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Evolution Won’t Stop Aging Any Time Soon, but Medicine Might


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#1 reason

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Posted 23 June 2021 - 07:11 PM


Today's open access paper offers one of a number of different perspectives on the present consensus regarding the causes of individual variance in life expectancy, of differences in species life span, and of changes in human life expectancy over time. Human life expectancy has increased greatly in the modern era, but this is largely due to improved control over infectious disease and other environmental factors that can cause early mortality and long-term health risks. Similarly, individual variance in life span near entirely arises from lifestyle choice and environmental factors. There is a component arising from slowed aging, but this has been an incidental side-effect of improved technologies, medical and otherwise.

The authors of the paper here suggest that life expectancy and mortality data shows that further improvements in the known environmental factors that impact health are unlikely to yield meaningful gains in human life expectancy. The lion's share of possible gains are already claimed, thanks to control of infectious disease and other outcomes of modern technologies. New approaches to age-related degeneration are needed, development programs and therapies that deliberately target the causative mechanisms of aging. Historical data says little about what human life expectancy will look like in the era of widespread use of senolytic treatments and other rejuvenation therapies now under development.

The long lives of primates and the 'invariant rate of ageing' hypothesis

The maximum human life expectancy has increased since the mid-1800s by ~3 months per year. These gains have resulted from shifting the majority of deaths from early to later and later ages, with no evidence of slowing the rate at which mortality increases with age (i.e. the 'rate of ageing'). Further substantial extensions of human longevity will depend on whether it is possible to slow the rate of ageing or otherwise reduce late life mortality. Consequently, the nature of biological constraints on ageing is a central problem in the health sciences and, because of its implications for demographic patterns, is also of long-standing interest in ecology and evolutionary biology.

Across species, rates of ageing are strongly correlated with other aspects of the life history-pre-adult mortality, age at first reproduction, birth rate, metabolic rate and generation time - as well as with morphological traits such as body size and growth rate. These correlations suggest that ageing evolves in concert with a suite of other traits, which may produce constraints on the rate of ageing within species. Indeed, researchers have long hypothesised that the rate of ageing is relatively fixed within species, not only in humans but also other animals.

This 'invariant rate of ageing' hypothesis has received mixed support. Understanding the nature and extent of biological constraints on the rate of ageing and other aspects of age-specific mortality patterns is critical for identifying possible targets of intervention to extend human lifespans, and for understanding the evolutionary forces that have shaped lifespans within and across species. Although no consensus has been reached about the invariant rate of ageing hypothesis, further evidence that biological constraints may shape human ageing comes from the remarkably consistent relationship between life expectancy at birth and lifespan equality in a diverse set of human populations. While life expectancy at birth (a measure of the 'pace' of mortality) describes the average lifespan in a population, lifespan equality (a measure of the 'shape' of mortality) describes the spread in the distribution of ages at death in a population.

To better understand biological constraints on ageing, here we answer two questions. First, is the highly regular linear relationship between life expectancy and lifespan equality in humans also evident in other primates? Second, if so, do biological constraints on ageing underlie this highly regular relationship? 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.

Can we humans slow our own rate of ageing? Our findings support the idea that, in historical population when life expectancies were low, mortality improvements for infants, and in age-independent mortality, were the central contributors to the decades-long trend towards longer human life expectancies and greater lifespan equality. These improvements were largely the result of environmental influences including social, economic, and public health advances. Since the middle of the 20th century, however, declines in the baseline level of adult mortality have very likely played an increasingly important role in industrialised societies. As we show here, improvements in the environment are unlikely to translate into a substantial reduction in the rate of ageing, or in the dramatic increase in lifespan that would result from such a change. 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.


View the full article at FightAging

#2 Steve H

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Posted 24 June 2021 - 01:05 PM

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.

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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

The post Evolution Won’t Stop Aging Any Time Soon, but Medicine Might first appeared on Lifespan.io.


View the article at lifespan.io




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