Nonpathological senescence arises from unsuitable external influences.


Journal Article (Review)

One of the most exciting events in current biogerontology is the elucidation of environmental control over the rate of aging. Many observations suggest that appropriate external stimuli can ameliorate the state of various biological entities and even rejuvenate them. Recent findings support the possibility that nonpathological aging of cells may be caused solely by external signals and moreover that this aging might be reversible. We have extended this principle to the level of the whole organism. We have suggested that a range of natural environmental conditions exists that corresponds to adequate vital activity within which an organism can maintain optimal functioning, renew itself, and remain ageless. But the environmental mortality of such organisms in natural niches is rather high. To reduce this mortality, the organism requires a milder but less stimulating environment in the presence of which (below some threshold level), the organism's renewal process becomes incomplete and the organism starts to age. Nevertheless, an age-dependent increase in the mortality rate due to senescence can be compensated for by a significant initial reduction in mortality due to environmental causes. The moderate present-day increase of life expectancy is the result of just such an initial mortality reduction. Living in a safe environment along with simulation of natural external positive influences or adequate responses to negative influences can decelerate, stop, and even reverse aging as well as considerably extend mean and extreme life span.

Full Text

Duke Authors

Cited Authors

  • Khalyavkin, AV; Yashin, AI

Published Date

  • November 2007

Published In

Volume / Issue

  • 1119 /

Start / End Page

  • 306 - 309

PubMed ID

  • 18056977

Pubmed Central ID

  • 18056977

Electronic International Standard Serial Number (EISSN)

  • 1749-6632

International Standard Serial Number (ISSN)

  • 0077-8923

Digital Object Identifier (DOI)

  • 10.1196/annals.1404.022


  • eng