7 Things People With Generalized Anxiety Disorder Wish Others Would Stop Saying

When Robin Williams Comforted Me in the Airport After My Husband’s Suicide

Target to Host Quiet Holiday Shopping Event for Those on the Autism Spectrum

It’s Never ‘Just a Migraine’

i can't keep calm because i have anxiety memeGeneralized anxiety disorder (GAD) is characterized by excessive, persistent and unrealistic worry, and caused by genetic factors, brain chemistry and personality. In fact, 40 million people in the United States are affected by an anxiety disorder, according to the Anxiety and Depression Association of America. As someone with GAD, here are 7 things I’d like to ask you to stop saying.

1. “Stop thinking about it.” Don’t you think if it was that easy I would not think about it? It maybe easy for you, but as a person with GAD I have to practice the coping strategies I’ve learned in therapy. And sometimes I can’t even do that. So telling me to not worry simply does not cut it.

Instead, try asking me to go for a walk or if there is anything you can do to help me process what is happening.

2. “Everyone feels anxious.” Yes, everyone feels anxious, and it is completely natural. Anxiety actually pushes us to get things done, but when your anxiety stops you from being able to function, guess what? That’s a problem. So please do not compare GADers (yes, I created this word) with non-GADers (this word too).

Instead, acknowledge what I’m going through. Say, “I see this is really hard for you. Would you like to talk about it?”

3. “I’m stressed too.” Not to discredit your stress, but you are certainly discrediting ours. What you do not understand is that we have a hard time controlling our thoughts, and whether you realize it or not, no matter how small it may seem to you, our anxiety tends to maximize everything.

Instead, try offering some words of encouragement.

4. “I know how you feel.” Unless you have GAD you do not know how I feel, so please stop saying that you do.

Instead, say, “I don’t understand exactly how you feel, but would you be willing to help me understand?”

5. “You need to calm down.” When people suffer from GAD, there are times when his/her anxiety is through the roof and it takes me time to calm down. It is always a three-ring circus going on in our heads. That advice is like telling someone who is sick to stop coughing. So no, we cannot calm down right now.

Instead say, “Is there anything I can do to help you?”

6. “You are doing too much.” (Translation: “You are being dramatic.”) Thank you for your words of comfort. We know our thoughts can be irrational at times, but that is how our brain works. Can you imagine 1,000 tabs on your computer are opened, and you cannot stop new tabs from opening? Well, that is how we feel. Just because our disorder is invisible does not mean it is not real.

Instead, ask me about what methods I use to ease anxiety (like breathing methods and yoga), and remind me what’s worked in the past.

7. “You worry too much.” Yes, we worry too much and we know that, but if you have not figured it out by now, we cannot control it. Telling us we worry too much does not help. We were already worrying about 50 things prior to this unnecessary statement, and now we are worrying about worrying.

Instead, say, “It’s OK to feel this way. I know your anxiety can be difficult, but I’m here for you.”  

New Understanding and Hope for Children on the Autism Spectrum: Based in Brain and Movement Sciences


Three Things You Can Do to Help Your Child with ASD

A new government survey of parents (November 2015) suggests that 1 in 45 children, ages 3 through 17, have been diagnosed with autism spectrum disorder(ASD). The official government estimate by the Centers for Disease Control and Prevention (CDC) is 1 in 68 American children are diagnosed with autism.

Autism spectrum disorder (ASD) is most commonly thought of as a brain disorder in the areas of cognition, language, communication, and social behaviors. Autism Speaks defines ASD as, “a group of complex disorders of brain development. These disorders are characterized, in varying degrees, by difficulties in social interaction, verbal and nonverbal communication and repetitive behaviors.”

Web MD defines it as, “a brain disorder that often makes it hard to communicate with and relate to others.”

Are these children doomed? Absolutely not! A variety of behavioral therapies, nutritional changes, and other interventions, can help the child on the autism spectrum make great strides. There are numerous anecdotal stories to that effect. Research is increasing our understanding of how the brain grows and learns, creating breakthrough possibilities for helping the child on the autism spectrum.

Symptoms such as compulsive and repetitive behaviors, lack of social connection, cognitive and learning challenges, and motor coordination challenges can be greatly reduced, and at times eliminated, by helping the brain do its job better and become the brilliant learning brain it is built to be.

How can you, the parent, teacher, or therapist help the brain of the child with ASD do its job better?

STEP #1: The first step is to stop trying to “fix” the child, to stop trying to have the child do what he or she cannot do. If he could, he would; if she could, she would. Drilling, lots of repetitions, and constant prompting may be sincere and well-meaning attempts that often do help the child with ASD improve some. However, they also often create great limitations in how much progress the child will make in the long run. Such repetitions and drilling deny the brain of what it needs most in order to learn and improve — new information, lots and lots of new information.

Moving away from trying to fix the child is not simple or easy to do. Trying to make the child do what other children can do when not challenged, is what most of us know to do. If we stop trying to “fix” the problems in our child, we may feel that we are neglecting him or her.

I suggest you take a day or two and simply observe the moments and times when you are in the “fixing” mode with your child, be it around academic learning, behavioral issues, or anything else. Don’t rush to try and change what you normally do. Give yourself some time to become aware of your own feelings and actions that are associated with trying to help your child.

STEP #2: Look to connect with your child instead of trying to fix her or him.You may be asking: “How can I connect with my child when one of the main challenges for the child with ASD is connecting with others?”

Allow me here a brief, yet important theoretical detour. The brain is an information system, i.e., it is an incredibly large, self-organizing, dynamic system that has a very important job: to put order in the disorder and to make sense out of the nonsense. The brain needs to make sense out of the constant barrage of external and internal stimuli coming at us. This is what allows us to perceive, feel, move, think, organize action, and interact with others successfully — that which is so hard for the child with ASD to do.


What is the source of information for the brain? Most people would say “stimulation,” and they’ll be right. However, stimulation alone is not enough. It is the perception of differences within the flow of stimulation, by the person exposed to the stimulation, that is the source of information. [1]

The more the brain can perceive differences, and the finer these perceived differences are, such as in sound (in pitch, intensity, quality, rhythm), sight, sensations coming from our muscles and joints, and the rest of our senses, the more information it has with which to create new connections in the brain that lead to the creation of new patterns, i.e., successful learning.

The brain of the child with ASD is challenged in its ability to perceive differences, (what is also called signal to noise ratio). The clearer the signal is relative to the background “noise” in the brain, the more the child is able to perceive a difference).[2]

When differences are not clearly perceived, the world is like a soup — it does not make sense.

When we create conditions that help the child’s brain perceive differences better, the brain gets new information with which the child can then make sense of herself, of her experiences, and of the world around her. When you do this, you are connecting with your child. She begins to get out of her fog and can begin to connect more with you.

The Story of Sammy

Sammy, a 5-year-old boy on the autism spectrum, was still wetting his pants and had to wear pull-up diapers. His parents, in collaboration with his teachers, tried everything to get Sammy potty trained, to no avail. Sammy, over a two-year period of working with us, had made great strides. Given his high level of functioning, I wondered why he still had this problem.

It occurred to me that aside from the possibility that Sammy didn’t want to be bothered going to the bathroom while he was busy doing other things, that perhaps his brain was not perceiving the difference between wet and dry clearly enough.

So the next session, I took two wash cloths, one that was wet and the other dry. I told Sammy to tell me, without looking, whether I was touching him with the wet cloth, or the dry one. I first touched him on the back of his lower legs. He misidentified both the wet and the dry.

At that point, I moved to his face where there is a lot more innervation between the face and the brain, i.e., a lot more potential for perception of differences. There, Sammy identified both the wet and the dry sensations accurately.

I then did the same on his legs, on his back, then the back of his pelvis, and the top of his buttocks. Not only did Sammy identify all correctly, he also got faster and faster and more refined in his identifications.

Sammy has not wet his pants since this session. Watch the video of Sammy here.

STEP #3: Intensify differences. Do not assume that your child sees, feels, or hears what you do. It is very important to realize that when you perceive a difference, for example, between a straight line and a curvy line, or between a loud sound and a softer sound, or between a rough movement and a gentle movement, that your child may not, even when it’s so obvious to you.

Actually when your child is having a hard time grasping information, doing something, or when your child is failing, I suggest that you always assume that he is not perceiving simple, obvious (to you) differences that are necessary for the brain to succeed.

Look for any opportunity, both in daily life, and in more formal teaching/learning situations, to increase the differences. For example, if you want your child to be more gentle when manipulating objects, have the child touch a safe object a lot harder, then even harder, until he feels that it is harder, and then go back to gentler.

It’s best to begin introducing differences to your child in areas where she has the least difficulty. (Remember, you are on a learning curve here too.) When your child has a hard time understanding or doing something, look for any aspect in that situation where you can amplify differences. Don’t worry whether “it’s working” or not. Just create as much opportunity for your child’s brain to experience perceiving differences, and thus get better at it.

The Technology That’s Giving Students With Autism a Greater Voice

Last year, Hanna Rosin, a well-known journalist for the Atlantic, wrote an articleabout her son’s Asperger’s diagnosis. He lived with this label for only four months, at which point the disorder was expunged from the DSM V. Now, her son is said to be on the “autism spectrum,” along with one out of every 68 children in the U.S.

Autism spectrum disorder (ASD), a newly popularized term which encompasses a breadth of social impairments, repetitive behaviors and communication “deficits,” reflects this different thinking. The flexibility of the spectrum means that it can be applied to children on either end, from highly functioning individuals to those who can’t speak or communicate even their most basic wishes.

According to Rosin, “the newly explicit spectrum thinking gives at least the illusion that there are no fixed boundaries at all. Taken to its logical extreme, the perspective implies an unbroken continuum among minds that extends from autism all the way into the realm of the normal.”

But with this flexibility comes ambiguity — especially in the classroom. The majority of teachers are not equipped to give students on various points across the autism spectrum the unique attention they require. For help, they have been turning to assistive technology.

Many children with autism learn well from visual media. Scene Speak, reviewed above, allows the user to make their own visual and audio books that can reflect real-life descriptions and relationships.

“Teachers are becoming more comfortable with technology,” Jules Csillag, a speech-language pathologist in New York City who focuses on technology and special education, told The Huffington Post. “More and more, it is allowing them to customize a curriculum for students [with ASD].”

According to Csillag, there are two main types of assistive technology for students with ASD: Teaching technologies and communication technologies. While both tools are exceptionally important, a student’s ability to communicate is tantamount to his or her success. “The tricky thing about classrooms is that there are so many unspoken rules,” she said. “I think one of the difficulties, even for high-functioning children, is knowing what the expectations are.”

Kathryn deBros, a special educator in Vermont working with children with behavior disorders, has voiced similar sentiments. “A huge part of going to school is learning how to navigate social situations,” she said. “[Students with ASD] are totally lost without a roadmap. Technology has been huge in allowing them to bridge that gap between them and the other kids.”


For students with ASD who are especially low-functioning communicators, Csillag recommends a group of apps called Visual Scene Displays — a type of augmentative and alternative communication (AAC) — that give detailed context to common situations. She cited an app called Scene Speak, as well as more dynamic ones likeTouchChat, Look2Learn and Tobii Sono Flex. The latter programs turn symbols into speech, allowing less-verbal children a better way to communicate.

As a more specialized classroom educator, deBros focuses on the tools geared around emotion for classroom support, such as Empatico, and organizational support, likeBoardmaker. “Some of these kids are lost in social situations,” she explained. “But with an iPad in front of them, it really just clicks.”

Assistive technology is helping those with ASD outside the classroom, as well. “Part of the ASD difficulty is that society is not built in a way that is easy [for the child] to be in,” Csillag says. She further explains that even a grocery store or movie theater can be filled with distractions and triggers that will continue to elicit autistic behaviors, regardless of how much improvement the child can make in his or her own communications. However, with a better understanding of what autism is, and newer tools that help those with ASD communicate with others, the societal factor is becoming less of an issue while the unique strengths of those with autism are being spotlighted.

The above tutorial explains how to make a communication board on Boardmaker, a design program that allows students with autism to communicate through symbols.

Despite the fact that employment rates for those with ASD have historically been abysmally low, companies like Microsoft are going out of their way to create work environments more friendly to people with autism. Mary Ellen Smith, a Microsoft VP whose son has ASD, announced the software company’s new hiring program for people with autism in a recent blog post. “People with autism bring strengths that we need at Microsoft,” she said, adding that “some have amazing ability to retain information, think at a level of detail and depth, or excel in math or code.”

Technology isn’t just helping those with autism learn; it is actually allowing them to thrive, and on some level, is becoming a more seamless component of their social selves. deBros compared the evolution of assistive technology to wearable devices: “In the future, technology will be much more integrated with the person,” she predicted. “It will allow them to function without the burden of going back and forth with the technology and the world around them.”

Love hormone ‘helps autistic brain’

Child with autism

The “love hormone” oxytocin alters the brain activity of children with autism and makes them more social, according to US researchers.

The role of the hormone in helping children with autism has been debated, with studies showing conflicting data.

Brain scans, reported in the Proceedings of the National Academy of Sciences, hint that there is an effect.

The National Autistic Society said research on oxytocin as a treatment was still in its infancy.

What is autism?

  • Autism and Asperger’s syndrome are part of a range of disorders that can cause difficulties with communication and social skills
  • The conditions can lead to isolation and emotional problems for those living with them
  • Conditions can vary from very mild, where the person can function as well as anyone else, to so severe they cannot take part in normal society
  • The conditions are collectively known as autistic spectrum disorders and affect more than 580,000 people in the UK

Oxytocin is naturally produced by the body, triggers labour and is involved in mother and baby bonding.

Seventeen children with autism, aged between eight and 16, were given two nasal spray – one containing oxytocin, the other no drugs at all.

After taking each one, the impact on brain activity was recorded in a scanner while the children were shown “social” pictures of human faces or “non-social” pictures of cars.

The parts of the brain normally associated with social situations appeared more active after the children had been given oxytocin.


One of the researchers, Prof Kevin Pelphrey, told the BBC: “We are very excited by the findings, all 17 showed a response, although the response was variable.

“There’s still lots of questions about oxytocin, but this suggests it enhances social brain functions and decreases non-social functions – helping kids to focus on socially relevant information.”

Larger trials are taking place to see what the side-effects and benefits of oxytocin might be in children with autism.

Exactly how the drug should be used is still up for debate, with some suggestions that it would be best used as an aid during current behavioural therapy rather than as a daily medication.

Prof Pelphrey said some parents were giving the drug to their children without medical advice and this was a “terrible idea”.

“It might have no effect or it might cause damage,” he said.

However, he added: “The most exciting finding is not oxytocin, but that you can show changes in the brain by a compound.

“It changes how we think of autism and how treatable it might be.”

Carol Povey, director of the National Autistic Society’s centre for autism, said: “Research investigating the impact oxytocin can have on people with autism is still in its very early stages.

“While the findings of this particular study are interesting, no hard and fast conclusions should be drawn.

“Autism is a very complex disability and can present a variety of challenges that extend beyond social difficulties.

“It’s crucial that those living with the condition have all their needs assessed so that they can access the appropriate support.”

Autism detectable ‘in first months’

An early indication of autism can be identified in babies under six months old, a study suggests.

US researchers, writing in Nature, analysed how infants looked at faces from birth to the age of three.

They found children later diagnosed with autism initially developed normally but showed diminished eye contact – a hallmark of autism – between two and six months of age.

A UK expert said the findings raise hope for early interventions.

In the study, researchers led by Emory University School of Medicine in Atlanta used eye-tracking technology to measure the way babies looked at and responded to social clues.

“Start Quote

These early markers are extremely important for us to identify – the earlier we can diagnose a child who has one of these disorders – such as autism – the earlier we can provide intervention and development”

Dr Deborah Riby Durham University

They found infants later diagnosed with autism had shown a steady decline in attention to the eyes of other people from the age of two months onwards, when watching videos of natural human interactions.

Lead researcher Dr Warren Jones told BBC News: “It tells us for the first time that it’s possible to detect some signs of autism in the first months of life.

“These are the earliest signs of autism that we’ve ever observed.”

The study, in collaboration with the Marcus Autism Center and Children’s Healthcare of Atlanta, followed 59 infants who had a high risk of autism because they had siblings with the life-long condition, and 51 infants at low risk.

Dr Jones and colleague Dr Ami Klin followed them to the age of three, when the children were formally assessed for autism.

Thirteen of the children were diagnosed with autism spectrum disorders – a range of disorders that includes autism and Asperger’s syndrome – 11 boys and two girls.

The researchers then went back to look at the eye-tracking data, and what they found was surprising.

“In infants with autism, eye contact is declining already in the first six months of life,” said Dr Jones.

But he added this could be seen only with sophisticated technology and would not be visible to parents.

“It’s not something that parents would be able to see by themselves at all. If parents have concerns they should talk to their paediatrician.”

Dr Deborah Riby, of the department of psychology at Durham University, said the study provided an insight into the timing of atypical social attention in children who might go on to develop autism.

Autism spectrum disorders

  • Autism and Asperger’s syndrome are part of a range of related developmental disorders known as autistic spectrum disorders (ASD)
  • They begin in childhood and last through adulthood.
  • ASD can cause a wide range of symptoms, which are grouped into three categories including problems with social interaction, impaired communication skills and unusual patterns of thought and behaviour

Source: NHS Choices

“These early markers are extremely important for us to identify – the earlier we can diagnose a child who has one of these disorders – such as autism – the earlier we can provide intervention and development,” she said.

Kay Hinton/Emory University

Caroline Hattersley, head of information, advice and advocacy at the National Autistic Society, said the research was “based on a very small sample and needs to be replicated on a far larger scale before any concrete conclusions can be drawn”.

“Autism is a very complex condition,” she said.

“No two people with autism are the same, and so a holistic approach to diagnosis is required that takes into account all aspects of an individual’s behaviour. A more comprehensive approach allows all of a person’s support needs to be identified.

“It’s vital that everyone with autism can access a diagnosis, as it can be key to unlocking the right support which can enable people with the condition to reach their full potential.”

Social Symptoms In Autistic Children Could Be Caused By Hyper-connected Neurons.

The brains of children with autism show more connections than the brains of typically developing children do. What’s more, the brains of individuals with the most severe social symptoms are also the most hyper-connected. The findings reported in two independent studies published in the Cell Press journal Cell Reports on November 7th are challenge the prevailing notion in the field that autistic brains are lacking in neural connections.

The findings could lead to new treatment strategies and new ways to detect autism early, the researchers say. Autism spectrum disorder is a neurodevelopmental condition affecting nearly 1 in 88 children.

“Our study addresses one of the hottest open questions in autism research,” said Kaustubh Supekar of Stanford University School of Medicine of his and his colleague Vinod Menon’s study aimed at characterizing whole-brain connectivity in children. “Using one of the largest and most heterogeneous pediatric functional neuroimaging datasets to date, we demonstrate that the brains of children with autism are hyper-connected in ways that are related to the severity of social impairment exhibited by these children.”

In the second Cell Reports study, Ralph-Axel Müller and colleagues at San Diego State University focused specifically on neighboring brain regions to find an atypical increase in connections in adolescents with a diagnosis of autism spectrum disorder. That over-connection, which his team observed particularly in the regions of the brain that control vision, was also linked to symptom severity.

“Our findings support the special status of the visual system in children with heavier symptom load,” Müller said, noting that all of the participants in his study were considered “high-functioning” with IQs above 70. He says measures of local connectivity in the cortex might be used as an aid to diagnosis, which today is based purely on behavioral criteria.

For Supekar and Menon, these new views of the autistic brain raise the intriguing possibility that epilepsy drugs might be used to treat autism.

“Our findings suggest that the imbalance of excitation and inhibition in the local brain circuits could engender cognitive and behavioral deficits observed in autism,” Menon said. That imbalance is a hallmark of epilepsy as well, which might explain why children with autism so often suffer with epilepsy too.

“Drawing from these observations, it might not be too far fetched to speculate that the existing drugs used to treat epilepsy may be potentially useful in treating autism,” Supekar said.

UNC child neurologist finds potential route to better treatments for Fragile X, autism.

When you experience something, neurons in the brain send chemical signals called neurotransmitters across synapses to receptors on other neurons. How well that process unfolds determines how you comprehend the experience and what behaviors might follow. In people with Fragile X syndrome, a third of whom are eventually diagnosed with Autism Spectrum Disorder, that process is severely hindered, leading to intellectual impairments and abnormal behaviors.

In a study published in the online journal PLoS One, a team of UNC School of Medicine researchers led by pharmacologist C.J. Malanga, MD, PhD, describes a major reason why current medications only moderately alleviate Fragile X symptoms. Using mouse models, Malanga discovered that three specific drugs affect three different kinds of neurotransmitter receptors that all seem to play roles in Fragile X. As a result, current Fragile X drugs have limited benefit because most of them only affect one receptor.

“There likely won’t be one magic bullet that really helps people with Fragile X,” said Malanga, an associate professor in the Department of Neurology. “It’s going to take therapies acting through different receptors to improve their behavioral symptoms and intellectual outcomes.”

Nearly one million people in the United States have Fragile X Syndrome, which is the result of a single mutated gene called FMR1. In people without Fragile X, the gene produces a protein that helps maintain the proper strength of synaptic communication between neurons. In people with Fragile X, FMR1 doesn’t produce the protein, the synaptic connection weakens, and there’s a decrease in synaptic input, leading to mild to severe learning disabilities and behavioral issues, such as hyperactivity, anxiety, and sensitivity to sensory stimulation, especially touch and noise.

More than two decades ago, researchers discovered that – in people with mental and behavior problems – a receptor called mGluR5 could not properly regulate the effect of the neurotransmitter, glutamate. Since then, pharmaceutical companies have been trying to develop drugs that target glutamate receptors. “It’s been a challenging goal,” Malanga said. “No one so far has made it work very well, and kids with Fragile X have been illustrative of this.”

But there are other receptors that regulate other neurotransmitters in similar ways to mGluR5. And there are drugs already available for human use that act on those receptors. So Malanga’s team checked how those drugs might affect mice in which the Fragile X gene has been knocked out.

By electrically stimulating specific brain circuits, Malanga’s team first learned how the mice perceived reward. The mice learned very quickly that if they press a lever, they get rewarded via a mild electrical stimulation. Then his team provided a drug molecule that acts on the same reward circuitry to see how the drugs affect the response patterns and other behaviors in the mice.

His team studied one drug that blocked dopamine receptors, another drug that blocked mGluR5 receptors, and another drug that blocked mAChR1, or M1, receptors. Three different types of neurotransmitters – dopamine, glutamate, and acetylcholine – act on those receptors. And there were big differences in how sensitive the mice were to each drug.

“Turns out, based on our study and a previous study we did with my UNC colleague Ben Philpot, that Fragile X mice and Angelman Syndrome mice are very different,” Malanga said. “And how the same pharmaceuticals act in these mouse models of Autism Spectrum Disorder is very different.”

Malanga’s finding suggests that not all people with Fragile X share the same biological hurdles. The same is likely true, he said, for people with other autism-related disorders, such as Rett syndrome and Angelman syndrome.

“Fragile X kids likely have very different sensitivities to prescribed drugs than do other kids with different biological causes of autism,” Malanga said.

Genetic Test for Autism Refuted.

A team of Australian scientists claimed to have developed a genetic test that predicts a person’s risk of developing autism spectrum disorder (ASD) with 72 percent accuracy. Writing in Molecular Psychiatry, the team led by Stan Skafidis and Carlos Pantelis from the University of Melbourne said that their panel of 237 genetic markers could “correctly classify ASD from non-ASD individuals” and “may provide a tool for screening at birth or during infancy to provide an index of at-risk status.”

But a new study, led by Benjamin Neale from Massachusetts General Hospital, suggests that those claims were overblown. Neale’s team replicated the Australian group’s research in a larger sample, and found that the proposed panel of markers did not accurately predict ASDs.

“The claims in the original manuscript were quite bold. If they were true, it really would have been quite a major advance for the field, with serious ramifications for patients and other risk populations,” said Neale. “I think it’s important to ensure that this kind of work is of the highest quality.”

“This is a convincing refutation that calls into question the original results on specific technical grounds, rather than simply a non-replication that leaves a puzzling discrepancy between the two studies,” said Leonid Kruglyak, a geneticist from the University of California, Los Angeles, who was not involved in either study.

In 2012, Skafidis’s team compared the genes of 732 European people with ASD from the Autism Genetic Resource Exchange database, with those of 123 neurotypical people from a different cohort. They searched for single nucleotide polymorphisms (SNPs) that were linked to ASD, especially those in genes with roles in relevant cellular pathways.

They eventually settled on 237 SNPs in 146 genes, which they used to create a classifier for predicting ASD risk. When they tested the classifier on 243 cases and 42 controls from the same databases, it correctly predicted ASD with an accuracy of 85.6 percent.

The team then tested the classifier on an independent group of people—525 with ASD taken from the Simons Foundation Autism Research Initiative and 2,620 controls from the Wellcome Trust Birth Cohort. It identified the ASD cases with an accuracy of 71.7 percent.

But to other geneticists, these results seemed too good to be true. They implied that this small set of SNPs can explain around 11 percent of the variation in ASD risk—an unprecedented figure for any psychiatric condition. If the set truly had such strong effects, genome-wide association studies (GWAS) should have identified those SNPs by now—and they had not. It will likely take a sample of hundreds of thousands of people to find SNPs with such predictive power, as has been the case for other traits like height. “The magnitude of the study you need is dramatically larger than what was presented,” said Neale.

Neale wrote to Skafidis’s team asking for the full list of 237 SNPs, but did not receive it. (Skafidis told The Scientist that they offered the code that they used to generate their results, which should have been even better.) As such, they focused on the 30 most important SNPs, which were detailed in the published paper.

By comparing 5,417 cases and 5,417 controls from the Psychiatric Genomics Consortium, Neale’s team found that none of the 30 SNPs were significantly associated with ASD risk. The researchers also combined the SNPs into a classifier, using methods detailed in the original paper, and tested it on 4,623 cases and 4,623 controls from the same group. Again, the set failed to predict ASDs any better than chance. Finally, they also showed that the cellular pathways which the Australian team identified are not significantly associated with ASDs. The team’s results were published as a letter to the editor on 22 October, also in Molecular Psychiatry.

Several factors could explain the differences between the two studies. The Melbourne team initially tested the accuracy of their risk classifier on the same group of people whom they used to identify their SNP set. This is bad practice. “To appropriately assess the accuracy of a classifier, the sample which is used to develop it must be fully distinct from the sample on which it is tested,” said Kruglyak.

The Australian researchers also drew their cases and controls from separate populations with subtly different ethnic compositions. The SNPs they identified could have reflected reflect random ancestral differences between the two groups, rather than meaningful differences in ASD risk. Daniel Geschwind from the University of California, Los Angeles, made the same argument in a letter regarding Skafidis’s paper, which was published in the same journal this April.

Kruglyak added a third possible explanation: “batch effects, in which cases and controls are genotyped at different times and on different technology platforms,” he proposed. This problem also plagued a similar recently-retracted paper, which identified a panel of SNPs that could supposedly predict longevity.

But Skafidis said that Neale’s team may have come to different conclusions because the group did not use the full set of SNPs, nor the code that was provided. His team has submitted a response to the new study, which is in revision with Molecular Psychiatry (and does list the full set of 237 SNPs).

Meanwhile, Neale emphasized that other research into the genetics of autism are yielding stronger results. Several studies have identified loss-of-function mutations, and differences in the number of copies of certain genes, that are linked to ASD risk. Promising GWAS results have been presented at conferences and are making their way into published papers. “Autism genetics shouldn’t be tarnished by science that hasn’t been robustly proven,” he said. “There are successes beginning to emerge, and that’s really exciting and important.”

Psychotropics Still Commonly Prescribed for Autism.

Children with autism spectrum disorder (ASD) are still commonly prescribed psychotropic medications alone and in combinations despite “minimal evidence” of their effectiveness, new research suggests.

A retrospective study of more than 33,000 children with ASD showed that 64% had been prescribed at least 1 psychotropic. In addition, 35% had been prescribed 2 or more classes of psychotropics concurrently, and 15% had been prescribed 3 or more classes.

“Our results indicate the need to develop standards of care around the prescription of psychotropic medications to children with ASD,” write Donna Spencer, PhD, from OptimumInsight, Life Sciences, in Eden Prairie, Minnesota, and colleagues.

They note that the study participants who had comorbidities such as bipolar disorder or attention-deficit disorders, who were older, or who had visited a psychiatrist were significantly more likely to use psychotropics.

New standards of care should be based on “a coordinated, multidisciplinary approach to improving the health and quality of life of children with ASD and their families,” write the investigators.

The study was published online October 21 in Pediatrics.

Few Treatment Options

As reported at the time by Medscape Medical News, a systematic review of 33 randomized controlled trials, which was published in 2011, showed that only 3 psychotropics (all of which were antipsychotics) “have established evidence” in treating symptoms of ASD.

These included aripiprazole and risperidone for irritability and hyperactivity, aripiprazole for stereotypy, and haloperidol for negative behavioral symptoms. Promising evidence of benefit was shown for methylphenidate, and preliminary evidence was shown for 5 other agents, including naltrexone and atomoxetine.

However, “the humbling or sobering news is that we still have no medicines that treat the core features of autism — social/interaction and language impairments and repetitive behaviors,” said Matthew Siegel, MD, medical director of the developmental disorders program at Spring Harbor Hospital, Maine Medical Center, in Westbrook, at the time.

Yet other studies have shown “increasing rates of psychotropic use and [polypharmacy] among children overall” as well as in children with ASD, note the current investigators.

Because there is a wide variance in use estimates of psychotropic medications and because many reports are based on a period of 1 year or less, are based on parent reports, and include small sample sizes, the researches sought to conduct a study that answered these concerns.

They assessed data from medical and pharmacy claims for 33,565 insured children and adolescents younger than 21 years with ASD (82% boys; 60% between the ages of 6 and 10 years, 22% between the ages of 11 and 17 years, 17% between the ages of 0 and 1 year).

Claims for all participants had been made at least 6 months prior to baseline, and all had at least 6 months of continuous care between January 2001 and December 2009.

For this study, the psychotropic medication classes included antidepressants, both stimulants and nonstimulants for treating attention-deficit disorder (ADD), antipsychotics, anxiolytics, lithium, anticholinergics, and anticonvulsants/antiepileptics.

“Polypharmacy was defined as at least 1 episode of multiclass polypharmacy,” explain the investigators, noting that “an episode of multiclass polypharmacy” denoted prescriptions that overlapped 2 or more classes for at least 30 days.

Increasing Use

Results showed that 63.56% of the participants had any psychotropic use, whereas 34.36% showed evidence of multiclass polypharmacy.

Psychotropic or polypharmacy use increased with the age of the children. A total of 34% of the 0- to 1-year age group had use of any psychotropic, and 10% had polypharmacy use.

These numbers jumped dramatically to 64% and 32%, respectively, for those in the 2- to 10-year age group; to 84% and 57% for those in the 11- to 17-year age group; and to 87% and 62% for those in the 18- to 20-year age group.

Of those in the polypharmacy subgroup, total episodes of multiclass polypharmacy averaged 5.63 per child. The average maximum number of medications per episode was 2.6, and the average maximum number of classes per episode was 3.3.

In addition, 10.4% of the entire study group had 3-class polypharmacy, and 4.5 had polypharmacy with 4 or more classes.

“Common class combinations were antidepressants and ADD medications (38% of subjects), antipsychotics and ADD medications (28%), antipsychotics and antidepressants (20%), and antipsychotic, antidepressant, and ADD medications (18%),” report the investigators.

The average total days of all episodes of polypharmacy was 525. The median was 346 days.

Interestingly, use of either psychotropics or polypharmacy was lower in the participants from the northeast and western regions of the United States and highest in the southern regions.

This raises questions “about the availability of nonpharmacologic, behaviorally based services and treatments in the south, where other health outcomes and health care services have been found to be poorer than in other parts of the country,” note the researchers.

The strongest predictor of psychotropic and polypharmacy use was having a comorbid condition, especially seizures, bipolar disorder, and ADD. Household income was not found be a significant factor.

Overall, the findings emphasize the need for more research of psychotropics in kids with ASD “to assess the value of these medications when weighed against their potential for harm,” conclude the investigators.

Source: Medscape.com



Study shows maths experts are ‘made, not born’

A new study of the brain of a maths supremo supports Darwin’s belief that intellectual excellence is largely due to “zeal and hard work” rather than inherent ability.

University of Sussex took fMRI scans of champion ‘mental calculatorYusnier Viera during arithmetical tasks that were either familiar or unfamiliar to him and found that his did not behave in an extraordinary or unusual way.

The paper, published this week (23 September 2013) in PloS One, provides scientific evidence that some calculation abilities are a matter of practice. Co-author Dr Natasha Sigala says: “This is a message of hope for all of us. Experts are made, not born.”

Cuban-born Yusnier holds world records for being able to name the days of the week for any dates of the past 400 years, giving his answer in less than a second. This is the kind of ability sometimes found in those with autism, although Yusnier is not on the autistic spectrum. Unlike those with autism or the related condition Asperger’s, he is able to explain exactly how he calculates his answers – and even teaches his system and has written books on the subject.

The study, carried out at the Clinical Imaging Sciences Centre on the University of Sussex campus, suggests that Yusnier has honed his ability to create short cuts to his answers by storing information in the middle part of the brain specialised for long-term (the and surrounding cortex). This type of memory helps us carry out tasks in our area of expertise with speed and efficiency.

Although the left side of his brain was activated during – which is normal for all brains – the scientists observed that something slightly different happened when Yusnier was presented with unfamiliar problems.

The scans showed marked connectivity of the anterior (prefrontal cortex), which are involved in decision making, during the unfamiliar calculations. This supports Yusnier’s report that he was building in an extra step to his mental processes to turn an unfamiliar problem into a familiar one. His answers to the unfamiliar questions had an 80 per cent degree of accuracy (compared with more than 90 per cent for familiar questions) and his responses were slightly slower.


Dr Sigala explains: “Although this kind of ability is seen among some people with autism, it is much rarer in those not on that spectrum. Brain scans of those with autism tend to show a variety of activity patterns, and autistic people are not able to explain how they reach their answer.

“With Yusnier, however, it is clear that his expertise is a result of long-term practice – and motivation.”

She adds: “It was beyond the scope of our paper to discuss the debate on deliberate practice vs. innate ability. But our study does not provide evidence for specific innate ability for mental calculations. As put by Charles Darwin to Francis Galton: ‘ […] I have always maintained that, excepting fools, men did not differ much in intellect, only in zeal and hard work; I still think this an eminently important difference.'”