Sober writes that John Arbuthnot noted in 1710 that there was a difference between birthrates of sons and daughters. He cites R.A.Fisher's 1930 analysis, in applying natural selection to this observation, as follows:
Arbuthnot could not have known that R.A. Fisher (1930) would bring sex ratio within the purview of the theory of natural selection. Fisher’s insight was to see that a mother’s mix of sons and daughters affects the number of grandoffspring she will have. Fisher demonstrated that when there is random mating in a large population, the sex ratio strategy that evolves is one in which a mother invests equally in sons and daughters (Sober 1993, p. 17). A mother will put half her reproductive resources into producing sons and half into producing daughters. This equal division means that she should have more sons than daughters, if sons tend to die sooner. Fisher’s model therefore predicts the slightly uneven sex ratio at birth that Arbuthnot observed. (p.5)This seriously baffled me – perhaps one of the well-informed commenters can help. Obviously, this is specifically addressed to sex ratios in human reproduction. Sex determination in humans comes from an X or Y chromosome in the sperm cell. To the best of my knowledge, the mother has no way of determining what sperm cell fertilizes an egg – either consciously or biologically.
Furthermore, if we are looking at grandoffspring, then surely there are much more important things to look at in biological terms than the age at which offspring die. For example: fertility rates; comparative rates of homosexuality/heterosexuality for the two genders (if such things are genetically coded, as we are told – if 10% of males are genetically homosexual and 5% of females are homosexual, and 5% differences in life expectancy have a natural selection effect, then one would assume that expected sexuality would have natural selection implications for the relative frequency of male and female offspring); comparative ages at which offspring become sexually active and cease being sexually active; and so on.
The analysis also implies that the death rates of different sex offspring are biologically hard-coded. Not only is there a mysterious mechanism present that results in a bias towards male offspring, but this mechanism works by somehow knowing about mortality rates.
The huge question that this proposition raises is: HOW??? If this comes about through natural selection (which, incidentally, I don't have a real problem with – I find Arbuthnot's argument unsatisfying as well), then what on earth is the mechanism?
What are the options?
Perhaps the gender distribution is hard-coded somehow into the species – but if so, what is the evolutionary basis for this? The neodarwinian paradigm insists that it ought to be DNA. If so, how? If it isn't known, then again we have a supposed natural selection “explanation” that is lacking a mechanism.
But the fact is that a natural selection story could be made up which would accommodate any observation about frequencies of sex distribution. Supposing female children were much more common than male children: this would work from a natural selection point of view because men are able to impregnate many women. Supposing male children were more common than female children: this would work from a natural selection point of view because it would allow females a greater say in the fitness of the father of their children. And so on.
The story isn't important – either in these cases, or in Fisher's case. What is important is the science that supports it. Fisher's supposed refutation of Arbuthnot's argument is apparently completely lacking in a mechanism – it simply doesn't square with what we know today about reproduction and evolution. And yet, here it is, being presented in refutation of an argument from design. If there is no mechanism, then it has no less, or more, power than Arbuthnot's argument which asserts that the distribution is a sign of divine involvement.