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By Benedict Carey At a recent visit to the Veterans Affairs clinic in the Bronx, Barry, a decorated Vietnam veteran, learned that he belonged to a very exclusive club. According to a new A.I.-assisted algorithm, he was one of several hundred V.A. patients nationwide, of six million total, deemed at imminent risk of suicide. The news did not take him entirely off guard. Barry, 69, who was badly wounded in the 1968 Tet offensive, had already made two previous attempts on his life. “I don’t like this idea of a list, to tell you the truth — a computer telling me something like this,” Barry, a retired postal worker, said in a phone interview. He asked that his surname be omitted for privacy. “But I thought about it,” Barry said. “I decided, you know, OK — if it’s going to get me more support that I need, then I’m OK with it.” For more than a decade, health officials have watched in vain as suicide rates climbed steadily — by 30 percent nationally since 2000 — and rates in the V.A. system have been higher than in the general population. The trends have defied easy explanation and driven investment in blind analysis: machine learning, or A.I.-assisted algorithms that search medical and other records for patterns historically associated with suicides or attempts in large clinical populations. Doctors have traditionally gauged patients’ risks by looking at past mental health diagnoses and incidents of substance abuse, and by drawing on experience and medical instinct. But these evaluations fall well short of predictive, and the artificially intelligent programs explore many more factors, like employment and marital status, physical ailments, prescription history and hospital visits. These algorithms are black boxes: They flag a person as at high risk of suicide, without providing any rationale. But human intelligence isn’t necessarily better at the task. “The fact is, we can’t rely on trained medical experts to identify people who are truly at high risk,” said Dr. Marianne S. Goodman, a psychiatrist at the Veterans Integrated Service Network in the Bronx, and a clinical professor of medicine at the Icahn School of Medicine at Mount Sinai. “We’re no good at it.” © 2020 The New York Times Company

Keyword: Depression
Link ID: 27600 - Posted: 11.30.2020

By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Keyword: Depression; Emotions
Link ID: 27599 - Posted: 11.30.2020

by Laura Dattaro Autistic boys with large brains in early childhood still have large brains in adolescence, according to a new study. Autistic girls, too, have brains that grow differently from those of their non-autistic peers. The findings challenge the long-standing idea that brain enlargement in autism is temporary. Previous studies indicated that young children on the spectrum have larger brains than their non-autistic peers but older people with autism do not. To explain the difference, researchers speculated that a pruning process follows early brain overgrowth. But the changes are a mirage, the researchers behind the new study say: Because having a large brain is associated with a low intelligence quotient (IQ) and severe autism traits, and because older children with such characteristics are often excluded from imaging studies, the prior results reflect only a lack of older participants with large brains. “This whole idea of this early overgrowth followed by normalization is just an artifact of sampling bias,” says lead investigator Christine Wu Nordahl, associate professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute. “It was sort of like, ‘Wow, why didn’t we ever think about this before?’ But it’s pretty clear that that’s what’s happening.” Autistic and non-autistic children also show different development patterns in their white matter — fibers that connect regions of the brain — in early childhood, a second study from Nordahl’s group shows. Some of the differences correlate with changes in the children’s autism traits over time. © 2020 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27598 - Posted: 11.30.2020

Janet M. Gibson Amusement and pleasant surprises – and the laughter they can trigger – add texture to the fabric of daily life. Those giggles and guffaws can seem like just silly throwaways. But laughter, in response to funny events, actually takes a lot of work, because it activates many areas of the brain: areas that control motor, emotional, cognitive and social processing. As I found when writing “An Introduction to the Psychology of Humor,” researchers now appreciate laughter’s power to enhance physical and mental well-being. People begin laughing in infancy, when it helps develop muscles and upper body strength. Laughter is not just breathing. It relies on complex combinations of facial muscles, often involving movement of the eyes, head and shoulders. Laughter – doing it or observing it – activates multiple regions of the brain: the motor cortex, which controls muscles; the frontal lobe, which helps you understand context; and the limbic system, which modulates positive emotions. Turning all these circuits on strengthens neural connections and helps a healthy brain coordinate its activity. By activating the neural pathways of emotions like joy and mirth, laughter can improve your mood and make your physical and emotional response to stress less intense. For example, laughing may help control brain levels of the neurotransmitter serotonin, similar to what antidepressants do. By minimizing your brain’s responses to threats, it limits the release of neurotransmitters and hormones like cortisol that can wear down your cardiovascular, metabolic and immune systems over time. Laughter’s kind of like an antidote to stress, which weakens these systems and increases vulnerability to diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Emotions; Neuroimmunology
Link ID: 27597 - Posted: 11.30.2020

By Concepción de León Pat Quinn, who helped raise $220 million to fight amyotrophic lateral sclerosis, or A.L.S., by promoting the Ice Bucket Challenge in 2014, died on Sunday, seven years after he learned he had the disease. He was 37. His death, at St. John’s Riverside Hospital in Yonkers, N.Y., was confirmed by the A.L.S. Association and in a post on his official Facebook page. Mr. Quinn did not create the challenge, in which people dumped buckets of ice water on their heads while pledging to donate money to fight A.L.S. But he and his friend Pete Frates, who also had A.L.S., are credited with amplifying it and helping to make it a sensation in the summer and fall of 2014, raising tens of millions of dollars for research and, perhaps nearly as important, wider awareness of the disease. “Pat changed the trajectory of the fight against A.L.S. forever,” Calaneet Balas, the president and chief executive of the A.L.S. Association, said in a statement on Sunday. “He inspired millions to get involved and care about people who are living with A.L.S.” A.L.S., also called Lou Gehrig’s disease, is a progressive neurodegenerative disorder that attacks the nerve cells that control voluntary muscle movements and leads to full paralysis. People with the disease typically live three to five years from the time of diagnosis, according to the National Institute of Neurological Disorders and Stroke. Shortly after Mr. Quinn learned he had A.L.S. in 2013, he created Quinn for the Win, a Facebook group, to raise awareness of the disease and to raise money to fight for a cure. Mr. Frates created his own page, Team Frate Train, with the same goal. In July 2014, Mr. Quinn and Mr. Frates saw another A.L.S. patient, Anthony Senerchia, do the Ice Bucket Challenge online. They created their own ice-bucket videos and shared the challenge with their followers. (Mr. Frates died last year at age 34.) In Her Words: Where women rule the headlines. From there, the campaign spread wildly, with Lady Gaga, Oprah Winfrey, LeBron James and scores of other celebrities participating and donating to the cause. The challenge raised $115 million for the A.L.S. Association and $220 million around the world for A.L.S. research in the span of just six weeks, the A.L.S. Association said. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27596 - Posted: 11.30.2020

by Josh Wilbur Jake Haendel was a hard-partying chef from a sleepy region of Massachusetts. When he was 28, his heroin addiction resulted in catastrophic brain damage and very nearly killed him. In a matter of months, Jake’s existence became reduced to a voice in his head. Jake’s parents had divorced when he was young. He grew up between their two homes in a couple of small towns just beyond reach of Boston, little more than strip malls, ailing churches and half-empty sports bars. His mother died of breast cancer when he was 19. By then, he had already been selling marijuana and abusing OxyContin, an opioid, for years. “Like a lot of kids at my school, I fell in love with oxy. If I was out to dinner with my family at a restaurant, I would go to the bathroom just to get a fix,” he said. He started culinary school, where he continued to experiment with opioids and cocaine. He hid his drug use from family and friends behind a sociable, fun-loving front. Inside, he felt anxious and empty. “I numbed myself with partying,” he said. After culinary school, he took a job as a chef at a local country club. At 25, Jake tried heroin for the first time, with a co-worker (narcotics are notoriously prevalent in American kitchens). By the summer of 2013, Jake was struggling to find prescription opioids. For months, he had been fending off the symptoms of opioid withdrawal, which he likened to “a severe case of the flu with an added feeling of impending doom”. Heroin offered a euphoric high, staving off the intense nausea and shaking chills of withdrawal. Despite his worsening addiction, Jake married his girlfriend, Ellen, in late 2016. Early in their relationship, Ellen had asked him if he was using heroin. He had lied without hesitation, but she soon found out the truth, and within months, the marriage was falling apart. “I was out of control, selling lots of heroin, using even more, spending a ridiculous amount of money on drugs and alcohol,” he said. In May 2017, Ellen noticed that he was talking funnily, his words slurred and off-pitch. “What’s up with your voice?” she asked him repeatedly.

Keyword: Consciousness; Drug Abuse
Link ID: 27595 - Posted: 11.27.2020

By Bethany Brookshire A hungry brain craves food. A lonely brain craves people. After spending a day completely isolated from anyone else, people’s brains perked up at the sight of social gatherings, like a hungry person’s brain seeing food, scientists report November 23 in Nature Neuroscience. Cognitive neuroscientist Livia Tomova, then at MIT, and her colleagues had 40 participants fast for 10 hours. At the end of the day, certain nerve cells in the midbrain fired up in response to pictures of pizza and chocolate cake. Those neurons — in the substantia nigra pars compacta and ventral tegmental area — produce dopamine, a chemical messenger associated with reward (SN: 8/27/15). On a different day, the same people underwent 10 hours of isolation (no friends, no Facebook and no Instagram). That evening, neurons in the same spot activated in response to pictures of people chatting or playing team sports. The more hunger or isolation the subject reported, the stronger the effect (SN: 10/4/17). In people who reported that they were generally more lonely, the social responses were blunted. “We don’t really know what causes that,” Tomova says. “Maybe being isolated doesn’t really affect them as much, because it’s something that is not that different, perhaps, from their everyday life.” The midbrain, which plays an important role in people’s motivation to seek food, friends, gambling or drugs, responds to food and social signals even when people aren’t hungry or lonely. After all, a person always could eat or hang out. But hunger and loneliness increased the reaction and made people’s responses specific to the thing they were missing. The findings “speak to our current state,” says Tomova, now at the University of Cambridge. COVID-19 has left many more socially isolated, putting mental as well as physical health at stake (SN: 3/29/20) and leaving people with cravings for more than food. “It’s important to look at the social dimension of this kind of crisis.” L. Tomova et al. Acute social isolation evokes midbrain craving responses similar to hunger. Nature Neuroscience. Published online November 23, 2020. doi: 10.1038/s41593-020-00742-z. = © Society for Science & the Public 2000–2020

Keyword: Stress; Obesity
Link ID: 27594 - Posted: 11.27.2020

By Lisa Feldman Barrett Five hundred million years ago, a tiny sea creature changed the course of history: It became the first predator. It somehow sensed the presence of another creature nearby, propelled or wiggled its way over, and deliberately ate it. This new activity of hunting started an evolutionary arms race. Over millions of years, both predators and prey evolved more complex bodies that could sense and move more effectively to catch or elude other creatures. Eventually, some creatures evolved a command center to run those complex bodies. We call it a brain. This story of how brains evolved, while admittedly just a sketch, draws attention to a key insight about human beings that is too often overlooked. Your brain’s most important job isn’t thinking; it’s running the systems of your body to keep you alive and well. According to recent findings in neuroscience, even when your brain does produce conscious thoughts and feelings, they are more in service to the needs of managing your body than you realize. And in stressful times like right now, this curious perspective on your mental life may actually help to lessen your anxieties. Much of your brain’s activity happens outside your awareness. In every moment, your brain must figure out your body’s needs for the next moment and execute a plan to fill those needs in advance. For example, each morning as you wake, your brain anticipates the energy you’ll need to drag your sorry body out of bed and start your day. It proactively floods your bloodstream with the hormone cortisol, which helps make glucose available for quick energy. Your brain runs your body using something like a budget. A financial budget tracks money as it’s earned and spent. The budget for your body tracks resources like water, salt and glucose as you gain and lose them. Each action that spends resources, such as standing up, running, and learning, is like a withdrawal from your account. Actions that replenish your resources, such as eating and sleeping, are like deposits. The scientific name for body budgeting is allostasis. It means automatically predicting and preparing to meet the body’s needs before they arise. © 2020 The New York Times Company

Keyword: Stress
Link ID: 27593 - Posted: 11.27.2020

By Katherine J. Wu For a rodent that resembles the love child of a skunk and a steel wool brush, the African crested rat carries itself with a surprising amount of swagger. The rats “very much have the personality of something that knows it’s poisonous,” says Sara Weinstein, a biologist at the University of Utah and the Smithsonian Conservation Biology Institute who studies them. In sharp contrast to most of their skittish rodent kin, Lophiomys imhausi lumber about with the languidness of porcupines. When cornered, they fluff up the fur along their backs into a tip-frosted mohawk, revealing rows of black-and-white bands that run like racing stripes down their flanks — and, at their center, a thicket of specialized brown hairs with a honeycomb-like texture. Those spongy hairs contain a poison powerful enough to bring an elephant to its knees, and are central to Dr. Weinstein’s recent research, which confirmed ideas about how this rat makes itself so deadly. Give them a chance and African crested rats will take nibbles from the branch of a poison arrow tree. It’s not for nutrition. Instead, they will chew chunks of the plants and spit them back out into their fur, anointing themselves with a form of chemical armor that most likely protects them from predators like hyenas and wild dogs. The ritual transforms the rats into the world’s only known toxic rodents, and ranks them among the few mammals that borrow poisons from plants. Dr. Weinstein’s research, which was published last week in the Journal of Mammalogy, is not the first to document the crested rats’ bizarre behavior. But the new paper adds weight to an idea described nearly a decade ago, and offers an early glimpse into the animals’ social lives. First documented in the scientific literature in 1867, the rarely-glimpsed African crested rat “has captured so much interest for so long,” said Kwasi Wrensford, a behavioral ecologist at the University of California, Berkeley who wasn’t involved in the study. “We’re now just starting to unpack what makes this animal tick.” © 2020 The New York Times Company

Keyword: Neurotoxins; Learning & Memory
Link ID: 27592 - Posted: 11.27.2020

By Lindsay Gray When Herbert Weinstein stood trial for the murder of his wife in 1992, his attorneys were struck by the measured calm with which he recounted her death and the events leading up to it. He made no attempt to deny that he was culpable, and yet his stoicism in the face of his wildly uncharacteristic actions led his defense to suspect that he might not be. Weinstein underwent neuroimaging tests, which confirmed what his attorneys had suspected: a cyst had impinged upon large parts of Weinstein’s frontal lobe, the seat of impulse control in the brain. On these grounds, they reasoned he should be found not guilty by reason of insanity, despite Weinstein’s free admission of guilt. Guilt is difficult to define, but it pervades every aspect of our lives, whether we’re chastising ourselves for skipping a workout, or serving on the jury of a criminal trial. Humans seem to be hardwired for justice, but we’re also saddled with a curious compulsion to diagram our own emotional wiring. This drive to assign a neurochemical method to our madness has led to the generation of vast catalogs of neuroimaging studies that detail the neural underpinnings of everything from anxiety to nostalgia. In a recent study, researchers now claim to have moved us one step closer to knowing what a guilty brain looks like. Since guilt carries different weight depending on context or culture, the authors of the study chose to define it operationally as the awareness of having harmed someone else. A series of functional magnetic resonance imaging (fMRI) experiments across two separate cohorts, one Swiss and one Chinese, revealed what they refer to as a “guilt-related brain signature” that persists across groups. Since pervasive guilt is a common feature in severe depression and PTSD, the authors suggest that a neural biomarker for guilt could offer more precise insight into these conditions and, potentially, their treatment. But brain-based biomarkers for complex human behaviors also lend themselves to the more ethically fraught discipline of neuroprediction, an emergent branch of behavioral science that combines neuroimaging data and machine learning to forecast how an individual is likely to act based on how their brain scans compare to those of other groups. © 2020 Scientific American,

Keyword: Stress; Brain imaging
Link ID: 27591 - Posted: 11.21.2020

by Peter Hess / Mutations in a top autism gene called SYNGAP1 slow the rate at which zebrafish digest food and pass waste. The findings may explain why some people with SYNGAP1 mutations have gastrointestinal (GI) problems. Researchers presented the unpublished work on Tuesday and Wednesday at the 2020 International SYNGAP1 Scientific Conference, which took place virtually because of the coronavirus pandemic. They also began recruiting people with SYNGAP1 mutations at the meeting for an ongoing study of gut function. “It’s been in the literature, this link between GI symptoms and [autism], for a long time, with not a lot of progress on the mechanisms,” says lead researcher Julia Dallman, associate professor of biology at the University of Miami in Florida, who presented the findings on Wednesday. In the brain, SYNGAP1 functions mainly at synapses, or the junctions between neurons, and helps the cells exchange chemical messages. Mutations in the gene are strongly linked to autism, seizures, intellectual disability and sleep problems. Prompted by families’ anecdotal reports of constipation, reflux and overeating in people with SYNGAP1 mutations, Dallman and her colleagues decided to explore the gene’s role in the gut. The young zebrafish’s transparent skin allowed the researchers to trace the movement of microscopic fluorescent beads — mixed into the fish’s food — through the gut. In this way, they measured how quickly and how strongly the digestive tract moves food and waste. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27590 - Posted: 11.21.2020

By Kashmir Hill and Jeremy White There are now businesses that sell fake people. On the website Generated.Photos, you can buy a “unique, worry-free” fake person for $2.99, or 1,000 people for $1,000. If you just need a couple of fake people — for characters in a video game, or to make your company website appear more diverse — you can get their photos for free on ThisPersonDoesNotExist.com. Adjust their likeness as needed; make them old or young or the ethnicity of your choosing. If you want your fake person animated, a company called Rosebud.AI can do that and can even make them talk. These simulated people are starting to show up around the internet, used as masks by real people with nefarious intent: spies who don an attractive face in an effort to infiltrate the intelligence community; right-wing propagandists who hide behind fake profiles, photo and all; online harassers who troll their targets with a friendly visage. The A.I. system sees each face as a complex mathematical figure, a range of values that can be shifted. Choosing different values — like those that determine the size and shape of eyes — can alter the whole image. For other qualities, our system used a different approach. Instead of shifting values that determine specific parts of the image, the system first generated two images to establish starting and end points for all of the values, and then created images in between. The creation of these types of fake images only became possible in recent years thanks to a new type of artificial intelligence called a generative adversarial network. In essence, you feed a computer program a bunch of photos of real people. It studies them and tries to come up with its own photos of people, while another part of the system tries to detect which of those photos are fake. The back-and-forth makes the end product ever more indistinguishable from the real thing. The portraits in this story were created by The Times using GAN software that was made publicly available by the computer graphics company Nvidia. © 2020 The New York Times Company

Keyword: Attention
Link ID: 27589 - Posted: 11.21.2020

Researchers at the National Eye Institute (NEI) have decoded brain maps of human color perception. The findings, published today in Current Biology, open a window into how color processing is organized in the brain, and how the brain recognizes and groups colors in the environment. The study may have implications for the development of machine-brain interfaces for visual prosthetics. NEI is part of the National Institutes of Health. “This is one of the first studies to determine what color a person is seeing based on direct measurements of brain activity,” said Bevil Conway, Ph.D., chief of NEI’s Unit on Sensation, Cognition and Action, who led the study. “The approach lets us get at fundamental questions of how we perceive, categorize, and understand color.” The brain uses light signals detected by the retina’s cone photoreceptors as the building blocks for color perception. Three types of cone photoreceptors detect light over a range of wavelengths. The brain mixes and categorizes these signals to perceive color in a process that is not well understood. To examine this process, Isabelle Rosenthal, Katherine Hermann, and Shridhar Singh, post-baccalaureate fellows in Conway’s lab and co-first authors on the study, used magnetoencephalography or “MEG,” a 50-year-old technology that noninvasively records the tiny magnetic fields that accompany brain activity. The technique provides a direct measurement of brain cell activity using an array of sensors around the head. It reveals the millisecond-by-millisecond changes that happen in the brain to enable vision. The researchers recorded patterns of activity as volunteers viewed specially designed color images and reported the colors they saw.

Keyword: Vision; Brain imaging
Link ID: 27588 - Posted: 11.21.2020

By Lisa Sanders, M.D. It started to drizzle just moments after the 24-year-old man crossed the finish line of the 2017 New York City Marathon. It was his first marathon, and he felt both elated and exhausted as the medal given for completing the brutal race was draped around his neck. A goody bag containing an energy drink was put in his left hand. It felt strangely heavy. His whole body ached and trembled with fatigue, but somehow that left arm felt even more tired. Unconcerned, he switched the bag to his right hand and went in search of his partner. Recovery took longer than he expected. It was a day and a half before his legs were strong enough for him to walk down stairs facing forward, rather than the sideways shuffle that his tired muscles insisted on. But by the end of the week he felt mostly normal. Only that left shoulder remained tired, sore and stiff. He went to a nearby walk-in clinic just south of City Hall. The nurse practitioner who examined him thought he had a rotator-cuff injury. She recommended a nonsteroidal anti-inflammatory like ibuprofen, physical therapy and time. The ibuprofen didn’t help much; neither did the physical therapy. That weekend he headed to the gym — his first workout since the race. He did his usual set of reps on his right biceps and triceps. But when he transferred the 25-pound dumbbell to his left hand, it seemed heavier. He struggled through two curls, but on the third the muscles in his arm turned wobbly. He grabbed the weight with his right hand and lowered it to the ground. By the time he got home, straightening his aching arm was excruciating, as if the muscles were too short to allow a full extension. That scared him. And it only got worse. The next day his whole arm was achy and tight. He couldn’t even work on his computer. Thinking back, the young runner questioned the assumption — shared by both him and the nurse practitioner — that the injury had occurred during the race. Now he suspected it started weeks earlier. © 2020 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27587 - Posted: 11.21.2020

Diana Kwon It all began with a cough. Three years ago Tracey McNiven, a Scottish woman in her mid-30s, caught a bad chest infection that left her with a persistent cough that refused to subside, even after medication. A few months later strange symptoms started to appear. McNiven noticed numbness spreading through her legs and began to feel that their movement was out of her control. When she walked, she felt like a marionette, with someone else pulling the strings. Over the course of two weeks the odd loss of sensation progressively worsened. Then, one evening at home, McNiven's legs collapsed beneath her. “I was lying there, and I felt like I couldn't breathe,” she recalls. “I couldn't feel below my waist.” McNiven's mother rushed her to the hospital where she remained for more than half a year. During her first few weeks in the hospital, McNiven endured a barrage of tests as doctors tried to uncover the cause of her symptoms. It could be a progressive neurodegenerative condition such as motor neuron disease, they thought. Or maybe it was multiple sclerosis, a disease in which the body's own immune cells attack the nervous system. Bafflingly, however, the brain scans, blood tests, spinal taps and everything else came back normal. McNiven's predicament is not uncommon. According to one of the most comprehensive assessments of neurology clinics to date, roughly a third of patients have neurological symptoms that are deemed to be either partially or entirely unexplained. These may include tremor, seizures, blindness, deafness, pain, paralysis and coma and can parallel those of almost any neurological disease. In some patients, such complications can persist for years or even decades; some people require wheelchairs or cannot get out of bed. Although women are more often diagnosed than men, such seemingly inexplicable illness can be found in anyone and across the life span. © 2020 Scientific American

Keyword: Attention; Emotions
Link ID: 27586 - Posted: 11.18.2020

Jon Hamilton During deep sleep, the brain appears to wash away waste products that increase the risk for Alzheimer's disease. A host of new research studies suggest that this stage of sleep — when dreams are rare and the brain follows a slow, steady beat – can help reduce levels of beta-amyloid and tau, two hallmarks of the disease. "There is something about this deep sleep that is helping protect you," says Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley. The research comes after decades of observations linking poor sleep to long-term problems with memory and thinking, Walker says. "We are now learning that there is a significant relationship between sleep and dementia, particularly Alzheimer's disease." The strongest evidence involves deep sleep, he says. That's when body temperature drops and the brain begins to produce slow, rhythmic electrical waves. So Walker and a team of scientists set out to answer a question: "Can I look into your future and can I accurately estimate how much beta-amyloid you're going to accumulate over the next two years, the next four years, the next six years, simply on the basis of your sleep tonight?" To find out, Walker's team studied 32 people in their 70s who had taken part in a sleep study that looked for the slow electrical waves that signal deep sleep. None of the participants had memory problems. the brain cells of people with Alzheimer's. © 2020 npr

Keyword: Sleep; Alzheimers
Link ID: 27585 - Posted: 11.18.2020

By Jessica Wapner We are living through an inarguably challenging time. The U.S. has been facing its highest daily COVID-19 case counts yet. Uncertainty and division continue to dog the aftermath of the presidential election. And we are heading into a long, cold winter, when socializing outdoors will be less of an option. We are a nation and a world under stress. But Andrew Huberman, a neuroscientist at Stanford University who studies the visual system, sees matters a bit differently. Stress, he says, is not just about the content of what we are reading or the images we are seeing. It is about how our eyes and breathing change in response to the world and the cascades of events that follow. And both of these bodily processes also offer us easy and accessible releases from stress. Huberman’s assertions are based on both established and emerging science. He has spent the past 20 years unraveling the inner workings of the visual system. In 2018, for example, his lab reported its discovery of brain pathways connected with fear and paralysis that respond specifically to visual threats. And a small but growing body of research makes the case that altering our breathing can alter our brain. In 2017 Mark Krasnow of Stanford University, Jack Feldman of the University of California, Los Angeles, and their colleagues identified a tight link between neurons responsible for controlling breathing and the region of the brain responsible for arousal and panic. This growing understanding of how vision and breathing directly affect the brain—rather than the more nebulous categories of the mind and feelings—can come in handy as we continue to face mounting challenges around the globe, across the U.S. and in our own lives. Scientific American spoke with Huberman about how it all works. © 2020 Scientific American

Keyword: Stress; Vision
Link ID: 27584 - Posted: 11.18.2020

Terry Gross Food science writer Harold McGee was in the middle of writing Nose Dive, his book about the science of smell, when he woke up one morning and realized that he couldn't smell his own coffee. Loss of smell has since become associated with COVID-19. In McGee's case, it was the byproduct of a sinus infection. McGee remembers feeling panicked. "I have friends in the kind of clinical side of taste and smell research. And so I immediately contacted them to find out what I could do and why this had happened," he says. "And they basically said, 'You're going to have to wait and see.' " Over the course of a few months, McGee's sense of smell gradually returned. But he still remembers what it was like to live in an odorless world. "It's the kind of thing where you don't notice something until it's gone," he says. "I spent less and less time cooking. There was no point in going out to restaurants because I wasn't really going to enjoy it." McGee's new book is about how smell is essential to our sense of taste, why things smell the way they do and the ways different chemicals combine to create surprising (and sometimes distasteful) odors. "One of the great pleasures of delving into smells in general was discovering over and over again that things that we enjoy in foods are actually found elsewhere in the world," he says. "And in as unlikely places as cat pee and human sweat, for example." © 2020 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27583 - Posted: 11.16.2020

Linda Geddes Many of the side-effects attributed to statins could be down to the “nocebo effect”, which occurs when someone expects to experience negative symptoms – even if the drug is a placebo – a study suggests. Statins are one of the most widely prescribed drugs in the UK, taken by nearly eight million people to reduce their risk of cardiovascular disease by lowering cholesterol levels. Yet, despite their effectiveness, up to a fifth of people stop taking them because of side-effects, such as fatigue, muscle aches, joint pain and nausea. Clinical studies have suggested, however, the incidence of side-effects is far lower. Researchers led by Frances Wood and Dr James Howard at Imperial College London recruited 60 patients who had been on statins, but stopped taking them owing to adverse effects. They were persuaded to resume treatment, and given four bottles containing atorvastatin, four bottles containing identical-looking placebo pills and four empty bottles, to be taken in a randomly prescribed order over the course of a year – including four months taking no pills. Each day, they recorded any side-effects on a smartphone, ranking their intensity from zero to 100. The researchers found 90% of symptoms experienced by the patients were present when they took placebo tablets. Also, 24 patients stopped taking tablets for at least one month of the trial, citing intolerable side-effects – amounting to 71 stoppages in total. Of these, 31 occurred during placebo months and 40 were during statin months. The results were published in the New England Journal of Medicine. © 2020 Guardian News & Media Limited

Keyword: Pain & Touch; Attention
Link ID: 27582 - Posted: 11.16.2020

By Catherine Zuckerman It’s 3 a.m. and you’ve been struggling for hours to fall asleep. Morning draws nearer and your anxiety about being exhausted the next day intensifies — yet again. If this sounds familiar, you’re not alone. Among the many disruptions of 2020, insomnia may rank high on the list. Data on how the pandemic has affected sleep is limited because biomedical research can take years to shake out and most studies to date have been small. But evidence from China and Europe suggests that prolonged confinement is altering sleep in adults as well as children. Doctors in the United States are seeing it too. “I think Covid and the election have affected sleep and could be considered a kind of trauma,” said Nancy Foldvary-Schaefer, director of the Cleveland Clinic Sleep Disorders Center. “A lot of people that I talk to — patients and non-patients and colleagues and family — have more anxiety generally now probably because of these two stressors, and high anxiety is clearly associated with insomnia.” Whether you’re suddenly tossing and turning at bedtime or waking up in the middle of the night, the first step toward better sleep is to figure out what’s triggering your insomnia. Once you do that, you can take action to prevent it from becoming chronic — a clinical sleep disorder that should be treated by a sleep-medicine specialist. Stressful and upsetting experiences like the death of a loved one or the loss of a job — two widespread realities of Covid-19 — are known psychological triggers for insomnia. If your insomnia is tied to such an event, the quickest way to get help is to call your doctor. One thing many doctors suggest is cognitive behavioral therapy, or C.B.T. C.B.T., or C.B.T.-I. for insomnia, is a standard treatment for both acute and chronic insomnia and includes a variety of techniques. Meditation, mindfulness and muscle relaxation can help people whose sleep problems are tied to a stressful event. C.B.T. for insomnia typically lasts from six to eight weeks and “works in about two-thirds to three-quarters of patients,” said Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles, David Geffen School of Medicine. © 2020 The New York Times Company

Keyword: Sleep; Stress
Link ID: 27581 - Posted: 11.16.2020