The biopsychosocial model of depersonalisation and derealisation: an updated framework

Depersonalisation (DP) and derealisation (DR) are dissociative phenomena involving detachment from the self (DP) or the external world (DR). Although relatively common, they remain under-researched, with existing studies largely limited to small clinical samples. This thesis adopts a biopsychosocial framework to investigate their development, maintenance, and severity. Chapter 1 reviews literature on DPDR, focusing on adverse childhood experiences (ACEs) and associated biological processes. The definition of ACEs was broadened beyond abuse and neglect to include household instability, emphasising the need to assess both individual ACE types and cumulative ACE clusters. The importance of distinguishing between DP and DR, and of considering secondary factors influencing DPDR, is highlighted. Using participant data from the Avon Longitudinal Study of Parents and Children (ALSPAC; N = 7,906), Chapter 2 examines ACEs in the first 11 years as predictors of DP and DR at ages 12, 17, and 24. Potential mediators (attachment, depression, anxiety, and perseverative cognition) are tested. Longitudinal analyses suggest ACEs are associated with DPDR from adolescence through to adulthood. Chapter 3 explores biological mechanisms, assessing whether interleukin-6 (IL-6) and C-reactive protein (CRP) predict DP and DR and mediate ACE–DPDR links. Sex, ethnicity, and social position are also examined as confounders. Longitudinal analyses demonstrated that CRP predicted DR over time, and IL-6 predicted DP. Chapter 4 investigates maintenance processes through thematic analysis of 368 self-help forum posts, identifying reactivation and persistence themes. Chapter 5 evaluates whether DPDR severity follows a dose-response relationship with ACEs and compares trait rumination with hyper-reflexivity as potential cognitive processes associated with DPDR. Quantitative analyses further tested maintenance themes identified qualitatively. Taken together, findings indicated that DP and DR may have distinct aetiologies: DP is strongly predicted by diverse ACEs and childhood IL-6, while DR is linked to selective ACEs and CRP dysregulation over time. Anxiety, depression, perseverative cognition, and rumination did not mediate ACE–DPDR relationships, while hyper-reflexivity emerged as a key feature of DPDR. Maintenance of DPDR appears driven by dysregulation of core systems, cognitive triggers, and environmental reactivity, helping explain their persistence.