Chapter 16. None
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by Agata Blaszczak-Boxe, LiveScience.com Unlike many humans, some monkeys are genuinely faithful to their mates. A species known as Azara's owl monkeys tends to be monogamous, according to a new study of these primates. The research also found that the monkeys' inclination to be faithful was related to the male monkeys' tendency to care for their offspring. "They [Azara's owl monkeys] live in pairs, so, in a group, we have only one adult male and one adult female, and both of them are faithful," study author Maren Huck, a professor at the University of Derby in England, told Live Science. "We found a link between... parental care and having few instances of cheating," Huck said. Researchers had known before this study that members of the Azara's species were socially monogamous, which means that males and females live in pairs. But in animals, including humans, social monogamy is not always equivalent to what researchers call genetic monogamy, where females and males only reproduce with their mates. One way researchers can check for genetic monogamy is to analyze the DNA of mating pairs, and check the paternity of the offspring. In the study, the researchers analyzed field observations of the monkeys' behavior, along with genetic samples from a total of 128 monkeys, including some that lived in groups, and others that were solitary "floaters." The material used by the research team included samples from 35 offspring that were born to 17 reproducing pairs. © 2014 Discovery Communications, LLC
By BENEDICT CAREY The relationship had become intolerably abusive, and after a stinging phone call one night, it seemed there was only one way to end the pain. Enough wine and pills should do the job — and would have, except that paramedics barged through the door, alerted by her lover. “I very rarely tell the story in detail publicly, it’s so triggering and sensational,” said Dese’Rae L. Stage, 30, a photographer and writer living in Brooklyn who tried to kill herself in 2006. “I talk about what led up to it, how helpless I felt — and what came after.” The nation’s oldest suicide prevention organization, the American Association of Suicidology, decided in a vote by its board last week to recognize a vast but historically invisible portion of its membership: people, like Ms. Stage, who tried to kill themselves but survived. About a million American adults a year make a failed attempt at suicide, surveys suggest, far outnumbering the 38,000 who succeed, and in the past few years, scores of them have come together on social media and in other forums to demand a bigger voice in prevention efforts. Plans for speakers bureaus of survivors willing to tell their stories are well underway, as is research to measure the effect of such testimony on audiences. For decades, mental health organizations have featured speakers with schizophrenia, bipolar disorder and depression. But until now, suicide has been virtually taboo, because of not only shame and stigma, but also fears that talking about the act could give others ideas about how to do it. “This is a real shift you’re seeing,” said Heidi Bryan, 56, of Neenah, Wis., who has been speaking for years about suicide attempts she made in the 1990s. “For people working in suicide prevention, they always told us not to talk about our own experience, like they were afraid to tip us over the edge or something. Honestly, we’re the ones who know what works and what doesn’t.” © 2014 The New York Times Company
Link ID: 19481 - Posted: 04.14.2014
By ALAN SCHWARZ With more than six million American children having received a diagnosis of attention deficit hyperactivity disorder, concern has been rising that the condition is being significantly misdiagnosed and overtreated with prescription medications. Yet now some powerful figures in mental health are claiming to have identified a new disorder that could vastly expand the ranks of young people treated for attention problems. Called sluggish cognitive tempo, the condition is said to be characterized by lethargy, daydreaming and slow mental processing. By some researchers’ estimates, it is present in perhaps two million children. Experts pushing for more research into sluggish cognitive tempo say it is gaining momentum toward recognition as a legitimate disorder — and, as such, a candidate for pharmacological treatment. Some of the condition’s researchers have helped Eli Lilly investigate how its flagship A.D.H.D. drug might treat it. The Journal of Abnormal Child Psychology devoted 136 pages of its January issue to papers describing the illness, with the lead paper claiming that the question of its existence “seems to be laid to rest as of this issue.” The psychologist Russell Barkley of the Medical University of South Carolina, for 30 years one of A.D.H.D.’s most influential and visible proponents, has claimed in research papers and lectures that sluggish cognitive tempo “has become the new attention disorder.” In an interview, Keith McBurnett, a professor of psychiatry at the University of California, San Francisco, and co-author of several papers on sluggish cognitive tempo, said: “When you start talking about things like daydreaming, mind-wandering, those types of behaviors, someone who has a son or daughter who does this excessively says, ‘I know about this from my own experience.’ They know what you’re talking about.” © 2014 The New York Times Company
Link ID: 19479 - Posted: 04.12.2014
Anne Trafton | MIT News Office Picking out a face in the crowd is a complicated task: Your brain has to retrieve the memory of the face you’re seeking, then hold it in place while scanning the crowd, paying special attention to finding a match. A new study by MIT neuroscientists reveals how the brain achieves this type of focused attention on faces or other objects: A part of the prefrontal cortex known as the inferior frontal junction (IFJ) controls visual processing areas that are tuned to recognize a specific category of objects, the researchers report in the April 10 online edition of Science. Scientists know much less about this type of attention, known as object-based attention, than spatial attention, which involves focusing on what’s happening in a particular location. However, the new findings suggest that these two types of attention have similar mechanisms involving related brain regions, says Robert Desimone, the Doris and Don Berkey Professor of Neuroscience, director of MIT’s McGovern Institute for Brain Research, and senior author of the paper. “The interactions are surprisingly similar to those seen in spatial attention,” Desimone says. “It seems like it’s a parallel process involving different areas.” In both cases, the prefrontal cortex — the control center for most cognitive functions — appears to take charge of the brain’s attention and control relevant parts of the visual cortex, which receives sensory input. For spatial attention, that involves regions of the visual cortex that map to a particular area within the visual field.
Link ID: 19478 - Posted: 04.12.2014
Scientists may have discovered how the most common genetic cause of Parkinson’s disease destroys brain cells and devastates many patients worldwide. The study was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS); the results may help scientists develop new therapies. The investigators found that mutations in a gene called leucine-rich repeat kinase 2 (LRRK2; pronounced “lark two” or “lurk two”) may increase the rate at which LRRK2 tags ribosomal proteins, which are key components of protein-making machinery inside cells. This could cause the machinery to manufacture too many proteins, leading to cell death. “For nearly a decade, scientists have been trying to figure out how mutations in LRRK2 cause Parkinson’s disease,” said Margaret Sutherland, Ph.D., a program director at NINDS. “This study represents a clear link between LRRK2 and a pathogenic mechanism linked to Parkinson’s disease.” Affecting more than half a million people in the United States, Parkinson’s disease is a degenerative disorder that attacks nerve cells in many parts of the nervous system, most notably in a brain region called the substantia nigra, which releases dopamine, a chemical messenger important for movement. Initially, Parkinson’s disease causes uncontrolled movements; including trembling of the hands, arms, or legs. As the disease gradually worsens, patients lose ability to walk, talk or complete simple tasks.
Link ID: 19477 - Posted: 04.12.2014
James Gorman Crows and their relatives, like jays and rooks, are definitely in the gifted class when it comes to the kinds of cognitive puzzles that scientists cook up. They recognize human faces. They make tools to suit a given problem. Sometimes they seem, as humans like to say, almost human. But the last common ancestor of humans and crows lived perhaps 300 million years ago, and was almost certainly no intellectual giant. So the higher levels of crow and primate intelligence evolved on separate tracks, but somehow reached some of the same destinations. And scientists are now asking what crows can’t do, as one way to understand how they learn and how their intelligence works. One very useful tool for this research comes from an ancient Greek (or perhaps Ethiopian), the fabulist known as Aesop. One of his stories is about a thirsty crow that drops pebbles into a pitcher to raise the level of water high enough that it can get a drink. Researchers have modified this task by adding a floating morsel of food to a tube with water and seeing which creatures solve the problem of using stones to raise the water enough to get the food. It can be used for a variety of species because it’s new to all of them. “No animal has a natural predisposition to drop stones to change water levels,” said Sarah Jelbert, a Ph.D. student at Auckland University in New Zealand, who works with crows. But in the latest experiment to test the crows, Ms. Jelbert, working with Alex Taylor and Russell Gray of Auckland and Lucy Cheke and Nicola Clayton of the University of Cambridge in England, found some clear limitations to what the crows can learn. And those limitations provide some hints to how they think. © 2014 The New York Times Company
|By Scott O. Lilienfeld and Hal Arkowitz A rabble-rousing patient on a psychiatric ward is brought into a room and strapped to a gurney. He is being punished for his defiance of the head nurse's sadistic authority. As he lies fully awake, the psychiatrist and other staff members place electrodes on both sides of his head and pass a quick jolt of electricity between them. Several orderlies hold the patient down while he grimaces in pain, thrashes uncontrollably and lapses into a stupor. This scene from the 1975 Academy Award–winning film One Flew Over the Cuckoo's Nest, starring Jack Nicholson as the rebellious patient, has probably shaped the general public's perceptions of electroconvulsive therapy (ECT) far more than any scientific description. As a result, many laypeople regard ECT as a hazardous, even barbaric, procedure. Yet most data suggest that when properly administered, ECT is a relatively safe and often beneficial last-resort treatment for severe depression, among other forms of mental illness. One Flew Over the Cuckoo's Nest is far from the only negative portrayal of ECT in popular culture. In a 2001 survey of 24 films featuring the technique, psychiatrists Andrew McDonald of the University of Sydney and Garry Walter of Northern Sydney Central Coast Health of New South Wales reported that the depictions of ECT are usually pejorative and inaccurate. In most cases, ECT is delivered without patients' consent and often as retribution for disobedience. The treatment is typically applied to fully conscious and terrified patients. Following the shocks, patients generally lapse into incoherence or a zombielike state. In six films, patients become markedly worse or die. Probably as a result of such portrayals, the general public holds negative attitudes toward ECT. © 2014 Scientific American
Link ID: 19475 - Posted: 04.12.2014
By Dominic Basulto The latest numbers from the Center for Disease Control showing a steep rise in the number of children with autism are so off the charts that it’s hard not to come to one of two conclusions: There’s something wrong in the way that we measure the data or there’s something extraordinary going on. 1 in 68 American children now has autism, up from 1 in 88 children just two years ago, an increase of 30 percent. A decade ago, one in 166 children were diagnosed as having autism. In 1975, it was 1 in 5000. Plot this as a graph using CDC data and you get a hockey stick curve showing exponential growth in autism over just the past decade. If you accept the first conclusion – that we’re simply not measuring autism correctly – there’s actually a fair amount of evidence to suggest that as much as 53 percent of the variation in data can be explained away by factors such as better diagnosis, better detection and better awareness. And it’s true that the very definition of “autism” continues to change to include a much wider description of symptoms along a spectrum, so it’s only natural to expect an increase in the number of cases if we’re making it easier to define people as having autism. There’s even a growing consensus in the scientific community that the current numbers are “no cause for alarm” and may actually underestimate the incidence of autism in the population, due to problems in collecting information in more rural areas and among some demographic groups. That still leaves approximately 50 percent of the rise in autism cases to explain through science. It won’t be easy. There may be as many as 60 different disorders that are associated with autism, and a multitude of factors at work, with most of them thought to be linked to changes in our environment or genetic factors resulting from increasing parental age. As a result, even the Chief Science Officer at Autism Speaks concedes that what causes autism remains a mystery. © 1996-2014 The Washington Post
Link ID: 19474 - Posted: 04.12.2014
By Dwayne Godwin and Jorge Cham ABOUT THE AUTHOR(S) Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2014 Scientific American
Link ID: 19473 - Posted: 04.12.2014
by Meghan Rosen Shaking off jet lag could be as easy as downloading an app. Researchers developed the iPhone app, called Entrain, using mathematical analyses of humans’ daily rhythms to calculate the quickest way to adjust to new time zones. Users plug in their destination and arrival time, and Entrain advises times of the day to soak up or stay out of the light. The schedules are surprisingly simple, says mathematical biologist Daniel Forger, of the University of Michigan in Ann Arbor. “They might say, ‘Hey you should keep the lights on in your room until midnight,’” he says. “Or ‘you should stay in darkness until 10 a.m.’” Scientists have previously created mathematical equations that describe how humans’ internal clocks respond to light, Forger says. He and a colleague used a computer program to solve the tricky problem of finding the best lighting schedules for more than 1,000 possible trips. To do so, the researchers asked a question: If a traveler wants to move their body’s clock from New York to London time, for instance, what lighting schedule gets them there fastest? The pair reports the results April 10 in PLOS Computational Biology. K. Serkh and D.B. Forger. Optimal schedules of light exposure for rapidly correcting circadian misalignment. PLOS Computational Biology. Vol.10, April 10, 2014, p. e1003525. Doi: 10.1371/journal.pcbi.1003523. © Society for Science & the Public 2000 - 2013.
Keyword: Biological Rhythms
Link ID: 19472 - Posted: 04.12.2014
By KATRINA KARKAZIS and REBECCA JORDAN-YOUNG In 2009, the South African middle-distance runner Caster Semenya was barred from competition and obliged to undergo intrusive and humiliating “sex testing” after fellow athletes at the Berlin World Championships questioned her sex. Ms. Semenya was eventually allowed to compete again, but the incident opened the world’s eyes to the process of sex testing and the distress it could bring to an athlete who had lived her whole life as a girl. When an endocrinologist, a gynecologist and a psychologist were brought in to determine whether the teenager was really a woman, she simply asserted, “I know who I am.” From 2011, major sports governing bodies, including the International Olympic Committee, the Fédération Internationale de Football Association and the International Association of Athletics Federations, instituted new eligibility rules that were intended to quell the outrage over the handling of the Semenya case. Instead, as recent cases attest, they may have made things worse. Rather than trying to decide whether an athlete is “really” female, as decades of mandatory sex tests did, the current policy targets women whose bodies produce more testosterone than is typical. If a female athlete’s T level is deemed too high, a medical team selected by the sport’s governing bodies develops a “therapeutic proposal.” This involves either surgery or drugs to lower the hormone level. If doctors can lower the athlete’s testosterone to what the governing bodies consider an appropriate level, she may return to competition. If she refuses to cooperate with the investigation or the medical procedures, she is placed under a permanent ban from elite women’s sports. © 2014 The New York Times Company
By GRETCHEN REYNOLDS It’s possible that some of us are born not to run. According to an eye-opening new genetics study of lab rats, published in The Journal of Physiology, the motivation to exercise — or not — may be at least partly inherited. For years, scientists have been bedeviled by the question of why so few people regularly exercise when we know that we should. There are obvious reasons, including poor health and jammed schedules. But researchers have begun to speculate that genetics might also play a role, as some recent experiments suggest. In one, published last year, sets of fraternal and identical adult twins wore activity monitors to track their movements. The results indicated that the twins were more alike in their exercise habits than a shared upbringing alone would explain. Their willingness to work out or sit all day depended to a large extent on genetics, the researchers concluded. But which genes might be involved and how any differences in the activity of those genes might play out inside the body were mysteries. So scientists at the University of Missouri recently decided to delve into those issues by creating their own avid- or anti-exercising animals. They accomplished this task by inter-breeding normal rats that had voluntarily run on wheels in the lab. The male rats that had run the most were bred with the female rats that also had run the most; those that had run the least were likewise mated. This scheme continued through many generations, until the scientists had two distinct groups of rats, some of which would willingly spend hours on running wheels, while the others would skitter on them only briefly, if at all. In their first experiments with these rats, the researchers found some intriguing differences in the activity of certain genes in their brains. In normal circumstances, these genes create proteins that tell young cells to grow up and join the working world. But if the genes don’t function normally, the cells don’t receive the necessary chemical messages and remain in a prolonged, feckless cellular adolescence. Such immature cells cannot join the neural network and don’t contribute to healthy brain function. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19470 - Posted: 04.10.2014
By Daisy Yuhas Greetings from Boston where the 21st annual meeting of the Cognitive Neuroscience Society is underway. Saturday and Sunday were packed with symposia, lectures and more than 400 posters. Here are just a few of the highlights. The bilingual brain has been a hot topic at the meeting this year, particularly as researchers grapple with the benefits and challenges of language learning. In news that will make many college language majors happy, a group of researchers led by Harriet Wood Bowden of the University of Tennessee-Knoxville have demonstrated that years of language study alter a person’s brain processing to be more like a native speaker’s brain. They found that native English speaking students with about seven semesters of study in Spanish show very similar brain activation to native speakers when processing spoken Spanish grammar. The study used electroencephalography, or EEG, in which electrodes are placed along the scalp to pick up and measure the electrical activity of neurons in the brain below. By contrast, students who have more recently begun studying Spanish show markedly different processing of these elements of the language. The study focused on the recognition of noun-adjective agreement, particularly in gender and number. Accents, however, can remain harder to master. Columbia University researchers worked with native Spanish speakers to study the difficulties encountered in hearing and reproducing English vowel sounds that are not used in Spanish. The research focused on the distinction between the extended o sound in “dock” and the soft u sound in “duck,” which is not part of spoken Spanish. The scientists used electroencephalograms to measure the brain responses to these vowel sounds in native-English and native-Spanish speakers. © 2014 Scientific American
Link ID: 19467 - Posted: 04.10.2014
Claudia Dreifus To Neil H. Shubin’s long résumé — paleontologist, molecular biologist, dean and professor of anatomy at the University of Chicago School of Medicine, best-selling author — can now be added “television host.” Dr. Shubin, 53, who helped discover the 375-million-year-old fish called Tiktaalik, hailed as a missing link between sea and land animals, will preside over “Your Inner Fish,” a three-part series on evolution (based on his book of the same title) that makes its debut Wednesday on PBS. We spoke in Chicago in February and in New York last month. What follows is an edited and condensed version of the conversations. Q. Where did you grow up? A. Suburban Philadelphia. My mom’s a retired nursing home administrator. My father, Seymour Shubin, is a fiction writer. He writes mysteries. My favorite is “The Captain”; it won an Edgar award. He’s an educated man, but science kind of scares him. So when I’m writing, my dad is my target audience. Whenever I hit a tricky scientific concept, I think, “How would I communicate this to him?” This is why my books are written, intentionally, without jargon, which can lead to some gyrations because jargon does have precision. The funny thing is, I’m not sure he always gets what I do. When I first started working on the book version of “Your Inner Fish,” he asked, “Neil, how did you become a scientist?” I thought, “All these years he’s seen me run off to the Arctic, but he’s never been quite sure what I do up there.” So let me ask you his question: How did you become a paleontologist? I was one of those kids with lots of hobbies: astronomy, dinosaurs, collecting rocks, collecting stamps. It all came together when I went to college in New York — Columbia — and volunteered at the American Museum of Natural History. That place was like a playground for me. © 2014 The New York Times Company
Link ID: 19466 - Posted: 04.10.2014
|By Bret Stetka The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s. Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity. Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields. © 2014 Scientific American
Julia Baird SYDNEY, Australia — PRETTY much the No. 1 question you are asked when you’re pregnant is: “Girl or boy?” If you choose not to find out, but to be deliciously surprised at birth, as I did, then you will be asked to guess: “What do you feel it is?” I used to scrunch up my eyes and try hard to draw on what people told me was an age-old female intuition: Which genitals were sprouting in my round belly? I could never tell, though. It is as though the entire world is trying to guess what, or who, is inside you. One oft-told tale is that girls steal your looks and make you fat, while boys just make your belly stick out straight. When I stood wearily bulging at one friend’s baby shower in Manhattan, a stylist confided that she thought our mutual friend was having a boy, because she looked so pretty. Then she looked me up and down: “I think you’re having a girl.” (I placed her in the same category as the neighbor who yelled, “Morning, Fatty!” over the side fence each day.) Why is whether a baby wears blue or pink the most pressing matter for adult acquaintances of a soon-to-be-born? Green is just fine, or white. But a 2007 Gallup poll found that most young Americans, and women under 50, would like to find out the sex of their baby before it is born. In some American fertility clinics, staff experts check the embryo’s sex before they implant it in the womb. So what will it do to our collective minds when forced to grasp that some people are neither gender? Not male, or female, but something else either encompassing, or rejecting, or just adapting from both? Last week, Australia had to grapple with just that after the High Court, in a historic decision, ruled that a person called Norrie May-Welby could register as “nonspecific” on official certificates. Now 52, Norrie was identified, physically, as male when she was born, in Scotland, but was drawn to the world of girls, playing with dolls at age 4 and tying her school tie around her head at night to create the illusion of long hair. She escaped into the library monitors’ group at school and made up adventures where she played six characters, five of whom were female: “I didn’t think there was any problem with this,” she says. “After all, just because I wasn’t really from Krypton, didn’t mean I couldn’t imagine being Supergirl.” © 2014 The New York Times Company
Keyword: Sexual Behavior
Link ID: 19462 - Posted: 04.09.2014
By: Larry Cahill, Ph.D. Early in 2013, the Food and Drug Administration (FDA) ordered the makers of the well-known sleep aid Ambien (zolpidem) to cut their recommended dose in half-but only for women. In essence, the FDA was acknowledging that despite extensive testing prior to the drug's release on the market, millions of women had been overdosing on Ambien for 20 years. On February 9, 2014, CBS's 60 Minutes highlighted this fact-and sex differences in general-by powerfully asking two questions: Why did this happen, and are men and women treated equally in research and medicine?1 The answer to the first question is that the biomedical community has long operated on what is increasingly being viewed as a false assumption: that biological sex matters little, if at all, in most areas of medicine. The answer to the second question is no, today's biomedical research establishment is not treating men and women equally. What are some of the key reasons for the biomedical community's false assumption, and why is this situation now finally changing? What are some of the seemingly endless controversies about sex differences in the brain generated by "anti-sex difference" investigators? And what lies at the root of the resistance to sex differences research in the human brain? For a long time, for most aspects of brain function, sex influences hardly mattered to the neuroscience mainstream. The only sex differences that concerned most neuroscientists involved brain regions (primarily a deep-brain structure called the hypothalamus) that regulate both sex hormones and sexual behaviors.2 Neuroscientists almost completely ignored possible sex influences on other areas of the brain, assuming that the sexes shared anything that was fundamental when it came to brain function. Conversely, the neuroscience mainstream viewed any apparent sex differences in the brain as not fundamental- something to be understood after they grasped the fundamental facts. By this logic, it was not a problem to study males almost exclusively, since doing so supposedly allowed researchers to understand all that was fundamental in females without having to consider the complicating aspects of female hormones. To this day, neuroscientists overwhelmingly study only male animals.3 © 2014 The Dana Foundation
Keyword: Sexual Behavior
Link ID: 19461 - Posted: 04.09.2014
By BENEDICT CAREY Therapists who specialize in autism often use a child’s own interests, toys or obsessions as a way to connect, and sometimes to reward effort and progress on social skills. The more eye contact a child makes, for example, the more play time he or she gets with those precious maps or stuffed animals. But now a group of scientists and the author of a new book are suggesting that those favorite activities could be harnessed in a deeper, more organic way. If a child is fascinated with animated characters like Thomas the Tank Engine, why not use those characters to prompt and reinforce social development? Millions of parents do this routinely, if not systematically, flopping down on the floor with a socially distant child to playact the characters themselves. “We individualize therapy to each child already, so if the child has an affinity for certain animated characters, it’s absolutely worth studying a therapy that incorporates those characters meaningfully,” said Kevin Pelphrey, director of the child neuroscience laboratory at Yale. He and several other researchers, including John D. E. Gabrieli of M.I.T., Simon Baron-Cohen of the University of Cambridge and Pamela Ventola of Yale, are proposing a study to test the approach. The idea came from Ron Suskind, a former Wall Street Journal reporter whose new book “Life, Animated” describes his family’s experience reaching their autistic son, Owen, through his fascination with Disney movies like “The Little Mermaid” and “Beauty and the Beast.” It was Mr. Suskind’s story that first referred to ‘“affinity therapy.” He approached the researchers to put together a clinical trial based on the idea that some children can develop social and emotional instincts through the characters they love. Experts familiar with his story say the theory behind the therapy is plausible, given what’s known from years of studying the effects of other approaches. © 2014 The New York Times Company
Link ID: 19459 - Posted: 04.08.2014
By Paul D. Thacker When the FDA denied Sprout Pharmaceutical’s bid last October to begin marketing flibanserin, a drug aimed at treating low sexual desire in women, women’s groups responded in anger. In January, representatives from eight different women’s groups, including the National Organization of Women, met with Janet Woodcock, the FDA’s head of pharmaceuticals, to protest the decision. Congress also got in on the act, with Reps. Debbie Wasserman Schultz, Chellie Pingree, Nita Lowey, and Louise Slaughter sending a letter to FDA Commissioner Margaret Hamburg to implore that, when evaluating drugs for female dysfunction (in medical terms Hypoactive Sexual Desire Disorder, or HSDD), Dr. Hamburg apply "the same standards of consideration given to the approved drugs for men in your risk/benefit evaluation." “We’ve now got 24 drugs for men for either testosterone replacement or erectile dysfunction,” Cindy Whitehead, Sprout’s chief operating officer told the Associated Press. “Yet there are zero drugs for the most common form of sexual dysfunction in women.” Anita H. Clayton, the interim chair of the department of psychiatry and neurobehavioral sciences at the University of Virginia School of Medicine, was more explicit, writing in a blistering column for the Huffington Post: “For the millions of women with HSDD, the FDA must overcome the problem of institutionalized sexism—unconscious and perhaps unintended, but damaging nonetheless.” The chorus was loud and clear: The FDA is sexist. The federal agency charged with approving drugs to protect and improve our health is now standing in the way of a woman’s right to have a satisfying sex life. This framing played out in numerous stories, with similar charges appearing in the American Prospect (“the FDA’s kinda sexist”), and the Washington Post (“Some critics say the agency—consciously or not—may be succumbing to society’s squeamishness about women’s sexual desires compared with those of men”). Not to be outdone with mere institutional sexism, a writer for the Wire mused whether “blatant, medieval sexism is also at play.” © 2014 The Slate Group LLC.
Keyword: Sexual Behavior
Link ID: 19458 - Posted: 04.08.2014
By JoNel Aleccia The engineer who drove a speeding commuter train off the rails in New York last year may have suffered from the most severe form of a dangerous sleep disorder, but health experts say he has plenty of company. As many as 22 million people in the U.S. — or up to 7 percent of the population — may suffer from obstructive sleep apnea, experts say. It’s a condition that causes airways to collapse during sleep, cutting off breathing dozens or sometimes hundreds of times a night, leaving them bleary-eyed and drowsy, even after a full night’s rest. William Rockefeller, 46, was diagnosed after the December 2013 crash that killed four and injured more than 70 with severe obstructive sleep apnea, documents released this week show. On a scale where as few as five sleep disruptions an hour can make someone sleepy, and 30 episodes are considered severe, Rockefeller logged about 66 arousals an hour, doctors said. “His sleep was really fragmented,” said Dr. Phyllis Zee, a sleep expert with the Northwestern Medicine Sleep and Circadian Rhythms Research Program. “Even if he were to sleep seven or eight hours, he would be sleep-deprived.” Zee and her colleagues suspected that Rockefeller might suffer from sleep deprivation. He was obese, records show, and there’s a certain fatigued look that she saw in news photos of the engineer. “That was one of my thoughts, ‘Oh my goodness, he has (OSA),’” she said.
Link ID: 19457 - Posted: 04.08.2014