Chapter 11. Emotions, Aggression, and Stress
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By Tania Rabesandratana Here’s one trick to make yourself feel happier: Listen to your own voice—digitally manipulated to make it sound cheery. That’s one potential application of a new study, in which researchers modified the speech of volunteers as they read a short story by Japanese writer Haruki Murakami. The team then altered the voice’s pitch, among other features, to make it sound happy, sad, or fearful. (Compare this normal voice with the same voice modified to sound afraid.) Listening to their own modified voices in real time through a headset, only 16 of 109 participants detected some kind of manipulation. The rest took the voice’s emotion as their own, feeling sad or happy themselves. (The result was less clear for fear.) The researchers suggest that emotions expressed through our voices are part of an ancient, unconscious primate communication system, whereas we have more conscious control over the words we utter. The voice manipulation software is available online, so anyone can experiment with it. The scientists speculate that emotion manipulation could help treat psychiatric disorders like depression. It could also change the mood of online meetings or gaming, they say, or even lend more emotional impact to singing performances. © 2016 American Association for the Advancement of Science
By Emily Underwood As long as she can remember, 53-year-old Rosa Sundquist has tallied the number of days per month when her head explodes with pain. The migraines started in childhood and have gotten worse as she’s grown older. Since 2008, they have incapacitated her at least 15 days per month, year-round. Head-splitting pain isn’t the worst of Sundquist’s symptoms. Nausea, vomiting, and an intense sensitivity to light, sound, and smell make it impossible for her to work—she used to be an office manager—or often even to leave her light-proofed home in Dumfries, Virginia. On the rare occasions when she does go out to dinner or a movie with her husband and two college-aged children, she wears sunglasses and noise-canceling headphones. A short trip to the grocery store can turn into a full-blown attack “on a dime,” she says. Every 10 weeks, Sundquist gets 32 bee sting–like injections of the nerve-numbing botulism toxin into her face and neck. She also visits a neurologist in Philadelphia, Pennsylvania, who gives her a continuous intravenous infusion of the anesthetic lidocaine over 7 days. The lidocaine makes Sundquist hallucinate, but it can reduce her attacks, she says—she recently counted 20 migraine days per month instead of 30. Sundquist can also sometimes ward off an attack with triptans, the only drugs specifically designed to interrupt migraines after they start. Millions of others similarly dread the onset of a migraine, although many are not afflicted as severely as Sundquist. Worldwide, migraines strike roughly 12% of people at least once per year, with women roughly three times as likely as men to have an attack. © 2016 American Association for the Advancement of Science.
By Erin Blakemore Despite all that neurotic clucking and scratching, domestic chickens are pretty unflappable. After all, we’ve bred them to be that way, preferring chill chicks to freaked-out fowl. But the behaviors of more anxious chickens could do more than ruffle a bunch of feathers: New research suggests that studying the genome of flustered birds could shed light on human mental disorders. In a new study published in the journal Genetics, evolutionary biologist Dominic Wright and his team looked at whether there’s a genetic connection between anxious behavior in chickens, mice and humans. Despite the compact size of the chicken genome — it’s just a third of the size of a human’s — the birds’ genes share surprising similarity to those of people. There's another reason why chickens are so great for genetic research. Because there are both wild and domesticated chickens, researchers can observe their contrasting behaviors and easily pin them to genetic differences. Wright bred wild red junglefowl chickens with their calmer cousins, white leghorn chickens, for the experiment. After eight generations, his team was able to run open field tests — experiments during which the birds were put in a brightly-lit arena and assessed for how much time they spent cowering on the periphery instead of strutting through the room. These behavioral tests helped the team identify brave and anxious birds, then narrow down areas of the genome related to variations in anxiety. They identified 10 candidate genes in the hypothalamus, an area of the brain which helps regulate anxiety.
Blocking the production of new immune cells in the brain could reduce memory problems seen in Alzheimer's disease, a study suggests. University of Southampton researchers said their findings added weight to evidence that inflammation in the brain is what drives the disease. A drug used to block the production of these microglia cells in the brains of mice had a positive effect. Experts said the results were exciting and could lead to new treatments. Up until now, most drugs used to treat dementia have targeted amyloid plaques in the brain which are a characteristic of people with the Alzheimer's disease. But this latest study, published in the journal Brain, suggests that in fact targeting inflammation in the brain, caused by a build-up of immune cells called microglia, could halt progression of the disease. Researchers found increased numbers of microglia in the post-mortem brains of people with Alzheimer's disease. Previous studies have also suggested that these cells could play an important role. Dr Diego Gomez-Nicola, lead study author from the university, said: "These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease. "The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans." © 2016 BBC
By Melinda Wenner Moyer There's a reason your mother told you to look people in the eye when you talk to them: eye contact conveys important social cues. Yet when someone holds your gaze for more than a few seconds, the experience can take on a different tenor. New work elucidates the factors that affect whether we like or loathe locking eyes for a lengthy period. Researchers have long known that eye contact is an important social signal. Our recognition of its import may even be hardwired. One study found that five-day-old babies prefer looking at faces that make direct eye contact compared with faces that have an averted gaze. “Eye contact provides some of the strongest information during a social interaction,” explains James Wirth, a social psychologist now at Ohio State University at Newark, because it conveys details about emotions and intentions. (Lack of eye contact is one of the early signs of autism in infants and toddlers.) The power of eye contact is so great that, according to a 2010 study co-authored by Wirth, if someone avoids your gaze for even a short period, you may feel ostracized. But what determines how we feel about prolonged eye contact? One recent study explored this question. In research presented in May 2015 at the Vision Sciences Society conference, psychologist Alan Johnston and his colleagues at University College London collected information from more than 400 volunteers about their personalities. Then the subjects indicated their comfort level while watching video clips of actors who appeared to be looking directly at them for varying lengths of time. © 2016 Scientific American
By Nicholas Bakalar Psychotherapy is effective in easing the symptoms of irritable bowel syndrome, researchers have found, even after therapy has ended. Irritable bowel syndrome can cause diarrhea, cramping, fever and sometimes rectal bleeding. The chronic ailment affects up to 11 percent of the population, and there is no cure or completely effective treatment. The study, in Clinical Gastroenterology and Hepatology, used data from 41 clinical trials that included 1,183 people assigned to psychotherapy and 1,107 controls. The approach was usually cognitive therapy, but some studies tested hypnotherapy, mindfulness, behavioral therapy or dynamic psychotherapy. The studies all used questionnaires at the start and end of the treatment, asking about severity and frequency of symptoms. Over all, the researchers found that 12 months after the end of treatment, 75 percent of the treatment group had greater symptom relief than the average member of the control group, although the benefits were modest. “I.B.S. is notoriously difficult to treat,” said the lead author, Kelsey T. Laird, a doctoral candidate at Vanderbilt University, “so the fact that these effects are just as strong six to 12 months later is very exciting — a significant effect, which did not decrease over time.” Whether a given individual will benefit from psychotherapy is still unknown, Ms. Laird said. But, she added, “We do know that this seems to be one of the best treatments out there. So I would recommend it.” © 2016 The New York Times Company
Link ID: 21740 - Posted: 01.02.2016
By Diana Kwon Pupils are a rich source of social information. Although changes in pupil size are automatic and uncontrollable, they can convey interest, arousal, helpful or harmful intentions, and a variety of emotions. According to a new study published in Psychological Science, we even synchronize our pupil size with others—and doing so influences social decisions. Mariska Kret, a psychologist now at the University of Amsterdam in the Netherlands, and her colleagues recruited 69 Dutch university students to take part in an investment game. Each participant decided whether to transfer zero or five euros to a virtual partner after viewing a video of their eyes for four seconds. The invested money is tripled, and the receiver chooses how much to give back to the donor—so subjects had to make quick decisions about how trustworthy each virtual partner seemed. Using an eye tracker, the investigators found that the participants' pupils tended to mimic the changes in the partners' pupils, whether they dilated, constricted or remained static. As expected, subjects were more likely to give more money to partners with dilating pupils, a well-established signal of nonthreatening intentions. The more a subject mirrored the dilating pupils of a partner, the more likely he or she was to invest—but only if they were of the same race. The Caucasian participants trusted Caucasian eyes more than Asian eyes—which suggests that group membership is important when interpreting these subtle signals. © 2015 Scientific American
By JOSEPH LEDOUX IN this age of terror, we struggle to figure out how to protect ourselves — especially, of late, from active shooters. One suggestion, promoted by the Federal Bureau of Investigation and Department of Homeland Security, and now widely disseminated, is “run, hide, fight.” The idea is: Run if you can; hide if you can’t run; and fight if all else fails. This three-step program appeals to common sense, but whether it makes scientific sense is another question. Underlying the idea of “run, hide, fight” is the presumption that volitional choices are readily available in situations of danger. But the fact is, when you are in danger, whether it is a bicyclist speeding at you or a shooter locked and loaded, you may well find yourself frozen, unable to act and think clearly. Freezing is not a choice. It is a built-in impulse controlled by ancient circuits in the brain involving the amygdala and its neural partners, and is automatically set into motion by external threats. By contrast, the kinds of intentional actions implied by “run, hide, fight” require newer circuits in the neocortex. Contemporary science has refined the old “fight or flight” concept — the idea that those are the two hard-wired options when in mortal danger — to the updated “freeze, flee, fight.” While “freeze, flee, fight” is superficially similar to “run, hide, fight,” the two expressions make fundamentally different assumptions about how and why we do what we do, when in danger. Why do we freeze? It’s part of a predatory defense system that is wired to keep the organism alive. Not only do we do it, but so do other mammals and other vertebrates. Even invertebrates — like flies — freeze. If you are freezing, you are less likely to be detected if the predator is far away, and if the predator is close by, you can postpone the attack (movement by the prey is a trigger for attack). © 2015 The New York Times Company
Bret Stetka In June of 2001 musician Peter Gabriel flew to Atlanta to make music with two apes. The jam went surprisingly well. At each session Gabriel, a known dabbler in experimental music and a founding member of the band Genesis, would riff with a small group of musicians. The bonobos – one named Panbanisha, the other Kanzi — were trained to play in response on keyboards and showed a surprising, if rudimentary, awareness of melody and rhythm. Since then Gabriel has been working with scientists to help better understand animal cognition, including musical perception. Plenty of related research has explored whether or not animals other than humans can recognize what we consider to be music – whether they can they find coherence in a series of sounds that could otherwise transmit as noise. Many do, to a degree. And it's not just apes that respond to song. Parrots reportedly demonstrate some degree of "entrainment," or the syncing up of brainwave patterns with an external rhythm; dolphins may — and I stress may — respond to Radiohead; and certain styles of music reportedly influence dog behavior (Wagner supposedly honed his operas based on the response of his Cavalier King Charles Spaniel). But most researchers agree that fully appreciating what we create and recognize as music is a primarily human phenomenon. Recent research hints at how the human brain is uniquely able to recognize and enjoy music — how we render simple ripples of vibrating air into visceral, emotional experiences. It turns out, the answer has a lot to do with timing. The work also reveals why your musician friends are sometimes more tolerant of really boring music. © 2015 npr
By Geoffrey S. Holtzman In November 1834, a 9-year-old boy named Major Mitchell was tried in Maine on one charge of maiming and one charge of felonious assault with intent to maim. He had lured an 8-year-old classmate into a field, beaten him with sticks, attempted to drown him in a stream, and castrated him with a piece of tin. Yet what makes this case so remarkable is neither the age of the defendant nor the violence of his crime, but the nature of his trial. Mitchell’s case marks the first time in U.S. history that a defendant’s attorney sought leniency from a jury on account of there being something wrong with the defendant’s brain. More recently, there has been an explosion in the number of criminals who have sought leniency on similar grounds. While the evidence presented by Mitchell’s defense was long ago debunked as pseudoscience (and was rightly dismissed by the judge), the case for exculpating Major Mitchell may actually be stronger today than it was 181 years ago. In a curious historical coincidence, recent advances in neuroscience suggest that there really might have been something wrong with Major Mitchell’s brain and that neurological deficits really could have contributed to his violent behavior. The case provides a unique window through which to view the relationship between 19th-century phrenology—the pseudoscientific study of the skull as an index of mental faculties—and 21st-century neuroscience. As you might expect, there is a world of difference between the two, but maintaining that difference depends crucially on the responsible use of neuroscience. Major Mitchell’s story cautions against overlooking neuroscience’s limitations, as well as its ability to be exploited for suspect purposes. © 2015 The Slate Group LLC.
Call it the optimism fallacy. It’s widely thought that staying happy and stress-free helps keep you healthy. But a massive study on the link between mood and mortality suggests that happiness actually has no effect on death rates. Other research that has found the opposite must have been mixing up cause and effect, says epidemiologist Richard Peto of the University of Oxford. “It’s likely that being ill makes you unhappy, rather than the other way round.” The power of positive thinking has passed into folklore, helping to fuel a large self-help industry – not to mention people who like to post “inspirational” quotes on social media. Some cancer bloggers complain that common advice to “fight” their illness by staying cheerful can be unhelpful. “Forcing optimism may have its own negative consequences,” says Gayle Sulik, who writes the “Pink Ribbon Blues” blog. “The emotional work to display optimism when a person does not feel it may add to stress.” To find out if there is indeed a link, Peto’s team conducted surveys with more than 700,000 UK women. At the start, they were asked questions about their health and how happy and relaxed they felt. A year later, the questionnaire was resent to a random sample of the women. Their responses suggested that most still felt the same as they did the year before. Ten years later, after allowing for any initial disparities in health, there turned out to be no difference in death rates between those who saw their glass as half-full or half-empty. © Copyright Reed Business Information Ltd.
Angus Chen Loneliness has been linked to everything from heart disease to Alzheimer's disease. Depression is common among the lonely. Cancers tear through their bodies more rapidly, and viruses hit them harder and more frequently. In the short term, it feels like the loneliness will kill you. A study suggests that's because the pain of loneliness activates the immune pattern of a primordial response commonly known as fight or flight. For decades, researchers have been seeing signs that the immune systems of lonely people are working differently. Lonely people's white blood cells seem to be more active in a way that increases inflammation, a natural immune response to wounding and bacterial infection. On top of that, they seem to have lower levels of antiviral compounds known as interferons. That seemed to provide a link to a lot of the poor health outcomes associated with loneliness, since chronic inflammation has been linked to everything from cancer to depression. The human body isn't built to hold a high level of inflammation for years. "That explains very clearly why lonely people fall at increased risk for cancer, neurodegenerative disease and viral infections as well," says Steve Cole, a genomics researcher at the University of California, Los Angeles, and lead author on the study published in the Proceedings of the National Academy of Sciences on Monday But it still doesn't explain how or why loneliness could change our bodies. To find that out, Cole and his collaborators tracked 141 people over five years. Every year, the researchers measured how lonely the participants felt and took blood samples to track the activity of genes involved with immunity and inflammation. © 2015 npr
By Virginia Morell Was that fish on your plate once a sentient being? Scientists have long believed that the animals aren’t capable of the same type of conscious thought we are because they fail the “emotional fever” test. When researchers expose birds, mammals (including humans), and at least one species of lizard to new environments, they experience a slight rise in body temperature of 1°C to 2°C that lasts a while; it’s a true fever, as if they were responding to an infection. The fever is linked to the emotions because it’s triggered by an outside stimulus, yet produces behavioral and physiological changes that can be observed. Some scientists argue that these only occur in animals with sophisticated brains that sense and are conscious of what’s happening to them. Previous tests suggested that toads and fish don’t respond this way. Now, a new experiment that gave the fish more choices shows the opposite. Researchers took 72 zebrafish and either did nothing with them or placed them alone in a small net hanging inside a chamber in their tank with water of about 27°C; zebrafish prefer water of about 28°C. After 15 minutes in the net, the team released the confined fish. They could then freely swim among the tank’s five other chambers, each heated to a different temperature along a gradient from 17.92°C to 35°C. (The previous study used a similar setup but gave goldfish a choice between only two chambers, both at higher temperatures.) The stressed fish spent more time—between 4 and 8 hours—in the warmer waters than did the control fish, and raised their body temperatures about 2°C to 4°C, showing an emotional fever, the scientists report online today in the Proceedings of the Royal Society B. Thus, their study upends a key argument against consciousness in fish, they say. © 2015 American Association for the Advancement of Science.
Laura Sanders In an unexpected twist, two antibodies designed to fight Alzheimer’s disease instead made nerve cells in mice misbehave more. The results, published online November 9 in Nature Neuroscience, highlight how little is known about how these drugs actually work, says study coauthor Marc Aurel Busche of Technical University Munich. “We need to understand what these antibodies do in the brains of patients better,” he says. The treatment approach relies on antibodies that target amyloid-beta, a protein that builds up in the brains of people with Alzheimer’s. One of the antibodies used in the new study, bapineuzumab, failed to show benefits in much-anticipated trials described in the New England Journal of Medicine in 2014. Despite that setback, some researchers say antibodies are still the best option to halt Alzheimer’s. The bapineuzumab trial was flawed, says neurologist Dennis Selkoe of Harvard Medical School and Brigham and Women’s Hospital. And the new results, which come from mice, have little relevance for ongoing tests of other antibodies in people, he says. “A-beta immunotherapy is the most promising approach right now, and nothing in their paper undercuts that,” he says. Several other antibodies have recently shown modest benefits in people with Alzheimer’s, he adds. Representatives from Eli Lilly and Biogen, pharmaceutical companies that are developing antibody treatments, declined to comment on the new study. © Society for Science & the Public 2000 - 2015
THINK twice before you tell that fib. By watching courtroom videos, a computer has learned to predict if someone is telling the truth or a lie. A machine learning algorithm trained on the faces of defendants in recordings of real trials, including that of Andrea Sneiderman (above) who was convicted of lying, correctly identified truth-tellers about 75 per cent of the time. Humans managed just 59.5 per cent. The best interrogators can reach 65 per cent. “We’re actually pretty bad lie detectors,” says Rada Mihalcea at the University of Michigan in Ann Arbor. Mihalcea and her colleagues took 121 videos from sources such as the Innocence Project, a non-profit group in Texas dedicated to exonerating people with wrongful convictions. This is superior to simulated conversation because the speakers are more invested in what they are saying. Transcriptions of the videos that included the speaker’s gestures and expressions were fed into a machine learning algorithm, along with the trial’s outcome. To hone it further, the team plans to feed in even more data. Such a system could one day spot liars in real-time in court or at airport customs, says Mihalcea, who will present the work at the International Conference on Multimodal Interaction this month in Seattle, Washington. © Copyright Reed Business Information Ltd.
Link ID: 21610 - Posted: 11.06.2015
Nancy Shute In September, we reported on a charming little study that found people who feel blue after watching sad videos have a harder time perceiving colors on the blue-yellow axis. Now the researchers may be feeling blue themselves. On Thursday they retracted their study, saying that errors in how they structured the experiment skewed the results. Shortly after the study was published online, commenters started looking skeptically at the results. And because the researchers had posted their data online, those commenters were able to run the numbers themselves. They didn't like what they found. As one blogger wrote: "A major problem is that the authors are claiming that they've found an interaction between video condition and color axis, but they haven't actually tested this interaction, they've just done a pair of independent t-tests and found different results." As the indefatigable crew at the Retraction Watch blog points out, it's not the first time scientists have messed this up. "This exact experimental oversight occurs all too often, according to a 2011 paper in Nature Neuroscience, which found that the same number of papers performed the procedure incorrectly as did it correctly." And there were other problems, too, such as not testing participants' color perception before the study. © 2015 npr
By Nicholas Bakalar A person with depression is at higher risk for heart disease, and a person with heart disease is at higher risk for depression. The link between the two diseases is complex and not entirely understood. Many of the effects of depression — feeling unable to exercise or eat properly, for example — and the behaviors associated with depression, like smoking and abusing alcohol, are well established risk factors for heart disease. Some studies have suggested that insomnia, another symptom of depression, may also increase the risk for cardiovascular illness. Depression can also make heart disease worse. Heart patients with depression may find it more difficult to take medications and comply with the behavioral demands of living with heart disease. Depression may also have destructive physiological effects on heart rhythm, blood pressure, stress hormone levels and blood clotting, studies have shown. These may be among the reasons why depressed patients with stable cardiovascular disease, or those who have survived a heart attack or had coronary bypass surgery, are at two to three times higher risk of dying than similar patients without depression. Treating depressed heart patients with drugs like Prozac may help. These drugs, known as selective serotonin reuptake inhibitors, or S.S.R.I.’s, in addition to relieving depression, have blood-thinning effects that may be beneficial against heart disease. “It is clear that treatment with an S.S.R.I. reduces cardiac mortality in depressed patients post heart attack,” said Dr. Steven P. Roose, a professor of psychiatry at Columbia. “What is not clear is whether the reduction in mortality results from the antidepressant effect of the medication or the anti-platelet effect of the medication.” © 2015 The New York Times Company
Your sense of smell might be more important than you think. It could indicate how well your immune system is functioning, a study in mice suggests. Evidence of a connection between the immune system and the olfactory system – used for sense of smell – has been building for some time. For instance, women seem to prefer the scent of men with different immune system genes to their own. Meanwhile, other studies have hinted that the robustness of your immune system may influence how extraverted you are. To investigate further, Fulvio D’Acquisto at Queen Mary University of London and his colleagues studied mice missing a recombinant activating gene (RAG), which controls the development of immune cells. Without it, mice lack a working immune system and some genes are expressed differently, including those involved in the olfactory system. “That rang bells, because people with immune deficiencies often lose their sense of smell,” says D’Acquisto. Systemic lupus erythematosus, an autoimmune disease in which the immune system mistakenly attacks tissues in the skin, joints, kidneys, brain, and other organs, is one such example. His team measured how long it took mice to find chocolate chip cookies buried in their cages. Those missing RAG took five times as long as normal mice. They also failed to respond to the scent of almond or banana, which mice usually find very appealing – although they did still react to the scent of other mice. Further study uncovered abnormalities in the lining of their noses; physical evidence that their sense of smell might be disrupted. © Copyright Reed Business Information Ltd.
Adam Cole Watch a scary movie and your skin crawls. Goose bumps have become so associated with fear that the word is synonymous with thrills and chills. But what on earth does scary have do to with chicken-skin bumps? For a long time, it wasn't well understood. Physiologically, it's fairly simple. Adrenaline stimulates tiny muscles to pull on the roots of our hairs, making them stand out from our skin. That distorts the skin, causing bumps to form. Call it horripilation, and you'll be right — bristling from cold or fear. Charles Darwin once investigated goose bumps by scaring zoo animals with a stuffed snake. He argued for the now accepted theory that goose bumps are a vestige of humanity's ancient past. Our ancestors were hairy. Goose bumps would have fluffed up their hair. When they were scared, that would have made them look bigger — and more intimidating to attackers. When they were cold, that would have trapped an insulating layer of air to keep them warm. We modern humans still get goose bumps when we're scared or cold, even though we've lost the advantage of looking scarier or staying warmer ourselves. And researchers have found that listening to classical music (or Phil Collins), seeing pictures of children or drinking a sour drink can also inspire goose bumps. There's clearly a link with emotion and reward, too. © 2015 npr
By Christian Jarrett Neuroscientists, for obvious reasons, are really interested in finding out what’s different about the brains of people with unpleasant personalities, such as narcissists, or unsavory habits, like porn addiction. Their hope is that by studying these people’s brains we might learn more about the causes of bad character, and ways to helpfully intervene. Now to the list of character flaws that've received the brain-scanner treatment we can apparently add sexism — a new Japanese study published in Scientific Reports claims to have found its neurological imprint. The researchers wanted to know whether there is something different about certain individuals’ brains that potentially predisposes them to sexist beliefs and attitudes (of course, as with so much neuroscience research like this, it’s very hard to disentangle whether any observed brain differences are the cause or consequence of the trait or behavior that’s being studied, a point I’ll come back to). More specifically, they were looking to see if people who publicly endorse gender inequality have brains that are anatomically different from people who believe in gender equality. In short, it seems the answer is yes. Neuroscientist Hikaru Takeuchi at Tohoku University and his colleagues have identified two brain areas where people who hold sexist attitudes have different levels of gray-matter density (basically, a measure of how many brain cells are packed into a given area), as compared with people who profess a belief in gender equality (their study doesn’t speak to any subconsciously held sexist beliefs). What’s more, these neural differences were correlated with psychological characteristics that could help explain some people’s sexist beliefs. © 2015, New York Media LLC.