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 affected individual. 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]
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]
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