Trying to extend life

Scientists have discovered a key link between DNA damage and the aging process, which could open up new avenues for treating diseases that cause premature aging. Studies in mice have revealed that a gene responsible for DNA repair plays a crucial role in organisms' lifespan. These findings could lead to the development of therapies that help children with progeria and promote healthy aging in adults. While complete immortality remains a fantasy, the theoretical possibility of extending lifespan is becoming increasingly realistic.

Here's a mystery older than Methuselah himself: why are we born only to die after reaching triple-digit age?

Scientists recently discovered how genetic damage to cells and their ability to regenerate determine how long we live. The research could lead to new treatments for terrifying diseases that cause young children to age and die prematurely; the first trials of such treatments are planned within the next year.

While the age of 969 and the Methuselah elixir of eternal life are still in the realm of belief and science fiction, researchers believe that at least theoretically it is possible to "significantly" extend lifespan.

It was once believed that the aging process was pre-programmed, adapted to the human condition, and that death was simply a matter of survival. However, average life expectancy in developed countries has stubbornly increased, by two years per decade, or five hours per day.

The journal Nature published details of a study on mice that aged and died within three weeks because they lacked a gene responsible for repairing damaged DNA and also had a disease that causes premature aging. Professor Laura Niedernhofer of the University of Pittsburgh, USA, said their findings showed that DNA damage and the ability to repair itself were crucial in determining the mice's lifespan.Damage, including DNA damage, causes the functional decline that we all experience as aging," said Professor Niedernhofer. "However, the response to this damage is genetically determined, primarily by genes that regulate growth hormone and insulin. Avoiding or reducing DNA damage caused by sources such as sunlight and cigarette smoke, as well as by metabolism, can also delay the aging process."

The key finding was that mice lacking the DNA repair gene and that died after three weeks underwent similar changes to those in mice that lived for two and a half years, showing that in the latter, the gene was active in the aging process.

Professor Jan Hoejimakers, chairman of the department of genetics at Erasmus University Medical Center Rotterdam, the Netherlands, said it was still "early days," but understanding why we age could open the door to new ways of treating age-related diseases.

"We could try to treat diseases that occur in young children who age too quickly to see if we can help these patients. Perhaps such a trial could take place within six months, maybe a year," Hoejimakers said.

In the long run, this might lead to old age in good health and to a longer lifespan that would probably be ended by disease or injury rather than old age, but we will never achieve immortality.

"We shouldn't talk about this as the secret to eternal life; that would be frivolous, to say the least," Hoejimakers said. "I think perfect repair is impossible; nothing in nature is perfect. There's always some damage that resists and causes cell death, which in turn contributes to aging. I think that theoretically it should be possible to significantly extend lifespan—if we had enough knowledge—but we're currently very far from that."The simple act of living causes cellular damage, which in turn leads to death. A byproduct of respiration is reactive oxygen, which causes DNA damage that must be constantly repaired. As the body ages, damage increases and metabolic changes occur, which are central to repair.

"There may be ways in which we can induce responses that increase cell longevity—that can cause healthier aging, trying to extend your lifespan—that could be through medications or chemicals, for example," Hoejimakers said.

A representative of the Roman Catholic Church said the study sounds "fascinating" and holds the potential for new treatments for diseases that cause premature aging.

"Regarding the alleged extension of life, it has more of a social than a theological significance. Life will still come to an end, however. We may have to wait a little longer to meet the Creator, but sooner or later we will choose it ourselves," he said.