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Researcher Profile - Christine Jasoni

Wednesday 29 June 2016 12:56pm

Associate Professor Christine Jasoni is a developmental biologist. Her team of postgraduate students and researchers are trying to determine the impact of maternal obesity on babies in the womb. “There is all sorts of public health data which shows that when a mother is in mental or physical adversity during her pregnancy her child is at a much higher risk for neurodevelopmental disorders,” Assoc Prof Jasoni explains, “we’re trying to figure out why that is.”

Children who are born to mothers who were obese or who experienced gestational diabetes are at a higher risk for obesity, metabolic imbalances, ADHD, anxiety, depression, autism, and schizophrenia. A similar pattern of developmental problems is observed in the children of mothers who were highly stressed during their pregnancy, had serious infections, or experienced a number of other complications. What we know is that for some reason when the hormone systems which regulate the body go out of alignment, developing babies are put at risk.

This risk isn’t always easy to see, or to understand. When the anti-nausea drug Thalidomide resulted in thousands of infants born with malformed limbs people could easily understand what had happened: A drug had been ingested by the mother and prevented her fetus from developing normally. By comparison, what Assoc Prof Jasoni and her team are dealing with is similar, in that the mother’s environment is impacting on the development of her fetus, however in these cases the impacts and pathways are not so easily identified as there are few, if any, external signs that something has gone wrong.

Associate Professor Jasoni and her team are trying to determine what it is about obesity that causes these neurodevelopmental issues. Unlike thalidomide these issues can’t be tracked to anything that is consumed by the mothers, and then goes on to directly interfere with fetal development, so it must be due to a change in their bodies. One of the main differences between individuals of average weight and those who are obese is the concentration of the hormone leptin.

Leptin is released as a signal for your body to stop eating, it stops you from feeling hungry. As your body-fat increases so does the concentration of leptin in your body. This high concentration eventually leads to leptin resistance, which leaves people feeling genuinely hungry at all times. The developing babies of obese mothers are exposed to very high levels of leptin, which in theory could cause leptin resistance prior to birth, but Assoc Prof Jasoni says this kind of leptin resistance is unlikely. “There is no evidence of classical leptin receptors being present or becoming active before birth,” she says, “so even if there is a high level of leptin in fetal brains, it shouldn’t have an effect.”

But she is not ruling out leptin resistance entirely. Hormones interact with the cells of your body in the same way as any other signalling chemical or molecule. They bind to receptors, and those receptors set off an effect within the cell. While these signalling chemicals and molecules are usually very different their effects can have overlaps. One group of molecules whose effect on cells overlaps with leptin are cytokines. “Immunological cytokines set off a very similar chain of cellular events,” Assoc Prof Jasoni says, “so it may be that these cells become resistant to leptin even before they can respond to it.” The presence of a high level of cytokines in the developing brain may cause leptin resistance and subsequent metabolic problems for that child. But what do cytokines have to do with obesity?

Cytokines are signalling molecules which are produced during an immune response or in response to inflammation in the body. People with obesity have a higher concentration of cytokines in their bodies than non-obese individuals. Associate Professor Jasoni and her team are currently examining whether exposure to elevated levels of cytokines during development could explain some of what we’re seeing in children of obese mothers. If this is the case, it would explain why the impact of obesity on developing babies is so similar to infection or to stress, two factors which also result in elevated cytokine levels.

Assoc Prof Jasoni and her team are also attempting to tackle the question of why these developmental disorders affect some children and not others. They’re in the process of identifying differences in the genes of mice who had obese mothers versus mice who did not. “Ideally, what we want is to be able to give people real information about what to expect on an individual level, but at the moment we have to stick with this general rule.” That rule is: early intervention works. Research has shown that children at risk of developing anxiety and depression, due to maternal stress, were able to eliminate those predispositions by learning how to manage their stress at an early age. At the moment, early intervention is the only way we have to minimise the risks to these children as they develop. And our work will lead to better identification of which children are at increased risk.

This work isn’t at all about shaming mothers; it’s about helping children and families navigate potential problems. In an ideal world people would be as healthy as humanly possible before becoming pregnant. In an ideal world, people wouldn’t get stressed, or sick, or be injured while they were pregnant. This isn’t an ideal world. Life happens. The best each of us can do is support those who need help, and where we can, support efforts to understand what factors put our children at risk and how we might navigate those risks. What is most important is that, no matter the adversity experienced by their mothers during pregnancy, we try to give these children the best start they can possibly have.

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