Chapter 15. Emotions, Aggression, and Stress

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Jef Akst Alan McElligott, an animal behavior researcher at the University of Roehampton in the UK, continues to be impressed by goats. Since he started studying the charismatic ungulates a decade ago, he’s found that mothers remember the calls of their kids several months after they’ve been separated, and that goats can solve a two-step puzzle box akin to those typically used in primate research—and remember how to do it a year later. Now his team has found that goats at the Buttercups Sanctuary in Kent, UK, can distinguish between happy and angry human expressions. “Given some of the other things that we’ve found out about goats, I guess we shouldn’t really be that surprised,” says McElligott, who’s hoping to improve welfare guidelines for the animals by revealing their smart and social nature. McElligott’s experiment was simple. Working with 20 goats at the sanctuary, he and his colleagues presented each with two black-and-white images—one of a person smiling, and the other of the same person making an angry expression—then sat back and watched what the animal did. “If the goats ignored the photographs, for example, or walked up to the photographs and ripped them off metal panels and chewed on them, would I have been shocked? Possibly not,” says McElligott. “But . . . the goats did seem to take the time to have a look at these photographs and actually study them, believe it or not.” And based on the time they spent interacting with each image, the goats seemed to prefer the happy snapshot (R Soc Open Sci, 5:180491, 2018). © 1986 - 2018 The Scientist

Keyword: Emotions; Attention
Link ID: 25777 - Posted: 12.12.2018

By Judi Ketteler A friend of mine who works for a jewelry company that makes necklaces inscribed with empowering sayings recently offered me one. “How about the ‘I am fearless’ one?” she asked. “I don’t think so,” I said. “I’m not fearless.” She laughed. I did too. Except I meant it. And I haven’t been able to stop thinking about it since. I suspect fearlessness is a concept invented by motivational speakers to sell books and command large audiences at events that feature fear-conquering exercises. I wonder, is being fearless even a real thing? “Talking about being fearless covers up where people really are with fear,” says Dr. Kerry Ressler, director of the Neurobiology of Fear Laboratory at McLean Hospital. “After all, fear is the most evolutionarily conserved behavioral reflex for survival.” Fear, he says, produces the same responses in people now as it did at the beginning of human history. We’ve needed fear to survive as a species, to run from the lion crouching in the brush, and we still need it. “The question,” he says, “is how do you not let the emotional response of the fear reflex run wild?” Dr. Ressler says the great majority of people — about 90 percent — are resilient after something frightening or tragic happens, like a car accident or the death of a loved one. They are left with a bad memory or with grief, but they have perspective. Yet about 10 percent of people generalize the fearful memory or the grief. Their brains continually get cues that the bad thing is still happening, and their bodies respond accordingly. “It becomes a black hole of emotion,” Dr. Ressler says. © 2018 The New York Times Company

Keyword: Emotions
Link ID: 25770 - Posted: 12.11.2018

By Benedict Carey In mid-October, researchers in California published a study of Civil War prisoners that came to a remarkable conclusion. Male children of abused war prisoners were about 10 percent more likely to die than their peers were in any given year after middle age, the study reported. The findings, the authors concluded, supported an “epigenetic explanation.” The idea is that trauma can leave a chemical mark on a person’s genes, which then is passed down to subsequent generations. The mark doesn’t directly damage the gene; there’s no mutation. Instead it alters the mechanism by which the gene is converted into functioning proteins, or expressed. The alteration isn’t genetic. It’s epigenetic. The field of epigenetics gained momentum about a decade ago, when scientists reported that children who were exposed in the womb to the Dutch Hunger Winter, a period of famine toward the end of World War II, carried a particular chemical mark, or epigenetic signature, on one of their genes. The researchers later linked that finding to differences in the children’s health later in life, including higher-than-average body mass. The excitement since then has only intensified, generating more studies — of the descendants of Holocaust survivors, of victims of poverty — that hint at the heritability of trauma. If these studies hold up, they would suggest that we genetically inherit some trace of our parents’ and even grandparents’ experience, particularly their suffering, which in turn modifies our own day-to-day health — and perhaps our children’s, too. But behind the scenes, the work has touched off a bitter dispute among researchers that could stunt the enterprise in its infancy. Critics contend that the biology implied by such studies simply is not plausible. Epigenetics researchers counter that their evidence is solid, even if the biology is not worked out. © 2018 The New York Times Company

Keyword: Epigenetics; Stress
Link ID: 25768 - Posted: 12.10.2018

Sara Reardon Infectious-disease researchers hunting for the cause of a mysterious illness that is paralysing children are combining machine learning with a new gene-sequencing technique to pin down the culprit. The disease, called acute flaccid myelitis (AFM), causes limb weakness and paralysis that resembles the symptoms of polio. The US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, has confirmed 134 cases of AFM in the United States so far this year. Many of those who develop the illness never recover. Most of the evidence suggests that an enterovirus called EV-D681 is causing the illness, but researchers haven’t been able to find the pathogen in the spinal fluid of sick children. Scientists are trying to identify the culprit by using a combination of host-response diagnostics — which look at how the immune system responds to pathogens — and machine-learning analysis. The approach could lead to better diagnostics and provide hints about new treatments. Host-response diagnostic tests haven’t been used in the clinic yet. But researchers are developing similar tests to help pinpoint other conditions that can be tricky to diagnose, including tuberculosis and bacterial meningitis. This year’s AFM outbreak started in October, and is the third in a series of outbreaks in the United States that began in 2014. They have occurred every other year since, though researchers have yet to find a definitive explanation for the pattern. It is also taking scientists an unusually long time to determine the cause of the illness, says William Weldon, a microbiologist at the CDC. © 2018 Springer Nature Publishing AG

Keyword: Movement Disorders; Neuroimmunology
Link ID: 25758 - Posted: 12.07.2018

By Jonathan D. Grinstein It is well known that a high salt diet leads to high blood pressure, a risk factor for an array of health problems, including heart disease and stroke. But over the last decade, studies across human populations have reported the association between salt intake and stroke irrespective of high blood pressure and risk of heart disease, suggesting a missing link between salt intake and brain health. Interestingly, there is a growing body of work showing that there is communication between the gut and brain, now commonly dubbed the gut–brain axis. The disruption of the gut–brain axis contributes to a diverse range of diseases, including Parkinson’s disease and irritable bowel syndrome. Consequently, the developing field of gut–brain axis research is rapidly growing and evolving. Five years ago, a couple of studies showed that high salt intake leads to profound immune changes in the gut, resulting in increased vulnerability of the brain to autoimmunity—when the immune system attacks its own healthy cells and tissues by mistake, suggesting that perhaps the gut can communicate with the brain via immune signaling. Now, new research shows another connection: immune signals sent from the gut can compromise the brain’s blood vessels, leading to deteriorated brain heath and cognitive impairment. Surprisingly, the research unveils a previously undescribed gut–brain connection mediated by the immune system and indicates that excessive salt might negatively impact brain health in humans through impairing the brain’s blood vessels regardless of its effect on blood pressure. © 2018 Scientific American

Keyword: Obesity; Neuroimmunology
Link ID: 25754 - Posted: 12.06.2018

By Lisa Sanders, M.D. “Something’s wrong,” the 27-year-old woman said to her new husband. “I think you need to take me to the hospital.” It was the day after their wedding. The woman’s husband and her best friend were car fanatics, and so the newlyweds had wanted to commemorate their union with pictures at a drift track in rural Toutle, Wash. The best friend would “drift cookies,” circling the couple in a tight, controlled skid. As another friend took pictures, the two embraced, wreathed by smoke and dust and barely contained chaos as the red Mustang fishtailed around them. In the photos, the couple look happy. But as they loaded up the car to go home, the young woman started to feel strange. She’d been a little jittery all day. She noticed she couldn’t stop talking. She figured it was just the excitement of the wedding’s aftermath. But suddenly her excitement felt out of control. Her heart, which was racing since she got up that morning, went into overdrive. It pounded so hard that it hurt her throat and chest. She couldn’t think. Her hands took on a life of their own — they opened and closed incessantly. Her new husband was confused and worried. They drove to a hospital a couple of towns over. It was a panic attack, they were told. Since the birth of the couple’s daughter a year before, the young woman had struggled with postpartum depression and anxiety. She’d just married and had these crazy pictures taken; it was no wonder she was panicking. The young woman accepted the diagnosis, but she couldn’t help feeling that this was different from the anxiety she sometimes experienced. She was given a medication to take if she had more symptoms and sent home. The pills didn’t seem to help. The next day she felt her heart pounding in her throat and the same spacy-headed jitters from the day before. She tried the medicine again but after that, her memory is just fragments. © 2018 The New York Times Company

Keyword: Schizophrenia; Neuroimmunology
Link ID: 25719 - Posted: 11.26.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Keyword: Obesity; Neuroimmunology
Link ID: 25710 - Posted: 11.24.2018

Bruce Bower Neandertals are shaking off their reputation as head bangers. Our close evolutionary cousins experienced plenty of head injuries, but no more so than late Stone Age humans did, a study suggests. Rates of fractures and other bone damage in a large sample of Neandertal and ancient Homo sapiens skulls roughly match rates previously reported for human foragers and farmers who have lived within the past 10,000 years, concludes a team led by paleoanthropologist Katerina Harvati of the University of Tübingen in Germany. Males suffered the bulk of harmful head knocks, whether they were Neandertals or ancient humans, the scientists report online November 14 in Nature. “Our results suggest that Neandertal lifestyles were not more dangerous than those of early modern Europeans,” Harvati says. Until recently, researchers depicted Neandertals, who inhabited Europe and Asia between around 400,000 and 40,000 years ago, as especially prone to head injuries. Serious damage to small numbers of Neandertal skulls fueled a view that these hominids led dangerous lives. Proposed causes of Neandertal noggin wounds have included fighting, attacks by cave bears and other carnivores and close-range hunting of large prey animals. Paleoanthropologist Erik Trinkaus of Washington University in St. Louis coauthored an influential 1995 paper arguing that Neandertals incurred an unusually large number of head and upper-body injuries. Trinkaus recanted that conclusion in 2012, though. All sorts of causes, including accidents and fossilization, could have resulted in Neandertal skull damage observed in relatively small fossil samples, he contended (SN: 5/27/17, p. 13). |© Society for Science & the Public 2000 - 2018.

Keyword: Evolution; Aggression
Link ID: 25686 - Posted: 11.15.2018

By Dana G. Smith SAN DIEGO—Robert King spent 29 years living alone in a six by nine-foot prison cell. He was part of the “Angola Three”—a trio of men kept in solitary confinement for decades and named for the Louisiana state penitentiary where they were held. King was released in 2001 after a judge overturned his 1973 conviction for killing a fellow inmate. Since his exoneration he has dedicated his life to raising awareness about the psychological harms of solitary confinement. “People want to know whether or not I have psychological problems, whether or not I’m crazy—‘How did you not go insane?’” King told a packed session at the annual Society for Neuroscience meeting here this week. “I look at them and I tell them, ‘I did not tell you I was not insane.’ I don’t mean I was psychotic or anything like that, but being placed in a six by nine by 12–foot cell for 23 hours a day, no matter how you appear on the outside, you are not sane.” There are an estimated 80,000 people, mostly men, in solitary confinement in U.S. prisons. They are confined to windowless cells roughly the size of a king bed for 23 hours a day, with virtually no human contact except for brief interactions with prison guards. According to scientists speaking at the conference session, this type of social isolation and sensory deprivation can have traumatic effects on the brain, many of which may be irreversible. Neuroscientists, lawyers and activists such as King have teamed up with the goal of abolishing solitary confinement as cruel and unusual punishment. © 2018 Scientific American

Keyword: Stress
Link ID: 25666 - Posted: 11.10.2018

By Kelly Servick SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating. “This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.” The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain. © 2018 American Association for the Advancement of Science

Keyword: Obesity; Neuroimmunology
Link ID: 25664 - Posted: 11.10.2018

Jon Hamilton Scientists may have caught a glimpse of what sadness looks like in the brain. A study of 21 people found that for most, feeling down was associated with greater communication between brain areas involved in emotion and memory, a team from the University of California, San Francisco reported Thursday in the journal Cell. "There was one network that over and over would tell us whether they were feeling happy or sad," says Vikaas Sohal, an associate professor of psychiatry at UCSF. The finding could lead to a better understanding of mood disorders, and perhaps new ways of treating them. Previous research had established that sadness and other emotions involve the amygdala, an almond-shaped mass found in each side of the brain. And there was also evidence that the hippocampus, which is associated with memory, can play a role in emotion. But Sohal and the other researchers were curious about precisely what these and other brain areas are doing when someone's mood shifts. "We really wanted to get at, you know, when you're feeling down or feeling happy, what exactly is happening in the brain at those moments," Sohal says. You can't get that information from brain scans, which don't capture changes that happen in fractions of a second. So the team studied 21 people who were in the hospital awaiting brain surgery for severe epilepsy. © 2018 npr

Keyword: Emotions; Brain imaging
Link ID: 25659 - Posted: 11.09.2018

By Richard A. Friedman Do politicians’ words, the president’s especially, matter? Since he has been in office, President Trump has relentlessly demonized his political opponents as evil and belittled them as stupid. He has called undocumented immigrants animals. His rhetoric has been a powerful contributor to our climate of hate, which is amplified by the right-wing media and virulent online culture. Of course, it’s difficult to prove that incendiary speech is a direct cause of violent acts. But humans are social creatures — including and perhaps especially the unhinged and misfits among us — who are easily influenced by the rage that is everywhere these days. Could that explain why just in the past two weeks we have seen the horrifying slaughter of 11 Jews in a synagogue in Pittsburgh, with the man arrested described as a rabid anti-Semite, as well as what the authorities say was the attempted bombing of prominent Trump critics by an ardent Trump supporter? You don’t need to be a psychiatrist to understand that the kind of hate and fear-mongering that is the stock-in-trade of Mr. Trump and his enablers can goad deranged people to action. But psychology and neuroscience can give us some important insights into the power of powerful people’s words. We know that repeated exposure to hate speech can increase prejudice, as a series of Polish studies confirmed last year. It can also desensitize individuals to verbal aggression, in part because it normalizes what is usually socially condemned behavior. At the same time, politicians like Mr. Trump who stoke anger and fear in their supporters provoke a surge of stress hormones, like cortisol and norepinephrine, and engage the amygdala, the brain center for threat. One study, for example, that focused on “the processing of danger” showed that threatening language can directly activate the amygdala. This makes it hard for people to dial down their emotions and think before they act. © 2018 The New York Times Company

Keyword: Emotions
Link ID: 25654 - Posted: 11.07.2018

Laura Sanders SAN DIEGO — A sleepless night can leave the brain spinning with anxiety the next day. In healthy adults, overnight sleep deprivation triggered anxiety the next morning, along with altered brain activity patterns, scientists reported November 4 at the annual meeting of the Society for Neuroscience. People with anxiety disorders often have trouble sleeping. The new results uncover the reverse effect — that poor sleep can induce anxiety. The study shows that “this is a two-way interaction,” says Clifford Saper, a sleep researcher at Harvard Medical School and Beth Israel Deaconess Medical Center in Boston who wasn’t involved in the study. “The sleep loss makes the anxiety worse, which in turn makes it harder to sleep.” Sleep researchers Eti Ben Simon and Matthew Walker, both of the University of California, Berkeley, studied the anxiety levels of 18 healthy people. Following either a night of sleep or a night of staying awake, these people took anxiety tests next morning. After sleep deprivation, anxiety levels in these healthy people were 30 percent higher than when they had slept. On average, the anxiety scores reached levels seen in people with anxiety disorders, Ben Simon said November 5 in a news briefing. What’s more, sleep-deprived people’s brain activity changed. In response to emotional videos, brain areas involved in emotions were more active, and the prefrontal cortex, an area that can put the brakes on anxiety, was less active, functional MRI scans showed. The results suggest that poor sleep “is more than just a symptom” of anxiety, but in some cases, may be a cause, Ben Simon said. Citations E. Ben Simon and M.P. Walker. Underslept and overanxious: The neural correlates of sleep loss-induced anxiety in the human brain. Society for Neuroscience Annual Meeting, San Diego, November 4, 2018. |© Society for Science & the Public 2000 - 2018

Keyword: Sleep; Emotions
Link ID: 25651 - Posted: 11.07.2018

Laura Sanders SAN DIEGO — Mice yanked out of their community and held in solitary isolation show signs of brain damage. After a month of being alone, the mice had smaller nerve cells in certain parts of the brain. Other brain changes followed, scientists reported at a news briefing November 4 at the annual meeting of the Society for Neuroscience. It’s not known whether similar damage happens in the brains of isolated humans. If so, the result have implications for the health of people who spend much of their time alone, including the estimated tens of thousands of inmates in solitary confinement in the United States and elderly people in institutionalized care facilities. The new results, along with other recent brain studies, clearly show that for social species, isolation is damaging, says neurobiologist Huda Akil of the University of Michigan in Ann Arbor. “There is no question that this is changing the basic architecture of the brain,” Akil says. Neurobiologist Richard Smeyne of Thomas Jefferson University in Philadelphia and his colleagues raised communities of multiple generations of mice in large enclosures packed with toys, mazes and things to climb. When some of the animals reached adulthood, they were taken out and put individually into “a typical shoebox cage,” Smeyne said. This abrupt switch from a complex society to isolation induced changes in the brain, Smeyne and his colleagues later found. The overall size of nerve cells, or neurons, shrunk by about 20 percent after a month of isolation. That shrinkage held roughly steady over three months as mice remained in isolation. |© Society for Science & the Public 2000 - 2018

Keyword: Stress; Learning & Memory
Link ID: 25649 - Posted: 11.06.2018

Serge Rivest The signals transmitted between neurons through synaptic connections are responsible for most, if not all, brain functions, from learning to decision-making. During brain development, synapses that are stimulated less often than others are eliminated through a process called pruning, whereas those that are highly stimulated are retained. This refines the brain’s ability to respond to stimuli and environmental cues. Microglia, the brain’s innate immune cells, have a key role in pruning — they engulf and digest synapses through a process called phagocytosis. But the mechanism that determines which synapses they avoid has been unclear. Writing in Neuron, Lehrman et al.1 describe a ‘don’t eat me’ signal, involving a protein called cluster of differentiation 47 (CD47), that prevents inappropriate synaptic pruning by microglia. About a decade ago, it was shown that synapses requiring elimination send an ‘eat me’ signal to microglia2 (Fig. 1a). This signal involves the proteins C1q and CR3, which are part of the complement cascade — a complex series of interactions that is best known for activating cells of the innate immune system to eliminate disease-causing organisms and damaged cells. ‘Don’t eat me’ signals act to limit the effects of ‘eat me’ signals in the immune system, but it was not known whether the same process occurs during synaptic pruning in the developing brain. CD47 is a cell-surface protein that has many immune functions, including acting as a ‘don’t eat me’ signal for macrophages3, microglia’s sister cells, which exist outside the brain. Lehrman et al. analysed whether CD47 is expressed in the dorsal lateral geniculate nucleus (dLGN), a region of the brain involved in vision. This region receives inputs from neurons called retinal ganglion cells (RGCs) that originate in the retina. The authors demonstrated in mice that, at five days after birth, synapses from RGCs to other neurons in the dLGN are being pruned at high levels. © 2018 Springer Nature Limited

Keyword: Development of the Brain; Neuroimmunology
Link ID: 25629 - Posted: 10.31.2018

By Karen Weintraub The stresses of everyday life may start taking a toll on the brain in relatively early middle age, new research shows. The study of more than 2,000 people, most of them in their 40s, found those with the highest levels of the stress-related hormone cortisol performed worse on tests of memory, organization, visual perception and attention. Higher cortisol levels, measured in subjects’ blood, were also found to be associated with physical changes in the brain that are often seen as precursors to Alzheimer’s disease and other forms of dementia, according to the study published Wednesday in Neurology. The link between high cortisol levels and low performance was particularly strong for women, the study found. But it remains unclear whether women in midlife are under more stress than men or simply more likely to have their stress manifested in higher cortisol levels, says lead researcher Sudha Seshadri. A professor of neurology, she splits her time between Boston University and The University of Texas Health Science Center at San Antonio, where she is the founding director of the Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases. Working on the study “made me more stressed about not being less stressed,” Seshadri says, laughing. But, she adds, the bottom line is serious: “An important message to myself and others is that when challenges come our way, getting frustrated is very counterproductive—not just to achieving our aims but perhaps to our capacity to be productive.” © 2018 Scientific American

Keyword: Stress; Learning & Memory
Link ID: 25620 - Posted: 10.26.2018

By Nicholas Bakalar People with high blood levels of cortisol, the “stress hormone,” may have poorer memory and thinking skills than those with lower levels. Cortisol is produced by the adrenal glands and is involved in regulating blood sugar levels, reducing inflammation, controlling salt and water balance and other body functions. Researchers gave tests for memory, abstract reasoning, visual perception and attention to 2,231 people, average age 49 and free of dementia. They recorded blood levels of cortisol and did M.R.I. examinations to assess brain volume. The study, in Neurology, controlled for age, sex, education, body mass index, blood pressure and many other variables, and found that compared with people with average levels of cortisol, those with the highest levels had lower scores on the cognitive tests. In women, but not in men, higher cortisol was also associated with reduced brain volume. There was no association of the lowest cortisol levels with either cognitive test scores or brain size. The lead author, Dr. Justin B. Echouffo-Tcheugui, an assistant professor of medicine at Johns Hopkins, said that the study suggests that even in people without symptoms, higher cortisol levels can be significant. Still, he said, “This is an initial study. The next step is a prospective study before we jump to the conclusion that this is really important. It’s premature now to consider intervention.” © 2018 The New York Times Company

Keyword: Stress; Learning & Memory
Link ID: 25616 - Posted: 10.26.2018

By Concepción de León I hear some people have trouble with therapy, that it can take years for them to open up to their doctors, let alone cry or break down. Not me. Day one, I told my therapist, Amy Bernstein, “I’ll just tell you everything, and we’ll go from there.” I was assigned to her after revealing, during an initial interview to determine the appropriate therapist for my needs, that I’d been touched as a child. I hadn’t planned to bring it up at all, but I was asked directly, so I said, yes, you could say that. (At the time, I avoided the word “molested.”) And yes, it still crossed my mind. To be honest, what happened had always felt like such a small thing. Many others have had it much worse; I counted myself lucky for only having been touched in subtle ways — a male relative digging his hands in my tiny skirt pockets to “feel around for change”; another bringing his hand to my crotch when he thought I was asleep. These were two of a handful of men who violated me. Amy recommended books to help me understand what had happened, but I put them down after just a few pages, thinking, “This isn’t for me! My thing is too small.” But then, as tends to be the case with therapy, things got harder before they got better. I returned to one of the books Amy had recommended, “The Body Keeps the Score: Brain, Mind and Body in the Healing of Trauma,” by Bessel van der Kolk, to try to understand my visceral response to remembering. Dr. van der Kolk is a Boston-based psychiatrist who specializes in post-traumatic stress disorder and has worked with a broad range of clients, from veterans to sexual assault survivors. “The Body Keeps the Score” hinges on his idea that trauma is stored in the body and that, for therapy to be effective, it needs to take the physiological changes that occur into account. Trauma produces “a re-calibration of the brain’s alarm system, an increase in stress hormone activity” and, also, “compromises the brain area that communicates the physical, embodied feeling of being alive,” Mr. van der Kolk writes. For survivors of sexual assault and other traumas, the amygdala, which initiates the body’s fight or flight response system whenever it perceives danger, can remain activated long after the threat has subsided. In the present, survivors relive their traumas in the form of fragmented images, sounds and emotion that the brain can’t register as belonging to the past. Many people also experience dissociation, which can manifest as literal desensitization in parts of the body or the inability to describe physical sensations. © 2018 The New York Times Company

Keyword: Stress
Link ID: 25590 - Posted: 10.18.2018

By Wajahat Ali Ever since I was young, my mind has gotten stuck. I’ll be flooded with intrusive thoughts. An image or an idea will transform into a burning question — “What if I left the stove on?” “What if the door is unlocked?” “What if I lose control and do something violent?” This plays on an endless loop. To cope, I constantly seek reassurance by reviewing my actions, trying to replace my thoughts or using logic to undo what is utterly illogical. But all those efforts fail, instead energizing the thought, resurrecting it like a zombie on steroids, making it more vicious, resistant and cruel. That’s a snapshot of living life with obsessive-compulsive disorder, an anxiety disorder that afflicts nearly 2 percent of the population. With O.C.D., the brain misfires, causing it to malfunction and react to disturbing thoughts, images and ruminations. The sufferer tries to manage his anxiety with compulsive rituals, which include excessive double-checking, counting, repeating a prayer or mantra, and engaging in mental reassurances that give a short-term relief but ultimately become addictive crutches, fueling an endless cycle of torment. O.C.D. has often been misunderstood, undiagnosed and exploited as a set of amusing quirks for Hollywood characters. I wish my O.C.D. was as fun and lovable as depicted in “Monk.” It’s not. At one point in my life, I endured an endless stream of tormenting thoughts about sex, overwhelmed by visions of every vile variation, partnership and arrangement imaginable. They would make Caligula blush. When this happened, feelings of guilt, disgust and shame would inevitably begin to overwhelm me. Self-doubt bubbled up and asked: “What sick person could imagine such things? Surely, there must be something wrong with you?” Here I am, a somewhat intelligent, moral, responsible individual fully aware that the thoughts are irrational, but nonetheless I must perform ridiculous rituals to try to feel safe and achieve relief. I think of it as God’s sick joke. © 2018 The New York Times Company

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 25573 - Posted: 10.15.2018

By Daniel Barron Lisa Barlow, whose name I have changed to protect her privacy, is at her kitchen table in Washington DC when she realizes that each Sunday, fifteen passenger trains depart for New Haven, CT. She’s a successful copy editor and has a meeting in New Haven early Monday morning. She has no plans Sunday, so doesn’t care when she arrives or how long it takes. She travels coach so has thirty tickets to choose from: fifteen departures each with two price options. Should she choose the more-expensive flexible ticket over the locked-in value ticket? Does she want to leave earlier or later? Brunch in DC or lunch in New Haven? She can’t decide. She scrolls the screen up and down, up and down, faster and faster. Her eyes dart about the webpage. She feels a rising tension in her chest. Her breathing shortens. Her thoughts race in and out of her mind like the breath in her lungs. She touches her face and notices the telltale sign: it’s numb. She reaches into her pocket, where she safeguards a small pill for moments like these. A pharmacologic reset button. Barlow has had panic attacks since High School—the first over a social drama, the second after her science teacher told her that if she refused to dissect a pig, she’d amount to nothing. She suspects her attacks have something to do with her parents, whose difficult marriage often forced her to choose between them. This, a therapist explained, was an “impossible choice,” one with permanent consequences yet no clear answer. Now as an adult, when faced with a decision that has no clear answer—even something as simple as booking a train ticket—her brain is programmed to panic. © 2018 Scientific American

Keyword: Emotions; Learning & Memory
Link ID: 25569 - Posted: 10.12.2018