The evidence they’re discovering shows that what goes on in those complicated molecules may hold important clues to extending our life expectancy. So, let’s take a peek at what these eye-opening investigations have found.
When researchers from the Wellcome Sanger Institute in England analyzed the DNA genomes of 16 species of mammals, including a variety of animals from giraffes to rodents as well as humans, the scientists discovered that all of them generally accumulated a similar number of genetic mutations by the time they reached the end of their life expectancy.1
Mutations Affect How Long You Can Expect to Live
The researchers began their investigation with the knowledge that mutations in genetic material, known as “somatic” mutations, continually occur during the life of an animal or human. These mutations occur in every cell and the average human cell experiences an average of about 47 mutations annually.Most of the mutations don’t cause any physiological issues, but some of them can be problematic. For example, they can cause a cell to turn cancerous or otherwise distort its normal functions.
For the past 70 years or so, researchers have been trying to pin down exactly how these mutations factor into the aging process. But it’s only recently that technological innovations have allowed researchers to follow and accurately record the progress of these mutations in normal tissues.
In the Wellcome Sanger Study, researchers generated whole-genome sequences from mammalian species – both animal and human. They used intestinal cells and measured the mutation rates in single cells. They found that similar mutational processes occurred in all the species.
They also discovered that species that had a longer life expectancy had slower rates of somatic mutations. And even though the animals were of many different sizes and life expectancy, the number of mutations that the cells in the animals acquired was relatively similar as the animals all reached the end of their usual lifespan.
For example, a giraffe is much bigger than a human and 40,000 times bigger than a mouse but the number of mutations that each species’ cells accumulated by the time they were close to death in old age was relatively similar (sort of like a built-in expiration date). So, while humans get, on average, around 47 mutations per year per cell, mice pick up about 500. Consequently, for mice, that more rapid buildup of mutations, the researchers believe, helps to shorten how long they live – which is often only about two years.
Fixing DNA May Extend Longevity
In line with these findings, a study in Italy shows that some long-lived people apparently possess cells that can resist mutations and may have bodies that also repair mutations more efficiently than people who don’t live that long.For their research, the Italian scientists focused their attention on the genomes of several groups of people – some who were older than 100, some older than 105, others whose average age was 68 and another group whose average age was 60.
They discovered that the oldest of the subjects in their study had genetic changes that were linked to repairing DNA damage more quickly, programming cells to die (apoptosis) when cellular dysfunction reached a certain level and keeping the amount of destructive reactive oxygen species – which cause oxidative stress – under tight control.2 They also found that folks over age 105 had a significantly lower “burden” of mutations in their cells.
"Our results suggest that DNA repair mechanisms and a low burden of mutations in specific genes are two central mechanisms that have protected people who have reached extreme longevity from age-related diseases," says researcher Claudio Franceschi, PhD, who teaches immunology at the University of Bologna.
