Like a Virgin (20 page)

It used to be thought that a baby in the womb somehow made itself completely invisible to the mother’s immune system, but this isn’t strictly true. What happens, instead, is that the
immune systems become interlocked. This means that diseases which are not normally transmissible between two adults can pass from mother to child. Diseases such as cancer.

In 2007, a twenty-eight-year-old Japanese woman gave birth to a girl. The pregnancy was uneventful, and the baby seemed perfectly healthy on delivery. When the baby was about one month old,
however, the mother had to be rushed back into hospital: she was bleeding uncontrollably from her vagina. She died not long after being admitted. Although she had not known it, the mother had
leukaemia, a cancer of the bone marrow and white blood cells, which is known to be a possible underlying cause of haemorrhaging after giving birth. Eleven months later, doctors found a huge tumour
trapped in the baby’s cheek.

Cancer cells tend to be pretty well skilled at making
themselves invisible to the immune system. Mostly, this is because they are actually our own cells, not foreign
invaders, and the disease comes from mutations that make the cells incapable of regulating their own growth. They divide and spread and expand in ways that would usually mark them for
self-destruction. But they grow on. That doesn’t explain, however, why the mother’s cancer cells would not be attacked by the baby’s immune system.

When the doctors studied the cancer cells in the Japanese baby and samples taken from her deceased mother, they found that the cancer cells were missing a large chunk of DNA from chromosome 6.
It is along this stretch of chromosome that the DNA normally produces the markers on to which our immune cells latch. In this case, the cancer cells passed from mother to child because the immune
cells were not able to attack, and there was nothing the baby – no matter how vigilant her immune system might be – could do about it.

Inside the watery world of the womb, the growing baby receives many cues that affect its health. The body is primed in the womb for the environment in which the mother already lives. That, in
turn, should increase the child’s own chances of growing to adulthood and reproducing successfully.

For example, if a mother eats too much or goes hungry, the foetus will adjust its nutritional needs in both the short and long term, preparing itself for a world in which it will either have
easy access to food or need to be ready to go without. Among the most well-publicized studies of nutrition in the womb are studies of rodents that have had their diets restricted. In particular,
scientists have been interested to find out how a mother’s calorie intake affects her fertility and the survival of her young. You might guess that a hungry mother rat would have fewer
nutrients to share with its foetuses, and that less food would mean less offspring. This isn’t the case. When female rats were fed
a calorie-restricted diet, the
mothers enjoyed a longer span of fertility, giving birth to pups at more advanced ages. And when these dieting rats gave birth, the survival rates of their pups were dramatically better than for
the offspring of rats that were allowed to eat to their heart’s content. For mother rats whose calorie intake was moderately restricted, over seventy-three percent of pups survived, whereas
only twenty-two percent of pups survived that were born to mothers with an unrestricted diet.

Like the propensity to be allergic, however, humans are also programmed in ways that can make us oversensitive to certain chemicals, putting us at risk for related diseases. Coronary heart
disease may also have its origins in the womb. Pregnant women who have impulsive, uncontrollable outbursts of temper (more incidents of slamming doors; loud, angry shouting; binge eating or
drinking; smashing dishes; etc.) secrete higher levels of stress hormones, such as cortisol, which can cross through the placenta and reach the baby in the womb. Once there, the hormones change the
way in which the
hypothalamic-pituitary-adrenal axis
, or HPA, and the autonomic nervous system work, and both the HPA and this part of the nervous system appear to be important for
programming disease into the foetus. Individuals who were overexposed to stress hormones in the womb exhibit long-term, stress-related behaviour as adults. These hormones also affect foetal heart
development and may increase the risk for developing cardiovascular disease later in life. Being overweight is associated with the release of inflammatory factors in the body, and these factors can
also affect the development of the lungs and the immune system in a foetus. So if a mother is overweight, her child may also have a higher risk of developing allergies and asthma.

Obesity, in particular, may be decided in the womb – long before a child gets around to putting anything into his or her
mouth. If a mother gains excessive weight or
has diabetes while she is pregnant, the foetus will adapt to an environment where there is an excess of sugar around. As a teenager, her child is more likely to have a high body mass index, or BMI,
even if the child does not eat fatty foods. Mice or rats that are put on a high-fat and high-sugar diet that makes them obese have pups that grow up to have increased body fat and abnormally large
appetites. In fact, even when these pups are kept on a healthy diet, their appetites mean they are far more likely to become obese on standard meals. They also have an abnormally high level in the
blood of the protein leptin, which has a starring role in the way food is consumed and then metabolized into energy by the body. Other experiments on animals indicate that if a mother’s
nutrition becomes imbalanced during pregnancy and breastfeeding, this permanently changes how – at the level of the brain – her offspring consume food as adults. The mother’s
patterns of consumption actually alter the developing hypothalamus, the almond-sized part of the brain that controls basic biological functions such as hunger, thirst, fatigue, and temperature. The
hypothalamus produces the hormones that control when we feel hungry and desire food, as well as those that control aggression and sexual behaviour.

Bizarrely, because of how imprinting works, a father also sways his child’s life after birth, through the timed influence of his genes. Some of a father’s genes, in
fact, only become expressed after a baby has been weaned, and they can have a significant effect at much later stages of life. For instance, the father’s genes have a say in whether or not a
child develops disorders related to food, possibly including obesity. Here, once again, we see the
battle between the father’s DNA and the mother’s body.

This is because those eighty genes that are subject to imprinting have an important say in the development of our brains. Those genes that are silenced when inherited from the mother but
expressed when inherited from the father inhibit our overall brain size; they contribute to the development of the hypothalamus – the impulse centre that makes us crave food. In contrast, the
imprinted genes that are expressed when inherited from the mother contribute to the cortex, the so-called grey matter of higher mental functions; the striatum, which is involved in decision-making
and risk-taking; and the hippocampus, the brain’s memory centre. Recent molecular analysis has shown that among people who carry defects or mutations in genes that are supposed to be
imprinted, there is a surprisingly large incidence of cognitive, behavioural, neurological, and psychiatric conditions. These include autism, bipolar affective disorder, epilepsy, schizophrenia,
and Tourette’s syndrome.

This sex divide in the role of imprinted genes on the brain is curious, because what happens in the hypothalamus is also believed to influence maternal behaviour. Studies in mice have shown that
mothers will neglect their offspring if the
PEG1
gene (paternally expressed gene 1) is removed from their fathers so that they are not able to inherit it. A related gene, called
PEG3
,
increases maternal care, too, and also regulates male sexual behaviour – meaning it ensures its own preservation. If a male mouse does not have the
PEG3
gene, then, no matter how much
sexual experience it gains, it is unable to improve its reproductive effectiveness; for example, no amount of experience will make the mouse better able to recognize the odours that female mice
secrete when they are ready to mate. It seems that a father can even directly influence how his daughter will behave towards her own children, through imprinted genes alone.

For mice and men (and women), evolution has pitched mother against father, father against mother, mother against child, and child against mother – our genetic
sources and our genetic creations are all battling for control. The outcome of these long-ago skirmishes is a treaty written in DNA: neither a mother nor a father may use all the genes at their
disposal, but both will have a genetic and a chemical voice that will continue whispering into the brains of their children – all the way into adulthood. Neither sex can do without the other.
At least, that is, while we are still constrained by the body.

But what comes next? Will those restrictions still hold when eggs and sperm and foetuses and wombs are no longer tied to biological packages of human anatomy? Because, if the past centuries of
discovery show anything, it is that once science stumbles upon an obstacle, the next step is to tear that obstacle to bits, find out how it works, and then see if we might get rid of it
altogether.

PART II

A NEW WAY OF MAKING BABIES

On 27 July 1978, the front page of the London
Evening News
carried a nearly life-sized photograph of a beautiful infant, a mere eighteen hours old. She was wide-eyed and
swaddled all in white, a perfect specimen of just-born humanity, and she was pictured below the headline – superbabe – that announced her birth.

Louise Joy Brown was no ordinary newborn, but ‘the world’s first test-tube arrival’, a child widely celebrated as a miracle of science. As her middle name testified, Louise was
an even greater miracle to her infertile mother, thirty-year-old Lesley Brown, whose grossly distorted and persistently blocked Fallopian tubes had made it impossible for her to become pregnant
over the course of nine arduous and depressing years. Louise was the first child to be born through
in vitro fertilization
, or IVF.

Medical science had been wrestling with infertility for quite some time. But because the subject has been (until very recently)
shrouded in secrecy, it is almost
impossible to say with any accuracy when artificial insemination in humans was first attempted by doctors. ‘Historically, artificial insemination is one of those rare medical entities which
cannot be traced back to Hippocrates,’ wrote one American obstetrician back in 1943. Yet, we can trace the practice to at least the middle of the fifteenth century, when a French doctor
called de Villeneuve performed artificial insemination for King Henry IV of Castile and his second wife, Joan of Portugal. The king was rather unkindly nicknamed ‘The Impotent’ –
and although local prostitutes confessed to a priest that their monarch was perfectly sexually capable, close examination confirmed that he could not, indeed, get an erection. Artificial
insemination, however, was not successful. De Villeneuve could not have known that King Henry was probably living with a pituitary tumour or a condition known as hypogonadism, either of which would
have rendered him completely sterile. So whatever ejaculate he could supply to his doctor contained little or no sperm. Even if de Villeneuve had managed to introduce the royal semen into
Joan’s womb, pregnancy would have been near impossible. Fortuitously, his wife took matters into her own hands and bore three children by natural donor insemination – that is to say,
the children were, reportedly, fathered in amorous liaisons with the Duke of Albuquerque and with the nephew of a Church bishop.