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      Respiratory sinus arrhythmia as a potential measure in substance use treatment-outcome studies : Psychophysiology and relapse prevention

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      Addiction
      Wiley-Blackwell

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d5256434e108">Background and Aims</h5> <p id="P1">Dysfunction of physiological regulation systems may underlie the disrupted emotional and self-regulatory processes among people with substance use disorder (SUD). This paper reviews evidence as to whether respiratory sinus arrhythmia (RSA), as a psychophysiological index of emotional regulation, could provide useful information in treatment-outcome research to provide insights into recovery processes. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d5256434e113">Methods</h5> <p id="P2">We reviewed use of RSA in clinical research and studies on SUD treatment. Search terms for the review of RSA in clinical research included respiratory sinus arrhythmia, heart rate variability, vagal, cardiac vagal control, psychophysiology, intervention, treatment, mindfulness, mind-body, mental health, substance use, chemical dependence, regulation, emotion regulation. For the review of RSA in intervention studies, we included only those that provided adequate description of psychophysiological methods, and examined RSA in the context of an intervention study. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d5256434e118">Results</h5> <p id="P3">RSA appears to be able to provide an index of self-regulatory capacity; however it has been little used in either intervention or treatment research. Of the four intervention studies included in this review, all were mindfulness-based interventions. Two studies were with substance using samples and both showed pre-post increases in RSA and related improved substance use outcomes. Two of the three studies were RCTs and both showed significant increases in RSA in the experimental compared to comparison condition. </p> </div><div class="section"> <a class="named-anchor" id="S4"> <!-- named anchor --> </a> <h5 class="section-title" id="d5256434e123">Conclusion</h5> <p id="P4">Respiratory sinus arrhythmia may be a useful index of emotional regulation in people with substance use disorder, and a potential measure of underlying mechanisms for SUD treatment studies, particularly mindfulness-based interventions. </p> </div>

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          The neuroscience of mindfulness meditation.

          Research over the past two decades broadly supports the claim that mindfulness meditation - practiced widely for the reduction of stress and promotion of health - exerts beneficial effects on physical and mental health, and cognitive performance. Recent neuroimaging studies have begun to uncover the brain areas and networks that mediate these positive effects. However, the underlying neural mechanisms remain unclear, and it is apparent that more methodologically rigorous studies are required if we are to gain a full understanding of the neuronal and molecular bases of the changes in the brain that accompany mindfulness meditation.
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            Addiction and the brain antireward system.

            A neurobiological model of the brain emotional systems has been proposed to explain the persistent changes in motivation that are associated with vulnerability to relapse in addiction, and this model may generalize to other psychopathology associated with dysregulated motivational systems. In this framework, addiction is conceptualized as a cycle of decreased function of brain reward systems and recruitment of antireward systems that progressively worsen, resulting in the compulsive use of drugs. Counteradaptive processes, such as opponent process, that are part of the normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to repeatedly drive the allostatic state. Excessive drug taking thus results in not only the short-term amelioration of the reward deficit but also suppression of the antireward system. However, in the long term, there is worsening of the underlying neurochemical dysregulations that ultimately form an allostatic state (decreased dopamine and opioid peptide function, increased corticotropin-releasing factor activity). This allostatic state is hypothesized to be reflected in a chronic deviation of reward set point that is fueled not only by dysregulation of reward circuits per se but also by recruitment of brain and hormonal stress responses. Vulnerability to addiction may involve genetic comorbidity and developmental factors at the molecular, cellular, or neurocircuitry levels that sensitize the brain antireward systems.
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              Cognitive neuroscience of self-regulation failure.

              Self-regulatory failure is a core feature of many social and mental health problems. Self-regulation can be undermined by failures to transcend overwhelming temptations, negative moods and resource depletion, and when minor lapses in self-control snowball into self-regulatory collapse. Cognitive neuroscience research suggests that successful self-regulation is dependent on top-down control from the prefrontal cortex over subcortical regions involved in reward and emotion. We highlight recent neuroimaging research on self-regulatory failure, the findings of which support a balance model of self-regulation whereby self-regulatory failure occurs whenever the balance is tipped in favor of subcortical areas, either due to particularly strong impulses or when prefrontal function itself is impaired. Such a model is consistent with recent findings in the cognitive neuroscience of addictive behavior, emotion regulation and decision-making. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Addiction
                Addiction
                Wiley-Blackwell
                09652140
                April 2016
                April 05 2016
                : 111
                : 4
                : 615-625
                Article
                10.1111/add.13232
                4801752
                26567088
                ec554101-9537-43e1-9a2c-12e70044a1f9
                © 2016

                http://doi.wiley.com/10.1002/tdm_license_1.1

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