Targeting cognitive-affective risk mechanisms in stress-precipitated alcohol dependence: an integrated, biopsychosocial model of automaticity, allostasis, and addiction.

摘要

This paper proposes a novel hypothetical model integrating formerly discrete theories of stress appraisal, neurobiological allostasis, automatic cognitive processing, and addictive behavior to elucidate how alcohol misuse and dependence are maintained and re-activated by stress. We outline a risk chain in which psychosocial stress initiates physiological arousal, perseverative cognition, and negative affect that, in turn, triggers automatized schema to compel alcohol consumption. This implicit cognitive process then leads to attentional biases toward alcohol, subjective experiences of craving, paradoxical increases in arousal and alcohol-related cognitions due to urge suppression, and palliative coping through drinking. When palliative coping relieves distress, it results in negative reinforcement conditioning that perpetuates the cycle by further sensitizing the system to future stressful encounters. This model has implications for development and implementation of innovative behavioral interventions (such as mindfulness training) that disrupt cognitive-affective mechanisms underpinning stress-precipitated dependence on alcohol.