web. 23 November 2016.
- ^ Russell, Christopher; Davies, John B.; Hunter, Simon C. (March 2011). "Treatment Providers' Beliefs About Addiction" (PDF). Journal of Substance Abuse Treatment. 40 (2): 150–164. doi:10.1016/j.jsat.2010.09.006. Retrieved 6 July 2017.
- ^ Tatarsky, Andrew (24 April 2003). "Harm reduction psychotherapy: Extending the reach of traditional substance use treatment" (PDF). Journal of Substance Abuse Treatment. 25: 249–256. doi:10.1016/s0740-5472(03)00085-0. Archived from the original (PDF) on 27 September 2011. Retrieved 11 July 2011.
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