Aging and the decline in health

Robin Holliday
DOI: 10.4236/health.2010.26092                

Abstract

The biological reasons for aging are now understood. Aging is the result of multiple stochastic events in molecules, cells, tissues and organs. These together produce the aged phenotype, senescence and ultimately death. Many of these changes can be directly linked to specific age-associated disease. However, there are also age-related changes that are not pathological. It can be said that aging has multiple causes, or is instead due to a general loss of molecular fidelity, that is, an increase in disorder. The complexity of organism means that they develop as ordered structures by obtaining energy from the environment. These ordered structures must be maintained by a wide variety of mechanisms which also depend on energy resources. Eventually these mechanisms fail, and senescence sets in. It is known that the efficiency of maintenance is correlated directly with the lifespan of different mammalian species. Also, these lifespans are inversely correlated with fecundity or reproductive potential. There is a trade off between investment of resources in maintenance of the body, or soma, and investment in reproduction.

Keywords

Aging; Senescence; Disease; Pathologies; Evolution

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	Hayflick, L. (1996) How and Why We Age. Ballantine Books, New York.
[2]	Holliday, R. (1995) Understanding Ageing. Cambridge University Press, Cambridge.
[3]	Austad, S.N. (1997) Why We Age. John Wiley, New York.
[4]	Hayflick, L. (2007) Biological aging is no longer an unsolved problem. Annals of the New York Academy of Sciences, 1100(1), 1-13.
[5]	Holliday, R. (2006) Aging is no longer an unsolved problem in biology. Annals of the New York Academy of Sciences, 1067(1), 1-9.
[6]	Kirkwood, T.B. (2005) Understanding the odd science of aging. Cell, 120(4), 437-447.
[7]	Evans, G.J., Franklin W.T., Beattie, B., Michel, J.P. and Wilcock, G.K. (2000) The Oxford Textbook of Geriatric Medicine. Oxford University Press, Oxford.
[8]	Hayflick, L., (2004) The not-so-close relationship between biological aging and age-associated pathologies in humans. Journal of Gerontology: Biological Sciences, 59 (6), 547-550.
[9]	Holliday, R. (2004) The close relationship between biological aging and age-associated pathologies in humans. Journal of Gerontology: Biological Sciences, 59(6), 543- 546.
[10]	Carnes, B.A., Staats, D.O. and Sonntag, W.G. (2009) Does senescence give rise to disease? Mechanisms of Ageing and Development, 129(12), 693-699.
[11]	Kirkwood, T.B.L. (1977) The evolution of ageing. Nature, 270(5635), 301-304.
[12]	Kirkwood, T.B. and Holliday, R. (1979) The evolution of ageing and longevity. Proceedings of the Royal Society London B: Biological Sciences, London, 205(1161), 532- 546.
[13]	Kirkwood, T.B.L. and Holliday, R. (1986) Ageing as a consequence of natural selection. In. Collins, K.J. and Bittles, A.H., Eds., Biology of Human Ageing, Cambridge University Press, Cambridge.
[14]	Holliday, R. (1994) Longevity and fecundity in eutherian mammals. In. Rose, M.R. and Finch, C.E. Eds., Genetics and the Evolution of Aging, Kluwer Academic, Dordrecht.
[15]	Holliday, R., (2004) The multiple and irreversible causes of aging. Journal of Gerontology: Biological Sciences, 59(6), 568-572.
[16]	Barja, G., (2004) Aging in vertebrates, and the effect of calorie restriction: a mitochondrial free radical production-DNA damage mechanism. Biological Reviews of the Cambridge Philosophical Society, 79(2), 235-251.
[17]	Kapahi, B., Boulton, M.E. and Kirkwood, T.B.L. (1999) Positive correlation between mammalian lifespan and cellular resistance to stress. Free Radical Biology and Medicine, 26(5-6), 495-500.
[18]	Yamauchi, M., Woodley, D.T. and Mechanic, G.L. (1988) Aging and cross-linking of skin collagen. Biochemical and Biophysical Research Communications, 152(2), 898- 903.
[19]	Ames, B.N., Saul, R.L., Schwiers, E., Adelman, R. and Cathcart, R. (1985) Oxidative damage as related to cancer and aging: the assay of thymine glycol, thymidine glycol and hydroxymethyl uracil in human and rat urine. In. Sohal, R.S., Birnbaum, L.S. and Cutler, R.G.., Eds., Molecular Biology of Aging, Raven Press, New York.
[20]	Morley, A.A., (1998) Somatic mutations and aging. Annals of the New York Academy of Sciences, 854, 20-22.
[21]	Pamplona, R., Portero-Ortin, M., Ruiz, C., Gredilla, R., Herrero, A. and Barja, G. (2000) Double bond content of phospholipids and lipid peroxidation negatively correlate with maximum longevity in the heart of mammals. Mechanisms of Ageing and Development, 112(3), 169- 183.
[22]	Barja, G. and Herrero, A. (2000) Oxidative damage to mitochondria is inversely correlated to maximum lifespan in the heart and brain of mammals. Journal of the Federation of American Societies for Experimental Biology, 14(2), 312-318.
[23]	Pamplona, R., Portero-Otin, M., Requena, J.R., Thorpe, S.R., Herrero, A. and Barja, G. (1999) A low degree of fatty acid unsaturation leads to lower lipid peroxidation and lipoxidation derived proteiun modification in heart mitochondria in the longevous pigeon than the short lived rat. Mechanisms of Ageing and Development, 106 (3), 283-296.
[24]	Pamplona, R., Portero-Otin, M., Riba, D., Gredilla, R., Herrero, A. and Barja, G. (1999) Heart fatty acid unsaturation and lipid peroxidation, and aging rate, are lower in the parakeet and canary than in the mouse. Aging Clinical and Experimental Research, 11, 44-49.
[25]	Lindahl, T. (1993) Instability and decay of the primary structure of DNA. Nature, 362(6422), 709-715
[26]	Fraga, M.F., Ballistar, E., Paz, M.F., et al. (2005) Epigenetic differences arise during the lifetime of monozygotic twins. Proc. Nat. Acad. Sci. USA, 102(30), 10604-10609.
[27]	Martin, G.M. (2005) Epigenetic drift in aging identical twins. Proceedings of the National Academy Science USA, 102, 10413-10414.
[28]	Tollefsbol, T. (2009) Epigenetics of aging. Springer Science, Humana Press, New Jersey.
[29]	Zurcher, C., Van Zwieten, M.J., Solleveld, H.A. and Hollander, C.F. (1982) Ageing research. In. Foster H. L., Small, J.D. and Fox, J.G. Eds., The Mouse in Biomedical Research, Academic Press, New York, 4, 11-35.
[30]	Smith, M.J. (1962) The causes of ageing. Proceedings of the Royal Society London B: Biological Sciences, London, 157(966), 115-127.
[31]	Schrodinger, E. (1944) What is life? Cambridge University Press. Cambridge