Our Lifespan Could Be Predicted by the Mutations We Collect in Our DNA

The number of genetic mutations we collect in our DNA over time may predict how long we will live, according to a study.

The research involved 603 people from 41 three-generation families who took part in a study in the 1990s to map the human genome. The total participants included 61 men and 61 women who were grandparents.

The authors of the new paper published in the journal Scientific Reports sequenced the participants' DNA. Next, they worked out the amount of mutations that parents passed to their children. If a mutation was found in the child's DNA but not their parents', the team surmised this mutation must have been emerged when the sperm and egg came together in the uterus. This enabled them to work out the number of mutations parents collected in their reproductive cells when they conceived. They also noted how the participants died, whether they developed cancer, and when the women had children and reached menopause.

Individuals who had collected more germline mutations, or those which could be passed on to their children, were found to have shorter lifespans. And people who had germline mutation rates in the lowest 25th percentile versus the 75th percentile lived for approximately 4.7 years longer, the study found.

In addition, the team uncovered a link between fertility in women and mutations. Women in the top two thirds of mutations gave birth to fewer children than those in the bottom third. Higher mutation rates were also linked with being younger when giving birth to their last child, which the authors said may indicate a decline in fertility.

However, the researchers found no association between germline mutations and the risk of cancer. This may be due to the fact that the grandparents had to reach an old enough age to achieve that status, and therefore may have had a lower risk of cancer in general.

Co-author Dr. Richard Cawthon, University of Utah Health research associate and professor of human genetics, said: "Compared to a 32-year-old man with 75 mutations, we would expect a 40-year-old with the same number of mutations to be aging more slowly.

"We'd expect him to die at an older age than the age at which the 32-year-old dies."

Cawthon said the DNA in our bodies is regularly damaged, and as we age our ability to fix these problems wanes and potentially harmful mutations collect. Therefore, parents who are older are more likely to pass on mutations to their children.

Co-author Lynn B. Jorde, chair of the Department of Human Genetics at University of Utah Health, said: "If the results from this small study are validated by other independent research, it would have tremendous implications.

"It would mean that we could possibly find ways to fix ourselves and live longer and better lives."

Cawthon said: "The ability to determine when aging starts, how long women can stay fertile, and how long people can live is an exciting possibility.

"If we can get to a point where we better understand what sort of developmental biology affecting mutation rates is happening during puberty, then we should be able to develop medical interventions to restore DNA repair and other homeostatic mechanisms back to what they were before puberty. If we could do that, it's possible people could live and stay healthy much longer."

Professor Joao Pedro de Magalhaes of the Institute of Ageing and Chronic Disease at the University of Liverpool who did not work on the paper told Newsweek: "this study fits the hypothesis that accumulation of DNA damage and mutations contributes to aging, although of course correlation does not imply causation, so it is not conclusive."

Magalhaes said: "I was surprised that, although people with higher germline mutation rates have a higher mortality, this is not related to cancer.

"Given that cancer is driven primarily by mutations, I would've thought that it would be one of the major factors at play here, but that doesn't seem to be the case."

Magalhaes said the study's major limitation was that it involved a relatively small number of people, which may explain the lack of a link to cancer. "It will be important to repeat the study in larger cohorts," he said.

Asked if this method could be used on members of the public so they could find out their potential lifespan, Magalhaes said this could be done if people sequenced their and their children's genomes.

"I don't think we are far away from this given that whole genome sequencing is becoming ever so cheap, costing less than $1000. I certainly think that everyone will have their genome sequenced in the not-too-distant future."

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