Arguing for Aging to Influence Natural Selection through Loss of Parental Contributions to Early Life Evolutionary Fitness

It seems that ever more people these days argue for aging to influence natural selection through effects on the group, or at least on offspring. The core argument made here, as I understand it, is that a sort of inverse Grandmother effect can allow a rapid pace of aging to reduce fitness in early life by reducing parental or grandparental contributions to survival. If the case, then this means that age-related diseases are not just side-effects of a relentless evolutionary focus on early life at the expense of later life, but are actively involved in selection in some way, perhaps as a buffer against more subtly harmful mutations. Like most of the more abstruse discussion of evolution, proof is hard to come by - most arguments at this level are a matter of model versus model and assumption versus assumption. The line between hypothesis and opinion is more blurred than it might be elsewhere in the life sciences.

During evolution, Muller's ratchet permanently generates deleterious germline mutations that eventually must be defused by selection. It seems widely held that cancer and aging-related diseases (ARDs) cannot contribute to this germline gene selection because they tail reproduction and thus occur too late, at the end of the life cycle. Here we posit however that by lessening the offspring's survival by proxy through diminishing parental care, they can still contribute to the selection.

The widespread occurrence of aging in animals suggests that it is an adaptation. But to what benefit? Aging seems to have only drawbacks. In humans, ARDs cause today almost all mortality; they include heart disease, cerebrovascular disease, Alzheimer's disease, kidney disease, and cancer. Compensation seems unthinkable.

For cancer, the author proposed in a previous study a benefit to the species: purifying selection against deleterious germline genes. We generalize, motivated by the parallels between cancer and aging, the purifying selection posited for cancer to aging. An ARD would be initiated in the organ by multicausal disruption of homeostasis, and be followed by dormancy and senescence until its onset near the end of the life cycle. Just as for cancer, the ARD gives a benefit to the species through the selection against germ line genes that disrupt homeostasis.

Link: https://doi.org/10.1016/j.mehy.2018.07.020

Comments

Aging does seem to be selected for , and actually it's not hard to see why. More rapid mixing of genes allows for more rapid evolution. Hence a short lived species can adapt more quickly than a long lived one. This is especially true when you consider how species compete or prey upon one another. A prey-predator evolution arms race is constantly under way. Stability of ecosystems seems to exist when prey live a shorter lifespan than predators, and you can see why it would be a disaster if it was the other way around.

Human beings aren't preyed on by anything, anymore - so are undoubtedly evolving longer lifespans, and this seems to be evident comparing us to our nearest genetic neighbours.

Posted by: Mark at August 29th, 2018 7:36 AM

Mark:

The problem is evolution doesn't work that way. It can't predict the long-term future and doesn't care about the species but only about the benefit of the unit of selection: the individual. In very united family groups it also cares about its family, but less (because time frames are longer).

Also, your argument is self-defeating. If aging were good per se, independently of context, only or mostly due to the rapid evolution it allows, then all species would be short-lived!

As I see it, longevity mainly depends on predatory pressure. Animals with lots of predators age fast, because they will die fast anyway, so there is low selective pressure for antiaging resistance. Animals with less predators age slower, because they can survive to old age (compared to other species) and thus get a benefit if they have strong defences against degeneration.

Posted by: Antonio at August 29th, 2018 10:15 PM

I agree with your last paragraph Antonio.

Evolution doesn't just occur at the level of individual 'unit' animal however. The reason is that if an individual evolves certain individually beneficial traits, such as being an awesome hunter or a very infectious pathogen for example, it will spread and reproduce very rapidly. This will be at the cost of the rest of the ecosystem however, and rapidly the predator will run out of prey, or the pathogen will kill all its hosts. Therefore the most deadly predators and pathogens perish or evolve to be less deadly.

Of course it is more complicated than this, but you should see my point - selection at the individual level has consequences for the species and it's ecological niche, and this can then lead to group effects. Gabish?

Posted by: Mark at August 30th, 2018 5:14 AM

Also, to your point that most species would be short lived, they are - or atleast most animals age, until such time as predatory pressure is removed, and they begin to evolve longer and longer lifespans, as you can see with squirrels or mole rats Vs rats, for example.

Posted by: Mark at August 30th, 2018 5:21 AM

I don't have anything else to add CD. I thought my explanation was simple enough. Selection at the individual level can nevertheless lead to group effects that appear in retrospect to be non-optimal for the individual. Doesn't mean those traits are programmed necessarily, more that all the animals whose genetic program evolved away aging are dead, so we don't see them (or atleast they are rare).

Posted by: Mark at August 30th, 2018 2:42 PM

Mark:

"selection at the individual level has consequences for the species and it's ecological niche, and this can then lead to group effects"

There are lots of examples were evolution takes the beneficial route for the individual at the expense of the benefit for the species. For example: https://en.wikipedia.org/wiki/Fisher%27s_principle

"Also, to your point that most species would be short lived, they are"

Huh?? There is a 2 orders of magnitude range in mammals lifespan alone, and around 7 orders of magnitude between macroscopic life.

Posted by: Antonio at August 31st, 2018 2:37 PM

That Fisher principle is a pefect example of what I'm talking about Antonio: individual selection balancing out through an 'unintended' group effect, in this case male and female numbers. That's all group selection is really. The same thing could be said for aging. As a species escapes from predation it has the chance to evolve a longer life. But this also mean it evolves more slowly and becomes more genetically homogenous - this makes them vulnerable to a change in circumstances, such as a new predator or disease. A changing environment will always pull lifespans back down, or make extinct those species who have become too long lived and inflexible.

Posted by: Mark at August 31st, 2018 3:57 PM

Then you understood nothing of Fisher's principle.

Posted by: Antonio at September 1st, 2018 10:55 AM

Might as well talk to a bloody wall.

Posted by: Mark at September 3rd, 2018 4:10 AM

(I am the author of the paper commented upon)
The paper is free access, so anyone can read it.

The paper describes a completely different point of view on aging and cancer: one has to get used to it.

The key idea: The paper argues that aging including cancer implement a weak selection against germline genes that disrupt homeostasis, resp. energy dissipation. Aging and cancer would do so by slightly accelerating death. The lessened care given to the offspring decreases its number.
In the long term this selection gives an advantage to the species/group, but at the cost of the individual.
Aging and cancer would be highly complex adaptations.

Posted by: Anthonie Muller at September 4th, 2018 2:24 PM

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