People who live past 105 have bodies that more efficiently mend DNA

Is THIS the key to a longer life? People who live past 105 have a unique genetic background that makes their bodies more efficient at mending DNA

  • Experts compared the genomes of 81 Italians aged 105+ with younger adults 
  • They found those in the older age groups tended to have certain genetic variants
  • These included genes for DNA repair, cellular health and killing damaged cells 
  • The findings may explain how some people avoid many age-related diseases

People who live for more than 105 years tend to have a unique genetic background that makes their bodies more efficient at repairing DNA, a study has found.

Researchers compared the sequenced genomes of 81 Italians aged 105 and over with healthy adults from the same region that were aged around 68.

They found that certain genetic changes, which were linked to DNA repair, cellular health and the death of damaged cells, were more common in people aged over 105.

The team said that the study represents the first time that the genomes of people with ‘extreme longevity’ have been decoded in such fine detail.

The findings shine a light on how some people manage to live such long lives while still avoiding the ravages of age-related diseases.

People who live for more than 105 years tend to have a unique genetic background that makes their bodies more efficient at repairing DNA, a study found


People who live to beyond 100 years of age are known as ‘centenarians’.

According to the United Nations, there are some 573,000 centenarians alive in 2021 — a number which is expected to rise as global life expectancies continue to increase alongside the growing world population.

The Office for National Statistics has predicted that around a third of babies born in the last decade will live to reach their 100 hundredth birthday.

Those who reach 110 are known as supercentenarians — a feat achieved by only 1 in 1000 centenarians.

In fact, only 2 in 100,000 women live to this ripe old age, and just 2 in 1,000,000 men.

Fewer than 100 people in recorded history are known to have lived longer than 115 years of age. 

‘Aging is a common risk factor for several chronic diseases and conditions,’ said paper author and medical researcher Paolo Garagnani of the University of Bologna.

‘We chose to study the genetics of a group of people who lived beyond 105 years old and compare them with a group of younger adults from the same area in Italy.

‘People in this younger age group tend to avoid many age-related diseases and therefore represent the best example of healthy aging.’

Specifically, the researchers recruited 81 so-called semi-supercentenarians (those aged 105 and older) and supercentenarians (those older than 110), and compared them with 36 healthy younger adults with an average age of 68 years old.

For each participant, the team took blood samples and conducted whole-genome sequencing, which allowed them to look for difference in the genes between the older and the younger participants.

Based on their analysis, Professor Garagnani and colleagues identified five common genetic changes  between two genes called ‘COA1’ and ‘STK17A’ that were present more often in the 105–110 and 120+ age groups.

These results were cross-checked against a previous study which had compared 333 Italian people aged over 100 and 358 younger adults aged around 60, revealing that the same genetic variants are also common in those aged over 100.

In the senior cohorts, the genetic changes were linked to increased activity in certain tissues of STK17A — a gene involved in cellular responses to DNA damage, levels of dangerous reactive oxygen species and the elimination of damaged cells. 

Activity of COA1, meanwhile, was seen to be reduced in some cells. This gene is key to maintaining proper communication between cell nuclei and mitochondria, which produce energy in cells and whose dysfunction is a key factor in aging.

Additionally, the team note, changes in this region of the genome are also liked to an increased expression of BLVRA in some tissues. This gene also plays a role in eliminating reactive oxygen species and is thus also important to cellular health.

‘Previous studies showed that DNA repair is one of the mechanisms allowing an extended lifespan across species. We showed that this is true also within humans.’ said biological anthropologist Cristina Giuliani, also of the University of Bologna.

‘Data suggest that the natural diversity in people reaching the last decades of life are, in part, linked to genetic variability that gives semi-supercentenarians the peculiar capability of efficiently managing cellular damage during their life course.’

As part of their study, the team also measured the number of naturally-occurring genetic mutations that each age group had accumulated throughout their life.

In six-out-of-seven genes tested, the subjects aged 105–110 or 100+ were found to have a less mutations than their younger counterparts. 

Disruptive mutations typically increase in number as one gets older and can contribute to various age-related conditions, including heart disease.

 The study represents the first time that the genomes of people with ‘extreme longevity’ have been decoded in such fine detail and it may help shine a light on how some people manage to live such long lives while still avoiding the ravages of age-related diseases. Pictured: Frenchwoman Jeanne Calment celebrating her 122 birthday. Calment is thought to have been the oldest known human on record, reaching a whopping 122 years and 164 days

‘This study constitutes the first whole-genome sequencing of extreme longevity,’ added paper author and geneticist Massimo Delledonne of University of Verona.

‘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,’ concluded immunologist Claudio Franceschi, also of Bologna.

The full findings of the study were published in the journal eLife.


Humans may live to 120 in just 60 years time, experts claimed in May 2017.

Research reveals it is possible to slow down our biological, or ‘inner’, ageing process, which could help us to live decades beyond the current life expectancy of 81.

Drugs that interact with our DNA maintain the function of our bodies for longer, the research suggests.

Experts stress, however, this must be combined with a healthy lifestyle for full effect.

Yet, how a 120-year-old life expectancy may impact people’s quality of life is unclear. The side effects of such treatments are also unknown.

Several European countries are in talks to start drug trials within the next three years.

Professor Vladimir Khavinson, head of the St. Petersburg Institute of Bioregulation and Gerontology, said: ‘It is important to understand that nobody would want to live a long and unhealthy life. 

‘The main goal for us now must be to allow people to stay healthy for as long as possible into their old age.’ 

Six of these drugs are already available in Russia.

These include Thymalin to maintain immune system function and Cortexin to preserve brain activity.

The drugs work on the so-called ‘peptide technology theory’, which states that interacting with DNA increases protein production that prolongs lifespan.

Speaking at the international symposium on longevity in Geneva, Professor Khavinson added: ‘One of the key indicators of ageing is the reduction of protein synthesis.

‘We have come to the conclusion that it is possible to restore it to a normal level with the use of peptide bioregulators and have found an optimal way to maintain natural peptide production of a sufficient quantity.

‘The technology developed by our scientific institute is based on the extraction of peptides from the tissues of young healthy animals that have the same structure as human tissues.’ 

A similar study conducted by researchers at the GLMED medical center in Moscow assessed 60 age markers throughout such drugs’ treatment in participants aged 31-to-72 years old.

Results suggested that, when combined with a healthy lifestyle, the drugs reduce a person’s biological age by an average of up to two years over 12 months. 

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