A flatworm (Pseudocerus liparus) crawling on a sponge – passing through a forest of hydroids and tunicates. (Image credit: Christa Rohrbach, CC BY-NC-SA 4.0)

Last week I posted an article about fascinating creatures that escape death almost completely, including the famous “immortal jellyfish” (link below). Yet while the jellyfish’s attitude to aging is awe-inspiring, its existence poses a more obvious, yet perplexing question: why do we age?

In aspiring for eternal youth, we tend to not see the wood for the trees. So why did aging and senescence evolve in the first place? At first, it might seem contradictory to our view of evolution: seemingly programmed decreasing fitness and death doesn’t make much sense when we only think about the survival of the fittest

Read More: A Story About Mortality: What Jellyfish Can Teach Us 

This also dazzled the mind of scientists. The first theory was mainly outlined by August Weismann (the same guy that described the species Turritopsis dohrnii – the “immortal jellyfish” –  in 1883) in the late 19^th century, but was earliest formulated by Alfred Russell Wallace in 1870. For those who haven’t heard of his name before, much of Wallace’s research laid the foundation for Darwin’s work The Origin of Species. Wallace and Weismann suggested that an individual’s death makes way for the next generation and thus limits the population size while increasing the evolutionary potential for the lineage. The theory wasn’t widely accepted at the time: individuals dying for the greater good flies in the face of what we know about evolution. 

Natural selection basically can’t act on a gene for aging in the wild due to the fact that most organisms don’t live long enough to grow old. Most animals die early because they get eaten, sick or can’t find enough food. Imagine a gene that leads to death at a specific age. It will never spread throughout a population because there are just not sufficient individuals living long enough for selection to work (i.e. it won’t be positively selected for). On top of this, even if a gene for aging did evolve, if only one individual in a population evolved an inactive type of this gene, it might live longer than the others (if it had the chance). This would lead to it producing more offspring and propagating the inactive gene – wiping out the gene for aging in the population over time.  

Theories about why we age

It took another 30 years until scientists tried a new attempt to solve the mystery of aging. Using mathematics, observations in human diseases and thinking deeply about the mechanisms behind evolution – finally a more conclusive theory was proposed independently by Peter Medawar and William Hamilton, named by Michael Rose later in 1982: Antagonistic pleiotropy. 

They concluded that if a gene that influences multiple traits in an organism (a pleiotropic gene) shows beneficial effects in early life, it would be still strongly selected for this gene even if it had bad effects later in life. So if a gene influences fitness positively in young age, even if it will lead to senescence and death in the older organism, that gene is still selected for. This theory gave way to the most recent views on the evolution of aging and was an important advancement in the field.

In combination with more recent findings it explains our limited years on earth. This age limit is due to a trade-off in the way of channeling resources in our bodies. Reproduction as well as protecting and repairing cells takes a lot of energy, and modern theories suggest that energy is either put into repairing cells constantly – and leading to a higher lifespan – or in reproduction, which leads to more offspring in a short time. This theory is also called disposable soma theory. 

There are still many things to explore when it comes to aging and senescence and much research is still ongoing in this field, continuing the work from Weismann, Hamilton and Co. A diverse repertoire of animals, such as cnidarians, flatforms, acoels or insects such as fruit flies can give us insights into a variety of biological processes. We can learn about important mechanisms that influence our life, the molecular basis for evolution and why things develop as they do. Also giving us a better understanding of aging and death.

Whether humans will ever come close to immortality is another story… this we had better leave to the jellies and polyps.

Lara Beckmann is a master’s student at the University of Stockholm in the program ‘Biodiversity & Systematics’ and is currently working on her thesis project at the University Museum of Bergen focusing on the diversity of hydrozoans. Follow Lara on Twitter here.

Literature and suggested reading

Rose, M. R., Burke, M. K., Shahrestani, P., & Mueller, L. D. (2008). Evolution of ageing since Darwin. Journal of genetics, 87 (4), 363. https://doi.org/10.1007/s12041-008-0059-6

Hiebert, L. S., Simpson, C., & Tiozzo, S. (2020). Coloniality, clonality, and modularity in animals: The elephant in the room. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. https://doi.org/10.1002/jez.b.22944

Kirkwood, T. B. L. (2008). Understanding ageing from an evolutionary perspective. Journal of internal medicine, 263(2), 117-127. https://doi.org/10.1111/j.1365-2796.2007.01901.x