I am in my 30s as I type this. And the idea of celebrating my 100th birthday is unthinkable. Even unimaginable. After some clinical experience with the elderly, I don’t even know whether to feel happy or sad when another centenarian is pestered by curious and anxious people looking for their secret. Because being 100 in 2017 means you go through pains of all sorts. Even if you appear smiling in the newspaper.
In other species it is possible to be 100 years old without any sign of damage. I refrained from using the word ‘pain’ because that is subjective. But if an animal or a plant shows no major signs of aging, then we can presume they have no ongoing pain. At least no age-related pain.
Such species are more frequent than you’d think. Outside nerd circles, nobody talks about them. And yet lots of peer-reviewed papers – often written by niche biologists and gerontologists and vets – describe the phenomenon of negligible senescence and/or extreme lifespans.
As most of you know, I got really curious about these species. Extreme lifespans are attained in species that don’t age but the reverse is not true.
The first thing that extreme lifespan record-breaking species do right is that they grow slowly. And most of them continue to grow after reaching adulthood.
Slow growth takes place in hostile environments. You could say that what doesn’t kill you will at least slow down your aging rate. Or even make the species evolve itself out of aging.
Environments where slow growth take place are harsh. Low in oxygen, low in nutrients and low in beautiful summers. These places prove to be just as harsh not only for the negligibly senescent species out there (like the Proteus anguinus olm), but also for their predators which could attack them or microorganisms which could infect them.
Slow growth can make the difference between living 80 years old and living 1653 years old as in the case of this white cedar tree.
But slow growth per se is not enough. The second thing that extreme lifespan record-breaking species do right is that they reproduce asexually, whether this is the only way they reproduce or whether they reproduce sexually as well. The reason this is important is that asexual reproduction would be impossible if most or all of the cells would lose their totipotency. How would you create a new individual then?
Before I go any further, let me be the devil’s advocate and tell you that not all species reproducing asexually live a long life and not all of them avoid aging. Sometimes, cell polarization takes place and clonal aging becomes the undesired result. Usually, that is when sexual reproduction saves the day.
Which brings me to the third thing that extreme lifespan record-breaking species do right: they are modular organisms. As their name suggests, these individuals are made of one module which they repeat as many times as their external environment allows. Modular organisms do several things right which increase their likelihood to avoid aging and have long lifespans. It’s not a rule that being modular allows you those two things, but it surely helps.
First of all, modular organisms are usually primitive. With simplicity come lots of advantages. Multicellular modular organisms organize their cells as a democracy. And like any democracy, the lower the number of individuals, the better. Or in this case the number of cells. It is important for a modular organism to be able to reproduce asexually, exclusively or not. So most of their cells have the right and the ability to divide and produce offspring. Not all of their cells are that flexible, but a couple of them are even as adults. Which is a big deal!
Multicellular unitary organisms – like you and me – run their cell populations as a monarchy. Most cells may have the right to divide, but not all cells have the right to produce offspring. Only germ cells are allowed to do that. They are the monarchy. And the rest of the cells must maintain those two germ cells.
Coming back to modular organisms, they do another thing right: they are poikilothermic. They’re not the only ones to do that, but couple that with no germ-soma segregation and things do add up. Poikilothermy makes you more dependant on the external environment. But if surrounding temperatures are low, lifespan increases take place in poikilothermic species, while effects in species that maintain some central body temperature are negligible at most. If you turn up your air conditioner you won’t live more than the rest of us. It’s only your electricity bill that will get up. The only time when humans are poikilothermic is when they sleep. And even then, only during REM sleep. And would poikilothermy in humans be compatible with having an energy-demanding brain? I doubt it.
To sum it up before I’ll end this blog post, the three things extreme lifespan record-breaking species do right are:
-they live in hostile environments which slow down their growth
-they are capable of asexual reproduction
-they are modular organisms
I know what you’re thinking right now even if you may not admit it in a comment below. Leaving aside the thorny problem of desirability, could humans ever live for millennia like brain corals and sponges and evergreen trees and many other species do?
I hate giving estimates because I am no witch predicting the future, but I put this blog post out there because it could give some ideas to some researcher out there. Aging is more complex than you’d think at first sight and it’s a pity to waste your time with incremental, slowing down aging research when there are species out there which don’t age and/or live for millennia.
There is not much you can do about the unitary design of humans. Least we’d stop being humans. But there is the field of regenerative medicine. Then there is cloning. There is much to be learned from asexually reproducing species because their cells need to maintain their flexibility even when differentiation is a necessity. At least a couple of their cells maintain totipotency as adults. Here is a case study to give you something to ponder: most coral colonies live for more than 4,000 years old, but the coral colony of Stylophora pistillata dies after a couple of years, with reproduction ceasing 6 months earlier.
As for slowing down growth, you could already achieve that to a certain degree with calorie restriction. Which is not only free, but it could also save you money on your food bill 🙂 Decreasing temperature may not work much because humans are endothermic. As for low oxygen levels, these do not differ in human societies with one exception: living at altitude. But before you start packing up to move in a mountain village, let me stop you by telling you species which are adapted to low oxygen levels are exposed to hypoxia intermittently. And that is when adaptation takes place. That is when free radicals are produced. Check out this Wiki article on reoxygenation and reperfusion injury. The organisms that slow down growth face intermittent oxygen levels in their natural environments. I’m thinking of the bowhead whale which needs to periodically dive in deep waters to catch its prey or the naked mole rat which lives in deep, underground tunnels.
So apart from calorie restriction on the short term, what I’d focus my energies in the next decade is regenerative medicine. And if you work in the field or you intend to and you’re reading this blog post, please check out the genetic expression of hydras, sponges, corals and many other beautiful creatures, some of which you could raise in an aquarium. It will be worth it, I promise.
Anca Ioviţă is the author of Eat Less Live Longer: Your Practical Guide to Calorie Restriction with Optimal Nutrition ,The Aging Gap Between Species and What Is Your Legacy? 101Ways on Getting Started to Create and Build One available on Amazon and several other places. If you enjoyed this article, don’t forget to sign up to receive updates on longevity news and novel book projects!
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Hi Anca,
interesting ideas, thanks.
“Aging is more complex than you’d think at first sight and it’s a pity to waste your time with incremental, slowing down aging research when there are species out there which don’t age and/or live for millennia.”
–But before we can get there, incremental increases are welcome, and likely much easier to achieve.
You mention growth limitation through caloric restriction — but what growth do you mean if humans don’t grow much after 20-25 anyway?
My opinion is that it would be useful to look at such species and for such adaptations that could be transferred to a living adult human, for the purpose of slowing down aging.
So then obviously we can’t transfer the 3 adaptations you mention (though I agree on the potential for ideas for regeneration research)
I think what would be very valuable for research is to find pairs species that
— age very differently,
but:
–live in same or similar environments,
— are evolutionarily close to one another,
— are evolutionarily closer to us (probably less important than the other 3 above)
For example, I read an article that compared 2 clams, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143345/ , which I think satisfy first 3 of the above criteria. I found it interesting that the authors attributed part of the longevity of one of the clams to resistance to oxidative stress — which in principle could be genetically engineered in people too (or not?)
Then to verify the alleged (genetic) cause of the difference in longevity in that pair, research would need to try to genetically engineer the other species to replicate the longevity trait. Then do so at an individual-level of that species.
Then proceed to try to replicate these results in species closer to us. Then eventually humans.
Thoughts?
Thank you for taking the time to comment!
Indeed, humans don’t grow after reaching adulthood. Most cells are either kept in check or they are not replenished anymore as they used to. But the hypertrophy common with old age is a form of growth that tried to compensate for organs such as the heart having fewer cells and having to make do with those. Those few cells increase in size now. Actually this may remind you of the phenotype of senescent cells which are larger than normal ones that divide properly. Obesity accelerates such hypertrophy because calories are abundant and cells can grow more in size. For this reason, I think calorie restriction with optimal nutrition is more useful after midlife when some organs (not all) grow in size.
Regarding close species that differ in the rate of aging, although I don’t know if they also differ in their lifespan, you may find this blog post useful on 2 such species of Hydra invertebrates: https://longevityletter.com/how-temperature-switches-aging-on-and-off-in-hydra-animals/
And as regards the two species of clams in that link, Arctica islandica is a special case but there are differences in its lifespan even between clams that live around Germany versus clams that live around Iceland. Arctica islandica grows very slowly because it can afford to (it is a clam that can burrow in the sand and that adds protection in addition to its shell) and it lives in cold waters (low temperature increases lifespan in invertebrates).
You could also test that idea by blocking a gene, this being easier than introducing a new gene in a growing animal. Check out the Laron syndrome in humans – it seems to mimic calorie restriction as such patients carry mutations of a gene coding for the growth hormone receptor and they are unable to use (much of) this hormone even when available. With calorie restriction you downregulate the synthesis of growth hormone through the lack of sufficient calories.
Thank you for explaining the growth you meant ( I actually hesitated to ask, fearing it would appear a silly question ). Hypertrophy, yes makes sense. I read somewhere long ago that a smaller heart in adults & olds is healthier than a bigger one – might be related to what you say.
I’m not doing actual calorie restriction nowadays (maybe I should resume some fasting), but I avoid overeating and have a habit of fasting overnight for 12 hours (not much I guess).
So those 2 clams both live in cold waters, but you’re suggesting that Arctica Islandica has the additional advantage of slower growth… I see. Well, then they could try to mutate a gene for growth hormone (as you mention later) in Mercenaria mercenaria to make that slower growing too.
I see that blocking a gene can be easier, but the ultimate goal is not just to understand the mechanism, but to engineer a organism to age slower, either by blocking or introducing genes.
Finally, through these discussions, I get to suspect that all these ideas most likely come to other researchers’ minds too.
And why then the anti-aging research is slow?… I guess because biologists are scattered across various topics, not just aging, and even when for aging, they don’t unite in bigger programs.
Or maybe it is slow because experiments take time and money and brains and everyone competes for these resources. Plus life.
Which is additional reason they should focus on aging research, and less on other things