Chapter 11. Emotions, Aggression, and Stress
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Annie Murphy Paul Twelve years ago, I tried to drive a stake into the heart of the personality-testing industry. Personality tests are neither valid nor reliable, I argued, and we should stop using them — especially for making decisions that affect the course of people's lives, like workplace hiring and promotion. But if I thought that my book, The Cult of Personality Testing, would lead to change in the world, I was keenly mistaken. Personality tests appear to be more popular than ever. I say "appear" because — today as when I wrote the book — verifiable numbers on the use of such tests are hard to come by. Personality testing is an industry the way astrology or dream analysis is an industry: slippery, often underground, hard to monitor or measure. There are the personality tests administered to job applicants "to determine if you're a good fit for the company;" there are the personality tests imposed on people who are already employed, "in order to facilitate teamwork;" there are the personality tests we take voluntarily, in career counseling offices and on self-improvement retreats and in the back pages of magazines (or, increasingly, online.) I know these tests are popular because after the book was published, most of the people I heard from were personality-test enthusiasts, eager to rebut my critique of the tests that had, they said, changed their lives. © 2016 npr
Link ID: 22359 - Posted: 06.25.2016
Ian Sample Science editor Brain scans have highlighted “striking” differences between the brains of young men with antisocial behavioural problems and those of their better-behaved peers. The structural changes, seen as variations in the thickness of the brain’s cortex or outer layer of neural tissue, may result from abnormal development in early life, scientists at Cambridge University claim. But while the images show how the two groups of brains differ on average, the scans cannot be used to identify individuals with behavioural issues, nor pinpoint specific developmental glitches that underpin antisocial behaviour. Led by Luca Passamonti, a neurologist at Cambridge, the researchers scanned the brains of 58 young men aged 16 to 21 who had been diagnosed with conduct disorder, defined by persistent problems that ranged from aggressive and destructive behaviour, to lying and stealing, carrying weapons or staying out all night. When compared with brain scans from 25 healthy men of the same age, the scientists noticed clear differences. Those diagnosed with conduct disorder before the age of 10 had similar variations in the thickness of the brain’s cortex. “It may be that problems they experience in childhood affect and delay the way the cortex is developing,” said Passamonti. But the brains of men diagnosed with behavioural problems in adolescence differed in another way. Scans on them showed fewer similarities in cortical thickness than were seen in the healthy men. That, Passamonti speculates, may arise when normal brain maturation, such as the “pruning” of neurons and the connections between them, goes awry. © 2016 Guardian News and Media Limited
Aggressive chemotherapy followed by a stem cell transplant can halt the progression of multiple sclerosis (MS), a small study has suggested. The research, published in The Lancet, looked at 24 patients aged between 18 and 50 from three hospitals in Canada. For 23 patients the treatment greatly reduced the onset of the disease, but in one case a person died. An MS Society spokeswoman said this type of treatment does "offer hope" but also comes with "significant risks". Around 100,000 people in the UK have MS, which is an incurable neurological disease. 'No relapses' The condition causes the immune system to attack the lining of nerves in the brain and spinal cord. Most patients are diagnosed in their 20s and 30s. One existing treatment is for the immune system to be suppressed with chemotherapy and then stem cells are introduced to the patient's bloodstream - this procedure is known as an autologous haematopoietic stem cell transplant (HSCT). But in this study, Canadian researchers went further - not just suppressing the immune system, but destroying it altogether. It is then rebuilt with stem cells harvested from the patient's own blood which are at such an early stage, they have not developed the flaws that trigger MS. The authors said that among the survivors, over a period of up to 13 years, there were no relapses and no new detectable disease activity. All the patients who took part in the trial had a "poor prognosis" and had previously undergone standard immunosuppressive therapy which had not controlled the MS - which affects around two million people worldwide. © 2016 BBC.
By ROBERT F. WORTH In early 2012, a neuropathologist named Daniel Perl was examining a slide of human brain tissue when he saw something odd and unfamiliar in the wormlike squiggles and folds. It looked like brown dust; a distinctive pattern of tiny scars. Perl was intrigued. At 69, he had examined 20,000 brains over a four-decade career, focusing mostly on Alzheimer’s and other degenerative disorders. He had peered through his microscope at countless malformed proteins and twisted axons. He knew as much about the biology of brain disease as just about anyone on earth. But he had never seen anything like this. The brain under Perl’s microscope belonged to an American soldier who had been five feet away when a suicide bomber detonated his belt of explosives in 2009. The soldier survived the blast, thanks to his body armor, but died two years later of an apparent drug overdose after suffering symptoms that have become the hallmark of the recent wars in Iraq and Afghanistan: memory loss, cognitive problems, inability to sleep and profound, often suicidal depression. Nearly 350,000 service members have been given a diagnosis of traumatic brain injury over the past 15 years, many of them from blast exposure. The real number is likely to be much higher, because so many who have enlisted are too proud to report a wound that remains invisible. For years, many scientists have assumed that explosive blasts affect the brain in much the same way as concussions from football or car accidents. Perl himself was a leading researcher on chronic traumatic encephalopathy, or C.T.E., which has caused dementia in N.F.L. players. Several veterans who died after suffering blast wounds have in fact developed C.T.E. But those veterans had other, nonblast injuries too. No one had done a systematic post-mortem study of blast-injured troops. That was exactly what the Pentagon asked Perl to do in 2010, offering him access to the brains they had gathered for research. It was a rare opportunity, and Perl left his post as director of neuropathology at the medical school at Mount Sinai to come to Washington. © 2016 The New York Times Company
By Rita Celli, This is what Jennifer Molson remembers doctors saying to her about the high-stakes procedure she would undergo in 2002 as part of an Ottawa study that has yielded some promising results in multiple sclerosis patients. The 41-year-old Ottawa woman was in a wheelchair before the treatment. She now walks, runs and works full time. "I had no feeling from my chest down. I could barely cut my food," Molson remembers. Molson was diagnosed with MS when she was 21, and within five years she needed full-time care. "It was scary. [The procedure] was my last shot at living." MS is among the most common chronic inflammatory diseases of the central nervous system, affecting an estimated two million people worldwide. New Canadian research led by two Ottawa doctors and published in The Lancet medical journal on Thursday suggests the high-risk therapy may stop the disease from progressing. "This is the first treatment to produce this level of disease control or neurological recovery" from MS, said The Lancet in a news release. But The Lancet also highlights the high mortality rate associated with the procedure — one patient out of 24 involved in the clinical trial died from liver failure. "Treatment related risks limit [the therapy's] widespread use," The Lancet concludes. Results 'impressive' Nevertheless, in the journal's accompanying editorial a German doctor calls the results "impressive." ©2016 CBC/Radio-Canada.
By JAMES GORMAN This summer’s science horror blockbuster is a remake: Return of the Leaping Electric Eel! If you have any kind of phobia of slimy, snakelike creatures that can rise from the water and use their bodies like Tasers, this story — and the accompanying video — may not be for you. The original tale (there was, alas, no video) dates to 1800 when the great explorer Alexander von Humboldt was in South America and enlisted local fishermen to catch some of these eels for the new (at the time) study of electricity. He wrote that the men herded horses and mules into a shallow pond and let the eels attack by pressing themselves against the horses. The horses and mules tried to escape, but the fishermen kept them in the water until the eels used up their power. Two horses died, probably from falling and drowning. Or so Humboldt said. Though the story was widely retold, no other report of this kind of fishing-with-horses phenomenon surfaced for more than 200 years, according to Kenneth Catania, a scientist with a passion for studying the eel species in question, electrophorus electricus. In 2014, he reported on how the eels freeze their prey. They use rapid pulses of more than 600 volts generated by modified muscle cells and sent through the water. These volleys of shocks cause the muscles of prey to tense at once, stopping all movement. The eels’ bodies function like Tasers, Dr. Catania wrote. But they can also project high-voltage pulses in the water in isolated couplets rather than full volleys for a different effect. The pairs of shocks don’t freeze the prey, but cause their bodies to twitch. That movement reveals the prey’s location, and then the eels send out a rapid volley to immobilize then swallow it. Dr. Catania noticed another kind of behavior, however. He was using a metal-handled net — wearing rubber gloves — while working with eels in an aquarium, and the eels would fling themselves up the handle of the net, pressing themselves to the metal and generating rapid electric shocks. © 2016 The New York Times Company
By LISA FELDMAN BARRETT WHEN the world gets you down, do you feel just generally “bad”? Or do you have more precise emotional experiences, such as grief or despair or gloom? In psychology, people with finely tuned feelings are said to exhibit “emotional granularity.” When reading about the abuses of the Islamic State, for example, you might experience creeping horror or fury, rather than general awfulness. When learning about climate change, you could feel alarm tinged with sorrow and regret for species facing extinction. Confronted with this year’s presidential campaign, you might feel astonished, exasperated or even embarrassed on behalf of the candidates — an emotion known in Mexico as “pena ajena.” Emotional granularity isn’t just about having a rich vocabulary; it’s about experiencing the world, and yourself, more precisely. This can make a difference in your life. In fact, there is growing scientific evidence that precisely tailored emotional experiences are good for you, even if those experiences are negative. According to a collection of studies, finely grained, unpleasant feelings allow people to be more agile at regulating their emotions, less likely to drink excessively when stressed and less likely to retaliate aggressively against someone who has hurt them. Perhaps surprisingly, the benefits of high emotional granularity are not only psychological. People who achieve it are also likely to have longer, healthier lives. They go to the doctor and use medication less frequently, and spend fewer days hospitalized for illness. Cancer patients, for example, have lower levels of harmful inflammation when they more frequently categorize, label and understand their emotions. © 2016 The New York Times Company
Link ID: 22285 - Posted: 06.06.2016
By Ann Griswold, Women who develop infections during pregnancy run an increased risk of having a child with autism. Most data indicate that an overactive maternal immune response underlies the risk. But a new analysis runs contrary to this view: It ties high levels of an inflammatory protein in pregnant women to a low risk of autism in their children, suggesting that a strong immune response is protective. Researchers looked at 1,315 mother-child pairs, including 500 children with autism and 235 with developmental delay. They found that healthy pregnant women with high levels of C-reactive protein (CRP), a marker of inflammation, are less likely to have a child with autism than are women with typical levels of the protein. The findings contradict a 2013 report from a large Finnish cohort that tied high CRP levels during pregnancy to an increased risk of having a child with autism. “It was the opposite of what we expected to find,” says senior researcher Lisa Croen, director of the Autism Research Program at Kaiser Permanente in Oakland, California. The work appeared in April in Translational Psychiatry. The results suggest that the strength of a woman’s immune system, rather than its response to infection, is the important factor in determining autism risk. Moderate or low baseline levels of CRP might indicate a relatively weak ability to fight off infection. And a less vigorous immune response might boost the risk in some women, the researchers say. © 2016 Scientific American,
By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.
By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American
By Andy Coghlan It’s a tear-jerker worthy of Hollywood – and one of the first examples of compassionate care and grief in a wild monkey. The alpha male of a group of snub-nosed monkeys and his dying partner spent a final, tender hour together beneath the tree from which she had fallen minutes earlier, cracking her head on a rock. Before she succumbed, he gently touched and groomed her. And after she was dead he remained by her side for 5 minutes, touching her and pulling gently at her hand, as if to try and revive her (for a full account of what happened, see “A monkey tends to his dying mate – as it unfolded”, below). “The case we’ve reported is particularly important because of the exclusively gentle nature of the interactions, and the special treatment of the dying female shown by the adult male,” says James Anderson of Kyoto University, Japan. “The events suggest that in the case of strongly bonded individuals at least, monkeys may show compassionate behaviour to ailing or dying individuals.” Together, the reports add to evidence that humans may not be the only species to display grieving behaviour following bereavement, or to show respect for dead individuals with whom they have forged ties. They also hint that animals have some recognition of the finality of death. “It seems likely that in long-lived species such as many primates, repeated exposure to death within the group leads to an understanding of the irreversibility of death,” says Anderson. “I believe the adult male and other members of his unit understood the dead female was no longer alive.” © Copyright Reed Business Information Ltd.
By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division
By Karen Weintraub There are case reports of people with no previously known risks having a heart attack after a nightmare, though they appear to be quite rare. No studies have been done to determine just how rare nightmare-induced heart attacks might be, and experts do not know whether they may result from the pulse-racing effects of the frightening dream itself. Nightmares are more commonly seen in the rapid eye movement, or REM, phase of sleep, which gets longer as the night progresses. Therefore, nightmares are more likely to occur in the early morning hours. Heart attacks, too, are most common in the early morning hours, when internal body clocks start secreting stress hormones and blood pressure tends to rise, said Dr. Mary Ann McLaughlin, a cardiologist at the Icahn School of Medicine at Mount Sinai in New York. If someone is at risk for a heart attack — because of high blood pressure, diabetes, sleep apnea, smoking or other factors — that attack is more likely to occur in the early morning. But “it’s rare for an otherwise healthy person to have a nightmare that causes a heart attack,” said Dr. McLaughlin. Nightmares can be triggered by alcohol, lack of sleep and medications, including some antidepressants and blood pressure medications, she said. Anxiety and depression have also been linked to increased risk of nightmares. On the flip side, patients with heart disease often have sleep apnea, a form of disordered breathing that can lead to fragmented sleep, and potentially more nightmares, said Dr. Neomi Shah, a sleep specialist, also at Mount Sinai. One 2013 study found that apnea patients with regular nightmares woke up more often than those who didn’t. Nightmares disappeared in more than 90 percent of the patients who used a continuous positive airway pressure, or CPAP, machine to treat their apnea. © 2016 The New York Times Company
Link ID: 22232 - Posted: 05.21.2016
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By Geraldine Dawson There’s a popular saying in the autism community: “If you’ve met one person with autism, you’ve met one person with autism.” Although this phrase is meant to convey the remarkable variation in abilities and disabilities among people with autism spectrum disorder (ASD), we’re learning that it also applies to the extraordinary variability in how ASD develops. When I first began doing research on autism decades ago, we thought of it as one condition and aimed to discover its “cause.” Now we know ASD is actually a group of lifelong conditions that can arise from a complex combination of multiple genetic and environmental factors. In the same way that each person with ASD has a unique personality and profile of talents and disabilities, each also has a distinct developmental history shaped by a specific combination of genetic and environmental factors. More evidence of this extraordinary variety will be presented this week in Baltimore, where nearly 2,000 of the world’s leading autism researchers will gather for the International Meeting for Autism Research (IMFAR). As president of the International Society for Autism Research, which sponsors the conference, I am more impressed than ever with the progress we are making. New findings being presented at the conference will highlight the importance of the prenatal period in understanding how various environmental factors such as exposure to alcohol, smoking and certain chemical compounds can increase risk for ASD. The impact of many environmental factors depends, however, on an individual’s genetic background and the timing of the exposure. Other research links inflammation—detected in blood spot tests taken at birth—with a higher likelihood of an ASD diagnosis later on. Researchers suggest that certain factors such as maternal infection and other factors during pregnancy may influence an infant’s immune system and contribute to risk. As our knowledge of these risk factors grows, so do the opportunities for promoting healthy pregnancies and better outcomes. © 2016 Scientific American
By Marta Zaraska Scientists and laypeople alike have historically attributed political beliefs to upbringing and surroundings, yet recent research shows that our political inclinations have a large genetic component. The largest recent study of political beliefs, published in 2014 in Behavior Genetics, looked at a sample of more than 12,000 twin pairs from five countries, including the U.S. Some were identical and some fraternal; all were raised together. The study reveals that the development of political attitudes depends, on average, about 60 percent on the environment in which we grow up and live and 40 percent on our genes. “We inherit some part of how we process information, how we see the world and how we perceive threats—and these are expressed in a modern society as political attitudes,” explains Peter Hatemi, who is a genetic epidemiologist at the University of Sydney and lead author of the study. The genes involved in such complex traits are difficult to pinpoint because they tend to be involved in a huge number of bodily and cognitive processes that each play a minuscule role in shaping our political attitudes. Yet a study published in 2015 in the Proceedings of the Royal Society B managed to do just that, showing that genes encoding certain receptors for the neurotransmitter dopamine are associated with where we fall on the liberal-conservative axis. Among women who were highly liberal, 62 percent were carriers of certain receptor genotypes that have previously been associated with such traits as extroversion and novelty seeking. Meanwhile, among highly conservative women, the proportion was only 37.5 percent. © 2016 Scientific American
By Jessica Lahey Before she became a neuroscientist, Mary Helen Immordino-Yang was a seventh-grade science teacher at a school outside Boston. One year, during a period of significant racial and ethnic tension at the school, she struggled to engage her students in a unit on human evolution. After days of apathy and outright resistance to Ms. Immordino-Yang’s teaching, a student finally asked the question that altered her teaching — and her career path — forever: “Why are early hominids always shown with dark skin?” With that question, one that connected the abstract concepts of human evolution and the very concrete, personal experiences of racial tension in the school, her students’ resistance gave way to interest. As she explained the connection between the effects of equatorial sunlight, melanin and skin color and went on to explain how evolutionary change and geography result in various human characteristics, interest blossomed into engagement, and something magical happened: Her students began to learn. Dr. Immordino-Yang’s eyes light up as she recounts this story in her office at the Brain and Creativity Institute at the University of Southern California. Now an associate professor of education, psychology and neuroscience, she understands the reason behind her students’ shift from apathy to engagement and, finally, to deep, meaningful learning. Her students learned because they became emotionally engaged in material that had personal relevance to them. Emotion is essential to learning, Dr. Immordino-Yang said, and should not be underestimated or misunderstood as a trend, or as merely the “E” in “SEL,” or social-emotional learning. Emotion is where learning begins, or, as is often the case, where it ends. Put simply, “It is literally neurobiologically impossible to think deeply about things that you don’t care about,” she said. © 2016 The New York Times Company
By Sarah Kaplan Scientists have known for a while that stereotypes warp our perceptions of things. Implicit biases — those unconscious assumptions that worm their way into our brains, without our full awareness and sometimes against our better judgment — can influence grading choices from teachers, split-second decisions by police officers and outcomes in online dating. We can't even see the world without filtering it through the lens of our assumptions, scientists say. In a study published Monday in the journal Nature Neuroscience, psychologists report that the neurons that respond to things such as sex, race and emotion are linked by stereotypes, distorting the way we perceive people's faces before that visual information even reaches our conscious brains. "The moment we actually glimpse another person ... [stereotypes] are biasing that processing in a way that conforms to our already existing expectations," said Jonathan Freeman, a psychology professor at New York University and one of the authors of the report. Responsibility lies in two far-flung regions of the brain: the orbital frontal cortex, which rests just above the eyes and is responsible for rapid visual predictions and categorizations, and the fusiform cortex, which sits in the back of the brain and is involved in recognizing faces. When Freeman and his co-author, Ryan Stolier, had 43 participants look at images of faces in a brain scanner, they noticed that neurons seemed to be firing in similar patterns in both parts of the brain, suggesting that information from each part was influencing the other.