Amsterdam Public Health Research Institute, Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands.
Brain Behav Immun. 2018 Oct;73:493-503. doi: 10.1016/j.bbi.2018.06.013. Epub 2018 Jun 18.
This study examined 1) the cross-sectional relationships between symptoms of depression/anxiety and immunometabolic risk factors, and 2) whether these relationships might be explained in part by cardiac vagal activity.
Data were drawn from the Adult Health and Behavior registries (n = 1785), comprised of community dwelling adults (52.8% women, aged 30-54). Depressive symptoms were measured with the Center for Epidemiological Studies Depression Scale (CES-D) and the Beck Depression Inventory-II (BDI-II), and anxious symptoms with the Trait Anxiety scale of the State-Trait Anxiety Inventory (STAI-T). Immunometabolic risk factors included fasting levels of triglycerides, high-density lipoproteins, glucose, and insulin, as well as blood pressure, waist circumference, body mass index, C-reactive protein, and interleukin-6. Measures of cardiac autonomic activity were high- and low-frequency indicators of heart rate variability (HRV), standard deviation of normal-to-normal R-R intervals, and the mean of absolute and successive differences in R-R intervals.
Higher BDI-II scores, in contrast to CES-D and STAI-T scores, were associated with increased immunometabolic risk and decreased HRV, especially HRV likely reflecting cardiac vagal activity. Decreased HRV was also associated with increased immunometabolic risk. Structural equation models indicated that BDI-II scores may relate to immunometabolic risk via cardiac vagal activity (indirect effect: β = .012, p = .046) or to vagal activity via immunometabolic risk (indirect effect: β = -.015, p = .021).
Depressive symptoms, as measured by the BDI-II, but not anxious symptoms, were related to elevated levels of immunometabolic risk factors and low cardiac vagal activity. The latter may exhibit bidirectional influences on one another in a meditational framework. Future longitudinal, intervention, an nonhuman animal work is needed to elucidate the precise and mechanistic pathways linking depressive symptoms to immune, metabolic, and autonomic parameters of physiology that predispose to cardiovascular disease risk.
本研究考察了 1）抑郁/焦虑症状与免疫代谢危险因素之间的横断面关系，以及 2）这些关系是否部分可以通过心脏迷走神经活动来解释。
数据来自成人健康和行为登记处（n=1785），包括社区居住的成年人（52.8%为女性，年龄 30-54 岁）。使用流行病学研究中心抑郁量表（CES-D）和贝克抑郁量表第二版（BDI-II）测量抑郁症状，使用状态特质焦虑量表（STAI-T）的特质焦虑量表测量焦虑症状。免疫代谢危险因素包括空腹甘油三酯、高密度脂蛋白、血糖和胰岛素水平，以及血压、腰围、体重指数、C 反应蛋白和白细胞介素-6。心脏自主活动的测量指标包括心率变异性（HRV）的高频和低频指标、正常到正常 R-R 间隔的标准差以及 R-R 间隔的绝对和连续差值的平均值。
与 CES-D 和 STAI-T 评分相比，BDI-II 评分较高与免疫代谢风险增加和 HRV 降低有关，尤其是 HRV 可能反映心脏迷走神经活动。HRV 降低也与免疫代谢风险增加有关。结构方程模型表明，BDI-II 评分可能通过心脏迷走神经活动与免疫代谢风险相关（间接效应：β=0.012，p=0.046），也可能通过免疫代谢风险与迷走神经活动相关（间接效应：β=-0.015，p=0.021）。
BDI-II 测量的抑郁症状，而不是焦虑症状，与免疫代谢危险因素水平升高和心脏迷走神经活动降低有关。在后一种情况下，它们可能在中介框架中彼此表现出双向影响。未来需要进行纵向、干预和非人类动物研究，以阐明将抑郁症状与易患心血管疾病风险的免疫、代谢和自主生理参数联系起来的确切和机制途径。
