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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
By DONNA DE LA CRUZ Some of the most troubling images of the opioid crisis involve parents buying or using drugs with their children in tow. Now new research offers a glimpse into the addicted brain, finding that the drugs appear to blunt a person’s natural parenting instincts. Researchers at the Perelman School of Medicine at the University of Pennsylvania scanned the brains of 47 men and women before and after they underwent treatment for opioid dependence. While in the scanner, the study subjects looked at various images of babies, and the researchers measured the brain’s response. The brain scans were compared with the responses of 25 healthy people. What the study subjects didn’t know was that the photos had been manipulated to adjust the “baby schema,” the term used to describe the set of facial and other features like round faces and big eyes that make our brains register babies as irresistible, kicking in our instinct to care for them. Sometimes the babies’ features were exaggerated to make them even more adorable; in others, the chubby cheeks and big eyes were reduced, making the faces less appealing. Studies show that a higher baby schema activates the part of the brain called the ventral striatum, a key component of the brain reward pathway. Compared with the brains of healthy people, the brains of people with opioid dependence didn’t produce strong responses to the cute baby pictures. But once the opioid-dependent people received a drug called naltrexone, which blocks the effects of opioids, their brains produced a more normal response. “When the participants were given an opioid blocker, their baby schema became more similar to that of healthy people,” said Dr. Daniel D. Langleben, one of the researchers. “The data also raised in question whether opioid medications may affect social cognition in general.” © 2016 The New York Times Company
Linda Geddes For the first time, a paralysed man has gained a limited sense of touch, thanks to an electric implant that stimulates his brain and allows him to feel pressure-like sensations in the fingers of a robotic arm. The advance raises the possibility of restoring limited sensation to various areas of the body, as well as giving people with spinal-cord injuries better control over prosthetic limbs. But restoring human-like feeling, such as sensations of heat or pain, will prove more challenging, the researchers say. Nathan Copeland had not been able to feel or move his legs and lower arms since a car accident snapped his neck and injured his spinal cord when he was 18. Now, some 12 years later, he can feel when a robotic arm has its fingers touched, because sensors on the fingers are linked to an implant in his brain. Brain implant restores paralysed man's sense of touch Rob Gaunt, a biomedical engineer at the University of Pittsburgh, performs a sensory test on a blindfolded Nathan Copeland. Nathan, who is paralysed, demonstrates his ability to feel by correctly identifying different fingers through a mind-controlled robotic arm. Video credit: UPMC/Pitt Health Sciences. “He says the sensations feel like they’re coming from his own hand,” says Robert Gaunt, a biomedical engineer at the University of Pittsburgh who led the study. © 2016 Macmillan Publishers Limited
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
By JOHN C. MARKOWITZ The United States government recently announced its new director of the National Institute of Mental Health, Dr. Joshua Gordon. If you think that’s just bureaucracy as usual, think again. Mental health research, under the leadership of the previous director, Dr. Thomas Insel, underwent a quiet crisis, one with worrisome implications for the treatment of mental health. I hope Dr. Gordon will resolve it. For decades, the National Institute of Mental Health provided crucial funding for American clinical research to determine how well psychotherapies worked as treatments (on their own as well as when combined with medications). This research produced empirical evidence supporting the effectiveness of cognitive behavioral therapy, interpersonal psychotherapy and other talking treatments. But over the past 13 years, Dr. Insel increasingly shifted the institute’s focus to neuroscience, strangling its clinical research budget. Dr. Insel wasn’t wrong to be enthusiastic about the possibilities of neuroscientific research. Compared with the psychiatric diagnoses listed in the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), which can be vague and flawed, brain-based research holds out the promise of a precise and truly scientific understanding of mental illness. Psychiatric diagnoses depend on clusters of signs and symptoms. For major depression, for example, some criteria are low mood; wanting to die; and sleep, appetite and energy changes. These diagnoses lack the specificity of the biological markers that neuroscience seeks to identify. If we could find a genetic, neuroimaging or brain-circuit explanation for a mental illness, it might even yield a cure, rather than just the treatment of what can be recurrent, chronic conditions. But where does that leave patients whom today’s treatments do not help? Can they wait for neuroscience developments that may take decades to appear, or prove illusory? Staking all your money on one bet, as the institute did under Dr. Insel, has consequences. © 2016 The New York Times Company
Link ID: 22757 - 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
By Jessica Boddy You’d probably never notice a jumping spider across your living room, but it would surely notice you. The arachnids are known for their brilliant eyesight, and a new study shows they have even greater sensory prowess than we thought: Jumping spiders can hear sounds even though they don’t have ears—or even eardrums. To find this out, researchers implanted tiny electrodes in a region of spiders’ brains that would show whether sound was being processed. Then they placed the spiders on a specially designed box to eliminate any vibrations from below—most spiders sense their surroundings through vibrations—and scared the heck out of them with a speaker-produced buzz of one of their predators, the mud dauber wasp. An out-of-earshot, high-frequency buzz and a silent control elicited no response from the spiders. But the 80-hertz wasp buzz made them freeze and look around, startled, just as they would do in the wild. What’s more, data from the electrodes showed a spike in brain activity with each buzz, revealing that spiders actually hear sounds, from a swooping mud dauber wasp to you crunching potato chips on your couch. The researchers, who publish their work today in Current Biology, say further study is needed to see exactly how spiders receive sounds without eardrums, but they believe sensitive hairs on their legs play a part. © 2016 American Association for the Advancement of Science.
Link ID: 22755 - Posted: 10.15.2016
By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,
Link ID: 22754 - Posted: 10.13.2016
By Smitha Mundasad Health reporter People who experience frequent drops in blood pressure or dizziness when suddenly standing up are at increased risk of dementia, scientists say. Writing in Plos Medicine they suggest that less blood reaches the brain during these moments, leading to brain cell damage over time. Dementia experts say this is a "robust study" and "plausible explanation" that needs further investigation. Charities point out that factors such as smoking carry higher risks. But they say the work adds to growing evidence that changes in blood pressure have an impact on the brain. Previous studies have linked high blood pressure to types of dementia. But in this paper scientists focused on transient periods of low blood pressure - also known as postural hypotension - which become more common in older age. These episodes can sometimes leave people feeling dizzy or give them "head rushes" when standing up suddenly. Researchers from the Erasmus Medical Center, in the Netherlands, tracked 6,000 people for an average of 15 years. They found those who suffered repeated periods of low blood pressure on standing were more likely to develop dementia in the years that followed. Researcher Dr Arfan Ikram said: "Even though the effect can be seen as subtle - with an increased risk of about 4% for people with postural hypotension compared to those without it - so many people suffer from postural hypotension as they get older that it could have a significant impact on the burden of dementia across the world." He told the BBC: "If people experience frequent episodes of dizziness on standing, particularly as they get older, they should see their GPs for advice." © 2016 BBC
Link ID: 22753 - Posted: 10.13.2016
Lauren Silverman It's been a wild ride for kratom lately. Since Aug. 31, when the Drug Enforcement Administration announced its intention to classify the plant as a Schedule I substance, a group of kratom vendors filed a lawsuit against the government to block the move, angry advocates took to social media in protest and scientists questioned whether they would be able to continue kratom research. Now, the DEA is withdrawing its notice of intent to put kratom in the most restrictive category of controlled substances, with drugs like LSD and heroin. The DEA says it will instead open an official public comment period — to last until Dec. 1, 2016 — for people to share their experiences using kratom as a medical treatment. It has also requested that the Food and Drug Administration expedite scientific research. DEA spokesman Russ Baer says the DEA received more than 2,000 phone calls since August, mostly in opposition to the plan to classify kratom as Schedule I. "So in a spirit of transparency, and to open this up to public dialogue, we withdrew our notice to temporarily schedule kratom," Baer says. "We will then give full consideration to those comments before we move forward with any action." Kratom is derived from the leaves of a tree native to Southeast Asia. It is a relative of the coffee plant. According to David Kroll, a pharmacologist and medical writer, farmers and indigenous people have used it for hundreds of years as both a stimulant to increase work output and also as a way to relax. © 2016 npr
Keyword: Drug Abuse
Link ID: 22752 - Posted: 10.13.2016
By MIKE IVES HONG KONG — President Rodrigo Duterte of the Philippines was elected in May after pledging to kill 100,000 criminals in his first six months in office, vowing that fish in Manila, the capital, would grow fat from eating the bodies of drug dealers and other “do nothings.” In Mr. Duterte’s first three months as president, his bloody campaign led to the killing of about 1,400 drug suspects by the police and hundreds of others by extrajudicial means, according to official estimates. He has also publicly accused thousands of government officials of being involved in the drug trade, in some cases offering no evidence. The campaign has taken particular aim at people who use or sell shabu, a cheap form of methamphetamine that has caused grave health and social problems across the country. Mr. Duterte has likened shabu addicts to zombies and claimed — absent evidence — that many are “no longer viable for rehabilitation” because abusing the drug shrinks their brains. What is methamphetamine? Methamphetamine is an addictive stimulant that can be made from ephedrine and other readily available chemicals. It typically comes in either tablets, called yaba in parts of Asia, or crystalline form. The first variety is common in mainland Southeast Asia, and the second — known as shabu, ice or crystal meth, among other names — is more popular in the Philippines and many other countries. It also tends to be more potent and more deeply intertwined with international drug manufacturing and smuggling networks, according to a report by the United Nations Office on Drugs and Crime. How does the drug affect people who use it? Smoking, snorting, ingesting or injecting methamphetamine can cause aggression, memory loss and a range of other health complications, including heart attack or sudden death. Links between methamphetamine abuse and crime, disease transmission and other social problems have also been documented. A study by the RAND Corporation found that the effects of methamphetamine abuse, including the burden of addiction and treatment, cost the United States $23.4 billion in 2005. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22751 - Posted: 10.13.2016
By peering into the eyes of mice and tracking their ocular movements, researchers made an unexpected discovery: the visual cortex — a region of the brain known to process sensory information — plays a key role in promoting the plasticity of innate, spontaneous eye movements. The study, published in Nature, was led by researchers at the University of California, San Diego (UCSD) and the University of California, San Francisco (UCSF) and funded by the National Eye Institute (NEI), part of the National Institutes of Health. “This study elegantly shows how analysis of eye movement sheds more light on brain plasticity — an ability that is at the core of the brain’s capacity to adapt and function. More specifically, it shows how the visual cortex continues to surprise and to awe,” said Houmam Araj, Ph.D., a program director at NEI. Without our being aware of it, our eyes are in constant motion. As we rotate our heads and as the world around us moves, two ocular reflexes kick in to offset this movement and stabilize images projected onto our retinas, the light-sensitive tissue at the back of our eyes. The optokinetic reflex causes eyes to drift horizontally from side-to-side — for example, as we watch the scenery through a window of a moving train. The vestibulo-ocular reflex adjusts our eye position to offset head movements. Both reflexes are crucial to survival. These mechanisms allow us to see traffic while driving down a bumpy road, or a hawk in flight to see a mouse scurrying for cover.
Link ID: 22750 - Posted: 10.13.2016
By Elizabeth Pennisi Although it has a face—and body—that only a mother could love, the naked mole rat has a lot to offer biomedical science. It lives 10 times longer than a mouse, almost never gets cancer, and doesn’t feel pain from injury and inflammation. Now, researchers say they’ve figured out how the rodents keep this pain away. “It’s an amazing result,” says Harold Zakon, an evolutionary neurobiologist at the University of Texas, Austin, who was not involved with the work. “This study points us to important areas … that might be targeted to reduce this type of pain.” Naked mole rats are just plain weird. They live almost totally underground in colonies structured like honey bee hives, with hundreds of workers servicing a single queen and her few consorts. To survive, they dig kilometers of tunnels in search of large underground tubers for food. It’s such a tough life that—to conserve energy—this member of the rodent family gave up regulating its temperature, and they are able to thrive in a low-oxygen, high–carbon dioxide environment that would suffocate or be very painful to humans. “They might as well be from another planet,” says Thomas Park, a neuroscientist at the University of Illinois, Chicago. Gary Lewin, a neuroscientist at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Berlin, began working with naked mole rats because a friend in Chicago was finding that the rodent's pain fibers were not the same as other mammals'. In 2008, the studies led to the finding that naked mole rats didn’t feel pain when they came into contact with acid and didn’t get more sensitive to heat or touch when injured, like we and other mammals do. Lewin was hooked and has been raising the rodents in his lab ever since. They are a little more challenging than rats or mice, he notes, because with just one female per colony producing young, he never really has quite enough individuals for his studies. © 2016 American Association for the Advancement of Science
By CASEY SCHWARTZ Have you ever been to Enfield? I had never even heard of it until I was 23 and living in London for graduate school. One afternoon, I received notification that a package whose arrival I had been anticipating for days had been bogged down in customs and was now in a FedEx warehouse in Enfield, an unremarkable London suburb. I was outside my flat within minutes of receiving this news and on the train to Enfield within the hour, staring through the window at the gray sky. The package in question, sent from Los Angeles, contained my monthly supply of Adderall. Adderall, the brand name for a mixture of amphetamine salts, is more strictly regulated in Britain than in the United States, where, the year before, in 2005, I became one of the millions of Americans to be prescribed a stimulant medication. The train to Enfield was hardly the greatest extreme to which I would go during the decade I was entangled with Adderall. I would open other people’s medicine cabinets, root through trash cans where I had previously disposed of pills, write friends’ college essays for barter. Once, while living in New Hampshire, I skipped a day of work to drive three hours each way to the health clinic where my prescription was still on file. Never was I more resourceful or unswerving than when I was devising ways to secure more Adderall. Adderall is prescribed to treat Attention Deficit Hyperactivity Disorder, a neurobehavioral condition marked by inattention, hyperactivity and impulsivity that was first included in the D.S.M. in 1987 and predominantly seen in children. That condition, which has also been called Attention Deficit Disorder, has been increasingly diagnosed over recent decades: In the 1990s, an estimated 3 to 5 percent of school-age American children were believed to have A.D.H.D., according to the Centers for Disease Control and Prevention; by 2013, that figure was 11 percent. It continues to rise. And the increase in diagnoses has been followed by an increase in prescriptions. In 1990, 600,000 children were on stimulants, usually Ritalin, an older medication that often had to be taken multiple times a day. By 2013, 3.5 million children were on stimulants, and in many cases, the Ritalin had been replaced by Adderall, officially brought to market in 1996 as the new, upgraded choice for A.D.H.D. — more effective, longer lasting. © 2016 The New York Times Company
By Gareth Cook According to the American Psychiatric Association, about 5 percent of American children suffer from Attention Deficit Hyperactivity Disorder (ADHD), yet the diagnosis is given to some 15 percent of American children, many of whom are placed on powerful drugs with lifelong consequences. This is the central fact of the journalist Alan Schwarz’s new book, ADHD Nation. Explaining this fact—how it is that perhaps two thirds of the children diagnosed with ADHD do not actually suffer from the disorder—is the book’s central mystery. The result is a damning indictment of the pharmaceutical industry, and an alarming portrait of what is being done to children in the name of mental health. What prompted you to write this book? In 2011, having spent four years exposing the dangers of concussions in the National Football League and youth sports for The New York Times, I wanted another project. I had heard that high school students in my native Westchester County (just north of New York City) were snorting Adderall before the S.A.T.'s to focus during the test. I was horrified and wanted to learn more. I saw it not as a "child psychiatry" story, and not as a "drug abuse" story, but one about academic pressure and the demands our children feel they're under. When I looked deeper, it was obvious that our nationwide system of ADHD treatment was completely scattershot—basically, many doctors were merely prescribing with little thought into whether a kid really had ADHD or not, and then the pills would be bought and sold among students who had no idea what they were messing with. I asked the ADHD and child-psychiatry establishment about this, and they denied it was happening. They denied that there were many false diagnoses. They denied that teenagers were buying and selling pills. They denied that the national diagnosis rates reported by the C.D.C.—then 9.5 percent of children aged 4-17, now 11 percent and still growing—were valid. They basically denied that anything about their world was malfunctioning at all. In the end, they doth protest too much. I wrote about 10 front-page stories for The New York Times on the subject from 2012-2014. © 2016 Scientific American,
By Christian Jarrett It’s been said that men and women are so unlike each other, it’s as if they’re from different planets – a claim that continues to amuse and irritate. John Gray’s original mega-selling book Men are from Mars, Women are from Venus, first published in the early 1990s, has sold millions, spawning numerous parodies (such as Katherine Black and Finn Contini’s Women May Be from Venus, But Men are Really from Uranus) and even comedy stage shows, such as Men are from Mars, Women are from Venus, Live! currently playing off Broadway.) While our physical differences in size and anatomy are obvious, the question of psychological differences between the genders is a lot more complicated and controversial. There are issues around how to reliably measure the differences. And when psychologists find them, there are usually arguments over whether the causes are innate and biological, or social and cultural. Are men and women born different or does society shape them that way? These questions are particularly thorny when you consider our differences in personality. Most research suggests that men and women really do differ on some important traits. But are these differences the result of biology or cultural pressures? And just how meaningful are they in the real world? One possibility is that most differences are tiny in size but that combined they can have important consequences. One of the most influential studies in the field, published in 2001 by pioneering personality researchers Paul Costa, Robert McCrae and Antonio Terracciano, involved over 23,000 men and women from 26 cultures filling out personality questionnaires. © 2016 BBC.
Keyword: Sexual Behavior
Link ID: 22746 - Posted: 10.12.2016
By Virginia Morell Human-produced noise in the ocean is likely harming marine mammals in numerous unknown ways, according to a comprehensive new report from the National Academies of Sciences, Engineering, and Medicine. That’s because there are insufficient data to determine how the ill effects of noise created by ships, sonar signals, and other activities interact with other threats, including pollution, climate change, and the loss of prey due to fishing. The report, which was sponsored by several government agencies and released on 7 October, provides a new framework for researchers to begin exploring these cumulative impacts. “There’s a growing recognition that interactions between stressors on marine mammals can’t right now be accurately assessed," said Peter Tyack, a marine mammal biologist at the University of St Andrews in the United Kingdom, in a webinar on the report. Tyack also chaired the committee that prepared the study, "Approaches to Understanding the Cumulative Effects of Stressors on Marine Mammals." Killer whales, for instance, are known to swim away from areas where they have encountered sonar signals of about 142 decibels, a sound level lower than currently allowed by the U.S. Navy for its ships, Tyack said, referring to a 2014 study in The Journal of the Acoustical Society of America that determined the mammals’ likely response. But scientists don’t yet know how other marine mammals might respond. They also don’t know whether or how other factors, such as encountering an oil spill or colliding with a ship, would—or would not—compound the cetaceans’ response to these sounds; or how or whether such combined stressors matter to the animals’ long-term health and overall population. © 2016 American Association for the Advancement of Science.
By GRETCHEN REYNOLDS Exercise may aid in weight control and help to fend off diabetes by improving the ability of fat cells to burn calories, a new study reports. It may do this in part by boosting levels of a hormone called irisin, which is produced during exercise and which may help to turn ordinary white fat into much more metabolically active brown fat, the findings suggest. Irisin (named for the Greek goddess Iris) entered the scientific literature in 2012 after researchers from Harvard and other universities published a study in Nature that showed the previously unknown hormone was created in working muscles in mice. From there, it would enter the bloodstream and migrate to other tissues, particularly to fat, where it would jump-start a series of biochemical processes that caused some of the fat cells, normally white, to turn brown. Brown fat, which is actually brown in color, burns calories. It also is known to contribute to improved insulin and blood sugar control, lessening the risk for Type 2 diabetes. Most babies, including human infants, are plump with brown fat, but we humans lose most of our brown fat as we grow up. By the time we are adults, we usually retain very little brown fat. In the 2012 study, the researchers reported that if they injected irisin into living mice, it not only turned some white fat into brown fat, it apparently also prevented the rodents from becoming obese, even on a high-fat, high-calorie diet. But in the years since, some scientists have questioned whether irisin affects fat cells in people to the same extent as it seems to in mice — and even whether the hormone exists in people at all. A study published last year in Cell Metabolism by the same group of researchers who had conducted the first irisin study, however, does seem to have established that irisin is produced in humans. They found some irisin in sedentary people, but the levels were much higher in those who exercise often. © 2016 The New York Times Company
Link ID: 22744 - Posted: 10.12.2016