Bigger creatures should have more cancer risk. However, Elephants do not have high rates of cancer. They have some kind of protection.
* elephants have 20 extra duplicates of p53, a tumor suppressor gene.
* they also duplicate copies of the LIF gene, which encodes for leukemia inhibitory factor.
Elephant cells commit suicide at the first hint of abnormality.
Above – Lucy Reading-Ikkanda/Quanta Magazine
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There is a kind of tumor against which éléphants are not protected: the human face…;-(
Your face in particular, is extra deadly to elephants.
If simple duplication of tumor suppressor genes provides such an effect then this could be a way to make people immune to cancer development. Genetic vaccine perhaps provided in utero will do this. There are other clues that it is true.. People with BRCA1 mutation have one copy of P53 TSG and as a result have drastically increased chances of Breast and Ovarian CA….
I would be shocked if it weren’t more complicated than that. Multiplication of tumor suppressor genes has to have some costs/downsides, or else it would be universal through all animal species.
Elephants have undoubtedly evolved some compensatory mechanism permitting that multiplication.
Big ears!
But seriously, in animals where there is a greater risk of some condition, there are often adaptations…and there is no logical reason there must be a cost. There could be, but it is not required.
Though that does not mean we can just copy and paste and expect it to work in humans.
If there is a cost, it is probably that cells can only multiply so many times (they reach the Hayflick limit). If cells suicide at the first hint of a problem, that might mean a faster turnover…and cells approaching that limit faster. I wonder if elephants have longer telomeres to compensate, or a way to extend them as needed.
I’ve been saying for a long while that we’re more likely to find hints on how to extend our longevity in longer lived mammals, than in mice and nematodes. They’ve already worked out strategies for longevity, and they might not be the same as our’s.
Sadly, large and long lived animals are orders of magnitude more difficult and more expensive to experiment with than small, short lived mice, nematodes and zebrafish.
I can just imagine writing a research proposal in which the university sets up an elephant breeding colony to conduct a 200 year longevity experiment. We will have to take over the main sports stadium and athletics ovals of course…
Not necessarily. With CRISPR we can just insert those genes into mice or rats…see if there is any effect on longevity…cancer rates or whatever.
And we already know the main 2 reasons some animals live longer than others. 1. Antioxidants: rats and mice have very poor built in antioxidant systems so that route is very effective on them. Humans however have very good antioxidant systems built in: SOD 1, 2 & 3, Glutathione peroxidase 1-8, and Catalase. In total we have a far more comprehensive antioxidant system with very high activity level. Though it is obviously incomplete requiring a number of vitamins from our food or supplemented, and some production does fall off as we age. This path though has been a big disappointment, because we don’t see the longevity gains with crazy amounts of antioxidants we see in rodents translate to humans.
2. The other method long lived animals have found is lower body temperature. Body temperature is a function of optimal enzyme activity…particularly the enzymes involved in making ATP via cellular respiration (the physics of the molecules dictates their temperature range of activity). Naked mole rats can operate at the temperature of the ground which is why they do not need hair to insulate themselves. Bowhead whales live over 200 years because their body temperature is a few degrees lower than ours (92.5F). Many fish/sharks live very long and some reptiles because their enzymes operate at a different temperature range.
Elephants are about 2 degrees cooler than humans, which I think is sufficient to explain their long lives.
The main group we have not adequately explained are the birds. There are many that both operate at a high temperature and live a long time, and often while operating at an intense activity level for very long periods that should shorten their lives but does not. I think that is the most promising direction to follow, because we have no idea how they are protecting their cells.
And some hydras’ ability to grow older and then younger and cycle is, of course, really special and interesting. Could that be applied to humans? I think that will be science fiction for a while. At least programing ourselves to do that naturally. A bunch of interventions turning back the clock? No longer that far fetched.
Yes, you’ve identified why doing longevity research in short-lived species is unlikely to be productive. Why do we live longer than they do? Because they don’t have a lot of longevity mechanisms we do.
You find an intervention that works in mice, usually you discover you’re just replicating something humans already do. And already do almost to the limit of what’s feasible. (For instance, why do humans get gout? Uric acid is an anti-oxidant! And we have much more of it in our systems than most species.)
The naked mole rats are an interesting case, a small, long lived animal. And we’ve already discovered some interesting things about them: They have a special error correcting mechanism in their ribosomes, for instance, which makes them much less error prone than other species.
Temperature regulation is an interesting approach, goes back a long ways. It has downsides, one reason we have such high body temperatures is that bacteria don’t handle heat well. That’s why our body temperatures go up higher to fight infections. Lower your body temperature a few degrees, and you might live longer, but maybe not if a bacterial infection kills you first.
Hydras are a bit of a dead end, I think. Sure, it would be keen to have hydra longevity, but at the price of periodically dissolving into undifferentiated cells, and reforming a new body without any memories? A bit harsh.
I think you’re right about the birds. Their lifestyle is so metabolically demanding, they’ve evolved all sorts of interesting adaptations. Counter-current exchange lungs, for instance. Brains that use neurons more efficiently.
Their longevity key seems to be better protection of mitochondria. But this may actually be a consequence of their high metabolic activity; Mitochondria naturally are conserved better in tissues with high metabolic activity and cell turnover.
It’s an interesting mechanism: Mitochondria have their own genes, and form reproducing populations subject to evolution within our cells. Sometimes a mitochondrion will mutate in such a way as to stop producing energy. It’s still capable of reproducing at a reduced rate, though, because it will get some energy from the other mitochondria in the cell.
Because these mutant mitochondria are not producing energy, they don’t take damage, and don’t get targeted for removal by cell cleanup mechanisms. This gives them a reproductive advantage, and eventually the mutants displace the functioning mitochondria, and that cell goes senescent.
But in tissues with high rates of cell turnover, the fact that the healthy mitochondria reproduce faster dominates, letting them out compete the mutants. So rapidly reproducing tissues tend not to go senescent.
I’d guess that birds either have high rates of cell turnover due to their energetic lifestyle, or have evolved better mechanisms for protecting against mutant mitochondria.
SENS, of course, has protecting against mutant mitochondria as one of it’s key strategies.
The drunk and the light post phenomenon: Looking where it’s easy to look, rather than where you’d rationally expect the car keys to have fallen.
A huge amount of medical research is done under the lamp post.
It isn’t such a bad idea if you know there are a lot more than one set of keys scattered around. Even if there is a higher key density in some areas of darkness, you’ll still have a higher success rate in the light.