Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Research Department of Clinical, Educational and Health Psychology, University College London, London, UK.
J Child Psychol Psychiatry. 2023 Feb;64(2):289-298. doi: 10.1111/jcpp.13725. Epub 2022 Dec 13.
Despite being considered a measure of environmental risk, reported life events are partly heritable. One mechanism that may contribute to this heritability is genetic influences on sensitivity, relating to how individuals process and interpret internal and external signals. The aim of this study was to explore the genetic and environmental overlap between self-reported life events and measures of sensitivity.
At age 17, 2,939 individuals from the Twins Early Development Study (TEDS) completed measures of anxiety sensitivity (Children's Anxiety Sensitivity Index), environmental sensitivity (Highly Sensitive Child Scale) and reported their experience of 20 recent life events. Using multivariate Cholesky decomposition models, we investigated the shared genetic and environmental influences on the associations between these measures of sensitivity and the number of reported life events, as well as both negative and positive ratings of life events.
The majority of the associations between anxiety sensitivity, environmental sensitivity and reported life events were explained by shared genetic influences (60%-75%), with the remainder explained by nonshared environmental influences (25%-40%). Environmental sensitivity showed comparable genetic correlations with both negative and positive ratings of life events (r = .21 and .15), anxiety sensitivity only showed a significant genetic correlation with negative ratings of life events (r = .33). Approximately 10% of the genetic influences on reported life events were accounted for by influences shared with anxiety sensitivity and environmental sensitivity.
Differences in how individuals process the contextual aspects of the environment or interpret their own physical and emotional response to environmental stimuli may be one mechanism through which genetic liability influences the subjective experience of life events.
尽管被认为是环境风险的一种衡量标准，但报告的生活事件在一定程度上是可遗传的。一种可能导致这种遗传性的机制是遗传对敏感性的影响，这与个体如何处理和解释内部和外部信号有关。本研究旨在探讨报告的生活事件与敏感性测量之间的遗传和环境重叠。
在 17 岁时，来自双胞胎早期发展研究（TEDS）的 2939 名个体完成了焦虑敏感性（儿童焦虑敏感性指数）、环境敏感性（高度敏感儿童量表）的测量，并报告了他们最近经历的 20 个生活事件。使用多变量 Cholesky 分解模型，我们研究了这些敏感性测量与报告的生活事件数量之间的关联，以及生活事件的负面和正面评价，共同遗传和环境影响。
焦虑敏感性、环境敏感性与报告的生活事件之间的大多数关联都受到共同遗传影响的解释（60%-75%），其余则由非共享环境影响解释（25%-40%）。环境敏感性与生活事件的负面和正面评价均显示出相似的遗传相关性（r 分别为.21 和.15），而焦虑敏感性仅与生活事件的负面评价显示出显著的遗传相关性（r 为.33）。报告的生活事件中约 10%的遗传影响归因于与焦虑敏感性和环境敏感性共享的影响。
个体处理环境的上下文方面或解释自己对环境刺激的身体和情绪反应的方式的差异，可能是遗传易感性影响生活事件主观体验的一种机制。
