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More sex by partners is good for offsprings to live disease-free life: Study

mutationNew research shows that the more we have sex, the better it is for offsprings as they could inherit the genes and avoid bad genetic mutations leading to less chances of developing diseases in offspring over time.

Canadian researchers from the University of Montreal and the Sainte-Justine University Hospital Research Centre have revealed how humans pass on genetic material to the progeny through sexual reproduction and any mutation in it results in disease-prone offsprings.

“This discovery gives us a better understanding of how we, as humans, become more or less at risk of developing or contracting diseases,” said lead author 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.

To be precise, the team discovered that the segments of the human genome that do not recombine carry greater proportion of the more disease-enabling genetic mutations.

Until chromosome recombination eventually occurs, these segments accumulate more and more bad mutations, passing on bad genes to the offspring that would be less resistant to diseases.

“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.

The study was made based on data available for years in the form of biological samples and genetic data from hundreds of individuals from Canada’s CARTaGENE genetic data repository and the multinational 1,000 Genomes Project.

The study found that the proportion of mutations associated with disease was significantly higher in low-recombining segments known as “coldspots” relative to highly-recombining regions, which 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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