How do we recover?

Mindfulness training targets neurocognitive mechanisms of addiction (Part 1).

The article on the effectiveness of Mindfulness that we cite and use excerpts from today (1) was published Frontiers in Psychiatry entitled “Mindfulness training targets neurocognitive mechanisms of addiction at the attention-appraisal-emotion interface” was designated in the 93rd percentile of 3,480,147 articles tracked by Altmetric. The Altmetric score is a measure of the quality and quantity of online attention that this article has received. The paper details the model depicted below.

In this review paper, they described how mindfulness-based interventions (MBIs) may target neurocognitive mechanisms of addiction at the attention-appraisal-emotion interface.

Empirical evidence is presented suggesting that MBIs ameliorate addiction by enhancing cognitive regulation of a number of key processes, including: clarifying cognitive appraisal and modulating negative emotions to reduce perseverative cognition and emotional arousal; enhancing metacognitive awareness to regulate drug-use action schema and decrease addiction attentional bias; promoting extinction learning to uncouple drug-use triggers from conditioned appetitive responses; reducing cue-reactivity and increasing cognitive control over craving; attenuating physiological stress reactivity through parasympathetic activation; and increasing “savoring” to restore natural reward processing.

“Prominent neuroscience models suggest that addictive behavior occurs when environmental stressors and drug-relevant cues activate a cycle of cognitive, affective, and psychophysiological mechanisms, including dysregulated interactions between bottom-up and top-down neural processes, that compel the user to seek out and use drugs. Mindfulness-based interventions (MBIs) target pathogenic mechanisms of the risk chain linking stress and addiction.

Although addiction has been a subject of societal concern for millennia, over the past several decades, discoveries from cognitive and affective neuroscience have deepened our understanding of this age-old, vexing, and pernicious problem. The perspective emerging from several lines of research is one in which addiction is seen as a cycle of compulsive drug-seeking behavior fueled by dysregulated neurocognitive processes (1, 2).

Key processes implicated in addiction include motivated attention, automaticity, reward processing, emotion regulation, stress reactivity, and inhibitory control. Studies suggest that these processes arise from individual differences in broadly distributed, functionally- and anatomically-integrated, cortico-limbic-striatal circuits that subserve acquisition, maintenance, and reinstatement of addictive behaviors (3).

This review offers a novel conceptual framework with which to understand how MBIs may ameliorate addiction, with a focus on how such interventions target pathogenic cognitive, affective, and neurobiological mechanisms that contribute to addictive behavior.

This framework is first grounded in a brief description of risk chain linking cue-reactivity, implicit cognition, and dysfunctional cognitive control efforts that drives the appetitive motivational states and drug-seeking behaviors characteristic of addiction.

Next, we propose a number of hypothetical neurocognitive targets of MBIs, and critique supporting empirical evidence from extant literature on mindfulness and addiction.

To promote future research in this area, we recommend behavioral tasks and psychophysiological measures that could be used as mechanistic probes of MBI treatment effects. Finally, we suggest how our neurocognitive framework might lead to optimization of the next generation of MBIs for persons suffering from addictive disorders.

A Neurocognitive Model of Addiction

Addictive Responses Arise from Automatic Habits and Unregulated Craving and Affect

Research with animals and humans demonstrates that chronic administration of psychoactive drugs results in adaptations in multiple neurotransmitter systems in the brain, consequentially altering functional neural circuitry that governs a broad array of interactive processes (e.g., affect and reward, habit learning and memory, and cognitive control over prepotent environmental stimuli). Though the neurobiological bases of the effects of chronic drug abuse on brain-behavior relations remain to be fully elucidated, current research suggests that the dopamine system plays a critical role in the progression from drug initiation to chronic and habitual self-administration. Psychoactive drug-use induces dopaminergic activity in the ventral striatum and ventral tegmental area (11), resulting in a robust form of positive reinforcement. However, following chronic use, drug administration effects on dopamine neurotransmission are attenuated in the ventral striatal-reward pathway and potentiated in the dorsal striatal-habit learning pathway (12).

Repeated use of psychoactive substances is believed to impart motivational significance to cues associated with drug-use episodes through sensitization of mesocorticolimbic brain regions (13). As such, drug-related cues come to evoke powerful, conditioned motivational responses that may be fully dissociable from the pleasure and reward elicited by drug use (14, 15).

This conditioned response to drug-related cues (i.e., cue-reactivity), manifests as a constellation of somatic sensations coupled with a broad array of physiological reactions including autonomic, corticolimbic, corticostriatal, and neuroendocrine responses (1619). The habitual behavioral response to drug-related cues is thought to be coordinated by drug-use action schemas, i.e., memory systems that drive drug seeking and drug use through automatized sequences of stimulus-bound, context-dependent behavior (20, 21). Importantly, cue-reactivity confers compulsivity to drug-seeking behaviors, motivating the addict to consume drugs even after long periods of abstinence and despite countervailing motivations to remain abstinent, particularly in contexts that elicit unregulated stress and negative affect (1). Indeed, stress biases behavior toward habitual responding (22).

Because obtaining and consuming psychoactive substances are motivationally salient goals in addiction, drug-use action schemas stored in memory guide implicit cognitive processing of stimuli associated with previous drug-use episodes. This implicit cognitive process is manifested as a preferential focus of attention toward drug-related cues, known as addiction attentional bias (23). When attention is focused on drug-related cues, motivation for drug-use increases, which then amplifies the salience of the cues (24). Thus, addiction attentional bias and craving are mutually excitatory processes (25) that can compel drug-use even in the absence of the volition or intent to use drugs. As such, an addict may find him or herself consuming drugs without awareness of the intention to use, in much the same way other complex goal-oriented, thought-action repertoires can be engaged habitually without conscious volition by conditioned contextual cues (26).

Dysregulation of Context-Dependent Prefrontally Mediated Control in Addiction

As the addictive habit becomes more entrenched, individuals struggling with addiction experience a loss of cognitive and behavioral control. Cognitive control deficits include those affecting attentional and inhibitory control (27) and deficits in cognitive regulation of stress and affect (1). Functional neuroanatomical correlates of the effects of substance abuse include alterations in cingulate and prefrontal cortices (PFCs), two brain structures crucial for error monitoring (28) and inhibitory control, respectively (29). For example, compared to healthy individuals, persons with substance use disorders exhibit hypoactivation in frontal cognitive control circuitry during inhibition of cognitive interference and conflict resolution (30, 31), as well as during processing of salient emotional information (3135). Acute withdrawal further dysregulates prefrontal brain function across an array of cognitive tasks (3641). Thus, as cognitive control over behavior becomes impaired due to neurocognitive changes that occur with the development of addiction, the addict progressively loses control over the addictive habit.

As a result of these cognitive control deficits, actively addicted persons may experience an intense, overwhelming compulsion and motivation to seek and use drugs that is difficult to regulate. Moreover, persons in recovery from addiction often experience the impulse to use substances as intrusive and incongruent with their desire to remain abstinent (42). Yet, due to deficient or atrophied proactive cognitive control, such individuals may attempt to reactively inhibit this upwelling of unbidden motivational drive by employing “willpower” to suppress the urge to engage in the addictive behavior. Thus the pendulum of prefrontal regulation swings from a context of under-control to one of over-control. Through such over-control, suppression may promote relapse insofar as this cognitive strategy inadvertently results in a “rebound effect,” i.e., an increased rate of the thoughts and emotions it is directed against (43, 44). When attention is deployed in search of undesirable mental content to be suppressed (e.g., a drug craving, negative affect), the ensuing positive feedback loop leads to hyperaccessibility of unwanted cognitions (45), amplifying their frequency and intensity under conditions of stress (46). Consistent with these deleterious effects of suppression on resolving emotional conflict, neuroimaging research demonstrates that unlike reappraisal of negative emotion which involves potentiated prefrontal response coupled with attenuated amygdala response (47, 48), suppression shifts the time-course of prefrontal response (i.e., delays) while potentiating amygdala response to negative emotional information (48). Furthermore, individuals who rely on suppression as a regulatory strategy exhibit greater amygdala activation in response to negative emotional information than individuals who tend to use reappraisal (49). Thus, while hypoactivation in cognitive control circuits may result in an inability to effectively inhibit automatized addictive responses, excessive and ill-timed hyper-activation of frontal-executive resources during suppression of negative emotions and urges may also fail to resolve emotional conflict. In contrast to context-dependent forms of prefrontal regulation that sensitively accommodate extant cognitive contexts to challenging mental contents (i.e., reappraisal), the use of suppression to rid oneself of craving or affective states once they have already arisen is costly in terms of neurocognitive resources and likely to fail.

This failure to resolve conflict between emotional drives (e.g., craving) and higher-order goals (e.g., the goal of abstinence) during attempted suppression may further bias cognitive processing toward drug-related cues and mental contents, inadvertently increasing attention to substance-related thoughts and urges (50, 51). Consequently, suppression of thoughts of substance use leads to greater enactment of consummatory behaviors (52, 53). When addictive urges are chronically suppressed over time, the neurocognitive resources for self-regulation are depleted, resulting in an inability to inhibit substance-related cognitions and an attentional bias toward drug-related cues (54). Ultimately, regulatory resource depletion that occurs during sustained suppression of urges may contribute to relapse.

Summary of the Neurocognitive Model of Addiction

In sum, the maintenance of drug addiction is a manifold process, putatively subserved via dysregulation within and between multiple, dynamic neurocognitive processes. Though not an exhaustive model of the time-course of addiction, we focus here on three primary systems where neuroscience models of addiction from the extant literature converge to shed light on dysregulated behavioral control: (1) habit responding-automaticity (Figure 1A), (2) unregulated craving (Figure1B), and (3) unregulated affect (Figure 1C). First, habitual or automatized drug-taking behavior is related to transfer from ventral to dorsal striatal mediation of motor commands, hyperactivity in ACC in response to drug-related cues, and weakened functional connectivity between a PFC-parietal attention network and striatal circuitry. Secondly, unregulated craving may result from disrupted feedback from the fronto-parietal attention network to broadly distributed yet highly interconnected circuits involved in contextual learning (hippocampus), interoception (insula), emotional reactivity and conditioning (amygdala), appraisal of emotionally salient stimuli (medial frontal cortex: MFC), emotion regulation and decision making (orbital-frontal cortex: OFC), and attention and conflict resolution (dorsal anterior cingulate cortex; dACC). Thirdly, unregulated affect may similarly result from dysfunctional fronto-parietal network feedback response, but in this context, ineffectively modulating amygdala reactivity to negative emotional information and ventral striatum (nucleus accumbens) during reward processing, coupled with aberrant ACC response. Common to all three dysregulated neural circuits are: (1) hyper-involvement of the dACC in the dysfunctional process, and (2) hypo-involvement of a fronto-parietal attention network necessary for exerting top-down regulation.”

We explore this articles suggestions on how mindfulness training targets neurocognitive mechanisms of addiction in Part 2 of this blog.

References

1. Garland, E. L., Froeliger, B., & Howard, M. O. (2013). Mindfulness  training targets neurocognitive mechanisms of addiction at the attention-appraisal-emotion interface. Frontiers in psychiatry, 4.

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