Unless you are a tree, a lobster, or some other sea creature, you are probably aging… which is another way of saying that beyond adulthood, your fitness decreases while your mortality risk increases over time. Though some pretend that aging is a well-understood process… from a scientific point of view, it largely remains a mystery.
There is plenty of room for debate, but there are generally two different ways to understand aging.
Some believe that aging is simply the result of an evolutionary neglect or compromise. That is, given that animals never get very old in the wild, their genes are simply not geared toward keeping them healthy and fertile for a long time. This is problematic as a theory because slightly older individuals in the wild are affected by aging (a 30-year-old man is less fit than a 25-year-old man) sufficiently to cause their death or prevent them from reproducing. We also know that many of our ancestors did live quite old and chances that many died in part due to the fact that they were weaker due to age. Others believe that aging is the result of some kind of compromise… the body exhausts all its energy on reproduction, and is incapable, as a consequence, of remaining fit. This is also problematic and I have written an entire blog post to explain why this appealing theory does not fit the facts.
There is also another entirely different theory that says that aging serves an evolutionary purpose. It is a population control mechanism. Without aging, the old and strong individuals would dominate, leaving little room from younger people with newer genes… and this would create a less adaptable population more likely go through extinction events. This theory is also problematic because if, in a given population, some people remain fitter and more fertile, their genes would spread more easily and they would come to dominate the population.
Thus, we are left with multiple theories, all of them with apparent disqualifying faults.
Vladimir Titorenko, a biology professor at Concordia University in Montreal, has come up with an experiment that seems to confirm that aging is the result of an evolutionary program. For his demonstration, Titorenko used yeast. Though you may not think of yeast as an animal lifeform, it is a well-established model for our biology. We have more in common with yeast than you may expect. Importantly, yeast ages.
In any case, Titorenko put yeast into some chemical (lithocholic acid) that Titorenko describes as aging-delaying. This created mutants that live five times longer while growing and reproducing just as well as normal yeast if you keep them separate from normal yeast.
In Titorenko’s view, this constitutes a validation of the programmed theory of aging. Indeed, if you are able to reprogram biology to significantly increase lifespan without affecting fitness, then you are “proving” that evolution had the option of much longer lived individuals but somehow selected against them.
We provide evidence that the dominant polygenic trait extending longevity of each of these mutants 1) does not affect such key features of early-life fitness as the exponential growth rate, efficacy of post-exponential growth and fecundity; and 2) enhances such features of early-life fitness as susceptibility to chronic exogenous stresses, and the resistance to apoptotic and liponecrotic forms of programmed cell death. These findings validate evolutionary theories of programmed aging. We also demonstrate that under laboratory conditions that imitate the process of natural selection within an ecosystem, each of these long-lived mutant strains is forced out of the ecosystem by the parental wild-type strain exhibiting shorter lifespan. (Aging 2016)
It is still unclear how the longer-lived individuals lose out to the normal years… but they speculate that normal yeast has some trick to penalize longer-lived individuals. That should be expected: for the programmed theory of aging the work, you need some robust approach to do away with longer-lived individuals (i.e., “cheaters”). In multicellular organisms like human beings, you can count on several builtin mechanisms to limit lifespan… but in something as simple as yeast, you probably need to count on the community because it is hard to build enough safeguards without a single cell.
Interesting times. I am not convinced that Titorenko proved the programmed theory of aging, but I am looking forward to reading his future work.
Further reading : Mitteldorf’s Cracking the Aging Code, Fossel’s The Telomerase Revolution, de Grey’s Ending Aging, Farrelly’s Biologically Modified Justice and Wood’s The Abolition of Aging.
Evolution favors evolution – as it works.
Evolution does not care if you die. If you were successful in procreating, your (perhaps) superior genes are present in your children. Evolution does not care whether you (an exceptionally long-lived individual) or your children pass along your superior genes.
This is a bit like software development. Do lots of small iterations, and hope to fail fast and early (for wrong paths).
OK … the above is a theory.
Ask a related question. How far back in evolution can we find organisms that age? If aging is a winning strategy for evolution, we should expect aging to appear very early.
Yeast is not exactly a recent organism. So we can safely say that organisms aged millions of years ago. I am not sure it proves anything, however.
If most folks died of an accident during their child-bearing years, then a minority population who lived longer and could still procreate would have an evolutionary advantage over those with less offspring – do I have that right?
(…) then a minority population who lived longer and could still procreate would have an evolutionary advantage over those with less offspring – do I have that right?
It would seem like this makes sense. And so natural selection would favor people with slower aging. But it does not seem to work that way.
Note that you the same “false” reasoning works with reproduction. There are two main ways to reproduce. You can clone yourself or you can proceed by sexual reproduction. Now suppose that a few individual develop, in addition to sexual reproduction, the ability to clone themselves. (For example, a woman could fertilize her own eggs.) That would seem advantageous. For example, in cloning, you preserve 100% of your genes, not just a fraction of them. Moreover, there are lots of cases where mates are not readily available, so cloning could allow you to reproduce when you otherwise couldn’t. So it would seem like evolution should favor cloning, but it does not.
I’m not sure you’re listing all the theories on aging? Specifically, I thought there was fairly strong evidence that aging is a defense against cancer, that it is a mechanism for controlling defections by individual cells, for limiting out-of-control cell growth. Am I mistaken?
This is important, as it suggests that aging can’t be eliminated without adding another defense against cancer. Any attempts to reduce the impact of aging, under this theory, would yield problematic increases in cancer rates. I thought this was widely accepted? Am I mistaken?
@Greg
I don’t know what aging is and I am pretty sure nobody really knows… so people are free to have theories.
Aging is remarkably preserved across species all the from yeast to us. Not all animals age… a few are ageless (lobsters die like trees because they grow too big… but they don’t age in the way we do).
This means that unicellular organisms (like yeast) that can’t have cancer also age. So it is difficult to see how cancer can be the reason behind aging…
I provide links to several books that describe several of the theories. I think I cover the main ones in my blog post but feel free to dig further.
You may refer to a variation on the telomere theory of aging whereas our cells can only divide so nany times (Hayflick limit). That might serve as a protection against cancer. However, it is unclear how it relates to aging. Mice age fast despite having long telomeres. Bats are very similar to mice, but live much longer. So do naked mole rats (who live long, with few cancers despite being very close to mive). It is unclear whether having long or short telomeres protects against cancer… In mutant mice with limited telomeres… we ended up getting more aging and more cancer… mutants mice with super long telomeres did not have more cancers… The data is all over the place.
Human beings who are born with very short telomeres undergo accelerated aging and they die young… so, certainly, it is not too good a protection to have super short telomeres.
In our bodies, we have stem cells that can elongate their telomeres (e.g., with telomerase), so I don’t think telomeres act as a limit that explains aging… though Fossel (see one of the books I reference) thinks it does… and he wants to try to elongate telomeres to, for example, cure Alzheimer’s. Maybe he is right.
I think at some point telomeres could be a limit for us, but I do not think that the loss of fitness we experience is caused by telomere shortening. At least not in our first few decades.
In human beings, cancer rates go up exponentially with age. They are very low when we are fast developing (e.g., teenage years) and have long telomeres. So cancer along with dementia and the cardiovascular diseases are what I refer to when I allude to the diseases of old age.
You could also refer to the theory that our body shuts down its activity to protect us from cancer. That’s a problematic theory as much of what happens with age makes cancer more likely… such as immunosenescence. If the body was trying to protect us against cancer as we age, we would at least maintain everything that protects us from cancer… maybe shutting down everything else… but that’s clearly not happening.
And this explanation relies on the belief that our bodies do everything they can to last longer. But is this true? If it were true, you could not reprogram biology to make aging organisms live much longer… but you can as with yeast here…
If you underfeed mice you can also make them live much older… showing that their biology leaves some longevity on the table.
You could describe aging as the cause (primary factor) of cancer in human beings. That is, many people believe (me included) that if we defeated aging, we would make cancer much less troublesome. Young people do die of cancer, but it is relatively rare and it is relatively easy for doctors to help young patients. It is much harder to treat elderly cancer patients.
aging can’t be eliminated without adding another defense against cancer
I guess we get into semantics here. What is aging? I defined it as a loss of fitness and increased risk of death with passing time. I think it is generally accepted that a comprehensive anti-aging therapy would have to stall cancer.
I don’t like to talk about eliminating aging however because of this exact problem… we don’t know what it means. Do we mean entering into a machine and getting out with a youthful look?
I prefer to talk about the possibility of getting the diseases of old age (cancer, Alzheimer’s…) under control.
So, yeah… if your risk of cancer keeps getting exponentially higher, I’d say you are aging… even if you look youthful.
Thanks, Daniel, I think we’re mostly agreeing, given what you said about anti-aging having to stall cancer.
And I appreciate your discussion here, as it forced me to back up what I was saying. A bunch of interesting articles came of that, some of which I had seen before, but, to focus on one, here’s a great survey of the latest, stating, at one point, “aging is a method that the body uses to attempt to escape from cancer”, which is again a point where I think we agree:
http://ascopubs.org/doi/full/10.1200/JCO.2014.55.1432
What predictions could we make to test this theory?
Well… fast aging organisms should be better protected from cancer…
Let us see…
Normal mice age fast and are very prone to cancers while naked mole rats age very slowly and are mostly cancer free.
We could look at families where we find many centenarians… I think you’ll find that they are not more prone to cancer in general.
What about lobsters, are they more prone to cancer? Nope.
What about long lived mammals like elephants? Nope. They rarely have cancer, despite the fact that they age slowly and have many more cells.
I don’t think you successfully argued against the evolutionary theory of aging. If an animal aged indefinitely and remained healthy, then evolution would suffer – since there would be fewer generations – in fact generations require aging.
Put another way – population would reach saturation, and the young would not be able to compete with the established. The “next generation” would effectively not occur, and the species would stagnate in an evolutionary sense.
I don’t think you successfully argued against the evolutionary theory of aging. If an animal aged indefinitely and remained healthy, then evolution would suffer – since there would be fewer generations – in fact generations require aging. (…) Put another way – population would reach saturation, and the young would not be able to compete with the established. The “next generation†would effectively not occur, and the species would stagnate in an evolutionary sense.
What you write sounds reasonable but it is not obvious that evolution would select in this manner (note that I am not saying you are wrong). You have to go back to how natural selection works. People who survive and reproduce pass on their genes, others do not.
Suppose that you have a community where some people live a bit longer. Say just 5 years longer, with 5 extra years of fertility. These high longevity people should, everything else being equal, be more successful in passing on their genes. So over a few generations, they should dominate the gene pool.
You argue that if that were the case, it would be bad for the species. Fine. But natural selection does not “think through the issues”. It is just an algorithm.
The experiment I report on shows that, somehow, yeast is able to select against long-lived individuals. This seems to support the evolutionary theory of aging. Maybe. I don’t know.