Here we have a comprehensive but hypothetical review of what effect mindfulness meditation may be having on the addicted brain.
First we look at areas of the brain effected in addiction and in relapse before looking at how mindfulness meditation may, via mediation based neuro plasticity alter the functioning and connectivity of these brain areas.
The authors look at addiction and mindfulness in terms of relapse vulnerability although there is mention also that mediation improves stress and emotion regulation. In fact with any type of cue based craving there is stress and emotion dysregulation implicated.
So using meditation to regulate stress and emotion appears to reduce the incidence of craving or attenuates its manifestation.
“A recently developed cognitive behavioral treatment for addiction, Mindfulness-Based Relapse Prevention (MBRP; Bowen, Chawla, & Marlatt, 2010; Witkiewitz, Marlatt, & Walker, 2005), was designed to target experiences of craving and negative affect and their role in the relapse process.
In the tradition of Mindfulness-Based Stress Reduction for chronic pain (MBSR; Kabat-Zinn, 1990) and Mindfulness-Based Cognitive Therapy for relapse to depression (MBCT; Segal, et al., 2002), MBRP integrates mindfulness meditation practices with cognitive behavioral relapse prevention skills (e.g., identifying high-risk situations; coping skills training; Marlatt & Gordon, 1985), retaining mindfulness practice as its primary focus (Bowen et al., 2010).
Other behavioral treatments that incorporate mindfulness practice, such as Acceptance and Commitment Therapy (ACT;Hayes, Strohsal, & Wilson, 1999) and Dialectical Behavior Therapy (DBT; Linehan, 1993), are similar to MBRP in that they involve practices emphasizing awareness and acceptance (Hayes, Follette, & Linehan, 2004). However ACT and DBT are dissimilar from MBRP and other mindfulness-based treatments in that they are multi-component therapies that include mindfulness as one element, rather than as the primary foundation.
The mindfulness practices in MBRP are intended to increase awareness of external triggers and internal cognitive and affective processes, increase the clients’ ability to tolerate challenging cognitive, affective, and physical experiences (Bowen et al., 2009), as well as enhance the clients’ metacognitive abilities (Teasdale et al., 2002).
Indeed, studies have shown that mindfulness practices taught in MBRP may lead to greater attentional (Chambers, Lo, & Allen, 2008) and inhibitory control (Hoppes, 2006) by teaching clients to observe challenging or uncomfortable emotional or craving states without habitually reacting.
In contrast to the various strategies commonly employed in substance abuse interventions (e.g., cognitive-behavioral interventions and twelve-step groups) such as thought-stopping, avoidance of negative or challenging experience and emotions, or reliance on will power, MBRP practices emphasize intentional awareness and acceptance of all experiences, including those that are uncomfortable or unwanted, and teach skills to better relate to these experiences. MBRP clients are taught to practice a curious and nonjudgmental approach to discomfort….rather than attempting to suppress or ameliorate the discomfort, fostering approach- vs. avoidance-based coping.
Mindfulness has been associated with reduced activation of craving-related bottom-up regions without the recruitment of the prefrontal regulatory regions that are involved in top-down processes (e.g., Way, Creswell, Eisenberger, & Lieberman, 2010; Westbrook et al., in press) suggesting that mindfulness may be operating on bottom-up when it comes to craving.
The goal of the current review is to propose hypothesized brain mechanisms that may underlie the effectiveness of MBRP. Our review builds on two recent reviews: one on the neural mechanisms of mindfulness meditation (Hölzel et al., 2011a) and the other on the neuroscience of treatments for addiction (Potenza et al., 2011).
First, we present an overview of recent data supporting the efficacy of MBRP, and of behavioral data from studies of MBRP that provide evidence in support of the hypothesized bottom-up and top-down brain mechanisms that may underlie the effectiveness of MBRP in the treatment of addictive behaviors. Second, we focus on the neurobiological correlates of addiction, addictive behavior relapse, craving, negative affect, and mindfulness meditation, with a specific focus on neuroimaging studies that have examined brain structure and function before and/or after mindfulness meditation.
Mindfulness-Based Relapse Prevention: Efficacy and Mechanisms of Change
Individuals who received these treatments reported reduced substance use or related improvements, such as reductions in craving and reduced reactivity to substance use cues (Bowen et al., 2009; Brewer et al., 2009; Vieten, Astin, Buscemi, & Galloway, 2010; Zgierska et al., 2008; see Bowen, Witkiewitz, Chawla, & Grow, 2011 for a review).
MBRP might be effective in part by reducing the subjective experience of craving potentially via … increased non-reactivity to salient craving cues by practicing acceptance (accepting the craving state) and nonjudgment (being non-critical of craving; Witkiewitz et al., in press), and by changing the way individuals respond to negative affect (Witkiewitz & Bowen, 2010). Although these changes have been observed at the level of self-reported behavior, it is hypothesized that the effects of MBRP may be observable at a neurobiological level via both top-down and bottom-up processes.
Neurobiology of Addiction
Numerous studies have identified key bottom-up and top-down processes involved in the development and maintenance of addictive behaviors (see Koob & Le Moal, 2005; Kuhn & Koob, 2010; Redish, Jensen, & Johnson, 2008). Neuroimaging studies have largely focused on two interconnected systems: the mesolimbic and the mesocortical systems, which together comprise the mesocorticolimbic system known as the brain reward system.
Regions within this system include the ventral tegmental area (VTA), the ventral striatum (including the nucleus accumbens), amygdala, and the medial prefrontal cortex (Feltenstein & See, 2008). While the neuropharmacological profiles of drugs of abuse are varied, they all share in common their ability to affect the nucleus accumbens, which is associated with reward-related processing (Di Chiara et al., 2004).
Subsequent neuroadaptations underlie compulsive drug seeking behaviors associated with abuse. For example, with repeated substance use, VTA input to the dorsal striatum (DS) is activated (Kauer & Malenka, 2007).”
The authors do not mention here that this is linked to severity of chronicity of addiction, with activation linked to more automatic or compulsive reward responding. For example this area is activated when more chronic alcoholics look at alcohol cues. Les severe individuals activate the ventral striatum, hence this shift in regions implicated in reward may also mark a shift in condition severity.
” Of particular interest within the dorsal striatum are the caudate nucleus and the putamen known for their roles in reward-based learning. This pathway from VTA to the dorsal striatum is often referred to as the habit circuit because of its vital role in conditioned learning.
…compulsive drug seeking and addiction is likely the result of bottom-up and top-down disruptions in the reward system as a whole, interacting …drive, conditioning, and inhibitory control aspects of executive functioning as coordinated by the prefrontal cortex (PFC; for overview of executive functions more generally see Cohen (2001) and Suchy (2009)…
There is consistent evidence across multiple drugs of abuse that PFC dysfunction is associated with abuse, and severity of drug use is correlated with top-down PFC dysfunction, including lack of inhibitory control and poor decision-making (for a review see Feil et al., 2010).
Neurobiology of Relapse
Most recently, a study by Cardenas and colleagues (2011) compared individuals who “relapsed” (defined as any alcohol use), in comparison to those who “abstained” (defined as no alcohol consumption) for approximately 8 months following entry to alcohol treatment using deformation-based morphometry. Individuals who relapsed had significantly smaller white matter volumes in the bilateral orbitofrontal cortex and smaller white matter … A prior study by Durazzo and colleagues (2011), found that relapsers had significantly lower total volume in the brain reward system than abstainers…
Considerable research has identified both cortical and subcortical areas of neural activation during craving (both drug cue-induced and stress-induced). The cortical areas include: the dorsolateral PFC (dlPFC) known for its role in working memory, top-down cognitive control over behavior, and executive cognitive functioning; the ventral PFC including both the ventromedial area and the orbitofrontal cortex (OFC) which are involved in evaluation and inhibition of behavior; and the cingulate cortex including the anterior portion…responsible for sustained attention, motivation, and conflict monitoring (i.e., processing of distracting events).
Subcortical structures implicated in craving include the ventral striatum (nucleus accumbens) which is a primary target of the VTA and the amygdala known for its role in stress and emotion processing (Heinz et al., 2008; Naqvi& Bechara, 2010; Sinha & Li, 2007; Wilson, Sayette, & Fiez, 2004).
Two recent meta-analyses of drug-cue activation and craving assessed using functional magnetic resonance imaging (fMRI) found that cue-related Blood Oxygen Level Dependent (BOLD) signal activation was consistently identified in the OFC, ventral striatum, and the amygdala (Chase, Eickhoff, Laird, & Hogarth, 2011). Moreover, the ventral striatum and anterior cingulate cortex (ACC) signals were associated with drug-cue reactivity and self-reported craving for nicotine, alcohol, and cocaine (Kühn & Gallinat, 2011).
Kober and colleagues (2010) found that individuals who were told to attend to the long-term consequences of smoking and overeating self-reported significantly less craving. Imaging results indicated significant dlPFC activity (as measured by BOLD) and regulation-related decreases in craving was mediated by ventral striatum activity. These results suggest that during craving, recruitment of dorsolateral PFC regions may temper craving in a top-down fashion by acting on craving-related brain regions…
A recent study by Westbrook and colleagues (in press) provided instructions similar to those in MBRP within an fMRI cue reactivity experiment. Participants were instructed to attend to smoking picture cues in two separate conditions: (1) relax and look at the pictures; or (2) “mindfully attend” to the pictures by actively and nonjudgmentally focusing on the thoughts, feelings, memories, and bodily sensations associated with the pictures.
Participants self-reported significantly less craving and distress when they were instructed to attend mindfully to smoking images, compared to when they were instructed to relax and look at the pictures. Imaging results indicated that subgenual ACC, a region typically activated during craving, showed reduced activity during mindful attention of smoking images compared to looking at the images. Importantly the reduced activity of the subgenual ACC during mindful attention was not explained by increased activity of the PFC.
Thus, neural reductions in reactivity to craving cues were observed without prefrontal top-down modulation of responses, supporting bottom-up changes. Furthermore, during mindful attention, there was significantly reduced functional connectivity between the subgenual ACC and other regions associated with craving, including the ventral striatum. These results suggest that nonjudgmental mindful attention to smoking cues may temper craving in a bottom-up fashion resulting in decreased activity in the subgenual ACC and by reducing functional coupling with other craving-related regions.
Westbrook and colleagues (in press) also found reduced functional connectivity between craving related regions (subgenual ACC and the bilateral insula) during mindful attention. The insula is associated with drug cue-induced activation in studies of cigarette, cocaine, alcohol, heroin, and marijuana craving (Filbey et al., 2009; see review by Naqvi & Bechara, 2010), which is particularly noteworthy given the well-known roles for the insula in bottom-up processing of salient stimuli. As such, it has been proposed that the insula may contribute to the somatic, interoceptive processes that result in the subjective experience of drug craving (Craig, 2009; Garavan, 2010).
More generally, research suggests that the insula plays a role in self-awareness and experiences that occur within the body in response to various stimuli, including emotional stimuli (Craig, 2009; Critchley et al., 2004; Damasio, 2000). The posterior insula provides the interoceptive representation of physiological sensations and the anterior insula is activated during subjective experiences of bodily sensations (e.g., craving) and emotions (e.g., negative affect; Craig, 2009; Kurth, Zilles, Fox, Laird, & Eickhoff, 2010). Results from resting state connectivity analyses indicated that the anterior insula is functionally connected to the ACC and mid-cingulate cortex, which together may form an emotional salience monitoring system (Taylor, Seminowicz, & Davis, 2009). As such, Naqvi and Bechara (2010) theorize that the insula may modulate the associations between brain regions activated during craving such as the ACC, amygdala, and the dorsomedial and ventromedial PFC.
Similarly, Goldstein and colleagues (2009) suggest that interoceptive awareness of the subjective experiences of drug craving (involving the insula), disadvantageous choice selection (involving the ACC), and the automaticity of drug seeking behavior in the presence of drug-cues or stimuli (involving the dorsal striatum) may explain lack of insight among individuals who relapse to substance use. One of the primary goals of a mindfulness approach is to disrupt this type of habitual stimulus-response cycle by increasing self-awareness and engaging approach versus avoidance systems in relation to triggering experiences.
Rather than a habitual avoidance-based behavior (e.g., substance use) following exposure to an aversive stimuli (e.g., negative affect), by which substance use is reinforced, clients are repeatedly exposed to challenging external and internal stimuli (e.g., substance cues) while remaining engaged with their experience. Over time, it is hypothesized that this repeated exposure without responding may reduce cue reactivity (Drummond, 1995). Based on the studies described above, we hypothesize that MBRP may be impacting the neurobiology of the habitual stimulus-response cycle from the top-down (as shown by Kober et al., 2010) and the bottom-up (as shown by Westbrook et al., in press).”
Part 2 considers how mindfulness mediation alters the functionality and connectivity of some of the brain regions mentioned above.
Witkiewitz, K., Lustyk, M. K. B., & Bowen, S. (2013). Retraining the addicted brain: A review of hypothesized neurobiological mechanisms of mindfulness-based relapse prevention. Psychology of Addictive Behaviors, 27(2), 351.
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