Using Neurofeedback to Understand the Relationship Between Stress and Alcohol Consumption

While it is well known and long acknowledged in scientific research that stress and alcohol consumption are closely linked, the actual relationship is complex, and the underlying mechanisms are only partially understood. To investigate the effects of acute stress under controlled conditions, experimental procedures, stress tests, and related paradigms are often employed. Studies on alcohol addiction generally indicate an increase in acute cravings following the experimental induction of stress. Neurologically, acute stress induction is associated with activation changes in widespread networks. In particular, research employing stress tests found increased activations in striatum, thalamus and limbic areas and deactivations in anterior cingulate cortex (ACC) as well as ventromedial prefrontal cortex (vmPFC), areas often associated with emotion regulation during stress induction. Given their role in emotion regulation, deactivations in these areas could reflect a reduction in emotional control during acute stress. Deactivation of these areas during experimentally induced stress has also been linked to problematic alcohol consumption and increased alcohol cravings. This study aims to elucidate how neurocognitive processes during stress influence alcohol cravings and consumption. To this end, participants with problematic alcohol consumption will be recruited. After having filled out various questionnaires pertaining to their biographical data, alcohol consumption and personality traits, participants will be experimentally stressed during a brain scan using functional Magnetic Resonance Imaging (fMRI). To reliably induce psychosocial stress, the ScanSTRESS test, a paradigm explicitly conceptualized for usage during MRI scanning, will be employed. Once the stress test is completed, participants will attempt to regulate their own neurological stress response through upregulation of the ACC using information about their current stress-induced brain activity (neurofeedback). Additionally, saliva samples will be regularly taken during the experiment to biologically observe the stress response through cortisol measurements. This will be followed by a 6-week follow-up phase, during which participants will be specifically asked about their alcohol cravings, alcohol consumption, and daily stress experiences. By employing real-time fMRI neurofeedback, this study creates experimental conditions in which participants can self-regulate the neural stress response of the targeted brain network. Nonspecific effects of the neurofeedback paradigm are controlled using a sham condition (Yoke-control group). Participants are randomly assigned to either the control group or the real neurofeedback group (experimental group). This approach allows for the investigation of the neural self-regulation abilities of emotional control networks and their role in the connection between stress, alcohol cravings, and drinking behavior in real life. In summary, this study aims to examine the relationship between the self-regulation abilities of neural stress responses and real-life drinking behavior. Investigators hypothesize that 1) the stress experiment significantly increases acute self-reported stress in participants, 2) specifically stress-induced patterns of neural activity, namely increased striatal and thalamic activity as well as decreased ACC activity, predict alcohol cravings and consumption, 3) the experimental neurofeedback group exhibits higher ACC activity during brain self-regulation than the control group, 4) the experimental group shows lower alcohol craving/consumption during the follow-up phase.