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  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 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. Written at a time when, in many places, miscegenation was outlawed and apartheid was actively enforced, the book raised several controversial issues surrounding the genetics of human offspring.

  Haldane asked whether inequality among men was fundamental and genetic, if the sterilization of genetic ‘defectives’ was appropriate or wrong, and what could be expected if mixed race children were accepted (and more regularly born into the world). He looked at whether certain races and certain social classes might be endowed with innate superiority, or stand as a ‘pure’ race – a belief he attacked. He wrote that recent learning about human inheritance had ‘been used to support proposals for very drastic changes in the structure of society’ – a clear reference to the treatment of Jews in contemporary Germany. He continued: ‘And the stringent measures which have been taken... are said to be based on biological facts. I do not believe that our present knowledge of human heredity justifies such steps.’

  After seventy-five years, the questions Haldane posed remain incendiary, and though our present knowledge of human heredity is growing exponentially each year, the sum total of accumulated data that has anything to do with race is minimal.

  In 2008, two members of Parliament called for a ban on marriages between first cousins in the UK. In large part, their reasoning was based on data suggesting that Pakistani families from the West Midlands of England accounted for about thirty-three percent of the recessive genetic disorders in the region, but only around 4.1 percent of total live births, a dramatic statistic. The disorders were recorded, in the language of medicine, as ‘recessive metabolic errors’. These are mistakes that only affect a child if that child inherits a copy of the ‘bad’, mutated, disorder-creating gene from both of his or her parents. And this is more likely to happen among parents who are closely related – who are consanguineous, that is, ‘share blood’.

  For several reasons, however, the statistics that the politicians used were skewed. There were problems with the way the data were gathered, and other studies over the years have shown that the risk of first cousins having a child with a recessive disease is quite low – no more than for the community overall. The issue wasn’t that first cousins were marrying, it was that everyone in this particular community was slightly more likely than the general population to carry the mutant gene.

  When epidemiologists want to investigate the chances that a certain group may be prone to recessive errors, they look at genetic load, the overall number of harmful mutations the average person is carrying, rather than specific gene mutations. Unfortunately, genetic load is not always simple to translate into morbidity and mortality rates – the chance that a foetus will not make it to full term, or that a child will have difficulty surviving into adulthood, let alone inheriting a genetic disorder. The medical statistics, for example, do not indicate that rare recessive genes are more likely to cause miscarriage than other factors. Moreover, imagine that one of the shared grandparents of two married cousins carried a gene for albinism, which would give each of the cousins’ offspring a fifty percent chance of being albino. That doesn’t necessarily mean that this grandparent carried any other recessive mutant gene, or that the children will automatically be unhealthy or have any other disorder – the genetic load would be small, but the chance of being albino would be relatively high. Finally, consanguineous marriages tend to be more prevalent among people with lower socio-economic status, which coincides, in and of itself, with higher rates of morbidity and mortality, as shown in Sir Michael Marmot’s famous study of Whitehall bureaucrats. The politicians’ motion was based on an oversimplified view of heredity and epidemiology, to say the least.

  Apart from the fact that the proposed law did not take into account all of this evidence, it would have turned a blind eye to risky reproductive behaviours that are currently accepted among many other groups. It is not questioned, for instance, that women nearing menopause should be able to procure fertility treatments, even though it is understood that older mothers are more likely to give birth to children with chromosomal abnormalities; nor that people with Huntington’s disease or other debilitating genetic disorders should retain the right to have children, despite an established fifty percent risk of the condition being inherited. Should a consenting adult be penalized for choosing a partner who might increase the risk of a genetic anomaly in his or her children? If so, would health services be required to screen potential reproductive partners, in the way that the charity Dor Yeshorim checks enrolled Orthodox Jewish families for a handful of recessive disorders before an arranged marriage goes forward? The law would have taken the choice of looking for a recessive trait out of the hands of the people having the child and put it in the hands of the government – a very drastic change in the structure of society. It would set a very disturbing precedent. Yet, the premise on which the law was proposed is quite basic: the premise that genetic variation is good and inbreeding is bad.

  Inbreeding, of course, is what we normally call it when close relations mate. Between the closest of relations, we brand this incest, from the Latin for unchaste or impure. Genetically speaking, this labelling could not be further from the truth, however, because inbreeding limits the genes available to create any offspring, and so maintains a relatively pure familial gene pool; no truly foreign DNA is
involved. As such, you could say that the ultimate form of inbreeding is making babies without a partner – that is, when reproduction does not involve sex at all.

  The incest taboo is universal, though what it means for a particular community depends on whom a group defines as being too close a relation for sexual relations. In many Western cultures, there is an informal taboo around marriages between first cousins or between uncles and nieces. These proscriptions may be fostered partly by religious laws, economic imperatives, or long-standing prejudices, including the socially taught belief that children who grow up together cannot (or should not) develop a sexual attraction to each other. Regardless, most Westerners would not hesitate to say that consanguineous liaisons (those between ‘blood’ relations) are inherently unhealthy, triggering a range of physical and mental deformities – such as the outsized ‘Hapsburg jaw’ you read about in school biology lessons, but also including infertility and early death. The conventional wisdom is so ingrained that, in recent decades, some scientists have begun to argue that the impetus to avoid inbreeding is itself genetic – that there is a gene that discourages inbreeding and promotes a taboo against incest in families that carry it.

  In many cultures, however, consanguineous marriages, including between cousins, remain widespread. These marriages are most prevalent in Arab countries, with India, Japan, Brazil, and Israel following them in the rate tables. The liaisons are more common among people with less education (as well as lower socio-economic status), perhaps because higher status groups are more likely to have been influenced by Western beliefs about ‘inbreeding’.

  Conventionally, consanguineous marriages are considered to carry social benefits, such as being able to aggregate family wealth and ensure better treatment of the bride, and thus increase stability and security for the whole family. Many arranged marriages occur between ‘blood’ relations. But while those social benefits may hold sway in many families, there can also be biological benefits to marrying within the family: marrying a close relative might save your lineage’s genes from extinction. In fact, there are cases in which inbreeding has actually facilitated a population’s adaptation to an inhospitable environment and parasite threats.