Iob, E;
Lacey, R;
Steptoe, A;
(2020)
Adverse childhood experiences and depressive symptoms in later life: Longitudinal mediation effects of inflammation.
Brain, Behavior, and Immunity
, 90
pp. 97-107.
10.1016/j.bbi.2020.07.045.
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Abstract
Background: Adverse childhood experiences (ACEs) have been associated with both inflammation and depression. However, few studies have examined the role of inflammation as a possible biological mechanism underlying the association of ACEs with depression in later life using longitudinal data. This study investigated the longitudinal mediation effects of inflammation in the relationship between ACEs and depressive symptoms in older adults. / Methods: We utilised data from the English Longitudinal Study of Ageing (N = 4382). ACEs (i.e. threat, family dysfunction, low parental bonding, loss experiences) were assessed retrospectively at wave 3 (2006/07). C-reactive protein (CRP), an inflammatory marker, was measured at waves 2 (2004/05), 4 (2008/09), and 6 (2012/13). Depressive symptoms were ascertained from wave 6 to 8 (2016/17). The mediation analysis was conducted using parallel process latent growth curve modelling. / Results: Greater ACEs cumulative exposure was associated with higher CRP and depressive symptoms at baseline (βCRPi = 0.066[0.030–0.102]; βDEPi = 0.149[0.115–0.183]) and with their increase over time (βCRPs = 0.205[0.095–0.315]; βDEPs = 0.355[0.184–0.526]). Baseline CRP levels were positively associated with baseline depressive symptoms (βDEPi = 0.145[0.104–0.186]) and their trajectory (βDEPs = 0.215[0.124–0.306]). The mediation analysis indicated that higher baseline CRP levels mediated respectively 7% and 5% of the total effect of ACEs cumulative exposure on the baseline value and change in depressive symptoms. These mediation effects were larger for Loss experiences (i.e. 20% and 12% respectively) than for other types of ACEs. In addition, they were independent of possible confounders and additional mediators including adult socioeconomic position and lifestyle factors. / Conclusion: ACEs were related to higher depressive symptoms partly via elevated CRP levels. Inflammation might be one of the psychobiological mechanisms underlying the link between ACEs and depression. Psychosocial and behavioural interventions to prevent and reduce the negative impact of ACEs might help to lower the risk of inflammation and depression in the population.
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