By John Horgan I’m already getting pushback against my free online book Mind-Body Problems: Science, Subjectivity & Who We Really Are. Tom Clark knocks me for not giving more credit to straight-forward materialism, or naturalism, as he prefers to call it. Meanwhile, Deepak Chopra, while defending an anti-materialistic view, compares my pluralistic approach “to giving every player in a junior soccer match a trophy.” Good one, Deepak! See “Discussion” for these and other comments. It was precisely because people have divergent views of the mind-body problem that I decided to write a book about it. The mind-body problem is the knottiest of all mysteries. It encompasses puzzles such as consciousness (which David Chalmers calls “the hard problem”), free will, the self, morality and the meaning of life (which Owen Flanagan, a subject of my book, calls “the really hard problem”). Another way of posing the mind-body problem is simply by asking, Who are we, really? Sages as diverse as Buddha, Plato, Kant and Douglas Hofstadter (to whom I devote a chapter of Mind-Body Problems) have offered answers to this question. In the early 1990s, Francis Crick said that science had finally given us the tools to solve the problem once and for all. In his 1994 book The Astonishing Hypothesis, he spells out the implications of his ultra-materialistic creed “You,” your joys and your sorrows, your memories and your ambitions, your sense of personal identity and free will, are in fact no more than the behavior of a vast assembly of nerve cells and their associated molecules. As Lewis Carroll’s Alice might have phrased it: “You’re nothing but a pack of neurons.” © 2018 Scientific American

Keyword: Consciousness
Link ID: 25543 - Posted: 10.08.2018

By Emily Underwood The ornately folded outer layer of the human brain, the cerebral cortex, has long received nearly all the credit for our ability to perform complex cognitive tasks such as composing a sonata, imagining the plot of a novel or reflecting on our own thoughts. One explanation for how we got these abilities is that the cortex rapidly expanded relative to body size as primates evolved — the human cortex has 10 times the surface area of a monkey’s cortex, for example, and 1,000 times that of a mouse. But the cortex is not the only brain region that has gotten bigger and more complex throughout evolution. Nestled beneath the cortex, a pair of egg-shaped structures called the thalamus has also grown, and its wiring became much more intricate as mammals diverged from reptiles. The thalamus — from the Greek thalamos, or inner chamber — transmits 98 percent of sensory information to the cortex, including vision, taste, touch and balance; the only sense that doesn’t pass through this brain region is smell. The thalamus also conducts motor signals and relays information from the brain stem to the cortex, coordinating shifts in consciousness such as waking up and falling asleep. Scientists have known for decades that the thalamus faithfully transmits information about the visual world from the retina to the cortex, leading to the impression that it is largely a messenger of sensory information rather than a center of complex cognition itself. But that limited, passive view of the thalamus is outdated, maintains Michael Halassa, a neuroscientist at the Massachusetts Institute of Technology who recently coauthored (with Ralf D. Wimmer and Rajeev V. Rikhye) an article in the Annual Review of Neuroscience exploring the thalamus’s role. © 2018 Annual Reviews, Inc

Keyword: Attention
Link ID: 25542 - Posted: 10.08.2018

By Jane E. Brody Jane R. Madell, a pediatric audiology consultant and speech-language pathologist in Brooklyn, N.Y., wants every parent with a child who is born hearing-impaired to know that it is now possible for nearly all children with severe hearing loss to learn to listen and speak as if their hearing were completely normal. “Children identified with hearing loss at birth and fitted with technology in the first weeks of life blend in so well with everyone else that people don’t realize there are so many deaf children,” she told me. With the appropriate hearing device and auditory training for children and their caregivers during the preschool years, even those born deaf “will have the ability to learn with their peers when they start school,” Dr. Madell said. “Eighty-five percent of such children are successfully mainstreamed. Parents need to know that listening and spoken language is a possibility for their children.” Determined to get this message out to all who learn their children lack normal hearing, Dr. Madell and Irene Taylor Brodsky produced a documentary, “The Listening Project,” to demonstrate the enormous help available through modern hearing assists and auditory training. Among the “stars” in the film, all of whom grew up deaf or severely hearing-impaired, are Dr. Elizabeth Bonagura, an obstetrician-gynecologist and surgeon; Jake Spinowitz, a musician; Joanna Lippert, a medical social worker, and Amy Pollick, a psychologist. All started out with hearing aids that helped them learn to speak and understand spoken language. But now all have cochlear implants that, as Ms. Lippert put it, “really revolutionized my world” when, at age 11, she became the first preteen to get a cochlear implant at New York University Medical Center. © 2018 The New York Times Company

Keyword: Hearing
Link ID: 25541 - Posted: 10.08.2018

Rhitu Chatterjee Paige Thesing has struggled with insomnia since high school. "It takes me a really long time to fall asleep — about four hours," she says. For years, her mornings were groggy and involved a "lot of coffee." After a year of trying sleep medication prescribed by her doctor, she turned to the internet for alternate solutions. About four months ago, she settled on a mobile phone meditation app called INSCAPE. "It's about a 30-minute soundtrack, and it starts with a woman kind of telling you to relax and instructing your breathing," explains Thesing. "Then it goes into sounds — relaxing noises. There's wind chimes, some atmospheric music playing..." She uses the app every night and falls asleep within 15 or 20 minutes. "So, definitely a big improvement from four hours," she says. Thesing is not alone. Chronic insomnia affects an estimated 10-15 percent of adults, and another 25-35 percent struggle with sleep issues occasionally. And like Thesing, a growing number of insomniacs are turning to mobile phone apps to lull them to sleep. On Twitter and Facebook, NPR asked its audience if they have used a mobile phone app to help manage insomnia. Nearly 100 people wrote back suggesting a range of apps, including podcasts created to put a listener to sleep. "These are usually relaxation strategies, white noise, meditation," Jason Ong, an associate professor of neurology specializing in sleep at Northwestern University's Feinberg School of Medicine. He studies non-pharmacological treatments for various sleep disorders and treats patients at the university's Sleep Medicine clinic. "It's not that there's something wrong with those apps. It's a reasonable first thing to try." © 2018 npr

Keyword: Sleep
Link ID: 25540 - Posted: 10.08.2018

Rory Cellan-Jones Technology correspondent Chinese tech giant Tencent and London medical firm Medopad have teamed up to use artificial intelligence in the diagnosis of Parkinson's Disease. A camera captures the way patients move their hands to determine the severity of their symptoms. The research team has trained the system with existing videos of patients who have been assessed by doctors, working with King's College Hospital in London. "We use the AI to measure the deterioration of Parkinson's disease patients without the patient wearing any sensors or devices," explains Dr Wei Fan, head of the Tencent Medical AI lab. The aim is to speed up a motor function assessment process, which usually takes more than half an hour. Using smartphone technology developed by Medopad, the hope is that patients could be assessed within three minutes - and might not even have to attend a hospital. Medopad is a London-based firm that has been developing apps and wearable devices to monitor patients with various medical conditions. It has been growing fast - but is a minnow compared with Tencent, which is spearheading China's huge investment in AI. Medopad's chief executive Dan Vahdat sais that there was no British company that could match what Tencent offered as a partner. "Our ambition is to impact a billion patients around the world - and to be able to get to that kind of scale we need to work with partners that have international reach," he told me. © 2018 BBC

Keyword: Parkinsons
Link ID: 25539 - Posted: 10.08.2018

By Neal Pollack AUSTIN, Tex. — My name is Neal, and I’m a marijuana addict. A year ago I wouldn’t have said that, because it would have meant giving up marijuana. I would rather have given up breathing. When I had my first cup of coffee in the morning, I pressed the little button on my vape pen, waited for the blue glow, took a huge inhale and then blew it into the mug so that I could suck in the THC and caffeine at the same time. Then I took another hit, and another. In the afternoons, I’d smoke a bowl, or pop a gummy bear, or both. At night, I got high before eating dinner or watching the ballgame. Maybe I’d stop getting stoned a little bit before bed, but what was the point? If I went to bed high, I could wake up high, too. What a time for people to get stoned! Marijuana has left the counterculture, exploded into the mainstream and transformed into a multibillion-dollar industry. Cannabis is now an essential part of any hip wellness and beauty regimen. Netflix offers a marijuana-themed cooking show. Cannabis should be legal. It has medical uses. Millions of people, most of them black and Latino men, have unjustly gone to jail for selling what should have been easily available in stores. States with the political courage to legalize it have seen their tax rolls bloom and have created thousands of jobs. Also, it’s delicious. But I’m not a child with intractable epilepsy, or a veteran with PTSD, or a person who just wants to chill a little, or Willie Nelson. Unless you count writing articles about marijuana, I’m not profiting from the industry. I’m just a middle-aged house dad with a substance-abuse problem. Like most pot addicts in denial, I spent years telling myself that marijuana isn’t addictive, and so I didn’t have a problem. But clearly I did. And I’m not the only one who suffers this way. © 2018 The New York Times Company

Keyword: Drug Abuse
Link ID: 25538 - Posted: 10.08.2018

By Erin Blakemore Are you depressed? If you’re not sure, it’s no surprise. Perpetual sadness isn’t the only symptom. Anger, back pain, sleep disturbances and even indecisiveness could all be signs of depression. One in six adults will experience depression in their life, but you can’t get help if you’re not sure you need it. Your doctor can screen for depression, so it’s worth asking on your next visit. Isolation and social withdrawal are common among people with depression. But it’s still possible to seek help during these periods. If you can’t face the thought of visiting your doctor, you can find information and assistance on your computer or smartphone. Screening for Mental Health’s online screening program gives a brief survey. It then tells you whether your answers are consistent with depression and provides materials to bring to your next doctor’s visit and a list of resources. Although it’s not a formal diagnosis, it’s a place to start to seek help. Crisis Text Line can connect you with a trained crisis counselor who can take you from crisis to cool down, all via text. The service is free and confidential. It’s available to people experiencing any kind of crisis. Text HOME to 741741 to get started. The National Alliance on Mental Illness can also connect you to mental-health resources, including help for depression. Visit nami.org/Find-Support or call the NAMI Helpline, 800-950-NAMI, between 10 a.m. and 6 p.m. Eastern. © 1996-2018 The Washington Post

Keyword: Depression
Link ID: 25537 - Posted: 10.08.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist

Keyword: Obesity; Neuroimmunology
Link ID: 25536 - Posted: 10.06.2018

By Elizabeth Pennisi The melodious call of many birds comes from a mysterious organ buried deep within their chests: a one-of-a-kind voice box called a syrinx. Now, scientists have concluded that this voice box evolved only once, and that it represents a rare example of a true evolutionary novelty. “It’s something that comes out of nothing,” says Denis Dubuole, a geneticist at the University of Geneva in Switzerland who was not involved with the work. “There is nothing that looks like a syrinx in any related animal groups in vertebrates. This is very bizarre.” Reptiles, amphibians, and mammals all have a larynx, a voice box at the top of the throat that protects the airways. Folds of tissue there—the vocal cords—can also vibrate to enable humans to talk, pigs to grunt, and lions to roar. Birds have larynxes, too. But the organ they use to sing their tunes is lower down—where the windpipe splits to go into the two lungs. The syrinx, named in 1872 after a Greek nymph who was transformed into panpipes, has a similar structure: Both are tubes supported by cartilage with folds of tissue. The oldest known syrinx belongs to a bird fossil some 67 million years old; that’s about the same time all modern bird groups became established. To figure out where the bizarre organ came from, Julia Clarke, a paleontologist at the University of Texas in Austin, who made the syrinx discovery in 2013, assembled a team of developmental biologists, evolutionary biologists, and other researchers. © 2018 American Association for the Advancement of Science.

Keyword: Animal Communication; Evolution
Link ID: 25535 - Posted: 10.06.2018

By Jim Hopper On Monday October 1, Republican senators released “Analysis of Dr. Christine Blasey Ford’s Allegations,” a memo written by Rachel Mitchell, the prosecutor they hired to question Christine Blasey Ford and review other evidence. Ms. Mitchell’s “analysis” includes descriptions of Ford’s memories as not “consistent,” lacking “key details,” and uncorroborated by people she said were at the “party.” In the final two weeks of September, many Americans learned from the media (e.g., USA Today, Rolling Stone, Vox, NBC News, NPR) the distinction that memory researchers make between “central” and “peripheral” details, terms that reflect the commonsense understanding that we remember things that had significance to us and got our attention. Many people have also learned that stress and trauma greatly enhance the differential storage of central over peripheral details, and that the central details of traumatic experiences can get burned into our brains for the rest of our lives. But most people already knew that too, even if they hadn’t stopped to think about it. Advertisement These past few weeks, I’ve tried to help with that learning, by talking with reporters and sharing the expert testimony on trauma and memory that I could have provided to senators and the country, which was published by Scientific American and on my blog with Psychology Today, Sexual Assault and the Brain. There I explain central versus peripheral details, that stress amplifies their differential encoding and storage, and how sexual assault survivors—like traumatized soldiers and police—may protect themselves by clinging for years to superficial descriptions of events, which keep the most disturbing details out of their minds. © 2018 Scientific American

Keyword: Learning & Memory; Stress
Link ID: 25534 - Posted: 10.06.2018

By Carl Zimmer People of Asian and European descent — almost anyone with origins outside of Africa — have inherited a sliver of DNA from some unusual ancestors: the Neanderthals. These genes are the result of repeated interbreeding long ago between Neanderthals and modern humans. But why are those genes still there 40,000 years after Neanderthals became extinct? As it turns out, some of them may protect humans against infections. In a study published on Thursday, scientists reported new evidence that modern humans encountered new viruses — including some related to influenza, herpes and H.I.V. — as they expanded out of Africa roughly 70,000 years ago. Some of those infections may have been picked up directly from Neanderthals. Without immunity to pathogens they had never encountered, modern humans were particularly vulnerable. “We were actually able to not only say, ‘Yes, modern humans and Neanderthals exchanged viruses,’” said David Enard, an evolutionary biologist at the University of Arizona and co-author of the new paper, published in the journal Cell. “We are able to start saying something about which types of viruses were involved.” But if Neanderthals made us sick, they also helped keep us well. Some of the genes inherited from them through interbreeding also protected our ancestors from these infections, just as they protected the Neanderthals. Lluis Quintana-Murci, a geneticist at the Pasteur Institute in Paris who was not involved in the new research, said that until now, scientists had not dreamed of getting such a glimpse at the distant medical history of our species. “Five years ago, we would never have imagined that,” he said. © 2018 The New York Times Company

Keyword: Evolution; Genes & Behavior
Link ID: 25533 - Posted: 10.05.2018

Doris Tsao is a neuroscientist who uses brain imaging technology, electrical recording techniques, and mathematical modeling. Though Tsao has explored several aspects of visual processing, such as the perception of depth and color, her most notable line of research has focused on uncovering the fundamental neural principles that underlie one of the brain’s most highly specialized and socially important tasks: recognizing a face. Prior neuroscientific research has identified regions in the inferior temporal cortex of monkeys that are particularly responsive to faces. These earlier studies, however, shed little light on how face-responsive cells within these regions might be organized and integrated into a system. Early in her career, Tsao confirmed with functional magnetic resonance imaging (fMRI) that the visual cortex of the macaque monkey shows face-selective activation in six small “patches” in each hemisphere of the brain. She then used data from fMRI brain scans as a map to guide the placement of single-neuron, electrical recording probes, which demonstrated that certain neurons display highly attuned sensitivity to faces, but not to other categories of objects, and that different patches across the brain’s cortex are integrated in a network dedicated to the visual processing of faces. Through other elegantly designed experiments, Tsao showed that the sensitivity of specific neurons can be further analyzed by measuring their responses to cartoon representations of faces with subtle variations in features and that certain features, such as facial shape and inter-eye distance, elicit particularly frequent and robust responses. © 2018 John D. and Catherine T. MacArthur Foundation

Keyword: Vision
Link ID: 25532 - Posted: 10.05.2018

By Benedict Carey Dr. Bernard J. Carroll, whose studies of severe depression gave psychiatry the closest thing it has to a “blood test” for a mental disorder, and who later became one of the field’s most relentless critics, helping to expose pervasive corruption in academic research, died on Sept. 10 at his home in Carmel, Calif. He was 77. His wife, Sylvia Carroll, said the cause was lung cancer. Dr. Carroll was all of 28 when he published a paper that seemed to herald a new age of psychiatry, one rooted in biology rather than Freudian theory. Trained both in endocrinology and psychiatry, he applied a test from that first specialty — the dexamethasone suppression test, or DST — to people with mood problems. The test measures the body’s ability to suppress its own surges of cortisol, a stress hormone. In a 1968 article in The British Medical Journal, Dr. Carroll announced that when the test was administered to people with the severest species of depression — a paralyzing gloom then called melancholia, or endogenous depression — their bodies were shown to have trouble suppressing the hormone. People with other kinds of mood disorders had normal scores. The test did not mean that failure to suppress cortisol caused depression, just that it was associated with it. “I thought of it as a confirmatory test, to support a diagnosis, not to make one,” Dr. Carroll, known as Barney, said, in a recent interview in his home, “and possibly as a way to monitor progress in treatment.” It didn’t happen. In 1980, experts revising psychiatry’s influential diagnostic manual eliminated distinctions in kinds of depression. Melancholia was lumped with many other mild and moderate conditions under the classification “major depressive disorder.” Soon after, modern antidepressants hit the market, and pharmaceutical companies paid top academics around the world to help interpret studies, massage data and promote their products. The field chased the drugs, and the money, and learned nothing about the biology of mental disorders. © 2018 The New York Times Company

Keyword: Depression
Link ID: 25531 - Posted: 10.05.2018

By Laura M. Holson Researchers from Johns Hopkins University have recommended that psilocybin, the active compound in hallucinogenic mushrooms, be reclassified for medical use, potentially paving the way for the psychedelic drug to one day treat depression and anxiety and help people stop smoking. The suggestion to reclassify psilocybin from a Schedule I drug, with no known medical benefit, to a Schedule IV drug, which is akin to prescription sleeping pills, was part of a review to assess the safety and abuse of medically administered psilocybin. Before the Food and Drug Administration can be petitioned to reclassify the drug, though, it has to clear extensive study and trials, which can take more than five years, the researchers wrote. The analysis was published in the October print issue of Neuropharmacology, a medical journal focused on neuroscience. The study comes as many Americans shift their attitudes toward the use of some illegal drugs. The widespread legalization of marijuana has helped demystify drug use, with many people now recognizing the medicinal benefits for those with anxiety, arthritis and other physical ailments. Psychedelics, like LSD and psilocybin, are illegal and not approved for medical or recreational use. But in recent years scientists and consumers have begun rethinking their use to combat depression and anxiety. “We are seeing a demographic shift, particularly among women,” said Matthew Johnson, an associate professor of psychiatry and behavioral sciences at Johns Hopkins and one of the study’s authors. Among the research he has conducted, he said, “we’ve had more females in our studies.” © 2018 The New York Times Company

Keyword: Depression
Link ID: 25530 - Posted: 10.04.2018

By Michael Shermer Anthony Bourdain (age 61). Kate Spade (55). Robin Williams (63). Aaron Swartz (26). Junior Seau (43). Alexander McQueen (40). Hunter S. Thompson (67). Kurt Cobain (27). Sylvia Plath (30). Ernest Hemingway (61). Alan Turing (41). Virginia Woolf (59). Vincent van Gogh (37). By the time you finish reading this list of notable people who died by suicide, somewhere in the world another person will have done the same, about one every 40 seconds (around 800,000 a year), making suicide the 10th leading cause of death in the U.S. Why? According to the prominent psychologist Jesse Bering of the University of Otago in New Zealand, in his authoritative book Suicidal: Why We Kill Ourselves (University of Chicago Press, 2018), “the specific issues leading any given person to become suicidal are as different, of course, as their DNA—involving chains of events that one expert calls ‘dizzying in their variety.’” Indeed, my short list above includes people with a diversity of ages, professions, personality and gender. Depression is commonly fingered in many suicide cases, yet most people suffering from depression do not kill themselves (only about 5 percent Bering says), and not all suicide victims were depressed. “Around 43 percent of the variability in suicidal behavior among the general population can be explained by genetics,” Bering reports, “while the remaining 57 percent is attributable to environmental factors.” Having a genetic predisposition for suicidality, coupled with a particular sequence of environmental assaults on one's will to live, leads some people to try to make the pain stop. In Bering's case, it first came as a closeted gay teenager “in an intolerant small Midwestern town” and later with unemployment at a status apex in his academic career (success can lead to unreasonably high standards for happiness, later crushed by the vicissitudes of life). Yet most oppressed gays and fallen academics don't want to kill themselves. “In the vast majority of cases, people kill themselves because of other people,” Bering adduces. “Social problems—especially a hypervigilant concern with what others think or will think of us if only they knew what we perceive to be some unpalatable truth—stoke a deadly fire.” © 2018 Scientific American

Keyword: Depression
Link ID: 25529 - Posted: 10.04.2018

Susan Milius It’s a lovely notion, but tricky to prove. Still, lemurs sniffing around wild fruits in Madagascar are bolstering the idea that animal noses contributed to the evolution of aromas of fruity ripeness. The idea sounds simple, says evolutionary ecologist Omer Nevo of the University of Ulm in Germany. Plants can use mouth-watering scents to lure animals to eat fruits, and thus spread around the seeds. But are those odors really advertising, or are they just the way fruits happen to smell as they ripen? For some wild figs and a range of other fruits in eastern Madagascar, a strong scent of ripeness does seem to have evolved in aid of allure, Nevo and his colleagues argue October 3 in Science Advances. A lot of fruit collecting and odor chemistry suggest that fruits dispersed by lemurs, with their sensitive noses, change more in scent than fruits that rely more on birds with acute color vision. Earlier studies had sniffed around several species, such as figs. But for a broader look, Nevo and his colleagues analyzed scents from 25 other kinds of fruits as well as five kinds of figs. All grew wild in a “really magnificent” mountainous rainforest preserved as a park in eastern Madagascar, Nevo says. The researchers classified 19 of the plants as depending largely on red-bellied and other local lemurs to spread seeds. Most of these lemurs are red-green color-blind, not great for spotting the ripe fruits among foliage. But the researchers following some lemurs foraging in daylight noticed that sniffing at fruits was a big deal for the primates. |© Society for Science & the Public 2000 - 2018

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 25528 - Posted: 10.04.2018

By Simon Makin Neuroscientists know a lot about how individual neurons operate but remarkably little about how large numbers of them work together to produce thoughts, feelings and behavior. They need a wiring diagram for the brain—known as a connectome—to identify the circuits that underlie the organ’s functions. Now researchers at Cold Spring Harbor Laboratory and their colleagues have developed an innovative brain-mapping technique and used it to trace the connections emanating from nearly 600 neurons in a mouse brain’s main visual area in just three weeks. This technology could someday be used to help understand disorders thought to involve atypical brain wiring, such as autism or schizophrenia. The technique works by tagging cells with genetic “bar codes.” Researchers inject viruses into mice brains, where the viruses direct cells to produce random 30-letter RNA sequences (consisting of the nucleotide “letters” G, A, U and C). The cells also create a protein that binds to these RNA bar codes and drags them the length of each neuron’s output wire, or axon. The researchers later dissect the mice brains into target regions and sequence the cells in each area, enabling them to determine which tagged neurons are connected to which regions. The team found that neurons in a mouse’s primary visual cortex typically send outputs to multiple other visual areas. It also discovered that most cells fall into six distinct groups based on which regions—and how many of them—they connect to. This finding suggests there are subtypes of neurons in a mouse’s primary visual cortex that perform different functions. “Because we have so many neurons, we can do statistics and start understanding the patterns we see,” says Cold Spring Harbor’s Justus Kebschull, co-lead author of the study, which was published in April in Nature. © 2018 Scientific American

Keyword: Brain imaging; Autism
Link ID: 25527 - Posted: 10.04.2018

By Gretchen Reynolds Are we born to be physically lazy? A sophisticated if disconcerting new neurological study suggests that we probably are. It finds that even when people know that exercise is desirable and plan to work out, certain electrical signals within their brains may be nudging them toward being sedentary. The study’s authors hope, though, that learning how our minds may undermine our exercise intentions could give us renewed motivation to move. Exercise physiologists, psychologists and practitioners have long been flummoxed by the difference between people’s plans and desires to be physically active and their actual behavior, which usually involves doing the opposite. Few of us exercise regularly, even though we know that it is important for health and well being. Typically, we blame lack of time, facilities or ability. But recently an international group of researchers began to wonder whether part of the cause might lie deeper, in how we think. For an earlier review, these scientists had examined past research about exercise attitudes and behavior and found that much of it showed that people sincerely wished to be active. In computer-based studies, for example, they would direct their attention to images of physical activity and away from images related to sitting and similar languor. But, as the scientists knew, few people followed through on their aims to be active. So maybe, the scientists thought, something was going on inside their skulls that dampened their enthusiasm for exercise. To find out, they recruited 29 healthy young men and women. All of the volunteers told the scientists that they wanted to be physically active, although only a few of them regularly were. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25526 - Posted: 10.04.2018

By Michael Mosley Horizon Could taking a placebo, a pill which contains nothing but ground rice, really help cure back pain? The placebo effect is well studied but at the same time something of a mystery. The word placebo comes from the Latin "I shall please" and is associated with images of quack doctors selling dodgy cures. Yet it is also an important part of modern clinical trials, where patients are given either a placebo (sometimes called a dummy pill) or an active drug (without knowing which is which) and researchers then look to see if the drug outperforms the placebo, or vice versa. But what if you decided to do a placebo-controlled trial on back pain, with a twist? The twist being that everyone, unknowingly, was getting placebo? Would people taking the pills get better anyway? That's what we set out to test for BBC2's Horizon programme, Can my brain cure my body? With the help of Dr Jeremy Howick. an expert on the placebo effect from University of Oxford, we set out to see if we could cure real back pain with fake pills. It would be the largest experiment of its kind ever carried out in the UK, with 100 people from Blackpool taking part. Some were asked to act as a "control" group. The rest were told that they were taking part in a study - where they might receive the placebo or a powerful new painkiller. What they weren't told was that they would all get placebos, capsules containing nothing but ground rice. The pills were authentic looking and based on years of research. They were blue-and-white-striped, because that has been shown to have a greatest painkilling effect. They came in bottles, carefully labelled, warning of potential side effects and sternly reminding patients to keep out of the hands of children. All very convincing. © 2018 BBC

Keyword: Pain & Touch
Link ID: 25525 - Posted: 10.04.2018

Sarah Boseley Health editor Half of all those taking antidepressants experience withdrawal problems when they try to give them up and for millions of people in England, these are severe, according to a new review of the evidence commissioned by MPs. Guidance from the National Institute of Health and Care Excellence (Nice), which says withdrawal symptoms “are usually mild and self-limiting over about one week” urgently needs to be changed, say the review authors. Dr James Davies from the University of Roehampton and Prof John Read from the University of East London say the high rate of withdrawal symptoms may be part of the reason people are staying on the pills for longer. They cannot cope, so carry on taking the drugs, or their doctors assume they have relapsed and write another prescription. The review was commissioned by the all-party parliamentary group for prescribed drug dependence and follows a long debate about the Nice guidance, which critics say is out of date. Modern antidepressants of the SSRI class, such as Prozac (fluoxetine) and Seroxat (paroxetine), were marketed in part on their safety. People were unable to harm themselves by overdosing as they could on benzodiazepines like valium and stopping the drugs was said to be easier. There have been plenty of anecdotal accounts of withdrawal symptoms, which include dizziness, vertigo, nausea, insomnia, headaches, tiredness and difficulties concentrating. But the Nice guidance said in 2004 that the withdrawal symptoms were slight and short-lived and was re-adopted without further evidence in 2009. It is similar to the US guidance, which says symptoms usually resolve within one to two weeks. © 2018 Guardian News and Media Limited

Keyword: Depression
Link ID: 25524 - Posted: 10.03.2018