Psychotic experiences are reported by 1 in 20 children at around 12 years of age and include paranoid thoughts, hearing or seeing things that others do not, and believing that others can read one’s mind. These experiences are often distressing and predictive of schizophrenia, other psychiatric disorders and suicide in adulthood, particularly if they persist during adolescence. Therefore, uncovering biomarkers associated with the onset and persistence of these childhood psychotic experiences is urgently required to facilitate early identification of individuals at increased risk in order to optimally target preventive interventions.

Changes in epigenetic processes, such as levels of DNA methylation, could be one potential biomarker of the emergence and persistence of childhood psychotic symptoms. These epigenetic processes have the potential to influence the degree to which our genes are expressed. Differential levels of DNA methylation at specific locations across the genome have been found between adult identical twins discordant for clinically-relevant psychosis and in a small sample of identical twin children discordant for childhood psychotic experiences. However, it is not yet known whether similar findings will be observed in a larger cohort of non-twin children, and which differences are indicative of the persistence of early psychotic symptoms. The proposed study will therefore explore whether there are specific genomic sites where levels of DNA methylation vary (at birth and across childhood) between individuals with and without psychotic experiences in childhood, and in those whose experiences persist compared to those whose experiences have remitted and those who have never had psychotic experiences.