Obesity: the role of fetal programming

Published on March 31, 2016   37 min

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Other Talks in the Series: Obesity: science, medicine and society

I'm Dr. Jess Buxton. I'm a researcher based at University College in London. My work involves investigating how genetic and environmental factors interact to affect disease risk. In this lecture, I'm going to be talking about the role of fetal programming in obesity.
So during this lecture, I'm going to describe what fetal programming is, and how it fits into the thrifty phenotype hypothesis in the wider research area of DOHaD. I'm going to also consider animal models of fetal programming, and some possible epigenetic mechanisms that explain this phenomenon. And finally, I'm going to look at the evidence for transgenerational effects of fetal programming.
So what causes obesity? We know that the causes are a complex mix of genetic and environmental factors, and an interaction between the two, often, including diet and low levels of physical activity. We also know that some genetic variations are involved and affect a person's risk of developing obesity. This talk is going to focus on the role of prenatal factors. So factors before birth that might affect our future risk of obesity in childhood and adulthood.
So fetal programming can be thought of as a particular set of environmental factors that affect disease risk. After all, our very first environment is the womb. But in particular, fetal programming is the concept that conditions in the womb during embryonic and fetal life can affect the development of tissues and organs, and that these changes can result in long-term consequences for health in childhood and adulthood.
What kinds of factors might affect the newborn baby cells? So, there are the obvious ones that we've known about for quite some time. Toxins such as cigarette smoke, tobacco. Some infections, such as rubella, German measles, can have long lasting effects on the development and health of the baby. Diet, maternal activity levels, and stress levels. So we know that all these things can affect the health and development the newborn baby. But what's become increasingly clear, since the early 1990s, is that some of these factors can have long-lasting effects on the health of the child and throughout its life into adulthood.
One of very first studies, and one of the first concrete examples of fetal programming, was this study carried out by David Barker and others, in which they looked at a very large group of men who were born in Hertfordshire between 1911 and 1930 in the UK. And very detailed records were kept of birth weight. The lower the birth rate, it seemed, the increased risk of death from heart disease. This population has been followed for quite some time now. And this was one of the first clues, really, that prenatal life may hold the key to adult health.
Several studies have since replicated the findings of this study in populations around the world, including this one carried out on men born in Finland during 1924 to 1933. This showed that the effects of low birth weight are particularly harmful when there's rapid catch up growth. So the study showed that in this group of men, those who were the thinnest as infants and who went on to gain the most in terms of their body mass index, by the age of 11 had the highest increased risk of coronary heart disease as adults. So they were five times more likely to die of heart disease as adults than the control group.
So these studies on low birth weight being associated with a high risk of coronary heart disease in adulthood led David Barker and others to develop what's known as the thrifty phenotype hypothesis. So this is the idea that poor nutrition, or other factors leading to poor fetal growth, which is reflected in a low birth weight, and the developing fetus is reacting to this environment, preparing itself for a harsh, nutrient-poor environment after birth, outside the womb. So these adaptations include things like restricted growth, which results in a lower birth weight, but also changes in the numbers and sizes of cells in some tissues and organs. This is thought to spare the brain. So the brain is the most important organ, so what nutrition there is goes to ensuring correct and full brain development, but at the expense of other organs, such as the pancreas, kidney, and liver, for example. But as well as these structural changes, there are also metabolic changes. So more efficient fat storage, increased appetite. So all these adaptations would be helpful if the environment in the womb is actually the same as the environment after birth. So the problem arises when there's a mismatch between these fetal and postnatal environments. And actually, once the child is born, there's good or overnutrition in both childhood and adulthood. And this mismatch between the environment that the fetus has been programmed to be ready for and the actual environment it encounters can lead to increased risk of obesity in childhood and increased risk of type 2 diabetes and heart disease in adulthood.

Obesity: the role of fetal programming

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