Few social ills are as pernicious and persistent as alcohol dependence. Despite more than a century of intervention efforts, 28.4% of persons ever treated for alcohol problems remain dependent on alcohol and 19.1% continue to exhibit alcohol abuse or subclinical dependence symptoms in the past year (
Dawson et al. 2005). Clearly, extant interventions are not effective for all alcohol misusers. Persons who drink to cope with stress have significantly higher rates of lifetime and current alcohol dependence symptoms than persons who drink for other reasons (
Schroder & Perrine 2007), and stress is known to increase risk of relapse (
Sinha 2007). Moreover, alcohol users have a comparatively high likelihood of experiencing serious life stressors: within the population of adult past-year drinkers, 72.5% reported experiencing at least one stressful life event in the past year, and 23.2% experienced 3 to 5 such stressors (
Dawson, Grant, & Ruan 2005). The experience of stressful life events significantly predicts quantity and frequency of alcohol consumption; for example, drinkers who reported experiencing six or more stressful events in the past year consumed, on average, more than three times the amount of ethanol per day than did alcohol users who denied experiencing any such stressors (
Dawson, Grant, & Ruan 2005). Congruent with such findings, an event-history analysis of 1786 young adults found that both distal and proximal exposure to stressful life events significantly predicted onset of alcohol dependence in a linear and additive fashion after controlling for socioeconomic status and history of psychiatric disorder, implicating a causal role for life stress in the etiology of the disorder (Lloyd & Turner 2008). Convergent evidence suggests that stress is a common precipitant of alcohol misuse and may play an important role in the pathogenesis of alcohol use disorders.
The central risk chain of stress-precipitated alcohol misuse, dependence, and relapse involves cognitive-affective mechanisms that may be explicated by an integrated biopsychosocial framework (for a review, see Garland, Boettiger, & Howard under review). In brief, stress appraisals coupled with deficits in coping resources result in psychophysiological reactivity, perseverative cognition, and negative affect, which in turn trigger automatized schemata to deploy sequences of maladaptive cognitive-behavioral processes that result in compulsive alcohol consumption in spite of often severe consequences for drinking.
Stress-activated engagement of alcohol use action schemata may result in implicit (i.e., unconscious) processing of salient stimuli, manifested as an involuntary attentional bias (AB) towards alcohol cues. Such alcohol approach bias is evident in visual probe tasks, in which heavy drinkers preferentially attend to alcohol cues, resulting in decreased reaction times (RTs) to probes replacing alcohol photographs presented for 500 and 2000 ms compared to probes replacing neutral photographs presented for the same duration (
Field, Mogg, Zetteler, & Bradley 2004). Conversely, although alcohol dependent patients have been shown to exhibit an AB toward alcohol cues presented for 50 ms (
Noel et al. 2006), they evidence AB away from alcohol cues presented for 500 ms (
Stormark, Field, Hugdahl, & Horowitz 1997;
Townshend & Duka 2007). Collectively, these findings suggest that alcohol dependent individuals in treatment, unlike their untreated counterparts, evince attentional disengagement from or avoidance of alcohol cues presented for longer stimulus durations (which allow for conscious mediation of attention), but continue to exhibit implicit appetitive attentional responses for short duration stimuli. Alcohol AB has been linked to subjective craving and alcohol consumption (
Field & Eastwood 2005). Moreover, among persons who drink to cope with dysphoria, stress enhances alcohol AB and craving (
Field & Powell 2007).
When attention is fixated on visual or olfactory alcohol cues, alcohol dependent individuals exhibit significant psychophysiological reactivity (
Carter & Tiffany 1999). In turn, this alcohol cue-reactivity may lead to increased craving, which can trigger alcohol consumption as a means of reducing distress. Many persons recovering from alcohol use disorders attempt to suppress cravings, which, paradoxically, can serve to increase intrusive, automatic alcohol-related cognitions (
Palfai, Monti, Colby, & Rohsenow 1997), dysphoria, and autonomic arousal (
Wenzlaff & Wegner 2000). Indeed, among alcohol dependent persons, thought suppression is negatively correlated with vagally-mediated heart rate variability (
Ingjaldsson, Laberg, & Thayer 2003), a putative index of emotion regulation and parasympathetic inhibition of stress reactions (
Thayer & Lane 2000). As thoughts of drinking intensify and are coupled with psychobiological distress, the impulse to consume alcohol as a form of palliative coping may overcome depleted self-regulation strength (
Muraven, Collins, & Nienhaus 2002;
Muraven & Shmueli 2006) leading to relapse. The attempt to avoid distress or allay its impact through compulsive alcohol consumption results in negative reinforcement conditioning that may perpetuate this cycle by further sensitizing the brain to future stressful encounters via allostatic dysregulation of neuroendocrine systems (
Koob 2003). Components of this risk chain may be especially malleable to targeted behavioral therapies.
Given that negative affect, autonomic arousal, automaticity, and attentional biases appear to be integral components of the risk chain for stress-precipitated alcohol misuse, dependence, and relapse, interventions targeting these mechanisms may hold promise for its treatment. One such intervention, mindfulness training, which originates from Buddhist traditions but has been co-opted by Western clinicians, has recently gained prominence in the psychological and medical literatures for its salutary effects on stress-related biobehavioral conditions (
Baer & Krietemeyer 2006;
Ludwig & Kabat-Zinn 2008). Mindfulness involves self-regulation of a metacognitive form of attention: a nonreactive, non-evaluative monitoring of moment-by-moment cognition, emotion, perception, and physiological state without fixation on thoughts of past or future (
Garland 2007). A growing body of research suggests that mindfulness affects implicit cognition and attentional processes (e.g.,
Jha, Krompinger, & Baime 2007;
Lutz, Slagter, Dunne, & Davidson 2008;
Wenk-Sormaz 2005) as well as heart rate variability indices of parasympathetic regulation (
Tang et al. 2009). This evidence, coupled with the knowledge that alcohol use disorders involve automaticity and attentional biases, suggests that mindfulness training may be an effective treatment for alcohol dependent persons coping with stress and dysphoria.
Mindfulness treatments may enhance clinical outcomes in substance-abusing populations. Using a nonrandomized pre-post comparison group design,
Bowen et al. (2007) found that mindfulness training of incarcerated inmates reduced post-release substance use, substance-related problems, and psychiatric symptoms to a greater extent than standard chemical dependency services offered at the prison. Other pilot studies of mindfulness-based interventions with substance abusers have found significant reductions in distress, negative affect, stress-related biomarkers, and substance use (
Marcus, Fine, & Kouzekanani 2001;
Marcus et al. 2003;
Zgierska et al. 2008). Despite this suggestive evidence that mindfulness interventions may ameliorate factors related to stress-precipitated alcohol misuse, future research should employ random assignment, as well as behavioral and psychophysiological indices of intervention-related change to overcome threats to validity and elucidate therapeutic mechanisms of action.
To that end, we conducted a pilot randomized controlled trial of a mindfulness intervention designed to disrupt cognitive, affective, and physiological risk mechanisms implicated in stress-precipitated relapse to alcohol consumption. A randomized, controlled design was used to compare the therapeutic effects of a mindfulness-oriented recovery enhancement (MORE) intervention to those of an evidence-based alcohol dependence support group (ASG) in a sample of low-income, primarily African American alcohol dependent adults recruited from a long-term, modified therapeutic community (TC).
We hypothesized that, relative to ASG, MORE would result in significantly greater decreases in perceived stress, impaired alcohol response inhibition, craving for alcohol, psychiatric symptoms, and thought suppression and significantly greater increases in mindfulness and in heart rate variability (HRV) recovery from stress-primed alcohol cues. Lastly, we hypothesized that mindfulness training would reduce alcohol AB, a presumed mechanism of change, by the intervention midpoint and prior to changes in clinical outcomes, such that, relative to ASG, MORE would result in significantly larger decreases in alcohol AB among participants with pre-treatment alcohol approach bias but not for those with baseline alcohol disengagement bias. This hypothesis was justified on the rationale that participants with pre-treatment alcohol disengagement bias entered our study with a pre-existing ability to disengage their attention from alcohol cues and would therefore exhibit a floor effect.