Chapter 15. Emotions, Aggression, and Stress
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T. M. Luhrmann AMERICANS are a pretty anxious people. Nearly one in five of us — 18 percent — has an anxiety disorder. We spend over $2 billion a year on anti-anxiety medications. College students are often described as more stressed than ever before. There are many explanations for these nerves: a bad job market, less cohesive communities, the constant self-comparison that is social media. In 2002 the World Mental Health Survey found that Americans were the most anxious people in the 14 countries studied, with more clinically significant levels of anxiety than people in Nigeria, Lebanon and Ukraine. To be clear, research suggests that anxiety is at least partially temperamental. A recent study of 592 rhesus monkeys found that some of them responded more anxiously than others and that as much as 30 percent of early anxiety may be inherited. Yet what is inherited is the potential for anxiety, not anxiety itself. Life events obviously play a role. Another, less obvious factor may be the way we think about the mind: as an interior place that demands careful, constant attention. Humans seem to distinguish between mind and body in all cultures, but the sharp awareness of mind as a possession, distinct from soul and body, comes from the Enlightenment. It was then, in the aftermath of the crisis of religious authority and the scientific revolution, that there were intense debates about the nature of mental events. Between 1600 and 1815, the place where mental stuff happened — the “thing that thinks,” to use Descartes’s phrase — came to seem more and more important, as George Makari, a psychiatrist and psychoanalyst, explains in his forthcoming book, “Soul Machine: The Invention of the Modern Mind.” From this, Mr. Makari writes, was developed the psychological mind and psychoanalysis and an expectation that personal thoughts and feelings are the central drivers of human action — not roles, not values, not personal sensation, not God. In the United States, the enormous psychotherapeutic and self-help industry teaches us that we must pay scrupulous attention to inner experience. To succeed and be happy, we are taught, we need to know what we feel. © 2015 The New York Times Company
Link ID: 21189 - Posted: 07.20.2015
By Claire Asher Even fish have role models. In a new study, researchers paired up inexperienced fathead minnows (Pimephales promelas, pictured) with two types of mentors: a minnow raised in an environment free of predators or a minnow raised in a dangerous one simulated by the odors of predatory pike and sturgeon. Fish from dangerous environments were fearful of the smell of both unknown and familiar predators, whereas fish that grew up in safety hid when they smelled a known predator but were curious about new smells. Both types of fish passed on their fears to their protégés: Minnows that spent time with fish raised in dangerous environments were scared of all smells they came across, but those that learned from fish raised in safety feared only specific predators and took new experiences in stride, the team reports online this week in the Proceedings of the Royal Society B. The authors say this is the first experiment to show that environment can influence the social transmission of fear and reveals how risk aversion can be learned. The researchers also suggest their study may shed light on how fear disorders such as post-traumatic stress disorder (PTSD) develop in humans, which research shows can be influenced by social environment; PTSD symptoms can be acquired from friends or family who have suffered trauma, for example. © 2015 American Association for the Advancement of Science
James Gorman Some animals just aren’t that social. Like octopuses. They don’t live in groups. They don’t have big chatterfests like prairie dogs. They don’t write, they don’t call. But new evidence shows that an octopus may signal its intentions when it is about to whomp another octopus. David Scheel, a biologist at Alaska Pacific University; Peter Godfrey-Smith, a philosopher of science who has appointments at City University of New York and the University of Sydney; and Matthew Lawrence, an Australian diver, collaborated to record interactions between common Sydney octopuses off the Australian island of Tasmania. Their method was to put cameras on the sea floor in areas where there were plenty of these octopuses and then comb through hours and hours of video. They aren’t done yet, but Dr. Scheel presented some of their initial findings in Anchorage at the annual meeting last month of the Animal Behavior Society, and they have about two dozen examples of octopuses signaling their aggressive intent. He showed video of one octopus moving swiftly toward another as it made itself look taller and turned very dark. Octopuses have a remarkable ability to change their coloration to blend in with their surroundings, like chameleons. But this color change is the opposite. A darkened octopus stands out against a sandy bottom like an avenging cephalopod. © 2015 The New York Times Company
Link ID: 21164 - Posted: 07.13.2015
By Nicholas Bakalar A short nap could reduce impulsive behavior and improve the ability to withstand frustration, a small study suggests. Researchers studied 40 people aged 18 to 50. After three nights of normal sleep, the participants took computer-based tests of frustration tolerance — which consisted of trying to complete an impossible task — and completed questionnaires on sleepiness, mood and impulsivity. Then they were randomly assigned to take an hour’s nap, or to watch a nature video. At the end of the process, they were tested again. The study appears in Personality and Individual Differences. Before the nap period, everyone spent about the same amount of time on the unsolvable task, but afterward nappers, who all reported having slept at least part of the time, spent significantly more time working at it than they had before their nap, while non-nappers gave up sooner. Nappers also rated their behavior as less impulsive than non-nappers. The lead author, Jennifer R. Goldschmied, a doctoral student at the University of Michigan, acknowledged that the sample is small, involved mainly college students and may not be applicable to other populations. The sleep calculations also did not use electronic devices to precisely measure sleep and wakefulness. Still, she said, “These results are valuable and have put us on the route to understanding how we can utilize naps. Now people are starting to understand how powerful short bursts of sleep can be.” © 2015 The New York Times Company
By Christian Jarrett We all know a narcissist or two — the often-annoying colleagues, friends, and family members who seem to be constantly talking about themselves and touting their own achievements. In some ways, these characters are a paradox. They seem to be in love with themselves — and when they’re asked in questionnaires, they claim to have very high self-esteem — but their behavior poses an obvious question: If you were genuinely happy with yourself, why would you feel the need to constantly boast and seek admiration from others? A new study in Social Cognitive and Affective Neuroscience potentially solves the mystery: Narcissists may talk and act confident, but their brains don’t lie. At a neural level, narcissists are needy. A research team led by David Chester at the University of Kentucky at Lexington recruited 50 undergrad students and had them complete a standard measure of narcissism. Participants who agreed with statements like “I think I am a special person” were allocated high narcissism scores. Next, the researchers invited the students to lie in a special kind of brain scanner that uses diffusion tensor imaging, a technology that measures the amount of connectivity between different brain areas. Such scans produce beautiful “wiring diagrams” of the brain, in contrast to structural MRI scans that show the brain’s gray matter, and functional MRI scans that measure neural activity — this allows researchers to better understand how much “conversation” there is between the brain’s various functional hubs.
Link ID: 21148 - Posted: 07.09.2015
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