The life-process model of addiction is an outdated view that addiction is not a disease but rather a habitual response and a source of gratification and security that can be understood only in the context of social relationships and experiences. This model of addiction is in direct opposition to the disease model of addiction. The proponents of the life-process model argue that the biological mechanisms that might account for addictive behavior have not been identified and thus do not support using the term disease, preferring to emphasize the individual's ability to overcome addiction by repairing relationships and personal strength of will.[medical citation needed]
The common biological mechanisms underlying all forms of addiction – CREB and ΔFosB – were reviewed by Eric J. Nestler in a 2013 review.
^Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin Neurosci15 (4): 431–43. PMC3898681. PMID24459410. "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]"Cite uses deprecated parameters (help)