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Written by Devin Juros Edited by Sisasenkosi Mandi  The year is 2050, you go to a brightly lit lab crowded with bustling scientists and shining technology scattered everywhere. After a few minutes of waiting, a scientist comes over with fifteen of the newly made LongeviPills© and says that each pill increases your lifespan by ten years. You can take some, all, or none of them, but this is your only chance to take the pills. How many LongeviPills© do you take? Would you want to live until the age of 250? With greater understanding of aging pathways, the question of how long you would want to live has become relevant beyond idle philosophical musings. Life-extending interventions may soon become a reality. One recent study by J. Lan increased the average lifespan of C. elegans (the nematode) by 250% [2]. This impressive feat was accomplished by developing C. elegans with mutations inhibiting the IIS pathway, decreasing insulin signaling (which decreases sugar uptake by cells), and the TOR pathway, decreasing cell growth. Mutating the IIS pathway alone leads to a 115% increase in average lifespan in C. elegans, while mutating the TOR pathway alone leads to a 15% increase in average lifespan. When both of these pathways are mutated at the same time, they have a synergistic effect that leads to a 250% increase in average lifespan. This is equivalent to the average human lifespan increasing from 73 years to 256 years [3]. Another recent study on mice with a mutated TOR pathway and consequent decrease in cell growth led to a 20% increase in median lifespan [4]. This is equivalent to the average human lifespan increasing from 73 years to 88 years. Though this is a less extreme increase in average lifespan, the ability to extend the lifespan of mice, a mammal more closely related to humans, makes increasing the human lifespan more viable. Yet, even if an intervention is developed to increase the human lifespan, would this actually be beneficial to individuals and society at large? One consideration is the accumulation of age-related diseases like Alzheimers, Parkinsons, arthritis, and cancer as you live longer. It is even possible that novel age-related diseases would occur that nobody has yet experienced because other cellular, systemic, or organismal mechanisms break down when humans live longer than they have thus far. All of these diseases would impact the quality of life of longer-living humans. Living longer would also impact society as our values are tied to different stages of life that people generally go through, like going to school through late childhood (until your late teens or early 20’s), getting a job in early adulthood (in your mid 20’s), building a family in mid-adulthood (in your late 20’s or 30’s), and retiring in late adulthood (in your 50’s, 60’s, or 70’s). Based on your age, there are certain values, goals, and responsibilities that you are expected to have in society. Over time, the average human lifespan has slowly increased, leading to a gradual shift in these time frames. But, what if, like C. elegans, we developed a drug to increase the average human lifespan by 250% from 73 years to 256 years? This sudden, massive increase in average lifespan would completely disrupt the general itinerary for human life. This groundbreaking shift in time frames would impact your values and what is important at different points in your life. This shift in time frames has a tangential effect on retirement-related benefits like social security. If people suddenly live longer, this financial support program would have to give benefits to a much larger group of people. If the retirement age did not increase by a similar proportion, an increase in average lifespan would strain the government and taxpayers to provide these benefits. A reduction in these benefits may decrease seniors’ ability to obtain adequate housing and nutrition. Though living longer may initially appear to be a tremendous boon to happiness, the reality of a longer-living society has numerous potential drawbacks. However, senolytics, an emerging area of research to prolong one’s “healthspan”, could mitigate some of the potential issues of living longer. Senolytics targets senescent cells, which are cells that have stopped dividing but remain active and release proinflammatory substances that can lead to many disease states correlated with old age, like osteoarthritis and glaucoma. By selectively destroying these senescent cells, researchers have had some success in improving health and reducing disease in older mice and humans [1]. Senolytics presents a potential way that healthspan could be extended along with lifespan, which could resolve the potential problem of an older population with accumulated age-related diseases. However, the impact of living longer on societal values and retirement benefits remain possible detriments that may make you think twice about taking all of LongeviPills©. Perhaps, your current lifespan is enough time to do all that you want. In the meantime, as lifespan-increasing interventions are developed, we will have to be content with the years that we do have. Works Cited:
[1] Fleming, A. (2019, September 2). The science of senolytics: how a new pill could spell the end of ageing. Retrieved March 17, 2020, from https://amp.theguardian.com/science/ 2019/sep/02/the-science-of-senolytics-how-a-new-pill-could-spell-the-end-of-ageing [2] Lan, J., Rollins, J. A., Zang, X., Wu, D., Zou, L., Wang, Z., … Chen, D. (2019, July 23). Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity. Retrieved March 7, 2020, from https://www.sciencedirect.com/science/article /pii/S2211124719308587?via=ihub [3] Roser, M., Ortiz-Ospina, E., & Ritchie, H. (2013, May 23). Life Expectancy. Retrieved March 7, 2020, from https://ourworldindata.org/life-expectancy [4] Wu, J. J., Liu, J., Chen, E. B., Wang, J. J., Cao, L., Narayan, N., … Finkel, T. (2013, September 12). Increased mammalian lifespan and a segmental and tissue-specific slowing of aging after genetic reduction of mTOR expression. Retrieved March 7, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784301/ [5] Image source: https://commons.wikimedia.org/wiki/File:Colorful,_fondness,_grandparent_Fortepan_57281.jpg
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