Programmed Aging Theory Information Wear and Tear Hypotheses
and Stochastic Hypothesis


Type: Non adaptive hypotheses

Definition: Aging is caused by the progressive accumulation of damage by various factors as: a) mechanical wear and tear; b) the progressive effects of the somatic accumulation of harmful mutations; c) random accumulation of errors in protein synthesis; d) oxidative stress by free radicals; e) somatic accumulation of mitochondrial DNA mutations, leading to the gradual loss of bioenergetic capacities; etc.

Proposers: There are so many proposers of hypotheses of this category that the writing up of a thorough list of them would be a boring and difficult task. However, some reviews provide a good description of these hypotheses and of their proposers and supporters (e.g.: Kowald & Kirkwood 1996; Kirkwood & Kowald 1997; Kirkwood 1998, 2002; Fossel 2004.

Empirical Evidence:
1) The existence of animals with negligible senescence is against these hypotheses.
2) The inverse correlation observed in the wild between extrinsic mortality rate and proportion of deaths due to intrinsic mortality is against these hypotheses.
3) The existence of mechanisms genetically determined and regulated limiting cell turnover and, therefore, lifespan is against these hypotheses.
4) The negative relation between caloric intake and lifespan is compatible with these hypotheses because a reduced metabolism caused by caloric restriction should slacken aging.

Conclusion: These hypotheses are strongly contradicted by empirical evidence (with the exclusion of caloric restriction effects) and are not plausible explanations of aging.

- Fossel, M.B. (2004) Cells, Aging and Human Disease. Oxford University Press, Oxford, USA. [Google Scholar]
- Kirkwood, T.B.L. (1998) Biological theories of aging: an overview. Aging (Milano) 10, 144-146. [PubMed] [Google Scholar]
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- Kirkwood, T.B.L. & Kowald, A. (1997) Network theory of aging. Exp. Gerontol. 32, 395-399. [PubMed]
- Kowald, A. & Kirkwood, T.B.L. (1996) A network theory of ageing: the interactions of defective mitochondria, aberrant proteins, free radicals and scavenger in the ageing process. Mutat. Res. 316, 209-236. [PubMed]

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