Disease model of addiction

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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]

Criticism[edit]

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:

See also[edit]

References[edit]

  1. ^ McLellan et al., Addiction is a Chronic Brain Disease (2000). Archived at the National Institute on Drug Abuse website.
  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. 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. ^ Tatarsky, Andrew (24 April 2003). "Harm reduction psychotherapy: Extending the reach of traditional substance use treatment". Journal of Substance Abuse Treatment 25: 249–256. doi:10.1016/s0740-5472(03)00085-0. Retrieved 11 July 2011.