Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.

Links 1 - 20 of 24427

By Emily Underwood When a 53-year-old man asked Dutch doctors to treat his obsessive-compulsive disorder (OCD) several years back, they suggested a new but promising surgical treatment: implanted electrodes that would stimulate deep brain tissue involved in decision-making, reward-seeking, and motivation. The treatment apparently helped him go off one of his psychiatric medications, but it came with a surprising side effect—it also seemed to improve his type 2 diabetes. Now, researchers think they know why. A new study suggests that a boost in the activity of dopamine, a neurotransmitter involved in motivation and pleasure, improves the body’s ability to process sugar. This is the first time such a pathway, previously seen in mice, has been found in humans, says Mike Michaelides, a neuroscientist at the National Institute on Drug Abuse in Baltimore, Maryland, who was not involved in the new research. That doesn’t make deep brain stimulation (DBS) realistic for most people with diabetes, but other, less invasive brain therapies that target dopamine might one day be feasible. Diabetes occurs when glucose, or sugar, in a person’s bloodstream remains in chronically high concentrations. Type 1, which typically begins in childhood, results when the immune system destroys the pancreatic cells that make insulin, the hormone that lets our cells use sugar as food. Type 2 diabetes, typically triggered by a combination of bad genes, poor eating habits, and a lack of exercise, also damages the body’s ability to produce its own insulin. As time goes on, cells are hard-pressed to remove sugar from the blood, and people require larger and larger amounts of insulin to keep their blood sugar stable. There is no cure for either disease. © 2018 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 25018 - Posted: 05.24.2018

By Chris Buckley and Gardiner Harris BEIJING — An American government employee posted in southern China has signs of possible brain injury after reporting disturbing sounds and sensations, the State Department said on Wednesday, in events that seemed to draw parallels with mysterious ailments that struck American diplomats in Cuba. The State Department warning, issued through the United States Consulate in Guangzhou, a city in southern China, advised American citizens in China to seek medical help if they felt similar symptoms. But it said that no other cases had been reported. “A U.S. government employee in China recently reported subtle and vague, but abnormal, sensations of sound and pressure,” the health alert said. “We do not currently know what caused the reported symptoms and we are not aware of any similar situations in China, either inside or outside of the diplomatic community.” The employee was working in Guangzhou, and “reported experiencing a variety of physical symptoms” from late 2017 until April, Jinnie Lee, a spokeswoman for the United States Embassy in Beijing, said in an emailed response to questions. Secretary of State Mike Pompeo told the House Foreign Affairs Committee on Wednesday that medical teams were heading to Guangzhou to address the issue. “The medical indications are very similar and entirely consistent with the medical indications that have taken place to Americans working in Cuba,” he said. The embassy was told on Friday “that the clinical findings of this evaluation matched mild traumatic brain injury,” according to Ms. Lee, who said she could not reveal any more details to protect the employee’s privacy. Mild traumatic brain injury can show up as headache, dizziness, nausea, poor memory and a general foggy sensation. The Chinese Ministry of Foreign Affairs did not immediately answer faxed questions about the ill American, but Mr. Pompeo said the Trump administration had asked the Chinese government for assistance in an investigation, “and they have committed to honoring their commitments under the Vienna convention.” The Vienna convention requires that countries protect diplomats stationed in their nations. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion; Hearing
Link ID: 25017 - Posted: 05.24.2018

Anya Kamenetz "I want The Three Bears!" These days parents, caregivers and teachers have lots of options when it comes to fulfilling that request. You can read a picture book, put on a cartoon, play an audiobook, or even ask Alexa. A newly published study gives some insight into what may be happening inside young children's brains in each of those situations. And, says lead author Dr. John Hutton, there is an apparent "Goldilocks effect" — some kinds of storytelling may be "too cold" for children, while others are "too hot." And, of course, some are "just right." Hutton is a researcher and pediatrician at Cincinnati Children's Hospital with a special interest in "emergent literacy" — the process of learning to read. For the study, 27 children around age 4 went into an FMRI machine. They were presented with stories in three conditions: audio only; the illustrated pages of a storybook with an audio voiceover; and an animated cartoon. All three versions came from the Web site of Canadian author Robert Munsch. While the children paid attention to the stories, the MRI, the machine scanned for activation within certain brain networks, and connectivity between the networks. "We went into it with an idea in mind of what brain networks were likely to be influenced by the story," Hutton explains. One was language. One was visual perception. The third is called visual imagery. The fourth was the default mode network, which Hutton calls, "the seat of the soul, internal reflection — how something matters to you." The default mode network includes regions of the brain that appear more active when someone is not actively concentrating on a designated mental task involving the outside world. In terms of Hutton's "Goldilocks effect," here's what the researchers found: © 2018 npr

Keyword: Language; Development of the Brain
Link ID: 25016 - Posted: 05.24.2018

Kelly Crowe · In a darkened room at Toronto's Krembil Research Institute, Dr. Donald Weaver is looking at a screen covered in green fluorescent dots. That's not a good thing. Those glowing green dots are exactly what this Alzheimer's researcher did not want to see. "Weeks if not months of work went into this compound and it failed," he said. "It's done." Weaver, a neurologist and chemist, was testing a compound to see if it could prevent the clumping of a protein called tau which creates distinctive tangles in the brains of people with Alzheimer's disease. If it had worked, it might have been a candidate for a new drug. But it didn't work, just like the thousands of others he's already tried. Failure is normal for researchers engaged in the frustrating search for drugs to treat Alzheimer's disease. "You have to be passionate," Weaver said. "This is a disease in which so many approaches have failed. You really have to deeply believe that your approach is correct just to get up every day and keep working at it." Many promising drugs have failed But after a series of high-profile drug failures over the past few years, scientists are facing the disturbing possibility that their leading theory of Alzheimer's might be fatally flawed. It's called the amyloid hypothesis, and it was an obvious target for researchers because the amyloid protein forms distinctive plaques in the brains of people with Alzheimer's. "That led to the conclusion it must be playing a pretty important role in the disease," Weaver said. The amyloid hypothesis was first proposed in 1992, and for the past 25 years research has focused on finding compounds that clear amyloid from the brain or slow down its production. ©2018 CBC/Radio-Canada.

Keyword: Alzheimers
Link ID: 25015 - Posted: 05.24.2018

By Darold A. Treffert How many children have “autism”? Is that number increasing? Is there an “epidemic” of autism or have we merely been continually refining it, expanding it and moving the goalposts since it was first described by Leo Kanner in 1943? I met my first child with autism in 1959, almost 60 years ago. I had the good fortune to learn about autism firsthand from Kanner himself, when he was a visiting professor at the University of Wisconsin Medical School and I was a medical student there. Then, in 1962, I started a Children’s Unit at Winnebago Mental Health Institute in Wisconsin, on which almost all the children were autistic. That’s also the unit on which I met my first savant. The question of autism prevalence engaged me even then. In 1970, I carried out the first U.S. study of the epidemiology of infantile autism, published in Archives of General Psychiatry. Actually, autism was then most commonly diagnosed formally as childhood schizophrenia. At that time, the Wisconsin Department of Health and Human services provided me with a printout listing all patients age 12 and under seen for evaluation or treatment and given a diagnosis of childhood schizophrenia between fiscal 1962 and 1967 in 30 community mental health and child guidance clinics; four state and county mental hospitals; three colonies NOT REAL NAMES and training schools; and the children’s treatment center, children’s diagnostic center and university hospitals. © 2018 Scientific American,

Keyword: Autism
Link ID: 25014 - Posted: 05.24.2018

By Dennis Normile SHANGHAI, CHINA—The nascent China Brain Project took another step toward reality last week with the launch of the Shanghai Research Center for Brain Science and Brain-Inspired Intelligence. The new center and its Beijing counterpart, launched 2 months ago, are expected to become part of an ambitious national effort to bring China to the forefront of neuroscience. But details of that 15-year project—expected to rival similar U.S. and EU efforts in scale and ambition—are still being worked out, 2 years after the government made it a priority. Preparation for the national effort “was taking quite a long time,” says Zhang Xu, a neuroscientist and executive director of the new center here. So Beijing and Shanghai got started on their own plans, he says. China’s growing research prowess and an increasing societal interest in neuroscience—triggered in part by an aging population—as well as commercial opportunities and government support are all coming together to make this “a good time for China’s brain science efforts,” Zhang says. Government planners called for brain research to be a key science and technology project in the nation’s 13th Five-Year Plan, adopted in spring 2016. The effort would have three main pillars, according to a November 2016 Neuron paper from a group that included Poo Mu-ming, director of Shanghai’s Institute of Neuroscience (ION), part of the Chinese Academy of Sciences (CAS). It would focus on basic research on neural mechanisms underlying cognition, translational studies of neurological diseases with an emphasis on early diagnosis and intervention, and brain simulations to advance artificial intelligence and robotics. Support under the 5-year plan was just the start of a 15-year program, the group wrote. © 2018 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 25013 - Posted: 05.23.2018

By Christof Koch Consciousness is everything you experience. It is the tune stuck in your head, the sweetness of chocolate mousse, the throbbing pain of a toothache, the fierce love for your child and the bitter knowledge that eventually all feelings will end. The origin and nature of these experiences, sometimes referred to as qualia, have been a mystery from the earliest days of antiquity right up to the present. Many modern analytic philosophers of mind, most prominently perhaps Daniel Dennett of Tufts University, find the existence of consciousness such an intolerable affront to what they believe should be a meaningless universe of matter and the void that they declare it to be an illusion. That is, they either deny that qualia exist or argue that they can never be meaningfully studied by science. If that assertion was true, this essay would be very short. All I would need to explain is why you, I and most everybody else is so convinced that we have feelings at all. If I have a tooth abscess, however, a sophisticated argument to persuade me that my pain is delusional will not lessen its torment one iota. As I have very little sympathy for this desperate solution to the mind-body problem, I shall move on. The majority of scholars accept consciousness as a given and seek to understand its relationship to the objective world described by science. More than a quarter of a century ago Francis Crick and I decided to set aside philosophical discussions on consciousness (which have engaged scholars since at least the time of Aristotle) and instead search for its physical footprints. What is it about a highly excitable piece of brain matter that gives rise to consciousness? Once we can understand that, we hope to get closer to solving the more fundamental problem. © 2018 Scientific American

Keyword: Consciousness
Link ID: 25012 - Posted: 05.23.2018

By Tanya Lewis Every few seconds a wave of electrical activity travels through the brain, like a large swell moving through the ocean. Scientists first detected these ultraslow undulations decades ago in functional magnetic resonance imaging (fMRI) scans of people and other animals at rest—but the phenomenon was thought to be either electrical “noise” or the sum of much faster brain signals and was largely ignored. Now a study that measured these “infraslow” (less than 0.1 hertz) brain waves in mice suggests they are a distinct type of brain activity that depends on an animal’s conscious state. But big questions remain about these waves’ origin and function. An fMRI scan detects changes in blood flow that are assumed to be linked to neural activity. “When you put someone in a scanner, if you just look at the signal when you don’t ask the subject to do anything, it looks pretty noisy,” says Marcus Raichle, a professor of radiology and neurology at Washington University School of Medicine in St. Louis and senior author of the new study, published in April in Neuron. “All this resting-state activity brought to the forefront: What is this fMRI signal all about?” To find out what was going on in the brain, Raichle’s team employed a combination of calcium/hemoglobin imaging, which uses fluorescent molecules to detect the activity of neurons at the cellular level, and electrophysiology, which can record signals from cells in different brain layers. They performed both measurements in awake and anesthetized mice; the awake mice were resting in tiny hammocks in a dark room. © 2018 Scientific American

Keyword: Consciousness
Link ID: 25011 - Posted: 05.23.2018

Hartmut Wekerle Some immunologists regard the central nervous system (CNS) as a no-man’s-land, avoided by immune cells and therefore uninteresting. But, in fact, the CNS has a vigorous immune potential that remains dormant in normal conditions but is awakened after injury. The switch that controls the brain’s immune microenvironment involves non-neuronal cells called glia — not only microglia, which are sometimes called the immune cells of the CNS, but also multifunctional cells called astrocytes1. In a paper in Nature, Rothhammer et al.2 describe how these two glial cell types communicate on a molecular level to influence inflammation in the CNS, and show that this interaction is controlled remotely by microbes that inhabit the gut. A decade ago, the group that performed the current study, along with another research group, discovered3,4 an unexpected immunoregulatory role for a ligand-activated transcription factor called the aryl hydrocarbon receptor (AHR), which at the time was best known as a receptor for environmental toxins5. The two groups showed that AHR modulates the progression of experimental autoimmune encephalomyelitis (EAE) — an autoimmune disease in mice in which the immune system becomes overactive and attacks the CNS. EAE is often used a model of multiple sclerosis (MS). Initially, the groups focused on how AHR might affect EAE by regulating pathogenic and protective subsets of immune cells outside the CNS. But it later emerged that AHR is also strongly expressed in the CNS, particularly in microglia and astrocytes6, raising the question of whether AHR in the CNS has a role in autoimmune diseases. © 2018 Macmillan Publishers Limited,

Keyword: Neuroimmunology; Obesity
Link ID: 25010 - Posted: 05.23.2018

by Lindsey Bever A rare, brain-damaging virus has killed at least 10 people in southern India, where medical crews are scrambling to manage the spread of the deadly disease — and to minimize panic. Health officials said Tuesday that 10 people who were exposed to the Nipah virus and showed symptoms have died. Two others have tested positive for Nipah and are considered critically ill, and more than three dozen people have been put into quarantine since the outbreak began in the Indian state of Kerala, according to BBC News. “This is a new situation for us; we have no prior experience in dealing with the Nipah virus,” said K.K. Shailaja, health minister of the state, according to Reuters. “We are hopeful we can put a stop to the outbreak.” Shailaja had said earlier the outbreak had been “effectively” contained and that there was no need for the public to panic. But the virus's spread — and the rapidly rising death toll — have prompted concern in the outbreak's epicenter, Kozhikode, a coastal city in Kerala, where people have been “swarming” hospitals with fevers and other illnesses to ensure they do not have the virus, a local government official told Reuters. “We’ve sought the help of private hospitals to tide over the crisis,” said the official, U.V. Jose. Gulf News reported that Kerala “is in a state of panic after many cases of the killer Nipah virus were detected.” © 1996-2018 The Washington Post

Keyword: Miscellaneous
Link ID: 25009 - Posted: 05.23.2018

By Ashley Yeager Twenty years ago, Ilyce Randell and her husband received devastating news: their son Maxie, who was a little over four months old at the time, had Canavan disease. Maxie would never walk or talk, and he likely wouldn’t live past age 10. Not much could be done to help their son, the couple was told, though a geneticist offhandedly remarked that researchers were developing a gene therapy that might lessen Maxie’s symptoms or extend his life. But the Randells also learned that there was no funding available for a clinical trial on the gene therapy. Recently married, the couple contacted the same people they had invited to their wedding. Randell wrote a letter describing her son’s illness and included a photo of Maxie grinning. “That was my first fundraising campaign,” she says. It was also the start of Canavan Research Illinois, the Randell family’s foundation. Canavan disease is caused by mutations to the ASPA gene, which encodes an enzyme, aspartoacylase, that breaks down N-acetyl-L-aspartic acid. Without aspartoacylase, the acid builds up in the brain’s neurons and prevents their axons from being coated in fatty myelin sheaths. As a result, electrical signals don’t travel as efficiently from nerve cell to nerve cell. Neurons in the brain break down, leaving the organ spongy and leading to intellectual disabilities, loss of movement, abnormal muscle tone, and seizures, among other symptoms. In the first US trial of a gene therapy for Canavan, researchers tried encasing healthy copies of ASPA in liposomes and injecting them into the brain through an intraventricular catheter attached to a small, plastic, dome-shaped reservoir placed just beneath the scalp. The researchers injected the gene therapy into the reservoir, and it then diffused into the cerebrospinal fluid. In 1999, Maxie became one of 16 patients to receive the treatment. Maxie and his cohort showed some improvements in vision and movement, but the children weren’t cured. © 1986-2018 The Scientist

Keyword: Development of the Brain
Link ID: 25008 - Posted: 05.23.2018

Nicola Davis Many people complain they do not get enough sleep, and it seems they are right to be concerned. Researchers have found that adults under the age of 65 who get five or fewer hours of sleep for seven days a week have a higher risk of death than those who consistently get six or seven hours’ shut-eye. However the effect of short sleeps over a few days may be countered by a later lie-in. The research found that individuals who managed just a few hours’ sleep each day during the week but then had a long snooze at weekends had no raised mortality risk, compared with those who consistently stuck to six or seven hours a night. “Sleep duration is important for longevity,” said Torbjörn Åkerstedt, first author of the study, at the Stress Research Institute, Stockholm University, and Karolinska Institute, also in the Swedish capital. The study, published in the Journal of Sleep Research, is based on data from more than 38,000 adults, collected during a lifestyle and medical survey conducted throughout Sweden in 1997. The fate of participants was followed for up to 13 years, using a national death register. Åkerstedt said researchers had previously looked at links between sleep duration and mortality but had focused on sleep during the working week. “I suspected there might be some modification if you included also weekend sleep, or day-off sleep.” Once factors such as gender, body mass index, smoking, physical activity and shift work, were taken into account, the results revealed that those under the age of 65 who got five hours of sleep or under that amount seven days a week had a 65% higher mortality rate than those getting six or seven hours’ sleep every day. But there was no increased risk of death for those who slept five or fewer hours during the week but then managed eight or more hours’ sleep on weekend days. 'Western society is chronically sleep deprived': the importance of the body's clock © 2018 Guardian News and Media Limited

Keyword: Sleep; Neuroimmunology
Link ID: 25007 - Posted: 05.23.2018

By Carl Zimmer James Priest couldn’t make sense of it. He was examining the DNA of a desperately ill baby, searching for a genetic mutation that threatened to stop her heart. But the results looked as if they had come from two different infants. “I was just flabbergasted,” said Dr. Priest, a pediatric cardiologist at Stanford University. The baby, it turned out, carried a mixture of genetically distinct cells, a condition known as mosaicism. Some of her cells carried the deadly mutation, but others did not. They could have belonged to a healthy child. We’re accustomed to thinking of our cells sharing an identical set of genes, faithfully copied ever since we were mere fertilized eggs. When we talk about our genome — all the DNA in our cells — we speak in the singular. But over the course of decades, it has become clear that the genome doesn’t just vary from person to person. It also varies from cell to cell. The condition is not uncommon: We are all mosaics. For some people, that can mean developing a serious disorder like a heart condition. But mosaicism also means that even healthy people are more different from one another than scientists had imagined. In medieval Europe, travelers making their way through forests sometimes encountered a terrifying tree. A growth sprouting from the trunk looked as if it belonged to a different plant altogether. It formed a dense bundle of twigs, the sort that people might fashion into a broom. Germans call it Hexenbesen: witches’ broom. As legend had it, witches used magic spells to conjure the brooms to fly across the night sky. The witches used some as nests, too, leaving them for hobgoblins to sleep in. In the 19th century, plant breeders found that if they cut witches’ broom from one tree and grafted it to another, the broom would grow and produce seeds. Those seeds would sprout into witches’ broom as well. © 2018 The New York Times Company

Keyword: Epigenetics
Link ID: 25006 - Posted: 05.22.2018

Nicola Davis With 26% of adults classified as obese in the UK in 2016, the hunt for causes and solutions to expanding waistlines is on. While public health messages have focused largely on the food we eat, some scientists suspect there is another factor at play: substances being dubbed as “obesogens” – found in our packaging, household goods and furnishings that might affect our hormones and the buildup of fat in the body. However, experts are sceptical, particularly in the light of one report this week. It has made the bold claim that “removing shoes when entering the house and swapping carpet for wooden floors could help people stay slim”, citing a talk by researchers at the universities of Aveiro and Beira Interior in Portugal, who have suggested that preventing obesogens accumulating in the house by frequently sweeping and dusting could stop us gaining weight. As Prof Russell Viner, president of the Royal College of Paediatrics and Child Health, says: “For some medical reasons, such as protection against allergies, yes, it’s advised to keep a dust-free home and so, too, is removing shoes to avoid bringing in dirt from outside, but these things will not make you a healthy weight. Only a balanced diet and regular exercise will do that.” It is not the first study to moot the idea of the existence of obesogens. Earlier this year, researchers at Harvard University suggested compounds called perfluoroalkyl substances (PFAS) – widely used in products such as stain repellents and known to have a number of negative effects on human health – might lead to weight gain. © 2018 Guardian News and Media Limited

Keyword: Obesity
Link ID: 25005 - Posted: 05.22.2018

by Juli Fraga Individuals with anorexia, binge eating disorder and bulimia often feel anxious and overwhelmed when surrounded by food. This anxiety can make grocery shopping and cooking a challenge. A new form of telemedicine in which people can video-chat with a nutritional counselor while at the supermarket aims to help. According to the National Institute of Mental Health, approximately 1 percent of Americans suffer from anorexia, a sometimes deadly psychiatric illness. Along with anorexia, millions of Americans also struggle with binge eating disorder. Jamie Lynn Pelletier, 28, of Greensboro, N.C., was just 13 when she began counting calories and skipping meals, behavior that eventually led to anorexia, which is characterized by food restriction, extreme weight loss and distorted body image. “In junior high, I began to feel unattractive and self-conscious about my body. To lose weight, I started dieting and overexercising,” Pelletier said. Since 2015, Pelletier has completed several residential and outpatient treatment programs in the battle to stop starving herself. Her struggle shows how tough it can be for anorexics to stop seeing food as the enemy. Recently, Pelletier’s dietitian recommended grocery store therapy, which allows her to connect with a dietitian via video chat. “Going to the grocery store is stressful because seeing foods labeled as low-carb and low-fat can make me feel like buying the real thing is not okay. With virtual therapy, I FaceTime with my dietitian at the store,” said Pelletier, referring to Apple’s video-chat application. “For privacy, I put in my headphones so I can talk to her discreetly while I’m shopping.” © 1996-2018 The Washington Post

Keyword: Anorexia & Bulimia
Link ID: 25004 - Posted: 05.22.2018

/ By Lynne Peeples Reaching behind a low bookshelf slightly taller than a typical 5-year-old — and one topped with a Seattle Seahawks gnome and stuffed kangaroo — Sara Barbee presses a button labeled “Alert.” Intense bluish light fills her classroom, and nearly all 17 kindergarteners respond with a collective “Whoooaaaaa.” Barbee, their teacher here at Renton Park Elementary School, walks back to the front of the classroom and ushers the students to sit “crisscross applesauce” on the perimeter of a brightly colored alphabet rug. Front-and-center rests a water tank atop a small blue table, which Barbee uses to teach her students about the buoyancy of objects in water. Indeed, it’s not the buoyancy lesson that has drawn me to this school just outside of Seattle, but those funky new lights, which are designed to mimic the shifting colors and intensities of the rising and setting sun. Scientists believe that exposure to bright, blue-rich white light during the day, and to softer, amber hues at night, helps restore the human body’s natural circadian rhythm, a deeply ingrained, physiological drumbeat that, many experts argue, has been disrupted to ill-effect by our constant exposure to standard incandescent or fluorescent lighting — and more recently, to the relentless glow of electronic screens. These are not, of course, new ideas, and doctors have long prescribed light boxes and related paraphernalia for seasonal affective disorder and other forms of depression. But it’s only now, proponents say — amid innovations in light-emitting diode, or LED, technology; amid calls for more energy-efficient lighting infrastructure overall; and amid a renaissance in scientific understanding of how human eyes, brains, and internal clocks interrelate — that a public health revolution, driven by more thoughtful lighting infrastructure, has the potential to unfold. Copyright 2018 Undark

Keyword: Biological Rhythms; Depression
Link ID: 25003 - Posted: 05.21.2018

Michaeleen Doucleff Six months ago, Melissa Nichols brought her baby girl, Arol, home from the hospital. And she immediately had a secret. "I just felt guilty and like I didn't want to tell anyone," says Nichols, who lives in San Francisco. "It feels like you're a bad mom. The mom guilt starts early, I guess." Across town, first-time mom Candyce Hubbell has the same secret — and she hides it from her pediatrician. "I don't really want be lectured," she says. "I know what her stance will be on it." The way these moms talk about their secret, you might think they're putting their babies in extreme danger. Perhaps drinking and driving with the baby in the car? Or smoking around the baby? But no. What they're hiding is this: They hold the baby at night while they sleep together in the bed. Here in the U.S., this is a growing trend among families. More moms are choosing to share a bed with their infants. Since 1993, the practice in the U.S. has grown from about 6 percent of parents to 24 percent in 2015. But the practice goes against medical advice in the U.S. The American Academy of Pediatrics is opposed to bed-sharing: It "should be avoided at all times" with a "[full-]term normal-weight infant younger than 4 months," the AAP writes in its 2016 recommendations for pediatricians. The organization says the practice puts babies at risk for sleep-related deaths, including sudden infant death syndrome, accidental suffocation and accidental strangulation. About 3,700 babies die each year in the U.S. from sleep-related causes. © 2018 npr

Keyword: Sleep; Development of the Brain
Link ID: 25002 - Posted: 05.21.2018

Robin McKie, science editor Fasting every other day to lose weight could have damaging side effects. That is the conclusion of a group of scientists speaking this weekend at the European Society of Endocrinology’s annual meeting. Their findings suggest that fasting-based diets may impair the action of sugar-regulating hormone insulin, and lead to increased risk of diabetes. Care should be taken before starting such programmes, say researchers. Ana Bonassa, whose team from the University of São Paulo in Brazil carried out the study, said: “This is the first study to show that, despite weight loss, intermittent fasting diets may actually damage the pancreas and affect insulin function in normal healthy individuals, which could lead to diabetes and serious health issues.” Advertisement In recent years intermittent fasting diets have gained popularity. Participants fast for two days out of seven, or on alternate days. However, evidence of their success has been contradictory and there is debate among doctors about their potential to trigger harmful long-term effects. Previous research has also shown that short-term fasting can produce molecules called free radicals, highly reactive chemicals that can cause damage to cells in the body and which may be associated with impaired organ function, cancer risk and accelerated ageing. © 2018 Guardian News and Media Limited

Keyword: Obesity
Link ID: 25001 - Posted: 05.21.2018

By Matthew Hutson Parents tend to favor children of one gender in certain situations—or so evolutionary biologists tell us. A new study used data on colored backpack sales to show that parental wealth may influence spending on sons versus daughters. In 1973 biologist Robert Trivers and computer scientist Dan Willard published a paper suggesting that parents invest more resources, such as food and effort, in male offspring when times are good and in female offspring when times are bad. According to the Trivers-Willard hypothesis, a son given lots of resources can outcompete others for mates—but when parents have few resources, they are more inclined to invest them in daughters, who generally find it easier to attract reproductive partners. Trivers and Willard further posited that parental circumstances could even influence the likelihood of having a boy or girl, a concept widely supported by research across vertebrate species. Studying parental investment after birth is difficult, however, and has produced conflicting results. The new study looked for a metric of such investment that met several criteria: it should be immune to inherent sex differences in the need for resources; it should measure investment rather than outcomes; and it should be objective rather than rely on self-reporting. Study author Shige Song, a sociologist at Queens College, City University of New York, examined spending on pink and blue backpacks purchased in China in 2015 from a large retailer, He narrowed the data to about 5,000 bags: blue backpacks bought by households known to have at least one boy and pink ones bought by households known to have at least one girl. The results showed that wealthier families spent more on blue versus pink backpacks—suggesting greater investment in sons. Poorer families spent more on pink packs than blue ones. The findings were published online in February in Evolution and Human Behavior. © 2018 Scientific American

Keyword: Evolution
Link ID: 25000 - Posted: 05.21.2018

Emine Saner On any given day in Cambridge, you may see numerous people jogging along the towpaths, and it’s not unreasonable to assume neuroscientists may be over-represented. “You see so many,” says Hannah Critchlow, a neuroscientist who likes to jog along the river. Physical fitness may be a secondary consideration, she says; what they are really trying to do is ramp up their neurogenesis – the birth of new nerve cells in the brain. “People used to think that once you were born, that was it, that was all the nerve cells you have throughout life,” she says. “Then, 20 years ago, Rusty Gage [a professor at the Salk Institute in California] discovered that you get neurogenesis in adults, in a region of the brain called the hippocampus, which is involved in learning and memory. It turns out that jogging is really good at increasing neurogenesis in the brain.” And so, Critchlow says with a laugh, she likes to run. “I go: ‘This is wonderful, my neurogenesis is really happy with me at the moment.’” We are sitting in her study at Magdalene College, Cambridge, where Critchlow is outreach fellow, tasked with public engagement. Once described by the Telegraph as “a sort of female Brian Cox”, she has given numerous talks, been a presenter on Tomorrow’s World Live, the interactive version of the BBC science show, appeared on TV, radio and podcasts and was named as a top 100 scientist for her work in science communication. She has just written a book on consciousness – part of the Ladybird Expert series aimed at adults, a brief but mindbending introduction to the brain and the idea of consciousness, taking in philosophy, famous neuroscience breakthroughs and brain facts. © 2018 Guardian News and Media Limited

Keyword: Consciousness
Link ID: 24999 - Posted: 05.19.2018