Like a Virgin Prasad, Aarathi (top 50 books to read .TXT) 📖

ovaries to release multiple eggs from their grip, these organs must be stimulated with a suite of hormones that the body itself uses for that purpose, but often at higher than normal doses. These include a drug to stop eggs from being released until they are mature (a gonadotropin-releasing hormone, or GnRH, agonist or antagonist; a follicle-stimulating hormone, or FSH, that kick-starts the development of multiple eggs; and human chorionic gonatotropin hormone, or HCG, which forces the eggs to mature properly (and is the hormone that causes over-the-counter tests to test positive for pregnancy). Without stimulating medications, the ovaries generally produce one egg a month. With them, they churn out anywhere from five to twenty-five eggs that might be harvested, and some young women have been reported to produce fifty to seventy eggs from one high-dose stimulation. This sounds like good news, but this stimulation can cause severe ovarian hyperstimulation syndrome, or OHSS – most likely as a result of too high a dose of HCG. When OHSS sets in, the woman’s blood vessels become much more permeable than they should be. This leads to a drop in blood volume, so that her blood thickens. It can lead to organ failure, and is a life-threatening condition.

The cocktail of medications served up in IVF and ICSI can also cause developmental problems in the babies they beget. FSH, if given in high doses, may lead to the production of eggs with too many or too few chromosomes or of eggs with chromosomal abnormalities. Having the right number of chromosomes is incredibly important; for example, in Down syndrome three copies of some genes are carried on chromosome number 21, rather than the usual two copies (an issue we will look at in more detail in the next chapter). High levels of FSH might also have a detrimental effect on the lining of the womb, which could compromise the growth and health of the baby growing in it. Children conceived in vitro, and even those conceived merely with the assistance of ovary-stimulating drugs, may also be more likely to be born with several syndromes. Babies with Beckwith-Wiedemann syndrome grow too large – both in the womb and outside it. This overgrowth can affect all systems of the body and cause diabetes, abdominal wall defects, kidney problems, and embryonal tumours. Another condition, Angelman syndrome, may express itself through severe mental retardation or delayed motor development, which means poor balance, jerky movements, and difficulties with speech. The growth disorder Silver-Russell syndrome leads to dwarfism. Fortunately, all of these conditions are rare in the general population, so an elevated risk after IVF or ICSI does not translate into an epidemic among scientifically fertilized offspring. Indeed, the absolute risk for a serious congenital malformation or chromosomal abnormality after IVF and ICSI appears to be small.

What is interesting from a medical perspective is that the last three syndromes are model ‘imprinting’ disorders – they result from changes in genes that work selectively depending on which parent provided them. Typically, of course, we inherit two complete sets of chromosomes, one from our mother and one from our father, and most genes are an expression of both of these sets. Imprinted genes, however, are expressed from only one of the pair of genes, the mother’s or the father’s, and as we saw earlier, many imprinted genes are critical in normal growth and development – hence the problems here with overgrowth and mental retardation.

Around half of all children diagnosed with Beckwith-Wiedemann syndrome have lost the key to a gene inherited from their mothers, and this change has been detected in almost one hundred percent of children with the syndrome who were conceived after any brand of ART. Experiments with laboratory animals indicate that imprinting disorders that occur as a result of IVF may be triggered by a few specific techniques – and so the risk might vary from clinic to clinic.

Remember that genetic imprinting was only discovered in 1984 – and the first child was born using IVF in 1978. For that reason alone, imprinting defects in IVF babies could not have been predicted from the start. Since then, reams of research have been compiled to compare the genetics of naturally- and laboratory-conceived children. But why should children born through ART be more susceptible to imprinting disorders? What is it about manipulating egg and sperm that leaves genes unable to ‘tell’ which parent they hail from, and whether and how they are supposed to go to work on developing the foetus?

Thus far, geneticists have learned that these imprints are erased in the cells that are specifically programmed to become eggs or sperm – a tantalizing piece towards solving the puzzle. While eggs and sperm are being made, the imprint is reset accordingly – in sperm, a certain subset of genes will be rendered non-functional; in eggs, a different set. It’s a reversible process that depends on the parent of origin, and determines the different functions of the eggs and sperm as they are developing. This means that the very process of making eggs and sperm is critical for the ‘right’ genetic imprinting, and ART procedures affect these developmental periods when genomic imprints are so vulnerable.

Genes are imprinted much earlier during the production of sperm than they are for eggs. For this reason, if you were to induce an egg to mature artificially, as happens in induced ovulation, you might disturb the genetic imprints that should be taking place in the egg, but are unlikely to affect the sperm. In fact, for growing eggs, the genetic imprints are not completed for some genes until just prior to ovulation. If this vital process is vulnerable to the hormones used, then it’s not surprising that in these developmental syndromes, the fault always lies with the egg. But even after fertilization has occurred, there is