Harmful changes to DNA in sperm become more common as men age, with a greater risk of older fathers “unknowingly” passing on a genetic mutation to their offspring.
Scientists say it is down to a form of natural selection which sees some mutations gain a competitive edge during the production of sperm.
Researchers used an ultra-accurate DNA sequencing method to study sperm from 81 healthy men who were aged between 24 and 75 years.
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The findings show that disease-causing mutations were found in around 2% of the sperm from men in their early 30s, increasing to 3-5% of sperm in men aged from 43 and 58 and from 59 to 74.
The results demonstrate how genetic risks to children increase the older the father is, but the findings could open up new areas of study looking at how lifestyle and environmental factors might impact genetic risks to future generations.
Co-author Professor Matt Hurles, Director of the Wellcome Sanger Institute, said: “Our findings reveal a hidden genetic risk that increases with paternal age. Some changes in DNA not only survive but thrive within the testes, meaning that fathers who conceive later in life may unknowingly have a higher risk of passing on a harmful mutation to their children.”
Changes to DNA – mutations – sees those cells gaining a competitive edge, leading to ‘cloned’ cells that contain the same mutations. When this happens in sperm and egg cells, the mutations can be transferred to offspring.
The latest research identified 40 genes where mutations are favoured during the production of sperm, showing this process is far more widespread than previously thought. Many of the mutations are linked to childhood diseases, severe neurodevelopmental disorders and inherited cancer risk.
In a separate, complementary study, scientists analysed mutations passed down to offspring.
They identified more than 30 genes where mutations led to a competitive edge in sperm cells, with many overlapping the genes seen in sperm.
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These findings also demonstrated that these changes significantly increase the rate of sperm mutation – around 500-fold – which helps to explain the emergence of genetic disorders when the parents are not carriers.
Senior author Dr Raheleh Rahbari, Group Leader at the Wellcome Sanger Institute, said:
“There’s a common assumption that because the germline has a low mutation rate, it is well protected. But in reality, the male germline is a dynamic environment where natural selection can favour harmful mutations, sometimes with consequences for the next generation.”
