Extending Healthy Life Span—From Yeast to Humans

  • Luigi Fontana
    Division of Geriatrics and Nutritional Science, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Linda Partridge
    Institute of Healthy Aging, and G.E.E., University College London, London WC1E 6BT, UK.
  • Valter D. Longo
    Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA.

書誌事項

公開日
2010-04-16
DOI
  • 10.1126/science.1172539
公開者
American Association for the Advancement of Science (AAAS)

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説明

<jats:title>Eat Less, Live Long</jats:title> <jats:p> Studies in several model organisms have shown that dietary restriction without malnutrition, or manipulation of nutrient-sensing pathways through mutations or drugs, can increase life span and reduce age-related disease. <jats:bold> Fontana <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="321" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1172539" xlink:type="simple">321</jats:related-article> ) review the ways in which nutrient-sensing pathways are central to aging. Studies of yeast, worms, rodents, and primates show that these pathways are conserved during evolution. Although data on the effects of dietary restriction in primates are very limited, in humans, the protective effects of dietary restriction against cancer, cardiovascular disease, and diabetes must be judged against potentially negative long-term effects. More work is needed to determine whether dietary restriction and the modulation of anti-aging pathways through drugs can extend life span and reduce pathologies in humans. </jats:p>

収録刊行物

  • Science

    Science 328 (5976), 321-326, 2010-04-16

    American Association for the Advancement of Science (AAAS)

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