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Psychophysiological adaptivity and the formation of paranoid delusions.

Subject Area Personality Psychology, Clinical and Medical Psychology, Methodology
Term from 2018 to 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 407085702
 
Due to considerable negative consequences caused by paranoid symptoms and the as of yet insufficient therapeutic benefits, a better understanding of the formation of delusions is necessary. In line with vulnerability-stress-models, research available to date points towards a dysregulated stress reaction, such as an increased negative affect, increased autonomic arousal and an aberrant cortisol response. It is not yet clear, however, how exactly a maladaptive stress reaction leads to symptoms. To answer this question, the neurovisceral integration model (Thayer & Lane, 2000) provides an important basis. In this model, vagal heart rate variability (HRV) is an indicator of a flexible adaptation of the organism. Moreover, HRV is conceptualized as an index of the effectivity of cortical-peripheral feedback loops, thereby linked to the functioning of the hypothalamic-pituitary-adrenal axis and emotion regulation abilities. In healthy individuals, research showed diminished HRV to be predictive of a reduced physiological adaptivity, which was particularly evident in a reduced recovery after a stressor. For participants with psychotic disorders, several studies have shown a substantially reduced HRV when compared to healthy controls. Based on this, the present project will investigate the association between low HRV and the psychophysiological adaptivity in participants with paranoid delusions. It is expected that due to the emotion regulation deficits related to a reduced HRV, reestablishment of homeostasis after a stressor is impaired and perceptions of threat are maintained.In a sample of participants with paranoid delusions (current or past; n=50) who will be compared to healthy controls (n=50), we plan to investigate (1) whether an altered adaptivity in participants with paranoid delusions is evident in a reduced recovery from a stressor; (2) whether less efficient recovery is associated with an increased reactivity to a new stressor; and (3) which mechanisms may explain the dysfunctional recovery and stress sensitivity, respectively whether these mechanisms (i.e., predictivity of a diminished baseline HRV, mediating and moderating role of emotion regulation, increased negative affect) are associated with an increase in paranoia. To test these assumptions, the planned project involves two stressor phases (bilateral feet-cold-pressor task plus paced serial addition task), each followed by a recovery period. The first recovery period will last 60 minutes to allow for salivary cortisol recovery to baseline. Along with enhancing the understanding of mechanisms to delusion formation, the project shall contribute to a better understanding of how reduced HRV may predict psychophysiological adaptivity and symptom formation. Based on this knowledge, targeted effective therapeutic interventions (e.g., biofeedback, emotion regulation focused therapy) could be inferred.
DFG Programme Research Grants
 
 

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