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Why the Sex Ratio is 1

Page history last edited by Alex Backer, Ph.D. 12 years, 3 months ago


Why The Male/Female Ratio is 1



In countries where the gender ratio is not artificially manipulated, such as in the U.S., the ratio of male to female human births is around 1.05. Higher male mortality leads to decreasing male-female sex ratios as the population segment gets older. In the whole population, these two effects roughly cancel each other out by reproductive age, leading to an overall male-female ratio close to 1. Why?

      Mammalian females go through prolonged periods, including gestation and lactation, during which they cannot produce offspring. Males, in contrast, can mate with practically arbitrarily high frequency. Thus, a species that had more females than males would be able to produce more offspring per unit time than a species with the same total numbers but an even distribution between males and females. Why hasn't this evolved?

      German biologist Carl Düsing was the first to arrive at the answer, but Sir Ronald Fisher was the first to disseminate it, in the 1920s (cited in The Red Queen, by Matt Ridley, pp. 118-128) or 1930s.

      The answer lies in the fact that evolution favors not what is good for the species as a whole, but rather genotypes that do better than their competitors. Fisher realized that a mother that produces an excess of the rarer sex (whichever this may be) will be favoured by natural selection. So, like a pendulum in motion that eventually comes to rest, the sex ratio will stabilize at an equilibrium where males and females are balanced with equal numbers.

      Assuming the males left every available female pregnant, a mutant which created more females than males among its offspring would generate more total offspring in the population. Which genotypes do these "extra" offspring carry? Therein lies the key to the puzzle: the "extra" offspring carry one haplotype (half a genotype) from the mutant that generates more females, and one haplotype from a genotype that generated a male. Thus, for every increase in the population of the mutation coding for more females, there will be an equal and corresponding increase in the population of genes coding for males. And if the ratio did shift toward females, there would be increased selection for genotypes favoring males, since every male would get multiple offspring per gestational period, while each females would get only one. Likewise, if the ratio shifted toward males, each male would on average get less than one offspring per gestational period, while females would get one, favoring females and bringing the ratio back to a 1:1 equilibrium.

      So while it would seem at first sight that, if each male could mate with a large number of females, a genotype could produce far more offspring if it produced more males than females, and that the gender ratio should over time have evolved to favor males, if males did start becoming more common, then the average male would not be able to mate with a large number of females. In equilibrium, at a 1:1 ratio, the average male fathers just as many children as the average female.


None of this precludes the proliferation of mutations that favor one gender over another

Note that none of this precludes the proliferation of mutations that favor one gender over another, as long as there is an equal and opposite proliferation of mutations that favor the opposite one. Thus, the fact that the ratio is 1:1 may be hiding families with genetic predisposition toward male or female progeny. Any such mutation has eluded animal breeders for millenia. Whether this has evolved or not in humans can be tested by looking at the statistics of census data.





Exceptions to the Rule

It is interesting to note that an hypothesis that led to our conclusions was that each offspring carries a male and a female haplotype. Where this rule is broken, such as in insects where unfertilized eggs can lead to live insects, gender biases can and do occur.


      Note also that the drive toward a 1:1 ratio derives from the fact that any benefit accorded to a female is accorded to a male of a different strain too, by virtue of the property of chromosomal sex determination that makes half the inherited material paternal and half maternal. When this does not hold, as in the interesting case of the lemmings with a male-inhibiting W chromosome, or in an incestuous population in which females copulated with their brothers, a genotype that produced more females than males would be beneficial, increasing the population growth speed for the genotype whilst not dimishing it via competition from rival genotypes also favored. Conversely, when the cost of males is much lower than the cost of females, more males are produced. More on this at .


Dominant and promiscuous individuals are better off as males

Trivers and Willard predicted in the 1960s that in species where male dominance was inherited more than female dominance (for example, if females left the population to join their male partner's), dominant individuals would tend to have more male progeny, and individuals of low social status would tend to have female progeny. There is some evidence that this may be true. But even if the inheritance of male and female dominance was equal, greater male than female promiscuity results in the same.





Y chromosomes like them male

It is interesting to note, as Bill Hamilton did in 1967, that it is in a Y chromosome's interest to produce only males, since females do not carry a Y chromosome --put better, Y chromosomes which produce more males will be selected for versus ones which produce females too at the expense of males. One of the ways in which this fate is avoided, for the benefit of most other genes, is by having Y chromosomes stripped of practically all their informational load, essentially shutting them off.




Further reading:

Sex Ratios, edited by I. C. W. Hardy (Cambridge University Press, 2002).

Sex Wars: Genes, Bacteria, and Biased Sex Ratios by Michael E. N. Majerus (Princeton University Press, 2003, 280 pp.).

The Red Queen, by Matt Ridley, pp. 104-128.

Up to Science.


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