Sperm cells in adolescent boys have unexpectedly high levels of DNA mutations which could explain why children born to teenage fathers are at higher risk of birth defects, research suggests.
Male germ cells undergo six times as many DNA mutations during their teenage years as women’s and 30 per cent more than when they are in their 20s, a study of 24,000 parents and their children found.
Peter Forster, who led the research, said the discovery is the first possible explanation as to why teenage boys are more likely to have children who suffer from conditions such as autism, schizophrenia and spina bifida.
Mutations, the result of DNA copying errors during cell division, can result in changes affecting a person’s offspring when they occur in sperm and egg cells.
Forster, a fellow of Murray Edwards College and the McDonald Institute at the University of Cambridge, said: “There’s a lot we can’t find out about reproduction for ethical reasons so this helps us to address something very basic but unknown.
“It appears that the male germ cells accumulate DNA errors unnoticed during childhood, or commit DNA errors at an especially high level at the onset of puberty.
“However, the reason for this is not yet clear.
“Possibly the DNA copying mechanism is particularly error-prone at the beginning of male puberty. Or sperm production in boys may undergo dozens more cell cycles, and therefore DNA copying errors, than has previously been suspected.”
Meanwhile, the DNA mutation rate in women is constant throughout their lives.
The risk to teenage fathers conceiving a baby with a birth defect is 0.5 per cent higher than the rest of the population, who face a risk of 1.5 per cent.
Forster said the increased risk is “nothing to worry about on a personal level” but is noticeable across national statistics. The London-born researcher is hopeful that the technique used to count the cell cycles during the study could be used to treat cancer patients by determining how old tumours are.
“For example, if a recovered patient has been diagnosed with a tumour for a second time, we would be able to see how old the tumour is and therefore whether the two are connected,” he said.
“If they were connected, we would know the first set of treatment didn’t work and to try another treatment.”
The research team used DNA from blood and saliva samples taken from 24,097 parents and their validated biological children from areas of Germany, Austria, the Middle East and West Africa over 20 years.
The research was carried out by the Institute of Forensic Genetics in Munster, Germany, and is published in the Proceedings of the Royal Society B: Biological Sciences.