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Pathways between early life adversity and adolescent self-harm: the mediating role of inflammation in the Avon Longitudinal Study of Parents and Children (ALSPAC)

Research output: Contribution to journalArticle

Original languageEnglish
JournalJournal of Child Psychology and Psychiatry
DateAccepted/In press - 25 Jun 2019

Abstract

Background 

Adverse childhood experiences (ACEs) such as physical and emotional abuse are strongly associated with self-harm, but mechanisms underlying this relationship are unclear.  Inflammation has been linked to both the experience of ACEs and self-harm or suicide in prior research. This is the first study to examine whether inflammatory markers mediate the association between exposure to ACEs and self-harm.

Methods

Participants were 4,308 young people from the Avon Longitudinal Study of Parents and Children (ALSPAC); a population-based birth cohort in the UK. A structural equation modelling approach was used to fit a mediation model with the number of ACEs experienced between ages 0-9 years, levels of the inflammatory markers interleukin-6 and c-reactive protein measured at 9.5 years, and self-harm reported at 16 years old.

Results

The mean number of ACEs young people experienced was 1.41 (SE 0.03). Higher ACE scores were associated with an increased risk of self-harm at 16 (direct effect Relative Risk (RR) per additional ACE 1.11, 95% CI 1.05, 1.18, p<0.001). We did not find evidence of an indirect effect of ACEs on self-harm via inflammation (RR 1.00, 95% CI 1.00, 1.01, p=0.38).

Conclusions

Young people who have been exposed to ACEs are a group at high risk of self-harm. The association between ACEs and self-harm does not appear to be mediated by an inflammatory process in childhood, as indexed by peripheral levels of circulating inflammatory markers measured in childhood. Further research is needed to identify alternative psychological and biological mechanisms underlying this relationship.

    Research areas

  • self-harm, suicide, ALSPAC, adverse childhood experiences, mediation, interleukin-6, c-reactive protein, inflammation

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  • Supplementary information PDF

    Accepted author manuscript, 335 KB, PDF document

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