Let’s explore the research behind a new life extension medicine under development.
While medical, scientific, and technological advancements have almost doubled human life expectancy over the last century, aging is still an inevitable part of life. Old age is the leading risk factor for diseases like cardiovascular disease, cancer, dementia, and arthritis. But why do some people live long, robust lives without much effort while others do everything they can and meet their fate at a young age? How was it possible that Jeanne Calment lived for 122 years, smoking a daily cigarette, while children under the age of one can die of cancer? The answer may lie within our cells. While cryopreservation is a type of medical technology that’s currently available to stop aging in its tracks (by stopping all sorts of cellular activity), there are new reports of a life extension medicine that could let you live 200 years or more. Here, we’ll take a deeper look into this aging research to see if it’s really worth the hype.
Biological age is different from chronological age. It refers to the vitality and health of your cells rather than the number of days since you were born. Technically, the prospect of delaying biological aging isn’t anything new. It’s something that’s been researched for years. By keeping cells healthy and reducing their “age,” life extension medicine could potentially eradicate age-related disease, reduce cellular deterioration, and even improve an individual’s overall quality of life. So, what’s the deal with this new “magical” pill that lets you live until you’re 200? Let’s find out.
Dr. Andrew Steele, scientist and author of Ageless: The New Science of Getting Older without Getting Old, is focusing his research on removing “zombie cells,” also referred to as senescent cells. He believes that there’s no real “biological reason” that humans couldn’t live until they’re 200 or more. His life extension medicine is focused on developing a compound that could eventually be taken in pill form to help flush out zombie cells. Although this sounds bizarre, human trials of senolytic drugs are already underway.
Another key player in this research is Dr. Peter Fedichev, a Russian molecular physicist. He holds similar beliefs, but understands that if lifespan was extended without doing anything to improve healthspan, there’d be no point. His primary focus is on enhancing the quality of life for as long as possible.
To understand the research of Dr. Steele and Dr. Fedichev, it’s important to gain a little background knowledge on these zombie cells everyone keeps talking about. As we briefly mentioned, zombie cells are the senescent cells. They’ve been given that nickname because they basically refuse to die, even though they’re damaged and providing absolutely no benefit to the body. Senescent (zombie) cells have actually stopped dividing altogether and just kind of hang around the body releasing harmful inflammatory compounds that accelerate aging. When we’re young, our immune system can eliminate these. However, the process of removing them becomes increasingly less efficient over time.
Therefore, the older we get, the more zombie cells accumulate within our body. This can lead to inflammation that affects metabolism, decreases overall stem cell function, and promotes aging and the health risks associated with it. This is one of the reasons that senescent cells are considered a driving force in the process of aging. Zombie cells contribute to chronic disorders, including those that account for morbidity, mortality, and health expenditures [2].
Removing the zombie cells is the key to life extension medicine. At least that’s what researchers claim. Senolytic drugs are a class of drugs that selectively clear senescent cells within the body [2]. They work by reducing unnecessary cellular death while simultaneously supporting the eradication of zombie cell build up. Senolytic drugs can “help delay, prevent, or alleviate frailty, cancers and cardiovascular, neuropsychiatric, liver, kidney, musculoskeletal, lung, eye, haematological, metabolic, and skin disorders as well as complications of organ transplantation, radiation, and cancer treatment” [2].
Early clinical trials of senolytic drugs on humans are already underway, but until these studies are completed, we can’t make any assumptions. However, there are quite a few promising studies on senolytics that deserve recognition.
While the idea of taking a pill in the future to slow, or even reverse aging might seem absurd, there is actually scientific research to back these claims. Some of the most promising studies on some of the possible drugs that could have anti-aging implications are as follows.
One study, conducted in 2016 by a team of researchers at the University of Washington, found that the FDA approved drug called rapamycin (currently used to prevent rejection of transplanted organs) could increase the lifespan of mice and even humans. It was found that, “three months of rapamycin treatment is sufficient to increase life expectancy by up to 60% and improve measures of healthspan in middle-aged mice” [3]. The combination of not only an elongated life, but also a higher quality life, which is essential in the race to treat aging.
Another study conducted in 2016 and led by the Mayo Clinic College of Medicine found that removing cells that contribute to senescence in mice by injecting them with a synthetic drug (AP20187) extended their life by up to 35%. This drug, AP20187 is an activator of sorts that triggers cell death (apoptosis), thus clearing many of the cells that contribute to age-related disease. The results of this study suggest that senescence is the primary driver of aging.
Researchers from the Mayo Clinic went on to test this strategy again. During the study, they “treated” mice and removed senescent cells with similar methodology. This led to an extension in median lifespan by 17% to 42% depending on their diet, sex, and genetic background. Mice who were treated and had senescent cells removed also tended to look healthier, increase activity level, and spark a sense of youthful curiosity. On a deeper level, scientists found that “the treatment slowed age-related changes in fat, kidney, and heart function. It also delayed tumor formation of a variety of cancers…” [4].
One of the most recent studies, which occurred in 2020, found some of the first evidence that senolytics had the potential to decrease senescent cells in humans. The study, published in EBioMedicine, demonstrated that a “short course of senolytics decreases the senescent cells in humans with drug-controlled diabetes mellitus and chronic kidney disease (CKD)” [6]. As a result, subjects experienced a reduced progression of diabetes and CKD.
Although interesting, there are also limitations to these studies. For example, in the Mayo Clinic follow up study that showed an improved lifespan in mice, there were no differences found between treated and untreated subjects in regard to memory, muscle strength/mass, metabolic features, motor coordination, or balance [4]. If used in humans, this could potentially increase overall lifespan, but there may not be the same impact on healthspan or quality of life. Trials need to be conducted, and finished, before any real implications can be drawn.
There’s also a fine line between researchers' success and failure in their test subjects. For instance, four genes that convert adult cells back to embryonic-like ones (known as the Yamanaka factors) can help clear senescent cells. However, in a study where these were activated, some mice who were treated continually ended up developing tumors and dying within a week, while those who only received two days of treatment lived [5]. Long-term effects in humans could be drastically different.
Finally, and arguably one of the most important challenges, is that no one in the history of time has ever tried to “treat” aging. This is new ground and is going to require research, more research, and then even more research. While the prospect of removing zombie cells seems straightforward, it’s a lot more complicated than what’s discussed on the surface. Don’t get me wrong, it’s interesting research in the field of longevity and aging, but don’t expect to buy it at your local drugstore any time soon. On the other hand, if you’re interested in longevity and realistic alternatives to anti-aging pills, cryopreservation is a great option to explore. As of today, it’s the only Plan B you can have in case none of this anti-aging technology becomes available during our lifetime.
Who knows, maybe this research could supplement cryopreservation in the future. It may even act as a bridge between cryopreservation and revival by providing key insight on how to cure aging before rewarming occurs. While it could be an exciting journey, we still have a long way to go on both fronts. If you want to allow yourself the possibility to see how these things play out in the future, sign up for biostasis with us today. You can also schedule a call to ask us all of your cryopreservation questions or learn more about the inevitable process of aging.
[1] Davies, J. (2022, June 27). Anti-ageing: Why living until you’re 200 really isn’t a pipe dream. Mail Online. https://www.dailymail.co.uk/health/article-10946839/Anti-ageing-living-youre-200-really-isnt-pipe-dream.html?ito=social-facebook&fs=e&s=cl
[2] Kirkland, J L, and T Tchkonia. (2020, November) Senolytic Drugs: From Discovery to Translation. Journal of Internal Medicine. John Wiley and Sons Inc., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7405395/
[3] Bitto, A., Ito, T. K., Pineda, V. V., LeTexier, N. J., Huang, H. Z., Sutlief, E., Tung, H., Vizzini, N., Chen, B., Smith, K., Meza, D., Yajima, M., Beyer, R. P., Kerr, K. F., Davis, D. J., Gillespie, C. H., Snyder, J. M., Treuting, P. M., & Kaeberlein, M. (2016, August 23). Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice. eLife. https://elifesciences.org/articles/16351
[4] Wein, H. (2016, July 13). Senescent cells tied to health and longevity in mice. National Institutes of Health (NIH). https://www.nih.gov/news-events/nih-research-matters/senescent-cells-tied-health-longevity-mice
[5] Weintraub, K. (2016, December 15). Aging Is Reversible—at Least in Human Cells and Live Mice. Scientific American. https://www.scientificamerican.com/article/aging-is-reversible-at-least-in-human-cells-and-live-mice/
[6] Ellison-Hughes, G. M. (2020). First evidence that senolytics are effective at decreasing senescent cells in humans. EBioMedicine, 56, 102473. https://doi.org/10.1016/j.ebiom.2019.09.053
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