This may spell bad news for those who believe that the ageing process can be reversed. Such “attempts are futile", assert two University of Arizona researchers who claim to have “proved that it’s mathematically impossible to halt ageing in multi-cellular organisms like humans".
“Aging is mathematically inevitable—like, seriously inevitable. There’s logically, theoretically, mathematically no way out," said Joanna Masel, professor of ecology and evolutionary biology at the University of Arizona, in a 30 October statement.
Masel and University of Arizona postdoctoral researcher Paul Nelson have outlined their findings on math and ageing in a new study titled “Intercellular Competition and Inevitability of Multicellular Aging," published in Proceedings of the National Academy of Sciences.
Love it, envy it, or hate it but immortality as a concept is very appealing to human beings. A simple web search for ‘immortality’ or ‘defying age’ will yield thousands of links that suggest different remedies to achieve the same, many of which border on quackery and even the occult.
Of course, there have also been several attempts to find scientific solutions to address this issue. But most of the research has been done on mice, which implies that the effect on human beings could differ vastly.
For instance, gene therapy has been used to lengthen telomeres (parts of human cells that affect how our cells age) in cultured cells and in mice, but never in a human patient. Our DNA is ‘written’ onto chromosomes, and the ends of each chromosome are known as telomeres, which also make it possible for cells to divide. Each time a cell divides, the telomeres get shorter. Hence, their length can be used as a proxy to measure ageing. When they get too short, the cell can no longer divide--this shortening process is associated with ageing, cancer, and a higher risk of death.
Scientists in the past have done a lot of research in this area. The efforts continue.
On 25 March, online magazine Sciencealert noted that researchers have identified a cellular mechanism that allows them to reverse ageing in mouse DNA and protect it from future damage. The researchers from the University of New South Wales (UNSW) in Australia and the Harvard Medical School in Boston demonstrated that by giving a particular compound to older mice, they can activate the DNA repair process and, thus, stem the effects of ageing.
A 26 July article in the Independent, said that researchers from the Albert Einstein College of Medicine in New York had published a study in the journal Nature, in which they said they had “identified a pea-sized part of the brain" that “may hold the key to extending human lifespans".
“Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates ageing," Cai was quoted saying. “But we also found that the effects of this loss are not irreversible. Ageing could be held back by replenishing these stem cells “or the molecules they produce," he added. The scientists believe humans are likely to respond to the influence of hypothalamus stem cells in just the same way as the mice, the article added.
Meanwhile, even big technology companies and some of their founders, too, are investing in anti-ageing research.However, the solution isn’t that simple, Masel and Nelson say. They explain that the current understanding of the evolution of ageing leaves open the possibility that ageing could be stopped if only science could figure out a way to make selection between organisms perfect. One way, they suggest, is to use competition between cells to eliminate poorly functioning “sluggish" cells linked to ageing, while keeping other cells intact.
However, Masel and Nelson found that even if natural selection were perfect, ageing would still occur, since cancer cells tend to cheat when cells compete.
“As you age, most of your cells are ratcheting down and losing function, and they stop growing, as well," said Nelson, lead author of the study. “But some of your cells are growing like crazy. What we show is that this forms a double bind—a Catch-22. If you get rid of those poorly functioning, sluggish cells, then that allows cancer cells to proliferate, and if you get rid of, or slow down, those cancer cells, then that allows sluggish cells to accumulate. So you’re stuck between allowing these sluggish cells to accumulate or allowing cancer cells to proliferate, and if you do one you can’t do the other. You can’t do them both at the same time."
“It’s not surprise that we’re all going to die; lots of things are obvious because they’re so familiar to us, but really, why is it that we age? We start to explain why," said Masel, who also teaches in the University of Arizona’s Graduate Interdisciplinary Program in Applied Mathematics.
“You might be able to slow down aging but you can’t stop it," Masel said. Nelson concluded: “It’s just something you have to deal with if you want to be a multicellular organism."