4.5 Article

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

Journal

JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
Volume 60, Issue 10, Pages 1094-1103

Publisher

WILEY
DOI: 10.1111/jcpp.13100

Keywords

Self-harm; suicide; Avon Longitudinal Study of Parents and Children; adverse childhood experiences; mediation; interleukin-6; C-reactive protein; Inflammation

Funding

  1. BBSRC [BB/I025263/1] Funding Source: UKRI
  2. ESRC [ES/N000498/1] Funding Source: UKRI
  3. MRC [G108/625, MC_PC_19009, MR/R004889/1, MC_UU_00011/5, MC_UU_12013/2] Funding Source: UKRI
  4. Medical Research Council [MC_PC_19009, G108/625, MC_UU_00011/5, MC_UU_12013/2, MR/R004889/1, G9815508, MC_PC_15018] Funding Source: Medline
  5. Wellcome [102215/2/13/2] Funding Source: Medline
  6. Wellcome Trust [GR067797MA, 208806/Z/17/Z] Funding Source: Medline
  7. University of Bristol [MC_UU_00011/1, MC_UU_00011/4] Funding Source: Medline
  8. MRF [MRF_MRF-058-0002-RG-MARS] Funding Source: Medline
  9. Department of Health [10/140/02] Funding Source: Medline

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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 United Kingdom. A structural equation modelling approach was used to fit a mediation model with the number of ACEs experienced between ages 0 and 9 years old (yo), levels of the inflammatory markers interleukin-6 and C-reactive protein measured at 9.5 yo, and self-harm reported at 16 yo. 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 yo (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.

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