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=4,382). 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.

中文翻译：

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童年的不良经历和晚年的抑郁症状：炎症的纵向中介效应

背景 童年不良经历 (ACE) 与炎症和抑郁症有关。然而，很少有研究使用纵向数据研究炎症作为 ACE 与晚年抑郁症关联的可能生物学机制的作用。本研究调查了炎症在老年人 ACE 与抑郁症状之间的关系中的纵向中介作用。方法 我们利用了英国老龄化纵向研究 (N=4,382) 的数据。在第 3 波 (2006/07) 中对 ACE（即威胁、家庭功能障碍、亲子关系低下、失去经历）进行了回顾性评估。在第 2 (2004/05)、第 4 (2008/09) 和第 6 (2012/13) 波测量 C 反应蛋白 (CRP)，一种炎症标志物。从第 6 波到第 8 波（2016/17）确定了抑郁症状。中介分析是使用平行过程潜在增长曲线模型进行的。结果 ACEs 累积暴露量越大，基线时的 CRP 和抑郁症状越高（βCRPi=0.066[0.030-0.102]；βDEPi=0.149[0.115-0.183]）并且随着时间的推移而增加（βCRPs=0.205[0.095-0. βDEPs=0.355[0.184-0.526])。基线 CRP 水平与基线抑郁症状 (βDEPi=0.145[0.104-0.186]) 及其轨迹 (βDEPs=0.215[0.124-0.306]) 呈正相关。中介分析表明，较高的基线 CRP 水平分别介导了 ACE 累积暴露对基线值和抑郁症状变化的总影响的 7% 和 5%。与其他类型的 ACE 相比，损失体验的这些中介效应（即分别为 20% 和 12%）更大。此外，它们独立于可能的混杂因素和其他中介因素，包括成人社会经济地位和生活方式因素。结论 ACE 与较高的抑郁症状相关，部分是通过升高的 CRP 水平。炎症可能是 ACE 与抑郁症之间联系的潜在心理生物学机制之一。预防和减少 ACE 负面影响的社会心理和行为干预可能有助于降低人群中炎症和抑郁的风险。