Like a Virgin by Prasad, Aarathi (recommended reading txt) 📕

nematode worm, and found that there was a significant correlation between chronic blood infections and the striking displays that scientists associate with bird mating: bright male plumage, bright female plumage, and ‘bright’ male song. As they looked deeper, they also discovered that female birds scrutinized mates based on these displays, and they chose males that were marked with health and vigour, that is, those that were more genetically resistant to disease. This finding came to be known as the ‘bright male hypothesis’. Perhaps the most spectacular avian plumage is the peacock’s, and the peacock has often been used as an exemplar of evolutionary selection at work. Of course, when it comes to a peahen’s mate, selection of a mate is relative. At the most basic level, healthy males are able to invest more bodily resources into maintaining healthy, vibrant plumes and engaging in elaborate courtship songs, dances, and other displays. Females may also tend to prefer less parasitized males in order to reduce their (and their babies’) risk of infection, and male attractiveness might offer a clue to a potential mate’s health.

Reproductive success has a genetic component in humans too. Men who carry a mutation in a gene on chromosome 7 that is linked with the gene for cystic fibrosis (the cftr gene) often experience infertility, sometimes because the vas deferens, a tube that should carry sperm towards the ejaculatory duct, may be absent or unable to provide the specific secretions needed for sperm to ready themselves for fertilization; and women with this mutation may have heavy mucus that prevents sperm from reaching the egg. A person with the genetic mutation may not have any other symptoms of cystic fibrosis, and may not be aware of the mutation until he or she has difficulty while trying to have a baby. The mutation causes a single change in a protein and seems to have benefits, however: the mutant CFTR protein is resistant to Salmonella typhi bacteria, the cause of typhoid fever. That change is more widespread among populations in Europe and Asia – in fact, one in twenty-five people of white European descent are carriers, meaning they have one of the two genes on that chromosome necessary for a person to have cystic fibrosis. So while the mutation can have serious consequences for a person’s health if it is inherited from both parents, it appears to be the product of positive natural selection. So through sex, the genes that increase fertility, and which give parents’ immune systems an enhanced ability to fend off parasites, are passed down to their children.

This isn’t true only of songbirds and ‘higher’ mammals, and that includes us. Female green stinkbugs, for example, also choose mates on the basis of the males’ potential genetic contributions to their young. These female bugs have a trickier time of it than peahens do, though, because large male stinkbugs, which are more likely to dominate energy resources and thus be more attractive to females than small males, are also more likely to suffer from parasitic infections. Even worse, it appears that body size is inherited, but only from the father – so there is more evolutionary pressure to prefer large males; larger offspring are more likely to survive against small bugs when resources are scarce. Being able to identify healthy large mates thus gives female stinkbugs a double advantage. Not only does the number of eggs they produce increase, but their male offspring have more success at attracting females and mating, a skill that seems to be inherited from the father, which potentially increases the number of descendants per ‘son’.

The Red Queen hypothesis assumes that only the healthiest (that is, parasite-free) creatures are able to reproduce. These healthy creatures pass on their DNA to produce a genetic range among their young, which also have a better chance of avoiding parasite infestation. This evolutionary tactic does not strictly favour sex above no sex; rather, it favours diversity, however generated, over no diversity. Even in animals that reproduce without sex, genes are shuffled to a certain degree, but in relative terms, sex does more to mix things up. Not being able to effect or incorporate change into your genome is, in this view, a one-way ticket to extinction.

For this reason, it is surprising that there is little or no direct evidence showing that accumulating mutations or a reduced ability to adapt in the face of environmental pressures causes increased extinction risk in animals that only reproduce without sex. In fact, asexual species do not just die out as the predictions say they should. Those that survive use a range of unusual biological tactics to alleviate the negative genetic effects of their chosen approach to reproduction. These include being able to disperse their offspring to wide geographical distributions (large, sometimes very diverse habitats) and dormant resting stages (periods with low activity, sexual and otherwise) – mechanisms of maintaining population equilibrium that help to increase the chances of long-term survival for an animal with low genetic diversity. These tactics take the place of natural selection through sex, which weeds out the genes that are least adapted to the environment.

Sex provides survival strategies, but it is by no means perfect. Among other things, sex does not allow the creation of a clone from a genetically super-successful parent, a parent that has the ideal make-up for meeting a particularly harsh environment. This, however, is a problem that can be circumvented by approximating asexual reproduction, say, through inbreeding.

What makes a baby healthy and bonny, that is, a ‘good’ baby? In 1938, the eminent biologist J. B. S. Haldane wrote Heredity and Politics, a book he described as being ‘addressed to such as are unacquainted with the science of genetics, but who are attracted or disturbed by eugenic doctrines’. The doctrines he discussed are disturbing indeed.