Like a Virgin (19 page)

This strategy is custom-made for polygamous reproduction. When each female regularly bears offspring of several different males, the mother has an equal genetic stake in each embryo and will
achieve the best outcome for her genes if resources are allocated equally to each one; the father is better served, however, if his particular embryos grow faster and extract a greater share of
resources from the mother than do the siblings in which he has no genetic stake. So silencing certain genes in the placenta ensures that every foetus has an equal chance of survival. The ability of
a father’s genes to influence how an embryo acquires resources from its mother is rare, but it does also appear in some plants. In these plants, including maize (
Zea mays
, or corn),
the mother nourishes the growing embryo for an extensive period after fertilization, whereas the father experiences negligible costs – just its seed.

In theory, imprinting does not make sense for a monogamous species. A father who intends to have multiple children with just one female partner should co-operate with her for resources rather
than try to extract everything he can for the benefit of his genes. Take, for example, what happens when a strait-laced oldfield mouse (
Peromyscus polionotus
) is crossed with its promiscuous
relative, the deer mouse (
Peromyscus maniculatus
). To be precise, the oldfield mouse is not strictly monogamous in the wild; it’s just that the females don’t change partners
nearly as often as their polygamous relatives. So when biologists decided to poke into the question of whether any monogamous animals have imprinted genes, the short answer was that they did, in
part because they are somewhat promiscuous and had fully polygamous ancestors. Nevertheless, the experiments still yielded some extremely interesting results.

In oldfield mice, the male and the female are about the same size, which is generally the case with monogamous species, and even though polygamous animals usually exhibit
a substantial difference in size and appearance between the sexes, deer mice are roughly the same size as oldfield mice. The animals seemed well suited to be mates. Despite this, when a female deer
mouse was crossed with a male oldfield mouse, their offspring grew up to be forty percent smaller than either parent. And when a male deer mouse was crossed with a female oldfield mouse, the babies
were oversized, bearing enlarged tongues that made it difficult for them to eat and swallow; for the most part, they did not survive. And it was not just that the embryos were overgrown – the
placentas that nurtured them were overgrown, too – around six times bigger than in a pregnancy involving two monogamous or two polygamous mice. As a consequence, oldfield mice mothers often
died in labour, while trying to push the babies out through the birth canal.

Though both mouse species had imprinted genes, the polygamous females were better equipped to do battle against the monogamous males’ genes. The embryos were restricted in taking resources
from the mother’s body. Similarly, the polygamous males were better able to extract nutrients from the mother for the offspring, building a supersized placenta to increase the foetuses’
(and the genes’) access to the resources. If there is a mismatch in the genes that are silenced between the mother and the father, however, fatal mistakes can result.

A pregnant woman’s body is constantly negotiating with the foetus over the share of nutrients each one gets. Among the body’s main energy-supplying fuels is the
sugar glucose. To
control glucose, you need to control the hormone essential in the body’s proper use of sugar: insulin. And when the body is not producing enough
insulin, or becomes resistant to its effects, you suffer from diabetes. Up to fourteen percent of women suffer with diabetes during pregnancy, and although the condition usually disappears after
the baby is born, nearly one in five of these women go on to develop Type 2 diabetes within nine years; they may also be at greater risk of developing heart disease. The reason for this lies with
imprinted genes.

During pregnancy, the placenta pumps out various hormones that block the usual action of insulin so that the foetus will gain greater access to the glucose circulating in the mother’s
blood. Effectively, the mother is left unable to control or use her own glucose, making her insulin-resistant, and glucose does not enter her own cells as it should. Glucose levels rise in her
bloodstream, and, in something of a vicious cycle, her body needs to produce more insulin to overcome this spike. If it does not, she develops diabetes for the duration of the pregnancy. In adults,
both the mother’s and the father’s copies of the human insulin gene, known as
INS
, work just as well as each other. In the embryo, however,
INS
is one of the small number
of genes that are imprinted, so that only the father’s copy of the gene functions. The same story plays out for a related gene called
IGF2
, which makes insulin-like growth factor-2.
The gene plays a vital role in the growth of the foetus and the placenta: too much insulin-like growth factor-2 makes huge placentas and severely oversized babies – rather like what happens
in the pairing of the monogamous oldfield mouse female with a polygamous deer mouse male.

Of course, sugar isn’t the only resource over which the mother and the foetus are fighting. By the sixth month of pregnancy, the mother’s body has produced an extra 1.4 litres (2.5
pints) of blood to support the foetus’s growing needs for oxygen
and other nutrients. Pumping this extra blood around the body requires some changes to the
woman’s circulatory system. Levels of the hormone progesterone increase, to relax and expand the blood vessels in an effort to accommodate the extra flow. In the best-case scenario, this
extra rush of blood makes a woman feel unusually hot and involves a drop in blood pressure, which might cause dizziness, or the occasional faint. But when there is a poor exchange of blood between
the mother and the foetus, the body has to find ways to push this extra blood in and out of the placenta, and brute force is the answer. Blood pressure rises in compensation. Approximately fifteen
million pregnant women experience high blood pressure around the world each year. And one of the reasons pregnant women are constantly having their blood pressure measured is to assess the chances
of a medical condition called pre-eclampsia.

Eclampsia in humans was recorded in early Egyptian, Chinese, and Indian medical texts dating as far back as four thousand years ago – not surprising, since the condition involves
spectacular, life-threatening complications that would be evident without any knowledge of the interior anatomy and genetic developments involved in pregnancy. If pre-eclampsia isn’t spotted
and prevented, sudden convulsions can develop during labour. When full eclampsia sets in, the mother’s mouth twitches and her body contracts, then becomes completely rigid; violent muscular
spasms break out and the woman foams at the mouth. So alarming is this complication that it probably prompted the first Caesarean sections to be conducted about two thousand years ago.
Unfortunately, eclampsia remains a serious, potentially fatal condition, and can harm a woman’s kidneys, liver, and blood vessels.

These terrible complications, however, do not affect all animals with placentas. In fact, they are only known to happen in three species alive today: patas monkeys, lowland gorillas, and us.
What distinguishes these three primates from other mammals is the extent to which the placenta penetrates the mother’s blood supply. If the placenta does not invade
deep enough, the mother’s heart has to work harder, increasing the pressure of the blood in order to keep the foetus alive.

The link between pre-eclampsia and high blood pressure has been acknowledged since 1896, when the inflatable arm-band for measuring blood pressure was invented, but doctors
still do not know exactly why, in some women, the placenta stops receiving blood as it should. The only risk factor that is universally accepted is being pregnant for the first time. Why should
that be?

Our immune systems evolved to protect us from a staggering variety of parasites – anything that is in our bodies that shouldn’t be. Once an outsider is recognized, the body’s
aim is to get rid of it. But we have seen that evolution has worked around this line of defence in many ways, for the simple reason that if a species is reproducing via sex, it benefits the
mother’s genes to become pregnant. Yet, it isn’t easy for foreign sperm to get to an egg. Out of the three hundred million sperm that might be released into a woman’s vagina, only
one, if any, will normally succeed in fertilizing an egg. All the barriers are in place to prevent it: to prevent infection, the woman’s vagina has an acidic pH that is also a killer for
sperm; to stop microbes from invading, the cervix is filled with compact mucus, which also makes it incredibly difficult for sperm to make it to the womb; and then, the womb is armed with the
soldiers of the immune system, white blood cells, which will physically engulf and destroy unwanted invaders, including most sperm. In
pre-eclampsia, it may be that the
woman’s immune system has put up yet another line of defence and refuses to accept the incursion of the placenta’s foreign DNA.

Pre-eclampsia occurs mostly in first-time pregnancies, but not all first-time pregnancies are the same. If a couple has had unprotected sex for less than four months before conception, the rate
of pre-eclampsia is approximately four out of five. This decreases to one in four among those couples who have been having unprotected sex for five to eight months, and further to one in twenty
among those who have been doing so for more than twelve months. Even a woman who has already conceived several children runs a heightened first-time-pregnancy risk when she takes a new male partner
who isn’t the father of her earlier children. Put simply, it may be that being exposed to a particular partner’s sperm ‘acclimatizes’ a woman’s immune system to his
genes, breaking down the defences against foreign intruders and improving the negotiations that take place between the womb and the child. Becoming tolerant of a partner’s sperm appears to
protect the mother and the embryo, once it implants in the woman’s womb.

So while humans may not ourselves be strictly monogamous, evolution has built women to have more successful pregnancies with long-term sexual partners.

During pregnancy, the mother, too, has an active role in protecting the foetus from her immune system’s attackers: substantial numbers of a woman’s immune cells
cross through the placenta and settle in the developing lymph nodes of the foetus, disguising the baby’s immune system from her own. In a way, the body is tricked into seeing the foetus as a
‘temporary self’. These cells
also serve to suppress the foetus’s immune system, which could be set against the mother’s blood.

These maternal immune cells have an incredibly long-lasting influence on the foetus, even long after the baby is born. As they cross from the mother to the child, the cells ‘teach’
the foetus how to balance the need for self-defence against the need for tolerance to the surrounding environment. This is a tricky balancing act. If the foetus is taught to be too tolerant, the
newborn baby may be left unprotected from a common but potentially lethal infection. If, on the other hand, the foetus’s self-defence mechanisms become too keen, a child may be overly
sensitive to certain foods and environments; worse, the body might start attacking itself – a condition called autoimmunity. Indeed, until at least early adulthood, a mother’s immune
cells influence how her child’s body regulates its own defences and how tolerant, or susceptible, it will be to allergies and infection.