Abstract
The aetiology of eating disorders (EDs) is unclear. It has been proposed that alterations in certain inflammatory processes could be a potential biological correlate of EDs, which may contribute to the development and/or maintenance of EDs. This thesis aimed to investigate the role of markers of these inflammatory mechanisms in EDs by (a) examining potential alterations in a broad range of cytokines and other inflammatory markers in people with anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED); (b) assessing whether longitudinal alterations in inflammatory markers co-occur with changes in ED psychopathology in patients with AN; and (c) exploring how stress, diet and genetic factors –all variables that have been reported to influence inflammatory marker concentrations in healthy and other clinical populations – are associated with inflammatory markers in people with EDs.The first aim was addressed in: a systematic review and meta-analysis exploring cytokine alterations in people with EDs, in comparison to healthy individuals (Chapter 2); two studies examining cross-sectional differences in inflammatory marker concentrations in people with AN and healthy comparison groups (Chapter 3); and a cross-sectional analysis of concentrations of C-reactive protein (CRP) in people with lifetime diagnoses of AN, BN, and BED (Chapter 6). The second aim was addressed in an observational longitudinal study, measuring inflammatory marker concentrations at three time points over a period of six months, in patients with AN undergoing specialist ED treatment (Chapter 4). The final aim was addressed in: three studies assessing the role of several types of event-related stress (exposure to traumatic and stressful life events, including childhood maltreatment) on inflammatory marker concentrations in people with current and/or a history of EDs (Chapter 5); two studies assessing the association between dietary inflammation (i.e., the inflammatory potential of an individual’s diet) and inflammatory markers in people with lifetime diagnoses of EDs and females with a current AN diagnosis (Chapter 6); and lastly, a nested case-control study using data from the UK Biobank, a population-based cohort, to explore the relationship between a polygenic risk score for CRP and ED status (Chapter 7).
The data provided some support for alterations of inflammatory markers, such as interleukin (IL)-6, IL-7 and C-reactive protein (CRP), as biological correlates of specific EDs; however, findings were inconsistent. It was further found that changes in certain cytokines (IL-6 and IL-7) co-occurred with improvements in ED symptoms in patients with AN, identifying possible state biomarkers of AN. Stress and the inflammatory potential of an individual’s diet were not related to concentrations of inflammatory markers in people with EDs. However, genetic factors may play a role in the relationship between inflammatory markers and EDs, as we reported that a polygenic risk score for circulating CRP was associated with having current and/or a lifetime BED diagnosis.
The findings extend current concepts related to biological correlates of EDs, and they provide direction for future research to explore the potential role of inflammatory markers as risk factors for EDs and as biomarkers of trait, state and treatment response in EDs.
| Date of Award | 1 Mar 2020 |
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| Original language | English |
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| Supervisor | Hubertus Himmerich (Supervisor), Ulrike Schmidt (Supervisor) & Gerome Breen (Supervisor) |