Self-harm in young people is a major public health concern. Recent community studies indicate that up to 1 in 6 adolescents have self-harmed at some point in their lives, with the incidence rising rapidly between 10 and 16 years of age. Self-harm is distressing for individuals, their friends, families, and carers, and is associated with a range of poor outcomes in early adulthood. It is also the strongest known risk factor for suicide. Although self-harm is very common in adolescence, we know little about what causes this behaviour. A better understanding of the factors that increase the risk for self-harm, and the mechanisms through which they operate is important in order to develop more effective treatments.
Many previous studies have identified early life adversity (such as physical abuse, sexual abuse, and emotional neglect) as an important risk factor for self-harm. However we don’t yet understand how exposure to adversity can trigger later self-harm behaviour. It is known that the social environment can have an impact on internal biological processes. This is of interest as there is growing evidence to suggest that biological factors are involved in suicide and self-harm. We aim to study whether experiences of early adversity are associated with three different biological processes (inflammation, onset of puberty, and DNA methylation) and explore whether these factors are, in turn, associated with self-harm in adolescence. This work can provide a model whereby early adversity can lead to self-harm through biological pathways. This could lead to identification of potential markers of future self-harm risk, as well as possible targets for treatment, and interventions to prevent people from developing self-harm. In order to investigate these pathways, it is necessary to establish the order in which events occur. To do this requires a large sample with information collected at multiple time points from childhood to adolescence. Our research will also investigate whether associations between inflammation, puberty, DNA methylation and self-harm are causal, or whether they might be explained by other factors (known as confounding).
To date, most studies of self-harm in adolescence have been based on small clinical samples – these are highly select groups, already known to medical services. In addition, existing studies have tended to focus only on suicide attempts, but only one quarter of self-harm episodes are carried out with expressed suicidal intent. An important question is whether suicidal and non-suicidal self-harm are distinct behaviours, or part of a continuum of risk. Previous studies have explored whether there are differences in risk-factors and outcomes for these behaviours. We aim to extend this work by providing new information about whether there are differences in their genetic architecture. This work will inform future research studies of self-harm, and help to inform decisions on how self-harm should be defined.