Disease model of addiction

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The disease model of addiction describes an addiction as a disease with genetic, biological, neurological or environmental origin. [1] The traditional medical model of disease requires only an abnormal condition causing distress, discomfort or dysfunction to an affected individual. The contemporary medical model partly attributes addiction to changes in the brain's mesolimbic pathway. [2] The model also considers these diseases as a result of other biological, psychological or sociological entities, despite an incomplete understanding of their mechanisms. The common biomolecular mechanisms underlying addiction – CREB and ΔFosB – were reviewed by Eric J. Nestler in a 2013 review. [3] Genetics and mental disorders may precipitate the severity of a drug addiction. It is estimated that 50% of healthy individuals developing an addiction can trace the cause to genetic factors. [4]

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Criticism

However, the model does not come without criticisms. Critics of the model, especially those subscribed to the life-process model of addiction, believe that labelling people as addicts prevents them from developing self-control and due to social stigmas. As noted by 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. [5]

See also

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Addiction vulnerability is an individual's risk of developing an addiction during their lifetime. There are a range of genetic and environmental risk factors for developing an addiction that vary across the population. Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction; the contribution from epigenetic risk factors to the total risk is unknown. Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time can result in an addiction. In other words, anyone can become an individual with a substance use disorder under particular circumstances. Research is working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability, including all factors at work in propensity for addiction.

References

  1. "McLellan et al., Addiction is a Chronic Brain Disease (2000). Archived at the National Institute on Drug Abuse website". Archived from the original on 19 February 2013. Retrieved 28 February 2013.
  2. Leshner, Alan I., Addiction Is a Brain Disease, and It Matters, Science 3 October 1997: Vol. 278. no. 5335, pp. 45 - 47
  3. Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin Neurosci. 15 (4): 431–43. doi:10.31887/DCNS.2013.15.4/enestler. 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]
  4. "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.
  5. Tatarsky, Andrew (24 April 2003). "Harm reduction psychotherapy: Extending the reach of traditional substance use treatment" (PDF). Journal of Substance Abuse Treatment. 25 (4): 249–256. doi:10.1016/s0740-5472(03)00085-0. PMID   14693253. Archived from the original (PDF) on 27 September 2011. Retrieved 11 July 2011.