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      Vanishing honey bees: Is the dying of adult worker bees a consequence of short telomeres and premature aging?

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      Medical Hypotheses
      Elsevier BV

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          Abstract

          Einstein is often quoted to have said that without the bee, mankind would have but 4years to live. It is highly unlikely that he made this comment, which was even mentioned in a Lancet article on honey bees. However, the current vanishing of the bees can have serious consequences for human health, because 35% of the human diet is thought to benefit from pollination. Colony collapse disorder (CCD) in honey bees is characterized by the rapid decline of the adult bee population, leaving the brood and the queen poorly or completely unattended, with no dead bodies in or around the hive. A large study found no evidence that the presence or amount of any individual pesticide or infectious agent occurred more frequently or abundantly in CCD-affected colonies. The growing consensus is that honey bees are suffering from comprised immune systems, which allow various infectious pathogens to invade. The question remains, what causes immunosuppression in many colonies of Apis mellifera in North America and Europe? Telomeres are protective DNA structures located at eukaryotic chromosome tips that shorten in the somatic tissues of animals with age. Lifelong tissue regeneration takes place in Apis mellifera, and worker bees have been shown to senesce. In humans, a vast amount of literature has accumulated on exhausted telomere reserves causing impaired tissue regeneration and age-associated diseases, specifically cancer and immunosuppression. Therefore, we propose a new causative mechanism for the vanishing of the bees: critically short telomeres in long-lived winter bees. We term this the telomere premature aging syndrome. Copyright 2010 Elsevier Ltd. All rights reserved.

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          Author and article information

          Journal
          Medical Hypotheses
          Medical Hypotheses
          Elsevier BV
          03069877
          October 2010
          October 2010
          : 75
          : 4
          : 387-390
          Article
          10.1016/j.mehy.2010.04.003
          20478660
          83501be8-b481-41ac-8236-d0a72c563d8d
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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