Hamilton Odessa S, Steptoe Andrew
Department of Behavioural Science and Health, Institute of Epidemiology and Health Care, University College London, 1-19 Torrington Place, London WC1E 7HB, UK.
medRxiv. 2024 Jul 24:2024.07.23.24310898. doi: 10.1101/2024.07.23.24310898.
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.
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.
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; <0.001) and longitudinally (RRR=1.31; 95%CI=1.02-1.68; =0.035), and it increased risk of belonging to the biomarker profile by 42% (95%CI=1.12-1.80; =0.004). Suboptimal sleep was not related to future risk of profile membership, nor did it moderate financial stress-biomarker profile associations.
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.
促炎介质和神经内分泌介质与疾病的病因发病机制有关。压力通过复杂的脑-体信号通路网络增加免疫-神经内分泌生物标志物的浓度。睡眠不足会通过改变使大脑对压力敏感的主要效应系统进一步调节这些过程。鉴于物质匮乏的普遍性和影响力，我们测试了经济压力和睡眠不足与这些分子过程之间的协同关联。
利用英国老龄化纵向研究（ELSA）的数据，对4940名参与者（约66±9.4岁）进行了为期四年（2008 - 2012年）的关联测试。通过分析三角剖分，我们测试了经济压力（资源不足>60%）和睡眠不足（≤5/≥9小时）是否与免疫-神经内分泌特征独立且交互相关，这些特征来自于对C反应蛋白、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的潜在类别分析（LPA）。
一个三类LPA模型提供了最大的简约性。在调整了遗传易感性、社会人口统计学、生活方式和健康因素后，经济压力与短期睡眠在横断面（RRR = 1.45；95%CI = 1.18 - 1.79；<0.001）和纵向（RRR = 1.31；95%CI = 1.02 - 1.68；= 0.035）上相关，并且它使属于该生物标志物特征的风险增加了42%（95%CI = 1.12 - 1.80；= 0.004）。睡眠不足与未来属于该特征类别的风险无关，也没有调节经济压力与生物标志物特征之间的关联。
研究结果通过揭示免疫-神经内分泌标志物在老年人群中的聚集方式以及随时间对经济压力的反应，推进了心理神经免疫学知识。经济压力与短期睡眠之间的关联得到了支持。睡眠不足作为暴露因素和中介因素在特征类别归属中的无效作用，为睡眠在免疫-神经内分泌过程中的动态作用提供了有价值的见解。
