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      Mechanisms of Behavior Change in Substance Use Disorder With and Without Formal Treatment

      1 , 2 , 2 , 3
      Annual Review of Clinical Psychology
      Annual Reviews

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          Abstract

          This article provides a narrative review of studies that examined mechanisms of behavior change in substance use disorder. Several mechanisms have some support, including self-efficacy, craving, protective behavioral strategies, and increasing substance-free rewards, whereas others have minimal support (e.g., motivation, identity). The review provides recommendations for expanding the research agenda for studying mechanisms of change, including designs to manipulate putative change mechanisms, measurement approaches that expand the temporal units of analysis during change efforts, more studies of change outside of treatment, and analytic approaches that move beyond mediation tests. The dominant causal inference approach that focuses on treatment and individuals as change agents could be expanded to include a molar behavioral approach that focuses on patterns of behavior in temporally extended environmental contexts. Molar behavioral approaches may advance understanding of how recovery from substance use disorder is influenced by broader contextual features, community-level variables, and social determinants of health.

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          Most cited references134

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          Diagnostic and Statistical Manual of Mental Disorders

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            Self-efficacy: Toward a unifying theory of behavioral change.

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              Neurobiology of addiction: a neurocircuitry analysis.

              Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction.
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                Author and article information

                Journal
                Annual Review of Clinical Psychology
                Annu. Rev. Clin. Psychol.
                Annual Reviews
                1548-5943
                1548-5951
                May 09 2022
                May 09 2022
                : 18
                : 1
                : 497-525
                Affiliations
                [1 ]Department of Psychology, University of New Mexico, Albuquerque, New Mexico, USA;
                [2 ]Center on Alcohol, Substance Use and Addictions, University of New Mexico, Albuquerque, New Mexico, USA
                [3 ]Department of Health Education & Behavior and Center for Behavioral Economic Health Research, University of Florida, Gainesville, Florida, USA
                Article
                10.1146/annurev-clinpsy-072720-014802
                35138868
                f4e50783-5bd0-4816-add4-3ae37213f116
                © 2022
                History

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