Chapter 7. Life-Span Development of the Brain and Behavior
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By Nicholas Bakalar A new study has found a simple way to significantly reduce teenage smoking: raise the tobacco sales age to 21. In 2005, Needham, Mass., did just that, while surrounding communities kept their age limit at 18. Researchers surveyed 16,000 high school students in Needham and 16 surrounding communities four times between 2006 and 2012, gathering data on their smoking habits. The study is in Tobacco Control. Over the seven years, the number of children under 18 buying cigarettes in Needham decreased to 11.6 percent from 18.4 percent, while in the surrounding communities it hardly changed — down to 19 percent from 19.4. In 2006, 12.9 percent of students in Needham and 14.8 percent of students in surrounding communities reported having smoked in the past 30 days. By 2010, 6.7 percent of Needham students reported smoking, compared with 12 percent in other towns. At the end of the study in 2012, smoking had declined to 5.5 percent in Needham and 8.5 percent outside. “More than 80 percent of smokers begin before 18,” said the lead author, Shari Kessel Schneider, project director at the Education Development Center in Waltham, Mass. “Our findings provide strong support for initiatives going on all across the country to increase the sales age as a means for decreasing youth access to cigarettes, initiation of smoking, and ultimately addiction.” © 2015 The New York Times Company
By James Gallagher Health editor, BBC News website Scientists have discovered a chemical in blood that indicates whether people will have declining brain function. Looking for the earliest signs of Alzheimer's disease, they analysed levels of 1,129 proteins circulating in the blood of more than 200 twins. These were compared with data from cognitive-function tests over the next decade, in Translational Psychiatry. And levels of one protein, MAPKAPK5, tended to be lower in those people whose brains declined. MAPKAPK5 is involved in relaying chemical messages within the body, although its connection with cognitive decline is unclear. Dementia cases are expected to treble globally by 2050, but there is no cure or treatment. It can take more than a decade from the first changes in the brain to culminate in symptoms such as memory loss, confusion and personality change. And drug companies believe they need to treat patients years before symptoms appear in order to protect the brain. Dr Steven Kiddle, a Medical Research Council scientist at King's College London, told the BBC News website: "People think it may be hard to reverse 20 years of potential damage to your brain. "But if you could start much earlier in that process, then you might be able to find something that works." He said a blood test could help identify people for clinical trials. But he added: "A test you could go in to your doctor to say, 'Do I have Alzheimer's disease or not?' I think that's a long way off." © 2015 BBC
Link ID: 21064 - Posted: 06.17.2015
by Meghan Rosen When we brought Baby S home from the hospital six months ago, his big sister, B, was instantly smitten. She leaned her curly head over his car seat, tickled his toes and cooed like a pro — in a voice squeakier than Mickey Mouse’s. B’s voice — already a happy toddler squeal — sounded as if she'd sucked in some helium. My husband and I wondered about her higher pitch. Are humans hardwired to chitchat squeakily to babies, or did B pick up vocal cues from us? (I don’t sound like that, do I?) If I’m like other mothers, I probably do. American English-speaking moms dial up their pitch drastically when talking to their children. But dads’ voices tend to stay steady, researchers reported May 19 in Pittsburgh at the 169th Meeting of the Acoustical Society of America. “Dads talk to kids like they talk to adults,” says study coauthor Mark VanDam, a speech scientist at Washington State University. But that doesn’t mean fathers are doing anything wrong, he says. Rather, they may be doing something right: offering their kids a kind of conversational bridge to the outside world. Scientists have studied infant- or child-directed speech (often called “motherese” or “parentese”) for decades. In American English, this type of babytalk typically uses high pitch, short utterances, repetition, loud volume and slowed-down speech. Mothers who speak German Japanese, French, and other languages also tweak their pitch and pace when talking to children. But no one had really studied dads, VanDam says. © Society for Science & the Public 2000 - 2015.
By Jessica Schmerler Approximately one in 68 children is identified with some form of autism, from extremely mild to severe, according to the U.S. Centers for Disease Control. On average, diagnosis does not occur until after age four, yet all evidence indicates that early intervention is the best way to maximize the treatment impact. Various tests that look for signs of autism in infants have not been conclusive but a new exercise could improve early diagnosis, and also help reduce worry among parents that they did not intervene as soon as possible. The two most widely used tests to measure symptoms, the Autism Observation Scale for Infants (AOSI) and the Autism Diagnostic Observation Schedule (ADOS), cannot be used before the ages of 12 or 16 months respectively. The AOSI measures precursors to symptoms, such as a baby’s response to name, eye contact, social reciprocity, and imitation. The ADOS measures the characteristics and severity of autism symptoms such as social affectation and repetitive and restrictive behaviors. Now a group of scientists at the Babylab at Birkbeck, University of London think they have identified a marker that can predict symptom development more accurately and at an earlier age: enhanced visual attention. Experts have long recognized that certain individuals with autism have superior visual skills, such as increased visual memory or artistic talent. Perhaps the most well known example is Temple Grandin, a high-functioning woman with autism who wrote, “I used to become very frustrated when a verbal thinker could not understand something I was trying to express because he or she couldn’t see the picture that was crystal clear to me.” © 2015 Scientific American
Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.
By Sue Bailey, The Canadian Press Scientific studies increasingly suggest marijuana may not be the risk-free high that teens — and sometimes their parents — think it is, researchers say. Yet pot is still widely perceived by young smokers as relatively harmless, said Dr. Romina Mizrahi, director of the Focus on Youth Psychosis Prevention clinic and research program at the Centre for Addiction and Mental Health. She cites a growing body of research that warns of significantly higher incidence of hallucinations, paranoia and the triggering of psychotic illness in adolescent users who are most predisposed. "When you look at the studies in general, you can safely say that in those that are vulnerable, it doubles the risk." Such fallout is increasingly evident in the 19-bed crisis monitoring unit at the Children's Hospital of Eastern Ontario in Ottawa. "I see more and more cases of substance-induced psychosis," said Dr. Sinthu Suntharalingam, a child and adolescent psychiatrist. "The most common substance that's abused is cannabis." One or two cases a week are now arriving on average. "They will present with active hallucinations," Suntharalingam said. "Parents will be very scared. They don't know what's going on. "They'll be seeing things, hearing things, sometimes they will try to self-harm or go after other people." Potential effects need to be better understood She and Mizrahi, an associate professor in psychiatry at University of Toronto, are among other front-line professionals who say more must be done to help kids understand potential effects. "They know the hard drugs, what they can do," Suntharalingam said. "Acid, they'll tell us it can cause all these things so they stay away from it. But marijuana? They'll be: 'Oh, everybody does it."' Mizrahi said the message isn't getting through. ©2015 CBC/Radio-Canada.
by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.
Rebecca Hersher Greg O'Brien sees things that he knows aren't there, and these visual disturbances are becoming more frequent. That's not uncommon; up to 50 percent of people who have Alzheimer's disease experience hallucinations, delusions or psychotic symptoms, recent research suggests. At first, he just saw spider-like forms floating in his peripheral vision, O'Brien says. "They move in platoons." But in the last year or so, the hallucinations have been more varied, and often more disturbing. A lion. A bird. Sprays of blood among the spiders. Over the past five months, O'Brien has turned on an audio recorder when the hallucinations start, in hopes of giving NPR listeners insight into what Alzheimer's feels like. For now, he says, "I'm able to function. But I fear the day, which I know will come, when I can't." Interview Highlights [It's] St. Patrick's Day, about 9 o'clock in the morning in my office, and they're coming again. Those hallucinations. Those things that just come into the mind when the mind plays games. And then I see the bird flying in tighter and tighter and tighter circles. And all of a sudden, the bird — beak first — it darted almost in a suicide mission, exploding into my heart. Today I'm just seeing this thing in front of me. It looks like a lion, almost looks like something you'd see in The Lion King, and there are birds above it. It's floating, and it disintegrates ... it disintegrates ... it disintegrates.
Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,
A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but... An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains. Sergiu Pasca, M.D. External Web Site Policy, of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods. Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.
Keyword: Development of the Brain
Link ID: 20998 - Posted: 05.30.2015
by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd
Children developed better fine-motor skills when the clamping of their umbilical cord at birth was delayed several minutes compared with just seconds, according to a new randomized trial. Delaying clamping allows fetal blood circulating in the placenta to be transfused to the infant, which has been shown to reduce iron deficiency at four to six months of age. Now the longer term benefits of a delay are becoming clearer. Researchers in Sweden randomly assigned 382 full-term infants born after low-risk pregnancies to be clamped at least three minutes after delivery or within 10 seconds of birth. When the children were four, a psychologist assessed them on standard tests of IQ, motor skills and behaviour. The parents also filled in questionnaires about their child's communication and social skills. "Delayed cord clamping compared with early cord clamping improved scores and reduced the number of children having low scores in fine-motor skills and social domains," the study's lead author, Dr. Ola Andersson of Uppsala University in Sweden, and his co-authors said in Tuesday's issue of JAMA Pediatrics. The fine-motor skill tests showed those in the delayed clamping group had a more mature pencil grip. There was also a difference in boys, who researchers said are generally more prone to iron deficiency than girls. Boys showed more improvements in fine-motor skills with delayed clamping. Andersson said delayed cord clamping can have quite an effect on the amount of iron in the blood, which is important for brain development just after birth. ©2015 CBC/Radio-Canada.
Keyword: Development of the Brain
Link ID: 20988 - Posted: 05.27.2015
By Tina Hesman Saey Combatants in the age-old battle of nature versus nurture may finally be able to lay down their arms. On average, both nature and nurture contribute roughly equally to determining human traits. Researchers compiled data from half a century’s worth of studies on more than 14 million pairs of twins. The researchers measured heritability — the amount of variation in a characteristic that can be attributed to genes — for a wide variety of human traits including blood pressure, the structure of the eyeball and mental or behavioral disorders. All traits are heritable to some degree, the researchers report May 18 in Nature Genetics. Traits overall had an average heritability of 49 percent, meaning it’s a draw between genes and environment. Individual traits can be more strongly influenced by one or the other. 100% Fraction of human traits with a genetic component 49% Fraction of variability in human traits determined by genes T.J.C. Polderman et al. Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature Genetics. Published online May 18, 2015. doi:10.1038/ng.3285. © Society for Science & the Public 2000 - 2015.
By Tara Haelle Thousands of infants each year die in their cribs from sudden infant death syndrome (SIDS) for reasons that have remained largely a mystery. A study published May 25 provides strong evidence that oxygen deprivation plays a big role. One reason the cause of SIDS has been so difficult to study is the sheer number of variables researchers have had to account for: whether the infant sleeps face down, breathes secondhand smoke or has an illness as well as whether the child has an unidentified underlying susceptibility. To isolate the effects of oxygen concentration, researchers from the University of Colorado compared the rate of SIDS in infants living at high altitudes, where the air is thin, to those living closer to sea level. Infants at high altitudes, they found, were more than twice as likely to die from SIDS. It was “very clever of the authors,” says Michael Goodstein, a pediatrician and member of the 2010–2011 Task Force on Sudden Infant Death Syndrome who was not involved in the study. “The authors did a good job controlling for other variables,” he adds. Beyond the risk of living at high altitudes, the study suggests a common link among different risk factors about the causes of SIDS. For example, the authors note that sleeping on the stomach and exposure to tobacco smoke can also contribute to hypoxia—insufficient oxygen reaching the tissues. Similarly, past research has suggested that sleeping on soft surfaces may shift the chin down, partly obstructing the airway, which might cause an infant to breathe in less oxygen. It’s unclear how hypoxia might contribute to SIDS but it could have to do with a buildup of carbon dioxide in the tissues when a child does not wake up. © 2015 Scientific American
Nala Rogers Alzheimer’s disease may have evolved alongside human intelligence, researchers report in a paper posted this month on BioRxiv1. The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development. This may have helped to increase the connectivity of neurons, making modern humans smarter as they evolved from their hominin ancestors. But that new intellectual capacity was not without cost: the same genes are implicated in Alzheimer's disease. Kun Tang, a population geneticist at the Shanghai Institutes for Biological Sciences in China who led the research, speculates that the memory disorder developed as ageing brains struggled with new metabolic demands imposed by increasing intelligence. Humans are the only species known to develop Alzheimer's; the disease is absent even in closely related primate species such as chimpanzees. Tang and his colleagues searched modern human DNA for evidence of this ancient evolution. They examined the genomes of 90 people with African, Asian or European ancestry, looking for patterns of variation driven by changes in population size and natural selection. Marked by selection The analysis was tricky, because the two effects can mimic each other. To control for the effects of population changes ― thereby isolating the signatures of natural selection — the researchers estimated how population sizes changed over time. Then they identified genome segments that did not match up with the population history, revealing the DNA stretches that were most likely shaped by selection. © 2015 Nature Publishing Group
Scientists at Mayo Clinic, Jacksonville, Florida created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), both of which are caused by a mutation in the a gene called C9ORF72. The study was partially funded by the National Institutes of Health and published in the journal Science. More than 30,000 Americans live with ALS, which destroys nerves that control essential movements, including speaking, walking, breathing and swallowing. After Alzheimer’s disease, FTD is the most common form of early onset dementia. It is characterized by changes in personality, behavior and language due to loss of neurons in the brain’s frontal and temporal lobes. Patients with mutations in the chromosome 9 open reading frame 72 (C9ORF72) gene have all or some symptoms associated with both disorders. “Our mouse model exhibits the pathologies and symptoms of ALS and FTD seen in patients with theC9ORF72 mutation,” said the study’s lead author, Leonard Petrucelli, Ph.D., chair and Ralph and Ruth Abrams Professor of the Department of Neuroscience at Mayo Clinic, and a senior author of the study. “These mice could greatly improve our understanding of ALS and FTD and hasten the development of effective treatments.” To create the model, Ms. Jeannie Chew, a Mayo Graduate School student and member of Dr. Petrucelli’s team, injected the brains of newborn mice with a disease-causing version of the C9ORF72 gene. As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms.
by Clare Wilson Does this qualify as irony? Our bodies need iron to be healthy – but too much could harm our brains by bringing on Alzheimer's disease. If that's the case, measuring people's brain iron levels could help identify those at risk of developing the disease. And since we already have drugs that lower iron, we may be able to put the brakes on. Despite intense efforts, the mechanisms behind this form of dementia are still poorly understood. For a long time the main suspect has been a protein called beta-amyloid, which forms distinctive plaques in the brain, but drugs that dissolve it don't result in people improving. Not so good ferrous Studies have suggested that people with Alzheimer's also have higher iron levels in their brains. Now it seems that high iron may hasten the disease's onset. Researchers at the University of Melbourne in Australia followed 144 older people who had mild cognitive impairment for seven years. To gauge how much iron was in their brains, they measured ferritin, a protein that binds to the metal, in their cerebrospinal fluid. For every nanogram per millilitre people had at the start of the study, they were diagnosed with Alzheimer's on average three months earlier. The team also found that the biggest risk gene for Alzheimer's, ApoE4, was strongly linked with higher iron, suggesting this is why carrying the gene makes you more vulnerable. Iron is highly reactive, so it probably subjects neurons to chemical stress, says team member Scott Ayton. © Copyright Reed Business Information Ltd
Link ID: 20957 - Posted: 05.20.2015
By PAM BELLUCKM The largest analysis to date of amyloid plaques in people’s brains confirms that the presence of the substance can help predict who will develop Alzheimer’s and determine who has the disease. Two linked studies, published Tuesday in JAMA, also support the central early role in Alzheimer’s of beta amyloid, the protein that creates plaques. Data from nearly 9,500 people on five continents shows that amyloid can appear 20 to 30 years before symptoms of dementia, that the vast majority of Alzheimer’s patients have amyloid and that the ApoE4 gene, known to increase Alzheimer’s risk, greatly accelerates amyloid accumulation. The findings also confirm that amyloid screening, by PET scan or cerebral spinal fluid test, can help identify people for clinical trials of drugs to prevent Alzheimer’s. Such screening is increasingly used in research. Experts say previous trials of anti-amyloid drugs on people with dementia failed because their brains were already too damaged or because some patients, not screened for amyloid, may not have had Alzheimer’s. “The papers indicate that amyloid imaging is important to be sure that the drugs are being tested on people who have amyloid,” said Dr. Roger Rosenberg, the director of the Alzheimer’s Disease Center at the University of Texas Southwestern Medical Center at Dallas, who wrote an editorial about the studies. Dr. Samuel Gandy, an Alzheimer’s researcher at Mount Sinai Hospital, who was not involved in the research, said doctors “can feel fairly confident that amyloid is due to Alzheimer’s.” But he and others cautioned against screening most people without dementia because there is not yet a drug that prevents or treats Alzheimer’s, and amyloid scans are expensive and typically not covered by insurance. © 2015 The New York Times Company
Link ID: 20956 - Posted: 05.20.2015
by Ashley Yeager This guest post is by SN's web producer Ashley Yeager, who can't remember ever not knowing how to swim. Sometimes my brother-in-law will scoop up my 2-year-old niece and fly her around like Superwoman. She’ll start kicking her legs and swinging her arms like she’s swimming — especially when we say, “paddle, paddle, paddle.” My niece, Baby D, loves the water. She often looks like one of the kids captured in famed photographer Seth Casteel’s new book, Underwater Babies. But she probably won’t remember her first trips to the pool — she was only a few months old when her mom first took her swimming. Part of my sister’s reasoning for such an early start was standard water safety. Every day in the United States, accidental drowning claims the lives of two children under the age of 14 years. Our family spends a lot of time at the pool and the beach, so making sure Baby D is protected is a priority. But there’s another reason my sister was keen to get Baby D to the pool. Loosely based on something our mother told us, it’s that learning to swim early in life may give kids a head start in developing balance, body awareness and maybe even language and math skills. Mom may have been right. A multi-year study released in 2012 suggests that kids who take swim lessons early in life appear to hit certain developmental milestones well before their nonswimming peers. In the study, Australian researchers surveyed about 7,000 parents about their children’s development and gave 177 kids aged 3 to 5 years standard motor, language, memory and attention tests. Compared with kids who didn’t spend much time in the water, kids who had taken swim lessons seemed to be more advanced at tasks like running and climbing stairs and standing on their tiptoes or on one leg, along with drawing, handling scissors and building towers out of blocks. © Society for Science & the Public 2000 - 2015.
Monica Tan The age-old question of whether human traits are determined by nature or nurture has been answered, a team of researchers say. Their conclusion? It’s a draw. By collating almost every twin study across the world from the past 50 years, researchers determined that the average variation for human traits and disease is 49% due to genetic factors and 51% due to environmental factors. University of Queensland researcher Beben Benyamin from the Queensland Brain Institute collaborated with researchers at VU University of Amsterdam to collate 2,748 studies involving more than 14.5 million pairs of twins. “Twin studies have been conducted for more than 50 years but there is still some debate in terms of how much the variation is due to genetic or environmental factors,” Benyamin said. He said the study showed the conversation should move away from nature versus nature, instead looking at how the two work together. “Both are important sources of variation between individuals,” he said. While the studies averaged an almost even split between nature and nurture, there was wide variation within the 17,800 separate traits and diseases examined by the studies. For example, the risk for bipolar disorder was found to be 68% due to genetics and only 32% due to environmental factors. Weight maintenance was 63% due to genetics and 37% due to environmental factors. In contrast, risk for eating disorders was found to be 40% genetic and 60% environmental, whereas the risk for mental and behavioural disorders due to use of alcohol was 41% genetic and 59% environmental. © 2015 Guardian News and Media Limited
Keyword: Genes & Behavior
Link ID: 20948 - Posted: 05.19.2015