Can we evolve to live forever?

What is known to be a gradual process of change and development, evolution takes credit for adaptations in heritable traits over successive generations, and is an ongoing process over millions of years which has allowed our species to survive. However, there is one thing that stands in the way of evolution; death. What could be considered an evolutionary paradox, the process of ageing is seemingly unstoppable; and so our ability to survive is thwarted by this inevitable deterioration of our physiological function with age. We can begin to question the reasons why age, as natural selection does not favour such a mechanism for dying, providing no obvious advantage. There are 2 theories to explain the evolution of ageing; Medawar’s mutation accumulation hypothesis details the declined effect of natural selection as deleterious mutations accumulate in populations by genetic drift, because they are only expressed in later life. Further, Williams’ antagonistic pleiotropy hypothesis shows that ageing is a maladaptive by-product of selection, to promote survival, and reproduction, during youth; genetic variants that are beneficial in early life ultimately prove detrimental later on. This second theory infers a complex debate, as certain Trade-Offs can arise; is it ethical to surrender reproductive abilities by silencing a gene in order to increase lifespan by a surplus of 10 years? A highly influential biochemist, Cynthia Kenyon has pioneered studies into the genetics of ageing. Through studies on C.elegans, a short-lived species of approximately 2 weeks, she discovered that a single mutation on their daf-2 gene was able to double a worm's lifespan, as well as its health-span. Having located a gene that seemingly caused ageing, the equivalent in mammals was studied, which codes for insulin or IGF-1 receptors; her experiment showed the same results in flies and mice, and there is building evidence for the same in humans due to the fact these species arose from a common evolutionary precursor. This coupled with the discovery of the FOXO protein, a gene regulator which is able to bind to the nucleus of cells to improve longevity by causing more DNA repair and a more active immune system, means there is hope that these receptor mutations could be stimulated through therapeutic pills to not only slow down ageing, but also age-related diseases such as cancer and Alzheimer’s. The research of Elizabeth Blackburn on tetrahymena cells, or pond scum, discovered that unlike how telomeres on our chromosomes shorten every time cells undergo division which ultimately leads to ageing, the presence of the enzyme telomerase prevented this deterioration, coding for a somewhat immortality. However, in this case it was not as simple as to just increase telomerase levels to ward off these effects of ageing; instead, after a psychologist suggested a study to look into the relationship between chronic stress and telomere health, a startling comparison was unearthed; people’s life events and how they responded to them had a direct effect on how their telomeres were maintained. A hopeful insight was taken from this- we have control over the way we age, and with this knowledge, lifespan could evolve to increase. Finally, one of the pioneers at the forefront of anti-ageing technology, David Sinclair, works on sirtuins, a group of longevity genes that sense the environment to fight to keep the body longer-lived, by controlling our epigenome (modifications to determine whether genes are turned on or off, often programmed by DNA methylation marks, leading to cell differentiation). Ageing is thought to be a consequence of epigenetic changes, which are thought to be reversible by clipping off chemical groups that turn on genes later in life which will be harmful, and by consequence, drastically increase the health span of humans. However, in harnessing this explosion of genetic technology, are we exploiting our free will, which could ultimately change the course of evolution forever. Since it could result in global amelioration of worldwide suffering, should it be our moral duty to explore its power? How different would the world look in 100 years if our populations had achieved ‘negligible senescence’?. A fascinating ethical dilemma is unearthed with this evolutionary science, which I believe will irreversibly change the course of the next century and beyond.