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The biology of human longevity: inflammation, nutrition and ageing in the evolution of lifespans

机译:人类长寿的生物学:寿命演变中的炎症,营养和衰老

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摘要

Those familiar with Caleb Finch’s previous Longevity, Senescencenand the Genome will not be surprised that 183 pages ofnthis 626 page volume are taken up with references to the literature.nFinch exemplifies the ideal of thorough scholarship,nand we should be grateful for his comprehensive summarynof ideas and data that bear upon the intriguing question ofnwhy humans live as long as they do. Finch reminds us thatnour species has undergone two successive doublings in averagenlife expectancy. First, over the short evolutionary timenspan since we shared a common ancestor with chimpanzees,nspecies–species average lifespan increased from around 20 ton40 years. Second, life expectancy has further doubled over thenlast two centuries as a result of improvements in sanitation,nnutrition, housing, education, technology and medicine. Itnis central to Finch’s thesis that common biological elementsnunderpin both these transformations and are to be foundnin the nexus of processes that connect infection, inflammationnand nutrition. The drive towards increased humannlongevity, which was associated with a shift towards meatneating, brought changes in the human population density andngenetics that led to a greater burden of infection and inflammation.nInflammation contributes non-specific damage toncells and tissues, driving age-related cardiovascular, neurodegenerativenand other diseases, as well as ageing itself. Finch’snnarrative in The Biology of Human Longevity is inevitably complex.nHowever, the discerning reader will be well rewarded.
机译:熟悉Caleb Finch先前的《长寿》,《衰老》和《基因组学》的人不会惊讶,在这626页的书中占据了183页,并参考了文献。nFinch体现了透彻的学术研究的理想,我们要感谢他对思想和思想的全面总结。这些数据引起了一个有趣的问题,即人类为什么会活得如此长久。芬奇提醒我们,平均物种平均寿命中,两种物种已经连续两次翻倍。首先,由于我们与黑猩猩有共同的祖先,所以在很短的进化时间内,物种的平均寿命从20吨40年左右增加。第二,由于卫生,营养,住房,教育,技术和医学的改善,预期寿命在过去两个世纪中进一步翻了一番。芬奇的理论认为,共同的生物学元素支撑着这两种转化,并且将在连接感染,炎症和营养的过程的联系中被发现,这是中心思想。延长人类寿命的动力,与转向肉食相关,带来了人口密度和遗传学的变化,从而导致更大的感染和炎症负担。炎症导致非特异性损伤扁桃体和组织,导致与年龄相关的心血管疾病,神经退行性疾病和其他疾病,以及自身老化。芬奇在《人类长寿生物学》中的叙事不可避免地很复杂。然而,有识之士们将得到丰厚的回报。

著录项

  • 来源
    《Age and Ageing》 |2009年第5期|p.636-636|共1页
  • 作者

    Tom Kirkwood;

  • 作者单位

    TOM KIRKWOODInstitute for Ageing and HealthNewcastle University,Newcastle Upon Tyne NE4 5PL, UKEmail: Tom.Kirkwood@ncl.ac.uk;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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