Sir

Westendorp and Kirkwood1 studied data on the British aristocracy and conclude (probably correctly) that there is an evolutionary trade-off between longevity and fecundity. There is another significant conclusion to be drawn, and that is that humans have a strong hereditary predisposition to infertility.

The tendency for low fecundity among the English aristocracy was in fact first studied systematically by Galton in 1869 (ref. 2). There was general concern at the time at the rate of extinction of English hereditary peerages. Galton examined the links between social status and reduced fecundity, and concluded that it was largely due to the tendency for peers — and the sons of peers — to marry heiresses as a means of accruing estates. He speculated that in a patrilineal society heiresses are more likely to arise in small families of reduced fertility, and that marriages with such women would also have a tendency for low fecundity.

Fisher3 later analysed Galton's data and other genealogical findings in some detail, and concluded that human reproductive success is extremely unevenly distributed and therefore subject to very strong selective pressures. In the 1912 Australian census, for example, 50 per cent of the children were the offspring of one in nine of the men and one in seven women. Three-fifths of all children that were born died unmarried and 11 per cent of marriages were sterile4.

While Fisher and Galton's writings were tarnished because of their links with the eugenics movement, one clear message is that subfertility is endemic within human populations — albeit hidden in ancestral communities by child-sharing and other devices such as serial polygamy5. Moreover, reduction of investment in reproduction is a powerful force for wealth consolidation within a family: a concept that Fisher3 traced back to Hesiod in the eighth century bc! The link between longevity and reduced fecundity is entirely consistent with the disposable-soma hypothesis discussed by Westendorp and Kirkwood1.

In an era when infertility is increasingly emergent as a social problem and is now eminently treatable by technological means, we should perhaps be aware of the evolutionary forces that may have helped amplify it.

For males, the strong selective pressure for critical genes controlling fertility on the Y chromosome6, coupled with highly uneven reproductive success between individuals in any generation, should be considered in any attempt to reconstruct genealogies based on Y sequences. Rather than differential migration rates between women and men, this could possibly explain part of the discordant convergent times for human Y sequences and mitochondrial DNA7. While Y chromosome variations are generally considered to be neutral, close scrutiny of actual patrilines reveals that long-term male reproductive success is strongly influenced by politics and social dominance8.