Teenage boys already have plenty to worry about: spots, girls and the size of their “thing”, as Adrian Mole might have put it. Does the problem of having genetically weak adolescent sperm really need to be added to this list?
Scientists at the University of Cambridge have suggested this is the case after carrying out a study involving more than 24,000 parents and their children. The analysis focused on tiny genetic differences between parents and offspring, which are assumed to be caused by copying errors in the egg or sperm cells.
The study shows that, on average, fathers pass on at least six times as many of these mutations to their children as mothers. This suggests sperm DNA is a less faithful replication of the father’s genetic sequence, probably because sperm cells have undergone more divisions than the female egg cell by the time conception occurs.
The more striking claim – and the one that got most attention – is that the error rate in the sperm cells of teenage boys is about 30% higher than that for young men.
The researchers say this could explain why children of teenage fathers have a higher risk for disorders such as autism, schizophrenia and spina bifida.
The paper’s author, Peter Forster, said: “Children of 15-year-old boys have about 30% more mutations than children of young men. It’s a J-shaped distribution.”
This probably translated to a risk of birth defects of about 2% for teenage boys, compared with an average risk of 1.5%, he said.
Forster said: “It could be that the whole sperm production system is more error prone at the start … that it just isn’t optimised yet.”
He said that the theory had even prompted the idea, by another journalist, that if teenage boys masturbated more, they might be able to work their way through this “suboptimal” period more rapidly.
Before teenagers heed this suggestion (don’t they already devote quite a lot of time to this activity?), it’s worth looking at the paper itself, in the Royal Society Journal Proceedings B.
The odd thing is the complete absence of the J-shaped curve. Here’s the graph, which looks like a straight line to me.
It is true that the data point for teenage boys may show a slightly higher number of mutations than that for the 20- to 30-year age range, but it still appears to overlap with the 95% confidence interval for the linear trend. I can’t see any reason to conclude that “the germ cells of adolescent boys are an exception to the ageing rule”, as the authors do.
If you were going to go down that route, you might also wonder why sperm goes a bit dodgy at 30, but then recovers again with the approach of middle age, because there seems to be a spike in the 30-35 category. A simpler explanation is that the data is just a bit noisy.
Allan Pacey, professor of andrology at the University of Sheffield, agrees: “This doesn’t make sense to me. I don’t see a J-shaped relationship and, in terms of biology, I can’t think of anything that would explain it.”
Forster points to several population studies, which hint that teenage fathers may be more likely to have children with various disorders. But it is hard to say whether such results are linked to direct genetic causes or social and environmental factors. For me, this latest studydoes not do much to resolve the issue. As Pacey puts it: “I don’t see any great concern for teenage dads.”
And for those teenage boys who are not dads, there are probably other reasons to wait until their 20s to embark on fatherhood.
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