Targeting cognitive-affective risk mechanisms in stress-precipitated alcohol dependence: An integrated, biopsychosocial model of automaticity, allostasis, and addiction
Introduction
Alcohol dependence remains prevalent despite a century of intervention efforts. Even with apparently efficacious behavioral and pharmacological treatments, relapse following treatment is the norm, and long-term recovery rates are low. According to the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), 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 over the past year [1]. Hence, certain risk chains leading to the development and maintenance of alcohol dependence may be intractable to extant interventions. One such pathway may involve positive feedback loops between stress appraisal, emotion dysregulation, physiological arousal, implicit cognition, and palliative coping with alcohol. As components of this stress-initiated risk chain may be malleable to novel behavioral therapies targeting cognitive-affective mediators of pathogenic gene-environment interactions, further explication of the pathways underpinning stress-precipitated alcohol dependence appears warranted.
The etiology of alcohol use disorders is multifactorial, involving interactions between genetic, environmental, interpersonal, and individual factors. Over time, as alcohol consumption becomes compulsive, automatic appetitive behaviors begin to supersede controlled, volitional alcohol use [2]. Once patterns of recurrent, heavy drinking in response to stress and negative affect are established, self-regulatory cognitive control mechanisms are hijacked by the addictive process, and consumption of alcohol is continued despite willful intent to abstain. Even repeated exposure to aversive consequences may be insufficient to prevent drinking in the alcohol dependent individual. The question of why alcohol consumption persists in spite of, and perhaps, due to, stress has been the subject of theory and scientific investigation.
Stress appears to be a key mechanism underlying alcohol dependence, intensifying alcohol consumption and precipitating relapse; indeed, persons who drink alcohol to cope with stress and negative affect evidence significantly higher rates of lifetime and current alcohol dependence symptoms than persons who drink for other reasons [3], and increases in stress can precipitate a shift towards heavy and more frequent alcohol consumption [4]. Epidemiological evidence for the link between stress and drinking behavior has been found through analyses of NESARC data. Among adult past-year drinkers, 72.5% reported experiencing at least one stressful life event in the past year, and 23.2% had experienced 3–5 such stressors [4]. Drinkers who reported experiencing six or more stressful life events had consumed more than three times the amount of daily ethanol and evidenced more than thrice the frequency of heavy drinking compared to drinkers who had not experienced life stressors in the past year [4]. Each experience of a past-year stressful life event was associated with an increase in frequency of heavy drinking by 24% for men and 13% for women, and increases in stress were associated with heavier patterns of alcohol consumption [4]. Congruent with these findings, an event-history analysis of urban, 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 even after controlling for socioeconomic status and history of psychiatric disorder, implicating a possible causal role for life stress in the etiology of alcohol use disorders [5]. Clearly, life stress is prevalent among alcohol users, and is an important correlate of heavy drinking and alcohol dependence.
Early motivational theories posited a relationship between alcohol consumption and stress. The tension reduction hypothesis, originating from animal experiments [6], claims that stressful life circumstances motivate alcohol consumption, and under such aversive or conflict-laden conditions, alcohol decreases anxiety, which then reinforces subsequent alcohol consumption [7]. This theory parallels clinical observations that alcohol is often used to “self-medicate” aversive cognitive-emotional and psychophysiological sequelae of the stress response [8]. Yet, despite its initial popularity, the tension reduction hypothesis lost favor because there was little agreement regarding the conditions under which alcohol dampens the stress response, and some aversive conditions actually decrease alcohol consumption, [9]. Inconsistent evidence of tension reduction-related drinking motivations in humans has been attributed to differences in alcohol expectancies, that is, beliefs about alcohol’s supposedly ameliorative effect on distress [10].
In an influential paper addressing the putative stress-response-dampening effects of alcohol in humans, Levenson et al. [11] raised the possibility that cognitive factors might mediate the pharmacological effects of alcohol on physiological reactivity. Concomitantly, sons of male alcoholics have been shown to exhibit heightened autonomic stress responses that are dampened by the effects of alcohol [12]; such stress-response dampening has been shown to be highly correlated with executive function deficits indicative of prefrontal cortical dysfunction in descendants of alcoholic probands [13]. Pihl, Peterson, and Finn [14] hypothesized that persons who drink alcohol to reduce stress have neurocognitive tendencies towards misattributing threatening significance to novel stimuli, resulting in augmented arousal, while exhibiting attenuated responses to stimuli that require sustained attention for processing.
The relationship between attentional factors and stress-response-dampening was addressed in Steele and Joseph’s attention-allocation model [15]. This model posited that drinking reduces stress via alcohol myopia, that is, a pharmacologically-induced impairment in controlled cognitive processing coupled with a narrowed attentional focus onto immediate internal and external cues. Such myopia is hypothesized to reduce capacity for cognitive processing of stressful content in the face of a demanding task, and to limit attention to proximal stimuli rather than to future threats. Hence, this model predicts that alcohol consumption will reduce stress when attention to stressors is restricted or divided by task demands, a prediction that has been supported by several studies [15], [16], [17], [18]. However, evidence suggests that, even without attentional manipulations, moderately high doses of alcohol can robustly reduce negative emotion [19]. Recent research has helped to reconcile this incongruity: using a social stress induction, alcohol was shown to exert direct stress-response-dampening effects on heart rate, galvanic skin response, and subjective anxiety, but the effects of drinking on stress-induced skin conductance responses were partially mediated by differences on a sustained attention task [20]. Hence, although the neuropharmacological properties of alcohol contribute to its anxiolytic effects, cognitive processes appear to be an important link in the association between stress and alcohol consumption.
Building on such earlier work, we argue that alcohol dependence is maintained, in part, by automatic and implicit cognitive processes which subvert and bypass the conscious desire to abstain from alcohol. We contend that stress and negative affect play a large role in activating appetitive automaticity and allostatic dysregulation underpinning alcohol dependence and relapse. We propose that the risk chain linking these pathogenic mechanisms may be explicated by a conceptual framework that integrates a transactional stress-coping model [21] with an allostatic model of alcohol dependence [22], a cognitive processing model of craving and compulsive alcohol use [23], and an affective processing model of negative reinforcement [24]. This integrated framework, which builds on our earlier conceptual model of stress, metacognition, and coping [25], describes a cybernetic system [26], that is, an informational circuit in which the causal flow loops back upon itself, with the output of the circuit (e.g., relapse) becoming its own input (i.e., a stressor) in further iterations of the cycle.
This article presents a new conceptual integration of formerly discrete theories of stress appraisal, neurobiological allostasis, automatic cognitive processing, and addictive behavior to explain how alcohol dependence is maintained and re-activated by stress. This conceptual framework has implications for development and implementation of innovative behavioral interventions that disrupt mechanisms underpinning stress-exacerbated dependence on alcohol.
Section snippets
The hypothetical model: An overview
According to our integrated conceptual framework (depicted in Fig. 1), the risk chain leading to stress-precipitated alcohol dependence involves a network of interlocking causal pathways between stress-reactivity, implicit cognitive operations, maladaptive cognitive control strategies, and reinforcement contingencies that organize and drive the appetitive, motivational states and drug-seeking behaviors that characterize this disorder. In brief, repeated alcohol misuse in the context of stress
Stress and cognitive appraisal activate the risk chain
Though some models of stress and addiction treat stress exposure as a monolithic concept, stress is a multicomponent process modulated by biopsychosocial factors. Among the numerous factors that influence the stress process, cognitive appraisal may be viewed as a central governor of the system. Although the stress concept derived from the physical sciences, biological organisms subjected to stressors are quite unlike inorganic objects which deform predictably and systematically under the
Conclusion
Stress appraisals coupled with an actual or perceived lack of problem-solving resources result in neurophysiological arousal, perseverative cognition, and negative affect. This reactivity may in turn trigger automatized schemata to deploy sequences of maladaptive cognitive-behavioral processes, including attentional biases towards affectively-charged stimuli, the urge to alleviate distress, and palliative coping attempts to avoid the stressor or allay its impact through impulsive behavior. When
Conflicts of interest statement
None declared.
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Cited by (0)
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ELG was supported by Grant No. T32AT003378 from the National Center for Complementary and Alternative Medicine, a Francisco J. Varela Research Grant from the Mind and Life Institute, and an Armfield-Reeves Innovation Grant from the UNC-Chapel Hill School of Social Work.
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CAB was supported by Award Number KL2RR025746 from the National Center for Research Resources. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health.