累积终生压力暴露与白细胞端粒长度损耗：压力持续时间和暴露时机的独特作用。
Cumulative lifetime stress exposure and leukocyte telomere length attrition: The unique role of stressor duration and exposure timing.
机构信息
Department of Psychiatry, University of California, San Francisco, CA, USA.
Department of Psychiatry, University of California, San Francisco, CA, USA.
出版信息
Psychoneuroendocrinology. 2019 Jun;104:210-218. doi: 10.1016/j.psyneuen.2019.03.002. Epub 2019 Mar 5.
BACKGROUND
Stress exposure occurring across the lifespan increases risk for disease, potentially involving telomere length shortening. Stress exposure during childhood and adulthood has been cross-sectionally linked with shorter telomere length. However, few longitudinal studies have examined telomere length attrition over time, and none have investigated how stressor duration (acute life events vs. chronic difficulties), timing (childhood vs. adulthood), and perceived severity may be uniquely related to telomere length shortening.
METHODS
To address these issues, we administered a standardized instrument for assessing cumulative lifetime stress exposure (Stress and Adversity Inventory; STRAIN) to 175 mothers of children with Autism Spectrum Disorder or neurotypical children and measured their leukocyte telomere length (LTL) at baseline and 2 years later.
RESULTS
Greater count of lifetime stressors was associated with shorter LTL at baseline and greater LTL attrition over time. When separating lifetime stressors into acute life events and chronic difficulties, only greater count of chronic difficulties significantly predicted shorter baseline LTL and greater LTL attrition. Similarly, when examining timing of stressor exposure, only greater count of chronic childhood difficulties (age < 18) significantly predicted shorter baseline LTL and greater LTL attrition over the 2-year period in mid-life. Importantly, these results were robust while controlling for stressors occurring during the interim 2-year period. Post-hoc analyses suggested that chronic difficulties occurring during earlier childhood (0-12 years) were associated with greater LTL attrition. Cumulative stressor severity predicted LTL attrition in a parallel manner, but was less consistently associated with baseline LTL.
CONCLUSIONS
These data are the first to examine the effects of different aspects of cumulative lifetime stress exposure on LTL attrition over time, suggesting that accumulated chronic difficulties during childhood may play a unique role in shaping telomere shortening in midlife.
背景
一生中经历的压力暴露会增加患病风险，这可能涉及端粒长度缩短。儿童期和成年期的压力暴露与端粒长度缩短呈横断面相关。然而，很少有纵向研究考察随着时间的推移端粒长度的消耗，也没有研究调查压力源持续时间（急性生活事件与慢性困难）、时间（儿童期与成年期）和感知严重程度如何与端粒长度缩短有独特的关系。
方法
为了解决这些问题，我们向 175 名自闭症谱系障碍或神经典型儿童的母亲发放了一份评估终生应激暴露的标准化量表（应激和逆境量表；STRAIN），并在基线和 2 年后测量了她们的白细胞端粒长度（LTL）。
结果
一生中应激源的数量与基线时的 LTL 较短和随时间的 LTL 消耗增加有关。当将一生中的应激源分为急性生活事件和慢性困难时，只有慢性困难的数量较多显著预测了基线时的 LTL 较短和随时间的 LTL 消耗增加。同样，当检查应激源暴露的时间时，只有慢性儿童期困难（年龄<18 岁）的数量较多显著预测了中年期 2 年内的基线 LTL 较短和随时间的 LTL 消耗增加。重要的是，这些结果在控制了中间 2 年内发生的应激源后仍然稳健。事后分析表明，早期儿童期（0-12 岁）发生的慢性困难与 LTL 消耗增加有关。累积应激源严重程度以类似的方式预测 LTL 消耗，但与基线 LTL 的相关性不太一致。
结论
这些数据首次研究了不同方面的终生累积应激暴露对随时间推移的 LTL 消耗的影响，表明儿童期累积的慢性困难可能在塑造中年期的端粒缩短方面发挥独特作用。
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