Evolution Wonât Stop Aging Any Time Soon, but Medicine Might – Article by Sedeer el-Showk
Sedeer el-Showk
Editor’s Note:Â The U.S. Transhumanist Party publishes this article by Sedeer el-Showk, originally featured by our allies at Lifespan.io, in order to highlight the fallacious nature of many media outlets’ responses to a recent study about the “invariant rate of aging”. As Mr. el-Showk eloquently explains, this study does not refute or undermine the possibility of pursuing the reversal of biological aging, but simply suggests that this needs to be done through medical and technological means, and that without such means, overcoming the limitations of the current maximum human lifespan would not be feasible. Many of us in the longevity advocacy community have known this for a long time already, but it is important to spread accurate information to prevent an unjustified decline in public confidence in the feasibility of radical life extension.
~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, July 25, 2021
Aging is not unstoppable, despite misinterpretations of the new study.
A new study [1] about the âinvariant rate of ageingâ has led to reports that aging is unstoppable and that we cannot cheat death. However, this reporting is based on a misunderstanding of what the study actually says.
The misinterpretations
The study shows that âimmortality and everlasting youth are the stuff of myths,â according to The Guardian. The article goes on to say that âan unprecedented study has now confirmed that we probably cannot slow the rate at which we get older because of biological constraints.â Other outlets published similar conclusions, with Futurism saying that the study shows âan âinvariant rate of agingâ that wonât slow downâ.
These reporters seem to have gotten tripped up on the idea of an âinvariant rateâ, which has the key implication that biological constraints determine the rate of human aging. This led to the conclusion that aging is fixed, inevitable, and immutable, but thatâs not at all what the study shows, as the paper itself directly says.
What the study actually says
The study aimed to investigate the âinvariant rate of ageingâ hypothesis, which proposes that the rate of aging is fixed within a species. The idea is that aging has evolved in concert with a suite of other traits, such as birth rate and metabolic rate, and this concerted evolution has led to the rate of aging being relatively fixed within a species.
In this context, âfixedâ is used as the opposite of âplasticâ. It doesnât mean âset in stoneâ. It means thereâs relatively limited variation in this trait within a species because biological factors have a stronger effect on it than environmental factors. A good example might be the number of digits on a limb â environmental factors donât really affect it, and thereâs very little (but some) variation.
To test this hypothesis, the researchers created a statistical model of the age-specific risk of death in species from seven primate genera. They used data from various studies to set the parameters of their model, which is how they tested the amount of variation.
The model included parameters for infant and juvenile mortality, age-independent mortality, and senescent mortality. Variation in the biological rate of aging would be reflected in the senescent mortality parameter, since it captures what we normally think of as âagingâ, while the infant and juvenile morality parameter reflects the misfortune of dying young.
The studyâs first finding is that most of the gain in human lifespan so far has come from reducing mortality at younger ages. Thereâs also variation in the infant and juvenile mortality parameter, both between societies and at different times.
This also shows up in the relationship between life expectancy and lifespan equality. Media reports generally got this part of the study right, and you can look at the report on SciTechDaily to get more details about these findings.
Unlike the infant and juvenile mortality parameter, the senescent mortality parameter varied very little within each species. In fact, changing this parameter in their model shifted the mortality and demographic data of one species to look like another.
Changing the other parameters led to minor shifts in age distribution, but changing senescent mortality made it look like data from a different species. What this means is that within a given species, biological factors are the ultimate determinants of longevity.
Changing the environment to reduce mortality at younger ages (as we have in most parts of the world) affects demographics, increasing life expectancy and lifespan equality. However, accomplishing more than that will require tackling the evolved biological constraints on lifespan.
This study, therefore, doesnât show that the rate of aging cannot be changed; it shows that thereâs a limit to how much change can be realized without biological interventions, which is precisely the challenge that longevity research aims to overcome.
The paper itself closes on that note, though you wouldnât know it from the way itâs been covered: âIt remains to be seen if future advances in medicine can overcome the biological constraints that we have identified here, and achieve what evolution has not.â
Abstract
Is it possible to slow the rate of ageing, or do biological constraints limit its plasticity? We test the âinvariant rate of ageingâ hypothesis, which posits that the rate of ageing is relatively fixed within species, with a collection of 39 human and nonhuman primate datasets across seven genera. We first recapitulate, in nonhuman primates, the highly regular relationship between life expectancy and lifespan equality seen in humans. We next demonstrate that variation in the rate of ageing within genera is orders of magnitude smaller than variation in pre-adult and age-independent mortality. Finally, we demonstrate that changes in the rate of ageing, but not other mortality parameters, produce striking, species-atypical changes in mortality patterns. Our results support the invariant rate of ageing hypothesis, implying biological constraints on how much the human rate of ageing can be slowed.
Conclusion
Ultimately, this wasnât a study about longevity or the inevitability of aging. It was research to understand what affects the rate of aging â how much it results from evolved biological processes versus the effects of the environment. Thatâs important science not only for longevity research but also for evolutionary biology. Itâs undoubtedly valuable, but unfortunately, its message has been misconstrued.
Far from showing that aging is inevitable, this research instead demonstrates that, ultimately, weâll run out of environmental improvements and will have to turn to biological interventions to affect aging.
Literature
[1] Colchero, F. et al. The long lives of primates and the âinvariant rate of ageingâ hypothesis. Nature Communications (2021), doi: 10.1038/s41467-021-23894-3
Sedeer el-Showk became a professional science writer after finishing a degree in biology. He also writes poetry and science fiction and fantasy, and somehow juggles an ever-growing list of hobbies from programming to knitting to gardening. Eternal curiosity and good fortune have taken him to many parts of the world, but heâs settled in Helsinki, Finland for the moment. He hopes heâll never stop learning new things.