By Andrew Friedland
The fountain of youth, the elixir of life, and the holy grail–Throughout all of human history, there has been a yearning for immortality. Despite thousands of years of research, however, no cure for aging has ever been discovered–until now.
Well, not quite–yet as days pass, we inch closer towards the ultimate goal of immortality. In the 1970s, Elizabeth Blackburn, Carol Greider, and Jack Szostak discovered telomeres, DNA sequences found at the end of genes, and telomerase, an enzyme responsible for maintaining telomere length. On January 14th, 2011, Masood A. Shammas uncovered a link between telomere length and aging. He also realized that epigenetic factors, the umbrella term environmental factors, such as “smoking, lack of physical activity, obesity, stress, exposure to pollution, etc. can potentially increase the rate of telomere shortening, cancer risk, and pace of aging”. By maintaining a healthy lifestyle, it was determined that the rate of telomere shortening could be decreased, thereby increasing lifespan. However, these findings only slow the rate of aging, but don’t cease it altogether.
On February 3rd, 2016, the journal Nature released a study, discovering that naturally occurring p16Ink4a cells effectively shorten healthy lifespan. The p16Ink4a cell is a “senescent cell”, a class of cells which accumulate in “various tissues and organs over time, and have been speculated to have a role in ageing”. By injecting mice with the compound AP20187, which induces apoptosis of p16Ink4a cells, the lifespan of both males and females increased. It was thus determined that p16Ink4a cells which accumulate during adulthood, confer a negative effect on lifespan. The therapeutic removal of such can then potentially lead to an increase in lifespan.
On December 9th, 2022, the journal Nature Aging released a study, tying aging to the length of genes, further compounding upon the efforts of Shammas. Essentially, genes with longer transcripts are correlated with a longer lifespan, whereas genes with a shorter transcript confer a shorter lifespan. The human body desires homeostasis, a state of balance between the long and short genes. However, when the activity of short and long genes shift, your body begins to exert more energy. Additionally, Thomas Stoeger, a researcher at Northwestern, corroborates that short genes are quite essential. For example, short genes “are called upon to help fight off pathogens”, and therefore “some short genes could have a short-term advantage on survival at the expense of ultimate lifespan”. Consequently, as our bodies endure the environment, the aging process is exacerbated. Thus, the researchers suggest that by targeting the imbalance in the genes, aging could be cured.
The culmination of these important findings are several therapeutic treatments. David Sinclair, an anti-aging expert at Harvard Medical School, asserts that as the body endures environmental conditions, “The cell panics, and proteins that normally would control the genes get distracted by having to go and repair the DNA”. However, he identified that the body has a backup copy of its DNA, and can fix the body’s damage “by tapping into a reset switch that restores the cell’s ability to read the genome correctly again, as if it was young”. Through this innovation, Sinclair has managed to help old mice regain eyesight, and develop younger, smarter brains and healthier tissue. What’s most notable about this finding is that young mice managed to prematurely age, proving devastating to their bodies. He’s also managed to find the inverse, capable of aging mice.
Despite these findings, it’ll be decades before clinical trials on humans will take place. It’s also imperative to note the implications of such findings. Achieving anti-aging technology in humans can potentially lead to a myriad of negative consequences for humanity. With an extended lifespan, humans will strain limited resources and aggravate existing issues like poverty, inequality, and environmental degradation. Moreover, anti-aging technologies may be limited to the privileged few as a product of cost and availability, thus intensifying social and economic disparities. Finally, an increase in population may overwhelm health care systems, resulting in higher expenses and higher demand.
Overall, anti-aging technology might just be over the horizon. With the development of AI and persistent scientific breakthroughs, the fountain of youth might be closer than we think. Yet, it’s important to note the potential consequences of such an opportunity, that may drastically change the world as we know it.
References:
Amaral, Luís A. N., et al. "Aging is driven by unbalanced genes." Northwestern Now, Northwestern University, 12 Dec. 2022, news.northwestern.edu/stories/2022/12/aging-is-driven-by-unbalanced-genes/.
Baker, David, Brian Childs, and Mark Durik. "Naturally occurring p16Ink4a-positive cells shorten healthy lifespan." Nature 529.7584 (2016): 489-493.
Blackburn, E. H., Greider, C. W., & Szostak, J. W. (2009). Telomeres and telomerase: the ends of chromosomes and the beginning of immortality. Nobelprize.org. Nobel Prize Outreach AB. Retrieved June 6, 2023, from https://www.nobelprize.org/prizes/medicine/2009/summary/
LaMotte, Sandee. “Old Mice Grow Young Again in Study. Can People Do the Same?” CNN, 13 Jan. 2023, www.cnn.com/2023/01/12/health/reversing-aging-scn-wellness/index.html.
Shammas, Masood A. "Telomeres, lifestyle, cancer, and aging." Current Opinion in Clinical Nutrition & Metabolic Care 14.1 (2011): 28-34.
Stoeger, Thomas, Robert A. Grant, Ashley C. McQuattie-Pimentel, et al. "Aging is associated with a systemic length-associated transcriptome imbalance." Nature Aging 2.6 (2022): 1191-1206.