Like a Virgin by Prasad, Aarathi (recommended reading txt) 📕

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