Like a Virgin (7 page)

Sex was born not for promoting change and diversity but for limiting them.

There is no doubt about it: sex is popular. The vast majority of species – 99.9 percent of higher animal species and about 92 percent of higher plants – reproduce
sexually, at least on an occasional basis. A tremendous amount of research has been devoted to asking why this is the case.

The magnitude of the question becomes apparent if you
consider that, for females especially, having sex is dangerous, expensive, and foolhardy. The act of mating can be
harmful, with sexual partners sustaining physical injuries or contracting sexually transmitted diseases. Finding a suitable partner involves an investment of time and energy – the work of
trying to dodge those physical dangers as well as the risk of picking a mate that, in the worst-case scenario, never produces a viable offspring.

Even if a woman meets her ‘soul mate’ (a very human way of describing the safety of a reproductive partner), mixing genes may be a disaster; sexual reproduction breaks apart
combinations of genes that work, after all, and they may not work in their new formation.

Moreover, because a sexually active female allows her mate’s foreign genes to enter her body (and thus her offspring), her own genetic contribution is diluted by one-half. That seems like
basic biology, but not all genes are created ‘equal’. Most mutations, those mistakes in the combined DNA, arise in sperm.

Recent estimates show that the rate of mutations in males compared to females is two times higher in rodents, six times higher in most primates, and ten times higher in our primate, humans
– which makes you question any concept that human evolution is the ultimate step in some hierarchical process. This comes down to a basic fact regarding how cells are made. Most mutations
arise from mistakes in copying the DNA in one cell when it divides to make two cells, and they divide to make four cells, and so on. In cells that divide more often than others, more mistakes are
likely to happen, simply because more copying is going on. It’s a bit like a game of Chinese Whispers – the more times a message is passed around a circle of people, the more likely it
is to get distorted. In men, cells divide to make ninety thousand sperm every
minute
– room for a lot of mistakes. And in the past century, geneticists have found that
most of these mutations that occur in copying are bad news, and that the mutations frequently interact with each other, with bad results. This means that the prolific production of
sperm is more likely to pass on harmful mutations than is the relatively more modest supply of eggs – and, of course, sperm pass their mutations on to offspring produced sexually.

So why, then, do females reproduce sexually, since it’s not optimal for them or their progeny? This long-standing puzzle in evolutionary biology is known as the paradox of sex.

One of the first to tackle an answer was the German biologist August Weismann, deemed by Ernst Mayr to be second only to Darwin among the pioneers of evolution. In 1885, Weismann delivered a
lecture series on the ‘Significance of Sexual Selection’. Weismann believed that the reason sex had evolved and was retained was because it provided the variation upon which natural
selection could act. Consider his example:

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 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’.