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Aging is a natural part of life, but that hasn't stopped people from embarking on efforts to stop the process. Unfortunately, perhaps, those attempts are futile, according to University of Arizona researchers who have proved that it's mathematically impossible to halt aging in multicellular organisms like humans. "Aging is mathematically inevitable - like, seriously inevitable. There's logically, theoretically, mathematically no way out," said Joanna Masel, professor of ecology and evolutionary biology and at the UA.
Masel and UA postdoctoral researcher Paul Nelson outline their findings on math and aging in a new study titled "Intercellular Competition and Inevitability of Multicellular Aging," published in Proceedings of the National Academy of Sciences.
Current understanding of the evolution of aging leaves open the possibility that aging could be stopped if only science could figure out a way to make selection between organisms perfect. One way to do that might be to use competition between cells to eliminate poorly functioning "sluggish" cells linked to aging, while keeping other cells intact. However, the solution isn't that simple, Masel and Nelson say.
Two things happen to the body on a cellular level as it ages, Nelson explains. One is that cells slow down and start to lose function, like when your hair cells, for example, stop making pigment. The other thing that happens is that some cells crank up their growth rate, which can cause cancer cells to form. As we get older, we all tend, at some point, to develop cancer cells in the body, even if they're not causing symptoms, the researchers say. Masel and Nelson found that even if natural selection were perfect, aging would still occur, since cancer cells tend to cheat when cells compete.
https://phys.org/news/2017-10-mathematically-impossible-aging-scientists.html
[Abstract]: Intercellular competition and the inevitability of multicellular aging
So, either you die of old age or you die of cancer. Choose wisely !!
(Score: 0) by Anonymous Coward on Tuesday October 31 2017, @10:16AM (8 children)
Im glad to see this basic conclusion anyone should be able to draw from the current conception of cancer is finally getting attention. The response to Tomasetti and Vogelstein a few years ago was really revealing about the current state of quantitative ignorance in biomed. You can see their most recent response here: https://www.ncbi.nlm.nih.gov/pubmed/28336671 [nih.gov]
The controversy that ensued from their 2015 paper was ridiculous. If you think cancer is caused by accumulated errors, then more divisions means more cancer. It is so obvious...
(Score: 4, Insightful) by aiwarrior on Tuesday October 31 2017, @11:00AM (7 children)
I am not biologist, but I remember that the current new understanding is that aging is not a purely entropic process where the information just gets degraded. It is in fact a feature that ensures people age and die for reasons of species fitness.
The reason age is not entropic, at least in regard to our lifespan's limitation, is that we have several million whole DNA copies which can be taken to rebuild damaged tissue a-la ship of Theseus. Can you point at how my reasoning is flawed?
(Score: 2, Insightful) by Anonymous Coward on Tuesday October 31 2017, @12:54PM (4 children)
Sure, although I would put this closer to "natural selection taking advantage of aging". Ie, I would think it is easier to select for aging than against it.
I don't think you can really go from DNA sequence -> functioning human body like that. All the tissues form under certain conditions in a certain order. Eg: https://en.wikipedia.org/wiki/Temperature-dependent_sex_determination [wikipedia.org]
Also, I doubt any two cells in an adult body have the exact same genome as the original fertilized egg. Say you have mutation rates of p = 1e-10 mutations/bp/division (I don't think anyone really knows this value, but that is probably on the low end, imo) and you have nBase = 6.4e9 basepairs.
The probability any one base is not mutated will be q = 1-p. The probability base[1] *and* base[2] do not mutate is q[1]*q[2] = q^2. The probability none of the bases mutate is q^nBase ~ .55, or 55%. If instead the mutation rate was 1e-9, it would be ~0.2%. And that is after only a single division. For more than one division, that would mean no mutation during division1 and division2, etc. We would use:
(Score: 0) by Anonymous Coward on Tuesday October 31 2017, @12:56PM
Oops, used the rounded nBase:
Anyway, same order of magnitude.
(Score: 2) by Reziac on Wednesday November 01 2017, @02:58AM (1 child)
According to one DNA researcher (who specializes in ancient DNA) humans average about 50 new mutations per generation (I believe he meant per descendant, not the aggregate), tho most don't change anything we'd notice.
And there is no Alkibiades to come back and save us from ourselves.
(Score: 0) by Anonymous Coward on Wednesday November 01 2017, @12:31PM
This is consistent, 1e-10 mutations/base/divisionX 6.4e9 bases X 100 divisions = 64. That assumption of 100 divisions seems to high though (its even above the hayflick limit). But this is circular since that type of data that was used to estimate the mutation rates...
The germline cells sperm/eggs) that make it into the next generation are also going to be a biased sample (due to selection), so I'm not sure the number of mutations that filter through that process can be used for more than a lower bound on the mutation rate.
(Score: 2) by aiwarrior on Thursday November 02 2017, @02:36PM
Well your premise seems wrong. According to [1]: "Recently reported estimates of the human genome-wide mutation rate. The human germline mutation rate is approximately 0.5×10−9 per basepair per year|
Look at the magnitude per year!! Your reasoning seems good in other aspects but with the odds so off i think it mostly fails. Am I missing something?
Thanks for the thorough answer by the way.
[1]Scally, Aylwyn (2016). "The mutation rate in human evolution and demographic inference". Current Opinion in Genetics & Development. 41: 36–43. ISSN 0959-437X. PMID 27589081. doi:10.1016/j.gde.2016.07.008.
(Score: 1, Interesting) by Anonymous Coward on Tuesday October 31 2017, @01:15PM
Another thing is that a good way to attack the aging and cancer problems may be to reduce the mutation rate a few orders of magnitude. However, that may have unintended consequences.
It is possible (I'd say very likely) that the mutations are actually taken advantage of to increase diversity. For example, there have been some reports that a large number of neurons actually have a different number of chromosomes (a type of large-scale mutation). Like most things in bio at this point the estimates vary widely, nobody really knows:
https://genomebiology.biomedcentral.com/articles/10.1186/s13059-016-0976-2 [biomedcentral.com]
(Score: 0) by Anonymous Coward on Tuesday October 31 2017, @02:29PM
What backs you up is the existence of large creatures like whales - whose cells would necessarily have undergone many more divisions than our cells would have, and yet aren't having the same cancer per division rates as we do.
Our cells probably don't have the same amount of "Error Correction and Control" as whale cells.
Works for the first zillion copies. But after while as more mistakes accumulate and spread how do we know which copies are still faithful to the originals?
So the workaround is a limit[1] on how many divisions before a self destruct.
And after a while there just aren't enough stem cells:
https://www.newscientist.com/article/dn25458-blood-of-worlds-oldest-woman-hints-at-limits-of-life/ [newscientist.com]
Maybe what you could do is donate stem cells to your future self. Genetic drift should not be a problem as long as stuff still works after all human chimeras can exist: https://en.wikipedia.org/wiki/Chimera_(genetics)#Humans [wikipedia.org]