aging is largely the consequence of cellular mechanisms that evolved to reduce or prevent cancer.
In this case, any animal that undergoes a statistically successful anti-aging intervention should ultimately die from cancer. At least, that would be expected for most of them. What about the rest of the animal kingdom? What about C. elegans?
Aging is evolutionary conseved => Molecular mechanism is evolutionary conseved. Any aging theory should propose a molecular mechanism of aging that can "kill" yeast, worm and any mammal.
And this is not about "damage" for sure.
I think that the idea has a correct core: there is a balance between rejuvenation and prevention of cancer in organisms. Eg telomer's limit. However, if evolution needs to suppress cancer without affecting life expectancy, it can do it but tweeking many anticancer defence mechanisms. Examples are whales and elephants. (Ineterstingly, crocodiles never have cancer - and aging - as they grow all life and die on starvation.)
Let's imagine, that we age for the Tumor Suppression reasons. Why didn't we develop a mechanism of reducing tumors, in the same way as bowhead whales or the naked mole rats?
Their existence suggests that the regeneration-cancer trade-off is not fixed. Moreover, transferring naked mole-rat Has2 into mice improved cancer resistance and extended lifespan. Why should comparable improvements in humans be considered futile rather than difficult but tractable engineering problems?
So, even if it can be the way to organise some of the hallmarks of aging, it means that there's some pressure, that prevents developing the mechanisms to prevent it.
Historically, evolutionary biology has explained the evolution of aging as the consequence of a mortality-driven decline in selection pressure at older age, meaning that aging is a product of neglect, not intent. Aging is then produced either by a genetic trade-offs between early-life fitness and late-life mortality (known as antagonistic pleiotropy), or as the consequence of restrained investment into somatic maintenance, causing molecular damage to accumulate over time (known as the disposable soma). None of these theories identify which genes or which kind of damage is important and actually causes aging.
The Tumor Suppression Theory of Aging (TSTA) proposes that aging proposes that in mammals, aging is largely the consequence of cellular mechanisms that evolved to reduce or prevent cancer. I show that most hallmarks of aging suppress tumorigenesis, and how they can be rearranged into a causal hierarchy instead of an arbitrary flat list. Furthermore, the hallmarks of aging are interconnected not by accident or due to evolutionary neglect, but because they interact synergistically to remove cells deemed to proliferate abnormally. A cell cannot magically detect oncogenic mutations, so evolution relied on the proxy signal of accelerated proliferation and associated metabolic and replicative stress to identify potentially dangerous cells exiting dormancy, and limit their proliferative potential. This leads to stem cell exhaustion as how mammals age and remaining cellular capacity as the primary store of biological age. Aging is not the consequence of evolutionary neglect or an artifact of domestication, but an unavoidable consequence of the instability of DNA producing oncogenic somatic mutations and the need to contain the cancer risk arising in animals with long lifespans and large body sizes.
The idea that tumor suppression mechanisms might cause aging originated decades ago, but was abandoned largely because caloric restriction (CR), drugs thought to slow aging and interventions into conserved aging pathways delay both aging and cancer, contradicting the idea. By explaining how CR slows aging via reducing proliferation rates, the tumor suppression theory of aging resolves this conundrum and identifies the instability of DNA giving rise to cancer as the ultimate reason why we age and the dominant factor constraining the evolution of very long, if not indefinite, lifespans in larger animals.
Because aging is not a consequence of evolutionary neglect, but it has been optimised by evolution, the TSTA suggests that trying to treat aging with drugs is a futile effort, similar to trying to treat stupidity with drugs. Healthy people don’t need drugs. There are no drugs that make us smarter, healthier or more resistant to disease. In the same way, there are no drugs that make us age slower. Except for drugs that cause us to eat less. Such drugs make us age slower relative to a control group that eats too much, which rodents do almost inevitably, because nutrient signalling accelerates proliferation, and therefore aging.
The TSTA also suggests that blaming aging on evolutionary neglect, i.e. that aging hasn’t been under effective selection, creates a universal excuse for shoddy theories of aging. Aging theories that blame aging on things that would be easily fixable, but suggest they aren’t fixed due to insufficient selection pressure, should be rejected as not making sense.
I would be particularly interested in opinions or arguments trying to prove this wrong. Several weaknesses are explained in the paper, available here:
https://www.researchgate.net/publication/403538169_How_Somatic_Mutations_cause_Aging_without_Causing_Aging
A previous version is available from SSRN, but please use the above Researchgate version, which contains several minor improvements. If possible, please try to read it first. Sorry, it isn’t short. Feel free to skip over the molecular details parts that might be excessively detailed.