Does the human lifespan have a limit?
Sambhavi Sneha Kumar considers scientific approaches to extending our lifespans
The maximum lifespan of an organism varies significantly between species, ranging from a single day for mayflies, to several hundred years for Greenland sharks. While the goal for most organisms at an evolutionary level is to reproduce, humanity continuously aimed at increasing our lifespan. Life expectancy is used as an indicator of a countries’ development, as well as a measure of social and scientific progress. A longer life would permit us to spend more time having valuable life experiences, make crucial contributions to our fields of work, potentially helping humanity progress further as a species.
Recent medical advances allow us to further pursue this quest. The average life expectancy in the U.K. is around 81 years currently – significantly higher than the 35 years it was in the 17th century. We now live in an era of diseases of old age, where degenerative disorders such as dementia are dubbed “the biggest health crisis of our time” in developed countries. This poses an important question – are our bodies biologically capable of sustaining the lifespans we strive for, or are we being overly ambitious?
Research into longevity is extremely complex and controversial. We only know of 48 people in history who have lived past the age of 115. It was already hypothesised in 1825 that mortality rates increase exponentially with age, implying that human life expectancy must tend towards a maximum value. A 2016 study claimed that even with a perfectly healthy lifestyle and access to medical interventions when necessary, the natural biological human age limit is approximately 115, with only a few individual outliers, in part due to their genetic architecture. This would imply that regardless of the technology we develop, it should be unable to increase our life expectancy past this limit.
This is a plausible suggestion when we consider ageing on a cellular level. The Hayflick limit refers to the number of times that most cells divide before entering ‘senescence’. Hayflick (currently a UCSF Professor of Anatomy at 91 years of age) proposed this theory in the 60s, after finding that a human cell population could only divide between 40 to 60 times in culture before entering senescence. Elizabeth Blackburn, Carol Greide and Jack Szostak went on to win a Nobel prize in 2009 for their discover that this correlates with telomeres (repetitive sequences of DNA at the ends of chromosomes that protect them) being reduced to a critical length, since these shorten after each cell division.
We only know of 48 people in history who have lived past the age of 115
Even if the body did not undergo any other processes of ageing, the accumulation of senescent cells would eventually cause death. Almost all senescent cells either self-destruct or are destroyed by the immune system, though a small number remain and have a strong signalling effect which can lead to chronic inflammation or disruption of nearby tissues and potentially even stimulate surrounding cells to become senescent. These processes are thought to be linked to the development of numerous age-related diseases, including Alzheimer’s and Type II diabetes. It appears that regardless of the condition the body is kept in, degenerative conditions will inevitably catch up with everyone.
Recent investigations carried out in Italy by observing lifespans of over 3,000 individuals over the age of 100 have revealed that annual mortality risks plateau by the age of 115 at around 50%. This is likely because any age related disorders that were to occur would have set in by this point. As a majority of diseases is associated with increasing age, we need to better understand what is driving ageing. We may be able to, through a mixture of medical, lifestyle, and environmental interventions push our life expectancy up.
But what about going further than, say, 115 years? While the early attempts at extending telomeres (using the enzyme telomerase) caused cells to become cancerous, more recent efforts using more controlled delivery systems are more promising at increasing lifespan without the added cancer risk. Promising results have recently arisen in the form of research carried out by the Spanish National Cancer Centre.
It could be possible for us to alter our susceptibility to the degenerative effects of age
The telomeres of mice embryonic stem cells were elongated beyond normal levels, and mice developing from these stem cells were generated. These mice had a 12.8% increase in median longevity, and an 8.4% increase in maximum longevity, compared to mice with normal telomere length. The mice also underwent less DNA damage as they aged, and showed lower cholesterol and LDL levels, as well as improved glucose and insulin tolerance.
Such research demonstrates that it could be possible for us to alter our susceptibility to the degenerative effects of age. Much remains to be discovered at what governs the rate of ageing, and then, whether reductions in the rate of ageing actually translate to longer lifespans, or simply to better health along the lifespan.
While many questions remain concerning the upper bound on lifespan, much could be done to increase life expectancy right now. In the last 100 years, the increase in life expectancy can be attributed to factors such as effective immunisation programs, antibiotics and public health initiatives around hygiene and sanitation. While life expectancies may appear to be approaching a plateau, many believe that developments in fields such as artificial intelligence and genetics could be responsible for our next surge in life expectancy by improving the ways in which we deliver healthcare. Some claim that it does not matter if our bodies degrade if we are able to develop technologies such as prosthesis and bionics.
While extending lifespan may seem like an exciting concept, this may pose additional challenges on both a societal and personal level. For instance, we are already struggling as a planet with overpopulation and its associated consequences, such as carbon emissions. Increased life expectancy has played a role in the development of this problem and may continue to do so. Many countries, such as Japan, have an aging population –individuals aged 65 and older in Japan make up a quarter of its total population, estimated to increase to a third by 2050. Therefore, the dependency ratio (the proportion of workers to non-workers) creates a need for more efficient social care provision and strategies. .
Ageing is a natural process, and it may not necessarily be possible to halt the clock. As a species, we seem to have more control over how long we live than many other species do. In modern society, it is becoming increasingly more likely that excess of food or age related degenerative disorders will kill us rather than starvation or disease. However, if we do strive to push our life expectancies to new limits, it is vital that we consider the challenges this will pose for our bodies and society.
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