Revision Point
If you are unsure of the structure of DNA and chromosomes, you might find it helpful to review this in your preferred textbook.
However, with each subsequent cell division the telomeres shorten. After many cycles of cell division, the telomeres are significantly reduced in size and no longer able to protect the chromosome. In the absence of this protective ‘cap’, the chromosomes themselves ‘fray’ and deteriorate over time, leading to a breakdown in the organism’s genetic material. This disruption in the chromosome prevents cells from replicating and can lead to cellular damage, cell death or cancer (Amella, 2004).
Telomerase is an enzyme found in abundance in cancerous cells but not in non-cancerous cells (Mauk, 2006; Meiner and Lueckenotte, 2006). This enzyme prevents the shortening of telomeres after cell division and therefore prevents the cell from dying after a finite number of divisions where the telomeres would have been used up (Lueckenotte, 2000). Cancerous cells are not governed by the same rules as non-cancerous cells (Siegel, 2008) and as such they maintain their telomeres and therefore can continue to divide indefinitely. This may account for the increasing incidence of cancers seen in older adults. It also opens up the possibility of treatments aimed at blocking the action of telomerase, thus preventing cancer cells from multiplying.
Theories | Description |
Error theory | Alteration in the sequencing of genes in DNA. Error theory suggests that this leads to decreased functional ability of the cell. |
Free radical theory | Free radicals are toxic compounds leading to oxidative stress that damages DNA. Accumulation of damage by the recurrent effects of free radicals within the body has been linked to the development of several chronic diseases. |
Immune theory | Decline in immune system functioning where age-related changes in cells may result in them no longer being recognised as ‘self’ and therefore seen as foreign and targeted by the immune system. Or an increase in autoimmune responses where altered proteins are viewed as ‘non-self’ triggering an immune response. |
Programmed theory of ageing: changes in cell replication | Loss of telomeres disrupts cell replication. This disruption in the chromosome prevents cells from replicating and can lead to cellular damage, cellular death or cancer. |
Neuroendocrine theory | The secretion of a range of hormones from the neuroendocrine system begins to fail with age. These changes result in an increase in disease in a number of body systems and organs. |
Neuroendocrine theory
We know that the nervous and endocrine systems play a key role in regulating normal growth, repair and development. It is postulated that as we age the regulatory pathways and the secretion of a range of hormones from the neuroendocrine system begin to fail. Notably, these include the hormones oestrogen, growth hormone and melatonin (Mauk, 2006). Plasma cortisol levels have also been shown to increase as a result of increased activation of the hypothalamus–pituitary–adrenal axis. The net effect of these changes is an increase in disease in a number of body systems and organs.
See Table 2.1 for a brief description of these ageing theories.
Effects of ageing on homeostasis and body function
Homeostasis is the maintenance of a constant internal environment which is necessary for effective physiological activity. Homeostasis involves a complex series of physiological and biochemical changes and responses. Nearly all organs and systems are involved in this process (Redfern and Ross, 2001). Whilst homeostasis is maintained in older adults, functional ability will decline over time. This decline may not be obvious or uniform and may not necessarily interfere with a person’s social functioning. However, a combination of stressors (internal or external) and ageing changes can have a deleterious effect on homeostasis. Such stressors can include illness, trauma, exposure to extreme environmental temperatures and strenuous exercise. These stressors may impact negatively on homeostasis in the older adult as although they have reserve capacity in organ systems, this capacity is reduced to the point where it cannot match the demands made by these stressors. In other words, systems which may normally function well most of the time can be overwhelmed by illness, trauma, infection and other stressors. When this occurs, the individual is no longer in homeostasis and problems ensue. When such a state is reached, it takes longer for the older adult to recover and return to the pre-stressor condition.
Reserve capacity is the spare capacity that systems have which ordinarily are not used but will be available if needed. A person uses their reserve capacity when there are increased health demands made on the body. Reduction in reserve capacity is an important consideration in frailty. Borz (2002) states that all organ systems of the body show evidence of redundant structure and function, stating that most systems have as much as a 70% margin of loss before signs of failure become apparent. Consequently, 30% of normal functioning is adequate for most needs. However, the reserve capacity becomes significant during episodes of stress, injury or illness, and as stated earlier, in older adults this reserve capacity is diminished, making it more likely that they succumb to illness.
Summary
Contrary to the impression that we often have of ageing, growing older is not synonymous with disease and infirmity. Regardless of which theory or theories of ageing proves to be correct, older adults can, for the most part, continue to lead a full and active life and maintain their usual daily activities.
However, the loss of ‘spare capacity’ in organs and systems may be significant when the older adult becomes unwell. Recovery from illness is slower in older adults and healthcare professionals need to plan accordingly.
It is also important to acknowledge that there is a psychological, social and spiritual as well as physiological dimension to growing older. It is not our intention in this text to examine these elements of ageing; however, the reader is directed to further reading if they wish to pursue this further.
For health-care professionals, knowledge of current theories of ageing should help them to advise adults about particular risks or compounding factors such as obesity or smoking. In this way, they can assist the ageing adult to maintain an optimum level of health for as long as possible and help them to adapt their activities of living when and if required.
References and further reading
Amelia, E.J. 2004. Presentation of illness in older adults. American Journal of Nursing 104(10), 40–51.
Arcavi, L. and Benowitz, N.L. 2004. Cigarette smoking and infection. Archives of Internal Medicine 164(20), 2206–2216.
Borz, W.M., II. 2002. A conceptual framework of frailty: a review. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 57(5), 283–288.
Farley, A.H., McLafferty, E. and Hendry, C. 2006. The physiological effects of ageing on the activities of living. Nursing Standard 20(45), 46–52.
Geng, Y., Savage, S.M., Johnson, L.J., Seagrave, J. and Sopori, M.L. 1995. Effects of nicotine on the immune response. I. Chronic exposure to nicotine impairs antigen receptor-mediated signal transduction in lymphocytes. Toxicology and Applied Pharmacology 135(2), 268–278.
Geng, Y., Savage, S.M., Razani-Boroujerdi, S. and Sopori, M.L. 1996. Effects of nicotine on the immune response. II. Chronic nicotine treatment induces T cell anergy. Journal of Immunology 156(7), 2384–2390.
Harman, D. 1956. Aging: a theory based on the free radical and radiation chemistry. Journal of Gerontology 11(3), 298–300.
House of Lords Science and Technology Committee. 2005. Scientific Aspects of Ageing. The Stationary Office, London.
Khaw, K. 1997. Healthy aging. British Medical Journal 315(7115), 1090–1096.
Kirkwood, T.B. 2003. The most pressing problem of our age. British Medical Journal 326(7402), 1297–1299.
Lueckenotte, A.G. 2000. Gerontologic Nursing. 2nd ed. Mosby, St. Louis, MO.
Matteson, M.A. 1997. Biological theories of ageing. In Matteson, M.A., McConnell, E.S. and Linton, A.D. (Eds). Gerontological Nursing: Concepts and Practice. 2nd ed. Saunders, Philadelphia, PA, pp. 159–171.
Mauk, K.L. 2006. Gerontological Nursing: Competencies for Care. Jones and Bartlett Publishers, Sudbury, MA.
Meiner, S.E. and Lueckenotte, A.G. 2006. Gerontologic Nursing. 3rd ed. Mosby Elsevier, St. Louis, MO.
Montague, S., Watson, R. and Herbert, R. 2005. Physiology for Nursing Practice. 3rd ed. Elsevier, Edinburgh.
Nowak, T.J. and Handford, A.G. 1996. Essentials of Pathophysiology. WC Brown Publishers, Dubuque, IA.
Redfern, S.J. and Ross, F.M. 2001. Nursing Older People. 3rd ed. Churchill Livingstone, Edinburgh.
Ricklefs, R.E. and Finch, C.E. 1995. Aging: A Natural History. Scientific American Library, New York, NY.
Seeley, R.R., Stephens, T.D. and Tate, P. 2003. Anatomy and Physiology. 6th ed. McGraw Hill, London.
Siegel, L.J. 2008. Are telomeres the key to aging and cancer. http://learn.genetics.utah.edu/content/begin/traits/telomeres/index.xhtml. Last accessed 4th May 2009.
Tortora, G. 2005. Principals of Human Anatomy. 10th ed. Wiley, Hoboken, NJ.
Woodrow, P. 2002. Ageing: Issues for Physical, Psychological and Social Health. Whurr, London.