https://www.myjoyonline.com/study-links-womb-environment-to-childhood-obesity/-------https://www.myjoyonline.com/study-links-womb-environment-to-childhood-obesity/
New evidence has linked the environment in the womb with increased body weight in later life. Scientists found changes around the DNA at birth which may result from a mother's diet or exposure to pollution or stress. They then linked these changes to a higher Body Mass Index (BMI) in children aged about nine years of age. But the researchers say more work is needed to definitively prove the link between these changes and obesity. Details are published in the journal Plos One. Childhood or adult obesity has many causes, not least childhood or adult diet, but scientists have previously linked specific genes, such as the FTO gene, with increased body weight. Others have looked at not the genes, but associated molecular changes - what are called epigenetics - which can play a role in how a gene functions in the body, switching genes on and off. These changes are thought to be caused in part by exposure to environmental factors such as diet, stress, smoking or hormones, particularly in the womb and during early childhood. While epigenetic changes in the womb have already been associated with later obesity, there is still little data to prove the link. Dr Caroline Relton, of Newcastle University, and colleagues took blood samples from 24 children aged 11 to 13 and looked for differences in the way genes are "expressed" or encoded into the many proteins which we need to grow and function. They identified epigenetic changes in 29 genes which could be associated with higher body mass among the children. They then looked at data from a larger study of 178 individuals, for whom there were both cord blood samples from birth, and body composition data from aged about nine. Prof Tim Spector of King's College London, explains what epigenetics are Among these individuals, epigenetic changes to nine of the 29 genes previously identified appeared to correspond to increased body weight, although only one of these associated changes withstood rigorous further analysis, admit the researchers. "Other studies have just taken genes at birth and looked at differences irrespective of whether they are differently expressed with different levels of obesity," Dr Relton told the BBC. "The difference between this study and others is that we had a reason to focus on the genes we looked at because we knew they were differently expressed in children with a higher BMI." However, Dr Relton says more research is needed to prove the epigenetic differences observed at birth and originating in the womb, are actually contributing to obesity. "While we have discovered an association between these genes and body size in childhood we need to carry out further studies to establish whether influencing the expression of these genes by altering epigenetic patterns is indeed a trigger to obesity." Early signals Commenting on the paper, Prof Gudrun Moore of University College London told BBC News: "The paper is an interesting study on epigentic variations and their potential association with body size indices." Prof Tim Spector of King's College London, said the paper represented "an exciting piece of research exploring new ways of looking at the causes of obesity". "Although it is limited by the small size and the fact that they only looked at 29 genes, the researchers found that a third of the genes they looked at contained epigenetic marks at birth that were related in some way to measures of later obesity. "This means that chemical signals that turn genes on or off at birth can influence susceptibility to being fat at age 10. "We know from differences in identical twins that genes and DNA are not the whole answer. Understanding how we could manipulate these signals in early life - via better understanding epigenetics - has great potential in battling the obesity epidemic," he said.

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DISCLAIMER: The Views, Comments, Opinions, Contributions and Statements made by Readers and Contributors on this platform do not necessarily represent the views or policy of Multimedia Group Limited.