At first glance, the Caenorhabditis elegans worms have nothing in common with us Homo Sapiens. These worms are only about 1 millimeter long, and you need to use a microscope to see them clearly.
However, deep within their genome, C. elegans shares a lot of genetic data with humans, including genes that cause aging. Recently, a group of Chinese and American scientists discovered two cellular pathways stemming from these genes, and they managed to alter them to extend the lifespan of C. elegans by 500%.
Coincidentally, the two genes we are talking about here, IIS and TOR, also exist in humans. Could this be an opportunity for us to quintuple our lifespan? Will gene editing techniques like CRISPR allow someone to live to 500 years old?

C. elegans is a species that primarily lives in soil, thriving in decaying plant matter. Sharing many genes with humans and living an average of 3-4 weeks, these roundworms are often used in genetic intervention experiments to influence lifespan.
In the latest research conducted by the MDI Laboratory of the Buck Institute for Research on Aging in the U.S. and Nanjing University in China, scientists discovered that the genes IIS and TOR of C. elegans are conserved through evolution and have been passed down to humans.
Two co-authors of the study, Dr. Jarod A. Rollins and Dr. Aric N. Rogers, stated that IIS is a gene that allows organisms to respond to environmental factors, such as food availability, to coordinate a response at the cellular level among different tissues of the organism.
IIS is also responsible for signaling insulin. When targeted and edited using CRISPR technology, the mutated C. elegans roundworms with altered IIS showed a 100% increase in lifespan.
Meanwhile, TOR is also a nutrient-sensing gene that allows cells to respond to changes in food availability. The pathway and mechanism of TOR are even older than hormonal signaling.
Researchers indicated that this gene is essential in the evolutionary process from unicellular to multicellular organisms. When manipulated alone, TOR can help an organism increase its lifespan by 30%.
However, the surprising result they found in their study is that manipulating both IIS and TOR genes simultaneously does not yield a 1+1=2 effect. By reducing the activity of both genes, C. elegans stopped growth responses and shifted to a body maintenance state.
This led to a fivefold increase in their lifespan, 500% compared to the 100% and 30% achieved by individual gene edits. Scientists refer to this effect as a synergistic effect.

Dr. Rollins commented: “The results of enhanced lifespan from the synergistic effect are impressive. The effect is not one plus one equals two, but one plus one equals five. Our findings demonstrate that nothing in nature exists in isolation. To develop the most effective anti-aging methods, we must consider networks rather than independent pathways leading to greater longevity.”
So, the question now is whether we can apply the same approach to humans to achieve similar results. In fact, C. elegans shares many genes and genetic pathways with us, including IIS and TOR.
With current studies, scientists believe that our lifespan is determined within the mitochondria. Mitochondria are the organelles responsible for energy conversion for cells, and their dysfunction is associated with the aging process.
Together with this hypothesis, the new research has helped explain why scientists have not been able to identify a single gene that enables us to live long and healthy lives.
Dr. Pankaj Kapahi, a co-author from the Buck Institute for Research on Aging, stated: “The discovery of the synergistic interaction [between the two genes IIS and TOR] may lead to combination therapies, each affecting a different pathway [of aging], to extend human lifespan just as we are using combination therapies to treat cancer and HIV.”
With the current results, researchers believe we can certainly envision a future where humans can extend their lifespan fivefold. “It is definitely possible; there are many examples in nature that show organisms living very long.” they stated. “However, the real focus of this field is to help people live as healthily as possible for as long as possible by preventing age-related health declines.”
This means that simply living longer is not a top priority for the near future; what scientists are concerned about here is increasing the healthy lifespan during life.

“The current refinement of similar genes in humans through drugs or other therapeutic methods may not immediately extend human lifespan by 500%, but it could create a similar synergistic response when both gene pathways are targeted simultaneously.” Dr. Rollins and Rogers explained.
“By analyzing the characteristics of these interactions, our scientists are paving the way for essential therapies to increase the healthy lifespan of our rapidly aging population.”
Currently, many countries are facing aging population rates and skyrocketing healthcare costs. This is the time when we should all seriously integrate preventive medical approaches on a broad scale to alleviate the prevalence and severity of age-related diseases.
Their new research has just been published in Cell Reports.
Source: Iflscience