The root of aging: Why do we die?
Dylan Ingham, Entrepreneurship, 2023
Humans hate dying. Since the beginning of civilization, people everywhere have struggled with the inevitability of their own mortality and tried countless experiments and strategies aimed at extending their lifespan. As time has progressed, the root causes of aging have revealed themselves to be more and more convoluted. But now, many scientists are focusing their attention on what may be the ultimate root of age-related disease and death: the human genome.
The genome is humanity’s biological code, containing all the information required to run the human body from birth until death. Extensive clinical evidence has shown that certain differentials in these lines of code can impact a specific person’s average life expectancy by as much as 40 percent. Additionally, these genetic sequences can have downstream effects, like a glitch in a website’s coding, that lead to age-related diseases in seemingly unrelated aspects of a person’s biology. There is a flipside, however; a greater understanding of the human genome has lead many scientists to utilize its possibilities for radical life-extension.
A greater understanding of the human genome has lead many scientists to utilize its possibilities for radical life-extension.
Earlier this year, researchers at Cornell used CRISPR, a method of gene editing involving genetically modified viruses, to enter the chromosome of a human stem cell and delete disease-causing genetic information. Using this same method, and with a growing understanding of the purposes and effects of all 20,000 genes in the human body, scientists could tackle the age-related genetic problem of epigenetic drift, a process where genes accumulate small changes in how and when they’re expressed that lead to larger physiological dysregulation. With a greater handle on the specific mechanics at play, these genetic changes could be mitigated and even eradicated in human cells.
Other researchers are taking different approaches. David Sinclair, a biologist at Harvard Medical School, is researching the effects of aging-preventative measures in mice. In a study published in Critical Reviews in Biochemistry and Molecular Biology last November, Sinclair discusses the positive benefits of the molecule rapamycin and the pharmaceutical drug metformin on preventing age-related epigenetic changes by activating certain genetic pathways associated with fasting. These ‘fasting genes’ provide many anti-aging benefits to the body, such as the cleanup of damaged proteins and the boosting of mitochondrial activity. Using similar supplementation that targets these genes might enable humans to mitigate epigenetic degradation and maintain youthful genetic homeostasis for a longer timeframe.
Fasting genes’ provide many anti-aging benefits to the body, such as the cleanup of damaged proteins and the boosting of mitochondrial activity…Supplementation that targets these genes might enable humans to mitigate epigenetic degradation and maintain youthful genetic homeostasis for a longer timeframe.
These realizations have not even come close to making immortality possible. The process of aging and death is still incredibly complicated, and it is a field that scientists will be grappling with for untold decades to come. But the gravity of these developments in such a short period of time is inspiring and hints at even more groundbreaking discoveries in the near future. So, while society may not be drinking from the Fountain of Youth anytime soon, many of the seemingly insurmountable diseases that we currently consider to be so problematic could soon become relics of the past.
Biochimica et Biophysica Acta (BBA) — Molecular Basis of Disease (2018), DOI: 10.1016/j.bbadis.2018.08.039
Molecular Cell (2019), DOI: https://doi.org/10.1016/j.molcel.2019.03.014
Critical Reviews in Biochemistry and Molecular Biology (2018), DOI: https://doi.org/10.1080/10409238.2019.1570075