Telomere Theory Classification
The telomere theory of aging completely changed the way researchers approach the process of aging. In studies of different populations, it has been found that as people get old, they have shorter telomeres, which eventually leads to the inability of cells to replicate. As a result, fewer telomeres in cells mean that older people will have tissue damage and other signs of decay. It is also important to mention that cancer cells do not die due to their ability to activate the telomerase cell, which then adds to telomeres during cell division. On the other hand, shorter telomeres can also be linked to diseases; it has been found that a shorter length of telomeres and lower activity of telomerase is linked to chronic conditions such as type 2 diabetes, obesity, depression, cardiovascular diseases, and several other disorders (Stibich, 2018). Based on the mechanism that aids in the production of telomeres within the body, a conclusion should be made in terms of linking the theory to either stochastic or non-stochastic theories of aging.
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On the one hand, stochastic theories (for example, free radical, orgel/error, wear and tear, and connective tissue theories) explain the process of aging as a series of events that take place at random and have accumulative effects that affect a human body over time. On the other hand, non-stochastic theories (for example, programmed, gene/biological clock, neuroendocrine, and immunologic/autoimmune theories), view aging as a predetermined process. Because it is still unclear why and how telomeres become shorter in some people but remain long in others with aging, the theory is more likely to be classified as stochastic.
Based on the characteristics of the telomere theory of aging, it can also be included in the free radical theory. The latter provided researchers with an ever-expanding theoretical “framework for an enormous amount of work leading to significant advances” in the understanding of aging (Viña, Borras, Abdelaziz, Garcia-Valles, & Gomez-Cabrera, 2013, p. 780). The theory includes considerations about the principle of metabolism, which produces free radicals as it occurs. After the accumulation of free radicals, the cell membrane is damaged, and thus its efficiency decreases. Since telomeres are directly involved in the process of cell division, it is possible to link the telomere theory to the free radical theory.
In addition, as mentioned by Viña et al. (2013) in their research, telomerase could be linked to the production of free radicals. This is so because telomerase activity is regulated by glutathione, a major intracellular reductant. The researchers also found that “telomerase prolonged lifespan in cancer protected animals […] without influencing oxidative stress” (Viña et al., 2013, p. 785). Overall, the telomere theory of aging is characterized as a stochastic theory of aging, because there is volatility in how cells divide in different individuals, which means that the process is not structured. On the other hand, the theory is somewhat confusing because it has some qualities in non-stochastic theories. For instance, the programmed theory implies that cells can divide a limited number of times. It has also been found that there is a limit to the number of telomeres in the body. Therefore, it can be concluded that the telomere theory of aging is multi-faceted and has characteristics of different approaches of researchers in terms of exploring the process of aging.
Stibich, M. (2018). The telomere theory of aging and longevity. Very Well Health. Web.
Viña, J., Borras, C., Abdelaziz, K. M., Garcia-Valles, R., & Gomez-Cabrera, M. C. (2013). The free radical theory of aging revisited: The cell signaling disruption theory of aging. Antioxidants & Redox Signaling, 19(8), 779-787.