Nell Greenfieldboyce Mosquitoes searching for a meal of blood use a variety of clues to track down humans, including our body heat and the carbon dioxide in our breath. Now, research shows that a certain olfactory receptor in their antennae also serves as a detector of humans, responding to smelly chemicals in our sweat. Targeting this receptor might offer a new way to foil blood-seeking mosquitoes and prevent the transmission of diseases including malaria, Zika virus and dengue, according to the study published Thursday in the journal Current Biology. "We found a receptor for human sweat, and we found that acidic volatiles that come off of us are really key for mosquitoes to find us," says Matthew DeGennaro, a neurogeneticist at Florida International University in Miami. "I think what's exciting about it is that finally we have evidence that there is some sort of pathway, in the sense of smell, that is required for mosquitoes to like us," says Lindy McBride, a scientist at Princeton University who studies mosquito behavior and was not part of the research team. It's long been known that mosquitoes rely on multiple clues to target humans. First, a mosquito will sense exhaled carbon dioxide from a distance that can be more than 30 feet. "After the carbon dioxide," DeGennaro explains, "then it begins to sense human odor." © 2019 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26092 - Posted: 03.29.2019

By James Gallagher Health and science correspondent, BBC News French scientists say they have proof that dogs can pick up the smell of an epileptic seizure. The University of Rennes team hope the findings could lead to ways to predict when people will have a seizure. These could include dogs or "electronic noses" that pick up the precise odour being given off during a seizure. Dogs have previously been shown to be able to sniff out diseases including cancers, Parkinson's, malaria and diabetes. Some people with epilepsy already rely on the animals. One sleeping in a child's bedroom can alert family members of a seizure in the middle of the night. The latest study, in the journal Scientific Reports, trained five dogs from Medical Mutts, in the US, to recognise the smell of sweat taken from a patient having a seizure. They were then given a choice of seven sweat samples taken from other patients while they were either relaxing, exercising or having a seizure. Two of the dogs found the seizure sample about two-thirds of the time and the other three were 100% accurate The report says: "The results are extremely clear and constitute a first step towards identifying a seizure-specific odour." © 2019 BBC

Keyword: Chemical Senses (Smell & Taste); Epilepsy
Link ID: 26091 - Posted: 03.29.2019

Ian Sample Science editor Doctors have identified a new mutation in a woman who is barely able to feel pain or stress after a surgeon who was baffled by her recovery from an operation referred her for genetic testing. Jo Cameron, 71, has a mutation in a previously unknown gene which scientists believe must play a major role in pain signalling, mood and memory. The discovery has boosted hopes of new treatments for chronic pain which affects millions of people globally. Cameron, a former teacher who lives in Inverness, has experienced broken limbs, cuts and burns, childbirth and numerous surgical operations with little or no need for pain relief. She sometimes leans on the Aga and knows about it not from the pain, but the smell. “I’m vegan, so the smell is pretty obvious,” she says. “There’s no other burning flesh going on in the house.” But it is not only an inability to sense pain that makes Cameron stand out: she also never panics. When a van driver ran her off the road two years ago, she climbed out of her car, which was on its roof in a ditch, and went to comfort the shaking young driver who cut across her. She only noticed her bruises later. She is relentlessly upbeat, and in stress and depression tests she scored zero. “I knew that I was happy-go-lucky, but it didn’t dawn on me that I was different,” she says. “I thought it was just me. I didn’t know anything strange was going on until I was 65.” © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Genes & Behavior
Link ID: 26090 - Posted: 03.28.2019

Amber Dance Robert Sorge was studying pain in mice in 2009, but he was the one who ended up with a headache. At McGill University in Montreal, Canada, Sorge was investigating how animals develop an extreme sensitivity to touch. To test for this response, Sorge poked the paws of mice using fine hairs, ones that wouldn’t ordinarily bother them. The males behaved as the scientific literature said they would: they yanked their paws back from even the finest of threads. But females remained stoic to Sorge’s gentle pokes and prods1. “It just didn’t work in the females,” recalls Sorge, now a behaviourist at the University of Alabama at Birmingham. “We couldn’t figure out why.” Sorge and his adviser at McGill University, pain researcher Jeffrey Mogil, would go on to determine that this kind of pain hypersensitivity results from remarkably different pathways in male and female mice, with distinct immune-cell types contributing to discomfort2. Sorge and Mogil would never have made their discovery if they had followed the conventions of most pain researchers. By including male and female mice, they were going against the crowd. At the time, many pain scientists worried that females’ hormone cycles would complicate results. Others stuck with males because, well, that’s how things were done. Today, inspired in part by Sorge and Mogil’s work and spurred on by funders, pain researchers are opening their eyes to the spectrum of responses across sexes. Results are starting to trickle out, and it’s clear that certain pain pathways vary considerably, with immune cells and hormones having key roles in differing responses. © 2019 Springer Nature Publishing AG

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 26089 - Posted: 03.28.2019

National Institutes of Health scientists studying the progression of inherited and infectious eye diseases that can cause blindness have found that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. In contrast, the study findings indicated that microglia might delay disease progression. The discovery could apply to studies of inherited photoreceptor degeneration diseases in people, known as retinitis pigmentosa. In retinitis pigmentosa cases, scientists find an influx of microglia near the photoreceptors, which led to the belief that microglia contribute to retina damage. These inherited diseases appear to damage the retina similarly to prion diseases. Prion diseases are slow degenerative diseases of the central nervous system that occur in people and various other mammals. No vaccines or treatments are available, and the diseases are almost always fatal. Prion diseases primarily involve the brain but also can affect the retina and other tissues. Expanding on work published in 2018, scientists at NIH’s National Institute of Allergy and Infectious Diseases (NIAID) used an experimental drug to eliminate microglia in prion-infected mice. They studied prion disease progression in the retina to see if they could discover additional details that might be obscured in the more complex structure of the brain. When the scientists examined their prion-infected study mice, they found that photoreceptor damage still occurred – even somewhat faster – despite the absence of microglia. They also observed early signs of new prion disease in the photoreceptor cells, which may provide clues as to how prions damage photoreceptors. Their work appears in Acta Neuropathologica Communications.

Keyword: Vision; Prions
Link ID: 26088 - Posted: 03.28.2019

By Richard Schiffman The patient, a 48-year-old real estate professional in treatment for anxiety and mild depression, revealed that he had eaten three dozen oysters over the weekend. His psychiatrist, Dr. Drew Ramsey, an assistant clinical professor of psychiatry at Columbia University, was impressed: “You’re the only person I’ve prescribed them to who came back and said he ate 36!” Dr. Ramsey, the author of several books that address food and mental health, is a big fan of oysters. They are rich in vitamin B12, he said, which studies suggest may help to reduce brain shrinkage. They are also well stocked with long chain omega-3 fatty acids, deficiencies of which have been linked to higher risk for suicide and depression. But shellfish are not the only food he is enthusiastic about. Dr. Ramsey is a pioneer in the field of nutritional psychiatry, which attempts to apply what science is learning about the impact of nutrition on the brain and mental health. Dr. Ramsey argues that a poor diet is a major factor contributing to the epidemic of depression, which is the top driver of disability for Americans aged 15 to 44, according to a report by the World Health Organization. Together with Samantha Elkrief, a chef and food coach who sits in on many of his patient sessions, he often counsels patients on how better eating may lead to better mental health. The irony, he says, is that most Americans are overfed in calories yet starved of the vital array of micronutrients that our brains need, many of which are found in common plant foods. A survey published in 2017 by the Centers for Disease Control and Prevention reported that only one in 10 adults meets the minimal daily federal recommendations for fruit and vegetables — at least one-and-a-half to two cups per day of fruit and two to three cups per day of vegetables. © 2019 The New York Times Company

Keyword: Depression
Link ID: 26087 - Posted: 03.28.2019

Jon Hamilton When you're thirsty, a swig of fresh water brings instant relief. But gulp down some salty sea water and you'll still feel parched. That's because your brain is trying to keep the concentration of salt in your body within a very narrow range, says Zachary Knight, an associate professor in physiology at the University of California, San Francisco and an investigator with the Howard Hughes Medical Institute. "If you experience, for example, a 10 percent change, you would be very sick," he says. "A 20 percent change and you could die." Knight and a team of researchers wanted to know how the brain keeps that from happening. They report the results of their search in an article published Wednesday in the journal Nature. "There has to be a mechanism for the brain to track how salty the solutions that you drink are and use that to fine-tune thirst," Knight says. "But the mechanism was unknown." So Knight's team began studying brain cells known as thirst neurons. First, the team piped fresh water directly into the stomachs of some thirsty mice. "Within a minute or two, infusing water into the stomach rapidly turns off these thirst neurons in the brain," says Chris Zimmerman, a graduate student in Knight's lab who conducted the experiment. "And not only that," Zimmerman says, "if we give [the mouse] access to water it doesn't drink at all." © 2019 npr

Keyword: Miscellaneous
Link ID: 26086 - Posted: 03.28.2019

By Nicholas Bakalar Urban air pollution is associated with an increased risk for psychotic experiences in teenagers, researchers report. A study published in JAMA Psychiatry included 2,063 British teenagers whose health had been followed from birth through age 18. Almost a third of them said they had at least one psychotic experience, ranging from a mild feeling of paranoia to a severe psychotic symptom, since age 12. Researchers linked air pollution data to locations where they spent most of their time — at home, school or work. Compared with teenagers who lived where pollution was lowest, those in the most polluted areas were 27 percent to 72 percent more likely to have psychotic experiences, depending on the type of pollutant; exposure to two pollutants, nitrogen dioxide and nitrogen oxides, accounted for 60 percent of the association. The study controlled for family psychiatric history, maternal psychosis, substance use, socioeconomic status, neighborhood social characteristics and other factors, but it is an observational study that does not prove causation. “From this one study, we can’t say that air pollution causes psychosis,” said the lead author, Helen L. Fisher, a research psychologist at King’s College London. “The study only says that these things commonly occur together.” © 2019 The New York Times Company

Keyword: Schizophrenia; Neurotoxins
Link ID: 26085 - Posted: 03.28.2019

Laura Sanders A few months back, a new storefront appeared in my small Oregon town. Its shelves were packed with tinctures, jars of salve, coffee beans, bath bombs — even beard oil. This motley collection shared a single star ingredient: CBD. Produced by the cannabis plant, CBD is the straitlaced cousin of marijuana’s more famous component — the THC that delivers a mind-swirling high. CBD, or cannabidiol, has no such intoxicating effects on the mind. Yet the molecule has captured people’s attention in a profound way, sold as a remedy for pain, anxiety, insomnia and other ailments — all without the high. That neighborhood shop, CBD Scientific, is far from alone in its efforts to sell people on the benefits of CBD, which is found in both marijuana and hemp, two versions of the Cannabis sativa plant. CBD is popping up in products in pet stores, coffee shops and the health and beauty sections of mainstream grocery stores. It’s even being brewed into beer. I left the shop with a $5 bottle of water infused with “5,000,000 nanograms” of CBD. So far, messages of CBD’s purported health benefits come from people trying to sell CBD products — not from scientists, says Margaret Haney, a neurobiologist who directs the Marijuana Research Laboratory at Columbia University. A gaping chasm separates the surging CBD market and the scientific evidence backing it. While there are reasons to be excited about CBD, the science just isn’t there yet, Haney says. |© Society for Science & the Public 2000 - 2019

Keyword: Drug Abuse; Sleep
Link ID: 26084 - Posted: 03.27.2019

Laura Sanders SAN FRANCISCO — Seizures during sleep can scramble memories — a preliminary finding that may help explain why people with epilepsy sometimes have trouble remembering. The sleeping brain normally rehashes newly learned material, a nocturnal rehearsal that strengthens those memories. Neuroscientist Jessica Creery and her colleagues forced this rehearsal by playing certain sounds while nine people with epilepsy learned where on a screen certain pictures of common objects were located. Then, while the subjects later slept, the researchers played the sounds to call up some of the associated memories. This sneaky method of strengthening memories, called targeted memory reactivation, worked as expected for five people who didn’t have seizures during the process. When these people woke up, they remembered the picture locations reactivated by a tone better than those that weren’t reactivated during sleep, said Creery, of Northwestern University in Evanston, Ill. She presented the research March 25 at the annual meeting of the Cognitive Neuroscience Society. The opposite was true, however, for four people who had mild seizures, detected only by electrodes implanted deep in the brain, while they slept. For these people, memory reactivation during sleep actually worsened memories, making the reactivated memories weaker than the memories that weren’t reactivated during sleep. The combination of seizures and memory reactivation “seems like it’s actually scrambling the memory,” Creery says, a finding that suggest that seizures somehow accelerate forgetting. |© Society for Science & the Public 2000 - 2019

Keyword: Sleep; Epilepsy
Link ID: 26083 - Posted: 03.27.2019

By Karen Weintraub If the memory center of the human brain can grow new cells, it might help people recover from depression and post-traumatic stress disorder (PTSD), delay the onset of Alzheimer’s, deepen our understanding of epilepsy and offer new insights into memory and learning. If not, well then, it’s just one other way people are different from rodents and birds. For decades, scientists have debated whether the birth of new neurons—called neurogenesis—was possible in an area of the brain that is responsible for learning, memory and mood regulation. A growing body of research suggested they could, but then a Nature paper last year raised doubts. Now, a new study published today in another of the Nature family of journals—Nature Medicine—tips the balance back toward “yes.” In light of the new study, “I would say that there is an overwhelming case for the neurogenesis throughout life in humans,” Jonas Frisén, a professor at the Karolinska Institute in Sweden, said in an e-mail. Frisén, who was not involved in the new research, wrote a News and Views about the study in the current issue of Nature Medicine. Not everyone was convinced. Arturo Alvarez-Buylla was the senior author on last year’s Nature paper, which questioned the existence of neurogenesis. Alvarez-Buylla, a professor of neurological surgery at the University of California, San Francisco, says he still doubts that new neurons develop in the brain’s hippocampus after toddlerhood. © 2019 Scientific American

Keyword: Neurogenesis
Link ID: 26082 - Posted: 03.26.2019

By Emily Underwood One of the thorniest debates in neuroscience is whether people can make new neurons after their brains stop developing in adolescence—a process known as neurogenesis. Now, a new study finds that even people long past middle age can make fresh brain cells, and that past studies that failed to spot these newcomers may have used flawed methods. The work “provides clear, definitive evidence that neurogenesis persists throughout life,” says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto, Canada. “For me, this puts the issue to bed.” Researchers have long hoped that neurogenesis could help treat brain disorders like depression and Alzheimer’s disease. But last year, a study in Nature reported that the process peters out by adolescence, contradicting previous work that had found newborn neurons in older people using a variety of methods. The finding was deflating for neuroscientists like Frankland, who studies adult neurogenesis in the rodent hippocampus, a brain region involved in learning and memory. It “raised questions about the relevance of our work,” he says. But there may have been problems with some of this earlier research. Last year’s Nature study, for example, looked for new neurons in 59 samples of human brain tissue, some of which came from brain banks where samples are often immersed in the fixative paraformaldehyde for months or even years. Over time, paraformaldehyde forms bonds between the components that make up neurons, turning the cells into a gel, says neuroscientist María Llorens-Martín of the Severo Ochoa Molecular Biology Center in Madrid. This makes it difficult for fluorescent antibodies to bind to the doublecortin (DCX) protein, which many scientists consider the “gold standard” marker of immature neurons, she says. © 2019 American Association for the Advancement of Science

Keyword: Neurogenesis
Link ID: 26081 - Posted: 03.26.2019

By Bernardo Kastrup In his 2014 book, Our Mathematical Universe, physicist Max Tegmark boldly claims that “protons, atoms, molecules, cells and stars” are all redundant “baggage.” Only the mathematical apparatus used to describe the behavior of matter is supposedly real, not matter itself. For Tegmark, the universe is a “set of abstract entities with relations between them,” which “can be described in a baggage-independent way”—i.e., without matter. He attributes existence solely to descriptions, while incongruously denying the very thing that is described in the first place. Matter is done away with and only information itself is taken to be ultimately real. This abstract notion, called information realism is philosophical in character, but it has been associated with physics from its very inception. Most famously, information realism is a popular philosophical underpinning for digital physics. The motivation for this association is not hard to fathom. Indeed, according to the Greek atomists, if we kept on dividing things into ever-smaller bits, at the end there would remain solid, indivisible particles called atoms, imagined to be so concrete as to have even particular shapes. Yet, as our understanding of physics progressed, we’ve realized that atoms themselves can be further divided into smaller bits, and those into yet smaller ones, and so on, until what is left lacks shape and solidity altogether. At the bottom of the chain of physical reduction there are only elusive, phantasmal entities we label as “energy” and “fields”—abstract conceptual tools for describing nature, which themselves seem to lack any real, concrete essence. © 2019 Scientific American

Keyword: Consciousness
Link ID: 26080 - Posted: 03.26.2019

By Roni Caryn Rabin Pot brownies and other cannabis “edibles” like gummy bears that are sold online and where marijuana is legal may seem like harmless fun, but new research indicates that edibles may be more potent and potentially more dangerous than pot that is smoked or vaped. The new study analyzed thousands of cannabis-triggered emergency room visits in the greater Denver area, and found that edibles induced a disproportionate number of pot-related medical crises. Edibles were also more likely than inhaled pot to cause severe intoxication, acute psychiatric symptoms in people with no history of psychiatric illness and cardiovascular problems. Pot smokers, on the other hand, were more likely to have gastrointestinal complaints, including a vomiting condition called cannabinoid hyperemesis syndrome, and they were more likely to be hospitalized if they needed emergency care. Emergency room doctors in Colorado started noticing several years ago that “there were a lot of visits associated with edibles, even though they were not the predominant product used, and they seemed to be sicker compared to those who inhaled,” said Dr. Andrew Monte, an associate professor of medicine and the lead author of the new study, published in Annals of Internal Medicine on Monday. He also noted that the only deaths in Colorado that have been definitively attributed to cannabis involved edibles, and those deaths were surprisingly violent. In all three incidents, including a murder and a suicide in 2014 and another suicide in 2015, the pot users exhibited extremely erratic behavior after consuming edibles, according to news reports and trial testimony. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26079 - Posted: 03.26.2019

Amy Fleming ‘This is what my brain looks like,” says David Nutt, showing me an intense abstract painting by a friend of his that is sitting on the windowsill in his office. Nutt’s base at Hammersmith hospital has a cosy, lived-in feel – a stark contrast to the gleaming white laboratory he oversees as director of the neuropsychopharmacology unit at Imperial College London. Lab coats hang on a hook by the door, an ancient kettle sits in the corner and next to the painting is an unruly collection of objects that offer clues to his research interests: brain-shaped awards, an atomic model of Nutt’s invention for detecting inflammation in the brain of Alzheimer’s and Parkinson’s patients, a poster for the 1967 film LSD Flesh of Devil and two carved wooden mushrooms – the final items hinting at his role at Imperial’s psychedelic research group. All that is missing is something to do with the demon drink, to reflect Nutt’s ambitious plan to bring a safe synthetic alcohol substitute called Alcarelle to the masses. Nutt has long been developing a holy grail of molecules – also referred to as “alcosynth” – that will provide the relaxing and socially lubricating qualities of alcohol, but without the hangovers, health issues and the risk of getting paralytic. It sounds too good to be true, and when I discuss the notion with two alcohol industry experts, they independently draw parallels with plans to colonise Mars. Yet Alcarelle finding its way into bars and shops is starting to look like a possibility. Seed funding was raised in November 2018, allowing Nutt and his business partner, David Orren, to attempt to raise £20m from investors to bring Alcarelle to market. “The industry knows alcohol is a toxic substance,” says Nutt. “If it were discovered today, it would be illegal as a foodstuff. The safe limit of alcohol, if you apply food standards criteria, would be one glass of wine a year.” © 2019 Guardian News & Media Limited

Keyword: Drug Abuse
Link ID: 26078 - Posted: 03.26.2019

By Malia Wollan “If you’re talking to a puppy, increase the pitch of your voice and slow the tempo,” says Mario Gallego-Abenza, a cognitive biologist and an author of a recent study analyzing canine response to human speech. People tend to use that high-register, baby-talk tone with all dogs, but it’s really only puppies under a year old that seem to like it. “With older dogs, just use your normal voice,” he says. Dogs can learn words. One well-studied border collie named Rico knew 200 objects by name and, like a toddler, could infer the names of novel objects by excluding things with labels he already knew. Use facial expressions, gestures and possibly food treats while you talk. “Maintain eye contact,” Gallego-Abenza says. Research shows that even wolves are attuned to the attention of human faces and that dogs are particularly receptive to your gaze and pointing gestures. Scientists disagree about whether dogs are capable of full-blown empathy, but studies suggest canines feel at least a form of primitive empathy known as “emotional contagion.” In one study, dogs that heard recordings of infants crying experienced the same spike in cortisol levels and alertness as their human counterparts. You might find yourself wondering: Is this dog even listening to me? Does it care? Look for the sorts of social cues you would seek in an attentive human listener. “Is the dog looking at you?” Gallego-Abenza says. “Is it getting closer?” You are a social animal; connection with other social animals can make you feel better about the world. Gallego-Abenza, no longer studying dogs, is now working on a doctorate at the University of Vienna focused on vocalizations between ravens. Last year, a couple contacted him, sure that they were able to converse with the birds in their garden. “Humans have this rich language, and we really want to communicate,” he says. “We think that every other animal is the same, but they’re not.” Go ahead and talk to dogs, but consider letting wild creatures alone to their own intraspecies squeaks, howls and whispers. © 2019 The New York Times Company

Keyword: Animal Communication
Link ID: 26077 - Posted: 03.26.2019

By Gina Kolata Lucas was 5 before his parents, Bill and Marci Barton of Grand Haven, Mich., finally got an explanation for his difficulties standing up or climbing stairs. The diagnosis: muscular dystrophy. Mr. Barton turned to Google. “The first thing I read was, ‘no cure, in a wheelchair in their teens, pass in their 20s,” Mr. Barton said. “I stopped. I couldn’t read any more. I couldn’t handle it.” Then he found a reason to hope. For the first time ever, there are clinical trials — nearly two dozen — testing treatments that might actually stop the disease. The problem, as Mr. Barton soon discovered, is that the enrollment criteria are so restrictive that very few children qualify. As a result, families like the Bartons often are turned away. “There is so much hope, but it’s not for them,” said Kristin Stephenson, vice president of policy and advocacy at the Muscular Dystrophy Association in Chicago. Even for the parents whose lucky child qualifies, good news may be followed by agonizing, life-or-death choices. What treatments seem most promising? Should he be enrolled in a trial with a placebo arm? Should he be placed in a less risky study that aims to slow the progress of the disease but will not stop it? Should the parents take their chances with a trial now — or wait a year or two, as their child’s condition worsens, until something better comes along? Often there is no easy way to decide. “We talk to families every day,” said Debra Miller who founded the advocacy group, Cure Duchenne, after her son was diagnosed with the disease. “So many times they are looking at us and saying, ‘What do I do?’” © 2019 The New York Times Company

Keyword: Movement Disorders; Muscles
Link ID: 26076 - Posted: 03.25.2019

By Sandra G. Boodman “She never cried loudly enough to bother us,” recalled Natalia Weil of her daughter, who was born in 2011. Although Vivienne babbled energetically in her early months, her vocalizing diminished around the time of her first birthday. So did the quality of her voice, which dwindled from normal to raspy to little more than a whisper. Vivienne also was a late talker: She didn’t begin speaking until she was 2. Her suburban Maryland pediatrician initially suspected that a respiratory infection was to blame for the toddler’s hoarseness, and counseled patience. But after the problem persisted, the doctor diagnosed acid reflux and prescribed a drug to treat the voice problems reflux can cause. But Vivienne’s problem turned out to be far more serious — and unusual — than excess stomach acid. The day she learned what was wrong ranks among the worst of Weil’s life. “I had never heard of it,” said Weil, now 33, of her daughter’s diagnosis. “Most people haven’t.” The chronic illness seriously damaged Vivienne Weil’s voice. The 8-year-old has blossomed recently after a new treatment restored it. Her mother says she is eagerly making new friends and has become “a happy, babbly little girl.” (Natalia Weil) At first, Natalia, a statistician, and her husband, Jason, a photographer, were reassured by the pediatrician, who blamed a respiratory infection for their daughter’s voice problem. Her explanation sounded logical: Toddlers get an average of seven or eight colds annually. © 1996-2019 The Washington Post

Keyword: Language
Link ID: 26075 - Posted: 03.25.2019

By Laura Parker In the coming adventure video game Sea of Solitude, the main character — a young woman named Kay — navigates a partly submerged city as she faces a multitude of red-eyed scaly creatures. None are as terrifying as her own personal demons. As the game progresses, Kay realizes the creatures she is encountering are humans who turned into monsters when they became too lonely. To save herself, she fights to overcome her own loneliness. Kay was modeled after the game’s creative director, Cornelia Geppert of Jo-Mei Games, an independent game studio, who struggled after a 2013 breakup. “I felt like I was trapped in a cage,” Ms. Geppert, 37, said of her experience. Sea of Solitude, which Electronic Arts will publish this year, is among a growing number of video games that are tackling mental health issues. Last year, a game called Celeste explored depression and anxiety through a protagonist who had to avoid physical and emotional obstacles. In 2017’s fantasy action-adventure video game Hellblade: Senua’s Sacrifice, a young Celtic warrior deals with psychosis. Other games in recent years, including Night in the Woods and Pry, have delved into self-identity, anger issues and post-traumatic stress disorder. All followed the 2013 interactive fiction game Depression Quest, which asked players to step into the shoes of a character living with depression. These games are a far cry from the industry’s better-known story lines of battlefield heroics or the zombie apocalypse. But as a cultural conversation around mental health grows louder, makers of content are responding. According to the National Institute of Mental Health, one in five American adults lives with a mental illness. “Mental health is becoming a more central narrative in our culture, with greater efforts to normalize mental health challenges,” said Eve Crevoshay, executive director of Take This, a nonprofit that educates video game developers on best practices around portraying mental health. “With that trend comes response from creative industries, including games.” (Take This was founded in 2013 after the suicide of a video game journalist prompted a debate about the issue.) © 2019 The New York Times Company

Keyword: Depression
Link ID: 26074 - Posted: 03.25.2019

By Marlene Cimons It can be difficult to sleep while pregnant. Any number of issues can interrupt sleep, including the frequent need to urinate, back pain, abdominal discomfort and shortness of breath, among others. Moreover, disruptive sleep during pregnancy can be risky for the fetus, contributing to curbing growth. But a recent study suggests that excessive, undisturbed sleep may be a problem, too. Sleeping continuously for nine or more hours may be related to the danger of late stillbirth, that is, the loss or death of a baby before or during delivery. “There’s been a lot of public attention paid to sleep deprivation and its impact on health, but not as much to lengthy — perhaps too much — sleep, especially when it comes to pregnancy,” said Louise O’Brien, research associate professor in the neurology sleep disorders center and in obstetrics and gynecology at the University of Michigan. “Women often worry when they wake up several times during the night when they are pregnant, but it may be protective in this case.” O’Brien and her colleagues analyzed online surveys from 153 women who had experienced a late stillbirth (on or after 28 weeks of pregnancy) during the month previous to answering the questionnaire and 480 women with an ongoing third-trimester pregnancy or who had recently delivered a live born baby during the same period. The findings, recently published in the journal Birth, suggest a connection between long periods of undisturbed maternal sleep and stillbirth, independent of other risk factors. Stillbirth affects about 1 percent of all pregnancies, or about 24,000 annually in the United States, many of them unexplained, according to the Centers for Disease Control and Prevention. © 1996-2019 The Washington Post

Keyword: Sleep
Link ID: 26073 - Posted: 03.25.2019