, Volume 19, Issue 1, pp 101–108 | Cite as

How regularities of mortality statistics explain why we age despite having potentially ageless somatic stem cells

  • Alexander V. KhalyavkinEmail author
  • Vyacheslav N. Krut’ko


Researchers working in the area of ageing have found numerous manifestations of this process at the molecular biological level, including DNA and protein damage, accumulation of metabolic by-products, lipids peroxidation, macromolecular cross-linking, non-enzymatic glycosylation, anti-oxidant/pro-oxidant misbalance, rising of pro-inflammatory cytokines, etc. This results in an increase in the proportion of cells in growth arrest, reduction of the rate of information processing, metabolic rate decrease, and decrease in rates of other processes characterizing dynamic aspects of the organism’s interaction with its environment. Such staggering multilevel diversity in manifestation of senescence precludes (without methodology of systems biology) development of a correct understanding of its primary causes and does not allow for developing approaches capable of postponing ageing or reducing organisms’ ageing rate to attain health preservation. Moreover, it turns out that damage production and damage elimination processes, the misbalance of which results in the ageing process, can to a large extent be regulated by external signals. The purpose of this report is to provide evidence supporting this view and its compatibility with the regularities of mortality statistics, because the main idea is very simple. Even potentially a non-senescent but certainly not immortal body must start to age under inadequate conditions (like a non-melting piece of ice taken out from the deepfreeze inevitably start to melt at the temperatures above zero Celsius). This conclusion is totally consistent with existing patterns of mortality and with agelessness potential of somatic stem cells. Therefore, there is no need to build up and explore too complicated, computational and sophisticated systems models of intrinsic ageing to understand the origin of this mainly extrinsic root cause of natural ageing, which is controlled by environmental signals. In our case, a simple phenomenological black-box approach with InputOutput analysis is ample. Here Input refers to the environmentally dependent initial force of mortality, whereas Output is a rate of age-related increase of mortality force.


Ageing plasticity Systems as units Reversibility of senescence External conditions Mortality patterns Adequate signalling Origin of ageing Environmental influences 



The reported study was funded by Ministry of Education and Science of the Russian Federation according to the research project # 14.607.21.0123 (Unique Project Identifier RFMEFI60715X0123).


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Copyright information

© Springer Science+Business Media B.V. 2017

Authors and Affiliations

  • Alexander V. Khalyavkin
    • 1
    • 2
    Email author
  • Vyacheslav N. Krut’ko
    • 2
    • 3
  1. 1.Emanuel Institute of Biochemical Physics of RASMoscowRussia
  2. 2.Federal Research Center «Computer Science and Control» of the Russian Academy of SciencesMoscowRussia
  3. 3.Sechenov First Moscow State Medical UniversityMoscowRussia

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