Telomere Aging Theory

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Aging remains one of the most complex physiological processes that has since attracted the attention of many scientists. Towards this end, theories have been suggested to explain aging. The two crucial concepts include stochastic and non-stochastic theories. According to Lange & Grossman (2010), stochastic model attributes aging to random episodic events in human life which eventually cause cell damage and aging. On the other hand, Lipsky & King (2015) pointed out that non-stochastic theories are limited to programmed causes of aging, and genetics detects the aging.
Telomere aging falls under the non-stochastic doctrine (programmed theory) since the entire process is programmed. Bernadotte et al. (2016) specified that during replication, a telomere drops off the chromosome. This occurs after a predetermined time, approximately one to two years. With time the telomere runs out, and the associated cells have to undergo programmed cell death because replication of the chromosome is not feasible (Connon et al., 2017).
When compared to stochastic models such as wear and tear, free radical and connective tissue theories, telomere aging is not random, and this disqualifies it from being a stochastic ideology. Telomere aging speculation is associated with timed functional changes that ultimately cause aging (Song & Johnson, 2018). Besides, unlike the stochastic theories, telomere aging theory is based on the genetic material of the individuals.

There are some non-stochastic theories as identified by Lipsky & King (2015); neuroendocrine, biological clock, and programmed theory. Telomere aging can be classified under the programme concept. When the chromosomes shorten due to the fall out of telomeres, the genes coding for apoptosis come to play and initiate the programmed death of the cells involved. The process is sequential, one thing leading to the other. Connon et al. (2017) identified the telomerase enzyme as a key determinant of the aging process since it detects the rate at which the telomeres fall off from the chromosomes.
Telomere aging can be explained by the programmed theory, which falls under non-stochastic theories.
References
Bernadotte, A., Mikhelson, V. M., & Spivak, I. M. (2016). The markers of cellular senescence. Telomere shortening as a marker of cellular senescence. Aging (Albany NY), 8(1), 3.
Connon, S. M., Einstein, G. P., & Tulp, O. L. (2017). Analysis of Telomere Length in Aging and Age-Related Illness. The FASEB Journal, 31(1 Supplement), 935-2.
Lange, J., & Grossman, S. (2010). Theories of aging. Gerontological nursing competencies for care, 50-73.
Lipsky, M. S., & King, M. (2015). Biological theories of aging. Disease-a-Month, 61(11), 460-466.
Song, S., & Johnson, F. B. (2018). Epigenetic Mechanisms Impacting Aging: A Focus on Histone Levels and Telomeres. Genes, 9(4), 201.