, 4 min read
Montreal researchers “prove” that aging is the result of a genetic program
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.