Genetic Mutation Could Increase The Lifespan Of Men By 10 Years

First Posted: Jun 22, 2017 05:07 AM EDT
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A new study reveals that a mutation in a growth hormone receptor gene could increase the lifespan of men by 10 years. The discovery could also lead to the development of drugs to slow aging. However, the mutation did not have the impact on women.

The discovery was described in the journal Science Advances. It was led by a team of researchers from the United States, France and Israel. The study indicated the list of gene variants that have the influence on human longevity, according to the The Globe and Mail.

Scientists examined the mutation deletions in growth hormone receptor exon 3. They discovered that males who express it could live on average 10 years longer. They were found to also grow on average an inch taller.

In the study, the researchers examined about 567 people of Ashkenazi Jews over age 60 and their children. They have sequenced their genes for growth hormone receptors. They discovered that the mutation was visible in 12 percent of men with age over 100. This was about three times higher than in 70-year-old men.

The researchers found that men with mutation lived on average 10 years longer compared to those without the mutation. Meanwhile, the mutation was not present in women. The team also examined other groups and they found the same effect, according to Medical Xpress.

Ali Torkamani, who is not involved in the study and the director of genome informatics at the Scripps Translational Science Institute in La Jolla, described the results as convincing. He further said that this was the first to establish a link between growth hormone receptors and longevity.

The growth hormones are molecules that are attached to other molecules. They are located on the surface of a cell. This trigger signals the cell to speed up its growth or eject molecules called as growth factors. In some people, there is a visibility of genetic mutation that inhibits the development of particular growth hormone receptor.

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