PDF(Pubmed)
Abstract：
UNASSIGNED: Proinflammatory and neuroendocrine mediators are implicated in disease aetiopathogenesis. Stress increases concentrations of immune-neuroendocrine biomarkers through a complex network of brain-body signalling pathways. Suboptimal sleep further modulates these processes by altering major effector systems that sensitise the brain to stress. Given the ubiquitous, impactful nature of material deprivation, we tested for a synergistic association of financial stress and suboptimal sleep with these molecular processes.
UNASSIGNED: With data drawn from the English Longitudinal Study of Ageing (ELSA), associations were tested on 4,940 participants (~66±9.4 years) across four-years (2008-2012). Through analytical triangulation, we tested whether financial stress (>60% insufficient resources) and suboptimal sleep (≤5/≥9 hours) were independently and interactively associated with immune-neuroendocrine profiles, derived from a latent profile analysis (LPA) of C-reactive protein, fibrinogen, white blood cell counts, hair cortisol, and insulin-like growth factor-1.
UNASSIGNED: A three-class LPA model offered the greatest parsimony. After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, financial stress was associated with short-sleep cross-sectionally (RRR=1.45; 95%CI=1.18-1.79; p<0.001) and longitudinally (RRR=1.31; 95%CI=1.02-1.68; p=0.035), and it increased risk of belonging to the high-risk biomarker profile by 42% (95%CI=1.12-1.80; p=0.004). Suboptimal sleep was not related to future risk of high-risk profile membership, nor did it moderate financial stress-biomarker profile associations.
UNASSIGNED: Results advance psychoneuroimmunological knowledge by revealing how immune-neuroendocrine markers cluster in older cohorts and respond to financial stress over time. Financial stress associations with short-sleep are supported. The null role of suboptimal sleep, as exposure and mediator, in profile membership, provides valuable insight into the dynamic role of sleep in immune-neuroendocrine processes.
UNASSIGNED: With data drawn from the English Longitudinal Study of Ageing (ELSA), associations were tested on 4,940 participants (~66±9.4 years) across four-years (2008-2012). Through analytical triangulation, we tested whether financial stress (>60% insufficient resources) and suboptimal sleep (≤5/≥9 hours) were independently and interactively associated with immune-neuroendocrine profiles, derived from a latent profile analysis (LPA) of C-reactive protein, fibrinogen, white blood cell counts, hair cortisol, and insulin-like growth factor-1.
UNASSIGNED: A three-class LPA model offered the greatest parsimony. After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, financial stress was associated with short-sleep cross-sectionally (RRR=1.45; 95%CI=1.18-1.79; p<0.001) and longitudinally (RRR=1.31; 95%CI=1.02-1.68; p=0.035), and it increased risk of belonging to the high-risk biomarker profile by 42% (95%CI=1.12-1.80; p=0.004). Suboptimal sleep was not related to future risk of high-risk profile membership, nor did it moderate financial stress-biomarker profile associations.
UNASSIGNED: Results advance psychoneuroimmunological knowledge by revealing how immune-neuroendocrine markers cluster in older cohorts and respond to financial stress over time. Financial stress associations with short-sleep are supported. The null role of suboptimal sleep, as exposure and mediator, in profile membership, provides valuable insight into the dynamic role of sleep in immune-neuroendocrine processes.
摘要：
背景。促炎和神经内分泌介质与疾病的病因有关。应激通过脑-体信号通路的复杂网络增加免疫-神经内分泌生物标志物的浓度。次优睡眠通过改变使大脑对压力敏感的主要效应系统来进一步调节这些过程。鉴于无处不在，物质剥夺的影响性质，我们测试了经济压力和不理想睡眠与这些分子过程的协同关联。方法。根据英国老龄化纵向研究(ELSA)的数据，在四年(2008-2012)中，对4,940名参与者(~66±9.4岁)进行了关联测试。通过分析三角剖分，我们测试了经济压力（>60％的资源不足）和睡眠欠佳（≤5/≥9小时）是否与免疫神经内分泌状况独立且交互相关，来自C反应蛋白的潜在谱分析（LPA），纤维蛋白原，白细胞计数,头发皮质醇,和胰岛素样生长因子-1.结果。三级LPA模型提供了最大的简约性。在调整遗传倾向后，社会人口统计学，生活方式,和健康，经济压力与短睡眠相关的横截面(RRR=1.45;95CI=1.18-1.79;p<0.001)和纵向(RRR=1.31;95CI=1.02-1.68;p=0.035)，它使属于高风险生物标志物的风险增加了42％（95CI=1.12-1.80；p=0.004）。不理想的睡眠与未来高风险成员资格的风险无关，它也没有缓和财务压力-生物标志物概况的关联。讨论。结果通过揭示免疫神经内分泌标志物如何在老年队列中聚集并随着时间的推移对经济压力做出反应来提高心理神经免疫学知识。支持与短期睡眠有关的财务压力。次优睡眠的无效作用，作为暴露和调解人，在个人资料成员中，提供了有关睡眠在免疫神经内分泌过程中的动态作用的宝贵见解。
