(photo credit: Wikimedia Commons)
A genetic mutation that contributes to longevity in men has been discovered by University of Haifa researchers.
“Now our aim is to understand completely the mechanism of the mutation so we can bring it to expression,” said Prof. Gil Atzmon, who heads the team. “This will make it possible to extend life while preserving quality of life.”
The mutation affects a gene for growth hormone receptors that contributes to living an average of a decade longer in men. “We knew in the past that genetic pathways associated with the growth hormone were also associated with longevity; now we have found a specific mutation whose presence or absence is directly related to it,” said Atzmon.
Some previous studies of Atzmon, who is head of the genetic and epigenetics of aging and longevity lab at the university, have shown dysfunction of biological pathways associated with the growth hormone and IGF-1 (insulin-like growth factor-1), which contributes to longevity.
But so far, the damage to these tracks has been done in the laboratory, and no mechanism has been found within the body that causes it.
The new study, which has just been published in the journal Science Advances, found the mutation that disrupts the activity of growth hormone and contributes to male longevity. The initial participants in the study were 102 American Jews over the age of 100 who were compared to other populations around the world in the same age grouping.
In all these groups, it was found that the mutation – which expressed the exclusion of axon 3 in the gene for the growth hormone receptor – was found to be significantly higher in men (and not in women 100 years of age and older) compared with the control group of men aged 70 years. They lived 10 years longer than people without the same mutation.
According to Atzmon, there is no doubt that the mutation is not the only factor for longevity.
Among the subjects there were also many who lived over the age of 100 without the mutation, but the presence of the mutation almost certainly ensured longevity.
From the examination of mutation activity, it became clear that the results of its activity are unusual. In nature, generally, lower forms of the same species live a longer period.
This is how ponies live longer than ordinary horses, and small dogs live longer than the larger ones, he explained.
“And this is also true among different insects. However, in the present case, the mutation in the receptor made it possible for the cells to absorb less growth hormone, but when the hormone was absorbed in the receptor, protein expression was increased several fold. The result was that the people who were born with the mutation and lived about a decade longer were also about three centimeters taller than those born without the receptor.
“This study makes it an established fact that there is a relationship between the function of the growth hormone and longevity. Our current goal is to fully understand the mechanism of the mutation we found to express it, so that we can allow longevity while maintaining quality,” Atzmon concluded.