School of Psychological Sciences, University of Indianapolis, 1400 East Hanna Avenue, Indianapolis, IN 46227, United States.
Department of Psychology, Indiana University-Purdue University Indianapolis, 402 N. Blackford St., LD 100E, Indianapolis, IN 46202, United States.
Brain Behav Immun. 2014 Oct;41:101-8. doi: 10.1016/j.bbi.2014.04.004. Epub 2014 May 22.
Because few studies have examined depression facets or potential moderators of the depression-inflammation relationship, our aims were to determine whether particular depressive symptom clusters are more strongly associated with C-reactive protein (CRP) levels and whether race/ethnicity moderates these relationships. We examined data from 10,149 adults representative of the U.S. population (4858 non-Hispanic White, 1978 non-Hispanic Black, 2260 Mexican American, 1053 Other Hispanic) who participated in the cross-sectional National Health and Nutrition Examination Survey between 2005 and 2010. Depressive symptoms were assessed by the Patient Health Questionnaire-9, and high-sensitivity serum CRP was quantified by latex-enhanced nephelometry. Total (p<.001), somatic (p<.001), and nonsomatic (p=.001) depressive symptoms were each positively related to serum CRP in individual models. However, in the simultaneous model that included both symptom clusters, somatic symptoms (p<.001), but not nonsomatic symptoms (p=.98), remained associated with serum CRP. Evidence of moderation by race/ethnicity was also observed, as six of the nine depressive symptoms×race/ethnicity interactions were significant (ps<.05). Among non-Hispanic Whites, the pattern of results was identical to the full sample; only somatic symptoms (p<.001) remained related to serum CRP in the simultaneous model. No relationships between total, somatic, or nonsomatic symptoms and serum CRP were observed among the non-Hispanic Black, Mexican American, or Other Hispanic groups. Our findings indicate that the link between depressive symptoms and systemic inflammation may be due to the somatic symptoms of sleep disturbance, fatigue, appetite changes, and psychomotor retardation/agitation and may be strongest among non-Hispanic Whites.
由于很少有研究检查抑郁方面或抑郁与炎症关系的潜在调节因素,我们的目的是确定特定的抑郁症状群是否与 C 反应蛋白 (CRP) 水平更密切相关,以及种族/民族是否调节这些关系。我们研究了代表美国人口的 10149 名成年人的数据(4858 名非西班牙裔白人、1978 名非西班牙裔黑人、2260 名墨西哥裔美国人、1053 名其他西班牙裔),他们参加了 2005 年至 2010 年期间的横断面全国健康和营养检查调查。抑郁症状采用患者健康问卷-9 进行评估,高敏血清 CRP 采用乳胶增强比浊法进行定量。在个体模型中,总(p<.001)、躯体(p<.001)和非躯体(p=.001)抑郁症状均与血清 CRP 呈正相关。然而,在包括两个症状群的同时模型中,只有躯体症状(p<.001),而非躯体症状(p=.98)与血清 CRP 仍然相关。种族/民族的调节作用也有证据,因为九个抑郁症状×种族/民族相互作用中有六个具有统计学意义(p<.05)。在非西班牙裔白人群体中,结果模式与全样本相同;只有躯体症状(p<.001)在同时模型中与血清 CRP 相关。在非西班牙裔黑人群体、墨西哥裔美国人群体或其他西班牙裔群体中,没有观察到总症状、躯体症状或非躯体症状与血清 CRP 之间的关系。我们的研究结果表明,抑郁症状与全身炎症之间的联系可能是由于睡眠障碍、疲劳、食欲变化和精神运动迟缓和激越等躯体症状引起的,并且在非西班牙裔白人群体中可能最强。