Chapter 15. Emotions, Aggression, and Stress
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Jessica Hamzelou Don't be too hard on them. Amoebas that weasel their way into our brains and chow down on our grey matter aren't welcome, but it's how our immune system reacts that's really lethal. Setting the story straight could help us deal with them better. Brain-eating amoebas (Naegleria fowleri) are found in warm freshwater pools around the world, feeding on bacteria. If someone swims in one of these pools and gets water up their nose, the amoeba heads for the brain in search of a meal. Once there, it starts to destroy tissue by ingesting cells and releasing proteins that make other cells disintegrate. The immune system launches a counter-attack by flooding the brain with immune cells, causing inflammation and swelling. It seldom works: of the 132 people known to have been infected in the US since 1962, only three survived. Brain-eating amoeba infections are more common elsewhere. "In Pakistan, we have something like 20 deaths per year," says Abdul Mannan Baig at the Aga Khan University in Karachi. There is no standard treatment. Doctors in the US have recently started trying to kill the amoebas with miltefosine, a drug known to work on the leishmaniasis parasite. Mannan thinks they should take a different approach, because the immune response may be more damaging than the amoeba itself. The problem is that enzymes released by the immune cells can also end up destroying brain tissue. And the swelling triggered by the immune system eventually squashes the brainstem, fatally shutting off communication between the body and the brain. © Copyright Reed Business Information Ltd
Link ID: 20917 - Posted: 05.13.2015
Tina Hesman Saey COLD SPRING HARBOR, N.Y. — Taming animals makes an impression on their DNA. Domesticated animals tend to have genetic variants that affect similar biological processes, such as brain and facial development and fur coloration. Alex Cagan of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, reported the results May 6 at the Biology of Genomes conference. Cagan and colleagues examined DNA in Norway rats (Rattus norvegicus) that had been bred for 70 generations to be either tame or aggressive toward humans. Docility was associated with genetic changes in 1,880 genes in the rats. American minks (Neovison vison) bred for tameness over 15 generations had tameness-associated variants in 525 genes, including 82 that were also changed in the rats. The researchers also compared other domesticated animals, including dogs, cats, pigs and rabbits, with their wild counterparts. The domestic species and the minks had tameness-associated changes in genes for epidermal growth factor and associated proteins that stimulate growth of cells. Those proteins are important for the movement of neural crest cells within an embryo. That finding seems to support a recent hypothesis that changes in neural crest cells could be responsible for domestication syndrome, physical traits, including floppy ears, spotted coats and juvenile faces, which accompany tameness in many domestic animals. © Society for Science & the Public 2000 - 2015.
Patricia Neighmond Terri Bradford has suffered debilitating headache pain all her life. Some days the pain is so bad, she says, "By 11 o'clock in the morning, I'm on the couch in a darkened room with my head packed in ice." Over the years, Bradford, who is 50 years old and lives in Bedford, Mass., has searched desperately for pain relief. She's been to the doctor countless times for countless tests. "Everything I've had, I've had twice," she says. "I've had two spinal taps; I've had so many nerve blocks I've lost count." Bradford is not alone. It's estimated that every year 12 million Americans go to the doctor seeking help for headaches. Nearly one quarter of the population suffers from recurrent severe tension headaches or migraines. People who go to the doctor for headache pain are more likely to be sent for advanced testing and treatment, a study finds. That testing is expensive, it may not be necessary and could even be harmful, says lead researcher Dr. John Mafi of Beth Israel Deaconess Medical Center in Boston. Mafi looked at the rates of advanced imaging like CT scans and MRIs in people with headaches, as well as referrals to other doctors, presumably specialists. He found that from 1999 to 2010, the number of diagnostic tests rose from 6.7 percent of all doctor visits to 13.9 percent. At the same time, referrals to other doctors increased from 6.9 percent to 13.2 percent. So almost double what it was a decade ago. Mafi says this isn't because more people are suffering headaches. The headache rate has remained virtually the same over the past decade. But what has changed is supply and demand. Today there are a lot more advanced diagnostic machines than there were a decade ago, and more patients are asking to be tested. © 2015 NPR
by Bethany Brookshire Certain images conjure up intense emotion: crying children, a bloody face, a snake rearing for a strike. When people take in pictures that hold deep meaning for them, they actually see the images more vividly. For them, emotion gives the world an extra burst of Technicolor and increases the odds that they will remember the scene. But the amount of visual boost — called emotionally enhanced vividness — varies from person to person. Some of this variability is in our genes, a new study finds, suggesting that people really do see the world in different ways. Many of us are familiar with the chemical messenger norepinephrine as a stress chemical. But it doesn’t just dictate whether we fight or flee, says Rebecca Todd, a cognitive neuroscientist at the University of British Columbia in Vancouver. Norepinephrine is also very important for emotional memory. “It’s important in the initial perception of emotional stimuli,” she explains. “It weighs down emotional memories so they burn brighter.” Norepinephrine is produced in an area of the brain called the locus coeruleus. In an ideal system, the cells in this area produce norepinephrine in response to a signal such as stress. The norepinephrine signals pass to other areas of the brain, but some chemical messenger remains, binding to receptors called alpha2b adrenoreceptors on cells in the locus coeruleus. These adrenoreceptors act as a brake, stopping the production of norepinephrine before things get out of hand. The receptors are produced by the gene ADRA2b. But a substantial proportion of Europeans and Africans have a variation on ADRA2b that deletes the alpha2b adrenoreceptor, possibly cutting some of the wires on the norepinephrine brakes. People with this deletion had stronger memories of emotionally charged events, a 2007 study found. Todd and graduate student Mana Ehlers wanted to see if this deletion might affect how people perceived emotional images. © Society for Science & the Public 2000 - 2015.
By Kira Peikoff I draw an uneasy breath as I step into a bright purple office on the 14th floor of Boston’s Prudential Building. I am shown to a small conference table, where I take a seat and await the experiment. A palm-size triangular module is affixed above my right eye. It connects to a single-use strip of electrodes stuck onto my forehead and running down the back of my neck. This is Thync, the latest in transcranial direct current stimulation, or tDCS. The manufacturer says the device, to come out later this year, can alter the user’s mood in minutes via electric current. With a connected smartphone app, the mood-impaired subject chooses one of two settings: “calm vibes” or “energy vibes.” I tap “calm vibes” and wait. Somehow, I am having a hard time picturing myself unwinding at home this way while my husband sips a glass of Merlot. Thync is the latest in a wave of wearable gadgets offering so-called noninvasive brain stimulation. Until recently, it was mostly hobbyists — nine-volt batteries stuck to their heads — who experimented with tDCS as a means of improving concentration, verbal and computation abilities, and creativity. But in the last few years, several companies have introduced slick consumer devices, among them Foc.us, whose headset and controller cost $298, and The Brain Stimulator, whose advanced starter kit costs $150. In January, the journal Brain Stimulation published the largest meta-analysis of tDCS to date. After examining every finding replicated by at least two research groups, leading to 59 analyses, the authors reported that one session of tDCS failed to show any significant benefit for users. © 2015 The New York Times Company
Link ID: 20891 - Posted: 05.05.2015
Paul Oswell “Cool” is a bit of a moving target. Sixty years ago it was James Dean, nonchalantly smoking a cigarette as he sat on a motorbike, glaring down 1950s conformity with brooding disapproval. Five years ago it was Zooey Deschanel holding a cupcake. In a phone interview with Steve Quartz, the co-author of the recently published Cool: How the Brain’s Hidden Quest for Cool Drives Our Economy and Shapes Our World, we skirted around a working definition. Defining cool turns out to be tricky even for someone who has just written an entire book examining the neurological processes behind it. Quartz’s most succinct definition was that cool is “the sweet spot between being innovative and unconventional, but not weird”. Quartz is the director of the Social Cognitive Neuroscience Laboratory at the California Institute of Technology. So when asked to describe what the lab does, he did not deliver a “cool” answer, but rather a precise one: it is, he said, “concerned with all the dimensions of decision making, from simple gambles and risk assessment right up to very complex reasoning and the nature of moral behaviour”. He wrote the book with his colleague Anette Asp, with whom he has long done research on “neuroeconomics” and “neuromarketing”. Those fields use imaging techniques to look at the ways our brains process the emotions and responses we have to brands and products. The results, as Quartz and Asp posit in the book, reflect primal instincts we have around ideas of status. Their technique gives results that are much more accurate about what the kids are into, these days, than traditional marketing focus groups have ever been able to give us. © 2015 Guardian News and Media Limited
Nala Rogers People who are ill often complain of changes in their sense of taste. Now, researchers report that this sensory shift may be caused by a protein that triggers inflammation. Mice that cannot produce the protein, called tumour necrosis factor-α (TNF-α), are less sensitive to bitter flavours than normal mice, according to a study published on 21 April in Brain, Behavior, and Immunity1. People with infections, autoimmune disease or other inflammatory conditions have higher levels of TNF-α than healthy people, and the protein has been shown to reduce food intake2. To investigate the influence of TNF-α on taste, researchers at the Monell Chemical Senses Center in Philadelphia, Pennsylvania, used engineered mice that could not produce the protein. The researchers offered the engineered mice and normal mice water that contained different types and concentrations of flavours. The mice that could not produce TNF-α had normal reactions to sweet, sour, salty and umami flavours, but were less sensitive to bitter ones. “Normal mice will pick up [that taste] at a much lower concentration. They will know this is bitter; they will not like it,” says Hong Wang, a molecular biologist at Monell and an author of the study. “But if the TNF-α gene is not there, then the mice will only start to avoid the bitter solution at higher concentrations.” © 2015 Nature Publishing Group
Neuroscientists have discovered brain circuitry for encoding positive and negative learned associations in mice. After finding that two circuits showed opposite activity following fear and reward learning, the researchers proved that this divergent activity causes either avoidance or reward-driven behaviors. Funded by the National Institutes of Health, they used cutting-edge optical-genetic tools to pinpoint these mechanisms critical to survival, which are also implicated in mental illness. “This study exemplifies the power of new molecular tools that can push and pull on the same circuit to see what drives behavior,” explained Thomas R. Insel, M.D., director of NIH’s National Institute of Mental Health (NIMH). “Improved understanding of how such emotional memory works holds promise for solving mysteries of brain circuit disorders in which these mechanisms are disrupted.” NIMH grantee Kay Tye, Ph.D. External Web Site Policy, Praneeth Namburi and Anna Beyeler, Ph.D., of the Massachusetts Institute of Technology (MIT), Cambridge, and colleagues, report their findings April 29, 2015 in the journal Nature. Prior to the new study, scientists suspected involvement of the circuits ultimately implicated, but were stumped by a seeming paradox. A crossroads of convergent circuits in an emotion hub deep in the brain, thebasolateral amygdala, seem to be involved in both fear and reward learning, but how one brain region could orchestrate such opposing behaviors – approach and avoidance – remained an enigma. How might signals find the appropriate path to follow at this fork in the road?
by Laura Sanders Here I am, fresh off of my second maternity leave ready to serve up lots of juicy fresh science about babies. And I would love to do that, if only I were sleeping more at night. With her intoxicating baby aroma, squishy face and sweet little coos, our newest little daughter is irresistible by day. Night is another story altogether. And it’s a sad one. Our tale begins and ends with her cries wrenching me from a dead sleep over and over again. Sometimes I lie in bed for a split second, deluding myself into thinking that maybe this time she’ll go back to sleep. That pause is long enough for me to notice all the ways her cries affect me: Pounding heart, sweaty hands and feet, and most importantly, a single-minded, maniacal focus on that sound. Evolution didn’t give babies many ways to communicate, but the method they have, crying, sure gets the job done. So I read with interest an April 23 study in Nature that explains one way in which baby cries sledgehammer a mother’s brain. Upon hearing a lost pup’s cries, mother mice promptly go and fetch the wayward pup by the scruff of its neck. But this behavior has to be learned — a first-time mom isn’t as attuned to the sounds of her pups’ cries. As she gets the hang of that whole mothering thing, the momma mouse’s brain gets better at picking the sound of a distant crying pup out of the background din. These pup cries bore their way into the mother’s brain in an interesting way, the researchers found. © Society for Science & the Public 2000 - 2015.
By Rachel E. Gross “By being a guy’s best first move … Axe is designed to keep guys a step ahead in the dating game,” boasts Unilever, the company that sells Axe products. Of course, if you don’t happen to be a gullible 13-year-old boy, you probably don’t believe that body spray or deodorant is a magic elixir with the power to turn nice girls naughty. But what if it were possible to change a person’s mood with just a scent? The idea may not be that far-fetched, according to a new study in the journal Psychological Science—reporting work that was funded by Unilever. The study found that it might be possible to subconsciously trigger a state of happiness using the scent of—deep breath now—human sweat. People send all kinds of secret messages through their secretions. When smelling chemicals in male sweat, women become more alert, and they can even tell whether that sweat was made by a guy who was particularly turned on. (Cautions the New York Times: “No man should imagine that based on these conclusions he can improve his sex life by refraining from bathing.”) But until now, most sweat studies have focused on sexual arousal or negative emotions like fear. For obvious reasons, these emotions are crucial to survival and evolutionary success. If your friend spots a puma, it may be helpful for you to be able to sniff out instant cues to be on the alert or flee for cover. Being able to transmit positive emotions may also have a profound social impact, says Gün Semin, a psychologist at Utrecht University in the Netherlands and lead researcher on the study. After all, “the pursuit of happiness is not an individual enterprise,” as he and his fellow researchers write rather eloquently in the new study. So Semin’s team decided to test whether people could communicate happiness via sweat.
Children who were often bullied by their peers may experience more anxiety and depression than children who were abused by adults, a finding that U.S. and British researchers say highlights an "imbalance" in school services to tackle bullying. Researchers followed the mental health of more than 4,000 children in Avon, south west England from birth to age 18 and 1,400 others in North Carolina from age nine up to age 26 through parent questionnaires and clinical interviews. In the Avon study, maltreatment was defined as physical, emotional, or sexual abuse or "maladaptive parenting" such as hitting, shouting and hostility. Children were interviewed about the frequency of bullying, which included overt threats, physical violence and nasty names as well as social exclusion or spreading lies or rumours. The results consistently showed an increased risk of anxiety, depression, self-harm and suicidal tendencies in children who were bullied, whether or not they had a history of abuse by adults, Prof. William Copeland, a clinical psychologist at Duke University School of Medicine in Durham, N.C. and his co-authors concluded in Tuesday's issue of Lancet Psychiatry. "What was a surprise was to see [the results] were as significant and pervasive as what we see for children that are physically abused, sexually abused or neglected," Copeland said. Government policies have focused almost exclusively on providing services for child abuse but much less attention and resources are devoted to bullying, the researchers said. Copeland's previous research showed long-term repercussions from bullying persist — and that includes impacts on physical health, dropping out of school and trouble with authorities. ©2015 CBC/Radio-Canada
By Nicholas Bakalar Many people consume sweets in response to stress. Now researchers may have discovered why. Sugar reduces levels of cortisol, the stress hormone. Scientists recruited 19 female volunteers. For 12 days, eight of them consumed beverages sweetened with aspartame, an artificial sweetener. The rest drank an identical beverage containing 25 percent sucrose, or table sugar. Before and after the experiment, researchers measured the volunteers’ saliva cortisol levels and performed functional M.R.I. scans while they took arithmetic tests designed to be just beyond their abilities — a procedure known to increase cortisol levels. The study, in the Journal of Clinical Endocrinology and Metabolism, found no differences in the tests between the two groups before the 12-day diet. But in tests afterward, cortisol levels were lower in the sugar consumers and higher in the aspartame group. The post-diet M.R.I. showed increased activity in the areas of the brain controlling fear and stress in the sugar group. The aspartame group showed decreased activity in those areas. The senior author, Kevin D. Laugero, a nutritionist with the federal Department of Agriculture, said no one should conclude that sugar should be used as a stress reducer. But, he said, “the finding is intriguing because it suggests that there is a metabolic pathway sensitive to sugar outside the brain that may expose new targets for treating neurobehavioral and stress-related conditions.” © 2015 The New York Times Company
Heidi Ledford An experimental antibody drug aimed at protecting nerves from the ravages of multiple sclerosis offers hope for a new way to combat the neurological disease — if researchers can definitively show that it works. The antibody, anti-LINGO-1, is intended to stimulate regrowth of the myelin sheath, the fatty protective covering on nerve cells that is damaged by multiple sclerosis. Its developer, Biogen of Cambridge, Massachusetts, will present results from a small clinical trial at an American Academy of Neurology meeting this week in Washington DC. If the initial promising results from the trial are confirmed, it will be the first such myelin-regeneration therapy. Other researchers are racing to find more targets and compounds that act similarly. “Once we get a positive result, the field will move very quickly,” says Jack Antel, a neurologist at McGill University in Montreal, Canada. But that excitement is tempered by practical hurdles: there is as yet no proven way to measure remyelination of nerve cells in living humans. Myelin sheaths insulate and support axons, the fibres that transmit signals between nerve cells. In multiple sclerosis, immune attack destroys these sheaths. Stripped of this protective coating, the axons gradually wither away, causing the numbness and muscle spasms that are characteristic of the disease. The 12 drugs approved in the United States to treat multiple sclerosis slow this immune attack — although sometimes with dangerous side effects. But none stops it, says Bruce Trapp, a neuroscientist at the Cleveland Clinic in Ohio. © 2015 Nature Publishing Group
By Smitha Mundasad Health reporter, BBC News A mindfulness-based therapy could offer a "new choice for millions of people" with recurrent depression, a Lancet report suggests. Scientists tested it against anti-depressant pills for people at risk of relapse and found it worked just as well. The therapy trains people to focus their minds and understand that negative thoughts may come and go. In England and Wales doctors are already encouraged to offer it. Patients who have had recurrent clinical depression are often prescribed long-term anti-depressant drugs to help prevent further episodes. And experts stress that drug therapy is still essential for many. In this study, UK scientists enrolled 212 people who were at risk of further depression on a course of mindfulness-based cognitive therapy (MBCT) while carefully reducing their medication. Patients took part in group sessions where they learned guided meditation and mindfulness skills. The therapy aimed to help people focus on the present, recognise any early warning signs of depression and respond to them in ways that did not trigger further reoccurrences. Researchers compared these results to 212 people who continued to take a full course of medication over two years. By the end of the study, a similar proportion of people had relapsed in both groups. And many in the MBCT group had been tapered off their medication. Scientists say these findings suggest MBCT could provide a much-needed alternative for people who cannot or do not wish to take long-term drugs. In their report, they conclude it "may be a new choice for millions of people with recurrent depression on repeat prescriptions." © 2015 BBC
Two drugs already on the market — an antifungal and a steroid — may potentially take on new roles as treatments for multiple sclerosis. According to a study published in Nature today, researchers discovered that these drugs may activate stem cells in the brain to stimulate myelin producing cells and repair white matter, which is damaged in multiple sclerosis. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. Specialized cells called oligodendrocytes lay down multiple layers of a fatty white substance known as myelin around axons, the long “wires” that connect brain cells. Myelin acts as an insulator and enables fast communication between brain cells. In multiple sclerosis there is breakdown of myelin and this deterioration leads to muscle weakness, numbness and problems with vision, coordination and balance. “To replace damaged cells, the scientific field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road. We asked if we could find a faster and less invasive approach by using drugs to activate native nervous system stem cells and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself,” said Paul J. Tesar, Ph.D., associate professor at Case Western Reserve School of Medicine in Cleveland, and senior author of the study. It is unknown how myelin-producing cells are damaged, but research suggests they may be targeted by malfunctioning immune cells and that multiple sclerosis may start as an autoimmune disorder. Current therapies for multiple sclerosis include anti-inflammatory drugs, which help prevent the episodic relapses common in multiple sclerosis, but are less effective at preventing long-term disability. Scientists believe that therapies that promote myelin repair might improve neurologic disability in people with multiple sclerosis.
By Sandra G. Boodman A Braced by her partner, Suzanne Tobin shuffled back to her car parked in the cavernous garage at Johns Hopkins Hospital late on the evening of Oct. 22, 2013, distraught about what might happen next. Tobin, then 60, had been driven by her partner, James Rapp, from their Germantown home to the Hopkins ER in hopes that doctors there could determine what was causing her relentless deterioration. Three months earlier, Tobin had held a full-time job as a copy editor at AARP in the District. She spent an hour before work striding around the Mall for exercise. Now she could no longer walk unassisted, her speech was nearly unintelligible and her left hand was so weak she could no longer hold a book. Doctors in suburban Maryland had diagnosed a stroke — or possibly a series of strokes — but were unable to explain why Tobin kept getting worse by the week. Her neurologist counseled patience and offered to prescribe antidepressants, drugs that Tobin had told him she had taken for years. An occupational therapist she’d been seeing had expressed alarm; stroke patients tended to plateau or even improve over time, not to experience a steady downward spiral. “You need to get a new neurologist,” she advised Tobin. Tobin and Rapp decided their best bet was to head to Hopkins in Baltimore. But after 12 hours and a battery of tests, including a CT, MRI and other scans, emergency physicians sent Tobin home. They found no new stroke — an earlier MRI that Rapp had brought along appeared to show an old one — nor any other problem that would require immediate hospitalization. They advised her to follow up with her regular doctors.
By LISA FELDMAN BARRETT and JOLIE WORMWOOD THE Justice Department recently analyzed eight years of shootings by Philadelphia police officers. Its report contained two sobering statistics: Fifteen percent of those shot were unarmed; and in half of these cases, an officer reportedly misidentified a “nonthreatening object (e.g., a cellphone) or movement (e.g., tugging at the waistband)” as a weapon. Many factors presumably contribute to such shootings, ranging from carelessness to unconscious bias to explicit racism, all of which have received considerable attention of late, and deservedly so. But there is a lesser-known psychological phenomenon that might also explain some of these shootings. It’s called “affective realism”: the tendency of your feelings to influence what you see — not what you think you see, but the actual content of your perceptual experience. Affective realism illustrates a common misconception about the working of the human brain. In everyday life, your brain seems to be a reactive organ. You stroll past a round red object in the produce section of a supermarket and react by reaching for an apple. A police officer sees a weapon and reacts by raising his gun. Stimulus is followed by response. But the brain doesn’t really work this way. The brain is a predictive organ. A majority of your brain activity consists of predictions about the world — thousands of them at a time — based on your past experience. These predictions are not deliberate prognostications like “the Red Sox will win the World Series,” but unconscious anticipations of every sight, sound and other sensation you might encounter in every instant. These neural “guesses” largely shape what you see, hear and otherwise perceive. © 2015 The New York Times Company
By VIRGINIA HEFFERNAN Most newly stylish coinages carry with them some evidence of grammatical trauma. Consider “affluencer,” “selfie,” “impactful.” Notes of cynicism and cutesiness come through. But every now and then a bright exception to this dispiriting routine appears. A rookie word makes its big-league debut, a stadium of pedants prepares to peg it with tomatoes and — nothing. A halfhearted heckle. The new word looks only passably pathetic. Maddeningly, it has heft. “Mindfulness” may be that hefty word now, one that can’t readily be dismissed as trivia or propaganda. Yes, it’s current among jaw-grinding Fortune 500 executives who take sleeping pills and have “leadership coaches,” as well as with the moneyed earnest, who shop at Whole Foods, where Mindful magazine is on the newsstand alongside glossies about woodworking and the environment. It looks like nothing more than the noun form of “mindful” — the proper attitude toward the London subway’s gaps — but “mindfulness” has more exotic origins. In the late 19th century, the heyday of both the British Empire and Victorian Orientalism, a British magistrate in Galle, Ceylon (now Sri Lanka), with the formidable name of Thomas William Rhys Davids, found himself charged with adjudicating Buddhist ecclesiastical disputes. He set out to learn Pali, a Middle Indo-Aryan tongue and the liturgical language of Theravada, an early branch of Buddhism. In 1881, he thus pulled out “mindfulness” — a synonym for “attention” from 1530 — as an approximate translation of the Buddhist concept of sati. The translation was indeed rough. Sati, which Buddhists consider the first of seven factors of enlightenment, means, more nearly, “memory of the present,” which didn’t track in tense-preoccupied English. “Mindfulness” stuck — but may have saddled the subtle sati with false-note connotations of Victorian caution, or even obedience. (“Mind your manners!”) © 2015 The New York Times Company
Link ID: 20818 - Posted: 04.20.2015
|By Julie Hecht Unlike porcupines, dogs are a relatively hands-on (actually, paws-on) species, both with one another and with us. YouTube has numerous videos of dogs essentially saying, “Just keep petting me, please. Yes, that’s it…more.” But this relationship is not one-sided. Many studies find that positive interactions between people and dogs can be beneficial for both species. Increases in β-endorphin (beta-endorphin), oxytocin and dopamine—neurochemicals associated with positive feelings and bonding—have been observed in both dogs and people after enjoyable interactions like petting, play and talking. Essentially, interacting with a dog, particularly a known dog, can have some of the same psychophysiological markers as when two emotionally attached people spend time together. But do certain types of interactions have an outsized impact? Dogs are incredibly attentive to human faces and, in some cases, even specific facial expressions. This seemingly routine, benign behavior—your dog turning to gaze on your beautiful face as you do his or hers—could actually hold a very important piece of the puzzle in our relationship with dogs, suggests a study published this week in Science. The new study, by Miho Nagasawa of Azabu University in Japan and colleagues, builds on Nagasawa’s previous work, published in Hormones and Behavior in 2009, that found owners and dogs sharing a long mutual gaze had higher levels of oxytocin in their urine than owners of dogs giving a shorter gaze. (Oxytocin, a humble peptide of nine amino acids that is sometimes called the “cuddle hormone,” has been implicated in social bonding and is instrumental to the cascade of hormonal changes leading up to and following birth.) Nagasawa and her colleagues concluded that their finding was “a manifestation of attachment behavior.” © 2015 Scientific American
Angus Chen A common pain medication might make you go from "so cute!" to "so what?" when you look at a photo of an adorable kitten. And it might make you less sensitive to horrifying things too. It's acetaminophen, the active ingredient in Tylenol. Researchers say the drug might be taking the edge off emotions – not just pain. "It seems to take off the highs of your daily highs and the lows off your daily lows," says Baldwin Way, a psychologist at Ohio State University and the principal investigator on the study, "It kind of flattens out the vicissitudes of your life." The idea that over-the-counter pain pills might affect emotions has been circulating since 2010, when two psychologists, Naomi Eisenberger and Nathan DeWall, led a study showing that acetaminophen seemed to be having both a psychological and a neurological effect on people. They asked volunteers to play a rigged game that simulated social rejection. Not only did the acetaminophen appear to be deflecting social anxieties, it also seemed to be dimming activity in the insula, a region of the brain involved in processing emotional pain. A brain that can let other thoughts bubble up despite being in pain might help its owner benefit from meditation or other cognitive therapies. "But [the insula] is a portion of the brain that seems to be involved in a lot of things," Way says. In older studies, scientists saw that people with damage in their insula didn't react as strongly to either negative or positive images. So Way and one of his students, Geoffrey Durso, figured that if acetaminophen is doing something to the insula, then it might be having a wider effect, too. © 2015 NPR