Chapter 15. Emotions, Aggression, and Stress

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Xiaomeng (Mona) Xu, assistant professor of experimental psychology, and Ariana Tart-Zelvin, If you have experienced the evolution from having a crush to falling in love, it may seem like the transition happens naturally. But have you ever wondered how we make such a huge emotional leap? In other words, what changes take place in our brains that allow us to fall deeply in love? Stephanie Cacioppo, a psychologist at the University of Chicago who has studied the neuroscience of romantic love for the past decade, explains that the process involves several complex changes, particularly in the brain’s reward system. More specifically, in a 2012 review of the love research literature Lisa Diamond and Janna Dickenson, psychologists at the University of Utah, found romantic love is most consistently associated with activity in two brain regions—the ventral tegmental area (VTA) and the caudate nucleus. These areas play an essential role in our reward pathway and regulate the “feel good” neurotransmitter dopamine. In other words, during the early stages of love you crave the person because he or she makes you feel so good. And over time these feelings persist. Our neuroimaging research and that of others suggests that once you are in love—as long as the relationship remains satisfying—simply thinking about your partner not only makes you feel good but can also buffer against pain, stress and other negative feelings. © 2017 Scientific American,

Keyword: Emotions; Sexual Behavior
Link ID: 23852 - Posted: 07.20.2017

By LISA FELDMAN BARRETT Imagine that a bully threatens to punch you in the face. A week later, he walks up to you and breaks your nose with his fist. Which is more harmful: the punch or the threat? The answer might seem obvious: Physical violence is physically damaging; verbal statements aren’t. “Sticks and stones can break my bones, but words will never hurt me.” But scientifically speaking, it’s not that simple. Words can have a powerful effect on your nervous system. Certain types of adversity, even those involving no physical contact, can make you sick, alter your brain — even kill neurons — and shorten your life. Your body’s immune system includes little proteins called proinflammatory cytokines that cause inflammation when you’re physically injured. Under certain conditions, however, these cytokines themselves can cause physical illness. What are those conditions? One of them is chronic stress. Your body also contains little packets of genetic material that sit on the ends of your chromosomes. They’re called telomeres. Each time your cells divide, their telomeres get a little shorter, and when they become too short, you die. This is normal aging. But guess what else shrinks your telomeres? Chronic stress. If words can cause stress, and if prolonged stress can cause physical harm, then it seems that speech — at least certain types of speech — can be a form of violence. But which types? This question has taken on some urgency in the past few years, as professed defenders of social justice have clashed with professed defenders of free speech on college campuses. Student advocates have protested vigorously, even violently, against invited speakers whose views they consider not just offensive but harmful — hence the desire to silence, not debate, the speaker. “Trigger warnings” are based on a similar principle: that discussions of certain topics will trigger, or reproduce, past trauma — as opposed to merely challenging or discomfiting the student. The same goes for “microaggressions.” © 2017 The New York Times Company

Keyword: Aggression; Brain imaging
Link ID: 23846 - Posted: 07.18.2017

Jon Hamilton Harsh life experiences appear to leave African-Americans vulnerable to Alzheimer's and other forms of dementia, researchers reported Sunday at the Alzheimer's Association International Conference in London. Several teams presented evidence that poverty, disadvantage and stressful life events are strongly associated with cognitive problems in middle age and dementia later in life among African-Americans. The findings could help explain why African-Americans are twice as likely as white Americans to develop dementia. And the research suggests genetic factors are not a major contributor. "The increased risk seems to be a matter of experience rather than ancestry," says Megan Zuelsdorff, a postdoctoral fellow in the Health Disparities Research Scholars Program at the University of Wisconsin-Madison. Scientists have struggled to understand why African-Americans are so likely to develop dementia. They are more likely to have conditions like high blood pressure and diabetes, which can affect the brain. And previous research has found some evidence that African-Americans are more likely to carry genes that raise the risk. But more recent studies suggest those explanations are incomplete, says Rachel Whitmer, an epidemiologist with Kaiser Permanente's Division of Research in Northern California. Whitmer has been involved in several studies that accounted for genetic and disease risks when comparing dementia in white and black Americans. "And we still saw these [racial] differences," she says. "So there is still something there that we are trying to get at." © 2017 npr

Keyword: Alzheimers; Stress
Link ID: 23841 - Posted: 07.17.2017

Brandie Jefferson It wasn't long ago that there were no treatments for multiple sclerosis. In the 1970s, some doctors used chemotherapy to treat the degenerative neurological disease. Since then, more than a dozen drugs have been developed or approved, including infusions, oral medications and self-administered shots. None of these are a magic bullet for a disease that can be disabling and deadly. But now there is a new drug, Ocrevus, that looks like a game-changer. It uses a novel approach to blocking the inflammation that drives the disease and looks as if it's spectacularly effective. It also costs $65,000 a year. I have MS. Should I take Ocrevus? That, I discovered, is not a simple question to answer. But because I'm an MS patient and a science journalist, I was determined to try to figure it out. In March, the FDA approved Ocrevus (ocrelizumab) for the treatment of relapsing-remitting multiple sclerosis, the most common form of the disease. People with RRMS tend to have flare-ups when their symptoms worsen, followed by periods of remission and, in some cases, a full or partial recovery. In two clinical trials sponsored by the drug's eventual manufacturer, F. Hoffmann-La Roche, RRMS patients who were given ocrelizumab had about 50 percent fewer relapses and up to 95 percent fewer new lesions on the brain and spinal cord than those who were given Rebif, a common therapy. MS is an autoimmune disease, meaning the body attacks itself. The body's nerve endings and the fatty tissue that coats them, called myelin, bear the brunt of the immune system's attacks. As a result, the central nervous system has difficulty communicating with the nerves, leading to a disease that manifests itself in different ways, such as pain, fatigue, disability and slurred speech. © 2017 npr

Keyword: Multiple Sclerosis
Link ID: 23838 - Posted: 07.14.2017

Hannah Devlin Science correspondent Brash, brawny and keen to impose their will on anyone who enters their sphere of existence: the alpha male in action is unmistakable. Now scientists claim to have pinpointed the biological root of domineering behaviour. New research has located a brain circuit that, when activated in mice, transformed timid individuals into bold alpha mice that almost always prevailed in aggressive social encounters. In some cases, the social ranking of the subordinate mice soared after the scientists’ intervention, hinting that it might be possible to acquire “alphaness” simply by adopting the appropriate mental attitude. Or as Donald Trump might put it: “My whole life is about winning. I almost never lose.” Prof Hailan Hu, a neuroscientist at Zhejiang University in Hangzhou, China, who led the work said: “We stimulate this brain region and we can make lower ranked mice move up the social ladder.” The brain region, called the dorsal medial prefrontal cortex (dmPFC), was already known to light up during social interactions involving decisions about whether to be assertive or submissive with others. But brain imaging alone could not determine whether the circuit was ultimately controlling how people behave. The latest findings answer the question, showing that when the circuit was artificially switched on, low-ranking mice were immediately emboldened. “It’s not aggressiveness per se,” Hu said. “It increases their perseverance, motivational drive, grit.” © 2017 Guardian News and Media Limited

Keyword: Aggression; Sexual Behavior
Link ID: 23836 - Posted: 07.14.2017

Ian Sample Science editor The secret to a good night’s sleep later in life is having a good reason to get up in the morning, according to US researchers who surveyed people on their sleeping habits and sense of purpose. People who felt they had a strong purpose in life suffered from less insomnia and sleep disturbances than others and claimed to rest better at night as a result, the study found. Jason Ong, a neurologist who led the research at Northwestern University in Chicago, said that encouraging people to develop a sense of purpose could help them to keep insomnia at bay without the need for sleeping pills. More than 800 people aged 60 to 100 took part in the study and answered questions on their sleep quality and motivations in life. To assess their sense of purpose, the participants were asked to rate statements such as: “I feel good when I think of what I’ve done in the past and what I hope to do in the future.” According to Ong, people who felt their lives had most meaning were less likely to have sleep apnea, a disorder that makes the breathing shallow or occasionally stop, or restless leg syndrome, a condition that compels people to move their legs and which is often worse at night. Those who reported the most purposeful lives had slightly better sleep quality overall, according to the study in the journal Sleep Science and Practice. © 2017 Guardian News and Media Limited

Keyword: Sleep; Attention
Link ID: 23819 - Posted: 07.11.2017

By Michael Price Male baboons that harass and assault females are more likely to mate with them, according to a new study, adding evidence that sexual intimidation may be a common mating strategy among promiscuous mammals. The study’s authors even argue that the findings could shed light on the evolutionary origins of our own species’ behavior, although others aren’t convinced the results imply anything about people. “I think the data and analyses in this study are first-rate,” says Susan Alberts, a biologist who studies primate behavior at Duke University in Durham, North Carolina. “[But] I also think it’s a big stretch to infer something about the origins of human male aggression towards women.” To conduct the research, Elise Huchard, a zoologist at the National Center for Scientific Research in Montpellier, France, and colleagues examined a group of chacma baboons (Papio ursinus) living in Tsaobis Nature Park in Namibia over a 9-year period. These brownish, dog-sized primates live in troops of dozens of males and females. Females will mate with multiple males throughout the year. The male chacma are about twice the size of females and aggressively fight one another and engage in howling competitions to establish dominance. The more dominant a male is, the more likely he is both to succeed in finding a mate and to sire offspring. Males rarely force females to mate, but after years spent observing the animals in the wild, Huchard noticed that a subtler form of sexual coercion appeared to be going on. “Males often chase and attack some females of their own group when meeting another group, and they generally target sexually receptive females on such occasions,” she says. “I spent a great deal of time studying female mate choice, and my main impression … was that females don't have much room to express any preference.” © 2017 American Association for the Advancement of Science

Keyword: Sexual Behavior; Aggression
Link ID: 23813 - Posted: 07.07.2017

Mike Mariani With its bright colors, anthropomorphic animal motif, and nautical-themed puzzle play mat, Dr. Kimberly Noble’s laboratory at Columbia University looks like your typical day care center—save for the team of cognitive neuroscientists observing kids from behind a large two-way mirror. The Neurocognition, Early Experience, and Development Lab is home to cutting-edge research on how poverty affects young brains, and I’ve come here to learn how Noble and her colleagues could soon definitively prove that growing up poor can keep a child’s brain from developing. Noble, a 40-year-old from outside of Philadelphia who discusses her work with a mix of enthusiasm and clinical restraint, is among the handful of neuroscientists and pediatricians who’ve seen increasing evidence that poverty itself—and not factors like nutrition, language exposure, family stability, or prenatal issues, as previously thought—may diminish the growth of a child’s brain. Now she’s in the middle of planning a five-year, nationwide study that could establish a causal link between poverty and brain development—and, in the process, suggest a path forward for helping our poorest children. It’s the culmination of years of work for Noble, who helped jump-start this fledgling field in the early 2000s when, as a University of Pennsylvania graduate student, she and renowned cognitive neuroscientist Martha Farah began exploring the observation that poor kids tended to perform worse academically than their better-off peers. They wanted to investigate the neurocognitive underpinnings of this relationship—to trace the long-standing correlation between socioeconomic status and academic performance back to specific parts of the brain. “There have been decades of work from social scientists, looking at socioeconomic disparities in broad cognitive outcomes—things like IQ or high school graduation rate,” she says. “But there’s no high school graduation part of the brain.” ©2017 Mother Jones and the Foundation for National Progress.

Keyword: Development of the Brain; Stress
Link ID: 23805 - Posted: 07.04.2017

Nicola Davis If you want your smile to appear pleasant, you might want to avoid a dazzling beam, research suggests. A study by scientists in the US has found that wide smiles with a high angle and showing a lot of teeth are not the best at creating a positive impression. “A lot of people don’t understand how important their smiles are and how important this aspect of communication we do with each other every day is,” said Stephen Guy, a co-author of the research from the University of Minnesota. The authors say the findings could prove valuable for clinicians working to restore facial movement and expression to those who have experienced facial paralysis. “When you have different surgical options, how do you choose which one is better?” Guy said, pointing out that some options might offer more extent of smile – referring to breadth – but others might improve the angle. “In order to do that, you need to say, ‘Oh, this smile is better or worse than that smile.’” To find the perfect smile, the team showed a 3D, computer-animated virtual face smiling in a range of different ways to 802 members of the public, ranging in age from 18 to 82. All had consumed fewer than six alcoholic drinks – the study was carried out at the Minnesota state fair. Each animation ran for 250 milliseconds and the faces showed differences in the angle of the smile, how broad it was, and the amount that teeth on show. In addition, the team took one smile – featuring a high angle, low extent and medium amount of dental show – and tinkered with the symmetry of the smile, changing the length of time it took the left side of the face to smile compared with the right. © 2017 Guardian News and Media Limited

Keyword: Emotions
Link ID: 23789 - Posted: 06.29.2017

/ By Rod McCullom Facebook has problem — a very significant problem — with the violent and gruesome content which has quickly found its way, in numerous instances, onto the social network and its Facebook Live feature, which was introduced to American users in January 2016. The disturbing litany of murders, suicides and assaults have already become macabre technological milestones. These include Robert Godwin Sr., the 74-year-old father of nine and grandfather of 14 who was selected by a gunman at random and then murdered in a video posted to Facebook in mid-April. One week later, a man in Thailand streamed the murder of his 11-month old daughter on Facebook Live before taking his own life. The beating and torture of an 18-year-old man with intellectual and development disabilities was live-streamed on the service in January, and the tragic shooting death of two-year-old Lavontay White Jr. followed a month later on Valentine’s Day. “At least 45 instances of violence — shootings, rapes, murders, child abuse, torture, suicides, and attempted suicides — have been broadcast via Live [since] December 2015,” Buzzfeed’s Alex Kantrowitz reported this month. “That’s an average rate of about two instances per month.” Copyright 2017 Undark

Keyword: Aggression; Robotics
Link ID: 23778 - Posted: 06.27.2017

By JANE E. BRODY It’s perfectly normal for someone to feel anxious or depressed after receiving a diagnosis of a serious illness. But what if the reverse occurs and symptoms of anxiety or depression masquerade as an as-yet undiagnosed physical disorder? Or what if someone’s physical symptoms stem from a psychological problem? How long might it take before the true cause of the symptoms is uncovered and proper treatment begun? Psychiatric Times, a medical publication seen by some 50,000 psychiatrists each month, recently published a “partial listing” of 47 medical illnesses, ranging from cardiac arrhythmias to pancreatic cancer, that may first present as anxiety. Added to that was another “partial listing” of 30 categories of medications that may cause anxiety, including, ironically, popular antidepressants like selective serotonin reuptake inhibitors, or S.S.R.I.s. These lists were included in an article called “Managing Anxiety in the Medically Ill” meant to alert mental health practitioners to the possibility that some patients seeking treatment for anxiety or depression may have an underlying medical condition that must be addressed before any emotional symptoms are likely to resolve. Doctors who treat ailments like cardiac, endocrine or intestinal disorders would do well to read this article as well lest they do patients a serious disservice by not recognizing an emotional cause of physical symptoms or addressing the emotional components of a physical disease. © 2017 The New York Times Company

Keyword: Depression; Stress
Link ID: 23773 - Posted: 06.26.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Neuroimmunology
Link ID: 23760 - Posted: 06.22.2017

By Diana Kwon Glioblastomas, highly aggressive malignant brain tumors, have a high propensity for recurrence and are associated with low survival rates. Even when surgeons remove these tumors, deeply infiltrated cancer cells often remain and contribute to relapse. By harnessing neutrophils, a critical player in the innate immune response, scientists have devised a way to deliver drugs to kill these residual cells, according to a study published today (June 19) in Nature Nanotechnology. Neutrophils, the most common type of white blood cell, home in to areas of injury and inflammation to fight infections. Prior studies in both animals and humans have reported that neutrophils can cross the blood-brain barrier, and although these cells are not typically attracted to glioblastomas, they are recruited at sites of tumor removal in response to post-operative inflammation. To take advantage of the characteristics of these innate immune cells, researchers at China Pharmaceutical University encased paclitaxel, a traditional chemotherapy drug, with lipids. These liposome capsules were loaded into neutrophils and injected in the blood of three mouse models of glioblastoma. When the treatment was applied following surgical removal of the main tumor mass, the neutrophil-carrying drugs were able to cross the blood-brain barrier, destroy residual cancer cells, and slow the growth of new tumors. Overall, mice receiving treatment lived significantly longer than controls. © 1986-2017 The Scientist

Keyword: Brain imaging; Neuroimmunology
Link ID: 23756 - Posted: 06.21.2017

By Timothy Revell Feeling sad? Soon your dolls will be able to tell. To demonstrate the power of a new chip that can run artificially intelligent algorithms, researchers have put it in a doll and programmed it to recognise emotions in facial images captured by a small camera. The doll can recognise eight emotions in total, including surprise and happiness, all while running on a small battery and without doing any processing in the cloud. The total cost of putting the new chip together is just €115 – an indicator of how easy it is becoming to give devices basic AI abilities. “In the near future, we will see a myriad of eyes everywhere that will not just be watching us, but trying to help us,” says project leader Oscar Deniz at the University of Castilla-La Mancha in Ciudad Real, Spain. Recent advances in AI mean we already have algorithms that can recognise objects, lip-read, make basic decisions and more. It’s only a matter of time before these abilities make their way on to little cheap chips like this one, and then put into consumer devices. “We will have wearable devices, toys, drones, small robots, and things we can’t even imagine yet that will all have basic artificial intelligence,” says Deniz. © Copyright New Scientist Ltd.

Keyword: Emotions
Link ID: 23752 - Posted: 06.20.2017

Heidi Ledford By 13 weeks of gestation, human fetuses have developed a much more unusual immune system than previously thought. A human fetus in its second trimester is extraordinarily busy. It is developing skin and bones, the ability to hear and swallow, and working on its first bowel movement. Now, a study published on 14 June in Nature finds that fetuses are also acquiring a functioning immune system — one that can recognize foreign proteins, but is less inclined than a mature immune system to go on the attack (N. McGovern et al. Nature http://dx.doi.org/10.1038/nature22795; 2017). The results add to a growing body of literature showing that the fetal immune system is more active than previously appreciated. “In general textbooks, you see this concept of a non-responsive fetus is still prevailing,” says immunologist Jakob Michaelsson at the Karolinska Institute in Stockholm. But the fetal immune system is unique, he says. “It’s not just immature, it’s special.” A developing fetus is constantly exposed to foreign proteins and cells, which are transferred from the mother through the placenta. In humans, this exposure is more extensive than in many other mammals, says immunologist Mike McCune at the University of California, San Francisco. As a result, laboratory mice have proved a poor model for studying the developing human fetal immune system. But fully understanding that development could reveal the reasons for some miscarriages, as well as explain conditions such as pre-eclampsia, which is associated with abnormal immune responses to pregnancy and causes up to 40% of premature births. © 2017 Macmillan Publishers Limited,

Keyword: Development of the Brain; Neuroimmunology
Link ID: 23746 - Posted: 06.15.2017

By ALEX WILLIAMS This past winter, Sarah Fader, a 37-year-old social media consultant in Brooklyn who has generalized anxiety disorder, texted a friend in Oregon about an impending visit, and when a quick response failed to materialize, she posted on Twitter to her 16,000-plus followers. “I don’t hear from my friend for a day — my thought, they don’t want to be my friend anymore,” she wrote, appending the hashtag #ThisIsWhatAnxietyFeelsLike. Thousands of people were soon offering up their own examples under the hashtag; some were retweeted more than 1,000 times. You might say Ms. Fader struck a nerve. “If you’re a human being living in 2017 and you’re not anxious,” she said on the telephone, “there’s something wrong with you.” It was 70 years ago that the poet W.H. Auden published “The Age of Anxiety,” a six-part verse framing modern humankind’s condition over the course of more than 100 pages, and now it seems we are too rattled to even sit down and read something that long (or as the internet would say, tl;dr). Anxiety has become our everyday argot, our thrumming lifeblood: not just on Twitter (the ur-anxious medium, with its constant updates), but also in blogger diaries, celebrity confessionals (Et tu, Beyoncé?), a hit Broadway show (“Dear Evan Hansen”), a magazine start-up (Anxy, a mental-health publication based in Berkeley, Calif.), buzzed-about television series (like “Maniac,” a coming Netflix series by Cary Fukunaga, the lauded “True Detective” director) and, defying our abbreviated attention spans, on bookshelves. With two new volumes analyzing the condition (“On Edge: A Journey Through Anxiety,” by Andrea Petersen, and “Hi, Anxiety,” by Kat Kinsman) following recent best-sellers by Scott Stossel (“My Age of Anxiety”) and Daniel Smith (“Monkey Mind”), the anxiety memoir has become a literary subgenre to rival the depression memoir, firmly established since William Styron’s “Darkness Visible” and Elizabeth Wurtzel’s “Prozac Nation” in the 1990s and continuing today with Daphne Merkin’s “This Close to Happy.” © 2017 The New York Times Company

Keyword: Depression; Stress
Link ID: 23732 - Posted: 06.12.2017

By JANE E. BRODY Hurray for the HotBlack Coffee cafe in Toronto for declining to offer Wi-Fi to its customers. There are other such cafes, to be sure, including seven of the eight New York City locations of Café Grumpy. But it’s HotBlack’s reason for the electronic blackout that is cause for hosannas. As its president, Jimson Bienenstock, explained, his aim is to get customers to talk with one another instead of being buried in their portable devices. “It’s about creating a social vibe,” he told a New York Times reporter. “We’re a vehicle for human interaction, otherwise it’s just a commodity.” What a novel idea! Perhaps Mr. Bienenstock instinctively knows what medical science has been increasingly demonstrating for decades: Social interaction is a critically important contributor to good health and longevity. Personally, I don’t need research-based evidence to appreciate the value of making and maintaining social connections. I experience it daily during my morning walk with up to three women, then before and after my swim in the locker room of the YMCA where the use of electronic devices is not allowed. The locker room experience has been surprisingly rewarding. I’ve made many new friends with whom I can share both joys and sorrows. The women help me solve problems big and small, providing a sounding board, advice and counsel and often a hearty laugh that brightens my day. © 2017 The New York Times Company

Keyword: Stress
Link ID: 23730 - Posted: 06.12.2017

By LISA SANDERS, M.D. She didn’t have any urgent medical problems, the woman told Dr. Lori Bigi. She was there because she had moved to Pittsburgh and needed a primary-care doctor. Bigi, an internist at the University of Pittsburgh Medical Center, quickly eyed her new patient. She was 31 and petite, just over five feet tall and barely 100 pounds. And she looked just as she described herself, pretty healthy. Doctors often rely on patients’ sense of their well-being, especially when their assessment matches their appearance. But as Dr. Bigi was reminded that day, patients aren’t always right. The patient did say that she had seen her old doctor for awful headaches she got occasionally. They felt like an ice pick through the top of her head, the patient explained, which, at least initially, usually came on while she was going to the bathroom. The headache didn’t last long, but it was intensely painful. Her previous doctor thought it was a type of migraine. He prescribed medication, but it didn’t help. Now her main problem was anxiety, and she saw a psychiatrist for that. Sudden Panic Anxiety is common enough, and because the patient was seeing a specialist, Bigi wasn’t planning to spend much time discussing it. But then the doctor saw that in addition to taking an antidepressant — a recommended treatment for anxiety — the patient was on a sedating medication called clonazepam. It wasn’t a first-line medication for anxiety, and this tiny woman was taking a huge dose of it. The young woman explained that for most of her life, she was not a particularly anxious person. Then, two years earlier, she started experiencing episodes of total panic for seemingly no reason. At the time she chalked it up to a new job — she worked in a research lab — and the pressures associated with a project they had recently started. But the anxiety never let up. © 2017 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 23721 - Posted: 06.08.2017

By EMILIE LE BEAU LUCCHESI Benjamin Stepp, an Iraq war veteran, sat in his graduate school course trying to focus on the lecture. Neither his classmates nor his professor knew he was silently seething. But his service dog, Arleigh, did. She sensed his agitation and “put herself in my lap,” said Mr. Stepp, 37, of Holly Springs, Miss. “I realized I needed to get out of class. We went outside, I calmed down. We breathed.” During his two deployments to Iraq, Mr. Stepp endured a traumatic brain injury and multiple surgeries on his ankle, and most days he suffers excruciating pain in his legs and lower back. He says he also returned from the war with a lot of anger, which wells up at unexpected times. “Anger kept us alive overseas,” Mr. Stepp said. “You learn that anger keeps you alive.” Now that he is back, though, that anger no longer serves a useful purpose. And Arleigh, a lab and retriever mix who came to Mr. Stepp from K9s For Warriors, a nonprofit organization that trains service dogs, has been helping him to manage it. The dog senses when his agitation and anxiety begin rising, and sends him signals to begin the controlled breathing and other exercises that help to calm him down. Pet owners and trainers have long been aware of a dog’s ability to sense a human’s emotions. In the last 10 years, researchers, too, have begun to explore more deeply the web of emotions, both positive and negative, that can spread between people and animals, said Natalia Albuquerque, an ethologist who studies animal cognition at the University of São Paulo in Brazil and the University of Lincoln in England. The spread of emotions between animals and people, or between animals — what researchers refer to as emotional contagion — is an emerging field of science. But “there are still many unanswered questions we need to address,” Ms. Albuquerque said. © 2017 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 23708 - Posted: 06.05.2017

Judith Ohikuare In 2005, James Fallon's life started to resemble the plot of a well-honed joke or big-screen thriller: A neuroscientist is working in his laboratory one day when he thinks he has stumbled upon a big mistake. He is researching Alzheimer's and using his healthy family members' brain scans as a control, while simultaneously reviewing the fMRIs of murderous psychopaths for a side project. It appears, though, that one of the killers' scans has been shuffled into the wrong batch. The scans are anonymously labeled, so the researcher has a technician break the code to identify the individual in his family, and place his or her scan in its proper place. When he sees the results, however, Fallon immediately orders the technician to double check the code. But no mistake has been made: The brain scan that mirrors those of the psychopaths is his own. After discovering that he had the brain of a psychopath, Fallon delved into his family tree and spoke with experts, colleagues, relatives, and friends to see if his behavior matched up with the imaging in front of him. He not only learned that few people were surprised at the outcome, but that the boundary separating him from dangerous criminals was less determinate than he presumed. Fallon wrote about his research and findings in the book The Psychopath Inside: A Neuroscientist's Personal Journey Into the Dark Side of the Brain, and we spoke about the idea of nature versus nurture, and what—if anything—can be done for people whose biology might betray their behavior. © 2017 by The Atlantic Monthly Group.

Keyword: Aggression; Emotions
Link ID: 23707 - Posted: 06.05.2017