Scientists have discovered 25 genetic mutations due to which our species was able to increase its lifespan.
Ana Vela died in Cordoba late last year at the age of 116. She was the oldest person in Europe, the third person on the planet, and a symbol of longevity in Spain. Our country ranks second after Japan in terms of life expectancy (at birth). Ana Vela is no exception, there are a sufficient number of people living in Spain, whose age has passed the century mark. According to the Institute of Statistics of Catalonia, this autonomous community has seen a continuous increase in the number of inhabitants over the past 35 years, which is more than 100 years old.
But what influences our life expectancy? What is the secret of the longevity of those people who live up to 120 years of age?
And why do humans live so long, while our closest evolutionary relatives, such as chimpanzees, live for about 50 years?
According to researchers from the Institute for Evolutionary Biology (UPF-CSIC), the Center for Genomic Regulation (CRG) at the University of Bristol and the University of Liverpool, who are led by Icrea Arcadi Navarro, the secret to longevity is contained in 25 genes.
The study, published in the journal Molecular Biology Evolution, examined the relationship between genomic variation and maximum lifespan among different primate species, including humans. Scientists have come to the conclusion that we have mutations in genes associated, for example, with the possibility of wound healing, coagulation and treatment of cardiovascular diseases, which, apparently, led to the lengthening of life.
According to scientists, these mutations are beneficial in the early stages of life, however, harmful in old age. For example, a mutation that allows calcium accumulation may be beneficial for bone formation in youth. However, in old age, a large amount of calcium contributes to the development of atherosclerosis.
This study attempts to explain the scientific theory, the so-called "antagonistic pleiotropy", put forward in the 50s of the XX century, which tried to answer such questions: why there are differences in life expectancy of different species, why hedgehogs live up to 200 years, while mice only live for two or three years?
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According to this theory, formulated by George Williams in 1957, certain genetic variants favor the individual in youth and have negative side effects later in life.
Depending on environmental conditions, there is a natural selection of mutations that are beneficial at the initial stage of life, but which become harmful with age.
Gerard Muntané, was one of the first scientists to study this problem at the Institute for Medical Research. Virgili. In a published press release, he claims that "there are mutations that can have different effects depending on the stage of life: some are useful to us, others with age, after the completion of the reproductive stage, harm us."
This study is based on material published last year in the journal Nature Ecology, which also addressed aging issues. In particular, we are talking about a comparative analysis of genomic data on human diseases, at the initial stage of his life and in old age.
“We saw that there are mutations that protect young people from diseases such as childhood glioma (a brain tumor in children). At the same time, they increase the risk of contracting other diseases in old age, says Navarro. - Thus, we have proved in practice the theory of George Williams. After the results are obtained, we would like to continue research and find out if these genes are directly related to aging."
To this end, scientists decided to study and compare the genes of different primate species. From an evolutionary biology perspective, primates are very interesting because, despite their very close kinship with humans, there are profound differences between species in terms of life expectancy.
Of all the species studied, only humans and two types of macaques live longer than their common ancestor, from which they descended three million years ago. According to the study authors, this proves that the process of increasing life expectancy was, in evolutionary terms, relatively fast.
Since the mutations found are associated with processes typical of cell aging, the researchers believe that the results of the study may contribute to the development of new therapeutic agents for treating diseases associated with aging, as well as demonstrate the potential of an evolutionary approach to medicine.
The researchers also warn that the individual mechanisms of aging in humans and mice are very different. Mice are most commonly used to study the causes of aging.
“We have to be very careful in our work in order to have a clear idea of what the results of our research could be used as a model,” said Navarro.
The scientist admitted that it has not yet been possible to establish why "homo sapiens" and primates have the same set of 25 mutations that allowed them to prolong life. There is also no answer to this question: "What factor played a decisive role in extending our life compared to our ancestors?"
“We do not yet have an answer to this question, there is only speculation,” Navarro said.
“Perhaps this is due to the fact that we have become dominant in our environment. Our species began to live and work in large groups. In difficult times, people defended each other and came to help. All this contributed to the increase in life expectancy. If before they died at 20, then later at 40,”Navarro said.
Of course, the selective movement towards the optimal period of our life was accompanied by adjustments in the vital activity of our body. Unlike gorillas and chimpanzees, humans have undergone radical environmental changes that may have led to an increase in our lifespan.
“The social factor was also superimposed on the electoral movement, thanks to 'engineering' we do not die at 60 from embolism, even if we have harmful mutations that are predisposed to this,” Rivero Navarro said.
Cristina Saez