A new study [1] about the ‘invariant rate of ageing’ 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 “immortality and everlasting youth are the stuff of myths,” according to The Guardian. The article goes on to say that “an unprecedented study has now confirmed that we probably cannot slow the rate at which we get older because of biological constraints.” Other outlets published similar conclusions, with Futurism saying that the study shows “an ‘invariant rate of aging’ that won’t slow down”.
These reporters seem to have gotten tripped up on the idea of an ‘invariant rate’, 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 that’s not at all what the study shows, as the paper itself directly says.
What the study actually says
The study aimed to investigate the ‘invariant rate of ageing’ 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, ‘fixed’ is used as the opposite of ‘plastic’. It doesn’t mean ‘set in stone’. It means there’s 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 – environmental factors don’t really affect it, and there’s 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 ‘aging’, while the infant and juvenile morality parameter reflects the misfortune of dying young.
The study’s first finding is that most of the gain in human lifespan so far has come from reducing mortality at younger ages. There’s 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, doesn’t show that the rate of aging cannot be changed; it shows that there’s 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 wouldn’t know it from the way it’s been covered: “It 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.”
Abstract
Is it possible to slow the rate of ageing, or do biological constraints limit its plasticity? We test the ‘invariant rate of ageing’ 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 wasn’t a study about longevity or the inevitability of aging. It was research to understand what affects the rate of aging – how much it results from evolved biological processes versus the effects of the environment. That’s important science not only for longevity research but also for evolutionary biology. It’s undoubtedly valuable, but unfortunately, its message has been misconstrued.
Far from showing that aging is inevitable, this research instead demonstrates that, ultimately, we’ll 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 ‘invariant rate of ageing’ hypothesis. Nature Communications (2021), doi: 10.1038/s41467-021-23894-3
