Cho Hyong Jin, Seeman Teresa E, Kiefe Catarina I, Lauderdale Diane S, Irwin Michael R
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, United States.
Division of Geriatrics, David Geffen School of Medicine at UCLA, United States.
Brain Behav Immun. 2015 May;46:319-26. doi: 10.1016/j.bbi.2015.02.023. Epub 2015 Feb 28.
Both sleep disturbance and social isolation increase the risk for morbidity and mortality. Systemic inflammation is suspected as a potential mechanism of these associations. However, the complex relationships between sleep disturbance, social isolation, and inflammation have not been examined in a population-based longitudinal study. This study examined the longitudinal association between sleep disturbance and systemic inflammation, and the moderating effects of social isolation on this association. The CARDIA study is a population-based longitudinal study conducted in four US cities. Sleep disturbance - i.e., insomnia complaints and short sleep duration - was assessed in 2962 African-American and White adults at baseline (2000-2001, ages 33-45years). Circulating C-reactive protein (CRP) was measured at baseline and follow-up (2005-2006). Interleukin-6 (IL-6) and subjective and objective social isolation (i.e., feelings of social isolation and social network size) were measured at follow-up. Sleep disturbance was a significant predictor of inflammation five years later after full adjustment for covariates (adjusted betas: 0.048, P=0.012 for CRP; 0.047, P=0.017 for IL-6). Further adjustment for baseline CRP revealed that sleep disturbance also impacted the longitudinal change in CRP levels over five years (adjusted beta: 0.044, P=0.013). Subjective social isolation was a significant moderator of this association between sleep disturbance and CRP (adjusted beta 0.131, P=0.002). Sleep disturbance was associated with heightened systemic inflammation in a general population over a five-year follow-up, and this association was significantly stronger in those who reported feelings of social isolation. Clinical interventions targeting sleep disturbances may be a potential avenue for reducing inflammation, particularly in individuals who feel socially isolated.
睡眠障碍和社会隔离都会增加发病和死亡风险。全身炎症被怀疑是这些关联的潜在机制。然而，睡眠障碍、社会隔离和炎症之间的复杂关系尚未在基于人群的纵向研究中得到检验。本研究考察了睡眠障碍与全身炎症之间的纵向关联，以及社会隔离对这种关联的调节作用。CARDIA研究是一项在美国四个城市进行的基于人群的纵向研究。在基线时（2000 - 2001年，年龄33 - 45岁），对2962名非裔美国人和白人成年人评估了睡眠障碍，即失眠主诉和睡眠时间短。在基线和随访时（2005 - 2006年）测量了循环C反应蛋白（CRP）。在随访时测量了白细胞介素 - 6（IL - 6）以及主观和客观社会隔离（即社会隔离感和社交网络规模）。在对协变量进行完全调整后，睡眠障碍是五年后炎症的显著预测因素（调整后的β值：CRP为0.048，P = 0.012；IL - 6为0.047，P = 0.017）。对基线CRP进行进一步调整后发现，睡眠障碍也影响了五年内CRP水平的纵向变化（调整后的β值：0.044，P = 0.013）。主观社会隔离是睡眠障碍与CRP之间这种关联的显著调节因素（调整后的β值0.131，P = 0.002）。在五年的随访中，睡眠障碍与普通人群中全身炎症加剧有关，并且这种关联在报告有社会隔离感的人群中明显更强。针对睡眠障碍的临床干预可能是减少炎症的潜在途径，特别是在那些感到社会隔离的个体中。
