Why Does Evolution Not Allow Us to Live Forever?
Image credits: WikiImagesPrior reading:
Why We Age and Die—Senescence: Part 2
Introduction
I discussed cellular senescence in two previous articles. Senescence is about the fact that cells undergo a gradual deterioration observable in the upsetting of normal tissue structures and age-related diseases via specific proteins, inflammation, and phenotypes.
A fascinating question is this: why does evolution allow cellular senescence to occur?
Dr. Michael Shermer talks about the fact that everything falls into disrepair because of thermodynamics and entropy. Allow me to detail how I understand him: We age and eventually die due to natural selection's limited allocation of resources that sustain us. Rearing offspring to their reproductive age/success is a parent's ultimate goal. Once that is achieved, there is less reason to keep you around. Due to scarcity of room and resources, older consumers must die off to make room for offspring to propagate their genes into the next generation. We can see natural selection's influence in the biological resources that are spent on quickly healing an infant's or toddler's wounds versus an adult's injuries that require more time. The quick healing ensures an infant's or toddler's survival to reproductive age [1].
If our genes are on a mission of generational propagation, with an importance that exceeds our eternal living, is there a "genetic program" driving the whole process of aging? It is strange that evolutionary theory could deny a "genetic program" as the driver for aging. Thomas B.L. Kirkwood and Simon Melov apparently denied it in 2011 when they stated that evolutionary theory does not support an adaptive basis for aging:
"The evolutionary theory of ageing is generally portrayed as rejecting the notion that ageing has an adaptive basis, i.e. that an age-related decline in survivorship and viability (including reproductive capacity) is favoured by natural selection. Nevertheless, the idea of 'programmed' ageing, with its implicit (or occasionally explicit) reliance on an adaptive role, reappears regularly and is commonly expressed by newcomers to the field. The reasons commonly suggested for ageing to be adaptive are: it avoids over-population; it eliminates post-reproductive individuals who would otherwise compete for resources with their younger kin; it facilitates ongoing evolutionary adaptation by promoting succession of generations; and it fits the purported existence of genes 'for ageing'. The evolutionary logic that establishes that these arguments are, in most cases, fallacious needs to be more widely understood, especially at a time when the discovery of genetic pathways that affect longevity is proceeding apace. At the same time, it needs to be recognised that evolutionary analysis does not, in fact, preclude the possibility that in special circumstances there may be tightly controlled aspects of ageing. Understanding the ways in which natural selection acts on the determinants of longevity is likely to be important in guiding further discoveries that might contribute to efforts to maximise health and wellbeing at later ages" [2].
Natural populations infrequently become biologically old. There is no evolutionary pressure or anti-reproductive success that necessitates bodily maintenance for everlasting living. So, why would evolution lead us to a destination scarcely seen? Natural selection should prevent instead of advance this event that is pernicious to the individual, as it seems that survival is more programmable for us [3].
Image credits: stevepb
Disposable soma theory would like to have us believe that organisms must evenly budget their energy across all domains of metabolism, reproduction, and repair/maintenance in such a way that prioritizes reproduction over everlasting maintenance. Inadequate refitting of the body throughout time eventually proves to be fatal for the organism [4].
This energy budgeting is observable in different species whose limitations in repair mechanisms are adjusted according to their different natural perils and threats based on the increased protection in cells from longer-lived species versus cells from shorter-lived species [3].
But some authors are admonishing us against the disposable soma theory, however. In 2010, Mikhail V. Blogosklonny firstly argued that the theory's title does not serve its definition well, and the theory does not distinguish itself apart from other theories. All soma (non-reproductive parts of an organism) are throwaways and recycled after continuous fixing. All theories of aging are about these throwaway parts. Although the sparsity of biological resources and buildup of random molecular destruction are relevant to soma, the Target of Rapamycin (TOR) is the primary driver of aging and death. TOR is an enzyme that uses signals from nutrients (amino acids and energy) to control cells and organs' growth and the progression of the cell cycle. This growth is a continual unplanned development that is not deactivated after finishing its task. This growth/development is chronic and hyperactivated. It causes cellular aging that leads to tissue, organ, and systematic damage before eventual organismal demise [5].
Secondly, he argued that disposable soma theory does not explain why women typically live longer than men. He expressed the premise that higher accidental deaths and physical brutality among men have perhaps given them greater size and robustness than women. He argued that the mechanistic target of rapamycin (another enzyme regulating cell growth) is hyperactivated in males, using testosterone to increase the growth of muscle cells (hypertrophy) and make males physically vigorous. Nutrients and resources are spent on physical vigor to preempt combat death and increase reproduction opportunities with accelerated aging as an expense for males [5].
Although aging is not programmed into us, there could be evolutionary programming in the aftereffects of our aging phenotype or our physical traits adapted to counteract the damage. Hence, our inflammation results from any wound or infection. Although inflammation feels deplorable in old age, it is important to recognize its advantage and origin during youth. Antagonistic pleiotropy becomes relevant in this discussion of evolution building a trait that is advantageous during youth but deplorable in old age [3].
It has been 60 years since George Williams proposed that genes in early life compromise with genes in later life. You enjoy your fitness-enhancing genes while you are young and lose them as you grow old. Your alleles (gene variants arising by mutation) that are the best contributors to procreation will prevail over those that are less contributory [6].
But why does natural selection not mold us in such a way to make aging impossible?
Huntington's disease is an excellent example of something that is always deadly and derived from your parents. Why does evolution not obliterate this from our gene pool? Firstly, its onset is late in life, either during or after your years of giving birth. A health-destroying allele that does not impact reproductive success flies under natural selection's radar. Natural selection will rarely fail to target the alleles that prevent your early life reproductive potential [6].
Sir Peter Medawar made this logic relevant to aging. He hypothesized that as undesirable mutations predominate over desirable ones and may affect late-life reproduction and survival, they slip under natural selection's radar and slip into the genome throughout generations [6].
George Williams was receptive to the idea but highlighted the alleles promoting survival and early life reproduction during which natural selection was favorable but allowed the disadvantages to creep in later. Williams stated natural selection could favor those alleles despite their disadvantages to later life. Thus, the idea of antagonistic pleiotropy was born to discuss the positive allelic effects in early life versus negative allelic effects in later life. The next proposition to automatically follow is that life-prolonging and age-slowing mutations are inimical to surviving and reproducing in early life [6].
Image credits: zoosnow Antagonistic Pleiotropy in Natural Populations
We can look to multitudes of reptiles, birds, and mammals to find examples of trade-offs between fecundity and longevity. The risk of death increases among Western gulls and red squirrels that copulate early in life compared to those who copulate later in life. However, mammals and birds that are held in captivity commonly do not have these trade-offs, indicating that antagonistic pleiotropy is more aggressive in the wild [6].
How does early-life reproduction negatively influence immunity? The large clutch size among female eider sea ducks diminishes their immunity and thereby declines their survival and reproduction. Small Drosophila fruit flies copulating in high numbers also have a diminished ability to fight off bacterial infections [6].
I want to apologize in advance for my accidental failure to mention any crucial aspects of this topic. I do not want to pretend to be comprehensive on this topic of evolutionary reasons for aging and dying. This topic is of ongoing interest to me, and I intend to address it numerous times again in the future as I improve my understanding.
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All information in this article is intended for educational/entertainment purposes only. This information should not be used as medical/therapeutic advice. Please seek a doctor/therapist for health advice.
Works cited:
[1] Scientifically speaking, this is why we die - Big Think
[3] On the evolution of cellular senescence - Kowald - 2020 - Aging Cell - Wiley Online Library
[4] 1503.07040.pdf (arxiv.org)
[5] Why the disposable soma theory cannot explain why women live longer and why we age (nih.gov)