Chapter 16. None
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By Tori Rodriguez Uric acid is almost always mentioned in the context of gout, an inflammatory type of arthritis that results from excessive uric acid in the blood. It may be surprising, then, that it has also been linked with a vastly different type of disease: bipolar disorder. Elevated uric acid has been observed in patients with acute mania, and reducing uric acid improves symptoms. New evidence supports its potential as a treatment target. Uric acid is a by-product of the breakdown of compounds called purines, found in many foods and manufactured by the body. High levels of uric acid can indicate that these compounds, such as the neurotransmitter adenosine, are being broken down too readily in the body. “Adenosine might play a key role in neurotransmission and neuromodulation, having sedative, anticonvulsant and antiaggressive effects,” says physician Francesco Bartoli, a researcher at the University of Milano-Bicocca in Italy. Bartoli's new study, published in May in the Journal of Psychosomatic Research, examined uric acid levels in 176 patients with bipolar disorder or another severe mental illness and 89 healthy controls. The results show that bipolar disorder was the only diagnosis significantly linked with levels of uric acid. Excess uric acid was found to be linked to male gender, metabolic syndrome, waist size and triglyceride levels. Beyond the too rapid breakdown of adenosine, other potential explanations for increased uric acid include the metabolic abnormalities often present in people with bipolar disorder and frequent consumption of purine-rich foods and drinks, such as liver, legumes, anchovies and alcohol. Fructose consumption can also be a problem because the sugar inhibits uric acid excretion. Dietary interventions may reduce levels, but medication is typically required if dietary changes are insufficient. © 2016 Scientific American
Link ID: 22790 - Posted: 10.26.2016
Andrew Solomon A new virtual-reality attraction planned for Knott’s Berry Farm in Buena Park, Calif., was announced last month in advance of the peak haunted-house season. The name, “Fear VR 5150,” was significant. The number 5150 is the California psychiatric involuntary commitment code, used for a mentally ill person who is deemed a danger to himself or others. Upon arrival in an ersatz “psychiatric hospital exam room,” VR 5150 visitors would be strapped into a wheelchair and fitted with headphones. “The VR headset puts you in the middle of the action inside the hospital,” an article in The Orange County Register explained. “One patient seems agitated and attempts to get up from a bed. Security officers try to subdue him. A nurse gives you a shot (which you will feel), knocking you out. When you wake up in the next scene, all hell has broken loose. Look left, right and down, bloody bodies lie on the floor. You hear people whimpering in pain.” Knott’s Berry Farm is operated by Ohio-based Cedar Fair Entertainment Company, and Fear VR 5150 was to be featured at two other Cedar Fair parks as well. Almost simultaneously, two similar attractions were started at Six Flags. A news release for one explained: “Our new haunted house brings you face-to-face with the world’s worst psychiatric patients. Traverse the haunted hallways of Dark Oaks Asylum and try not to bump into any of the grunting inmates around every turn. Maniacal inmates yell out from their bloodstained rooms and deranged guards wander the corridors in search of those who have escaped.” The Orange County branch of the National Alliance on Mental Illness (NAMI) sprang into action, and Doris Schwartz, a Westchester, N.Y.-based mental-health professional, immediately emailed a roster of 130 grass-roots activists, including me, many of whom flooded Cedar Fair and Six Flags with phone calls, petitions and emails. After some heated back-and-forth, Fear VR 5150 was shelved, and Six Flags changed the mental patients in its maze into zombies. © 2016 The New York Times Company
Richard Harris Researchers have launched an innovative medical experiment that's designed to provide quick answers while meeting the needs of patients, rather than drug companies. Traditional studies can cost hundreds of millions of dollars, and can take many years. But patients with amyotrophic lateral sclerosis, or Lou Gehrig's disease don't have the time to wait. This progressive muscle-wasting disease is usually fatal within a few years. Scientists in an active online patient community identified a potential treatment and have started to gather data from the participants virtually rather than requiring many in-person doctor's visits. How is that possible? In this case, doctors and patients alike got interested in an extraordinary ALS patient whose symptoms actually got better, which rarely occurs. He'd been taking a dietary supplement called lunasin, "and lo and behold six months later, [his] speech [was] back to normal, swallowing back to normal, doesn't use his feeding tube, [and he was] significantly stronger as measured by his therapists," said Richard Bedlack, a neurologist who runs the ALS clinic at Duke University. Of course, it could just be a coincidence that the man who got better happened to be taking these supplements. To find out, Bedlack teamed up to run a study with Paul Wicks, a neuropsychologist and vice president for innovation at a web-based patient organization called PatientsLikeMe. © 2016 npr
Keyword: ALS-Lou Gehrig's Disease
Link ID: 22788 - Posted: 10.26.2016
Laura Sanders When small lies snowball into blizzards of deception, the brain becomes numb to dishonesty. As people tell more and bigger lies, certain brain areas respond less to the whoppers, scientists report online October 24 in Nature Neuroscience. The results might help explain how small transgressions can ultimately set pants aflame. The findings “have big implications for how lying can develop,” says developmental psychologist Victoria Talwar of McGill University in Montreal, who studies how dishonest behavior develops in children. “It starts to give us some idea about how lying escalates from small lies to bigger ones.” During the experiment, researchers from University College London and Duke University showed 80 participants a crisp, big picture of a glass jar of pennies. They were told that they needed to send an estimate of how much money was in the jar to an unseen partner who saw a smaller picture of the same jar. Each participant was serving as a “well-informed financial adviser tasked with advising a client who is less informed about what investments to make,” study coauthor Neil Garrett of University College London said October 20 during a news briefing. Researchers gave people varying incentives to lie. In some cases, for instance, intentionally overestimating the jar’s contents was rewarded with a bigger cut of the money. As the experiment wore on, the fibs started flying. People lied the most when the lie would benefit both themselves and their unseen partner. But these “financial advisers” still told self-serving lies even when it would hurt their partner. |© Society for Science & the Public 2000 - 2016
Link ID: 22784 - Posted: 10.25.2016
Robin McKie New visions of the brain and body’s detailed operations will be unveiled by a suite of medical scanners being opened this week. The newly refurbished Wolfson Brain Imaging Centre in the University of Cambridge has been equipped with some of the world’s most powerful magnetic resonance imaging (MRI) and positron emission tomography (PET) scanners and will give its researchers unprecedented power to make images of cancers, study the precise makeup of the cortex and analyse how chemicals in the brain – known as neurotransmitters – underpin the development of schizophrenia and depression. “It is a remarkable set of machines,” says Professor Ed Bullmore, head of neuroscience at Cambridge University. “We will be able to address clinical issues such as the detailed progression of Parkinson’s disease. At the same time, we will be able to address basic issues about the mind. How does the brain develop? How does the adult brain perform its functions?” At the heart of the refurbished centre – funded by the Medical Research Council, Wellcome Trust and Cancer Research UK – are three groundbreaking devices. Only a handful of these exist at institutions outside Cambridge and no institution – other than Cambridge – has all three. “The devices we have assembled are primarily for studying humans and will have a strong research focus,” Bullmore says. A key example is provided by the 7T MRI scanner. Current devices have magnetic fields that have strengths of around 3T (tesla) and can see structures 2-3 mm in size. By contrast, the new Cambridge scanner with its 7T field will have a resolution of around 0.5mm. © 2016 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 22782 - Posted: 10.24.2016
by Bethany Brookshire Most of us spend our careers trying to meet — and hopefully exceed — expectations. Scientists do too. But the requirements for success in a job in academic science don’t always line up with the best scientific methods. The net result? Bad science doesn’t just happen — it gets selected for. What does it mean to be successful in science? A scientist gets a job and funding by publishing a lot of high-impact papers with novel findings. Those papers and findings beget awards and funding to do more science — and publish more papers. “The problem that we face is that the incentive system is focused almost entirely on getting research published, rather than on getting research right,” says Brian Nosek, a psychologist at the University of Virginia in Charlottesville. This idea of success has become so ingrained that scientists are even introduced when they give talks by the number of papers they have published or the amount of grant funding they have, says Marc Edwards, a civil engineer at Virginia Polytechnic Institute and State University in Blacksburg. But rewarding researchers for the number of papers they publish results in a “natural selection” of sloppy science, new research shows. The idea of scientific “success” equated as number of publications promotes not just lazy science but also unethical science, another paper argues. Both articles proclaim that it’s time for a culture shift. But with many scientific labs to fund and little money to do it, what does a new, better scientific enterprise look like? © Society for Science & the Public 2000 - 2016
Link ID: 22779 - Posted: 10.24.2016
By Kensy Cooperrider, Rafael Núñez “What is the difference between yesterday and tomorrow?” The Yupno man we were interviewing, Danda, paused to consider his answer. A group of us sat on a hillside in the Yupno Valley, a remote nook high in the mountains of Papua New Guinea. Only days earlier we had arrived on a single-engine plane. After a steep hike from the grass airstrip, we found ourselves in the village of Gua, one of about 20 Yupno villages dotting the rugged terrain. We came all the way here because we are interested in time—in how Yupno people understand concepts such as past, present and future. Are these ideas universal, or are they products of our language, our culture and our environment? As we interviewed Danda and others in the village, we listened to what they said about time, but we paid even closer attention to what they did with their hands as they spoke. Gestures can be revealing. Ask English speakers about the difference between yesterday and tomorrow, and they might thrust a hand over the shoulder when referring to the past and then forward when referring to the future. Such unreflective movements reveal a fundamental way of thinking in which the past is at our backs, something that we “leave behind,” and the future is in front of us, something to “look forward” to. Would a Yupno speaker do the same? Danda was making just the kinds of gestures we were hoping for. As he explained the Yupno word for “yesterday,” his hand swept backward; as he mentioned “tomorrow,” it leaped forward. We all sat looking up a steep slope toward a jagged ridge, but as the light faded, we changed the camera angle, spinning around so that we and Danda faced in the opposite direction, downhill. With our backs now to the ridge, we looked over the Yupno River meandering toward the Bismarck Sea. “Let's go over that one more time,” we suggested. © 2016 Scientific American,
Link ID: 22778 - Posted: 10.22.2016
By Laura Wright, Researchers have the clearest-ever picture of the receptor that gives humans the 'high' from marijuana, which could lead to a better understanding of how the drug affects humans. Scientists have long known that molecules from THC, the psychoactive component of marijuana, bind to and activate the receptor known as CB1. But now they know that it has a three-dimensional crystal structure. The authors of the paper, which was published Thursday in the journal Cell, say this information is crucial to improve our understanding of this receptor as marijuana use becomes widespread and, in many places, legalized. Now that they know the shape of the receptor, they can get a better idea of how different molecules bind to it, which is what causes reactions in humans. "What is important is to understand how different molecules bind to the receptor, how they control the receptor function, and how this can affect different people," said Raymond Stevens, co-author of the study. Dr. Mark Ware, the executive director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research at the Alan Edwards pain management unit at the McGill University Health Centre, called the discovery a "breakthrough." "Suddenly we've been given the design of the building," he explained. "We can work out ways to get in the building, we know where the windows and doors and stairs are, and we know kind of how the building is structured now." They both said that knowing the receptor's design can lead to better drug design. K2 synthetic pot It's also a key step to understanding the differences between natural cannabinoids, found in the marijuana plant, and synthetic cannabinoids, made in labs. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22776 - Posted: 10.22.2016
By Agata Blaszczak-Boxe Some rodents have a sweet tooth. And sometimes, you need to get crafty to reach your sugar fix. Rats have been filmed for the first time using hooked tools to get chocolate cereal – a manifestation of their critter intelligence. Akane Nagano and Kenjiro Aoyama, of Doshisha University in Kyotanabe, Japan, placed eight brown rats in a transparent box and trained them to pull small hooked tools to obtain the cereal that was otherwise beyond their reach. In one experiment they gave them two similar hooked tools, one of which worked well for the food retrieval task, and the other did not. The rats quickly learned to choose the correct tool for the job, selecting it 95 per cent of the time. The experiments showed that the rats understood the spatial arrangement between the food and the tool. The team’s study is the first to demonstrate that rats are able to use tools, says Nagano. The rats did get a little confused in the final experiment. When the team gave them a rake that looked the part but with a bottom was too soft and flimsy to move the cereal, they still tried to use it as much as the working tool that was also available. But, says Nagano, it is possible their eyesight was simply not good enough for them to tell that the flimsy tool wasn’t up to the task. The rodents’ crafty feat places them in the ever-growing club of known tool-using animals such as chimps, bearded capuchin monkeys, New Caledonian crows, alligators and even some fish. © Copyright Reed Business Information Ltd.
By Catherine Caruso Imagine you are faced with the classic thought experiment dilemma: You can take a pile of money now or wait and get an even bigger stash of cash later on. Which option do you choose? Your level of self-control, researchers have found, may have to do with a region of the brain that lets us take the perspective of others—including that of our future self. A study, published today in Science Advances, found that when scientists used noninvasive brain stimulation to disrupt a brain region called the temporoparietal junction (TPJ), people appeared less able to see things from the point of view of their future selves or of another person, and consequently were less likely to share money with others and more inclined to opt for immediate cash instead of waiting for a larger bounty at a later date. The TPJ, which is located where the temporal and parietal lobes meet, plays an important role in social functioning, particularly in our ability to understand situations from the perspectives of other people. However, according to Alexander Soutschek, an economist at the University of Zurich and lead author on the study, previous research on self-control and delayed gratification has focused instead on the prefrontal brain regions involved in impulse control. “When you have a closer look at the literature, you sometimes find in the neuroimaging data that the TPJ is also active during delay of gratification,” Soutschek says, “but it's never interpreted.” © 2016 Scientific American
Link ID: 22772 - Posted: 10.20.2016
Hannah Devlin Science correspondent Monkeys have been observed producing sharp stone flakes that closely resemble the earliest known tools made by our ancient relatives, proving that this ability is not uniquely human. Previously, modifying stones to create razor-edged fragments was thought to be an activity confined to hominins, the family including early humans and their more primitive cousins. The latest observations re-write this view, showing that monkeys unintentionally produce almost identical artefacts simply by smashing stones together. The findings put archaeologists on alert that they can no longer assume that stone flakes they discover are linked to the deliberate crafting of tools by early humans as their brains became more sophisticated. Tomos Proffitt, an archaeologist at the University of Oxford and the study’s lead author, said: “At a very fundamental level - if you’re looking at a very simple flake - if you had a capuchin flake and a human flake they would be the same. It raises really important questions about what level of cognitive complexity is required to produce a sophisticated cutting tool.” Unlike early humans, the flakes produced by the capuchins were the unintentional byproduct of hammering stones - an activity that the monkeys pursued decisively, but the purpose of which was not clear. Originally scientists thought the behaviour was a flamboyant display of aggression in response to an intruder, but after more extensive observations the monkeys appeared to be seeking out the quartz dust produced by smashing the rocks, possibly because it has a nutritional benefit. © 2016 Guardian News and Media Limited
Link ID: 22771 - Posted: 10.20.2016
Tina Hesman Saey VANCOUVER — Zika virus’s tricks for interfering with human brain cell development may also be the virus’s undoing. Zika infection interferes with DNA replication and repair machinery and also prevents production of some proteins needed for proper brain growth, geneticist Feiran Zhang of Emory University in Atlanta reported October 19 at the annual meeting of the American Society of Human Genetics. Levels of a protein called p53, which helps control cell growth and death, shot up by 80 percent in human brain cells infected with the Asian Zika virus strain responsible for the Zika epidemic in the Americas, Zhang said. The lab dish results are also reported in the Oct. 14 Nucleic Acids Research. Increased levels of the protein stop developing brain cells from growing and may cause the cells to commit suicide. A drug that inactivates p53 stopped brain cells from dying, Zhang said. Such p53 inhibitors could help protect developing brains in babies infected with Zika. But researchers would need to be careful giving such drugs because too little p53 can lead to cancer. Zika also makes small RNA molecules that interfere with production of proteins needed for DNA replication, cell growth and brain development, Zhang said. In particular, a small viral RNA called vsRNA-21 reduced the amount of microcephalin 1 protein made in human brain cells in lab dishes. The researchers confirmed the results in mouse experiments. That protein is needed for brain growth; not enough leads to the small heads seen in babies with microcephaly. Inhibitors of the viral RNAs might also be used in therapies, Zhang suggested. |© Society for Science & the Public 2000 - 2016
Keyword: Development of the Brain
Link ID: 22770 - Posted: 10.20.2016
By Meredith Knight In June, international diabetes organizations endorsed provocative new guidelines suggesting physicians should consider gastric bypass surgery for a greatly expanded number of diabetics—those with a body mass index of 30 and above as opposed to just those with a BMI of 40 or more. Research has shown that the surgery helps people lose more weight, maintain the loss longer and achieve better blood glucose levels than those who slim down by changing diet and exercise habits. Now a study in mice suggests the effectiveness of bariatric surgery may stem in part from changes it causes in the brain. According to the study, published in the International Journal of Obesity, gastric bypass surgery causes the hyperactivation of a neural pathway that leads from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, an area in the midbrain that receives sensory information from the body, and then to the amygdala, the brain's emotion- and fear-processing center. The obese mice underwent so-called Roux-en-Y bypass surgery, in which surgeons detach most of the stomach, leaving only a tiny pouch connected to the small intestine. Shortly after the surgery, the mice begin to show increased activation in this neural pathway, along with reduced meal size and a preference for less fatty food. They also begin to secrete higher levels of satiety hormones. Similar behavioral and hormonal patterns are found in humans after bypass surgery, suggesting that the brain changes may also be similar—but the authors say looking at this particular circuit in humans with brain imaging is difficult because the resolution is not up to the task. © 2016 Scientific American,
Link ID: 22768 - Posted: 10.19.2016
By MARC SANTORA The morning after Christine Grounds gave birth to her son Nicholas, she awoke to find a neurologist examining her baby. It was summer 2006, and Nicholas was her first child. There had been no indication that anything was wrong during her pregnancy, but it was soon clear that there was a problem. “Did you know he has microcephaly?” she remembers the doctor asking matter-of-factly. Confused, she replied, “What is microcephaly?” This was before the Zika virus had spread from Brazil across South and Central America and the Caribbean and reached Florida. It was before doctors had determined that the virus could cause microcephaly, a birth defect in which children have malformed heads and severely stunted brain development. And it was before people had seen the devastating pictures of scores of newborns with the condition in Brazil and elsewhere that shocked the world this year. Ms. Grounds, a 45-year-old psychotherapist, and her husband, Jon Mir, who live in Manhattan, had no idea what microcephaly would mean for them or for their child. “We had a diagnosis but no prognosis,” recalled Mr. Mir, 44, who works in finance. The doctors could offer few answers. “We don’t know if he will walk,” the couple recalled being told. “We don’t know if he will talk. He might be in a vegetative state.” But the truth was, even the doctors did not know. As mosquito season draws to a close in much of the country, taking with it the major risk of new Zika infections, there are still more than 2,600 pregnant women who have tested positive for the virus in the United States and its territories, according to the Centers for Disease Control and Prevention. They, and thousands more around the world, face the prospect of giving birth to a child with microcephaly. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22766 - Posted: 10.19.2016
By Meredith Wadman The second century C.E. Greek physician and philosopher Galen advised patients suffering from disorders of the spirit to bathe in and drink hot spring water. Modern day brain scientists have posited that Galen’s prescription delivered more than a placebo effect. Lithium has for decades been recognized as an effective mood stabilizer in bipolar disease, and lithium salts may have been present in the springs Galen knew. Yet exactly how lithium soothes the mind has been less than clear. Now, a team led by Ben Cheyette, a neuroscientist at the University of California in San Francisco (UCSF), has linked its success to influence over dendritic spines, tiny projections where excitatory neurons form connections, or synapses, with other nerve cells. Lithium treatment restored healthy numbers of dendritic spines in mice engineered to carry a genetic mutation that is more common in people with autism, schizophrenia, and bipolar disorder than in unaffected people, they report today in Molecular Psychiatry. The lithium also reversed symptoms in these mutant mice—lack of interest in social interactions, decreased motivation, and increased anxiety—that mimic those in the human diseases. “They showed there’s a correlation between the ability of lithium to reverse not only the behavioral abnormalities in the mice, but also the [dendritic] spine abnormalities,” says Scott Soderling, a neuroscientist at Duke University in Durham, North Carolina, who studies how dysfunctions in signaling at brain synapses and lead to psychiatric disorders. Soderling adds that the work also sheds light on the roots of these diseases. “It gives further credence to this idea that these spine abnormalities are functionally linked to the behavioral disorders.” © 2016 American Association for the Advancement of Science.
Link ID: 22764 - Posted: 10.18.2016
Laura Sanders When the body’s internal sense of time doesn’t match up with outside cues, people can suffer, and not just from a lack of sleep. Such ailments are similar in a way to motion sickness — the queasiness caused when body sensations of movement don’t match the external world. So scientists propose calling time-related troubles, which can afflict time-zone hoppers and people who work at night, “circadian-time sickness.” This malady can be described, these scientists say, with a certain type of math. The idea, to be published in Trends in Neurosciences, is “intriguing and thought-provoking,” says neuroscientist Samer Hattar of Johns Hopkins University. “They really came up with an interesting idea of how to explain the mismatch.” Neuroscientist Raymond van Ee of Radboud University in the Netherlands and colleagues knew that many studies had turned up ill effects from an out-of-whack circadian clock. Depression, metabolic syndromes and memory troubles have been found alongside altered daily rhythms. But despite these results, scientists don’t have a good understanding of how body clocks work, van Ee says. Van Ee and colleagues offer a new perspective by using a type of math called Bayesian inference to describe the circadian trouble. Bayesian inference can be used to describe how the brain makes and refines predictions about the world. This guesswork relies on the combination of previous knowledge and incoming sensory information (SN: 5/28/16, p. 18). In the case of circadian-time sickness, these two cues don’t match up, the researchers propose. |© Society for Science & the Public 2000 - 2016
Link ID: 22763 - Posted: 10.18.2016
By PERRI KLASS, M.D. It’s a classic which-came-first question: Is the child not getting enough sleep because of problem behaviors, especially at bedtime, or is the child behaving problematically because of not getting enough sleep? The answers are most likely yes and yes, and the back-and-forth currents can drag a child down developmentally. In an editorial in JAMA Pediatrics in 2015, Michelle M. Garrison, a research assistant professor at the University of Washington in the division of child and adolescent psychiatry, described this intersection of sleep and behavior problems in early childhood as a “feedback whirlpool.” Dr. Garrison was commenting on a longitudinal study of more than 32,000 Norwegian mothers and their children who were followed from birth to age 5; the children with sleep problems at 18 months, including short sleep duration (sleeping 10 hours or less) or frequent nocturnal awakenings (three times a night or more) had more emotional and behavioral problems at the age of 5. This held true even when the researchers adjusted for emotional and behavioral problems already present in the 18-month-olds; compared to children at the same behavioral baseline, the kids with sleep problems ran into more difficulties as they developed. “Sleep really does drive behavior problems and behavior problems are driving sleep problems, it really is bidirectional,” Dr. Garrison said. “A child can start having problems with emotional regulation, melting down more, and that makes it more difficult for the family to do all the things they have to do so the child can get good sleep. Sleep gets worse; behavior gets worse. It can really be an awful cycle for the kid and the family both.” Dr. Oskar Jenni, a professor of developmental pediatrics at Zurich University Children’s Hospital, said that there is a great deal of variation in the individual sleep needs of children at any given age. Parents need to understand their children’s sleep needs and rhythms, since behavior problems can also arise when children are compelled to spend more time in bed than they actually need. “My main message is adjusting bedtime to the needs of the children in both directions,” he said. © 2016 The New York Times Company
Link ID: 22762 - Posted: 10.18.2016
By Michael Price When you’re smiling, it may feel like the whole world is smiling with you, but a new study suggests that some facial expressions may not be so universal. In fact, several expressions commonly understood in the West—including one for fear—have very different meanings to one indigenous, isolated society in Papua New Guinea. The new findings call into question some widely held tenets of emotional theory, and they may undercut emerging technologies, like robots and artificial intelligence programs tasked with reading people’s emotions. For more than a century, scientists have wondered whether all humans experience the same basic range of emotions—and if they do, whether they express them in the same way. In the 1870s, it was the central question Charles Darwin explored in The Expression of the Emotions in Man and Animals. By the 1960s, emeritus psychologist Paul Ekman, then at the University of California (UC) in San Francisco, had come up with an accepted methodology to explore this question. He showed pictures of Westerners with different facial expressions to people living in isolated cultures, including in Papua New Guinea, and then asked them what emotion was being conveyed. Ekman’s early experiments appeared conclusive. From anger to happiness to sadness to surprise, facial expressions seemed to be universally understood around the world, a biologically innate response to emotion. That conclusion went virtually unchallenged for 50 years, and it still features prominently in many psychology and anthropology textbooks, says James Russell, a psychologist at Boston College and corresponding author of the recent study. But over the last few decades, scientists have begun questioning the methodologies and assumptions of the earlier studies. © 2016 American Association for the Advancement of Science.
Link ID: 22761 - Posted: 10.18.2016
Bruce Bower Scientists, politicians, clinicians, police officers and medical workers agree on one thing: The U.S. mental health system needs a big fix. Too few people get the help they need for mental ailments and emotional turmoil that can destroy livelihoods and lives. A report in the October JAMA Internal Medicine, for instance, concludes that more than 70 percent of U.S. adults who experience depression don’t receive treatment for it. Much attention focuses on developing better psychiatric medications and talk therapies. But those tactics may not be enough. New research suggests that the longstanding but understudied problem of stigma leaves many of those suffering mental ailments feeling alone, often unwilling to seek help and frustrated with treatment when they do. “Stigma about mental illness is widespread,” says sociologist Bernice Pescosolido of Indiana University in Bloomington. And the current emphasis on mental ills as diseases of individuals can unintentionally inflame that sense of shame. An effective mental health care system needs to address stigma’s suffocating social grip, investigators say. “If we want to explain problems such as depression and suicide, we have to see them in a social context, not just as individual issues,” Pescosolido says. |© Society for Science & the Public 2000 - 2016
Link ID: 22758 - Posted: 10.15.2016
Analysis of a trial that used the drug canagliflozin found that as people lost weight, their appetite increased proportionately, leading to consumption of more calories and weight loss plateau (leveling off). The findings provide the first measurement in people of how strongly appetite counters weight loss as part of the body’s feedback control system regulating weight. Results are currently available on BioRxiv (link is external) and will publish in Obesity during Obesity Week 2016. A team led by the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) analyzed data from a year-long, placebo-controlled, double-blind trial in people with type 2 diabetes who could eat and drink without restriction by the study. Of the 242 participants, 153 received canagliflozin, a drug that caused a substantial increase in the amount of glucose excreted in their urine. Those people were not directly aware of that calorie loss, which caused a gradual decrease in weight averaging about eight pounds. The team used a validated math model to calculate the changes in the amount of calories consumed during the study. They found no long-term calorie intake changes in the 89 people who got a placebo. However, for every pound of lost weight, the people treated with canagliflozin consumed about 50 calories per day more than they were eating before the study. This increase in appetite and calorie intake led to slowing of weight loss after about six months. The measurements are consistent with the researchers’ analysis of data from a separate trial on a commercial weight loss program not involving canagliflozin. In the weight loss program trial, despite the dieters’ consistent efforts to reduce calorie intake, their increased appetite resulted in a progressive increase in calorie intake — three times stronger than the changes in caloric expenditure that typically accompany weight loss — and weight loss plateau. Findings from the analyses suggest that persistent effort is required to avoid weight regain.
Link ID: 22756 - Posted: 10.15.2016