B4283 - How are Adverse Childhood Experiences Linked to Depersonalisation Biological Mediators and Psychosocial Risk Factors - 27/03/2023

B number: 
B4283
Principal applicant name: 
Katie Daughters | University of Essex
Co-applicants: 
Evelyn Dilkes
Title of project: 
How are Adverse Childhood Experiences Linked to Depersonalisation? Biological Mediators and Psychosocial Risk Factors
Proposal summary: 

Depersonalisation disorder (DPD) is a distressing condition that typically emerges in young adulthood, characterised by detachment from one’s body and self, and/or one’s environment. Individuals with DPD retrospectively report adverse childhood experiences (ACEs) and are objectively evidenced to have a dysfunctional biological stress system. However, no research has looked at the biological mechanisms that translate ACEs into DPD later in life. Using self-report and biological data of parent-child dyads from the Avon Longitudinal Study of Parents and Children (ALSPAC), I aim to fulfil this research gap. Within the ALSPAC data, instances of childhood sexual, emotional, and physical abuse, emotional neglect and family dysfunction are reported separately by both parents (during annual assessment of the child’s development), and by the child (later in life), which can be combined, creating a measure of ACEs that doesn’t rely solely on retrospective reports. Stress system dysfunction is measured by cortisol (a stress hormone) level, interleukin-6 and C-reactive protein (measures of inflammation). At ages 12 (N = 6832), 17 (N = 5217) and 24 (N = 4021), symptoms of DPD were assessed. Using statistical modelling, I am examining whether the accumulation and the timing of childhood abuse translates into DPD symptoms, mediated by abnormal cortisol and inflammation levels. Additionally, factors with potential to provide risk for, or resilience against, developing DPD symptoms are also being evaluated to provide a comprehensive representation of how DPD symptoms may develop. These include sleep, drug use, attachment, maladaptive cognitions and social position.

Impact of research: 
The investigation of the mediating roles of cortisol and inflammation between childhood abuse and depersonalisation later in life holds extensive implications. With respect to cortisol, further research can provide insights into the underlying mechanisms of depersonalisation development. This includes investigating the relationship between cortisol levels and depersonalisation symptoms, as well as exploring statistical models such as mediated multi-level modelling to examine the role of confounding variables in the relationship between cortisol and depersonalisation. The findings can identify potential treatment targets for depersonalisation, with the possibility of informing pharmacological treatments and cognitive-behavioral therapy to develop more effective interventions. Moreover, this research has broader implications for the treatment of other stress and cortisol-related mental health conditions, such as anxiety and depression. Similarly, the investigation of low-grade, chronic inflammation's role in depersonalisation development can shed light on the relationship between inflammation and depersonalisation. Although early evidence suggests a possible association, further research can identify the extent of this relationship and pave the way for the development of interventions to treat depersonalisation. These interventions may include anti-inflammatory medications, dietary changes, or lifestyle modifications to improve treatment effectiveness. Ultimately, a finding that low-grade, chronic inflammation plays a role in depersonalisation development would contribute to the development of a new research model in studying depersonalisation, similar to how inflammation impacts depression.
Date proposal received: 
Wednesday, 8 March, 2023
Date proposal approved: 
Monday, 27 March, 2023
Keywords: 
Mental health - Psychology, Psychiatry, Cognition, Mental health, Statistical methods, Biomarkers - e.g. cotinine, fatty acids, haemoglobin, etc.