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Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.
The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.
Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.
Photo credit: Yoichi Araki, Ph.D.
By Virginia Morell Like many newborn mammals, baby mice cry to get their mother’s attention. But the mother doesn’t instinctively recognize these calls; she must learn the sounds of her offspring—just as human parents must learn the cries of their infants. Now, a team of researchers has discovered that the hormone oxytocin, which has been tied to trust and maternal bonding, holds the key to how this learning occurs. Only after oxytocin tweaks the brain of a female mouse does she respond with a mother’s concern and attentiveness to crying pups. “It’s an exciting study with implications that … could be helpful to certain disorders, such as autism,” says Larry Young, a neuroscientist at Emory University in Atlanta who was not involved in the work. To understand the role oxytocin plays in a mother mouse’s brain, scientists at New York University School of Medicine first investigated how female mice in general respond to the distress calls of baby mice. Pups emit ultrasonic cries when they are separated from the nest, which sometimes happens when a mother carries her babies to a new location. (Moms change nest locations regularly to elude predators.) When a mother hears these cries, she runs to the lost pup, picks it up, and carries it back to her nest. Other scientists have shown that moms respond even to the distress cries of pups that aren’t their own, readily approaching loudspeakers that broadcast the calls. Most virgin female mice, though, couldn’t care less; they seem completely indifferent to the pups’ cries for help. And yet, some virgin females that have either been housed with a mother and her litter or have been injected with oxytocin will retrieve crying infants. © 2015 American Association for the Advancement of Science.
Angus Chen A common pain medication might make you go from "so cute!" to "so what?" when you look at a photo of an adorable kitten. And it might make you less sensitive to horrifying things too. It's acetaminophen, the active ingredient in Tylenol. Researchers say the drug might be taking the edge off emotions – not just pain. "It seems to take off the highs of your daily highs and the lows off your daily lows," says Baldwin Way, a psychologist at Ohio State University and the principal investigator on the study, "It kind of flattens out the vicissitudes of your life." The idea that over-the-counter pain pills might affect emotions has been circulating since 2010, when two psychologists, Naomi Eisenberger and Nathan DeWall, led a study showing that acetaminophen seemed to be having both a psychological and a neurological effect on people. They asked volunteers to play a rigged game that simulated social rejection. Not only did the acetaminophen appear to be deflecting social anxieties, it also seemed to be dimming activity in the insula, a region of the brain involved in processing emotional pain. A brain that can let other thoughts bubble up despite being in pain might help its owner benefit from meditation or other cognitive therapies. "But [the insula] is a portion of the brain that seems to be involved in a lot of things," Way says. In older studies, scientists saw that people with damage in their insula didn't react as strongly to either negative or positive images. So Way and one of his students, Geoffrey Durso, figured that if acetaminophen is doing something to the insula, then it might be having a wider effect, too. © 2015 NPR
By Nicholas Bakalar Breathing problems during sleep may be linked to early mental decline and Alzheimer’s disease, a new study suggests. But treating apnea with a continuous positive airway pressure machine can significantly delay the onset of cognitive problems. In a group of 2,470 people, average age 73, researchers gathered information on the incidence of sleep apnea, a breathing disorder marked by interrupted breathing and snoring, and the incidence of mild cognitive impairment and Alzheimer’s disease. After adjusting for a range of variables, they found that people with disordered breathing during sleep became cognitively impaired an average of about 10 years sooner than those without the disorder. But compared with those whose sleep disorder was untreated, those using C.P.A.P. machines delayed the appearance of cognitive impairment by an average of 10 years — making their age of onset almost identical to those who had no sleep disorder at all. The lead author, Dr. Ricardo S. Osorio, a research professor of psychiatry at New York University, said the analysis, published online in Neurology, is an observational study that does not prove cause and effect. “But,” he added, “we need to increase the awareness that sleep disorders can increase the risk for cognitive impairment and possibly for Alzheimer’s. Whether treating sleep disorders truly slows the decline is still not known, but there is some evidence that it might.” © 2015 The New York Times Company
by Jessica Hamzelou An exoskeleton that enables movement and provides tactile feedback has helped eight paralysed people regain sensation and move previously paralysed muscles "I FELT the ball!" yelled Juliano Pinto as he kicked off the Football World Cup in Brazil last year. Pinto, aged 29 at the time, lost the use of his lower body after a car accident in 2006. "It was the most moving moment," says Miguel Nicolelis at Duke University in North Carolina, head of the Walk Again Project, which developed the thought-controlled exoskeleton that enabled Pinto to make his kick. Since November 2013, Nicolelis and his team have been training Pinto and seven other people with similar injuries to use the exoskeleton – a robotic device that encases the limbs and converts brain signals into movement. The device also feeds sensory information to its wearer, which seems to have partially reawakened their nervous system. When Nicolelis reassessed his volunteers after a year of training, he found that all eight people had regained sensations and the ability to move muscles in their once-paralysed limbs. "Nobody expected it at all," says Nicolelis, who presented the results at the Brain Forum in Lausanne, Switzerland, on 31 March. "When we first saw the level of recovery, there was not a single person in the room with a dry eye." When a person's spinal cord is injured, the connection between body and brain can be damaged, leaving them unable to feel or move parts of their body. If a few spinal nerves remain, people can sometimes regain control over their limbs, although this can involve years of rehabilitation. © Copyright Reed Business Information Ltd.
Link ID: 20805 - Posted: 04.16.2015
|By Cari Nierenberg and LiveScience Women who develop gestational diabetes early in their pregnancy have a higher chance of having a child with autism than women who don't develop the condition, a new study suggests. Researchers found that mothers-to-be who developed gestational diabetes — high blood sugar during pregnancy in women who have never had diabetes — by their 26th week of pregnancy were 63 percent more likely to have a child diagnosed with an autism spectrum disorder (ASD) compared with women who did not have gestational diabetes at any point during their pregnancy (and who also did not have type 2 diabetes prior to pregnancy). The finding does not mean that autism is common among children born to women who had gestational diabetes. "Autism is still rare," said study co-author Anny Xiang, a research scientist at Kaiser Permanente Southern California in Pasadena. The findings show that, although the risk of having a child with autism is still low among women who have gestational diabetes early in pregnancy (before 26 weeks), the study did find a relationship between these women and an increased risk that the child would have autism, Xiang said. The study, published today (April 14) in the Journal of the American Medical Association, looked at more than 320,000 children born in Southern California between 1995 and 2009. About 8 percent of the kids were born to mothers who had pregnancy-related diabetes, and 2 percent had mothers with type 2 diabetes. © 2015 Scientific American
By Neuroskeptic According to a large study just published in the Journal of Autism and Developmental Disorders, there’s no correlation between brain anatomy and self-reported autistic traits. Dutch researchers P. Cedric M. P. Koolschijn and colleagues looked at two samples of young Dutch adults: an ‘exploration’ sample of 204, and a separate ‘validation’ group of 304 individuals. Most of the participants did not have autism. The researchers looked for associations between various aspects of brain structure and autistic traits, using the AQ questionnaire, a popular self-report measure. Autistic traits are personality or behavior features similar to (but generally milder than) autism symptoms. For example, the first item on the AQ is “I prefer to do things with others rather than on my own.” If you disagree with that, you get a point. More points means more autistic traits. Koolschijn et al. used VBM, vertex-based cortical thickness analysis, and diffusion weighted imaging to explore different aspects of brain grey and white matter anatomy. However, although AQ scores were weakly correlated with the volume of a few brain areas in the exploration sample, none of these correlations were confirmed in the larger validation sample, suggesting that they were just false positives caused by the large number of multiple comparisons.
A study using mice has uncovered a possible cause of Alzheimer’s disease, and suggests that a drug currently being investigated in human clinical trials to treat cancer could prevent the illness. The research has been heralded as offering hope of finding new treatments for dementia, an illness that affects 850,000 people in the UK. The findings, by Duke University in America and published in the Journal of Neuroscience, are surprising, according to one of the authors, as they contradict current thinking on the disease. The research suggests that in mice with Alzheimer’s disease certain immune cells that normally protect the brain begin abnormally to consume an important nutrient called arginine. By blocking this process using the drug difluoromethylornithine (DFMO), memory loss and a buildup of sticky proteins known as brain plaques were prevented. The study used a type of mouse in which a number of important genes had been swapped to make the animal’s immune system more similar to a human’s. Senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences, said: “If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease.” It was previously thought the brain releases molecules that ramp up the immune system, apparently damaging the brain, but the study found a heightened expression of genes associated with the suppression of the immune system. Author Matthew Kan said: “It’s surprising because [suppression of the immune system is] not what the field has been thinking is happening in AD [Alzheimer’s disease].” © 2015 Guardian News and Media Limited
Link ID: 20802 - Posted: 04.15.2015
Jon Hamilton There's new evidence that the brain's activity during sleep isn't random. And the findings could help explain why the brain consumes so much energy even when it appears to be resting. "There is something that's going on in a very structured manner during rest and during sleep," says Stanford neurologist Dr. Josef Parvizi, "and that will, of course, require energy consumption." For a long time, scientists dismissed the brain's electrical activity during rest and sleep as meaningless "noise." But then studies using fMRI began to reveal patterns suggesting coordinated activity. To take a closer look, Parvizi and a team of researchers studied three people awaiting surgery for epilepsy. These people spent several days with electrodes in their brains to help locate the source of their seizures. And that meant Parvizi's team was able to monitor the activity of small groups of brain cells in real time. "We wanted to know exactly what's going on during rest," Parvizi says, "and whether or not it reflects what went on during the daytime when the subject was not resting." In the study published online earlier this month in Neuron, the team first studied the volunteers while they were awake and answering simple questions like: Did you drive to work last week? "In order to answer yes or no, you retrieve a lot of facts; you retrieve a lot of visualized memories," Parvizi says. © 2015 NPR
By JAMES GORMAN Studies of hunters and gatherers — and of chimpanzees, which are often used as stand-ins for human ancestors — have cast bigger, faster and more powerful males in the hunter role. Now, a 10-year study of chimpanzees in Senegal shows females playing an unexpectedly big role in hunting and males, surprisingly, letting smaller and weaker hunters keep their prey. The results do not overturn the idea of dominant male hunters, said Jill D. Pruetz of Iowa State University, who led the study. But they may offer a new frame of reference on hunting, tools and human evolution. “We need to broaden our perspective,” she said. Among the 30 or so chimps Dr. Pruetz and her colleagues observed, called the Fongoli band, males caught 70 percent of the prey, mostly by chasing and running it down. But these chimps are very unusual in one respect. They are the only apes that regularly hunt other animals with tools — broken tree branches. And females do the majority of that hunting for small primates called bush babies. Craig Stanford, an anthropologist at the University of Southern California who has written extensively on chimp hunting and human evolution, said the research was “really important” because it solidified the evidence for chimps hunting with tools, which Dr. Pruetz had reported in earlier papers. It also clearly shows “the females are more involved than in other places,” he said, adding that it provides new evidence to already documented observations that female chimps are “much more avid tool users than males are.” All chimpanzees eat a variety of plant and animal foods, including insects like termites. And all chimpanzees eat some other animals. The most familiar examples of chimpanzee hunting are bands of the apes chasing red colobus monkeys through the trees in the rain forests of East Africa. © 2015 The New York Times Company
By Laura Sanders To drive a rat to drink, make it smoke first. Rats dependent on nicotine escalate their drinking more quickly than rats that haven’t been exposed to nicotine, researchers report in the April 15 Journal of Neuroscience. The results help explain why alcohol and tobacco addictions in people often go hand in hand. After nicotine injections, rats that had previously been exposed to alcohol dosed themselves with more alcohol than rats unexposed to nicotine did. Scientists were able to curb this booziness: Rats injected with a compound that made brain cells ignore nicotine did not boost their intake of alcohol. The double whammy of nicotine and alcohol dependence may be due to a select group of nerve cells throughout the rat brain that respond to this nicotine-aided drinking, Olivier George of the Scripps Research Institute in La Jolla, Calif., and colleagues found. If a similar response happens in humans, studying these particular nerve cells might ultimately lead to better ways to curb both alcohol and tobacco dependencies, the researchers write. R. Leão et al. Chronic nicotine activates stress/reward-related brain regions and facilitates the transition to compulsive alcohol drinking. Journal of Neuroscience. Vol. 35, April 15, 2015. doi:10.1523/JNEUROSCI.3302-14.2015. © Society for Science & the Public 2000 - 2015.
Keyword: Drug Abuse
Link ID: 20799 - Posted: 04.15.2015
Daniel Cressey Experiments that use only a small number of animals are common, but might not give meaningful results. Replace, refine, reduce: the 3 Rs of ethical animal research are widely accepted around the world. But now the message from UK funding agencies is that some experiments use too few animals, a problem that leads to wastage and low-quality results. On 15 April, the research councils responsible for channelling government funding to scientists, and their umbrella group Research Councils UK, announced changes to their guidelines for animal experiments. Funding applicants must now show that their work will provide statistically robust results — not just explain how it is justified and set out the ethical implications — or risk having their grant application rejected. The move aims to improve the quality of medical research, and will help to address widespread concerns that animals — mostly mice and rats — are being squandered in tiny studies that lack statistical power. “If the study is underpowered your results are not going to be reliable,” says Nathalie Percie du Sert, who works on experimental design at the National Centre for the Replacement, Refinement and Reduction (NC3Rs) of Animals in Research in London. “These animals are going to be wasted.” © 2015 Nature Publishing Group
Keyword: Animal Rights
Link ID: 20798 - Posted: 04.15.2015
By VIRGINIA HEFFERNAN Most newly stylish coinages carry with them some evidence of grammatical trauma. Consider “affluencer,” “selfie,” “impactful.” Notes of cynicism and cutesiness come through. But every now and then a bright exception to this dispiriting routine appears. A rookie word makes its big-league debut, a stadium of pedants prepares to peg it with tomatoes and — nothing. A halfhearted heckle. The new word looks only passably pathetic. Maddeningly, it has heft. “Mindfulness” may be that hefty word now, one that can’t readily be dismissed as trivia or propaganda. Yes, it’s current among jaw-grinding Fortune 500 executives who take sleeping pills and have “leadership coaches,” as well as with the moneyed earnest, who shop at Whole Foods, where Mindful magazine is on the newsstand alongside glossies about woodworking and the environment. It looks like nothing more than the noun form of “mindful” — the proper attitude toward the London subway’s gaps — but “mindfulness” has more exotic origins. In the late 19th century, the heyday of both the British Empire and Victorian Orientalism, a British magistrate in Galle, Ceylon (now Sri Lanka), with the formidable name of Thomas William Rhys Davids, found himself charged with adjudicating Buddhist ecclesiastical disputes. He set out to learn Pali, a Middle Indo-Aryan tongue and the liturgical language of Theravada, an early branch of Buddhism. In 1881, he thus pulled out “mindfulness” — a synonym for “attention” from 1530 — as an approximate translation of the Buddhist concept of sati. The translation was indeed rough. Sati, which Buddhists consider the first of seven factors of enlightenment, means, more nearly, “memory of the present,” which didn’t track in tense-preoccupied English. “Mindfulness” stuck — but may have saddled the subtle sati with false-note connotations of Victorian caution, or even obedience. (“Mind your manners!”) © 2015 The New York Times Company
Link ID: 20797 - Posted: 04.14.2015
By Lenny Bernstein Children with two of the most severe forms of epilepsy can suffer scores of seizures each day, as well as long-term physical and cognitive problems. The two conditions, Dravet and Lennox-Gastaut syndromes, are quite rare but unfortunately very resistant to treatment with current epilepsy drugs. Now a compound found in marijuana plants has shown promising results in a preliminary study, during which it sharply reduced the number of seizures suffered by these children. Some were even seizure-free after three months of taking the drug, cannabidiol, the research showed. "We're very encouraged by the data," said Orrin Devinsky, director of the NYU Langone Comprehensive Epilepsy Center and leader of the research. A more rigorous study of cannabidiol's impact has begun and will help determine how effective it really is, he said. In making cannabidiol, the marijuana plant's psychoactive material (THC) was removed. A 99 percent pure liquid version of the drug was given for three to six months to 137 people with the two syndromes. Most were children (the subjects ranged in age from 2 to 26), and before the experiment they suffered a disturbing average of 95.3 convulsive seizures every month. Convulsive seizures are the more severe, violent kind; people with epilepsy can experience a wide variety of seizures, including some mild enough that they appear to be merely staring into space for a few seconds. Some of the subjects had taken as many as 10 different epilepsy drugs, with little success.
Fred Powledge I think I knew what was happening even before my head bounced off the hard kitchen counter on its way to the even harder stone floor. I was rapidly losing my connection with reality. My wife, Tabitha, later estimated that I was out for 10 minutes. When I emerged from unconsciousness I heard the sirens on the street in front of the house. It seemed as if half of Tucson's fire department was streaming through the front door. I was scared. At my age, which is old, you laugh at any childlike faith in your immortality. In this case, what brought on the unconsciousness was apparently a quick turn of my head while reaching for an onion to peel for the night's dinner, followed by the knockout blow from hitting the floor. I was scared. At my age, which is old, you laugh at any childlike faith in your immortality. An enormous hook and ladder and an ambulance were drawn up in front of the house, sirens winding down. The commotion was embarrassing, but it was comforting to know that my wife was in the next room, had called for help, and that 911 had responded to her call as it was supposed to. The emergency room doctor said I had a concussion — a blow to the head that our new and improved language calls a MTBI. This scared me as much as the ambulance ride itself, since it stands for "Mild Traumatic Brain Injury." © 2015 NPR
Keyword: Brain Injury/Concussion
Link ID: 20795 - Posted: 04.14.2015
by Penny Sarchet You've got a splitting migraine. If you were offered a sugar pill, would you bother taking it? What if you were told your genetic make-up means it is very likely to make you feel better? This is one of the questions raised by the burgeoning effort to understand which genes influence the placebo effect, and how these genes – collectively known as the placebome – determine a person's susceptibility to the phenomenon. There are tremendous differences in the placebo effect between individuals, says Kathryn Hall of Harvard Medical School. "It can vary from no measurable response to someone getting significantly better." Having drawn together all the studies carried out so far, Hall says there is reasonable evidence for at least 11 genes that influence a person's susceptibility. This is enough to warrant discussing the use of genetic screening to assess how likely a person is to respond to a placebo treatment, such as a sugar pill or saline injection. The idea is that this could lead to more personalised treatments for conditions like pain syndromes, migraines, depression, irritable bowel syndrome and even Parkinson's disease, symptoms of which seem to be relieved by placebo in some individuals. It could also lead to the design of more balanced clinical trials. Your personality can help you guess whether you're among the estimated third of the population who are placebo responders. Being agreeable, extroverted and open to new experiences all appear to be associated with placebo susceptibility. Although brain imaging techniques can also indicate a person's likely susceptibility, a genetic read-out would offer a convenient, easily applicable and clearly codified measure. © Copyright Reed Business Information Ltd
Keyword: Pain & Touch
Link ID: 20794 - Posted: 04.14.2015
|By Andrea Alfano To scratch an itch is to scratch many itches: placing nails to skin brings sweet yet short-lived relief because it often instigates another bout of itchiness. The unexpected culprit behind this vicious cycle, new research reveals, is serotonin, the so-called happiness hormone. Scientists thought itch was merely a mild form of pain until 2009, when Zhou-Feng Chen and his colleagues at the Center for the Study of Itch at Washington University in St. Louis discovered itch-specific neurons in mice. Though not identical, itch and pain are closely related; they share the same pathways in certain brain areas. Because of the doubling up, activating one suppresses the other, which is why scratching blocks the itch sensation momentarily. The act, however, also triggers the release of the chemical serotonin, which helps to alleviate pain. It is that burst that makes scratching feel good, but recent work by Chen's group showed that it exacerbates the itch-scratch cycle, too. Itch-sensing neurons have a set of receptors that facilitates pain relief and another that induces itch. Serotonin can bind only to the pain-related receptor, but because the two sets sit close to each other and physically interact, the chemical's arrival indirectly enhances the itch pathway. When Chen and his colleagues activated both receptors simultaneously in mice, the rodents scratched much more than if the itch-inducing receptor was turned on alone. In another experiment, mice lacking the cells that produce serotonin scratched less than normal mice when exposed to a skin irritant. The findings were published in the journal Neuron. © 2015 Scientific American
Keyword: Pain & Touch
Link ID: 20793 - Posted: 04.14.2015
Boer Deng Universities in the United States employ many more male scientists than female ones. Men are paid more, and in fields such as mathematics, engineering and economics, they hold the majority of top-level jobs. But in a sign of progress, a 13 April study finds that faculty members prefer female candidates for tenure-track jobs in science and engineering — by a ratio of two to one. That result, based on experiments involving hypothetical job seekers, held true regardless of the hirer’s gender, department, career status or university type, researchers report in the Proceedings of the National Academy of Sciences1. “We were shocked,” says Wendy Williams, a psychologist at Cornell University in Ithaca, New York, and a co-author of the study. With fellow Cornell psychologist Stephen Ceci, she surveyed 873 tenure-track faculty members in biology, psychology, economics and engineering at 371 US universities. One experiment presented participants with three hypothetical job candidates, of which two were identical except for their gender. Another experiment added descriptions of marital and parental status, to test whether underlying assumptions about gender choices affected hiring. “You don’t frequently see that level of attention and sophistication” in statistical analysis, says Robert Santos, vice-president of the American Statistical Association in Alexandria, Virginia. Nothing seemed to sway study participants’ preference for female job candidates. The authors say that this is interesting given their previous finding that a relatively low percentage of female PhDs in the social and biological sciences secure academic positions — in part because they are less likely than men to apply for these jobs. Other research suggests that in the physical sciences, women and men are just as likely to secure a tenure-track position within five years of earning a PhD. © 2015 Nature Publishing Group
Keyword: Sexual Behavior
Link ID: 20792 - Posted: 04.14.2015
By David Grimm The U.S. Department of Agriculture has launched an investigation into Harvard University’s New England Primate Research Center after several suspicious deaths at the Southborough, Massachusetts, facility. The inquiry coincides with a series of articles published by The Boston Globe, which has uncovered a number of potential animal welfare violations at the center, including a dozen dehydrated squirrel monkeys found dead in their cages or euthanized because of poor health between 1999 and 2011. In several cases it appears that the animals were not given water or were unable to drink due to malfunctioning water lines. In one incident, a monkey’s tooth caught in her jacket, preventing her from drinking. Some of these animals were the subject of a 2014 Veterinary Pathology paper on the impact of dehydration on lab animals. The journal says it is now investigating this study. The primate center is set to close at the end of next month, though—according to the Globe—the university blames finances, not animal care problems. © 2015 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 20791 - Posted: 04.14.2015
By STEVEN QUARTZ and ANETTE ASP THE gaping inequality of America’s first Gilded Age generated strong emotions. It produced social reformers like Jane Addams, anarchist agitators like Emma Goldman, labor leaders like Eugene V. Debs and Progressive politicians like Theodore Roosevelt. By the 1920s, sweeping legislation regulating food and drugs and breaking up corrupt trusts had been passed. The road to the New Deal was paved. But our current Gilded Age has been greeted with relative complacency. Despite soaring inequality, worsened by the Great Recession, and recent grumbling about the 1 percent, Americans remain fairly happy. All of the wage gains since the downturn ended in 2009 have essentially gone to the top 1 percent, yet the proportion of Americans who say they are “thriving” has actually increased. So-called happiness inequality — the proportion of Americans who are either especially miserable or especially joyful — hit a 40-year low in 2010 by some measures. Men have historically been less happy than women, but that gap has disappeared. Whites have historically been happier than nonwhites, but that gap has narrowed, too. In fact, American happiness has not only stayed steady, but converged, since wages began stagnating in the mid-1970s. This is puzzling. It does not conform with economic theories that compare happiness to envy, and emphasize the impact of relative income for happiness — how we compare with the Joneses. A new neuroscience of consumer behavior reinforces our argument. In one experiment, we used functional magnetic resonance imaging (fMRI) to understand our brains’ reaction to perceived coolness. We selected students from the Art Center College of Design in Pasadena, Calif., and asked them to rate, from uncool to cool, hundreds of images from the following categories: bottled water, shoes, perfumes, handbags, watches, cars, chairs, personal electronics and sunglasses. We also included images of celebrities (actors and musicians). The cooler objects typically weren’t the more expensive ones: our subjects rated a Kia hatchback above a Buick sedan, for example. © 2015 The New York Times Company
Link ID: 20790 - Posted: 04.13.2015
By MALIA WOLLAN “A polygraph is nothing more than a psychological billy club used to coerce and intimidate people,” says Doug Williams, a former Oklahoma City police detective and polygraph examiner who for 36 years has trained people to pass the lie-detector test. The first step is not to be intimidated. Most tests include two types of questions: relevant ones about a specific incident (“Did you leak classified information to The New York Times?”) and broader so-called control questions (“Have you ever lied to anyone who trusted you?”). The test assumes that an innocent person telling the truth will have a stronger reaction to the control questions than to the relevant ones. Before your test, practice deciphering between the two question types. “Go to the beach” when you hear a relevant question, Williams says. Calm yourself before answering by imagining gentle waves and warm sand. When you get a control question, which is more general, envision the scariest thing you can in order to trigger physiological distress; the polygraph’s tubes around your chest measure breathing, the arm cuff monitors heart rate and electrodes attached to you fingertips detect perspiration. What is your greatest fear? Falling? Drowning? Being buried alive? “Picture that,” Williams says. He used to advise trainees to clench their anus but has since concluded that terrifying mental imagery works better. Williams, who is 69, may be among the more vitriolic critics of polygraphs, which he refers to as “insidious Orwellian instruments of torture,” but their reliability has long been questioned elsewhere, too. Federal legislation prohibits most private employers from using polygraphs. The U.S. Supreme Court has ruled that lower courts can ban them as evidence, and the scientific community has repeatedly raised concerns about their ability to accurately detect lies. © 2015 The New York Times Company
Link ID: 20789 - Posted: 04.13.2015