Shalev Idan, Belsky Jay
Department of Biobehavioral Health, Pennsylvania State University, University Park, PA, USA.
Department of Human Ecology, University of California, Davis, CA, USA.
Med Hypotheses. 2016 May;90:41-7. doi: 10.1016/j.mehy.2016.03.002. Epub 2016 Mar 11.
Two seemingly independent bodies of research suggest a two-hit model of accelerated aging, one highlighting early-life stress and the other reproduction. The first, informed by developmental models of early-life stress, highlights reduced longevity effects of early adversity on telomere erosion, whereas the second, informed by evolutionary theories of aging, highlights such effects with regard to reproductive cost (in females). The fact that both early-life adversity and reproductive effort are associated with shorter telomeres and increased oxidative stress raises the prospect, consistent with life-history theory, that these two theoretical frameworks currently informing much research are tapping into the same evolutionary-developmental process of increased senescence and reduced longevity. Here we propose a mechanistic view of a two-hit model of accelerated aging in human females through (a) early-life adversity and (b) early reproduction, via a process of telomere erosion, while highlighting mediating biological embedding mechanisms that might link these two developmental aging processes.
两项看似独立的研究表明了加速衰老的双打击模型,其中一项强调生命早期应激,另一项强调繁殖。第一项研究以生命早期应激的发育模型为依据,强调早期逆境对端粒侵蚀的寿命缩短影响,而第二项研究以衰老的进化理论为依据,强调(女性)生殖成本方面的此类影响。生命早期逆境和生殖努力都与较短的端粒和增加的氧化应激相关这一事实,与生命史理论一致,提出了这样一种前景,即目前为许多研究提供信息的这两个理论框架正在探究衰老加剧和寿命缩短的同一进化发育过程。在此,我们通过(a)生命早期逆境和(b)早期生殖,经由端粒侵蚀过程,提出了人类女性加速衰老双打击模型的一种机制观点,同时强调可能将这两个发育衰老过程联系起来的中介生物嵌入机制。