Miller Gregory E, Stetler Cinnamon A, Carney Robert M, Freedland Kenneth E, Banks William A
Department of Psychology, Washington University, St. Louis, Missouri 63130, USA.
Am J Cardiol. 2002 Dec 15;90(12):1279-83. doi: 10.1016/s0002-9149(02)02863-1.
Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 +/- 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 +/- 0.5 vs 2.5 +/- 5 mg/L, p = 0.04) and interleukin-6 (3.0 +/- 0.3 vs 1.9 +/- 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers. These findings indicate that in otherwise healthy adults, depression is associated with heightened expression of inflammatory markers implicated in the pathogenesis of CHD. Increased body mass appears to be partially, although not completely, responsible for this relation.
尽管越来越多的证据表明,精神抑郁症会增加心脏发病和死亡的风险,但对于这种关联背后的机制却知之甚少。本研究调查了抑郁症与冠心病(CHD)发病机制中涉及的炎症风险标志物表达之间的关系。招募了100名成年人(68%为女性,48%为白种人,48%为非裔美国人,平均年龄30±2岁)。50名受试者符合临床抑郁症的诊断标准;其余50名是在人口统计学上匹配的对照组,无精神疾病史。所有受试者健康状况良好,定义为除口服避孕药外,无急性传染病、慢性疾病或常规药物治疗方案。与对照组相比,抑郁症患者的炎症标志物C反应蛋白(3.5±0.5 vs 2.5±5 mg/L,p = 0.04)和白细胞介素-6(3.0±0.3 vs 1.9±0.2 pg/ml,p = 0.007)水平显著更高。旨在确定促成这种关联途径的中介分析表明,吸烟、巨细胞病毒或肺炎衣原体的亚临床感染均与此无关。然而,抑郁症患者的体重比对照组更大,分析结果表明肥胖在临床抑郁症与炎症标志物表达增加之间的关系中占了一部分原因。这些发现表明,在其他方面健康的成年人中,抑郁症与冠心病发病机制中涉及的炎症标志物表达增加有关。体重增加似乎部分(尽管不是全部)导致了这种关系。