Suzanne Dworak-Peck School of Social Work, University of Southern California, Los Angeles, California, USA.
Edward R. Roybal Institute on Aging, University of Southern California, Los Angeles, California, USA.
J Gerontol A Biol Sci Med Sci. 2023 Aug 2;78(8):1417-1426. doi: 10.1093/gerona/glac213.
Loneliness precedes the onset of cognitive impairment (CI) in older adults. Although the mechanisms through which loneliness "gets under the skin" to influence the risk of developing CI have been conceptually proposed, they are rarely empirically examined. The Evolutionary Theory of Loneliness posits that loneliness as a stressor could cause dysregulations in multiple physiological systems. The current study investigated whether inflammatory, cardiovascular, and kidney biomarkers mediate the longitudinal association between loneliness and CI.
Cross-lagged panel models were used to examine the hypothesized relationships, using 2006, 2010, and 2014 waves of data from the Health and Retirement Study (N = 7,037). Loneliness was measured with the 3-item UCLA loneliness scale. CI was assessed with the modified telephone interview for cognitive status. Biomarkers included HbA1C, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, C-reactive protein, and Cystatin C. Using a stepwise model-building approach, first, the model included only loneliness, CI, and biomarker variables; then, sociodemographic covariates were added; lastly, health status were controlled for.
In unadjusted and partially adjusted models, loneliness was associated with higher odds of worse cognitive status in an 8-year follow-up. Only HbA1C mediated the longitudinal association between loneliness and CI. However, after further controlling for health status, all associations became nonsignificant.
Examining a large number of participants and linking a limited number of biological markers with cognition and loneliness longitudinally, our empirical data did not support theoretical propositions, highlighting the critical importance of controlling for confounders in future studies examining longitudinal mediational relationships underlying loneliness and CI.
孤独感先于老年人认知障碍（CI）的发生。虽然孤独感“深入骨髓”影响发生 CI 的风险的机制已被概念化提出，但很少有经验性的检验。孤独的进化理论认为，孤独作为一种应激源可能导致多个生理系统失调。本研究调查了孤独感与 CI 之间的纵向关联是否由炎症、心血管和肾脏生物标志物介导。
使用健康与退休研究（N=7037）的 2006、2010 和 2014 年的数据进行交叉滞后面板模型，检验假设关系。孤独感采用 UCLA 孤独量表的 3 项条目进行测量。CI 采用改良电话认知状态测试进行评估。生物标志物包括 HbA1C、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、C 反应蛋白和胱抑素 C。采用逐步模型构建方法，首先，模型仅包含孤独感、CI 和生物标志物变量；然后，加入社会人口统计学协变量；最后，控制健康状况。
在未调整和部分调整的模型中，孤独感与 8 年随访中认知状态恶化的几率增加相关。只有 HbA1C 介导了孤独感与 CI 之间的纵向关联。然而，进一步控制健康状况后，所有关联均变得无统计学意义。
在对大量参与者进行检查并将有限数量的生物标志物与认知和孤独感进行纵向关联时，我们的经验数据不支持理论假设，突出了在未来研究中检查孤独感和 CI 之间的纵向中介关系时控制混杂因素的重要性。
