Chapter 15. Emotions, Aggression, and Stress
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by Jessica Griggs Manoeuvring the colourful tiles of Tetris can help block flashbacks of traumatic events, even after the memory has fixed itself in your mind. Playing the game could be an easy way to reduce the risk of post-traumatic stress disorder (PTSD). After any event, there is a window of about six hours where memories are consolidated and cemented in the mind, says Emily Holmes at the Medical Research Council Cognition and Brain Sciences Unit in Cambridge, UK. Sleeping on the memory strengthens it further. If an event is particularly traumatic, vivid memories of it can reoccur. These intrusive flashbacks are distressing for anyone, but in a proportion of cases they can persist and contribute to PTSD. For example, about half of people who have been raped go on to develop PTSD, as do a number of asylum seekers and people who have been tortured. About 20 per cent of people who have been in a serious car accident are affected by the condition. There are effective treatments for people who are diagnosed with PTSD, but nothing currently exists to help prevent people from developing it in the days and weeks after the initial trauma. Holmes and her colleagues think a dose of Tetris could be the answer. In 2009, they showed that playing the game four hours after being exposed to trauma reduced the number of subsequent flashbacks. But getting the game into a person's hands immediately after they have been raped, for example, won't always be practical, so the team tested whether it could still work a day later – after the memory had been consolidated and slept on. © Copyright Reed Business Information Ltd.
By DACHER KELTNER and PAUL EKMAN FIVE years ago, the writer and director Pete Docter of Pixar reached out to us to talk over an idea for a film, one that would portray how emotions work inside a person’s head and at the same time shape a person’s outer life with other people. He wanted to do this all in the mind of an 11-year-old girl as she navigated a few difficult days in her life. As scientists who have studied emotion for decades, we were delighted to be asked. We ended up serving as scientific consultants for the movie, “Inside Out,” which was recently released. Our conversations with Mr. Docter and his team were generally about the science related to questions at the heart of the film: How do emotions govern the stream of consciousness? How do emotions color our memories of the past? What is the emotional life of an 11-year-old girl like? (Studies find that the experience of positive emotions begins to drop precipitously in frequency and intensity at that age.) “Inside Out” is about how five emotions — personified as the characters Anger, Disgust, Fear, Sadness and Joy — grapple for control of the mind of an 11-year-old girl named Riley during the tumult of a move from Minnesota to San Francisco. (One of us suggested that the film include the full array of emotions now studied in science, but Mr. Docter rejected this idea for the simple reason that the story could handle only five or six characters.) Riley’s personality is principally defined by Joy, and this is fitting with what we know scientifically. Studies find that our identities are defined by specific emotions, which shape how we perceive the world, how we express ourselves and the responses we evoke in others. © 2015 The New York Times Company
Link ID: 21139 - Posted: 07.07.2015
By Kelly Servick How many times would you give your neighbor an electric shock to earn a few extra bucks? Your answer could be more malleable than you think. A new study finds that two common drugs—an antidepressant and a treatment for Parkinson’s disease—can influence moral decisions, a discovery that could help unravel specific mechanisms behind aggression and eventually help researchers design treatments for antisocial behavior. Previous research has linked two neurotransmitters, the brain’s signaling molecules, to our willingness to inflict harm. Serotonin appears to help keep us civil; it’s reduced in the brains of violent offenders, for example. Dopamine, meanwhile, has been shown to prompt aggression in animals, and it’s elevated in a certain part of the brain in people with psychopathic behavior. But measuring how these neurotransmitters contribute to moral decision-making is hard to do in the lab. Many studies rely on theoretical questions like the so-called trolley dilemma, which asks a person whether they would redirect an oncoming train to kill someone if it would save the lives of several others in its path. A person’s answer might not always reflect how they would behave in real life, however. So neuroscientist Molly Crockett of the University of Oxford in the United Kingdom and her colleagues developed a lab test with real consequences. They asked subjects to make a series of decisions about how many moderately painful electric shocks to deliver to themselves or to others. Half the questions gave volunteers a chance to earn money by inflicting self-harm. (For example: “Would you rather endure seven shocks to earn $10 or 10 shocks to earn $15?”) The other half offered the same type of decision, except that someone else stood to be shocked. At the end of the experiment, one of these choices was randomly selected and carried out: The decision-maker got paid, and either they or another person—waiting in a different room—got a series of painful zings on the wrist. Any answer could be the one with real consequences, so “people have to sort of put their money where their mouth is,” Crockett says. © 2015 American Association for the Advancement of Science
Link ID: 21131 - Posted: 07.04.2015
By Victoria Gill Science reporter, BBC News Cat v mouse: it is probably the most famous predator-prey pairing, enshrined in idioms and a well-known cartoon. And cats, it turns out, even have chemical warfare in their anti-mouse arsenal - contained in their urine. Researchers found that when very young mice were exposed to a chemical in cat urine, they were less likely to avoid the scent of cats later in life. The findings were presented at the Society for Experimental Biology's annual meeting in Prague. The researchers, from the AN Severtov Institute of Ecology and Evolution in Moscow, had previously found that the compound - aptly named felinine - causes pregnant mice to abort. Dr Vera Voznessenskaya explained that mice have a physiological response to this cat-specific compound. Chemical-sensing mouse neurons in the mouse's brain pick up the scent, triggering a reaction which includes an increase in the levels of stress hormones. "It's something that has existed in cats and mice for thousands of years," said Dr Voznessenskaya. This new study revealed that baby mice exposed to the compound during a "critical period" in their development would, as adults, react quite differently to their arch enemy's smell. The team exposed one-month-old mice to the chemical over two weeks. When they were tested later for their reaction, they were much less likely to flee the same scent. The interaction between cats and mice has a long history "Their physical sensitivity [to the chemical] was actually actually much higher," Dr Voznessenskaya explained. "More of their receptors detect the compound and they produce higher levels of stress hormone." Despite this though, mice raised around the unmistakable scent of cat pee are less inclined to show signs of fear, or to flee when they sniff it out. © 2015 BBC.
By Gretchen Vogel The 2009 H1N1 influenza pandemic left a troubling legacy in Europe: More than 1300 people who received a vaccine to prevent the flu developed narcolepsy, an incurable, debilitating condition that causes overpowering daytime sleepiness, sometimes accompanied by a sudden muscle weakness in response to strong emotions such as laughter or anger. The manufacturer, GlaxoSmithKline (GSK), has acknowledged the link, and some patients and their families have already been awarded cpmpensation. But how the vaccine might have triggered the condition has been unclear. In a paper in Science Translational Medicine (STM) this week, researchers offer a possible explanation. They show that the vaccine, called Pandemrix, triggers antibodies that can also bind to a receptor in brain cells that help regulate sleepiness. The work strongly suggests that Pandemrix, which was given to more than 30 million Europeans, triggered an autoimmune re action that led to narcolepsy in some people who are genetically at risk. “They put together quite a convincing picture and provide a plausible explanation for what has happened,” says Pasi Penttinen, who heads the influenza program at the European Centre for Disease Prevention and Control in Stockholm. “It’s really the kind of work we’ve been waiting for for 5 years.” But the results still need to be confirmed in a larger study, the authors and other narcolepsy researchers say. A 2013 paper in STM by another group, documenting a different type of vaccine-triggered autoimmune re action, was retracted after the results proved irreproducible (Science, 1 August 2014, p. 498). © 2015 American Association for the Advancement of Science
by Andy Coghlan "I was completely revitalised," says Karen. "Suddenly, I could be sociable again. I would go to work, go home, eat dinner and feel restless." Karen (not her real name) experienced this relief from chronic fatigue syndrome while taking a drug that is usually used to treat the blood cancer lymphoma and rheumatoid arthritis (see "Karen's experience", below). She was one of 18 people with CFS who reported improvements after taking rituximab as part of a small trial in Bergen, Norway. The results could lead to new treatments for the condition, which can leave people exhausted and housebound. Finding a cause for CFS has been difficult. Four years ago, claims that a mouse virus was to blame proved to be unfounded, and some have suggested the disease is psychosomatic. The latest study implicates the immune system, at least in some cases. Rituximab wipes out most of the body's B-cells, which are the white blood cells that make antibodies. Øystein Fluge and Olav Mella of the Haukeland University Hospital in Bergen noticed its effect on CFS symptoms in 2004, when they used the drug to treat lymphoma in a person who happened to also have CFS. Several months later, the person's CFS symptoms had disappeared. A small, one-year trial in 2011 found that two-thirds of those who received rituximab experienced relief, compared with none of the control group. The latest study, involving 29 people with CFS, shows that repeated rituximab infusions can keep symptoms at bay for years. © Copyright Reed Business Information Ltd
Vaughan Bell Marketing has discovered neuroscience and the shiny new product has plenty of style but very little substance. “Neuromarketing” is lighting up the eyes of advertising executives and lightening the wallets of public relations companies. It promises to target the unconscious desires of consumers, which are supposedly revealed by measuring the brain. The more successful agencies have some of the world’s biggest brands on their books and these mega-corporations are happy to trumpet their use of brain science in targeting their key markets. The holy grail of neuromarketing is to predict which ads will lead to most sales before they’ve been released but the reality is a mixture of bad science, bullshit and hope. First, it’s important to realise that the concept of neuroscience is used in different ways in marketing. Sometimes, it’s just an empty ploy aimed at consumers – the equivalent of putting a bikini-clad body next to your product for people who believe they’re above the bikini ploy. A recent Porsche advert apparently showed a neuroscience experiment suggesting that the brain reacts in a similar way to driving their car and flying a fighter jet, but it was all glitter and no gold. The images were computer-generated, the measurements impossible, and the scientist an actor. In complete contrast, neuromarketing is also a serious research area. This is a scientifically sound, genuinely interesting field in cognitive science, where the response to products and consumer decision-making is understood on the level of body and mind. This might involve looking at how familiar brand logos engage the memory systems in the brain, or examining whether the direction of eye gaze of people in ads affects how attention-grabbing they are, or testing whether the brain’s electrical activity varies when watching subtly different ads. Like most of cognitive neuroscience, the studies are abstract, ultra-focused and a long way from everyday experience. © 2015 Guardian News and Media Limited
Link ID: 21105 - Posted: 06.29.2015
By PETER ANDREY SMITH Eighteen vials were rocking back and forth on a squeaky mechanical device the shape of a butcher scale, and Mark Lyte was beside himself with excitement. ‘‘We actually got some fresh yesterday — freshly frozen,’’ Lyte said to a lab technician. Each vial contained a tiny nugget of monkey feces that were collected at the Harlow primate lab near Madison, Wis., the day before and shipped to Lyte’s lab on the Texas Tech University Health Sciences Center campus in Abilene, Tex. Lyte’s interest was not in the feces per se but in the hidden form of life they harbor. The digestive tube of a monkey, like that of all vertebrates, contains vast quantities of what biologists call gut microbiota. The genetic material of these trillions of microbes, as well as others living elsewhere in and on the body, is collectively known as the microbiome. Taken together, these bacteria can weigh as much as six pounds, and they make up a sort of organ whose functions have only begun to reveal themselves to science. Lyte has spent his career trying to prove that gut microbes communicate with the nervous system using some of the same neurochemicals that relay messages in the brain. Inside a closet-size room at his lab that afternoon, Lyte hunched over to inspect the vials, whose samples had been spun down in a centrifuge to a radiant, golden broth. Lyte, 60, spoke fast and emphatically. ‘‘You wouldn’t believe what we’re extracting out of poop,’’ he told me. ‘‘We found that the guys here in the gut make neurochemicals. We didn’t know that. Now, if they make this stuff here, does it have an influence there? Guess what? We make the same stuff. Maybe all this communication has an influence on our behavior.’’ Since 2007, when scientists announced plans for a Human Microbiome Project to catalog the micro-organisms living in our body, the profound appreciation for the influence of such organisms has grown rapidly with each passing year. Bacteria in the gut produce vitamins and break down our food; their presence or absence has been linked to obesity, inflammatory bowel disease and the toxic side effects of prescription drugs. Biologists now believe that much of what makes us human depends on microbial activity. © 2015 The New York Times Company
Helen Shen Boosting activity in neurons that have stored happy memories might help to treat depression — at least according to results in mice. In a study published today (17 June) in Nature, neuroscientist Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology in Cambridge report how they reversed a depression-like state in rodents by using light to stimulate clusters of brain cells believed to have stored memories of a positive experience1. The findings are preliminary, but they hint that areas of the brain involved in storing memories could one day be a target to treat mental disorders in humans, says Tonegawa. “I want to be very careful not to give false expectations to patients. We are doing very basic science,” he adds. “This is exactly the type of work that psychiatry needs right now,” says Robert Malenka, a behavioural scientist at Stanford University in California. “This is an elegant paper.” The work has grown out of studies by Tonegawa’s lab and others that aimed to locate the memory ‘engram’ — the physical trace of a memory, thought to be encoded in an ensemble of neurons2–6. In 2012, Tonegawa and his team provided one of the clearest demonstrations of an engram. They engineered mice with light-sensitive proteins that were expressed when neurons fired. As a result, they could track any neurons that activated while the mice were given a fearful memory by being trained with repeated electric shocks to be scared of a cage3. The researchers later used blue flashes of light to make the same neurons fire again — a technique known as optogenetics — and found that they could make the animals freeze up, presumably because the fearful memory had been reawoken. © 2015 Nature Publishing Group
By Greg Toppo On the morning of August 12, 2013, nearly eight months after 20-year-old Adam Lanza shot his way into Sandy Hook Elementary School in Newtown, Conn., and killed 26 people, Michael Mudry, an investigator with the Connecticut State Police, drove to nearby Danbury to try to solve a little mystery. Police had found a Garmin GPS unit in Lanza's house, and its records showed that the gunman had driven to the same spot nine times in April, May and June 2012, arriving around midnight each time and staying for hours. The GPS readout took Mudry to the vast parking lot of a suburban shopping center, about 14 miles west of Lanza's home. Workers at a movie theater there immediately recognized Lanza from a photograph. He was at the theater constantly, they told Mudry, but never to see movies. He came to the lobby to play an arcade game, the same one, over and over again, sometimes for eight to 10 hours a night. Witnesses said he would whip himself into a frenzy, and on occasion the theater manager had to unplug the game to get him to leave. Police had been scouring Lanza's home since the shootings, and on his computer hard drive they found information on weapons magazine capacities, images of Columbine killers Eric Harris and Dylan Klebold, copies of the violent movies Bloody Wednesday and Rampage, and a list of ingredients for TNT. And like many teenaged boys, Lanza owned the typical first-person shooter, fighting and action games: Call of Duty, Dead or Alive, Grand Theft Auto. © 2015 Scientific American,
Link ID: 21068 - Posted: 06.18.2015
By Tori Rodriguez Joint flexibility is an oft-coveted trait that provides a special advantage to dancers and athletes, but there can be too much of this good thing. A growing body of research suggests a surprising link between high levels of flexibility and anxiety. A study published last year in the journal Frontiers in Psychology is among the most recent to confirm the association, finding that people with hypermobile joints have heightened brain activity in anxiety regions. Joint hypermobility, which affects approximately 20 percent of the population, confers an unusually large range of motion. Hypermobile people can often, for instance, touch their thumb to their inner forearm or place their hands flat on the floor without bending their knees. The trait appears to be genetic and is a result of variation in collagen, the main structural protein of connective tissue. Being double-jointed has long been linked with an increased risk for asthma and irritable bowel syndrome, among other physical disorders. “Joint hypermobility has an impact on the whole body and not just joints,” says Jessica Eccles, a psychiatrist and researcher at the University of Sussex in England. It was only a matter of time before scientists also looked at whether joint hypermobility was linked to mental disorders. The investigation began in 1993 and heated up in 1998 when researcher Rocío Martín-Santos, now at the Hospital Clinic of the University of Barcelona, and her colleagues discovered that patients with anxiety were 16 times more likely to have lax joints. Their findings have since been replicated numerous times in large populations. © 2015 Scientific American
Sara Reardon Traumatic experiences, such as those encountered during warfare, can cause long-lasting stress. Tweaking the immune system could be key to treating, or even preventing, post-traumatic stress disorder (PTSD). Research in rodents suggests that immunizing animals can lessen fear if they are later exposed to stress. Researchers have known for some time that depression and immune-system health are linked and can affect each other. Early clinical trials have shown that anti-inflammatory drugs can reduce symptoms of depression1, raising hopes that such treatments might be useful in other types of mental illness, such as PTSD. “I think there’s kind of a frenzy about inflammation in psychiatry right now,” says Christopher Lowry, a neuroscientist at the University of Colorado Boulder. He presented results of experiments probing the link between fearful behaviour and immune response at a meeting in Victoria, Canada, last week of the International Behavioral Neuroscience Society. Studies of military personnel suggest that immune function can influence the development of PTSD. Soldiers whose blood contains high levels of the inflammatory protein CRP before they are deployed2, or who have a genetic mutation that makes CRP more active3, are more likely to develop the disorder. To directly test whether altering the immune system affects fear and anxiety, Lowry and colleagues injected mice with a common bacterium, Mycobacterium vaccae, three times over three weeks to modulate their immune systems. The scientists then placed these mice, and a control group of unimmunized mice, in cages with larger, more aggressive animals. © 2015 Nature Publishing Group
Dogs do not like people who are mean to their owners and will refuse food offered by people who have snubbed their master, Japanese researchers have said. The findings reveal that canines have the capacity to cooperate socially – a characteristic found in a relatively small number of species, including humans and some other primates. Researchers led by Kazuo Fujita, a professor of comparative cognition at Kyoto University, tested three groups of 18 dogs using role plays in which their owners needed to open a box. In all three groups, the owner was accompanied by two people whom the dog did not know. In the first group, the owner sought assistance from one of the other people, who actively refused to help. In the second group, the owner asked for, and received, help from one person. In both groups, the third person was neutral and not involved in either helping or refusing to help. Neither person interacted with the dog’s owner in the control – third – group. After watching the box-opening scene, the dog was offered food by the two unfamiliar people in the room. Dogs that saw their owner being rebuffed were far more likely to choose food from the neutral observer, and to ignore the offer from the person who had refused to help, Fujita said on Friday. Dogs whose owners were helped and dogs whose owners did not interact with either person showed no marked preference for accepting snacks from the strangers. “We discovered for the first time that dogs make social and emotional evaluations of people regardless of their direct interest,” Fujita said. If the dogs were acting solely out of self-interest, there would be no differences among the groups, and a roughly equal number of animals would have accepted food from each person. © 2015 Guardian News and Media Limited
By Lisa Sanders On Thursday, we challenged Well readers to figure out why a previously healthy 31-year-old woman suddenly began having strokes. I thought this was a particularly tough case – all the more so since I had never heard of the disease she was ultimately diagnosed with. Apparently I was not alone. Only a few dozen of the 400 plus readers who wrote in were able to make this difficult diagnosis. The correct diagnosis is: Susac’s syndrome The first person to identify this rare neurological disorder was Errol Levine, a retired radiologist from South Africa, now living in Santa Fe, N.M. The location of the stroke shown — in a part of the brain known as the corpus callosum — was a subtle clue, and Dr. Levine recalled reading of an autoimmune disease characterized by strokes in this unusual area of the brain. This is Dr. Levine’s second win. Well done, sir! Susac’s syndrome is a rare disorder first described in 1979 by Dr. John Susac, a neurologist in Winter Haven, Fla. Dr. Susac described two women, one 26 years old, the other 40, who he encountered within weeks of one another. Both had the same unusual triad of psychiatric symptoms suggestive of some type of brain inflammation, hearing loss, and patchy vision loss caused by blockages of the tiniest vessels of the retina known as branch retinal arteries. A few years later, Dr. Susac encountered two more cases and presented one of these at a meeting as a mystery diagnosis. The doctor who figured it out called the disorder Susac’s syndrome, and the name stuck. Seen primarily in young women, Susac’s is thought to be an autoimmune disorder in which antibodies, the foot soldiers of the immune system, mistakenly attack tissues in some of the smallest arteries in the brain. The inflammation of these small vessels blocks the flow of blood, causing tiny strokes. © 2015 The New York Times Company
By Tori Rodriguez Heart disease and depression often go hand in hand. Long-term studies have found that people with depression have a significantly higher risk of subsequent heart disease, and vice versa. Recent research has revealed that the link begins at an early age and is probably caused by chronic inflammation. A new study in the November 2014 issue of Psychosomatic Medicine by researchers in the U.S., Australia and China examined data from an ongoing study of health among Australians. The researchers looked at the scores of 865 young adults on a questionnaire that assesses depression symptoms and other measures of mental health. They also examined measurements of the internal diameter of the blood vessels of the retina, a possible marker of early cardiovascular disease. After controlling for sex, age, smoking status and body mass index, the investigators found that participants with more symptoms of depression and anxiety had wider retinal arterioles than others, which could reflect the quality of blood vessels in their heart and brain. “We don't know if the association is causal,” explains study co-author Madeline Meier, a psychology professor at Arizona State University. “But our findings suggest that symptoms of depression and anxiety may identify youth at risk for cardiovascular disease.” Other research shows that people with depression have more inflammation throughout their body and nervous system. “One theory is that stress and inflammation could play a causal role in depression,” Meier says. Such chronic inflammation is also a risk factor for cardiovascular disease. The relationship is complex: in some people, inflammation seems to precede depression and heart disease; in others, the disorders seem to cause or exacerbate the inflammation. © 2015 Scientific American
by Jessica Hamzelou IF YOU knew you were about to go through a stressful experience, would you pop a pill to protect yourself from its knock-on effects? It's an idea that has been mooted after a drug seemed to make mice immune to the negative impacts of stressful events. But could we rationalise prescribing such a drug? We all experience stress during our lives, whether it be a one-off event, such as a loved one dying, or chronic, low-level stress that results from struggling to make ends meet, for example. While most people find ways to cope, for some a particularly stressful event can trigger depression. What if there was a way to boost our stress resilience and thus shield us from depression? Rebecca Brachman at Columbia University in New York stumbled across the idea while she was giving ketamine to mice with the symptoms of depression. Even though the ketamine-taking mice had been chronically stressed, when they were dropped in a pool of water – a one-off stressful event – they were unperturbed and swam to an exit. Mice not given the drug made no attempt to escape, a classic sign of depression in rodents. There was also no change in the ketamine-taking animals' cognitive abilities or metabolism – both of which are altered in human depression. "It's really remarkable," says Brachman. "They basically look like mice that haven't been stressed." A single dose of ketamine protected mice from developing the symptoms of depression after stressful events for four weeks. But the drug only seemed to stop the symptoms of depression – some of the animals still exhibited anxiety behaviours. "It seems to protect against depression rather than anxiety," says Brachman, who controversially describes it as a depression "vaccine". The work will be published in Biological Psychiatry. © Copyright Reed Business Information Ltd
By Neuroskeptic | Neuroscientists might need to rethink much of what’s known about the amygdala, a small brain region that’s been the focus of a lot of research. That’s according to a new paper just published in Scientific Reports: fMRI measurements of amygdala activation are confounded by stimulus correlated signal fluctuation in nearby veins draining distant brain regions. The amygdala is believed to be involved in emotion, especially negative emotions such as fear. Much of the evidence for this comes from fMRI studies showing that the amygdala activates in response to stimuli such as images of scared faces. However, according to the authors of the new paper, Austrian neuroscientists Roland N. Boubela and colleagues, there’s a flaw in these fMRI studies. The problem, they say, is that the amygdala happens to be located next to a large vein, called the basal vein of Rosenthal (BVR). fMRI works by detecting blood oxygenation, so changes in the oxygen level in the blood within the BVR could produce signal changes that could be mistaken for activation in the amygdala. Because the BVR drains blood from several brain regions, some of which are themselves involved in emotion processing, the BVR could act as a proxy for emotion-related neural activation elsewhere in the brain, which is then projected onto the amygdala. Neuroscientists have long been aware of potential large vein contributions to the fMRI signal, but it hasn’t generally been seen as a serious concern. According to Boubela et al., however, the problem is serious, when it comes to the amygdala.
Michael C. Corbalis In the quest to identify what might be unique to the human mind, one might well ask whether non-human animals have a theory of mind. In fiction, perhaps, they do. Eeyore, the morose donkey in Winnie-the-Pooh, at one point complains: ‘A little consideration, a little thought for others, makes all the difference.’ In real life, some animals do seem to show empathy toward others in distress. The primatologist Frans de Waal photographed a juvenile chimpanzee placing a consoling arm around an adult chimpanzee in distress after losing a fight, but suggests that monkeys do not do this. However, one study shows that monkeys won’t pull a chain to receive food if doing so causes a painful stimulus to be delivered to another monkey, evidently understanding that it will cause distress. Even mice, according to another study, react more intensely to pain if they perceive other mice in pain. It is often claimed that dogs show empathy toward their human owners, whereas cats do not. Cats don’t empathise—they exploit. Understanding what others are thinking, or what they believe, can be complicated, but perceiving emotion in others is much more basic to survival, and no doubt has ancient roots in evolution. Different emotions usually give different outward signs. In Shakespeare’s “Henry V,” the King recognises the signs of rage, urging his troops to . . . imitate the action of the tiger; Stiffen the sinews, summon up the blood, Disguise fair nature with hard-favour’d rage; Then lend the eye a terrible aspect . . . The human enemy will read the emotion of Henry’s troops, just as the antelope will read the emotion of the marauding tiger. Perhaps the best treatise on the outward signs of emotion is Charles Darwin’s “The Expression of the Emotions in Man and Animals,” which details the way fear and anger are expressed in cats and dogs, although he does not neglect the positive emotions: © 2015 Salon Media Group, Inc.
Richard Harris American medicine is heading into new terrain, a place where a year's supply of drugs can come with a price tag that exceeds what an average family earns. Pharmacy benefit manager Express Scripts says last year more than half a million Americans racked up prescription drug bills exceeding $50,000. Barbara Haedtke of Portland, Ore., knows this all too well. When she was diagnosed with multiple sclerosis in 2001 at the age of 35, she was prescribed Avonex, at a cost of around $10,000 a year. Her health insurance paid most of that until she and her husband found themselves without jobs during an economic downturn. "We were in the hole, and so $10,000 was a lot of money," she says. "Under the best circumstances it's a lot of money, but then particularly it was really difficult." Barbara Haedtke says she's grateful for a drug-company program that helps cover copays, but doesn't know how long she'll get that benefit. The drug company gave her the medication at no charge until she once again had a job with insurance, and for that, she says, she's really grateful. But the story doesn't end there. Haedtke used Avonex for about a decade and watched with disbelief as the price more than tripled. She's now taking a new drug, Tecfidera, that's priced even higher — $66,000 a year, according to her pharmacy receipt. The drug is supposed to help reduce the number of episodes that characterize multiple sclerosis, a disease in which nerve fibers gradually degenerate, causing muscle weakness, numbness, loss of balance and even paralysis. © 2015 NPR
Dan Sung A 10-year study has revealed a startling link between high levels of anxiety and an increased risk of death from liver disease. The research, carried out by scientists at the University of Edinburgh, took account for obvious sociological and physiological factors such as alcohol consumption, obesity, diabetes and class, but still the data pointed to a clear relationship between the psychological conditions of stress and depression and the physical health of the hepatic system. There were over 165,000 participants surveyed for mental distress. They were each tracked for over a decade during which time the causes of death for those who passed on were recorded and categorised. What was found was that those who’d scored highly for signs of depression and stress were far more likely to suffer fatal liver disease. “This study provides further evidence for the important links between mind and body, and of the damaging effects psychological distress can have on physical wellbeing,” said Dr Tom Russ of the Centre for Clinical Brain Sciences. The work did not uncover any reasons for direct cause and effect but is the first to identify such a link between mental states and liver damage. Previous research has described how psychological conditions can lead to increased risk of cardiovascular disease which, in turn, may develop into obesity, raised blood pressure and then eventually to liver failure but, with this methodology controlling for such factors, it appears that the link is more direct than was previously thought.