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Firstly, it greatly depends on how you define immortality. If you define it as living forever and being indestructible as in a comic book, then, no, it is highly unlikely. However, if you define it in terms of showing no decline of survival characteristics, no increase in disease incidence and no increase in mortality with advancing age, then yes. The first is a science-fiction fantasy; the second is based on real-world biology that evolution has already selected for in certain species. We call this state negligible senescence.

Senescence and negligible senescence

Senescence refers to the gradual deterioration of aging and is typically very obvious in almost every species. More accurately, senescence refers to a decline of survival characteristics, such as strength, mobility, senses, and age-related increases in mortality along with a decrease in reproductive capability. Mortality rates for humans and most animals increase dramatically with age beyond reaching reproductive maturity.

A few species are more unusual and exhibit negligible senescence (NS). An organism is considered negligibly senescent if it does not show any loss of survival characteristics, such as strength, mobility, and senses, an increased mortality rate with advancing age, or a loss of reproductive capability with age.

Species

Recorded lifespan

Rougheye rockfish 205 years[1-2]
Aldabra Giant Tortoise 255 years
Lobsters 100+ years (Presumed NS)
Naked mole rat (Heterocephalus glaberis) 28 years
Sea anemones 60–80 years
Freshwater pearl mussel 210–250 years[3]
Ocean Quahog clam 507 years[4]
Greenland Shark 400 years
Lake sturgeon (Acipenser fulvescens) 152 years (Presumed NS)
Clams such as Panopea generosa 160 years (Presumed NS)

It is worth noting that even though these species do not age or age immeasurably slowly, they are still vulnerable to predation, accidents, starvation, environmental dangers, changes to their environmental niche and diseases. This means that extremely old examples of these species are very rare, especially in the wild.

To further complicate matters, we often need to sacrifice the animal in order to measure its age by examining the deep tissues and marks inside bones, much like measuring rings in a tree trunk. This means that we cannot know the maximum age that might be achieved by these species, so the above numbers are based on what information we have; there could well be considerably older examples out there. The point here is that NS species do not deteriorate with age and may live considerably longer than has been recorded.

Possibly even more intriguing is the hydra, a species that is observed to have no lifespan limit, as it regenerates very quickly. Barring predation and changes to its environment, it is one of the few species for which the phrase “biological immortality” would be appropriate[5]. The hydra is quite unique in how its cells work, and it is quite unlike the majority of other organisms on the planet; it is a true oddball but fascinating all the same.

Strategies for Engineered Negligible Senescence.

Well this is great news if you happen to be a lobster and avoid the fisherman’s pot long enough to reach a ripe old age, but what about us; how can we benefit from the same advantages that negligibly senescent species do?

It is clear that we would have to wait a long time, perhaps forever, before evolution selected the same traits in humans, so something a little more direct is needed.

Some scientists, such as Dr. Aubrey de Grey, propose that we can engineer negligible senescence by using a repair-based approach to the damage that aging causes. This is the basis of SENS, the Strategies for Engineered Negligible Senescence, and is being pursued by the SENS Research Foundation.

Should negligible senescence be achieved in humans through SENS or other, similar, repair approaches, it would potentially mean the end of age-related diseases and ill health, a most worthy goal indeed.

The inevitability of multicellular aging

Recently, a great deal of fuss has been made about humans achieving negligible senescence, with a number of articles suggesting that it is impossible. The reason is that the popular media has interpreted this recent paper very badly, assuming that the authors imply that because aging is inevitable, we cannot do anything about it[6].

The media has been filled with articles almost smugly proclaiming in some cases that aging is unstoppable and mathematically impossible to defeat. The problem with this interpretation is that it is just plain wrong. The original paper is, strictly speaking, correct in that aging damage is indeed inevitable, but it makes no assumptions about interventions. The publication says a great deal about what evolution has done and is likely to do based on observation, but that says nothing about what medicine may achieve in the future.

One cannot apply such thinking when it comes to engineering negligible senescence in humans through the periodic repair of age-related damage. So, quite simply, publications like this make little difference to work in this field, and they change the plausibility of us achieving negligible senescence in no way whatsoever.

Conclusion

There is a clear difference between Hollywood style immortality and negligible senescence, with the latter being a plausible goal in the next few decades. Evolution has already demonstrated that negligible senescence is indeed possible; now, the next big challenge is to use an engineering approach to aging to see if we can emulate in people what nature has done in a few lucky species. 

Literature

[1] Munk, K. M. (2001). Maximum ages of groundfishes in waters off Alaska and British Columbia and considerations of age determination. Alaska Fish. Res. Bull, 8(1), 12-21.

[2] Cailliet, G. M., Andrews, A. H., Burton, E. J., Watters, D. L., Kline, D. E., & Ferry-Graham, L. A. (2001). Age determination and validation studies of marine fishes: do deep-dwellers live longer?. Experimental gerontology, 36(4), 739-764.

[3] Ziuganov, V., Miguel, E. S., Neves, R. J., Longa, A., Fernández, C., Amaro, R., … & Johnson, T. (2000). Life span variation of the freshwater pearl shell: a model species for testing longevity mechanisms in animals. AMBIO: A Journal of the Human Environment, 29(2), 102-105.

[4] Munro, D., & Blier, P. U. (2012). The extreme longevity of Arctica islandica is associated with increased peroxidation resistance in mitochondrial membranes. Aging cell, 11(5), 845-855.

[5] Martı́nez, D. E. (1998). Mortality patterns suggest lack of senescence in hydra. Experimental gerontology, 33(3), 217-225.

[6] Nelson, P., & Masel, J. (2017). Intercellular competition and the inevitability of multicellular aging. Proceedings of the National Academy of Sciences, 201618854.

About the author
mm

Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies Steve has provided the community with multiple educational articles, interviews and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).
  1. November 7, 2017

    What a great article. Immorality is possible!

    • mm
      November 8, 2017

      Immorality is always possible ;)

  2. November 8, 2017

    The claim that there must be a trend to either sluggish cells or cancer assumes that cell activity is driven only by internal processes in the cells and competition between cells. That ignores the possibility of extracellular forced reprogramming of cells. This can account for the age reversal in Turritopsis, which uses transdifferentiation of cells en masse.

  3. November 8, 2017

    I suspect that I might volunteer as an NS study subject. Travis

    Note : I tried to answer a “captcha” question (correctly) as 101 but she no work.

  4. November 10, 2017

    Good article, although SENS is not about translating nature NS examples to human since it will involve much change of biochemistry (because NS species already NS, and need no repair medicine). SENS uses NS species merely as a proof. Also it is interesting how authors of the original paper deal with NS in their model. :3

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