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By Aaron E. Carroll More people in the United States are on antidepressants, as a percentage of the population, than any other country in the world. And yet the drugs’ efficacy has been hotly debated. Some believe that the short-term benefits are much more modest than widely thought, and that harms may outweigh benefits in the long run. Others believe that they work, and that they can be life-changing. Settling this debate has been much harder than you might think. It’s not that we lack research. Many, many studies of antidepressants can be found in the peer-reviewed literature. The problem is that this has been a prime example of publication bias: Positive studies are likely to be released, with negative ones more likely to be buried in a drawer. In 2008, a group of researchers made this point by doing a meta-analysis of antidepressant trials that were registered with the Food and Drug Administration as evidence in support of approvals for marketing or changes in labeling. Companies had to submit the results of registered trials to the F.D.A. regardless of the result. These trials also tend to have less data massaging — such as the cherry-picking of outcomes — than might be possible in journals. The researchers found 74 studies, with more than 12,500 patients, for drugs approved between 1987 and 2004. About half of these trials had “positive” results, in that the antidepressant performed better than a placebo; the other half were “negative.” But if you looked only in the published literature, you’d get a much different picture. Nearly all of the positive studies are there. Only three of the negative studies appear in the literature as negative. Twenty-two were never published, and 11 were published but repackaged so that they appeared positive. © 2018 The New York Times Company
Keyword: Depression
Link ID: 24739 - Posted: 03.12.2018
Emily Hanford Dyslexia is the most common learning disability, affecting tens of millions of people in the United States. But getting help for children who have it in public school can be a nightmare. "They wouldn't acknowledge that he had a problem," says Christine Beattie about her son Neil. "They wouldn't say the word 'dyslexia.' " Other parents, she says, in the Upper Arlington, Ohio, schools were having the same problem. The district in a suburb of Columbus wasn't identifying their children's dyslexia or giving them appropriate help. So, in 2011, the parents pooled their resources and hired a lawyer. "I was not surprised there was a group of students with dyslexia who were not getting the kind of instruction that they really needed," says Kerry Agins, an Ohio special education attorney who represented the Upper Arlington parents. She says the issue of public schools failing to address the needs of students with dyslexia is widespread, in Ohio and across the country. Agins advised the parents to file a group complaint against the district. Parents typically fight special education cases alone, seeking remedies one by one. But a group complaint, Agins told them, could force the school system to make broader change. Nineteen people signed the complaint, including parents, students and graduates of the Upper Arlington public schools. © 2018 npr
Keyword: Dyslexia
Link ID: 24738 - Posted: 03.12.2018
Researchers say they may have worked out why there is a natural loss of muscle in the legs as people age - and that it is due to a loss of nerves. In tests on 168 men, they found that nerves controlling the legs decreased by around 30% by the age of 75. This made muscles waste away, but in older fitter athletes there was a better chance of them being 'rescued' by nerves re-connecting. The scientists published their research in the Journal of Physiology. As people get older, their leg muscles become smaller and weaker, leading to problems with everyday movements such as walking up stairs or getting out of a chair. It is something that affects everyone eventually, but why it happens is not fully understood. Prof Jamie McPhee, from Manchester Metropolitan University, said young adults usually had 60-70,000 nerves controlling movement in the legs from the lumbar spine. But his research showed this changed significantly in old age. "There was a dramatic loss of nerves controlling the muscles - a 30-60% loss - which means they waste away," he said. "The muscles need to receive a proper signal from the nervous system to tell them to contract, so we can move around." The research team from Manchester Metropolitan University worked with researchers from the University of Waterloo, Ontario, and the University of Manchester. They looked at muscle tissue in detail using magnetic resonance imaging (MRI) and they recorded the electrical activity passing through the muscle to estimate the numbers and the size of surviving nerves. The good news is that healthy muscles have a form of protection: surviving nerves can send out new branches to rescue muscles and stop them wasting away. This is more likely to happen in fit people with large, healthy muscles, Prof McPhee said. © 2018 BBC.
Keyword: Movement Disorders; Development of the Brain
Link ID: 24737 - Posted: 03.12.2018
By George Musser, Satsuki Ayaya remembers finding it hard to play with other children when she was young, as if a screen separated her from them. Sometimes she felt numb, sometimes too sensitive; sometimes sounds were muted, sometimes too sharp. As a teenager, desperate to understand herself, she began keeping a journal. “I started to write my ideas in my notebooks, like: What’s happened to me? Or: What’s wrong with me? Or: Who am I?” she says, “I wrote, wrote, wrote. I filled maybe 40 notebooks.” Today, at 43, Ayaya has a better sense of who she is: She was diagnosed with autism when she was in her early 30s. As a Ph.D. student in the history and philosophy of science at the University of Tokyo, she is using the narratives from her teen years and after to generate hypotheses and suggest experiments about autism — a form of self-analysis called Tojisha-Kenkyu, introduced nearly 20 years ago by the disability-rights movement in Japan. In Ayaya’s telling, her autism involves a host of perceptual disconnects. For example, she feels in exquisite detail all the sensations that typical people readily identify as hunger, but she can’t piece them together. “It’s very hard for me to conclude I’m hungry,” she says. “I feel irritated, or I feel sad, or I feel something [is] wrong. This information is separated, not connected.” It takes her so long to realize she is hungry that she often feels faint and gets something to eat only after someone suggests it to her. © 2018 American Association for the Advancement of Science
Keyword: Autism
Link ID: 24736 - Posted: 03.10.2018
Ari Shapiro Millions of Americans use opioids to relieve pain. But many also struggle with addiction. This week, a report in JAMA, the journal of the American Medical Association, found that nonopioid painkillers — like acetaminophen and ibuprofen — were as effective as opioids at treating chronic back, hip and knee pain, and with fewer side effects. The findings raise a lot of questions about the right approach to managing pain, particularly chronic pain. So earlier this week, we asked listeners on Facebook and Twitter to share their questions about treating chronic pain. For answers, NPR's Ari Shapiro turned to Dr. Ajay Wasan, professor and vice chair for pain medicine at the University of Pittsburgh Medical Center. Isn't it true that ... acetaminophen can be very damaging to the liver, particularly with daily long-term use? — Emma Juneau For treatment of chronic pain, especially arthritis pain, higher doses of acetaminophen have been recommended, and there are good studies supporting that it can be quite effective for pain. You get a cumulative effect with the higher doses. Those can also be associated with a rise in liver enzymes for some people. It would be very rare for those enzymes to reach a toxic level that would cause liver damage, but we don't know what percent of people get that little rise in liver enzymes, or the chances that a slight increase in liver enzymes will lead to liver damage. It raises a very excellent point, that nonopiate medications have some side effects as well. We know anti-inflammatories can have significant side effects — in general the side effects of opioids are greater — but both nonopioids and opioids do have side effects. © 2018 npr
Keyword: Pain & Touch; Drug Abuse
Link ID: 24735 - Posted: 03.10.2018
By Elizabeth Pennisi Although it’s hard to believe that delicate nervous tissues could persist for hundreds of millions of years, that’s exactly what happened to the brains and eyes of some 15 ancestors of modern-day spiders and lobsters, called Kerygmachela kierkegaardi (after the famous philosopher Søren Kierkegaard). Found along the coast of north Greenland, the 518-million-year-old fossils contained enough preserved brains and eyes to help researchers write a brand-new history of the arthropod nervous system. Until now, many biologists had argued that ancient arthropods—which gave rise to today’s insects, spiders, and crustaceans—had a three-part brain and very simple eyes. Compound eyes, in which the “eye” is really a cluster of many smaller eyes, supposedly evolved later from a pair of legs that moved into the head and was modified to sense light. But these new fossils, which range from a few centimeters to 30 centimeters long, had a tiny, unsegmented brain, akin to what’s seen in modern velvet worms, researchers report today in Nature Communications. Despite the simple brain, Kerygmachela’s eyes were probably complex, perhaps enough to form rudimentary images. The eyes, indicated by shiny spots in the fossil’s small head, appear to be duplicated versions of the small, simple eyes seen today in soft, primitive arthropods called water bears and velvet worms. © 2018 American Association for the Advancement of Science.
Keyword: Evolution
Link ID: 24734 - Posted: 03.10.2018
Giorgia Guglielmi Every day, the human hippocampus, a brain region involved in learning and memory, creates hundreds of new nerve cells — or so scientists thought. Now, results from a study could upend this long-standing idea. A team of researchers has found that the birth of neurons in this region seems to stop once we become adults. A few years ago, the group looked at a well-preserved adult brain sample and spotted a few young neurons in several regions, but none in the hippocampus. So they decided to analyse hippocampus samples from dozens of donors, ranging from fetuses to people in their 60s and 70s. They concluded that the number of new hippocampal neurons starts to dwindle after birth and drops to near zero in adulthood. The results1, published in Nature on 7 March, are already raising controversy. If confirmed, the findings would be a “huge blow” not only to scientists in the field, but also to people with certain brain disorders, says Ludwig Aigner, a neuroscientist at Paracelsus Medical University in Salzburg, Austria. This is because researchers had hoped to harness the brain’s ability to generate new neurons to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s, he says. But Aigner and other neuroscientists are not fully persuaded by the findings, which contradict multiple lines of evidence that the hippocampus keeps producing neurons throughout a person’s life. “I wouldn’t close the books on [that],” says neuroscientist Heather Cameron of the US National Institute of Mental Health in Bethesda, Maryland. © 2018 Macmillan Publishers Limited
Keyword: Neurogenesis; Learning & Memory
Link ID: 24733 - Posted: 03.08.2018
By Ruth Williams When optogenetics burst onto the scene a little over a decade ago, it added a powerful tool to neuroscientists’ arsenal. Instead of merely correlating recorded brain activity with behaviors, researchers could control the cell types of their choosing to produce specific outcomes. Light-sensitive ion channels (opsins) inserted into the cells allow neuronal activity to be controlled by the flick of a switch. Nevertheless, MIT’s Edward Boyden says more precision is needed. Previous approaches achieved temporal resolution in the tens of milliseconds, making them a somewhat blunt instrument for controlling neurons’ millisecond-fast firings. In addition, most optogenetics experiments have involved “activation or silencing of a whole set of neurons,” he says. “But the problem is the brain doesn’t work that way.” When a cell is performing a given function—initiating a muscle movement, recalling a memory—“neighboring neurons can be doing completely different things,” Boyden explains. “So there is a quest now to do single-cell optogenetics.” Illumination techniques such as two-photon excitation with computer-generated holography (a way to precisely sculpt light in 3D) allow light to be focused tightly enough to hit one cell. But even so, Boyden says, if the targeted cell body lies close to the axons or dendrites of neighboring opsin-expressing cells, those will be activated too. © 1986-2018 The Scientist
Keyword: Brain imaging
Link ID: 24732 - Posted: 03.08.2018
Children and adults who spend a lot of time outside in the summer may be less likely to develop multiple sclerosis years later, a U.S. study suggests. Sun exposure is thought to lessen the risk of MS, a chronic disease in which a person's immune system targets nerve cells in the brain and spinal cord, leading to damage. It is estimated Canada may have among the highest prevalence of MS in the world. While the disease is common, little is known about its causes. But for more than 10 years, sun exposure has been thought to be linked to MS risk. Previously, researchers focused on how UV-B rays from sunlight seem protective during childhood years. Now, University of British Columbia neurology professor Helen Tremlett and her co-authors have taken a broader view, extending the association into adulthood. In Wednesday's online issue of the journal Neurology, Tremlett and her team report combing through data on 151 women with MS and 235 others of similar age without the disease who were all participating in the Nurses' Health Study based in Boston. The long-running U.S. study is one of the largest investigations into risk factors such as diet, hormones, and environment for major chronic diseases in women. "We found that just generally going out in the summer was a beneficial thing and didn't matter so much if you were exposing yourself to direct sunlight. It was just going out in the summer that was associated with a reduced risk," Tremlett said in an interview. ©2018 CBC/Radio-Canada.
Keyword: Multiple Sclerosis; Biological Rhythms
Link ID: 24731 - Posted: 03.08.2018
By Michelle Roberts Health editor, BBC News online Four dementia scientists have shared this year's 1m Euro brain prize for pivotal work that has changed our understanding of Alzheimer's disease. Profs John Hardy, Bart De Strooper, Michel Goedert, based in the UK, and Prof Christian Haass, from Germany, unpicked key protein changes that lead to this most common type of dementia. On getting the award, Prof Hardy said he hoped new treatments could be found. He is donating some of his prize money to care for Alzheimer's patients. Much of the drug discovery research that's done today builds on their pioneering work, looking for ways to stop the build-up of damaging proteins, such as amyloid and tau. Alzheimer's and other dementias affect 50 million people around the world, and none of the treatments currently available can stop the disease. Path to beating Alzheimer's Prof Hardy's work includes finding rare, faulty genes linked to Alzheimer's disease. These genetic errors implicated a build-up of amyloid as the event that kick-starts damage to nerve cells in Alzheimer's. This idea, known as the amyloid cascade hypothesis, has been central to Alzheimer's research for nearly 30 years. Together with Prof Haass, who is from the University of Munich, Prof Hardy, who's now at University College London, then discovered how amyloid production changes in people with rare inherited forms of Alzheimer's dementia. How one woman and her family transformed Alzheimer's research Prof Goedert's research at Cambridge University, meanwhile, revealed the importance of another damaging protein, called tau, while Prof De Stooper, who is the new director of the UK Dementia Research Institute at UCL, discovered how genetic errors that alter the activity of proteins called secretases can lead to Alzheimer's processes. Dr David Reynolds, Chief Scientific Officer at Alzheimer's Research UK, said: "Our congratulations go to all four of these outstanding scientists whose vital contributions have transformed our understanding of the complex causes of Alzheimer's disease. © 2018 BBC.
Keyword: Alzheimers
Link ID: 24730 - Posted: 03.08.2018
By CADE METZ SAN FRANCISCO — Machines are starting to learn tasks on their own. They are identifying faces, recognizing spoken words, reading medical scans and even carrying on their own conversations. All this is done through so-called neural networks, which are complex computer algorithms that learn tasks by analyzing vast amounts of data. But these neural networks create a problem that scientists are trying to solve: It is not always easy to tell how the machines arrive at their conclusions. On Tuesday, a team at Google took a small step toward addressing this issue with the unveiling of new research that offers the rough outlines of technology that shows how the machines are arriving at their decisions. “Even seeing part of how a decision was made can give you a lot of insight into the possible ways it can fail,” said Christopher Olah, a Google researcher. A growing number of A.I. researchers are now developing ways to better understand neural networks. Jeff Clune, a professor at University of Wyoming who now works in the A.I. lab at the ride-hailing company Uber, called this “artificial neuroscience.” Understanding how these systems work will become more important as they make decisions now made by humans, like who gets a job and how a self-driving car responds to emergencies. First proposed in the 1950s, neural networks are meant to mimic the web of neurons in the brain. But that is a rough analogy. These algorithms are really series of mathematical operations, and each operation represents a neuron. Google’s new research aims to show — in a highly visual way — how these mathematical operations perform discrete tasks, like recognizing objects in photos. © 2018 The New York Times Company
Keyword: Learning & Memory; Robotics
Link ID: 24729 - Posted: 03.07.2018
Bruce Bower People have evolved to sleep much less than chimps, baboons or any other primate studied so far. A large comparison of primate sleep patterns finds that most species get somewhere between nine and 15 hours of shut-eye daily, while humans average just seven. An analysis of several lifestyle and biological factors, however, predicts people should get 9.55 hours, researchers report online February 14 in the American Journal of Physical Anthropology. Most other primates in the study typically sleep as much as the scientists’ statistical models predict they should. Two long-standing features of human life have contributed to unusually short sleep times, argue evolutionary anthropologists Charles Nunn of Duke University and David Samson of the University of Toronto Mississauga. First, when humans’ ancestors descended from the trees to sleep on the ground, individuals probably had to spend more time awake to guard against predator attacks. Second, humans have faced intense pressure to learn and teach new skills and to make social connections at the expense of sleep. As sleep declined, rapid-eye movement, or REM — sleep linked to learning and memory (SN: 6/11/16, p. 15) — came to play an outsize role in human slumber, the researchers propose. Non-REM sleep accounts for an unexpectedly small share of human sleep, although it may also aid memory (SN: 7/12/14, p. 8), the scientists contend. “It’s pretty surprising that non-REM sleep time is so low in humans, but something had to give as we slept less,” Nunn says. |© Society for Science & the Public 2000 - 2018.
Keyword: Sleep; Evolution
Link ID: 24728 - Posted: 03.07.2018
By VERONIQUE GREENWOOD Ears are a peculiarly individual piece of anatomy. Those little fleshy seashells, whether they stick out or hang low, can be instantly recognizable in family portraits. And they aren’t just for show. Researchers have discovered that filling in an external part of the ear with a small piece of silicone drastically changes people’s ability to tell whether a sound came from above or below. But given time, the scientists show in a paper published Monday in the Journal of Neuroscience, the brain adjusts to the new shape, regaining the ability to pinpoint sounds with almost the same accuracy as before. Scientists already knew that our ability to tell where a sound is coming from arises in part from sound waves arriving at our ears at slightly different times. If a missing cellphone rings from the couch cushions to your right, the sound reaches your right ear first and your left ear slightly later. Then, your brain tells you where to look. But working out whether a sound is emanating from high up on a bookshelf or under the coffee table is not dependent on when the sound reaches your ears. Instead, said Régis Trapeau, a neuroscientist at the University of Montreal and author of the new paper, the determination involves the way the sound waves bounce off outer parts of your ear. Curious to see how the brain processed this information, the researchers set up a series of experiments using a dome of speakers, ear molds made of silicone and an fMRI machine to record brain activity. Before being fitted with the pieces of silicone, volunteers heard a number of sounds played around them and indicated where they thought the noises were coming from. In the next session, the same participants listened to the same sounds with the ear molds in. This time it was clear that something was very different. © 2018 The New York Times Company
Keyword: Hearing
Link ID: 24727 - Posted: 03.07.2018
By Michael Price When you hear a B-flat music note, do you see the color blue? Do the words in this sentence look red or green? If so, you may have synesthesia, a mysterious condition in which one sense consistently mingles with another. Now, for the first time, scientists have identified a handful of genes that might predispose people to synesthesia, offering a window to better understand disorders such as autism, which is also thought to involve abnormal brain connections. “It’s very exciting,” says Romke Rouw, a cognitive psychologist who studies synesthesia at the University of Amsterdam but who wasn’t involved in the study. “It provides a fascinating suggestion of a link between particular genetic variations and hyperconnectivity in the synesthetic brain.” For decades, many psychologists and neuroscientists were reluctant to research synesthesia. Some refused to acknowledge its existence, whereas others believed the phenomenon’s individual, subjective nature made it virtually impossible to study. But increasingly sophisticated survey methods have allowed scientists to confirm that some people—it’s unclear how many—do consistently and involuntarily experience this unusual condition. Synesthesia is thought to be at least somewhat heritable, as it frequently clusters within families. But genomic investigations so far have failed to turn up individual genes that might be responsible for it. © 2018 American Association for the Advancement of Science
Keyword: Development of the Brain
Link ID: 24726 - Posted: 03.06.2018
By DOUGLAS QUENQUA Claudio Mello was conducting research in Brazil’s Atlantic Forest about 20 years ago when he heard a curious sound. It was high-pitched and reedy, like a pin scratching metal. A cricket? A tree frog? No, a hummingbird. At least that’s what Dr. Mello, a behavioral neuroscientist at Oregon Health and Science University, concluded at the time. Despite extensive deforestation, the Atlantic Forest is one of Earth’s great cradles of biological diversity. It is home to about 2,200 species of animals, including about 40 species of hummingbirds. The variety of hummingbirds makes it difficult to isolate specific noises without sophisticated listening or recording devices. In 2015, Dr. Mello returned to the forest with microphones used to record high-frequency bat noises. The recordings he made confirmed that the calls were coming from black jacobin hummingbirds. The species is found in other parts of South America, too, and researchers are unsure whether the sound is emitted by males, females or both, although they have confirmed that juvenile black jacobins do not make them. When Dr. Mello and his team analyzed the noise — a triplet of syllables produced in rapid succession — they discovered it was well above the normal hearing range of birds. Peak hearing sensitivity for most birds is believed to rest between two to three kilohertz. (Humans are most sensitive to noises between one and four kilohertz.) “No one has ever described that a bird can hear even above 8, 9 kilohertz,” said Dr. Mello. But “the fundamental frequency of those calls was above 10 kilohertz,” he said. “That’s what was really amazing.” © 2018 The New York Times Company
Keyword: Hearing; Animal Communication
Link ID: 24725 - Posted: 03.06.2018
By Shawna Williams In recent years, US society has seen a sea change in the perception of transgender people, with celebrities such as Caitlyn Jenner and Laverne Cox becoming the recognizable faces of a marginalized population. Transgender rights have also become a mainstream political issue, and the idea that people should be referred to by the names and pronouns they find most fitting—whether or not these designations match those on their birth certificates, or align with the categories of male and female—is gaining acceptance. Yet a biological understanding of the contrast between the natal sex and the gender identity of transgender people remains elusive. In recent years, techniques such as functional magnetic resonance imaging (fMRI) have begun to yield clues to possible biological underpinnings of the condition known as gender dysphoria. In particular, researchers are identifying similarities and differences between aspects of the structure and function of the brains of trans- and cisgender individuals that could help explain the conviction that one’s gender and natal sex don’t match. The results may not have much effect on how gender dysphoria is diagnosed and treated, notes Baudewijntje Kreukels, who studies gender incongruence at VU University Medical Center in Amsterdam. “It’s really important that it will not be seen as, ‘When you see [gender dysphoria] in the brain, then it’s true.’” But the insights from such research could go a long way toward satisfying the desire of some transgender people to understand the roots of their condition, she adds. “In that way, it is good to find out if these differences between them and their sex assigned at birth are reflected by measures in the brain.” © 1986-2018 The Scientist
Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 24724 - Posted: 03.06.2018
By JANE E. BRODY When The New York Times hired me to write about science and health 52 years ago, I was 40 pounds overweight. I’d spent the previous three years watching my weight rise as I hopped from one diet to the next in a futile attempt to shed the pounds most recently gained. No amount of exercise, and I did plenty of it, could compensate for how much I ate when I abandoned the latest weight loss scheme. I had become a living example of the adage: A diet is something one goes on to go off. Even daylong fasting failed me. When I finally ate supper, I couldn’t stop eating until I fell asleep, and sometimes awoke the next morning with partly chewed food in my mouth. I had dieted myself into a binge-eating disorder, and that really scared me. Clearly, something had to change. I finally regained control when I stopped dieting. I decided that if I was going to be fat, at least I could be healthy. I made a plan to eat three nutritious, satisfying meals every day with one small snack, which helped me overcome the temptation to binge in response to deprivation. Much to my surprise, a month later I had lost 10 pounds — eating! Eating good food, that is, and plenty of it. I continued the regimen without difficulty because it was not a diet. It was a way to live and a healthy one at that. And I continued to lose, about two pounds a month. Two years later, all the excess weight was gone. I never gained it back and never again went on a diet. (Even with a twin pregnancy, I gained only 36 pounds and lost them all when my sons were born at 6 pounds 13 ounces each.) The greatest challenge to lasting weight loss, especially for someone like me with a food addiction, is the fact that no one can give up eating. Rather, one has to learn a better — and permanent — way to handle food. © 2018 The New York Times Company
Keyword: Obesity
Link ID: 24723 - Posted: 03.06.2018
By Virginia Morell A dog searching for a lost child is typically given an item of clothing to smell. But what does that scent “look” like? To find out, scientists tested 48 dogs, half of which had special police or rescue training. In a laboratory room, the scientists slid each dog’s favorite toy across the floor to a hiding place, while the dog waited in another room. One researcher then brought the dog to the testing room and pointed at the starting point of the odor trail and told the dog, “Look for it! Bring it!” In one trial, the dog found either its favored toy or—surprise!—a different item. Many of the surprised dogs continued searching for the toy used to lay the scent trail—an indication that they had a mental representation of what they expected to find, the scientists report today in the Journal of Comparative Psychology. Both family dogs and working dogs scored about the same on the tests, confirming previous studies showing that education doesn’t necessarily improve a dog’s performance. Previous studies have shown that horses have mental images of their owners and other horses—based on the sounds of their voices and whinnies. But scientists know little about how smell and cognition are linked in animals that rely heavily on smell—such as dogs, elephants, and rats. Now, we have a better idea at least for our pooches: They picture what they’re searching for. © 2018 American Association for the Advancement of Science.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 24722 - Posted: 03.06.2018
Simon Parkin In an unprecedented attack of candour, Sean Parker, the 38-year-old founding president of Facebook, recently admitted that the social network was founded not to unite us, but to distract us. “The thought process was: ‘How do we consume as much of your time and conscious attention as possible?’” he said at an event in Philadelphia in November. To achieve this goal, Facebook’s architects exploited a “vulnerability in human psychology”, explained Parker, who resigned from the company in 2005. Whenever someone likes or comments on a post or photograph, he said, “we… give you a little dopamine hit”. Facebook is an empire of empires, then, built upon a molecule. A neuroscientist explains: the need for ‘empathetic citizens’ - podcast Dopamine, discovered in 1957, is one of 20 or so major neurotransmitters, a fleet of chemicals that, like bicycle couriers weaving through traffic, carry urgent messages between neurons, nerves and other cells in the body. These neurotransmitters ensure our hearts keep beating, our lungs keep breathing and, in dopamine’s case, that we know to get a glass of water when we feel thirsty, or attempt to procreate so that our genes may survive our death. In the 1950s, dopamine was thought to be largely associated with physical movement after a study showed that Parkinsonism (a group of neurological disorders whose symptoms include tremors, slow movement and stiffness) was caused by dopamine deficiency. In the 1980s, that assumption changed following a series of experiments on rats by Wolfram Schultz, now a professor of neuroscience at Cambridge University, which showed that, inside the midbrain, dopamine relates to the reward we receive for an action. Dopamine, it seemed, was to do with desire, ambition, addiction and sex drive.
Keyword: Drug Abuse
Link ID: 24721 - Posted: 03.05.2018
By Dina Fine Maron After Richard Hodges pleaded guilty to cocaine possession and residential burglary, he appeared somewhat dazed and kept asking questions that had nothing to do with the plea process. That’s when the judge ordered that Hodges undergo a neuropsychological examination and magnetic resonance imaging (MRI) testing. Yet no irregularities turned up. Hodges, experts concluded, was faking it. His guilty plea would stand. But experts looking back at the 2007 case now say Hodges was part of a burgeoning trend: Criminal defense strategies are increasingly relying on neurological evidence—psychological evaluations, behavioral tests or brain scans—to potentially mitigate punishment. Defendants may cite earlier head traumas or brain disorders as underlying reasons for their behavior, hoping this will be factored into a court’s decisions. Such defenses have been employed for decades, mostly in death penalty cases. But as science has evolved in recent years, the practice has become more common in criminal cases ranging from drug offenses to robberies. Advertisement “The number of cases in which people try to introduce neurotechnological evidence in the trial or sentencing phase has gone up by leaps and bounds,” says Joshua Sanes, director of the Center for Brain Science at Harvard University. But such attempts may be outpacing the scientific evidence behind the technology, he adds. © 2018 Scientific American
Keyword: Consciousness
Link ID: 24720 - Posted: 03.05.2018


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