A Unifying Theory of Aging between Modern Medicine and Traditional Chinese Medicine
- 1 Division of Life Science, Hong Kong University of Science & Technology, Hong Kong, China
- 2 Division of Life Science, Hong Kong University of Science & Technology, Hong Kong, China
- 3 Division of Life Science, Hong Kong University of Science & Technology, Hong Kong, China
Abstract
With the increasing aging population around the world as a result of birth rates and advances in medical technologies, there is an urgent need to unravel the primary cause of aging, in the hope of developing a rational approach to retard the aging process. This is crucial to reduce the societal impact of aging. Although modern medicine and traditional Chinese medicine view the process of aging from different perspectives, this article aims to develop a common understanding between these two distinct medical systems in relation to the aging process. As such, a unified approach can hopefully be developed to effectively slow down the aging process. Modern medicine has proposed the “mitochondrial theory” of aging, which implicates a causal relationship between the rate of mitochondrial reactive oxygen species generation and lifespan as noted in a wide spectrum of primate species, while traditional Chinese medicine views aging as the result of a gradual depletion of congenital primordial Qi, which can be spared by the sufficient generation of postnatal pectoral Qi. By amalgamating the knowledge of modern medicine with that of traditional Chinese medicine in relation to aging, it is suggested that while Chinese tonifying herbs can be used to restore the balance of body functions enabling the generation of sufficient pectoral Qi, active ingredients isolated from Chinese tonifying herbs or other plant sources capable of inducing mitohormesis and mitophagy, as well as senolysis, can be used to retard the aging process.
- da Costa, J.P., Vitorino, R., Silva, G.M., Vogel, C., Duarte, A.C. and Santos, T.R. (2016) A Synopsis on Aging—Theories, Mechanisms and Future Prospects. Ageing Research Review, 29, 90-112. https://doi.org/10.1016/j.arr.2016.06.005
- Veith, I. (1972) The Yellow Emperor’s Classic of Internal Medicine. University of California Press, Berkeley, Los Angeles, London, 15.
- Barja, G. (2019) Towards a Unified Mechanistic Theory of Aging. Experimental Gerontology, 124, 110627. https://doi.org/10.1016/j.exger.2019.05.016
- Chabi, B., de Cararet, B.M., Chevrollier, A., Boisgard, S. and Stephen, G. (2005) Random mtDNA Deletion and Functional Consequence in Aged Human Skeletal Muscle. Biochemica Biophysica Research Communication, 332, 542-549. https://doi.org/10.1016/j.bbrc.2005.04.153
- Caro, A., Gómez, J., Arduini, A., González-Sánchez, M., González-García, M., Borrás, C., Vina, J., Puertas, M.J., Sastre, J. and Barja, G. (2010) Mitochondrial DNA Sequences Are Present Inside Nuclear DNA in Rat Tissues and Increase with Age. Mitochondrion, 10, 479-486. https://doi.org/10.1016/j.mito.2010.05.004
- Macedo, J.C., Vaz, S. and Bakker, B. (2018) FoxM1 Repression during Human Aging Leads to Mitotic Decline and Aneuploidy-Driven Full Senescence. Nature Communication, 9, Article No. 2834. https://doi.org/10.1038/s41467-018-05258-6
- Pamplona, R. and Barja, G. (2006) Mitochondrial Oxidative Stress, Aging and Caloric Restriction: The Protein and Methionine Connection. Biochimica et Biophysica Acta (BBA)—Bioenergetics, 1757, 496-508. https://doi.org/10.1016/j.bbabio.2006.01.009
- Nakamura, S. and Yoshimori, T. (2018) Autophagy and Longevity. Molecules and Cells, 41, 65-72.
- Ashrafi, G. and Schwarz, T.L. (2013) The Pathways of Mitophagy for Quality Control and Clearance of Mitochondria. Cell Death and Differentiation, 20, 31-42. https://doi.org/10.1038/cdd.2012.81
- Bárcena, C., Mayoral, P. and Quirós, P.M. (2018) Mitohormesis, an Antiaging Paradigm. International Review of Cell and Molecular Biology, 340, 35-77. https://doi.org/10.1016/bs.ircmb.2018.05.002
- Yun, J. and Finkel, T. (2014) Mitohormesis. Cell Metabolism, 19, 757-766. https://doi.org/10.1016/j.cmet.2014.01.011
- Regulski, M.J. (2017) Cellular Senescence: What, Why, and How. Wounds: A Compendium of Clinical Research and Practice, 29, 168-174.
- Hickson, L.J., LanghiPrata, L.G.P., Bobart, S.A., Evans, T.K., Giorgadze, N., Hashmi, S.K., Herrmann, S.M., Jensen, M.D., Jia, Q., Jordan, K.L., Kellogg, T.A., Khosla, S., Koerber, D.M., Lagnado, A.B., Lawson, D.K., LeBrasseur, N.K., Lerman, L.O., McDonald, K.M., McKenzie, T.J., Passos, J.F., Pignolo, R.J., Pirtskhalava, T., Saadiq, I.M., Schaefer, K.K., Textor, S.C., Victorelli, S.G., Volkman, T.L., Xue, A., Wentworth, M.A., Wissler Gerdes, E.O., Zhu, Y., Tchkonia, T. and Kirkland, J.L. (2019) Senolytics Decrease Senescent Cells in Humans: Preliminary Report from a Clinical trial of Dasatinib plus Quercetin in Individuals with Diabetic Kidney Disease. Ebiomedicine, 47, 446-456. https://doi.org/10.1016/j.ebiom.2019.08.069