Links for Keyword: Epigenetics

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By Helen Briggs BBC News A mother's diet around the time of conception can permanently influence her baby's DNA, research suggests. Animal experiments show diet in pregnancy can switch genes on or off, but this is the first human evidence. The research followed women in rural Gambia, where seasonal climate leads to big differences in diet between rainy and dry periods. It emphasises the need for a well-balanced diet before conception and in pregnancy, says a UK/US team. Scientists followed 84 pregnant women who conceived at the peak of the rainy season, and about the same number who conceived at the peak of the dry season. Nutrient levels were measured in blood samples taken from the women; while the DNA of their babies was analysed two to eight months after birth. Lead scientist Dr Branwen Hennig, from the London School of Hygiene & Tropical Medicine, said it was the first demonstration in humans that a mother's nutrition at the time of conception can change how her child's genes will be interpreted for life. She told BBC News: "Our results have shown that maternal nutrition pre-conception and in early pregnancy is important and may have implications for health outcomes of the next generation. "Women should have a well-balanced food diet prior to conception and during pregnancy." BBC © 2014

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 19556 - Posted: 04.30.2014

Virginia Hughes When Brian Dias became a father last October, he was, like any new parent, mindful of the enormous responsibility that lay before him. From that moment on, every choice he made could affect his newborn son's physical and psychological development. But, unlike most new parents, Dias was also aware of the influence of his past experiences — not to mention those of his parents, his grandparents and beyond. Where one's ancestors lived, or how much they valued education, can clearly have effects that pass down through the generations. But what about the legacy of their health: whether they smoked, endured famine or fought in a war? As a postdoc in Kerry Ressler's laboratory at Emory University in Atlanta, Georgia, Dias had spent much of the two years before his son's birth studying these kinds of questions in mice. Specifically, he looked at how fear associated with a particular smell affects the animals and leaves an imprint on the brains of their descendants. Dias had been exposing male mice to acetophenone — a chemical with a sweet, almond-like smell — and then giving them a mild foot shock. After being exposed to this treatment five times a day for three days, the mice became reliably fearful, freezing in the presence of acetophenone even when they received no shock. Ten days later, Dias allowed the mice to mate with unexposed females. When their young grew up, many of the animals were more sensitive to acetophenone than to other odours, and more likely to be startled by an unexpected noise during exposure to the smell. Their offspring — the 'grandchildren' of the mice trained to fear the smell — were also jumpier in the presence of acetophenone. What's more, all three generations had larger-than-normal 'M71 glomeruli', structures where acetophenone-sensitive neurons in the nose connect with neurons in the olfactory bulb. In the January issue of Nature Neuroscience1, Dias and Ressler suggested that this hereditary transmission of environmental information was the result of epigenetics — chemical changes to the genome that affect how DNA is packaged and expressed without altering its sequence. © 2014 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19325 - Posted: 03.05.2014

Stephen S. Hall Hochelaga was the original Iroquoian name for the village that ultimately became Montreal, but it is also the name of a rough-hewn French–Canadian neighbourhood located east of — and a world away from — the cosmopolitan city centre. The district's tidy two- and three-storey brick duplexes, adorned with Montreal's characteristic wrought-iron staircases, predominantly house families that have, because of poverty and lack of education, never quite attained thriving middle-class status. During the 1980s, public-school officials identified Hochelaga and many other impoverished neighbourhoods in the eastern part of Montreal as places where kindergarten children disproportionately displayed severe behavioural problems, such as physical aggression. The school system asked a young University of Montreal psychologist named Richard Tremblay for help. “Their parents didn't have a high-school diploma, and many of the mothers had their first child before the age of 20,” Tremblay says of the families he began to study, as he walks along Rue Ontario in Hochelaga on a sunny afternoon in September. Those were the women, he adds, “most at risk of having children who have problems”. Over the past three decades, Hochelaga and similar neighbourhoods have served as living laboratories in the study of the roots of aggression. Since 1984, Tremblay and his collaborators have followed more than 1,000 children from 53 schools in the city from childhood into adulthood. And in 1985, he initiated a ground-breaking experiment in which some families of at-risk children were given support and counselling to help curb bad behaviour. His research overturned ideas about when aggressive behaviour first emerges, and showed that early intervention can deflect children away from adult criminality. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory, Learning, and Development
Link ID: 19082 - Posted: 12.31.2013

by Bethany Brookshire “You are what you eat.” We’ve all heard that one. What we eat can affect our growth, life span and whether we develop disease. These days, we know that we also are what our mother eats. Or rather, what our mothers ate while we were in the womb. But are we also what our father eats? A new study shows that in mice, a dietary deficiency in dad can be a big downer for baby. The dietary staple in the study was folic acid, or folate. Folate is one of the B vitamins and is found in dark leafy greens (eat your kale!) and has even been added to some foods like cereals. It is particularly essential to get in the diet because we cannot synthesize it on our own. And it plays roles in DNA repair and DNA synthesis, as well as methylation of DNA. It’s particularly important during development. Without adequate folate, developing fetuses are prone to neural tube disorders, such as spina bifida. Some of the neural tube disorders caused by folate deficiency could result from breaks in the DNA itself. But folic acid is also important in the epigenome. Epigenetics is a mechanism that allows cells to change how genes are used without changing the genes themselves. Instead of altering the DNA itself, epigenetic alterations put chemical “marks” or “notes” —methyl or acetyl groups — on the DNA and the proteins associated with it. The marks can either make a gene more accessible (acetylation) or less accessible (methylation), making it more or less likely to be made into a protein. This means that each cell type can have a different epigenome, allowing a neuron to function differently than a muscle cell, even though they contain the same DNA. Folate affects DNA synthesis, but it can also affect DNA methylation. In fact, DNA methylation requires the presence of folate. So low folate could affect whether genes are turned off or on and by how much. In a developing fetus, that could contribute to developmental problems. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19035 - Posted: 12.14.2013

By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19017 - Posted: 12.11.2013

Ewen Callaway Certain fears can be inherited through the generations, a provocative study of mice reports1. The authors suggest that a similar phenomenon could influence anxiety and addiction in humans. But some researchers are sceptical of the findings because a biological mechanism that explains the phenomenon has not been identified. According to convention, the genetic sequences contained in DNA are the only way to transmit biological information across generations. Random DNA mutations, when beneficial, enable organisms to adapt to changing conditions, but this process typically occurs slowly over many generations. Yet some studies have hinted that environmental factors can influence biology more rapidly through 'epigenetic' modifications, which alter the expression of genes, but not their actual nucleotide sequence. For instance, children who were conceived during a harsh wartime famine in the Netherlands in the 1940s are at increased risk of diabetes, heart disease and other conditions — possibly because of epigenetic alterations to genes involved in these diseases2. Yet although epigenetic modifications are known to be important for processes such as development and the inactivation of one copy of the X-chromsome in females, their role in the inheritance of behaviour is still controversial. Kerry Ressler, a neurobiologist and psychiatrist at Emory University in Atlanta, Georgia, and a co-author of the latest study, became interested in epigenetic inheritance after working with poor people living in inner cities, where cycles of drug addiction, neuropsychiatric illness and other problems often seem to recur in parents and their children. “There are a lot of anecdotes to suggest that there’s intergenerational transfer of risk, and that it’s hard to break that cycle,” he says. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 18990 - Posted: 12.02.2013

By Puneet Kollipara Identical twin mice sharing the same mazelike environment develop distinct personalities based on how much they explore their surroundings, researchers report in the May 10 Science. After death, those differences were reflected in the animals’ brains. The study “highlights something for which we had some intuition before, but actually quantifies it,” says Fred Gage, a neuroscientist at the Salk Institute for Biological Studies in La Jolla, Calif. Some character and biological differences between identical twins may originate as early as pregnancy. But twins become more and more different as life goes on, even when they grow up together. Scientists have recognized that having distinct experiences within the same environment might boost such personality differences, but that’s difficult to test in humans. Studying it in animals has multiple benefits. “You can keep the genes constant and also keep the environment constant,” says Gerd Kempermann of the Center for Regenerative Therapies Dresden in Germany. “It’s much more controlled than in a human situation.” Researchers led by Kempermann put 40 genetically identical female mice in an elaborate cage and observed their behavior. The cage had multiple levels linked together by tubes and contained toys and other features that the animals could explore. The researchers equipped each mouse with a microchip that tracked its location, using the animals’ movements as a measure of exploratory behavior. Initially, the mice differed only slightly in their tendency to roam. As they grew older, all tended to explore more often, but the differences among the mice grew more pronounced. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18145 - Posted: 05.11.2013

By Tina Hesman Saey Like many women with parents of the Mad Men generation, Susan Murphy grew up in a household full of cigarette smoke. Both dad and mom smoked heavily, even while Murphy was still in her mother’s womb. “That explains a lot,” Murphy quips, poking fun at herself. But Murphy isn’t worried about her own health. She’s fine. Her children aren’t, though. One boy died of cancer as a toddler. Another has autism. And her daughter has attention deficit disorder. Murphy knows the scientific evidence isn’t in yet, but she still can’t help wondering whether their fates might have been affected by her exposure to tobacco smoke before she was born. Murphy, a researcher at Duke University, studies links between a mother’s diet and chemical exposures during pregnancy with the child’s later health. She and others have established that the womb is the antithesis of Las Vegas; what happens there not only doesn’t stay there, it can influence a child’s health for life. Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring. Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17934 - Posted: 03.23.2013

By GINA KOLATA It has been one of the toughest problems in genetics. How do investigators figure out not just what genes are involved in causing a disease, but what turns those genes on or off? What makes one person with the genes get the disease and another not? Now, in a pathbreaking paper, researchers at the Johns Hopkins University School of Medicine and the Karolinska Institute in Sweden report a way to evaluate one gene-regulation system: chemical tags that tell genes to be active or not. Their test case was of patients with rheumatoid arthritis, a crippling autoimmune disease that affects 1.5 million Americans. It was an investigation of epigenetics, a popular area of molecular biology that looks for modifications of genes that can help determine disease risk. “This is one of the first studies that looks for an epigenetic disease association in a really rigorous fashion,” said Dr. Bradley Bernstein of Harvard, who was not associated with the study. Kun Zhang of the University of California, San Diego, made a similar observation. “I am quite impressed with their level of rigor and sophistication,” he said. In previous genomic studies, researchers with papers in leading journals “have made major claims, but after a few months or a year they were retracted,” he said. Those investigators, Dr. Zhang added, “did not treat their data very carefully.” In the new study, researchers compared 354 newly diagnosed rheumatoid arthritis patients and 337 healthy people who served as controls. The goal was to review both groups’ white blood cells, examining their DNA for chemical tags — methyl groups — that could attach themselves to genes and turn them on or off. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17703 - Posted: 01.22.2013

Sujata Gupta Two things are thought to be crucial for evolutionary adaptation: genetic diversity and long periods of time, in which advantageous mutations accumulate. So how do invasive species, which often lack genetic diversity, succeed so quickly? Some ecologists are beginning to think that environmental, or ‘epigenetic’, factors might be modifying genes while leaving the genome intact. “There are a lot of different ways for invasive species to do well in novel environments and I think epigenetics is one of those ways,” says Christina Richards, an evolutionary ecologist at the University of South Florida in Tampa. Although biomedical researchers have been investigating the links between epigenetics and human health for some time, evolutionary biologists are just beginning to take up the subject. Richards, who helped to organize a special symposium on ecological epigenetics at a meeting of the Society for Integrative and Comparative Biology (SICB) in San Francisco this month, says that the field has the potential to revolutionize the study of evolutionary biology. The nascent field of ecological epigenetics has plenty of challenges standing in its way. The genomes of most wild animals and plants have not been sequenced so ecologists can’t pinpoint which genes have been modified. And, because they tend to work outside of controlled laboratory conditions, researchers have trouble linking those gene modifications to behavioural changes. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17674 - Posted: 01.12.2013

By Laura Sanders When sociologist Mike Tomlinson began combing through the health records of people in Northern Ireland, he wasn’t interested in suicide. He was on the hunt for links between poverty and international conflict. But he came across a startling trend. From 1998 to 2008, the rate at which men in their mid-30s to mid-50s were committing suicide rose alarmingly fast, more quickly than the rate for the rest of Northern Ireland’s population. At first, that spike made no sense. A peace agreement reached in 1998 transformed Northern Ireland into a prosperous and tranquil place. Economic indicators had been surprisingly good. Suicide rates in neighboring countries were all gently falling. Nothing seemed to explain why so many of these men were killing themselves. But Tomlinson found a hint in the men’s pasts. They had all grown up in the late 1960s and the 1970s, during some of the worst violence Northern Ireland had ever experienced. Called the Troubles, this warlike period brought religious and political fighting that pitted neighbor against neighbor. Children of the Troubles lived with terrorism, house-to-house searches, curfews and bomb explosions. Trauma early in life had rendered men more vulnerable to taking their own lives later, Tomlinson proposed in July in International Sociology. “If you were younger then, you carry that through,” says Tomlinson, of Queen’s University Belfast. This idea, that something that happened long ago could have such a profound effect today, seemed to resonate with others. When he described his idea to a suicide prevention group in Northern Ireland, “they just lit on it, and said it speaks so much to what they were seeing.” © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17391 - Posted: 10.20.2012

By Tina Hesman Saey Identical twins aren’t perfect carbon copies of each other even at birth. Twins emerge from the womb carrying different chemical marks on their DNA that influence the activity of individual genes, a new study shows. Known as epigenetic markers, these alterations don’t change the underlying genetic information. But by regulating the activity of certain genes, they can profoundly influence how the DNA blueprint is used to create and operate a living organism. Past research has shown that identical twins bear some differences in epigenetic markers. But those differences were thought to arise after birth, as twins have different life experiences and encounter different environments. The new study — the first to measure epigenetic profiles in newborns — suggests that subtle differences in conditions within the womb can leave marks on fetal DNA that may have long-term consequences for adult health. These differing chemical tags may help explain why identical twins look slightly different, have their own personalities and may have different susceptibility to diseases. Jeffrey Craig, a molecular and cell biologist at Murdoch Childrens Research Institute in Parkville, Australia, and his colleagues report the findings online July 15 in Genome Biology. Identical twins are on average more epigenetically similar than fraternal twins, the researchers found. The similarity was probably not due to sharing a womb, but could be attributed partially to genetics and partially to chance, they suggest. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17054 - Posted: 07.18.2012