Chapter 11. Emotions, Aggression, and Stress
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|By Jill U. Adams Our noses are loaded with bitter taste receptors, but they're not helping us taste or smell lunch. Ever since researchers at the University of Iowa came to this conclusion in 2009, scientists have been looking for an explanation for why the receptors are there. One speculation is that they warn us of noxious substances. But they may play another role too: helping to fight infections. In addition to common bitter compounds, the nose's bitter receptors also react to chemicals that bacteria use to communicate. That got Noam Cohen, a University of Pennsylvania otolaryngologist, wondering whether the receptors detect pathogens that cause sinus infections. In a 2012 study, his team found that bacterial chemicals elicited two bacteria-fighting responses in cells from the nose and upper airways: movement of the cells' projections that divert noxious things out of the body and release of nitric oxide, which kills bacteria. The findings may have clinical applications. When Cohen recently analyzed bitter taste receptor genes from his patients with chronic sinus infections, he noticed that practically none were supertasters, even though supertasters make up an estimated 25 percent of the population. Supertasters are extra sensitive to bitter compounds in foods. People are either supertasters or nontasters, or somewhere in between, reflecting the genes they carry for a receptor known as T2R38. Cohen thinks supertasters react vigorously to bacterial bitter compounds in the nose and are thus resistant to sinus infections. In nontasters the reaction is weaker, bacteria thrive and sinus infections ensue. These results suggest that a simple taste test could be used to predict who is at risk for recurrent infections and might need more aggressive medical treatment. © 2014 Scientific American
Carl Zimmer An unassuming single-celled organism called Toxoplasma gondii is one of the most successful parasites on Earth, infecting an estimated 11 percent of Americans and perhaps half of all people worldwide. It’s just as prevalent in many other species of mammals and birds. In a recent study in Ohio, scientists found the parasite in three-quarters of the white-tailed deer they studied. One reason for Toxoplasma’s success is its ability to manipulate its hosts. The parasite can influence their behavior, so much so that hosts can put themselves at risk of death. Scientists first discovered this strange mind control in the 1990s, but it’s been hard to figure out how they manage it. Now a new study suggests that Toxoplasma can turn its host’s genes on and off — and it’s possible other parasites use this strategy, too. Toxoplasma manipulates its hosts to complete its life cycle. Although it can infect any mammal or bird, it can reproduce only inside of a cat. The parasites produce cysts that get passed out of the cat with its feces; once in the soil, the cysts infect new hosts. Toxoplasma returns to cats via their prey. But a host like a rat has evolved to avoid cats as much as possible, taking evasive action from the very moment it smells feline odor. Experiments on rats and mice have shown that Toxoplasma alters their response to cat smells. Many infected rodents lose their natural fear of the scent. Some even seem to be attracted to it. Manipulating the behavior of a host is a fairly common strategy among parasites, but it’s hard to fathom how they manage it. A rat’s response to cat odor, for example, emerges from complex networks of neurons that detect an odor, figure out its source and decide on the right response in a given moment. © 2014 The New York Times Company
By JAMIE EDGIN and FABIAN FERNANDEZ LAST week the biologist Richard Dawkins sparked controversy when, in response to a woman’s hypothetical question about whether to carry to term a child with Down syndrome, he wrote on Twitter: “Abort it and try again. It would be immoral to bring it into the world if you have the choice.” In further statements, Mr. Dawkins suggested that his view was rooted in the moral principle of reducing overall suffering whenever possible — in this case, that of individuals born with Down syndrome and their families. But Mr. Dawkins’s argument is flawed. Not because his moral reasoning is wrong, necessarily (that is a question for another day), but because his understanding of the facts is mistaken. Recent research indicates that individuals with Down syndrome can experience more happiness and potential for success than Mr. Dawkins seems to appreciate. There are, of course, many challenges facing families caring for children with Down syndrome, including a high likelihood that their children will face surgery in infancy and Alzheimer’s disease in adulthood. But at the same time, studies have suggested that families of these children show levels of well-being that are often greater than those of families with children with other developmental disabilities, and sometimes equivalent to those of families with nondisabled children. These effects are prevalent enough to have been coined the “Down syndrome advantage.” In 2010, researchers reported that parents of preschoolers with Down syndrome experienced lower levels of stress than parents of preschoolers with autism. In 2007, researchers found that the divorce rate in families with a child with Down syndrome was lower on average than that in families with a child with other congenital abnormalities and in those with a nondisabled child. © 2014 The New York Times Company
By PAM BELLUCK Memories and the feelings associated with them are not set in stone. You may have happy memories about your family’s annual ski vacation, but if you see a tragic accident on the slopes, those feelings may change. You might even be afraid to ski that mountain again. Now, using a technique in which light is used to switch neurons on and off, neuroscientists at the Massachusetts Institute of Technology appear to have unlocked some secrets about how the brain attaches emotions to memories and how those emotions can be adjusted. Their research, published Wednesday in the journal Nature, was conducted on mice, not humans, so the findings cannot immediately be translated to the treatment of patients. But experts said the experiments may eventually lead to more effective therapies for people with psychological problems such as depression, anxiety or post-traumatic stress disorder. “Imagine you can go in and find a particular traumatic memory and turn it off or change it somehow,” said David Moorman, an assistant professor of psychological and brain sciences at the University of Massachusetts Amherst, who was not involved in the research. “That’s still science fiction, but with this we’re getting a lot closer to it.” The M.I.T. scientists labeled neurons in the brains of mice with a light-sensitive protein and used pulses of light to switch the cells on and off, a technique called optogenetics. Then they identified patterns of neurons activated when mice created a negative memory or a positive one. A negative memory formed when mice received a mild electric shock to their feet; a positive one was formed when the mice, all male, were allowed to spend time with female mice. © 2014 The New York Times Company
by Penny Sarchet Memory is a fickle beast. A bad experience can turn a once-loved coffee shop or holiday destination into a place to be avoided. Now experiments in mice have shown how such associations can be reversed. When forming a memory of a place, the details of the location and the associated emotions are encoded in different regions of the brain. Memories of the place are formed in the hippocampus, whereas positive or negative associations are encoded in the amygdala. In experiments with mice in 2012, a group led by Susumo Tonegawa of the Massachusetts Institute of Technology managed to trigger the fear part of a memory associated with a location when the animals were in a different location. They used a technique known as optogenetics, which involves genetically engineering mice so that their brains produce a light-sensitive protein in response to a certain cue. In this case, the cue was the formation of the location memory. This meant the team could make the mouse recall the location just by flashing pulses of light down an optical fibre embedded in the skull. The mice were given electric shocks while their memories of the place were was being formed, so that the animals learned to associate that location with pain. Once trained, the mice were put in a new place and a pulse of light was flashed into their brains. This activated the neurons associated with the original location memory and the mice froze, terrified of a shock, demonstrating that the emotion associated with the original location could be induced by reactivating the memory of the place. © Copyright Reed Business Information Ltd.
Erin Allday It's well established that chronic pain afflicts people with more than just pain. With the pain come fatigue and sleeplessness, depression and frustration, and a noticeable disinterest in so many of the activities that used to fill a day. It makes sense that chronic pain would leave patients feeling weary and unmotivated - most people wouldn't want to go to work or shop for a week's worth of groceries or even meet friends for dinner when they're exhausted and in pain. But experts in pain and neurology say the connection between chronic pain and a lousy mood may be biochemical, something more complicated than a dour mood brought on from persistent, long-term discomfort alone. Now, a team of Stanford neurologists have found evidence that chronic pain triggers a series of molecular changes in the brain that may sap patients' motivation. "There is an actual physiologic change that happens," said Dr. Neil Schwartz, a post-doctoral scientist who helped lead the Stanford research. "The behavior changes seem quite primary to the pain itself. They're not just a consequence of living with it." Schwartz and his colleagues hope their work could someday lead to new treatments for the behavior changes that come with chronic pain. In the short term, the research improves understanding of the biochemical effects of chronic pain and may be a comfort to patients who blame themselves for their lack of motivation, pain experts said. © 2014 Hearst Communications, Inc.
By ANNA NORTH “You can learn a lot from what you see on a screen,” said Yalda T. Uhls. However, she told Op-Talk, “It’s not going to give you context. It’s not going to give you the big picture.” Ms. Uhls, a researcher at the Children’s Digital Media Center in Los Angeles, was part of a team that looked at what happened when kids were separated from their screens — phones, iPads, laptops and the like — for several days. Their findings may have implications for adults’ relationship to technology, too. For a paper published in the journal Computers in Human Behavior, the researchers studied 51 sixth-graders who attended a five-day camp where no electronic devices were allowed. Before and after the camp, they tested the kids’ emotion-recognition skills using photos of facial expressions and sound-free video clips designed to measure their reading of nonverbal cues. The kids did significantly better on both tests after five screen-free days; a group of sixth-graders from the same school who didn’t go to camp showed less or no improvement. Ms. Uhls, who also works for the nonprofit Common Sense Media, told Op-Talk that a number of factors might have been at play in the campers’ improvement. For instance, their time in nature might have played a role. But to her, the most likely explanation was the sheer increase in face-to-face interaction: “The issue really is not that staring at screens is going to make you bad at recognizing emotions,” she said. “It’s more that if you’re looking at screens you’re not looking at the world, and you’re not looking at people.” Many adults have sought out the same Internet-free experience the kids had, though they usually don’t go to camp to get it. The novelist Neil Gaiman took a “sabbatical from social media” in 2013, “so I can concentrate on my day job: making things up.” © 2014 The New York Times Company
Link ID: 20006 - Posted: 08.28.2014
By Michael Balter Humans are generally highly cooperative and often impressively altruistic, quicker than any other animal species to help out strangers in need. A new study suggests that our lineage got that way by adopting so-called cooperative breeding: the caring for infants not just by the mother, but also by other members of the family and sometimes even unrelated adults. In addition to helping us get along with others, the advance led to the development of language and complex civilizations, the authors say. Cooperative breeding is not unique to humans. Up to 10% of birds are cooperative breeders, as are meerkats and New World monkeys such as tamarins and marmosets. But our closest primate relatives, great apes such as chimpanzees, are not cooperative breeders. Because the human and chimpanzee lineages split between 5 million and 7 million years ago, and humans are the only apes that engage in cooperative breeding, researchers have puzzled over how this helping behavior might have evolved all over again on the human line. In the late 1990s, Sarah Blaffer Hrdy, now an anthropologist emeritus at the University of California, Davis, proposed the cooperative breeding hypothesis. According to her model, early in their evolution humans added cooperative breeding behaviors to their already existing advanced ape cognition, leading to a powerful combination of smarts and sociality that fueled even bigger brains, the evolution of language, and unprecedented levels of cooperation. Soon after Hrdy’s proposal, anthropologists Carel van Schaik and Judith Burkart of the University of Zurich in Switzerland began to test some of these ideas, demonstrating that cooperatively breeding primates like marmosets engaged in seemingly altruistic behavior by helping other marmosets get food with no immediate reward to themselves. © 2014 American Association for the Advancement of Science.
by Bethany Brookshire When a laboratory mouse and a house mouse come nose to nose for the first time, each one is encountering something it has never seen before. They are both Mus musculus. But the wild mouse is facing a larger, fatter, calmer and less aggressive version of itself that’s the result of brother-to-sister inbreeding for generations, resulting in mice that are almost completely genetically identical. Laboratory mice are incredibly valuable tools for research into diseases from Alzheimer’s to Zellweger syndrome. Scientists have a deep understanding of lab mouse DNA, and can use that knowledge to study how specific genes may control certain behaviors and underlie disease. But with all the inbreeding comes some traits that, while desirable in a lab mouse, may not reflect the behavior of an animal in the wild. So for some questions, and some behaviors, scientists might need something a bit wilder. A new study takes lab mice back to their roots and along the way uncovers a new gene function. Lea Chalfin and colleagues at the Weizmann Institute of Science in Rohovot, Israel, bred laboratory mice with wild mice for 10 generations. The result was a mouse with wild mouse genes and wild mouse behavior — with a few important lab mouse genes mixed in. The technique allows scientists to place specific mutations in a wild mouse. The results have interesting implications for studying the mouse species, and might provide some new ways to study human disease as well. Chalfin and her colleagues were especially interested in behaviors linked to female aggression. © Society for Science & the Public 2000 - 2013
|By Christie Nicholson Children who experience neglect, abuse and poverty have a tougher time as adults than do well-cared-for kids. Now there’s evidence that such stress can actually change the size of brain structures responsible for learning, memory and processing emotion. The finding is in the journal Biological Psychiatry. [Jamie L. Hanson et al, Behavioral Problems After Early Life Stress: Contributions of the Hippocampus and Amygdala] Researchers took images of the brains of 12-year-olds who had suffered either physical abuse or neglect or had grown up poor. From the images the scientists were able to measure the size of the amygdala and hippocampus—two structures involved in emotional processing and memory. And they compared the sizes of these structures with those of 12-year-old children who were raised in middle-class families and had not been abused. And they found that the stressed children had significantly smaller amygdalas and hippocampuses than did the kids from the more nurturing environments. Early stress has been associated with depression, anxiety, cancer and lack of career success later on in adulthood. This study on the sizes of brain regions may offer physiological clues to why what happens to toddlers can have such a profound impact decades later. © 2014 Scientific American
Greta Kaul It was a rainy day, and earthworms wriggled out of the ground and began to arrange themselves on the pavement as Julian Plumadore walked to his community college zoology class in 1991. They spelled out messages only he could read. "I was very frightened to be a custodian of that kind of cosmic information and be able to do absolutely nothing about it," Plumadore said. Other times, there were voices - demons screaming - telling him he was going to hell. Plumadore was eventually diagnosed as having schizoaffective disorder, a psychosis that combines the hallucinations of schizophrenia with a mood disorder like depression. People with psychotic disorders, of which schizophrenia is the most severe, have hallucinations, like the voices Plumadore was hearing, that are divorced from reality. Now, a Stanford researcher suggests that the voices he experienced might have been different if he had grown up somewhere other than the U.S. If he were from India, he might have heard family members telling him to do household chores. If he were from Ghana, he might have heard the voice of God guiding him. For a study published in June, Tanya Luhrmann, a Stanford anthropologist, and other researchers interviewed 60 people who met the criteria for schizophrenia: 20 from in and around San Mateo, 20 from India and 20 from Ghana. Though the patients heard both positive and negative voices no matter where they were from, those in India and in Ghana tended to have less negative experiences than Americans: They could more often identify who was talking to them and had less violent hallucinations. Though the study isn't conclusive, Luhrmann believes the differences in voice-hearing between cultures may be a clue into how social expectations and environment shape the way people hear those imaginary voices. © 2014 Hearst Communications, Inc.
By NATALIE ANGIER SOUTH LUANGWA NATIONAL PARK, ZAMBIA — We saw the impala first, a young buck with a proud set of ridged and twisted horns, like helical rebar, bounding across the open plain at full, desperate gallop. But why? A moment later somebody in our vehicle gasped, and the answer became clear. Rising up behind the antelope, as though conjured on movie cue from the aubergine glow of the late afternoon, were six African wild dogs, running in single file. They moved with military grace and precision, their steps synchronized, their radio-dish ears cocked forward, their long, puppet-stick legs barely skimming the ground. Still, the impala had such a jump on them that the dogs couldn’t possibly catch up — could they? We gunned the engine and followed. The pace quickened. The dogs’ discipline held steady. They were closing the gap and oh, no, did I really want to watch the kill? To my embarrassed relief, the violence was taken off-screen, when prey and predators suddenly dashed up a hill and into obscuring bushes. By the time we reached the site, the dogs were well into their communal feast, their dark muzzles glazed with bright red blood, their white-tipped tails wagging in furious joy. “They are the most enthusiastic animals,” said Rosie Woodroffe of the Institute of Zoology in London, who has studied wild dogs for the last 20 years. “Other predators may be bigger and fiercer, but I would argue that there is nothing so enthusiastic as a wild dog,” she said. “They live the life domestic dogs wish they could live.” In 1997, while devising an action plan to help save the wild dog species, Lycaon pictus, Dr. Woodroffe felt anything but exuberant. Wild dogs were considered among the most endangered of Africa’s mammals; Dr. Woodroffe had yet to see one in the wild, and she feared she never would. © 2014 The New York Times Company
Helen Shen Most people gradually recover from trauma, but a small fraction of individuals develop post-traumatic stress disorder (PTSD) — prompting scientists to look for the biological underpinnings of this extreme response to traumatic situations such as warfare, car accidents and natural disasters. Research published on 11 August in Proceedings of the National Academy of Sciences identifies up to 334 genes that may be involved in vulnerability to post-traumatic stress in rats1. Most animal studies of stress use intense stimuli such as electric shocks, designed to produce large, group differences between exposed and unexposed animals. But Nikolaos Daskalakis and his colleagues tried a subtler approach to elicit a wide range of individual responses in rats that had all experienced the same trauma — more closely mimicking the variability of human responses to disturbing events. "We wanted to capture the differences between a susceptible individual and one that is not susceptible to the same experience," says Daskalakis, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York. The researchers exposed around 100 rats to soiled cat litter — which evokes a feared predator — and tested the animals one week later for lingering effects of the trauma. About one-quarter of the exposed animals were classified as 'extreme' responders, showing high levels of anxiety and startling easily on hearing loud noises. Another quarter of the animals were 'minimal' responders, and exhibited anxiety levels similar to those of non-exposed rats. © 2014 Nature Publishing Group
By DANIEL J. LEVITIN THIS month, many Americans will take time off from work to go on vacation, catch up on household projects and simply be with family and friends. And many of us will feel guilty for doing so. We will worry about all of the emails piling up at work, and in many cases continue to compulsively check email during our precious time off. But beware the false break. Make sure you have a real one. The summer vacation is more than a quaint tradition. Along with family time, mealtime and weekends, it is an important way that we can make the most of our beautiful brains. Every day we’re assaulted with facts, pseudofacts, news feeds and jibber-jabber, coming from all directions. According to a 2011 study, on a typical day, we take in the equivalent of about 174 newspapers’ worth of information, five times as much as we did in 1986. As the world’s 21,274 television stations produce some 85,000 hours of original programming every day (by 2003 figures), we watch an average of five hours of television per day. For every hour of YouTube video you watch, there are 5,999 hours of new video just posted! If you’re feeling overwhelmed, there’s a reason: The processing capacity of the conscious mind is limited. This is a result of how the brain’s attentional system evolved. Our brains have two dominant modes of attention: the task-positive network and the task-negative network (they’re called networks because they comprise distributed networks of neurons, like electrical circuits within the brain). The task-positive network is active when you’re actively engaged in a task, focused on it, and undistracted; neuroscientists have taken to calling it the central executive. The task-negative network is active when your mind is wandering; this is the daydreaming mode. These two attentional networks operate like a seesaw in the brain: when one is active the other is not. © 2014 The New York Times Company
Simon Makin Fish that have been exposed to a common anti-anxiety drug are more active and have better chances of survival than unexposed fish, researchers report in Environmental Research Letters1. The results suggest that standard methods for assessing the environmental impact of pharmaceuticals in waterways might miss some of the drugs' effects because they focus exclusively on harms, according to the authors. In the study, researchers led by Jonatan Klaminder at Umeå University in Sweden exposed Eurasian perch (Perca fluviatilis) to oxazepam, one of a widely used class of anti-anxiety drugs called benzodiazepines. Standard ecotoxicology experiments use unstressed, healthy fish that have been bred in labs. Control groups are designed to have 100% survival rates so that decreases in survival in the test group are easy to detect by comparison. But it is difficult to detect any increase in survival rates when the control group already has nearly complete survival. So Klaminder and his colleagues used the opposite approach. They exposed fish to the drug at two sensitive life stages: two-year-old wild fish taken from a Swedish lake that had only recently thawed after winter, and strings of roes — fish eggs that contain embryos undergoing development. These are more realistic conditions, the researchers say, as animals in the wild often experience high mortality. The researchers used oxazepam at a high concentration of 1,000 micrograms per litre and at a low concentration of 1 μg l−1. The low dose is relevant to aquatic environments in urban areas, because oxazepam concentrations of 1.9 μg l−1 have been measured in effluents from wastewater treatment plants. © 2014 Nature Publishing Group,
Link ID: 19928 - Posted: 08.09.2014
By DOUGLAS QUENQUA A tiny part of the brain keeps track of painful experiences and helps determine how we will react to them in the future, scientists say. The findings could be a boon to depression treatments. The habenula (pronounced ha-BEN-you-la), a part of the brain less than half the size of a pea, has been shown in animal studies to activate during painful or unpleasant episodes. Using M.R.I.s to produce powerful brain scans, researchers at University College London tracked the habenulas in subjects who were hooked up to electric shock machines. The subjects were presented with a series of photographs, some of which were followed by increasingly strong shocks. Soon, when the subjects were shown pictures associated with shocks, their habenulas would light up. “The habenula seems to track the associations with electric shocks becoming stronger and stronger,” said Jonathan Roiser, a neuroscientist at the college and an author of the study, published in The Proceedings of the National Academy of Sciences. The habenula appeared to have an effect on motivation, too. The subjects had been asked to occasionally press a button, just to show they were awake. They were much slower to do so when their habenula was active. In fact, the more slowly they responded, the more reliably their habenulas tracked associations with shocks. In animals, the habenula has been shown to suppress production of dopamine, a chemical that drives motivation. Perhaps, the researchers say, an overactive habenula can cause the feelings of impending doom and low motivation common in people with depression. © 2014 The New York Times Company
Emily Underwood Since swine flu swept the globe in 2009, scientists have scrambled to determine why a small percentage of children in Europe who received the flu vaccine Pandemrix developed narcolepsy, an incurable brain disorder that causes irresistible sleepiness. This week, a promising explanation was dealt a setback when prominent sleep scientist Emmanuel Mignot of Stanford University in Palo Alto, California, and colleagues retracted their influential study reporting a potential link between the H1N1 virus used to make the vaccine and narcolepsy. Some researchers were taken aback. “This was one of the most important pieces of work on narcolepsy that has come out,” says neuroimmunologist Lawrence Steinman, a close friend and colleague of Mignot’s, who is also at Stanford. The retraction, announced in Science Translational Medicine (STM), “really caught me by surprise,” he says. Others say that journal editors should have detected problems with the study’s methodology. The work provided the first substantiation of an autoimmune mechanism for narcolepsy, which could explain the Pandemrix side effect, researchers say. The vaccine, used only in Europe, seems to have triggered the disease in roughly one out of 15,000 children who received it. The affected children carried a gene variant for a particular human leukocyte antigen (HLA) type—a molecule that presents foreign proteins to immune cells—considered necessary for developing narcolepsy. In the 18 December 2013 issue of STM, Mignot and colleagues reported that T cells from people with narcolepsy, but not from healthy controls, are primed to attack by hypocretin, a hormone that regulates wakefulness. They also showed molecular similarities between fragments of the H1N1 virus and the hypocretin molecule and suggested that these fragments might fool the immune system into attacking hypocretin-producing cells. © 2014 American Association for the Advancement of Science
By Caelainn Hogan A simple blood test could determine a person’s risk of suicide and provide a future tool of prevention to stem suicide rates. In a study published online Wednesday in the American Journal of Psychiatry, researchers say they have discovered a genetic indicator of a person’s vulnerability to the effects of stress and anxiety and, therefore, the risk of suicidal thoughts or attempts. The Johns Hopkins researchers looked at how a group of chemicals known as methyls affect the gene SKA2, which modifies how the brain reacts to stress hormones. If the gene’s function is impaired by a chemical change, someone who is stressed won’t be able to shut down the effect of the stress hormone, which would be like having a faulty brake pad in a car for the fear center of the brain, worsening the impact of even everyday stresses. Researchers studied about 150 postmortem brain samples of healthy people and those with mental illness, including some who had committed suicide. They found that those who died by suicide had significantly higher levels of the chemical that altered the SKA2 gene. As a result of the gene’s modification, it was not able to “switch off” the effect of the stress hormone. The researchers then tested sets of blood samples from more than 325 participants in the Johns Hopkins Center for Prevention Research study to see whether they could determine those who were at greater risk of suicide by the same biomarker. They were able to guess with 80 to 90 percent accuracy whether a person had thoughts of suicide or made an attempt by looking at the single gene, while accounting for age, gender and levels of stress or anxiety.
By ANNA NORTH What does it mean to be lonely? It’s tempting to equate the feeling with a dearth of social interaction, but some people are now saying that it’s more complicated than that — and that true loneliness might be dangerous. In a story at Medium, Robin Marantz Henig busts some common loneliness myths. Lonely people aren’t necessarily weird or uncool: Ms. Henig cites a study of Ohio State undergrads showing that “those who called themselves lonely had just as much ‘social capital’ — defined by physical attractiveness, height, weight, socioeconomic status, and academic achievement — as their non-lonely peers.” And they may not be actually alone: “The students at Ohio State who were lonely belonged to as many clubs and had as many roommates as those who were ‘socially embedded.’ And while some studies indicate that living alone puts people at greater risk for loneliness, living with a spouse is not necessarily any protection.” Rather, loneliness may be psychological. The lonely, writes Ms. Henig, are more likely than others “to feel put upon and misunderstood” in social situations, to see “social danger even where none might exist.” She writes: “People grow lonely because of the gloomy stories they tell themselves. And, in a cruel twist, the loneliness itself can further distort their thinking, making them misread other people’s good intentions, which in turn causes them to withdraw to protect themselves from further rejection — and causes other people to keep them at arm’s length.” This distancing can have a physical impact; Ms. Henig argues that loneliness deserves further study, in part because it may increase the risk of high blood pressure, sleep problems and Alzheimer’s disease. © 2014 The New York Times Company
|By Fikri Birey What’s the difference between you and a rat? The list is unsurprisingly long but now, we can cross a universal human experience — feelings of regret — off of it. A new study shows for the first time that rats regret bad decisions and learn from them. In addition to existentialist suggestions of a rat’s regret — and what that takes away from, or adds to, being “human” — the study is highly relevant to basic brain research. Researchers demonstrated that we can tap into complex internal states of rodents if we hone in on the right behavior and the right neurons. There is a significant literature on what brain regions are representative of certain states, like reward predictions and value calculations, but the study, powered by a novel behavioral test, is able to put together such discrete behavioral correlates into a “rat” definition of regret. Finding better animal models of human behavior constitute a long-standing challenge in neuroscience: It has been difficult to authentically recapitulate mental states in animal models of neuropsychiatric disorders: For example, an attempt to model depression in rodents can often go no further than relatively coarse approximations of the core symptoms like guilt or sadness, which often translates to behaviors like social avoidance or anhedonia in rodents. The inability to efficiently approach the questions of mental abnormalities is a major problem. Depression is currently ranked as the leading cause of disability globally, and it’s estimated that by 2020, depression will lead 1.5 million people to end their lives by suicide. Now, thanks to a simple yet well-conceived series of experiments by Steiner and Redish, a compound behavior like regret is fully open to investigation. The investigators use a spatial decision-making set-up called “Restaurant Row”: an arena with four zones where four different flavors of food (banana, cherry, chocolate or unflavored) are introduced in sequence. © 2014 Scientific American