Links for Keyword: Autism

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By Karen Weintraub The four members of Asperger’s Are Us decided a long time ago that their main goal would be to amuse themselves. But after nearly a decade of laughing and writing punch lines together, Asperger’s Are Us, which is probably the only comedy troupe made up of people on the autism spectrum, is on the cusp of comedic success. A documentary about the group premiered at the SXSW conference in Austin in March and was recently sold to Netflix. The troupe is also preparing for its first national tour this summer. Comedy might be a surprising choice for someone with Asperger’s syndrome, since stereotypically, people with autism are generally regarded as socially awkward loners. But the four men in the group bonded at summer camp 11 years ago, when one was a counselor and the other three were campers, and are clearly great friends. An “Aspergers Are Us” performance from 2011. Talking recently via Skype, Noah Britton, the former counselor, settles giant black rabbit ears onto his head. Jack Hanke, another member of the troupe, dons his favorite sombrero – the black one he took with him to Oxford University during his recent junior year abroad – accessorized with a red sombrero on top. They slip into their usual banter when asked what they thought of the film, named for the group, which will be shown publicly for the first time on Friday at the Somerville Theater outside of Boston. “I liked the four weird guys in it,” Mr. Britton said. “It was better than ‘Jaws 2,’ but not as good as ‘Jaws 3,’” Mr. Hanke insisted. “I found it kind of annoying myself,” added Ethan Finlan, another member of the group. The fourth member, who changed his first name to New Michael to distinguish himself from his father, Michael Ingemi, didn’t want to join the call. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22169 - Posted: 05.03.2016

New York's Tribeca Film Festival will not show Vaxxed, a controversial film about the MMR vaccine, its founder Robert De Niro says. As recently as Friday, Mr De Niro stood by his decision to include the film by anti-vaccination activist Andrew Wakefield in next month's festival. The link the film makes between the measles, mumps and rubella vaccine and autism has been widely discredited. "We have concerns with certain things in this film," said Mr De Niro. Mr De Niro, who has a child with autism, said he had hoped the film would provide the opportunity for discussion of the issue. But after reviewing the film with festival organisers and scientists, he said: "We do not believe it contributes to or furthers the discussion I had hoped for." Image caption Wakefield published his controversial study in 1998 Vaxxed was directed and co-written by Mr Wakefield, who described it as a "whistle-blower documentary". In a statement issued following the Tribeca Film Festival's decision, he and the film's producer Del Bigtree said that "we have just witnessed yet another example of the power of corporate interests censoring free speech, art and truth". The British doctor was the lead author of a controversial study published in 1998, which argued there might be a link between MMR and autism and bowel disease. Mr Wakefield suggested that parents should opt for single jabs against mumps, measles and rubella instead of the three-in-one vaccine. His comments and the subsequent media furore led to a sharp drop in the number of children being vaccinated against these diseases. But the study, first published in The Lancet, was later retracted by the medical journal. Mr Wakefield's research methods were subsequently investigated by the General Medical Council and he was struck off the medical register.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22037 - Posted: 03.28.2016

John Consentino After multiple doctors had conflicted about ADHD, I decided to move away from psychiatry and seek a neuropsychologist. I thought that autism made sense, but what ultimately led me to seek help was my focus problem. When I was 8 years old, it would take me HOURS to do homework. On Wednesdays, we got out of school at noon, and I wouldn't finish homework until about 8 p.m. No one understood why this was happening, and with all of the screaming and punishments I withstood, nothing improved. I still had GPAs near the high 90s, so all was OK, supposedly. I struggled with eye contact during that time, and this is very much apparent now. I struggled speaking to waiters/waitresses, to teachers, to family members. Speaking to members of the opposite sex was a near-impossible task. I never understood social groups. I went through all of high school in the same fashion. However, my family felt that everything was OK. I still had a mid-90 GPA, and I had made numerous friends. Unfortunately, my GPA had dropped by about 15-plus points by my senior year. I struggled badly during my first two years of college. I was constantly unhappy, and I made little to no friends. My GPA was horrid, and my time at the university was dwindling. I dropped out of school twice, and my future felt bleak. After transferring schools, I did great. So, everything was OK yet again. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22036 - Posted: 03.28.2016

Nicola Davis The same genes involved in predisposing people to autism appear to influence social skills in the wider population, suggesting that the autism spectrum has no clear cut-off point, scientists have discovered. Researchers have previously shown that autism is linked not just to one or two powerful genes, but to the combined effect of many small genetic changes. The latest findings, published in Nature Genetics, suggest that social charm, empathy and the ability to make friends is about more than just practice and upbringing, but is also affected by how many of these autism risk gene variants we possess. Dr Elise Robinson, from Harvard University and a lead author on the paper, said: “This is the first study that specifically shows that ... factors that we have unambiguously associated with autism are also very clearly associated with social communication differences in the general population.” Rather than viewing a person as either having or not having such a disorder, Robinson believes our social skills are better viewed as sitting on a sliding scale across the whole population. “The primary implication is that the line at which we say people are affected or unaffected is arbitrary,” said Robinson. “There is no clear objective point either in terms of genetic risk or in terms of behavioural traits, where you can say quite simply or categorically that you’re affected or unaffected. It’s like trying to pick a point where you say someone is tall or not.” © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22014 - Posted: 03.22.2016

By Emily Underwood People with autism spectrum disorder (ASD) die on average 18 years before the general population, according to a report released today by Autistica, a philanthropic group based in the United Kingdom. People with both ASD and an intellectual disability die even younger, on average 30 years earlier than those without the conditions. Fatal accidents—often by drowning, when a child or adult with ASD wanders away from caregivers—are one of the classic causes of premature death in people who have both ASD and an intellectual disability, says Sven Bölte, a clinical psychologist at the Karolinksa Institute in Stockholm, whose research is cited in the Autistica report. Epilepsy, along with several other neurological disorders, is another common cause of death among people with both ASD and learning difficulties, suggesting that early disruption of neurodevelopment is to blame. These “classic” causes of premature death in autism, however, do not fully account for a decades-long life span gap between autistic and nonautistic people, or the difference in mortality between autistic people with and without an intellectual disability, Bölte says. To explore these gaps, in 2015 Bölte’s group published a large epidemiological study of more than 27,000 Swedish people with ASD, 6500 of whom had an intellectual disability. They found that risk of premature death was about 2.5 times higher for the entire group, a gap largely due to increased prevalence of common health problems such as diabetes and respiratory disease. Patients may be being diagnosed too late because they do not know how to express health concerns to their doctors, Bölte says, making it “extremely important” for general practitioners to thoroughly explore autistic patients’ symptoms and histories. © 2016 American Association for the Advancement of Scienc

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22010 - Posted: 03.19.2016

By John Elder Robison What happens to your relationships when your emotional perception changes overnight? Because I’m autistic, I have always been oblivious to unspoken cues from other people. My wife, my son and my friends liked my unflappable demeanor and my predictable behavior. They told me I was great the way I was, but I never really agreed. For 50 years I made the best of how I was, because there was nothing else I could do. Then I was offered a chance to participate in a study at Beth Israel Deaconess Medical Center, a teaching hospital of Harvard Medical School. Investigators at the Berenson-Allen Center there were studying transcranial magnetic stimulation, or T.M.S., a noninvasive procedure that applies magnetic pulses to stimulate the brain. It offers promise for many brain disorders. Several T.M.S. devices have been approved by the Food and Drug Administration for the treatment of severe depression, and others are under study for different conditions. (It’s still in the experimental phase for autism.) The doctors wondered if changing activity in a particular part of the autistic brain could change the way we sense emotions. That sounded exciting. I hoped it would help me read people a little better. They say, be careful what you wish for. The intervention succeeded beyond my wildest dreams — and it turned my life upside down. After one of my first T.M.S. sessions, in 2008, I thought nothing had happened. But when I got home and closed my eyes, I felt as if I were on a ship at sea. And there were dreams — so real they felt like hallucinations. It sounds like a fairy tale, but the next morning when I went to work, everything was different. Emotions came at me from all directions, so fast that I didn’t have a moment to process them. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22009 - Posted: 03.19.2016

By Lisa Rapaport Mothers who are obese during pregnancy have almost twice the odds of having a child with autism as women who weigh less, a U.S. study suggests. When women are both obese and have diabetes, the autism risk for their child is at least quadrupled, researchers reported online January 29 in Pediatrics. "In terms of absolute risk, compared to common pediatric diseases such as obesity and asthma, the rate of autism spectrum disorder (ASD) in the U.S. population is relatively low, however, the personal, family and societal impact of ASD is enormous," said senior study author Dr. Xiaobin Wang, a public health and pediatrics researcher at Johns Hopkins University in Baltimore. About one in 68 children have ASD, according to the U.S. Centers for Disease Control and Prevention, or about 1.5 percent of U.S. children. The study findings suggest the risk rises closer to about 3 percent of babies born to women who are obese or have diabetes, and approaches 5 percent to 6 percent when mothers have the combination of obesity and diabetes. Wang and colleagues analyzed data on 2,734 mother-child pairs followed at Boston Medical Center between 1998 and 2014. Most of the children, 64 percent, weren't diagnosed with any other development disorders, but there were 102 kids who did receive an ASD diagnosis. © 2016 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21843 - Posted: 02.01.2016

Ian Sample Science editor Genetically modified (GM) monkeys that develop symptoms of autism have been created to help scientists discover treatments for the condition. The macaques carry a genetic fault that causes a rare disorder in humans called MeCP2 duplication syndrome. This produces a wide range of medical conditions, some of which mirror those seen in autism, such as difficulties with social interactions. Researchers say groups of the GM monkeys could be used to identify brain circuits involved in common autistic behaviours and to test new treatments designed to alleviate the symptoms. Because the monkeys pass the genetic defects on to their offspring, scientists can breed large populations of the animals for medical research. A group of 200 monkeys has been established at the scientists’ lab in China. The research, described in the journal Nature, paves the way for more varieties of GM monkeys that develop different mental and psychiatric problems which are almost impossible to study in other animals. “The first cohort of transgenic monkeys shows very similar behaviour to human autism, including increased anxiety, but most importantly, defects in social interactions,” said Zilong Qiu who led the research at the Institute of Neuroscience in Shanghai. © 2016 Guardian News and Media Limited or it

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21824 - Posted: 01.26.2016

By Melinda Wenner Moyer There's a reason your mother told you to look people in the eye when you talk to them: eye contact conveys important social cues. Yet when someone holds your gaze for more than a few seconds, the experience can take on a different tenor. New work elucidates the factors that affect whether we like or loathe locking eyes for a lengthy period. Researchers have long known that eye contact is an important social signal. Our recognition of its import may even be hardwired. One study found that five-day-old babies prefer looking at faces that make direct eye contact compared with faces that have an averted gaze. “Eye contact provides some of the strongest information during a social interaction,” explains James Wirth, a social psychologist now at Ohio State University at Newark, because it conveys details about emotions and intentions. (Lack of eye contact is one of the early signs of autism in infants and toddlers.) The power of eye contact is so great that, according to a 2010 study co-authored by Wirth, if someone avoids your gaze for even a short period, you may feel ostracized. But what determines how we feel about prolonged eye contact? One recent study explored this question. In research presented in May 2015 at the Vision Sciences Society conference, psychologist Alan Johnston and his colleagues at University College London collected information from more than 400 volunteers about their personalities. Then the subjects indicated their comfort level while watching video clips of actors who appeared to be looking directly at them for varying lengths of time. © 2016 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21746 - Posted: 01.04.2016

By Andrea Anderson Mom's ovaries could hold clues to some autism cases, new research suggests—and this time it's not because of genetic vulnerabilities carried in her eggs. A new, large-scale study out of Sweden suggests that women with polycystic ovarian syndrome (PCOS)—an endocrine disorder that affects 5 to 10 percent of women of childbearing age—have an increased risk of giving birth to children with autism spectrum disorder (ASD). The Karolinska Institute's Renee Gardner, along with colleagues from Sweden and the U.S., tapped into a Swedish national population health database to look at potential ties between PCOS and ASD. As they reported online December 8 in Molecular Psychiatry, the team looked at 23,748 individuals with ASD and nearly 209,000 unaffected individuals, all born in Sweden between 1984 and 2007. Although identifying information about the individuals was removed, the researchers had access to information about their relationships to others in the database as well as documented diagnoses and use of health care services. The group found that ASD was 59 percent more prevalent in children born to women with PCOS—a relationship that was independent of PCOS complications such as increased neonatal distress or C-section delivery. This risk level is roughly comparable with that of having a father over age 50 (estimated to be 66 percent) but lower than it is in those with certain rare genetic syndromes or mutations. The authors of the analysis believe PCOS increases ASD risk in offspring to a greater extent than maternal infection, one of many factors previously implicated in autism. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21694 - Posted: 12.12.2015

By Darold A. Treffert The headlines read “New study suggests autism can be outgrown”, or “outgrowing autism: a doctor’s surprise and wonder.” The stories are based on studies reporting that 7-9% of children with a documented early autistic syndrome disorder (ASD) have no symptoms of the disorder on follow-up later in childhood or adolescence. That is good news. The question is how to account for it. Is it possible to simply “outgrow” autism? Was the initial diagnosis wrong? Did some interventions work? Or might there be other explanations for this welcome news? "In an earlier column titled “Oops. When “autism” isn’t autistic disorder,” I outlined three types of hyperlexia, or precocious reading ability, which is sometimes an element of a diagnosis of ASD. Type 1 are neurotypical children who simply read way ahead of their chronological age. Listening to a 4 year old reading books to his or her nursery school classmates is a startling experience. Type 2 are children in which intense fascination with letters and numbers, along with early reading and remarkable memory represent ‘splinter skills’ as a part of autistic syndrome disorder (ASD) Type 3 are children who likewise show intense fascination and preoccupation with numbers and letters very early, along with precocious reading skills and remarkable memory. They do have “autistic-like” symptoms or behaviors but those disappear over time as the child gets older. The outcome in these children is much more positive than those with ASD to their benefit and the great relief of their parents. Following the “Oops” article I received numerous reports from parents who identified with hyperlexia 3. “You just described my child,” the puzzled, and relieved parents would write as they read the case examples in my Wisconsin Medical Journal article in December, 2011. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21689 - Posted: 12.10.2015

By Jennie Baird Last week’s news that Sesame Street was introducing the first autistic Muppet was met in my house with a resounding, “Huh?” “But there already is an autistic Muppet,” my high-functioning 14-year-old said. “Fozzie Bear.” I had never thought of Fozzie that way, but my son had a point. Fozzie is not good at taking social cues; he doesn’t read a room well and he tends to monologue and perseverate (to repeat himself long after the need has passed). He interprets figurative language as literal — remember that fork in the road in “The Muppet Movie?” He has a verbal tic he falls back on, “wokka-wokka.” And he hates to be separated from his hat for no obvious reason. I’ve tested this theory on friends and have seen the light bulb of recognition go off every time. Of course Fozzie has autism! One friend, a mother whose son is also on the spectrum even told me her family had the exact same conversation. Sesame Street hopes children will identify with their new character Julia, described as a “friend who has autism,” and appearing, for now, only in the book “We’re Amazing 1-2-3!” There is no question, the mere presence of Julia is a positive development. But she also introduces a rarely discussed complication of autism. Let’s call it the Fozzie Conundrum. I’m particularly sensitive to the Fozzie Conundrum now that my son attends regular honors classes in a regular public high school. Naturally sociable and charismatic — and with eight years of support and interventions from a team of terrific teachers and therapists at specialized schools — he can easily “pass” as a regular, funny, quirky teenager. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21590 - Posted: 11.02.2015

Elizabeth Blair The muppet Julia has not yet made her TV debut, but the wide-eyed little girl with a big smile is the star of her own "digital storybook" called "We're Amazing, 1,2,3." For over a year now, Sesame Street has been working with organizations such as Autism Speaks and Autism Self Advocacy to help reduce the stigma associated with autism spectrum disorder. As part of the campaign "See Amazing in All Children," the adorable muppet Abby Cadabby explains in one YouTube video, "Lots of kids have autism and that just means their brains work a little differently." Julia is not the first fictional media character with autism. But Michael Robb, Director of Research for Common Sense Media, an organization that rates and reviews media aimed at children, says Sesame Street's move is "pretty groundbreaking." "It can be difficult to start a conversation about children with disabilities. It's even harder when that difference isn't visible," he says. After looking through "We're Amazing, 1,2,3," Robb says the story could help children be more understanding of how Julia is different. "It's very real in terms of talking in simple language. It spells out these things in concrete ways that kids can understand. It shows ways she's just like other kids. It shows how making simple accommodations can help Julia." According to Dr. Jeanette Betancourt, Senior Vice President of U.S. Social Impact at Sesame Workshop, says Sesame Street producers are waiting to hear back from the autism community before introducing Julia to the show on TV. © 2015 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21557 - Posted: 10.24.2015

By Brook Borel and Spectrum In a lab in Sacramento, California, a wall of plastic boxes lined with corncob bedding holds around 800 mice. Even in this clean and bright room, the smell of so many mice concentrated in one place is overpowering — pungent, and familiar to anyone who has spent time with a pet hamster or gerbil. Most of the boxes hold four adult mice, which flit about, noses twitching as they stare out at the humans staring in. But in one of the boxes, a sleek white mouse is tucked in a corner suckling her litter of half a dozen or so squirmy, dark-furred pups. In most research labs, the fate of these pups would be determined by their sex. The males would spend their lives as test subjects. The females would either be kept for breeding or simply euthanized because they’re not ideal for experiments: They’re supposedly more difficult to work with and generate less consistent data than males do, and it costs too much to maintain both males and females, which must be housed separately. Or so the rationale has gone. But these little female pups are different. The lab where they live is run by Jill Silverman and Mu Yang, researchers at the University of California, Davis (UC Davis) MIND Institute. The two scientists study the behavior of about 15 autism mouse models, and they have always included both males and females in their work. When the pups get older, they will learn to paddle through water mazes or bury black marbles in their bedding, giving researchers insight into how their memory and behavior compare with that of typical mice. Finding the best animal behavioral models of autism is essential because behavior is at the heart of the disorder. In people, autism is diagnosed based on behavioral criteria: abnormal social interactions, difficulties with communication and repetitive actions. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21531 - Posted: 10.20.2015

By ANDREW SOLOMON INEXPLICABLE violence is the hardest kind to accept. The human wish to insert logic where there is none often drives bystanders to psychic violence of their own. This happened again last week, after it was reported that the shooter at Umpqua Community College in Oregon, Christopher Harper-Mercer, who killed nine people and injured several others, may have been autistic. Although there is no established connection between autism and murder, some eagerly leapt to causality and scapegoating. The killer’s “diagnosis” was based primarily on posts on Yahoo made over the last decade by his mother, Laurel Harper, in which she characterized both herself and her son as having Asperger’s syndrome — a category no longer in medical use that describes autistic people with advanced verbal skills. Mr. Harper-Mercer attended a school that caters to children with special needs, including autism. While Ms. Harper is not a doctor, her descriptions of her son across his childhood are consistent with the syndrome. A Facebook page called “Families Against Autistic Shooters” ranted about “the soulless, dead eyes of autistic children,” and characterized them as “cold, calculating killing machines with no regard for human life!” Its author announced: “What do all shooters over the last few years have in common? A lack of empathy and compassion due to Autism!” If Mr. Harper-Mercer were rumored to have been diabetic or afflicted with male-pattern baldness, no such “explanations” of his behavior would have surfaced. But despite a huge increase in awareness of autism among the public, those with the condition are often subject to this type of disparagement. This was evident in both the Facebook page and the response to it by Facebook’s management, who, despite the site’s anti-bullying policy, initially refused to remove it on grounds that it did not target named individuals. “Families Against Autistic Shooters” remained accessible until last Monday, by which time escalating media attention and a petition on Change.org with nearly 5,000 signatures embarrassed administrators into action. For the time it was viewable, the page stigmatized a population far more likely to be attacked than to attack, far less likely to receive justice when injured, and far more likely to be misunderstood. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory, Learning, and Development
Link ID: 21501 - Posted: 10.12.2015

By Somer Bishop Subtle, significant. In a nutshell, these two words capture the symptoms of many girls with autism. Like many in my field, I’ve seen this subtlety firsthand. One 6-year-old girl I met several years ago seemed, at first, to have good social skills. She responded appropriately when I introduced myself, complimented my outfit, and politely answered all of my questions. It was only when I saw her again a few days later that I understood her family’s concerns: She made nearly identical overtures, as if our interaction were part of a play she had rehearsed. I also met a teenage girl with autism who was highly intelligent. Because she could not relate to the other girls at her high school, she began interacting exclusively with boys, whose social behaviors she found easier to imitate. She even went through a period of wanting to become a boy, reasoning that she might have more success navigating the social world as a male. The past several years have seen an explosion of studies aimed at backing up these one-off observations about how autism presents differently in girls than in boys. This is a welcome development, as understanding the unique presentation of autism in girls will help us to better identify and treat the disorder. Consistently recognizing autism in girls can be challenging, however. This is not only because girls with autism are as diverse as any other group of individuals with the disorder but also because most autism screening and diagnostic tools were developed based primarily on observations of behaviors in boys. © 2015 The Slate Group LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21487 - Posted: 10.08.2015

By Elizabeth Landau Ask a physician what the hormone vasopressin is good for, and she will explain that it regulates the volume of water in your body and also affects blood pressure. But since the 1990s, vasopressin has been a hot topic in a very different field: social behavior. And recently it has emerged as a possible target for treating autism spectrum disorders (ASD), which are characterized by social, behavioral and communication impairments. The research is still in early stages, however, and has yielded more questions than answers. Given that one out of 68 children in the U.S. has an autism spectrum disorder, researchers are scrambling to figure out what in the brain might be related to the symptoms, and how they might design an effective treatment. Vasopressin may be a key player in the disorder. But scientists do not yet know whether too much or too little of the hormone—or perhaps some combination of both—is tied to autism. New clinical trials may yield insights. “I think that the work is exciting and important” says Suma Jacob, who leads an autism research laboratory at the University of Minnesota. “I also think we still have a lot more work to do in this field as a whole.” Previous research has shown that vasopressin, like the hormone oxytocin, is associated with parenting behavior and social bonding, including falling in love. In fact, the two hormones are structurally very similar, and there are receptors in the brain that interact with both of them. But high levels of vasopressin are also associated with anxiety and aggression. Intriguingly, some animal studies have found that higher levels of vasopressin increased aggression specifically in males. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 21402 - Posted: 09.12.2015

By Siri Carpenter Alex, age 10, bounds onto his bed to pose with his Aaron Rodgers poster, grinning as proudly as if he had recruited the Green Bay Packers’ quarterback himself. Continuing the tour of his suburban New York bedroom, he points out his Packers-themed alarm clock, his soccer trophy, his Boy Scout trophy, and then the big reveal: a homemade foam box in Packers green and gold. “Mmm, very nice,” I say. Alex grins—part shy, part sly—as he turns it around to show me the message on the back: “Jets stink.” Even though he seems to be an entirely ordinary boy, there’s something unusual about Alex: He once had autism, and now he does not. There was a time when Alex’s parents didn’t know if he would ever speak in full sentences, let alone joke around with a stranger. His autism, they suspected, might prevent any such future. Alex’s parents began to worry about him before he was even a year old. He wasn’t learning to sit, crawl, or stand as his fraternal twin brother was. Even more striking was how much less social he was than his brother. “Alex was an expressionless child,” says his mother, Amy. (Alex’s and Amy’s names have been changed to protect their privacy.) She remembers a friend trying in vain to get Alex to laugh—jumping up and down, gesturing wildly, making silly faces. “His brother would be in belly laughs, and Alex would be just glazed over,” Amy says. © 2015 The Slate Group LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21393 - Posted: 09.10.2015

In 1938, an Austrian pediatrician named Hans Asperger gave the first public talk on autism in history. Asperger was speaking to an audience of Nazis, and he feared that his patients — children who fell onto what we now call the autism spectrum — were in danger of being sent to Nazi extermination camps. As Asperger spoke, he highlighted his "most promising" patients, a notion that would stick with the autistic spectrum for decades to come. "That is where the idea of so-called high-functioning versus low-functioning autistic people comes from really — it comes from Asperger's attempt to save the lives of the children in his clinic," science writer Steve Silberman tells Fresh Air's Terry Gross. Silberman chronicles the history of autism and examines some of the myths surrounding our current understanding of the condition in his new book, NeuroTribes. Along the way, he revisits Asperger's calculated efforts to save his patients. Steve Silberman's articles have been published in Wired, The New Yorker, Nature and Salon. Silberman shies away from using the terms high-functioning and low-functioning, because "both of those terms can be off base," he says. But he praises Asperger's courage in speaking to the Nazis. "I would literally weep while I was writing that chapter," he says. NeuroTribes also explores how a 1987 expansion of the medical definition of autism (which was previously much narrower and led to less frequent diagnoses) contributed to the perception that there was an autism epidemic. © 2015 NPR

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21378 - Posted: 09.03.2015

By Roni Caryn Rabin For years experts have urged physicians to screen infants and toddlers for autism in order to begin treatment as early as possible. But now an influential panel of experts has concluded there is not enough evidence to recommend universal autism screening of young children. The findings, from a draft proposal by the U.S. Preventive Services Task Force published Monday, are already causing consternation among specialists who work with autistic children. “I was in a meeting when I read this, and I started feeling like I’d have chest pain,” said Dr. Susan E. Levy, a pediatrician who helped write the American Academy of Pediatrics guidelines urging universal screening of all babies, with standardized screening tools at both 18 and 24 months. “I would hate to see people stop screening.” Dr. David Grossman, a pediatrician and vice chairman of the U.S. Preventive Services Task Force, emphasized that the panel’s draft proposal was a call for more research and not intended to change practices. About half of all pediatricians routinely screen toddlers for autism. “This doesn’t mean ‘don’t screen.’ ” Dr. Grossman said. “It means there is not enough evidence to make a recommendation.” Dr. Grossman also noted that the panel’s conclusion applied only to routine screening of healthy children without symptoms. A child displaying symptoms associated with autism should always be evaluated, he said. “If a parent comes in and says, ‘My child isn’t looking at me,’ that’s not a screening,” Dr. Grossman said. “You hear that as a doctor and you say, ‘That needs to be looked at,’ and you embark on a series of tests.” Despite those reassurances, autism experts worry that the panel’s lack of support for early autism screening could undermine efforts to identify and treat children as early as possible. The task force is an independent panel of experts in prevention and primary care appointed by the federal Department of Health and Human Services. The task force wields enormous influence in the medical community. In 2009, the panel issued controversial screening guidelines for breast cancer, stating that routine mammograms should start at 50 rather than 40. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21262 - Posted: 08.04.2015