Why Do We Get Old Instead Of Living Forever? ‘Evolutionary Oversight’

The same mechanism in living organisms that promote health and fitness in young age is responsible for ageing, scientists have found, identifying for the first time the genes responsible for the mechanism called autophagy. It is also the first genetic evidence for the fact that evolution has worked in a quirky way that makes us old instead of making us live forever.

Theoretically advancing Charles Darwin’s work on evolution — which posits that nature selects individuals from any given environment who are most capable of successfully reproducing and passing on their genes — could lead to the conclusion that individuals would evolve to live forever, thereby being able to pass on their genes indefinitely to the next generations. But in practice, that is far from the truth, since individuals of all species age (albeit in different ways) and eventually die, contradictory to the logical extension of evolution which would preclude ageing.

A theory from 1953 by George C. William offered an explanation, saying that natural selection cared only for genes that promoted reproductive success and ignored the negative effects on individuals’ longevity, and that this held true only when the negative effects started after the beginning of the individual’s reproductive stage. What that would mean is a large number of descendants of an individual were more likely to carry on the individual’s genes than the lone individual, and therefore if the genes responsible for reproductive success actually shortened the individual’s lifespan, that was of no great consequence. But there had been no genes-based evidence to back up this theory, called the hypothesis of antagonistic pleiotropy (AP). Until now, that is.

“Evolution becomes blind to the effects of mutations that promote ageing as long as those effects only kick in after reproduction has started. Really, ageing is an evolutionary oversight. … These AP genes haven't been found before because it's incredibly difficult to work with already old animals, we were the first to figure out how to do this on a large scale,” Jonathan Byrne, a researcher at the Institute of Molecular Biology (IMB) in Mainz, Germany, and co-lead author of a paper on the subject, said in a statement Friday.

Byrne and his colleagues were looking at genes in old worms of the C. elegans variety, in which genes had been found earlier that promoted ageing but were also essential for other functions. All the genes found by the IMB team only promoted ageing among the old worms.

“Considering we tested only 0.05 percent of all the genes in a worm this suggests there could be many more of these genes out there to find,” Byrne added.

Further, the researchers shut down the genes responsible for autophagy and found that the worms lived longer, although crippled, lives.

“Autophagy is nearly always thought of as beneficial even if it’s barely working. We instead show that there are severe negative consequences when it breaks down and then you are better off bypassing it all together,” Holger Richly, the principal investigator of the study, said in the statement.

The study was titled “Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans” and appeared in the journal Genes & Development.