Wednesday, July 9th, 2014
A point against the idea that there’s a good-at-math gene you’re lacking—scientists have discovered that many of the genes that influence a child’s math ability also impact their skill at reading. The study, published in the journal Nature Communications, compared DNA and math and reading test results for nearly 2,800 12-year-olds in the UK, looking for DNA differences and how skills matched up.
Of course, there isn’t complete overlap (could that account for the lack of math or language prowess in an otherwise brilliant person?)—and the study authors also found that nurture can also play a role in whether your child becomes the next Einstein or Shakespeare.
“We looked at this question in two ways, by comparing the similarity of thousands of twins, and by measuring millions of tiny differences in their DNA. Both analyses show that similar collections of subtle DNA differences are important for reading and maths,” study author Oliver Davis, of University College London, said in a school news release.
“However, it’s also clear just how important our life experience is in making us better at one or the other. It’s this complex interplay of nature and nurture as we grow up that shapes who we are.”
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Education, Must Read, New Research, Parents News Now
Thursday, June 5th, 2014
British researchers are close to developing a new medical technique in which genetic material from two women and one man are used to create an embryo that would not face the risk of mitochondrial diseases. The technique, if successful, would enable women who are carriers for mitochondrial genetic mutations to bear children. More from NPR:
“I think that [two years] is not a bad estimation,” Robin Lovell-Badge of the Medical Research Council tells . “The other sorts of experiments that we thought were necessary, again it will take about two years to complete all of those.”
The procedure targets problems in mitochondria, the energy-producing organelles that have their own DNA. Their genome is both prone to mutation and inherited maternally — characteristics that have led researchers to think up ways to help women who carry mutated genes to have healthy children.
The British panel has been reviewing two treatment methods that involve using either a donor embryo or a donor egg from a woman with normal mitochondria. The parents would contribute nuclear DNA, but the mitochondrial DNA would come from a donor.
Before that process occurs in Britain, it would have to be made legal. And as you might imagine, the review panel is also considering ethical and safety consequences.
“The direction of travel still suggests that it is all safe, but we don’t know what’s round the corner so we’re being a little cautious,” says Lovell-Badge, who is on a review board of Britain’s Human Fertilization and Embryology Authority.
The HFEA group saying evidence “does not suggest that these techniques are unsafe,” but that more experiments need to be conducted before clinical treatments begin. (You can ).
The process under review is often called oocyte modification, or more generally, three-parent IVF. In the U.S., convened meetings about a similar procedure in February, seeking expert and public comment.
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Friday, May 2nd, 2014
The types of foods a mother-to-be eats just before she becomes pregnant may have an effect on her baby’s genetic development–especially if there are nutritional deficiencies in the mother’s diet. More from NPR on a new study published in the journal Nature Communications:
The study, published in Nature Communications, is the first to show that an environmental factor during the first few days of development can change DNA long term.
The researchers didn’t look at how these genetic changes affect overall fetal development or the baby’s health later in life. And they analyzed only six genes.
But there’s growing from other studies that similar types of genetic changes may help determine a child’s risk for some diseases, including diabetes, mental disorders and autism.
“Can diet affect other genes? What’s the biological impact of those [DNA] modifications? At the moment we don’t know the answer to those questions,” says nutritionist , who contributed to the study. “But subsequent research we have — and haven’t [yet] published — says it does matter.”
Now we’re not talking about altering the DNA code itself — you know, the building blocks of genes, the ? Rather, Prentice says the dietary effects he and his team have found seem to be changing whether genes are turned on or off in that earliest stage of embryonic development.
This on-and-off switch is controlled by decorating the DNA with a special tag, called . How much the six genes got tagged in the developing embryo depended on the levels of a few micronutrients in the mom’s blood at the time of conception, Prentice and his team found.
The team examined several B vitamins and nutrients associated with them. They couldn’t pinpoint exactly which ones were most important. But in general, when several of these nutrients, including vitamin B2, were at lower levels in mom’s blood, the six genes had less methylation.
“The vitamin levels [in all the women] weren’t way out of the normal range either,” Prentice says. “If you took the blood to your doctor, he would say they were normal.”
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Wednesday, March 26th, 2014
Researchers have developed a test children can take around the age of five that may help identify children that are at risk for becoming obese. The test would analyze the PGC1a gene, which controls fat storage. The study leaders hope this test will help those kids with an increased risk to learn more about healthy living from an earlier age. More from the University of Southampton:
Scientists have found that a simple blood test, which can read DNA, could be used to predict obesity levels in children.
Researchers at the Universities of Southampton, Exeter and Plymouth used the test to assess the levels of epigenetic switches in the PGC1a gene – a gene that regulates fat storage in the body.
Epigenetic switches take place through a chemical change called DNA methylation which controls how genes work and is set during early life.
The Southampton team found that the test, when carried out on children at five years old, differentiates between children with a high body fat and those with a low body fat when they were older. Results showed that a rise in DNA methylation levels of 10 per cent at five years was associated with up to 12 per cent more body fat at 14 years. Results were independent of the child’s gender, their amount of physical activity and their timing of puberty.
Dr Graham Burdge, of the University of Southampton who led the study with colleague Dr Karen Lillycrop, comments: “It can be difficult to predict when children are very young, which children will put on weight or become obese. It is important to know which children are at risk because help, such as suggestions about their diet, can be offered early and before they start to gain weight.
“The results of our study provide further evidence that being overweight or obese in childhood is not just due to lifestyle, but may also involve important basic processes that control our genes. We hope that this knowledge will help us to develop and test new ways to prevent children developing obesity which can be introduced before a child starts to gain excess weight. However, our findings now need to be tested in larger groups of children.”
The study, which also involved Professor Terence Wilkin at the University of Exeter and Dr Joanne Hosking at the University of Plymouth, is published in the journal Diabetes. The researchers used DNA samples from 40 children who took part in the EarlyBird project, which studied 300 children in Plymouth from the age of five until they were 14 years old.
Led by Professor Wilkin, the study assessed the children in Plymouth each year for factors related to type 2 diabetes, such as the amount of exercise they undertook and the amount of fat in their body. A blood sample was collected and stored. The Southampton team extracted DNA from these blood samples to test for epigenetic switches.
Professor Wilkin says: “The EarlyBird study has already provided important information about the causes of obesity in children. Now samples stored during the study have provided clues about the role of fundamental processes that affect how genes work, over which a child has no control. This has shown that these mechanisms can affect their health during childhood and as adults.”
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Monday, December 9th, 2013
Fifteen-year-old Hayley Mogul and her 9-year-old sister both extremely rare genetic disorders–so rare, that a cure isn’t even being sought by scientists–that has had severe neurological and metabolic consequences for the sisters. But their participation in cutting edge research that combines stem cell and genetic techniques may give hope to future generations. NBC News reports:
There’s no cure for their rare disorders, caused by unique genetic mutations. But for once, there’s an advantage to having conditions so rare that drug companies cannot even think of looking for a cure. The sisters are taking part in a whole new kind of experiment in which scientists are literally turning back the clock on their cells.
They’re using an experimental technique to transform the cells into embryonic form, and then growing these baby cells in lab dishes.
The goal is the get the cells to misfire in the lab in just the same way they are in Hayley’s and Bari’s bodies. It’s a new marriage of genetics and stem cell research, and represents one of the most promising applications of so-called pluripotent stem cells.
“One day these two girls will probably change the face of medicine as we know it,” said their father, Steven Mogul.
Steven and Robyn Mogul don’t understand why both their daughters ended up with the rare mutations, which cause a range of neurological and metabolic problems.
“We have been tested,” said Mogul, a 45-year-old wealth manager living in Chicago. “We don’t have any mutations, and there are no developmental issues. We have no idea how it happened. “
The girls need special schooling and physical therapy. They must wear diapers, and when they get a cold or the flu, they can develop dangerously low blood sugar. “When the kids get sick, get colds or flu, we have to get them to the hospital,” Mogul said.
Hayley, 15, has a mutation in a gene called RAI1, which can cause Smith-Magenis syndrome. The syndrome affects 1 in 25,000 people and can disturb sleep patterns, cause obesity and behavioral issues. But Hayley’s mutation is unique and puzzling. Bari, 9, has an RAI1 mutation and a similarly unique mutation in the GRIN2B gene, which can cause learning disabilities.
“Bari doesn’t talk,” Mogul said. “She walks around, she gets around and lets you know what she wants. She is eating baby food and she is drinking from bottles.”
Hayley can attend school and can read, but lacks the fine motor skills needed to write. It’s especially unusual for two children in the same family to end up with such rare, and different, mutations.
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