Humans have been searching for immortality and slowed or reversed aging since the beginning of human civilization. Humanity’s interest in longevity spans from “immortal realms” such as the concept of Heaven in Abrahamic religions to immortal heroes in Taoist, Sumerian, and Greek mythology. Upper-class Romans during the Late Republic strived to practice a lifestyle of healthy diets rich in seafood and vegetables and a healthy psyche with training and sufficient sleep. Later in the High Middle Ages, numerous doctors believed that diseases could spread through water and air into the pores of the human body. As a result, they vehemently opposed baths as catalysts for disease and aging while encouraging deliberate dirtiness (allowing soils to plug the pores, preventing the insertion of disease vectors). During the Age of Enlightenment, after Darwin proposed the revolutionary theory of evolution, many academics came to understand that the human body is not a perfect creation of God but a flawed automaton with vestigial features left over from previous evolution, such as wisdom teeth, tailbones, and the external ear. Physicians like William Arbuthnot Lane claimed that the removal of some of these “disease-harboring organs” can reduce diseases and extend lifespans. He went on a crusade to excise all sorts of organs he considered unhealthy from his patients. His most notorious practice is the complete removal of the colon, connecting the small intestine directly to the rectum. Unsurprisingly, his quackery did not produce satisfactory results. The kaleidoscope of methods to extend lifespan across human history reveals a human’s undying pursuit of a long life.
Adhering to this historical obsession, a common story exists on the internet claiming that lobsters are biologically immortal. The claim stems from the continued production of the enzyme telomerase in the lobster’s body. All living organisms are composed of individual cells. These cells sometimes become damaged or worked out. In eukaryote organisms that have linear chromosomes, there are telomeres at the ends of the chromosomes. Due to the mechanisms of cellular replication, a portion of the DNA at the end of the chromosome cannot be replicated, so the telomeres function as buffers to prevent important genes from being left out. As eukaryote organisms age, the telomeres become progressively shorter until they completely wear out. This will lead to a scenario where each replication deletes some genes from the DNA. As a result, these old organisms will experience various cellular defects that will ultimately lead to aging and death. Human cells on average can only be replicated around forty to sixty times before the telomeres become too short to protect the critical genetic information. Lobsters are divergent. Their cells produce the enzyme telomerase, an enzyme that extends and repairs the chromosome’s telomeres continuously. This means that the DNA in lobster cells can seemingly replicate indefinitely without fear of damage.
However, proponents of this story fail to take into account other factors that can damage DNAs such as oxidative stress from free radicals and glycation from glucose inhibitors binding to the genetic code.
If lobsters cannot provide a consistent window in the quest for longevity, what can? Recently, biologists discovered that mitochondria from tissues around the body will communicate with each other to repair injured cells. The traditional understanding of mitochondria confines it as the “powerhouse of the cell”. The association with the definition is so strong it has now become a semi-cliché. Mitochondria, however, also plays an important role in intercellular signaling. Chemical signals released by mitochondria are ferried through the body (and interestingly, across germline cells) to other mitochondria. These signals were found to harbor impacts on how rapidly organisms age. This research continues a line of studies that previously established an independent network of communications between mitochondria in the organism’s body. This should not come as a surprise given the fact that mitochondria likely originated from the internalization of prokaryotic proto-mitochondria bacteria. In simple terms, according to the endosymbiosis theory, mitochondria may be ancient bacteria living inside eukaryotic cells. Researchers discovered that damage to mitochondria in brain cells initiated a signal cascade that was progressively amplified to influence all mitochondria in the organism. The test subjects in the experiment, worms, experienced a fifty percent lifespan extension following mitochondrial repair. Preliminary trials on human cells in vitro yielded promising results. This research on mitochondria’s influence on aging comes as an addition to a long train of similar research on extra-genetic influences on aging, hyperbaric oxygen therapy, stem cell regression, and DNA methylation. This new discovery opens up new avenues for research into aging influences at a molecular level
Sources:
Dillin, Andrew, et al. “Rates of behavior and aging specified by mitochondrial function during development.” Science 298.5602 (2022): 2398-2401.
Morris, Mackenzie, et al. “William Arbuthnot Lane (1856–1943): Surgical Innovator and His Theory of Autointoxication.” The American Surgeon 83.1 (2017): 1-2.
Shen, Koning, et al. “Mitochondria as cellular and organismal signaling hubs.” Annual review of cell and developmental biology 38 (2022): 179-218.
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ME Research UK