Adverse childhood experiences and depressive symptoms in later life: Longitudinal mediation effects of inflammation
Adverse childhood experiences and depressive symptoms in later life: Longitudinal mediation effects of inflammation
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DOI：
10.1016/j.bbi.2020.07.045
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发表时间：
2020-11-01
影响因子：
15.1
通讯作者：
Steptoe, Andrew
中科院分区：
文献类型：
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作者：
Iob, Eleonora;Lacey, Rebecca;Steptoe, Andrew
背景：不良童年经历（ACE）与炎症和抑郁症有关。然而，很少有研究使用纵向数据来检验炎症作为 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 与抑郁症状之间关系中的纵向中介效应。方法：我们利用英国老龄化纵向研究 (N = 4382) 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、失去经历）进行了回顾性评估。反应蛋白（CRP）是一种炎症标志物，在第 2 波（2004/05）、第 4 波（2008/09）和第 6 波（2012/13）进行了测量。抑郁症状是从第 6 波至第 8 波（2016/17）确定的。使用并行过程潜在生长曲线模型进行中介分析。结果：较高的 ACE 累积暴露与基线时较高的 CRP 和抑郁症状相关（β(CRPi) = 0.066[0.030-0.102]；β(DEPi) = 0.149[0.115-0.183]），并且随着时间的推移而增加（β(CRPs) = 0.205[0.095-0.315]；β(DEP) = 0.355[0.184-0.526])。基线 CRP 水平与基线抑郁症状 (beta(DEPi) = 0.145[0.104-0.186]) 及其轨迹 (beta(DEPs) = 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 ACE 累积暴露对基线值和抑郁症状变化总效应的 7% 和 5%。损失经历的中介效应（分别为 20% 和 12%）比其他类型的 ACE 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 与较高的抑郁症状部分相关，部分是通过升高的 CRP 水平实现的。炎症可能是 ACE 与抑郁症之间联系的心理生物学机制之一。预防和减少 ACE 负面影响的心理社会和行为干预措施可能有助于降低人群患炎症和抑郁的风险。
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). Creactive 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 (beta(CRPi) = 0.066[0.030-0.102]; beta(DEPi) = 0.149[0.115-0.183]) and with their increase over time (beta(CRPs) = 0.205[0.095-0.315]; beta(DEPs) = 0.355[0.184-0.526]). Baseline CRP levels were positively associated with baseline depressive symptoms (beta(DEPi) = 0.145[0.104-0.186]) and their trajectory (beta(DEPs) = 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.