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such a colour existed previously in certain individuals, it follows that those with other shades of green would be gradually exterminated, while the former alone will survive.

This idea that, through sex, species are better placed to adapt rapidly should environmental conditions change or become hostile has dominated the discussion of the evolution of sex for more than a century.

Yet, natural selection on its own doesn’t entirely account for the invention of sex, since random mutations also play a role – for instance, if our insect found itself saddled with a mutation that just happened to make it the same shade of green as the new food plant. Mutations perturb the genetic blender of sex, sometimes to the detriment of an individual offspring but sometimes to its benefit. There have to be other plausible explanations as to why sex is the number one way to make babies despite its drawbacks.

One modern hypothesis emphasizes the comparatively efficient way in which sex rids offspring of harmful mutations. Because genes are reshuffled among individuals in each subsequent generation, fewer bad mutations accumulate in a line of descendants. Sex makes it possible to ‘reverse’ a deleterious mutation by mixing DNA with a mate’s. These mutations do not need to be harmful in and of themselves; they may simply provide an easy target.

Which brings us to the second reason why having sex to reproduce may be better than going without: it’s all about ecology. In a fluctuating environment, sexual reproduction offers a short-term advantage since the genetic variability produced through sex offers chances to be better able to adapt. Indeed, the most popular of the ecological theories is the Red Queen hypothesis, which focuses on the advantages that sex provides in thwarting the threat of parasites.

Parasites are smaller and shorter-lived than their hosts, and so in general also reproduce more frequently and accumulate mutations more quickly than their host organisms. No matter how well adapted the target species’ immune system might be, or how quickly it can change itself to deflect a threat, the parasites change even faster. They do not want to be made homeless, after all. To fight off potential assaults from numerous parasites successfully, host species create, on the scale of evolutionary time, an array of different gene combinations that throw up barriers against parasites.

The most important genetic weapons against parasites are our mhc genes, which encode instructions for the major histocompatibility complex, which is responsible for how white blood cells – the foot soldiers of our immune system – interact with one another, with other cells in the body, and with foreign objects. It will come as little surprise that mhc genes are the most variable genes contained in the genome of vertebrate animals; the range of forms in which the genes can appear is quite spectacular. Mhc variants determine how well our immune systems recognize invaders; how susceptible we are to infectious and autoimmune diseases; and even how we respond to odours, including body odours, and therefore things like our mating preferences and our recognition of others as kin (with whom we generally wish to co-operate). Mhc genes also influence the outcome of a pregnancy.

In their job as part of the immune system, MHC molecules on the surface of cells latch on to foreign molecules – known as antigens – from viruses, bacteria, transplanted organs, tumours, and other ‘pathogens’ that are not supposed to be in the body. The molecules present these invaders to a subset of white blood cells, called the T lymphocytes, which in turn initiate an appropriate immune response. T cells do everything from destroying infected or tumorous cells, to remembering previous infectious attacks in order to call up a quick response to a repeat invader, to turning on other T cells and immune-system responders.

Mhc genes fall into two classes tied to these various immune-system tasks. Virtually all cells have mhc class I genes, which mainly provide immune protection from internal pathogens – pathogens, like viruses and bacteria, that have already made their way inside our cells. A few specialized cells, such as the antigen-presenting B cells and macrophages, have mhc class II genes. These cells engulf offending parasites. The MHC class II molecules bind to proteins on parasites and present the proteins to cells, which digest them all up, destroying the threat. There is a rare MHC class II variant that may give a particular advantage when it comes to parasites. Called supertype 7, it has been shown in lemurs to help protect the body against multiple parasites at once, and it is presumed to have a similar role in other primates, including humans. So, the more shuffling there is in mhc genes, the more chances a species has to ‘out-think’ pathogen threats.

In as far as the Red Queen hypothesis presumes that hosts and parasites are engaged in an evolutionary arms race, with nimble parasites able to produce more generations (and change) more quickly, the mhc variants that provide more resistance to parasites will be more likely to spread through a population. To stay ahead of the parasites, mhc genes will diversify, creating new combinations and rare types, like the supertype 7. The more variation, the better. And swapping genes through sex is a tested way of creating new combinations and rare types, and thus provides greater protection from a greater range of environmental pathogens.

Thwarting parasitic infection has knock-on effects when it comes to sexual behaviour itself. Among the males of some animal species, those individuals less infected with parasites typically have more energy to allocate to attracting mates. A landmark study, published in 1982 by British naturalist W. D. Hamilton and American evolutionary ecologist Marlene Zuk in the journal Science, investigated this question by looking at blood parasites infecting songbirds. Hamilton and Zuk looked at seven surveys of bird parasites, including several kinds of protozoa and one