Sex guarantees disease-free life in offspring

Montreal: The more we have sex, the more we avoid bad genetic mutations leading to less chances of developing diseases in offspring over time, finds an interesting study.

Researchers from the University of Montreal and the Sainte-Justine University Hospital Research Centre in Canada have revealed how humanity's predispositions to disease gradually decrease the more we mix our genetic material together through sexual reproduction.

Sex guarantees disease-free life in offspring
Representational picture

"This discovery gives us a better understanding of how we, as humans, become more or less at risk of developing or contracting diseases," said study leader Philip Awadalla from the University of Montreal.

"It also tells scientists more precisely where to look in the human genome to find disease-enabling mutations which should speed up the discovery and identification of mutations associated with specific diseases," he added.

More specifically, the team discovered that the segments of the human genome that do not recombine carry a significantly greater proportion of the more disease-enabling genetic mutations.

Until chromosome recombination eventually occurs, these segments accumulate more and more bad mutations.

In other words, as far as susceptibility to disease is concerned, our genetic material actually worsens before it gets better.

"Thankfully, disease-enabling mutations are eventually shuffled off our genetic code through sexual reproduction. But since these mutations rest on less dynamic segments of our genome, the process can potentially take many hundreds of generations," Awadalla explained.

This discovery was made possible by the availability in recent years of repositories of biological samples and genetic data from different populations around the globe.

Awadalla and his team studied the sequenced genomes of hundreds of individuals from Canada's CARTaGENE genetic data repository and the multinational 1,000 Genomes Project.

They found that the proportion of mutations associated with disease was significantly higher in low-recombining segments known as "coldspots" relative to highly-recombining regions.

The bad mutations in these "coldspots" were generally more damaging than the mutations in the highly recombining segments.

"Researchers and health authorities will be able to apply this new information to develop more effective treatments and prevention programmes," Awadalla added.

The paper appeared in the journal Nature Genetics.

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