Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, 1240 N. 10th Street, Milwaukee, WI, USA; Epidemiology Branch, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA.
Epidemiology Branch, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA.
Psychoneuroendocrinology. 2022 Oct;144:105876. doi: 10.1016/j.psyneuen.2022.105876. Epub 2022 Jul 23.
Telomere length, a biomarker of cell division and cellular aging, has been associated with multiple chronic disease endpoints. Experienced trauma over the life course may contribute to telomere shortening via mechanisms of stress embodiment. However, it is unclear how patterns of co-occurring trauma during sensitive periods (e.g., early life) throughout the life course may influence telomere shortening. We examine the relationship between co-occurring early life trauma on adult telomere length and the extent to which adulthood trauma, socioeconomic position, and health and lifestyle factors may mediate this relationship.
We use data from a sample of participants in the Sister Study (N = 740, analytic sample: n = 602), a prospective cohort of U.S. self-identified females aged 35-74 years at enrollment (2003-2009) for whom leukocyte telomere length was measured in baseline blood samples. Participants reported their experience of 20 different types of trauma, from which we identified patterns of co-occurring early life trauma (before age 18) using latent class analysis. We estimated the direct and indirect effects of early life trauma on leukocyte telomere length using structural equation modeling, allowing for mediating adult pathways.
Approximately 47 % of participants reported early life trauma. High early life trauma was associated with shorter telomere length compared to low early life trauma (β = -0.11; 95 % CI: -0.22, -0.004) after adjusting for age and childhood socioeconomic position. The inverse association between early life trauma and adult leukocyte telomere length was largely attributable to the direct effect of early life trauma on telomere length (β = -0.12; 95 %CI: -0.23, -0.01). Mediating indirect pathways via adult trauma, socioeconomic position, and health metrics did not substantively contribute the overall association.
These findings highlight the role of patterns of co-occurring early life trauma on shortened telomere length independent of adult pathways.
端粒长度是细胞分裂和细胞衰老的生物标志物，与多种慢性疾病终点有关。生命过程中经历的创伤可能通过压力体现机制导致端粒缩短。然而，目前尚不清楚生命过程中敏感时期（如早期生活）同时发生的创伤模式如何影响端粒缩短。我们研究了早期生活中共同发生的创伤与成人端粒长度之间的关系，以及成年期创伤、社会经济地位以及健康和生活方式因素在多大程度上可能调节这种关系。
我们使用了来自姐妹研究（N=740，分析样本：n=602）的参与者的数据，这是一项在美国进行的前瞻性队列研究，招募了年龄在 35-74 岁之间的自我认定的女性（2003-2009 年入组），在基线血液样本中测量白细胞端粒长度。参与者报告了他们经历的 20 种不同类型的创伤，我们使用潜在类别分析确定了早期生活创伤（18 岁之前）的共同发生模式。我们使用结构方程模型估计早期生活创伤对白细胞端粒长度的直接和间接影响，允许存在成人途径的中介作用。
大约 47%的参与者报告了早期生活创伤。与低早期生活创伤相比，高早期生活创伤与较短的端粒长度相关（β=-0.11；95%CI：-0.22，-0.004），调整年龄和儿童社会经济地位后。早期生活创伤与成人白细胞端粒长度之间的负相关主要归因于早期生活创伤对端粒长度的直接影响（β=-0.12；95%CI：-0.23，-0.01）。通过成年创伤、社会经济地位和健康指标的中介间接途径并没有实质性地增加整体关联。
这些发现强调了共同发生的早期生活创伤模式对端粒缩短的作用，独立于成人途径。
