Cacioppo John T, Cacioppo Stephanie, Capitanio John P, Cole Steven W
Department of Psychology, University of Chicago, Chicago, Illinois 60637; email:
Annu Rev Psychol. 2015 Jan 3;66:733-67. doi: 10.1146/annurev-psych-010814-015240. Epub 2014 Aug 22.
Social isolation has been recognized as a major risk factor for morbidity and mortality in humans for more than a quarter of a century. Although the focus of research has been on objective social roles and health behavior, the brain is the key organ for forming, monitoring, maintaining, repairing, and replacing salutary connections with others. Accordingly, population-based longitudinal research indicates that perceived social isolation (loneliness) is a risk factor for morbidity and mortality independent of objective social isolation and health behavior. Human and animal investigations of neuroendocrine stress mechanisms that may be involved suggest that (a) chronic social isolation increases the activation of the hypothalamic pituitary adrenocortical axis, and (b) these effects are more dependent on the disruption of a social bond between a significant pair than objective isolation per se. The relational factors and neuroendocrine, neurobiological, and genetic mechanisms that may contribute to the association between perceived isolation and mortality are reviewed.
在过去二十五年多的时间里,社会孤立已被公认为人类发病和死亡的主要风险因素。尽管研究重点一直放在客观的社会角色和健康行为上,但大脑是与他人形成、监测、维持、修复和替代有益联系的关键器官。因此,基于人群的纵向研究表明,感知到的社会孤立(孤独感)是发病和死亡的风险因素,与客观的社会孤立和健康行为无关。对可能涉及的神经内分泌应激机制进行的人类和动物研究表明:(a)长期社会孤立会增加下丘脑-垂体-肾上腺皮质轴的激活;(b)这些影响更多地取决于重要配对之间社会联系的中断,而非客观孤立本身。本文综述了可能导致感知到的孤立与死亡率之间关联的关系因素以及神经内分泌、神经生物学和遗传机制。