Persistent depressive symptoms, HPA-axis hyperactivity, and inflammation: the role of cognitive-affective and somatic symptoms
Persistent depressive symptoms, HPA-axis hyperactivity, and inflammation: the role of cognitive-affective and somatic symptoms
复制标题
DOI：
10.1038/s41380-019-0501-6
复制
发表时间：
2020-05-01
影响因子：
11
通讯作者：
Steptoe, Andrew
中科院分区：
文献类型：
--
作者：
Iob, Eleonora;Kirschbaum, Clemens;Steptoe, Andrew
下丘脑-垂体-肾上腺（HPA）轴过度活跃和炎症被认为是抑郁症的主要病因。虽然荟萃分析已经证实了这种关系，但不同研究的效应量存在相当大的差异。这可能是由于这种生物系统在躯体与认知情感抑郁症状中的不同作用，这在很大程度上尚未探索。此外，迄今为止，大多数纵向研究都集中在短暂的而不是持续的抑郁症状。在目前的研究中，我们调查了头发皮质醇和血浆C-反应蛋白（CRP）与抑郁症状的纵向持久性和尺寸（认知情感与躯体）超过14年的时间使用特质状态场合（TSO）结构方程模型。这些数据来自英国老龄化纵向研究的老年人的大样本。从第1波（2002-03）到第8波（2016-17）评估抑郁症状。在第6波（2012-13）中测量毛发皮质醇（N = 4761）和血浆CRP（N = 5784）。协变量包括人口统计学、社会经济学、生活方式、慢性病和药物治疗数据。我们的结果表明，在整个研究期间，较高的皮质醇和CRP水平与持续的抑郁症状显着相关。值得注意的是，这两种生物标志物与躯体症状的关系比与认知情感症状的关系更强。与躯体症状的关联也独立于相关混杂因素。与此相反，在调整所有协变量后，它们与认知情感症状的关联很弱。这些不同的协会揭示了在未来的研究中考虑特定的影响，病理生理机制的重要性。最终，这将有可能推进抑郁症生物标志物的研究，并促进更有针对性的治疗。
Hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity and inflammation are thought to be prominent in the aetiology of depression. Although meta-analyses have confirmed this relationship, there is considerable variability in the effect sizes across studies. This could be attributed to a differential role of such biological systems in somatic versus cognitive-affective depressive symptoms which remains largely unexplored. Furthermore, most longitudinal research to date has focused on transient rather than persistent depressive symptoms. In the current study, we investigated the associations of hair cortisol and plasma C-reactive protein (CRP) with the longitudinal persistence and dimensions (cognitive-affective versus somatic) of depressive symptoms over a 14-year period using Trait-State-Occasion (TSO) structural equation modelling. The data came from a large sample of older adults from the English Longitudinal Study of Ageing. Depressive symptoms were assessed from wave 1 (2002-03) to wave 8 (2016-17). Hair cortisol (N = 4761) and plasma CRP (N = 5784) were measured in wave 6 (2012-13). Covariates included demographic, socioeconomic, lifestyle, chronic disease, and medication data. Our results revealed that higher cortisol and CRP levels were significantly associated with persistent depressive symptoms across the study period. Notably, both biomarkers exhibited stronger relationships with somatic than with cognitive-affective symptoms. The associations with somatic symptoms were also independent of relevant confounding factors. In contrast, their associations with cognitive-affective symptoms were weak after adjustment for all covariates. These distinct associations reveal the importance of considering symptom-specific effects in future studies on pathophysiological mechanisms. Ultimately, this will have the potential to advance the search for biomarkers of depression and facilitate more targeted treatments.