Wu E Lydia, LeRoy Angie S, Heijnen Cobi J, Fagundes Christopher P
Department of Psychological Sciences, Rice University, Houston, TX, USA.
Department of Symptom Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Psychoneuroendocrinology. 2021 Jun;128:105206. doi: 10.1016/j.psyneuen.2021.105206. Epub 2021 Mar 27.
Major depressive disorder (MDD) is an important contributor to the total disease burden because of its high comorbidity with chronic illnesses. Many people with high levels of depressive symptoms exhibit elevated systemic inflammation, but inflammation is not a necessary determinant of depression onset. Among those who recently experienced the death of a spouse, we investigated whether (a) inflammation assessed early in bereavement predicted future depressive symptoms and whether (b) inflammation predicted change in depressive symptoms from baseline to follow-up. Ninety-nine spousally bereaved individuals (M=68.61, SD=10.70) from a larger study were evaluated at baseline (3 months post-death) and follow-up (6 months post-death). Subjects received a venous blood draw and completed the Center for Epidemiologic Studies Depression Scale (CES-D). Stimulated T-cell derived cytokines (IL-6, TNF-α, and IFN-γ) were assessed individually and as a pro-inflammatory composite index. After controlling for confounding factors (i.e., age, sex, body mass index, race, ethnicity, anti-inflammatory medication, days since spousal death, smoking status, comorbidities), individuals with higher levels of IL-6, TNF-α, and IFN-γ at baseline exhibited more depressive symptoms (composite index, p = .05) and an increased probability of experiencing clinical levels of depression (CES-D score ≥16) (composite index, p = .04). Inflammatory levels were not predictive of change in depressive symptoms or in clinical depression status from baseline to follow-up. Among individuals who did not experience clinical levels of depression at baseline, baseline inflammatory levels predicted clinical levels of depression 3 months later (p = .03). This study provides support for an inflammatory mechanism underlying depression following bereavement. It suggests that one's inflammatory profile following a significant social stressor in older adulthood can be prognostic of depression risk months later. These findings add to our understanding of the physiological and mental health risks experienced by the bereaved population and provide insight into identifying vulnerable widow(er)s at risk for maladaptive grief coping.
重度抑郁症（MDD）因其与慢性病的高共病率，成为疾病总负担的一个重要因素。许多有高水平抑郁症状的人表现出全身炎症升高，但炎症并非抑郁症发作的必要决定因素。在那些最近经历配偶死亡的人群中，我们调查了：（a）丧亲早期评估的炎症是否能预测未来的抑郁症状；以及（b）炎症是否能预测从基线到随访期间抑郁症状的变化。来自一项更大规模研究的99名丧偶个体（M = 68.61，SD = 10.70）在基线（死亡后3个月）和随访（死亡后6个月）时接受了评估。受试者接受静脉采血，并完成流行病学研究中心抑郁量表（CES - D）。分别评估了刺激T细胞衍生的细胞因子（IL - 6、TNF - α和IFN - γ）以及作为促炎复合指数的情况。在控制了混杂因素（即年龄、性别、体重指数、种族、民族、抗炎药物、配偶死亡后的天数、吸烟状况、共病情况）后，基线时IL - 6、TNF - α和IFN - γ水平较高的个体表现出更多的抑郁症状（复合指数，p = 0.05），且出现临床水平抑郁（CES - D评分≥16）的概率增加（复合指数，p = 0.04）。炎症水平并不能预测从基线到随访期间抑郁症状或临床抑郁状态的变化。在基线时未经历临床水平抑郁的个体中，基线炎症水平可预测3个月后临床水平的抑郁（p = 0.03）。本研究为丧亲后抑郁症潜在的炎症机制提供了支持。这表明在成年后期经历重大社会应激源后的炎症特征可以预测数月后的抑郁风险。这些发现增进了我们对丧亲人群所经历的生理和心理健康风险的理解，并为识别有适应不良悲伤应对风险的易损寡妇/鳏夫提供了见解。
