Department of Psychiatry, University of California San Diego, La Jolla, CA, USA; Sam and Rose Stein Institute for Research on Aging, University of California San Diego, La Jolla, CA, USA; Veterans Affairs San Diego Healthcare System, San Diego, CA, USA.
Sam and Rose Stein Institute for Research on Aging, University of California San Diego, La Jolla, CA, USA.
J Psychiatr Res. 2021 Feb;134:8-14. doi: 10.1016/j.jpsychires.2020.12.019. Epub 2020 Dec 13.
Premature mortality and increased physical comorbidity associated with bipolar disorder (BD) may be related to accelerated biological aging. Sleep disturbances and inflammation may be key mechanisms underlying accelerated aging in adults with BD. To our knowledge, these relationships have not been examined rigorously. This cross-sectional study included 50 adults with BD and 73 age- and sex-comparable non-psychiatric comparison (NC) subjects, age 26-65 years. Participants were assessed with wrist-worn actigraphy for total sleep time (TST), percent sleep (PS), and bed/wake times for 7 consecutive nights as well as completing scales for subjective sleep quality. Within-individual variability in sleep measures included intra-individual standard deviation (iSD) and atypicality of one evening's sleep. Blood-based inflammatory biomarkers included interleukin (IL)-6, C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). Linear regression analyses tested relationships of mean and iSD sleep variables with inflammatory marker levels; time-lagged analyses tested the influence of the previous evening's sleep on inflammation. BD participants had worse subjective sleep quality, as well as greater TST iSD and wake time iSD compared to the NC group. In all participants, higher TST iSD and lower mean PS were associated with higher IL-6 levels (p = 0.04, η = 0.042; p = 0.05, η = 0.039, respectively). Lower mean PS was associated with higher CRP levels (p = 0.05, η = 0.039). Atypicality of the previous night's TST predicted next day IL-6 levels (p = 0.05, η = 0.04). All of these relationships were present in both BD and NC groups and remained significant even after controlling for sleep medications. Overall, sleep measures and their variability may influence inflammatory markers in all adults. Thus, sleep may be linked to the inflammatory processes believed to underlie accelerated aging in BD.
生物标志物与双相障碍患者睡眠的关系
生物标志物与双相障碍患者睡眠的关系
双相障碍（BD）患者的过早死亡率和身体合并症增加可能与生物衰老加速有关。睡眠障碍和炎症可能是 BD 成人加速衰老的关键机制。据我们所知，这些关系尚未得到严格检查。本横断面研究纳入了 50 名 BD 成年患者和 73 名年龄和性别匹配的非精神科对照组（NC）患者，年龄 26-65 岁。参与者连续 7 晚佩戴腕戴式活动记录仪评估总睡眠时间（TST）、睡眠百分比（PS）和上床/起床时间，并完成主观睡眠质量量表。睡眠测量的个体内变异性包括个体内标准差（iSD）和一晚上睡眠的非典型性。基于血液的炎症生物标志物包括白细胞介素（IL）-6、C 反应蛋白（CRP）和肿瘤坏死因子-α（TNF-α）。线性回归分析测试了平均和 iSD 睡眠变量与炎症标志物水平的关系；时间滞后分析测试了前一天晚上睡眠对炎症的影响。BD 患者的主观睡眠质量较差，TST iSD 和唤醒时间 iSD 高于 NC 组。在所有参与者中，较高的 TST iSD 和较低的平均 PS 与较高的 IL-6 水平相关（p=0.04，η=0.042；p=0.05，η=0.039）。较低的平均 PS 与较高的 CRP 水平相关（p=0.05，η=0.039）。前一天晚上 TST 的非典型性预测第二天的 IL-6 水平（p=0.05，η=0.04）。所有这些关系在 BD 和 NC 组中均存在，即使在控制睡眠药物后仍具有统计学意义。
总体而言，睡眠测量及其变异性可能会影响所有成年人的炎症标志物。因此，睡眠可能与被认为导致 BD 中加速衰老的炎症过程有关。
