Stressful life events, inflammation and emotional and behavioural problems in children: A population-based study

•We test if inflammatory markers (IL-6, CRP) explain the link between adverse life events and child mental health.•Only IL-6 is associated with adverse life events.•IL-6 explains part of the path from events to later internalising symptoms.•IL-6 does not explain the opposite association (from internalising symptoms to later events)•IL-6 does not explain either direction of the link between events and externalising problems. To test the hypothesis that higher plasma levels of inflammatory markers due to exposure to adverse life events may lead to internalising and externalising symptoms in children. Using data from the Avon Longitudinal Study of Parents and Children, a general population birth cohort, we explored if inflammatory markers [serum C-reactive protein (CRP) and interleukin-6 (IL-6)] at age 9 years explain the longitudinal association between adverse life events (at ages 1–9 and 9–11 years) and internalising and externalising symptoms (at ages 9 and 11 years). Data (n = 4583) were analysed using cross-lagged panel modelling to take into account reciprocal associations and reverse causality, and path analyses to test for mediation. Gender, ethnicity, body mass index, maternal education, paternal social class and maternal depression were used as potential confounders. CRP was not associated with adverse life events. There was evidence for partial mediation by IL-6 such that exposure to adverse life events was associated with increased levels of IL-6 later, in turn associated with later internalising symptoms. These associations were robust to adjustment for confounders. IL-6 did not explain part of the opposite association, that of earlier internalising symptoms and later life events, nor did it explain either direction of the association between life events and externalising symptoms. Our findings suggest a pathway that may connect early psychosocial adversity and childhood internalising symptoms via higher plasma levels of inflammatory markers, such as IL-6.