Chapter 16. None

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By LISA SANDERS, M.D. On Thursday, we challenged Well readers to take on the complicated case of a 50-year-old woman who felt feverish and couldn’t stop vomiting and who ended up losing a lot of weight. Like the doctors who saw her as she searched for a diagnosis, many of you focused on her recent journey to Kenya as the source of her symptoms. It was a completely reasonable approach, and one that was extensively explored by the doctors who cared for her. But ultimately it was incorrect. This was a really tough case. Indeed, only three of you got it right. The correct diagnosis was: Hyperthyroidism Thyroid hormone controls metabolism. The more of this hormone flowing in the body, the harder the body works. Because this hormone plays such an important role in how we function, the body tightly regulates how much of it is released and when. But just like every other system in the body, that regulatory mechanism can mess up, releasing either too little hormone (hypothyroidism) or, as in this case, too much. The usual symptoms of hyperthyroidism are pretty apparent: The heart races; patients are sweaty, shaky, itchy and sometimes feverish. The appetite increases, but because the entire body is revved up, there is often weight loss. Bowel movements become more frequent and sleep harder to come by. Frequent and uncontrolled vomiting is less common but has been reported. This patient had all of these symptoms. The most common cause of hyperthyroidism is an autoimmune disorder known as Graves’ disease, named after Dr. Robert Graves, a 19th-century Irish physician who wrote about the phenomenon of rapid and violent palpitations associated with an enlarged thyroid gland. In the 20th century it was discovered that the symptoms result when antibodies, the foot soldiers of the immune system, cause excess stimulation of the thyroid gland, resulting in the uncontrolled production and release of thyroid hormone. © 2016 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 22624 - Posted: 09.03.2016

By JOHN P. GLUCK Albuquerque, N.M. — Five years ago, the National Institutes of Health all but ended biomedical and behavioral research on chimpanzees, concluding that, as the closest human relative, they deserved “special consideration and respect.” But chimpanzees were far from the only nonhuman primates used in research then, or now. About 70,000 other primates are still living their lives as research subjects in labs across the United States. On Wednesday, the N.I.H. will hold a workshop on “continued responsible research” with these animals. This sounds like a positive development. But as someone who spent decades working almost daily with macaque monkeys in primate research laboratories, I know firsthand that “responsible” research is not enough. What we really need to examine is the very moral ground of animal research itself. Like many researchers, I once believed that intermittent scientific gains justified methods that almost always did harm. As a graduate student in the late 1960s, I came to see that my natural recoil from intentionally harming animals was a hindrance to how I understood scientific progress. I told myself that we were being responsible by providing good nutrition, safe cages, skilled and caring caretakers and veterinarians for the animals — and, crucially, that what we stood to learn outweighed any momentary or prolonged anguish these animals might experience. The potential for a medical breakthrough, the excitement of research and discovering whether my hypotheses were correct — and let’s not leave out smoldering ambition — made my transition to a more “rigorous” stance easier than I could have imagined. One of my areas of study focused on the effects of early social deprivation on the intellectual abilities of rhesus monkeys. We kept young, intelligent monkeys separated from their families and others of their kind for many months in soundproof cages that remained lit 24 hours a day, then measured how their potential for complex social and intellectual lives unraveled. All the while, I comforted myself with the idea that these monkeys were my research partners, and that by creating developmental disorders in monkeys born in a lab, we could better understand these disorders in humans. © 2016 The New York Times Company

Keyword: Animal Migration
Link ID: 22622 - Posted: 09.03.2016

Laura Sanders An experimental drug swept sticky plaques from the brains of a small number of people with Alzheimer’s disease over the course of a year. And preliminary results hint that this cleanup may have staved off mental decline. News about the new drug, an antibody called aducanumab, led to excitement as it trickled out of recent scientific meetings. A paper published online August 31 in Nature offers a more comprehensive look at the drug’s effects. “Overall, this is the best news that we’ve had in my 25 years doing Alzheimer’s clinical research,” study coauthor Stephen Salloway of Brown University said August 30 at a news briefing. “It brings new hope for patients and families most affected by the disease.” The results are the most convincing evidence yet that an antibody can reduce amyloid in the brain, says Alzheimer’s researcherRachelle Doody of Baylor College of Medicine in Houston, who was not involved in the study. Still, experts caution that the results come from 165 people, a relatively small number. The seemingly beneficial effects could disappear in larger clinical trials, which are under way. “These new data are tantalizing, but they are not yet definitive,” says neuroscientist John Hardy of University College London. Like some other drug candidates for Alzheimer’s, aducanumab is an antibody that targets amyloid-beta, a sticky protein that accumulates in the brains of people with the disease. Delivered by intravenous injection, aducanumab appeared to get inside the brains of people with mild Alzheimer’s (average age about 73) and destroy A-beta plaques, the results suggest. After a year of exposure to the drug, A-beta levels had dropped. This reduction depended on the dose — the more drug, the bigger the decline in A-beta. In fact, people on the highest dose of the drug had almost no A-beta plaques in their brains after a year. |© Society for Science & the Public 2000 - 2016.

Keyword: Alzheimers
Link ID: 22621 - Posted: 09.01.2016

By CATHERINE SAINT LOUIS In seven countries that recently experienced Zika outbreaks, there were also sharp increases in the numbers of people suffering from a form of temporary paralysis, researchers reported Wednesday. The analysis, published online in The New England Journal of Medicine, adds to substantial evidence that Zika infections — even asymptomatic ones — may bring on a paralysis called Guillain-Barré syndrome. The syndrome can be caused by a number of other factors, including infection with other viruses. Researchers studying the Zika epidemic in French Polynesia had estimated that roughly 1 in 4,000 people infected with the virus could develop the syndrome. The Centers for Disease Control and Prevention has said that the Zika virus is “strongly associated” with Guillain-Barré, but has stopped short of declaring it a cause of the condition. The new data suggest a telling pattern: Each country in the study saw unusual increases in Guillain-Barré that coincided with peaks in Zika infections, the researchers concluded. “It’s pretty obvious that in all seven sites there is a clear relationship,” said Dr. Marcos A. Espinal, the study’s lead author and the director of communicable diseases at the Pan American Health Organization, which collected data on confirmed and suspected cases of Zika infection and on the incidence of Guillain-Barré. “Something is going on.” In Venezuela, officials expected roughly 70 cases of Guillain-Barré from December 2015 to the end of March 2016, as mosquitoes were spreading the virus. Instead, there were 684 cases. Similarly, during five months in which the Zika virus was circulating in Colombia, officials recorded 320 cases of Guillain-Barré when there should have been about 100. From September 2015 to March 2016, while Zika infections peaked in El Salvador, cases of Guillain-Barré doubled to 184 from 92. © 2016 The New York Times Company

Keyword: Movement Disorders
Link ID: 22618 - Posted: 09.01.2016

By JAMES GORMAN Who’s a good dog? Well, that depends on whom you’re asking, of course. But new research suggests that the next time you look at your pup, whether Maltese or mastiff, you might want to choose your words carefully. “Both what we say and how we say it matters to dogs,” said Attila Andics, a research fellow at Eotvos Lorand University in Budapest. Dr. Andics, who studies language and behavior in dogs and humans, along with Adam Miklosi and several other colleagues, reported in a paper to be published in this week’s issue of the journal Science that different parts of dogs’ brains respond to the meaning of a word, and to how the word is said, much as human brains do. Photo A dog waiting for its brain activity to be measured in a magnetic resonance imaging machine for research reported in the journal Science. Credit Enik Kubinyi As with people’s brains, parts of dogs’ left hemisphere react to meaning and parts of the right hemisphere to intonation — the emotional content of a sound. And, perhaps most interesting to dog owners, only a word of praise said in a positive tone really made the reward system of a dog’s brain light up. The experiment itself was something of an achievement. Dr. Andics and his colleagues trained dogs to enter a magnetic resonance imaging machine and lie in a harness while the machine recorded their brain activity. A trainer spoke words in Hungarian — common words of praise used by dog owners like “good boy,” “super” and “well done.” The trainer also tried neutral words like “however” and “nevertheless.” Both the praise words and neutral words were offered in positive and neutral tones. The positive words spoken in a positive tone prompted strong activity in the brain’s reward centers. All the other conditions resulted in significantly less action, and all at the same level. © 2016 The New York Times Company

Keyword: Language; Evolution
Link ID: 22617 - Posted: 08.31.2016

Laurel Hamers The brains of human ancestors didn’t just grow bigger over evolutionary time. They also amped up their metabolism, demanding more energy for a given volume, a new study suggests. Those increased energy demands might reflect changes in brain structure and organization as cognitive abilities increased, says physiologist Roger Seymour of the University of Adelaide in Australia, a coauthor of the report, published online August 31 in Royal Society Open Science. Blood vessels passing through bones leave behind holes in skulls; bigger holes correspond to bigger blood vessels. And since larger vessels carry more blood, scientists can use hole size to estimate blood flow in extinct hominids’ brains. Blood flow in turn indicates how much energy the brain consumed. (In modern humans, the brain eats up 20 to 25 percent of the energy the body generates when at rest.) Seymour and colleagues focused on the carotid arteries, the vessels that deliver the bulk of the brain’s blood. The team looked at nearly three dozen skulls from 12 hominid species from the last 3 million years, including Australopithecus africanus, Homo neanderthalensis and Homo erectus. In each, the researchers compared the brain’s overall volume with the diameter of the carotid artery’s tiny entrance hole at the base of the skull. “We expected to find that the rate of blood flow was proportional to the brain size,” Seymour says. “But we found that wasn’t the case.” Instead, bigger brains required more blood flow per unit volume than smaller brains. |© Society for Science & the Public 2000 - 2016.

Keyword: Evolution
Link ID: 22616 - Posted: 08.31.2016

By Alison F. Takemura | In mice, severely restricting caloric intake promotes the transformation of white fat into brown fat, which contains cells that burn energy faster, according to a study published today (August 25) in Cell Metabolism. The innate immune system, researchers from the University of Geneva, Switzerland, and their colleagues reported, mediates this fat cell-transforming effect. “The paper nicely characterizes this phenomenon,” said Ajay Chawla of the University of California, San Francisco, who was not involved in the work. “And it mechanistically seems to identify a pathway that we had identified.” Whereas the present study found diet induced a “beiging” phenotype—in which white adipose tissue starts to express more energy-expending brown fat cells—Chawla and colleagues had previously shown that cold temperatures, another extreme condition, can produce the same effect. Scientists are keenly interested in learning how to generate brown fat cells. A treatment could help stem the obesity epidemic. “Finding some mechanism to activate this response—ideally, in obese or diabetic individuals—is really attractive,” said postdoctoral researcher Salvatore Fabbiano of the University of Geneva who led the present study. Several conditions are already known to make white fat tissue more brown—cold temperatures, microbe loss, and gastric bypass surgery among them. Fabbiano and colleagues hypothesized that the common feature of all these experiences was an increased expenditure of calories compared to intake. © 1986-2016 The Scientist

Keyword: Obesity
Link ID: 22615 - Posted: 08.31.2016

By RACHEL RABKIN PEACHMAN New research shows that athletes who leave the game immediately after a concussion recover twice as fast as athletes who keep playing. Credit Fabrizio Costantini for The New York Times High school athletes who kept playing in the minutes after a concussion took nearly twice as long to recover as those who left the game immediately after the head trauma, a new study shows. The finding, published in the journal Pediatrics, is believed to be the first to focus on one of the most difficult social challenges of treating concussions: a pervasive sports culture that encourages young athletes to keep playing through pain. Medical guidelines call for benching the athlete immediately after the head injury to prevent long-term complications and the potentially devastating consequences of a second hit. “Kids are often reluctant to acknowledge a concussion,” said Dawon Dicks, a youth football coach with CoachUp in Andover, Mass. “The kid may want a scholarship and want to go to college, or it could be that ‘Dad or Coach wants me to play.’ That’s when they’re going to start to be a little dishonest in what they’re truly feeling.” The latest study tracked the neurological symptoms of 69 athletes who visited the University of Pittsburgh Medical Center Sports Medicine Concussion Program after suffering head trauma during a contact sport. The athletes, who ranged from 12 to 19 years old, came from football, soccer, ice hockey, volleyball, field hockey, basketball, wrestling and rugby. The sample included 35 athletes who were removed from games right after getting a concussion and compared their symptoms and recovery to 34 athletes who kept playing in the game or match after taking a hit. The study found that players who stayed in the game after head trauma took an average of 44 days to recover. By comparison, athletes who left a game immediately after signs of concussion took only an average of 22 days to recover. © 2016 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 22614 - Posted: 08.30.2016

By Will Boggs MD NEW YORK (Reuters Health) - Most adults in the U.S. who screen positive for depression are not being treated for depression, according to results from Medical Expenditure Panel Surveys (MEPS). "With the recent increase in prescribing of antidepressant medications, many physicians might assume that undertreatment of depression is no longer a widespread problem," Dr. Mark Olfson from College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute in New York City told Reuters Health by email. "This study makes clear, however, that most American adults who screen positive for depression receive no treatment for their symptoms." Surveys from the early 2000s show that about half of U.S. adults with a lifetime medical history of major depressive disorder had never received treatment for depression. Still, little is known about the extent to which adults with depression in the U.S. receive depression care and the extent to which such patients are matched based on their illness severity to appropriate treatments and healthcare professionals. Dr. Olfson and colleagues used data from the 2012 and 2013 MEPS to examine the prevalence and treatment of adults with screen-positive depression (a Patient Health Questionnaire-2 score of 3 or less). They also assessed whether serious psychological distress was associated with more intensive treatment. © 2016 Scientific American

Keyword: Depression
Link ID: 22613 - Posted: 08.30.2016

Laura Sanders Despite its name, the newly identified GluMI cell (pronounced “gloomy”) is no downer. It’s a nerve cell, spied in a mouse retina, that looks like one type of cell but behaves like another. Like neighboring retina nerve cells that subdue, or deaden, activity of other nerve cells, GluMI cells have a single arm extending from their body. But unlike those cells, GluMI cells actually seem to ramp up activity of nearby cells in a way that could aid vision. GLuMIs don’t seem to detect light firsthand, but they respond to it, Luca Della Santina of the University of Washington in Seattle and colleagues found. GluMIs are among a growing list of unexpected and mysterious cells found in the retinas of vertebrates, the researchers write August 8 in Current Biology. Citations L. Della Santina et al. Glutamatergic monopolar interneurons provide a novel pathway of excitation in the mouse retina. Current Biology. Vol. 26, August 8, 2016. doi:10.1016/j.cub.2016.06.016. |© Society for Science & the Public 2000 - 2016

Keyword: Vision
Link ID: 22610 - Posted: 08.30.2016

By Daniel Engber In the spring of 2013, a 63-year-old social psychologist in Wurzburg, Germany, made a bold suggestion in a private email chain. For months, several dozen of his colleagues had been squabbling over how to double-check the scientific literature on “social priming,” the idea that even very subtle cues—the height of a chair, the temperature of a cup of coffee, the color of a printed word—can influence someone’s behavior or judgment. Now the skeptics in the group wanted volunteers: Who among the priming experts and believers would help them with a large-scale replication effort, in which a major finding would be tested in many different labs at once? Who—if anyone—would agree to put his research to this daunting test? The experts were reluctant to step forward. In recent months their field had fallen into scandal and uncertainty: An influential scholar had been outed as a fraud; certain bedrock studies—even so-called “instant classics”—had seemed to shrivel under scrutiny. But the rigidity of the replication process felt a bit like bullying. After all, their work on social priming was delicate by definition: It relied on lab manipulations that had been precisely calibrated to elicit tiny changes in behavior. Even slight adjustments to their setups, or small mistakes made by those with less experience, could set the data all askew. So let’s say another lab—or several other labs—tried and failed to copy their experiments. What would that really prove? Would it lead anyone to change their minds about the science?

Keyword: Emotions
Link ID: 22609 - Posted: 08.29.2016

Doctors describe 16-year-old Sebastian DeLeon as a walking miracle — he is only the fourth person in the U.S. to survive an infection from the so-called brain-eating amoeba. Infection from Naegleria fowleri is extremely rare but almost always fatal. Between 1962 and 2015, there were only 138 known infections due to the organism, according to the Centers for Disease Control and Prevention. Just three people survived. This summer, two young people, one in Florida and one in North Carolina, became infected after water recreation. Only one had a happy ending. DeLeon is a 16-year-old camp counselor. The Florida Department of Health thinks he got the infection while swimming in unsanitary water on private property in South Florida before his family came to visit Orlando's theme parks. So many things had to go right for DeLeon to survive. On a Friday, he had a bad headache. The next day, his parents decided this was way more than just a migraine and took him to the emergency room at Florida Hospital for Children. Doctors persuaded the family to do a spinal tap to rule out meningitis, even though he didn't have a stiff neck, the telltale symptom. Sheila Black, the lab coordinator, looked at the sample and assumed she saw white blood cells. But then she took a second, longer look. "We are all detectives," Black said. "We literally had to look at this and study it for a while and watch for the movement because the amoeba can look like a white cell. So unless you're actually visually looking for this and looking for the movement, you're going to miss it." © 2016 npr

Keyword: Miscellaneous
Link ID: 22608 - Posted: 08.29.2016

By KATE MURPHY We’ve all seen them, those colorful images that show how our brains “light up” when we’re in love, playing a video game, craving chocolate, etc. Created using functional magnetic resonance imaging, or fM.R.I., these pictures are the basis of tens of thousands of scientific papers, the backdrop to TED talks and supporting evidence in best-selling books that tell us how to maintain healthy relationships, make decisions, market products and lose weight. But a study published last month in the Proceedings of the National Academy of Sciences uncovered flaws in the software researchers rely on to analyze fM.R.I. data. The glitch can cause false positives — suggesting brain activity where there is none — up to 70 percent of the time. This cued a chorus of “I told you so!” from critics who have long said fM.R.I. is nothing more than high-tech phrenology. Brain-imaging researchers protested that the software problems were not as bad nor as widespread as the study suggested. The dust-up has caused considerable angst in the fM.R.I. community, about not only the reliability of their pretty pictures but also how limited funding and the pressure to publish splashy results might have allowed such a mistake to go unnoticed for so long. The remedial measures some in the field are now proposing could be a model for the wider scientific community, which, despite breathtaking technological advances, often produces findings that don’t hold up over time. “We have entered an era where the kinds of data and the analyses that people run have gotten incredibly complicated,” said Martin Sereno, the chairman of the cognitive neuroimaging department at the University of California, San Diego. “So you have researchers using sophisticated software programs that they probably don’t understand but are generally accepted and everyone uses.” © 2016 The New York Times Company

Keyword: Brain imaging
Link ID: 22607 - Posted: 08.29.2016

By Usha Lee McFarling @ushamcfarling LOS ANGELES — A team of physicians and neuroscientists on Wednesday reported the successful use of ultrasound waves to “jump start” the brain of a 25-year-old man recovering from coma — and plan to launch a much broader test of the technique, in hopes of finding a way to help at least some of the tens of thousands of patients in vegetative states. The team, based at the University of California, Los Angeles, cautions that the evidence so far is thin: They have no way to know for sure whether the ultrasound stimulation made the difference for their young patient, or whether he spontaneously recovered by coincidence shortly after the therapy. But the region of the brain they targeted with the ultrasound — the thalamus — has previously been shown to be important in restoring consciousness. In 2007, a 38-year-old man who had been minimally conscious for six years regained some functions after electrodes were implanted in his brain to stimulate the thalamus. The ultrasound technique is a “good idea” that merits further study, said Dr. Nicholas Schiff, a pioneer in the field of using brain stimulation to restore consciousness who conducted the 2007 study. “It’s intriguing and it’s an interesting possibility,” said Schiff, a neuroscientist at Weill Cornell Medicine. The UCLA procedure used an experimental device, about the size of a teacup saucer, to focus ultrasonic waves on the thalamus, two walnut-sized bulbs in the center of the brain that serve as a critical hub for information flow and help regulate consciousness and sleep.

Keyword: Consciousness
Link ID: 22606 - Posted: 08.27.2016

By Amy Ellis Nutt Before iPhones and thumb drives, before Google docs and gigabytes of RAM, memory was more art than artifact. It wasn’t a tool or a byproduct of being human. It was essential to our character and therefore a powerful theme in both myth and literature. At the end of Book 2 of the “Divine Comedy,” with Paradise nearly in reach, Dante is dipped into the River Lethe, where the sins of the self are washed away in the waters of forgetfulness. To be truly cleansed of his memories, however, Dante must also drink from the river of oblivion. Only then will he be truly purified and the memories of his good deeds restored to him. Before we can truly remember, according to Dante, we must forget. In “Patient H.M.: A Story of Memory, Madness, and Family Secrets,” author Luke Dittrich seems to be saying that before we can forgive, we must remember. The terrible irony is that H.M., the real-life character around whom Dittrich’s book revolves, had no memory at all. In prose both elegant and intimate, and often thrilling, “Patient H.M.” is an important book about the wages not of sin but of science. It is deeply reported and surprisingly emotional, at times poignant, at others shocking. H.M., arguably the single most important research subject in the history of neuroscience, was once Henry Molaison, an ordinary New England boy. When Henry was 9 years old, he was hit by a bicyclist as he walked across the street in his home town, Hartford, Conn. © 1996-2016 The Washington Post

Keyword: Learning & Memory
Link ID: 22604 - Posted: 08.27.2016

By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.

Keyword: Movement Disorders
Link ID: 22603 - Posted: 08.25.2016

By Sara Chodosh When a single neuron fires, it is an isolated chemical blip. When many fire together, they form a thought. How the brain bridges the gap between these two tiers of neural activity remains a great mystery, but a new kind of technology is edging us closer to solving it. The glowing splash of cyan in the photo above comes from a type of biosensor that can detect the release of very small amounts of neurotransmitters, the signaling molecules that brain cells use to communicate. These sensors, called CNiFERs (pronounced “sniffers”), for cell-based neurotransmitter fluorescent engineered reporters, are enabling scientists to examine the brain in action and up close. This newfound ability, developed as part of the White House BRAIN Initiative, could further our understanding of how brain function arises from the complex interplay of individual neurons, including how complex behaviors like addiction develop. Neuroscientist Paul Slesinger at Icahn School of Medicine at Mount Sinai, one of the senior researchers who spearheaded this research, presented the sensors Monday at the American Chemical Society’s 252nd National Meeting & Exposition. Current technologies have proved either too broad or too specific to track how tiny amounts of neurotransmitters in and around many cells might contribute to the transmission of a thought. Scientists have used functional magnetic resonance imaging to look at blood flow as a surrogate for brain activity over fairly long periods of time or have employed tracers to follow the release of a particular neurotransmitter from a small set of neurons for a few seconds. But CNiFERs make for a happy medium; they allow researchers to monitor multiple neurotransmitters in many cells over significant periods of time. © 2016 Scientific American

Keyword: Brain imaging
Link ID: 22600 - Posted: 08.25.2016

James Hamblin Like ​The Atlantic? Subscribe to ​the Daily​, our free weekday email newsletter. Elite tennis players have an uncanny ability to clear their heads after making errors. They constantly move on and start fresh for the next point. They can’t afford to dwell on mistakes. Peter Strick is not a professional tennis player. He’s a distinguished professor and chair of the department of neurobiology at the University of Pittsburgh Brain Institute. He’s the sort of person to dwell on mistakes, however small. “My kids would tell me, dad, you ought to take up pilates. Do some yoga,” he said. “But I’d say, as far as I’m concerned, there's no scientific evidence that this is going to help me.” Still, the meticulous skeptic espoused more of a tennis approach to dealing with stressful situations: Just teach yourself to move on. Of course there is evidence that ties practicing yoga to good health, but not the sort that convinced Strick. Studies show correlations between the two, but he needed a physiological mechanism to explain the relationship. Vague conjecture that yoga “decreases stress” wasn’t sufficient. How? Simply by distracting the mind? The stress response in humans is facilitated by the adrenal glands, which sit on top of our kidneys and spit adrenaline into our blood whenever we’re in need of fight or flight. That stress response is crucial in dire circumstances. But little of modern life truly requires it (especially among academic scientists). Most of the time, our stress responses are operating as a sort of background hum, keeping us on edge. Turn that off, and we relax. © 2016 by The Atlantic Monthly Group

Keyword: Stress
Link ID: 22599 - Posted: 08.25.2016

By Alice Callahan As new parents, Penn State researcher Doug Teti and his wife were co-sleepers, sharing their bed at night with all three of their children, now grown. So when Dr. Teti, a professor of human development and family studies, embarked on an usual study of co-sleeping, bringing cameras into the bedrooms of 139 Pennsylvania couples, he did not expect to see co-sleeping associated with family stress. But to his surprise, many of the parents in the study who co-slept with their children beyond 6 months of age, a group he called “persistent co-sleepers,” did show signs of stress, particularly the mothers. Dr. Teti emphasized that the research isn’t an indictment against co-sleeping, but does suggest that a number of factors, including cultural pressures and an unsupportive spouse, can make longer-term co-sleeping a more stressful experience for some families. “Co-sleeping is simply a practice, just like solitary sleep is a practice,” he said. “It is important for parents to be on the same page about whatever practices with their children they choose to put into effect.” The study, published this month in the journal Developmental Psychology, was unusual in that it tracked 139 couples, mostly married or living together, who generously allowed researchers to peek into their bedrooms with video cameras, recording nighttime interactions with their new babies at five time points in the first year of life. Co-sleeping — defined in this study as room-sharing or bed-sharing, often a mix of the two — was surprisingly common in early infancy. Nearly 75 percent of the parents co-slept with infants early on, and about half were still co-sleeping three months after the birth. But once the babies reached 6 months of age, only one in four babies continued to share a bed or a room with their parents. © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22598 - Posted: 08.25.2016

By PAM BELLUCK The images tell a heartbreaking story: Zika’s calamitous attack on the brains of babies — as seen from the inside. A study of brain scans and ultrasound pictures of 45 Brazilian babies whose mothers were infected with Zika in pregnancy shows that the virus can inflict serious damage to many different parts of the fetal brain beyond microcephaly, the condition of unusually small heads that has become the sinister signature of Zika. The images, published Tuesday in the journal Radiology, also suggest a grim possibility: Because some of the damage was seen in brain areas that continue to develop after birth, it may be that babies born without obvious impairment will experience problems as they grow. “It really brings to the forefront the importance of truly understanding the impact of Zika virus and the fact that we need to follow children who not only are exposed to Zika in pregnancy, but even those who don’t appear to have any complications at birth,” said Dr. Catherine Y. Spong, chief of the pregnancy and perinatology branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, who was not involved in the study. Most of the babies in the study were born with microcephaly, although three were not. Each also suffered other impairments, almost all of which emerge earlier than microcephaly because a smaller head is really a consequence of brain that has failed to develop fully or has been damaged along the way, experts said. “The brain that should be there is not there,” said Dr. Deborah Levine, an author of the study and a professor of radiology at Harvard Medical School in Boston. “The abnormalities that we see in the brain suggest a very early disruption of the brain development process.” © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22594 - Posted: 08.24.2016