Antonella Trotta1, Louise Arseneault1, Andrea Danese1, Terrie Moffit1,2, Avshalom Caspi1,2, Helen Fisher1; 1Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, Psychology & Neuroscience, King's College London, 2Department of Psychology & Neuroscience, Duke University
Background: Both human and animal studies suggest that childhood exposure to stress can trigger a persistent inflammatory response, similar to the response the body has in the case of physical injury. A significant etiological role for immune-related processes and inflammation has been showed also in psychosis. We hypothesized that maltreated children who also experienced psychotic symptoms at the time of inflammation assessment would show elevated high-sensitivity (hs) CRP levels. Methods: The sample included 172 children from the E-Risk Longitudinal Twin Study. Childhood victimisation was measured prospectively from birth to age 12 years. Each child was privately interviewed at age 12 about seven psychotic symptoms pertaining to delusions and hallucinations. Inflammation at age 12 was assessed based on levels of hsCRP collected through blood spots. Independent samples t-tests were conducted to calculate mean differences in age-12 hsCRP in children exposed to severe victimisation with and without psychotic symptoms and children with no exposure to victimisation with and without psychotic symptoms. Results: We found significant mean differences in hsCRP between groups. Severely victimised children with psychotic symptoms showed a significant mean elevation in hsCRP levels compared with victimised children without psychotic symptoms [t(98)=3.04, p=0.003]. In contrast, non-victimised children with psychotic symptoms showed mean hsCRP levels similar to their peers without psychotic symptoms [t(70)=0.40, p=0.687]. Conclusions: Children experiencing severe victimisation and psychotic symptoms showed significantly elevated inflammation levels. The present study therefore provides the first evidence that the origins of these abnormalities in stress-sensitive systems could be traced back to the childhood years.
