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Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.