In this research project, the aim is to discover the role specific brain networks play in the relationship between stress reactions and the desire for alcohol and alcohol consumption. To investigate this question, various brain imaging methods as well as cognitive tasks are combined. Various questionnaires are sampled and brain scans are conducted.

Individuals interested in participating in the study have to fulfill certain criteria...

• no serious medical or mental health diagnosis

• problematic alcohol drinking habits

• interested in improving drinking habits

  ...and undergo various non-invasive procedures

• filling out several questionnaires concerning personality and habits

• undergoing a mental performance task while being in a brain scanner (MRI)

• attempting to regulate their own brain activity while lying in the MRI scanner

• filling out an electronic diary for 6 weeks - concerning daily mood, stress, and alcohol habits

Participants will be randomly allocated to either one of 2 experimental groups. Both groups undergo the same tasks, receive the same instructions and only differ regarding some aspects of the brain self-regulation task .

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.

Inclusion Criteria:

• Age 18-65 years
• Presence of 2 to a maximum of 5 criteria for alcohol use disorder according to DSM-5
• no clinical necessity for detoxification treatment
• participants may have a moderate cannabis use disorder and tobacco use disorder
• Capacity for consent and ability to use self-assessment scales
• Sufficient knowledge of German
• Willingness to use a mobile phone with Android operating system

Exclusion Criteria:

• Lifetime diagnosis of bipolar or psychotic disorder or a substance use disorder according to Diagnostical and Statistical Manual of Mental Disorders - 5 (DSM-5) that is not alcohol, cannabis, or tobacco use disorder
• Current substance use other than cannabis and tobacco
• Current diagnosis of one of the following conditions according to DSM-5: (hypo)manic episode, major depression, generalized anxiety disorder, post-traumatic stress disorder, borderline personality disorder, or obsessive-compulsive disorder
• History of severe head trauma or other severe central neurological disorders (dementia, Parkinson's disease, multiple sclerosis)
• Pregnancy or lactation
• Use of medications known to interact with the central nervous system within the last 10 days; testing at least four half-lives after the last dose
• Exercising the prerogative of the "Right not to know" in the context of incidental findings during an examination or investigation

There will be collaborative data processing, sharing of data and storage of data at different locations as specified below.

Research data will be stored on secure servers of the Center for Information Services and High-Performance Computing at the Dresden University of Technology (ZIH; Zellescher Weg 12, 01069 Dresden) and the ZI Mannheim. The data will be retained for 10 years after the completion or termination of the research project. Participants' data will be protected against unauthorized access, and anonymization will occur once the research purpose allows it. Data will be deleted at the latest after 10 years.

Coding method: Double coding, access by project staff, emergency decoding possible during the project duration (MRT scans).

Transfer of pseudonymized biomaterials/data to third parties: Name: Dresden University of Technology Address: Zellescher Weg 19, 01069 Dresden. There will be a transfer of pseudonymized saliva samples for cortisol level determination.

The biomaterials will be destroyed immediately after the completion of the work. All other data will become available at the start of the study and will be deleted 10 years after the completion of the study. Data sharing will not be possible 10 years after completion of the study.

Next to the investigator and participants, research assistants as well as medical technical radiology assistants (MTRAs) will be blinded to the conditions. Only after the 6-week long ecological momentary assessment is completed are participants as well as investigators, MTRAs and research assistants debriefed concerning the participants group assignment (experimental or Yoke-control group).