The Wall_Spring 2023_Issue 9

Josh Titchen , (he/him), LVI, discusses science’s possible answer to immortality, examining its feasibility and what it could mean for humanity.

It has been discovered that a person’s lifespan is dictated by the number of times a human cell can divide. The number of divisions is around 75 - 100 and once this limit is reached the cell enters a phase called senescence, whereby it starts to deteriorate.This information has led to research into extending the human lifespan. The tips of a cell’s chromosomes are called telomeres.Their function is not dissimilar to the plastic cap at the end of a shoelace that stops it from fraying. This is where the ticking clock of death is found.Telomeres are made up of bases of DNA and have evolved to prevent the infinite growth of cells by limiting their life span.We can look at the telomere as a candle wick; each time a cell divides the wick slightly reduces in length.

this inevitable fate, by activating an en zyme called telomerase, which may help maintain telomere length. However, this research comes with issues and disagreements over the safety of the method.The main cause for concern is the potential for promoting cancer.Approximately 85-95% of all cancers express telomerase activity. So it may seem ridiculous that we would want to intentionally increase telomerase activity. However, some scientists argue that data shows telomerase is not the cause of cancer. Cancer is a mutation in an ordinary cell that causes it to divide by mitosis exponentially.This is known as replicative immortality.When a cell becomes cancerous, telomerase is activated and this allows cancerous cells and tumours to persist, as the telomere length is maintained.Therefore the cell does not die. Looking at this it seems that although cancerous cells turn on telomerase, this does not cause a cell to become cancerous. There are also strong reasons to believe that longer telomeres are better in reducing the risk of cancer, especially in older patients, because short telomeres may even be one of the major causes of cancer.When telomeres are short, they have a higher chance of inducing chromosome rearrangements. This can lead to the abnormal expres sion of oncogenes (mutated genes that have the potential to cause cancer) as well as repression of tumour-suppressor

keeping telomeres long could decrease the incidence of cancer and help our immune systems to fight cancer. However, many scientists argue that cancer would still be a real risk.Adult human bodies have many “runaway” cells that have activated oncogenes and inactivated tumour-suppressor genes, but these have stalled due to being mortal (pre-malignant growths that halt because they have a limited lifespan). If we were to reset cellular ageing to extend lifespan, it would have to be carefully designed to increase the probability of human longevity without exposing people to cancer risk. Even if we did achieve the lengthening of telomeres, cancer would still be an issue as it would become more prevalent. Ultimately, cancer is a random mutation: the longer you live, the more likely your cells are to mutate into being cancerous. The good news is that modern advances in medical research are leading to unprecedented discoveries into the actual mechanisms of human ageing. But it is very difficult to carry out clinical trials.We don’t yet know the repercussions of extending lifespan in terms of health and medicines. is whether we can even sustain a population that ages more slowly, given the current state of the healthcare system and state of our planet.Would the extension of human life, even if biologically possible, really be ethical? Arguably, the bigger question

Remedies have recently been

developed that could be the answer to alleviate, abol ish, or even reverse

genes. Furthermore, our im mune cells show decreased abilities to target and destroy cancerous cells when tel omeres are short.Therefore, there is a possibility that

Artwork: Jake Beament, S9

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