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Thursday, October 31, 2013

Children Quick To Judge Peers With Autism, Study Finds


By Michelle Diament
October 23, 2013

Typically-developing kids often see their peers with autism as less friendly and less trustworthy, new research suggests, and they’re making these assessments quickly based on appearance alone.

Researchers found that typically-developing children formed their impressions of those with autism in as little as 30 seconds.

The findings come from a study of 44 typically-developing 11-year-olds who viewed a series of short, silent videos featuring other children their age who were filmed while responding to simple questions from an interviewer. They were not told that some of the kids in the videos had autism.

Nonetheless, when the children participating in the study were asked to rate the kids in the videos, they indicated that those with autism were not as trustworthy as the typically-developing children in the films.

What’s more, study participants were less likely to say that they wanted to play with or be friends with the video subjects on the spectrum, according to the findings published this month in the journal Autism.

“Children with autism spend many years learning about facial expressivity, but our research shows that by the age of 11, their slower development in this area is already marking them out amongst their typically-developing peers,” said Steven Stagg of Anglia Ruskin University in England, who led the study.

“It is therefore important that schools work with typically-developing children to educate them about autism, in order to break through the negative impressions that can be formed through a moment’s contact.”

National Network To Focus On Severe Autism


By Michelle Diament
October 18, 2013

A first-of-its-kind research network is forming with an eye toward better understanding autism by studying kids who are most severely affected by the developmental disorder.

Six inpatient psychiatric facilities across the country that specialize in treating individuals with autism and other developmental disorders are coming together to form the new initiative known as the Autism and Developmental Disorders Inpatient Research Collaborative.

While significant resources have been devoted to autism research in recent years, those behind the new effort say large studies have generally failed to include individuals at the severe end of the spectrum.

“There is so much that remains unknown about autism … and those most severely affected by the disorder both deserve our attention and are likely to provide us clues for understanding the core features of autism,” said Matthew Siegel of Spring Harbor Hospital and the Maine Medical Center Research Institute, who is working with his colleague Susan Santangelo to spearhead the new project.

The network will be looking to better understand the genetics behind the communication, intellectual and psychiatric components of autism in hopes of developing more individualized treatments for the disorder, organizers said.

In addition to Spring Harbor Hospital in Westbrook, Maine, the network will include Bradley Hospital in East Providence, R.I., Hampstead Hospital in Hampstead, N.H., Sheppard Pratt Hospital in Baltimore, The Children’s Hospital Colorado in Aurora, Colo. and Western Psychiatric Institute & Clinics in Pittsburgh.

The new effort is funded with a two-year $1.2 million grant from the Simons Foundation and the Nancy Lurie Marks Family Foundation. In that time, researchers plan to enroll 500 individuals at the hospitals in their study.

“In the short term, this will raise the standard of care in the participating hospital units and inform best practices for psychiatry units in the U.S. and abroad,” Santangelo said. “Ultimately we intend to make this study the launching point for future autism research that will unlock some of the mystery surrounding this disorder.”

Wednesday, October 30, 2013

Warily, Schools Watch Students on the Internet

From The New York Times

By Somini Sengupta
October 28, 2013

For years, a school principal’s job was to make sure students were not creating a ruckus in the hallways or smoking in the bathroom. Vigilance ended at the schoolhouse gates.

Now, as students complain, taunt and sometimes cry out for help on social media, educators have more opportunities to monitor students around the clock. And some schools are turning to technology to help them. Several companies offer services to filter and glean what students do on school networks; a few now offer automated tools to comb through off-campus postings for signs of danger.

For school officials, this raises new questions about whether they should — or legally can — discipline children for their online outbursts.

The problem has taken on new urgency with the case of a 12-year-old Florida girl who committed suicide after classmates relentlessly bullied her online and offline.

Two girls — ages 12 and 14 — who the authorities contend were her chief tormentors were arrested this month after one posted a Facebook comment about her death.

Educators find themselves needing to balance students’ free speech rights against the dangers children can get into at school and sometimes with the law because of what they say in posts on Facebook, Twitter and Tumblr. Courts have started to weigh in.

In September, a federal appeals court in Nevada, for instance, sided with school officials who suspended a high school sophomore for threatening, through messages on Myspace, to shoot classmates. In 2011, an Indiana court ruled that school officials had violated the Constitution when they disciplined students for posting pictures on Facebook of themselves at a slumber party, posing with rainbow-colored lollipops shaped like phalluses.

“It is a concern and in some cases, a major problem for school districts,” said Daniel A. Domenech, executive director of the American Association of School Administrators, which represents public school superintendents.

Surveillance of students’ online speech, he said, can be cumbersome and confusing. “Is this something that a student has the right to do, or is this something that flies against the rules and regulations of a district?”

Interviews with educators suggest that surveillance of students off campus is still mostly done the old-fashioned way, by relying on students to report trouble or following students on social networks. Tracking students on social media comes with its own risks: One principal in Missouri resigned last year after accusations that she had snooped on students using a fake Facebook account. “It was our children she was monitoring,” said one Twitter user who identified herself as Judy Rayford, after the news broke last year, without, she added, “authorization” from children or parents.

But technology is catching on.

In August, officials in Glendale, a suburb in Southern California, paid Geo Listening, a technology company, to comb through the social network posts of children in the district. The company said its service was not to pry, but to help the district, Glendale Unified, protect its students after suicides by teenagers in the area.

Chris Frydrych founded a company, Geo Listening, that
reviews the posts of students for school administrators.

Students mocked the effort on Twitter, saying officials at G.U.S.D., the Glendale Unified School District, would not “even understand what I tweet most of the time, they should hire a high school slang analyst #shoutout2GUSD.”

“We should be monitoring GUSD instead,” one Twitter user wrote after an instructor was arrested on charges of sexual abuse; the instructor pleaded not guilty.

Chris Frydrych, the chief executive of Geo Listening, based in Hermosa Beach, also in Southern California, declined to explain how his company’s technology worked, except to say that it was “a sprinkling of technology and a whole lot of human capital.” He said Geo Listening looked for keywords and sentiments on posts that could be viewed publicly. It cannot, for instance, read anyone’s Facebook posts that are designated for “friends” or “friends of friends.”

But with Facebook’s announcement this month that teenagers will be permitted to post public status updates and images, Geo Listening and similar services will potentially have access to more information on that social network.

Glendale has paid Geo Listening $40,500 to monitor the social media posts. Mr. Frydrych declined to say which other schools his company works with, except to predict that by the end of the year, his company would have signed up 3,000 schools.

David Jones of CompuGuardian, based in Salt Lake City, said his product let school officials monitor whether students were researching topics like how to build bombs or discussing anorexia. His customers include five schools, but he, too, is optimistic about market growth.

“It helps you boil down to what students are having what problems,” he said. “And then you can drill down.”

But when does protecting children from each other or from themselves turn into chilling free speech?

John G. Palfrey Jr., head of Phillips Academy in Massachusetts, said he favored a middle ground. He follows his students on Twitter if they follow him, for instance, but he is wary of automated tools that try to conduct what he called National Security Agency-style surveillance.

John G. Palfrey Jr. of Phillips Academy said he was cautious about
Internet tools that allowed too much surveillance of students.

He briefly contended with this question last year when students created a blog where they could anonymously share “secrets.” Many posts were on the fringe, Mr. Palfrey recalled, and some teachers and students were concerned that children’s identities could be determined from their writing patterns.

The blog’s student founders were persuaded to add a note of caution, warning participants that their identities could be discovered.

Mr. Palfrey offered an offline analogy. “We wouldn’t want to record every conversation they are having in the hallway,” he said. “The safety and well-being of our students is our top priority, but we also need for them to have the time and space to grow without feeling like we are watching their every move.”

That fine line seems to be equally confounding the courts.

In the Nevada case, a 16-year-old boy bragged on Myspace about having guns at home, and threatened to kill fellow students on a particular date. He also cited the 2007 massacre at Virginia Tech, in which a troubled student killed 32 people.

The boy ended up spending 31 days in a local jail and was suspended from school for 90 days. He then sued the district, saying his free speech rights had been violated.

The Ninth Circuit Court of Appeals dismissed the claim. It called his threats “alarming” and so specific that they presented “a real risk of significant disruption” to the school. Administrators were justified, the court ruled, for penalizing what was ostensibly off-campus speech.

“It’s going to be more and more of legal issues,” said Gretchen Shipley, a lawyer who represents school districts. “The ability to monitor is growing so quickly.”

The Indiana case offers a contrast. In the summer of 2009, two incoming 10th graders at Churubusco High School posted what the court called “raunchy” pictures of themselves. Once school officials found out, the girls were suspended from extracurricular activities for the school year. The girls sued, saying their free speech rights had been violated. The school contended that its student handbook bars conduct that could “discredit” or “dishonor” it.

The court found that prohibition too broad. The students’ pictures, “juvenile” though they were, did not cause “substantial disruption” at school, the court ruled, and even though it was just “crude humor,” it was protected speech. “No message of lofty social or political importance was conveyed, but none is required,” the court said.

Tuesday, October 29, 2013

Research Finds Brain Scans May Aid in Diagnosis of Autism

From NN -

By Kelli Hewett Taylor
October 18, 2013

Joint research from the University of Alabama at Birmingham Department of Psychology and Auburn University indicates that brain scans show signs of autism that could eventually support behavior-based diagnosis of autism and effective early intervention therapies. The findings appear online today in Frontiers in Human Neuroscience as part of a special issue on brain connectivity in autism.

“This research suggests brain connectivity as a neural signature of autism and may eventually support clinical testing for autism,” said Rajesh Kana, Ph.D., associate professor of psychology and the project’s senior researcher. “We found the information transfer between brain areas, causal influence of one brain area on another, to be weaker in autism.”

The investigators found that brain connectivity data from 19 paths in brain scans predicted whether the participants had autism, with an accuracy rate of 95.9 percent.

This brain scan from Kana’s study shows weaker neural connectivity in
participants with autism compared with participants without autism.

Kana, working with a team including Gopikrishna Deshpande, Ph.D., from Auburn University’s MRI Research Center, studied 15 high-functioning adolescents and adults with autism, as well as 15 typically developing control participants ages 16-34 years. Kana’s team collected all data in his autism lab at UAB that was then analyzed using a novel connectivity method at Auburn.

The current study showed that adults with autism spectrum disorders processed social cues differently than typical controls. It also revealed the disrupted brain connectivity that explains their difficulty in understanding social processes.

“We can see that there are consistently weaker brain regions due to the disrupted brain connectivity,” Kana said. “There’s a very clear difference.”

Participants in this study were asked to choose the most logical of three possible endings as they watched a series of comic strip vignettes while a functional MRI scanner measured brain activity.

The scenes included a glass about to fall off a table and a man enjoying the music of a street violinist and giving him a cash tip. Most participants in the autism group had difficulty in finding a logical end to the violinist scenario, which required an understanding of emotional and mental states. The current study showed that adults with autism spectrum disorders struggle to process subtle social cues, and altered brain connectivity may underlie their difficulty in understanding social processes.

“We can see that the weaker connectivity hinders the cross-talk among brain regions in autism,” Kana said.

Kana plans to continue his research on autism.

“Over the next five to 10 years, our research is going in the direction of finding objective ways to supplement the diagnosis of autism with medical testing and testing the effectiveness of intervention in improving brain connectivity,” Kana said.

Autism is currently diagnosed through interviews and behavioral observation. Although autism can be diagnosed by 18 months, in reality, earliest diagnoses occur around ages 4-6 as children face challenges in school or social settings.

“Parents usually have a longer road before getting a firm diagnosis for their child now,” Kana said. “You lose a lot of intervention time, which is so critical. Brain imaging may not be able to replace the current diagnostic measures; but if it can supplement them at an earlier age, that’s going to be really helpful.”

The findings of this study build on Kana’s research collaborations with Auburn that began in 2010. Lauren Libero, a graduate student in the UAB Department of Psychology, assisted in the research.

Original Research

Full open access research for “Identification of neural connectivity signatures of autism using machine learning” by Gopikrishna Deshpande, Lauren E. Libero, Karthik R. Sreenivasan, Hrishikesh D. Deshpande and Rajesh K. Kana in Frontiers in Human Neuroscience. Published online October 17 2013 doi:10.3389/fnhum.2013.00670

Monday, October 28, 2013

Current Trends in Special Education

From the Education Week Blog "Education Futures"

By Matthew Lynch
October 21, 2013

The way that K-12 learners are taught is in rapid flux, particularly when it comes to students in special education programs.

According to a report by the Fordham Insititute, special education participation by K-12 students represented 13.1 percent of the nation's student population in 2010. From 2000 to 2010, students in special education categories like learning disabilities, intellectual disabilties and emotional disturbances dropped in numbers. Cases of autism spiked dramatically, though, quadrupling over the 10-year span.

Combine these statistics with the way classroom technology has changed since the year 2000 and it makes sense that special education is in an adjustment period. The way that students are served through special education initiatives is evolving, as it should. Here are a just a few of the trends in K-12 education:


Language Acquisition through Motor Planning, or LAMP, is an approach that connects neurological and motor learning in a way that makes communication easier for students with autism and related disorders. These principles are proving especially helpful for students who do not speak or have very limited verbal skills. Paired with technology, LAMP principles empower a growing student population with autism to effectively communicate and reach higher academic achievements. LAMP is present in technology - from specially made computers to learning apps.

Assistive Technology

The tools needed for academic success when it comes to students with physical disabilities are progressing. The same is true of students that may have learning disabilities, or a combination of both. Assistive technology can help any student with any number of issues. The technology can be as common as using an e-reader instead of a traditional book or as advanced as a computer that responds to the eye movements of the student as commands. It can be argued that while assistive technology certainly enhances the learning process for traditional students, it gives those in special education access to learning that would not exist without the technology.

Early Detection

Of course, discovering disabilities early in life is nothing new but it has become more than simply a labeling game. Groups like Easter Seals are behind the cultural push to fund programs that specialize in early detection of developmental delays that can often be helped with intervention programs. The Centers for Disease Control reports that 11 percent of the children who are served in federally funded early intervention programs (before Kindergarten, as young as 24 months) end up not needing any special education in the school years. Despite this, the CDC also reports that the median age for diagnosis of spectrum disorders like autism is older than 6.

It will take a change in thinking at all levels - from parents to lawmakers - for kids to receive the help they need in early childhood and improve special education through adulthood.

Classroom Integration

Long gone are the days when special education students were placed in separate classrooms, perhaps even in completely different parts of a school. Special education students are often now sitting alongside their traditional student peers for at least part of the day. The amount of time spent in a regular education classroom is determined by the particular disability but more special education students are in classrooms than in the past - giving them the common school experience of their classmates.

Student-Led Planning

When special education students reach high school, they are being called upon more and more to have input into their individual education plans. This is to prepare these students for more independence in adulthood. It also gives teachers more insight into the methods these students favor when it comes to learning. Instead of dictating what and how special education students should learn, student-led input helps chart the course toward academic and life skills.

Overall, special education is becoming a more normalized experience for the students. Our tech-hungry culture is the perfect backdrop for the tools that these special education learners need to succeed in K-12 classrooms.

What changes have other educators noticed in special education over the past decade or so?


Dr. Matthew Lynch is the author of the upcoming textbook, The Call to Teach: An Introduction to Teaching. To pre-order it via Amazon, please click on the following link.

Sound Response May Explain Language Problems in Autism

From - The Simons Foundation Autism Research Initiative

By Virginia Hughes
December 9, 2008

Children with autism process sounds a split second slower than typically developing children, according to a new study that measured the magnetic fields emitted from the children's brains.

While preliminary, the findings may partly explain the language and communication problems that burden so many with the disorder, the researchers say.

"The findings [show a delay of] only fractions of a second, but those really matter in spoken speech," says Timothy Roberts, vice chair of radiology research at Children's Hospital of Philadelphia, who presented the data last week at the annual meeting of the Radiological Society of North America in Chicago. "Our thought here is these delays kind of cascade through later and later processing," Roberts says.

Cumulative effect: For children with autism,
even a delay of 50 milliseconds in processing sound could translate
to serious problems with language and communication.

Many parents and clinicians report a delay in language acquisition or a loss of previously learned language in young children with autism. Reflecting the diversity of the disorder, some people with autism are also extremely sensitive to normal sounds, whereas others are insensitive to extremely loud sounds1.

Roberts and his team were the first, about nine years ago, to explore these auditory deficits using magnetoencephalography (MEG), a brain imaging technique used to measure magnetic fields produced by the electrical activity of neurons. MEG is routinely used to pinpoint the misfiring brain areas that cause seizures in individuals with epilepsy.

Using MEG to study autism was "just the convergence of a problem and a solution," Roberts says.

Many researchers hypothesize that autism is a communication failure between neighboring brain regions.

But the difficulty with proving this theory is that electrical signaling between brain regions occurs over a few hundredths of a second ― much too rapid to be picked up by functional magnetic resonance imaging (fMRI) or positron emission tomography (PET), which detect temporal differences on the order of seconds or minutes.

Like those methods, MEG can pinpoint the region of activity, but is much more sensitive to changes over short periods of time. "MEG's real-time capability seemed to be ideally suited to look at autism," Roberts says.
Short lag:

In 1999, Roberts led MEG experiments on 15 children with autism and 17 healthy controls2,3 which were the first to show that the brain response to sound in children with autism lags behind that of typically developing children.

In July 2007, a $1.25 million grant from the National Institutes of Health allowed the researchers to broaden these experiments to a much larger number of children.

For the scans, participants sit in a large and comfortable chair, their heads under a large MEG helmet that resembles "one of those old-fashioned hair dryers," Roberts says.

The children watch a soundless movie, while tiny earphones play a series of beeps or vowel sounds. Each frequency evokes an automatic electrical 'signature' in the brain. This little bit of electrical activity generates a magnetic field, which passes through the skull and is immediately sensed by the 275 detectors lining the inside of the helmet.

At last week's conference, Roberts reported results from 64 children aged 6 to 15, including 30 who have autism. In the first set of experiments, the children heard beeps of different frequencies, and the MEG detectors recorded the brainʼs response to each sound.

In children with autism, this response is delayed by about 20 milliseconds compared with the response in typically developing children, Roberts found.

In a second ‘mismatchʼ experiment, the children heard three successive speech sounds, such as ‘ah, ah, ah,ʼ followed by a different speech sound, such as ‘ouʼ. Compared with the control group, children with autism respond to the novel sound with a delay of about 50 milliseconds.

People normally speak at a rate of about four syllables per second, or 250 milliseconds per syllable, meaning that a delay of 50 milliseconds could be “quite catastrophic,” Roberts says.

“If you're saying 'elephant,' they'd be stuck on the 'el' when you're on the 'ant'. If the brain can't catch up, can't cope with the constant stream of information, then that might be why spoken speech presents such difficulties,” he says.
Diagnostic tool:

Roberts is still recruiting participants, hoping to enroll a total of 300 before the grant expires in 2012. He has not yet submitted the results to a journal for publication.

In future experiments, he plans to test young toddlers, in hopes of using MEG signatures as a diagnostic tool for autism. “We'd like to predict if there's some sort of abnormal brain function even before they get a diagnosis [of autism],” he says.

Other experts agree that auditory processing should be studied in much younger children Studies in the past year have shown that the perception of native speech sounds begins in babies as young as 7 or 8 months of age4.

“Those studies have shown now that language process is developing very, very early, and that auditory processing is much linked to language learning,” says Eira Jansson-Verkasalo, a professor at the University of Oulu, in Finland. Jansson-Versakalo has used electroencephalography (EEG), a cousin of MEG, to identify millisecond delays in sound processing in people with Asperger's syndrome5,6.

“It will be very important to study these children as infants, because when we find it early enough, we can teach or rehabilitate the child so that these difficulties don't get worse,” she says. MEG is a great technique for studying babies, she adds, because it's non-invasive and doesn't require them to perform specific cognitive tasks.

The biggest downside to using MEG as a diagnostic tool is cost. The machines cost about as much as an fMRI machine, roughly $3 million. There are only about 100 machines worldwide; of the 30 in the U.S., only 2 are in pediatric hospitals.

“It's expensive, but when you're thinking about rehabilitation, that's expensive as well,” Jansson-Verkasalo says. “I think if we find these children early enough, then this rehab will be cheaper.”

  • O'Neill M. and Jones R.S. J. Autism Dev. Disord. 27, 283-293 (1997) PubMed
  • Gage N.M. et al. Neuroreport 14, 2047-2051 (2003) PubMed
  • Gage N.M., Siegel B. and Roberts T.P. Brain Res. Dev. Brain Res. 144, 201-209 (2003) PubMed
  • Kuhl P.K. et al. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 363, 979-1000 (2008) PubMed
  • Jansson-Verkasalo E. et al. Neurosci Lett. 338, 197-200 (2003) PubMed
  • Jansson-Verkasalo E. et al. Eur. J. Neurosci. 22, 986-990 (2005) PubMed

Sunday, October 27, 2013

Soccer Players Show Signs of Brain Damage

From Scientific American's MIND Blog

By Ajai Raj
October 19, 2013

Frequently hitting the ball with the head may impair memory.

Football has become notorious for the degeneration it causes in players' brains. Now a preliminary study of soccer players has found that frequently hitting the ball with the head may adversely affect brain structure and cognition.

The study imaged the brains of 37 amateur soccer players, 21 to 44 years old, and found that players who reported “heading the ball” more frequently had microstructural changes in the white matter of their brains similar to those observed in patients with traumatic brain injury. These players also performed poorly on cognitive tests, compared with players who reported heading the ball less.

The study, published online in June in Radiology, found evidence of a threshold—1,800 headings—above which the effects on memory begin to manifest. Neuro-radiologist Michael Lipton of the Albert Einstein College of Medicine of Yeshiva University, who led the study, says the findings may indicate that heading causes mild concussions, even when players do not show symptoms.

The results are noteworthy but far from conclusive, comments Jonathan French, a neuropsychologist in the Sports Medicine Concussion Program at the University of Pittsburgh Medical Center, who was not involved in the study. “The majority of soccer players who are concussed don't have any functional problems in everyday life,” he says.

The structural changes detected in the study, he points out, are "so microscopic that we don't know what they actually mean” for long-term function.

Lipton agrees more work is needed to determine the significance of the brain changes, but he hopes to call attention to the potential risk because soccer is the most popular sport in the world.

Saturday, October 26, 2013

Stress of Childhood Poverty May Have Long Effect on Brain

From Bloomberg News

By Nicole Ostrow
October 21, 2013

Children raised in poverty or in orphanages experience chronic stress early in life that can have long-lasting effects on the brain, setting them up for future mental and physical ailments as adults, two studies found.

The stress of poverty may affect regions in a child’s brain that control emotion, according to research published today in the journal Proceedings of the National Academy of Sciences. A second study found that children who had lived in an orphanage were more anxious than those who hadn’t.

In childhood, the brain is still immature and developing rapidly so it is more sensitive to high-stress situations than an adult brain, said Pilyoung Kim, lead study author of the childhood poverty study. The findings from both papers suggest that early intervention programs to address chronic stress may benefit these children, the authors said.

“Long-term exposure to chronic stress is likely to cause wear and tear in children’s physical and psychological systems for coping with stress over time,” said Kim, an assistant professor and director of the Family and Child Neuroscience Lab at the University of Denver, in an October 20 e-mail.

“Living in poverty at a young age can cause long-lasting changes in brain development, which contribute to difficulties in regulating of emotions and future devastating health outcomes, including mental illness and high mortality and morbidity in adulthood.”

Poverty Effects

Researchers in the poverty study looked at 54 adults at age 24. Half of those in the study were considered low income when they were 9 years old and half were not.

Using brain imaging, they found that adults who were poor as children were less able than other participants to minimize their emotional reactions to negative images by reinterpreting scenes as less harmful or mentally distancing themselves. The findings were the same even when the researchers controlled for income as adults.

In the second paper, researchers from the Weill Cornell Medical College in New York studied 16 children ages 11 and younger who had been reared in an orphanage and 10 children who hadn’t.

The researchers also created a mouse model in which the maternal care of newborn mice was disrupted. This experiment enabled the researchers to simulate the orphanage experience, observe the behavior of the animals and look into their brains.

The findings suggested that the unpredictable care children receive in orphanages may alter their behavior and, as seen in the mouse model, is an early-life stress that can affect brain development.

Altered Behavior

“When growing up in an unpredictable situation such as an orphanage, you are altering the way the brain allocates resources to interpret the world around it,” said Matthew Cohen, who conducted the research as part of his doctoral work at Weill Cornell. “By doing so, you end up altering the behavior of the animal or humans later on.”

Early stressful experiences in childhood lead to higher rates of anxiety and depression, he said. “It’s definitely more difficult to reverse the older the individual,” Cohen said in a telephone interview. “The changes are more widespread if the children are in the orphanage longer.”

The results suggest early intervention is needed for orphanage-reared children to help reduce risk of psychological illness, the authors wrote. About 8 million children live in orphanages worldwide, the paper said.

Discovery at UNC Points to Possible Environmental Cause of Autism

From The News & Observer

By Mary-Russell Roberson
October 20, 2013

Researchers at UNC School of Medicine have discovered a potential environmental cause of autism in a type of chemotherapy drug, and they are investigating the effects of other non-chemo drugs that work by a similar mechanism.

Professors Mark Zylka and Benjamin Philpot made the discovery while studying a drug that’s effective against cancer, but also shows potential as a treatment for a genetic disease called Angelman syndrome. In the process, they made some new observations that seem to point to a cause of autism. “That’s science,” says Zylka. “You’re trying to do something and you find something else.”

The duo, along with colleagues at UNC Chapel Hill and the University of Connecticut, published their results in the journal Nature on Aug. 28.

On Sept. 30, the National Institutes of Health awarded Zylka a Pioneer Award to continue the autism work. Only about a dozen researchers receive the annual award, which provides up to $2.5 million over five years. According to the NIH website, the award supports researchers of “exceptional creativity, who propose pioneering and possibly transforming approaches to major challenges in biomedical and behavioral research.”

Zylka and Philpot are both associate professors in the department of cell biology and physiology at UNC’s School of Medicine, but they might never have worked together if it weren’t for the proximity of their labs. Zylka studies the neurology of pain; Philpot studies Angelman syndrome, a genetic disorder that is sometimes misdiagnosed as autism or cerebral palsy. The two often discussed their work when they saw each other in the halls or at lunch.

They started collaborating on projects related to the perception of pain in people with Angelman syndrome. Recently, they broadened their collaboration by pooling funds to purchase a genome sequencing machine, which they used to investigate how the cancer drug topotecan affects specific genes. This project grew out of work Philpot did a couple of years ago that showed topotecan might be useful in treating Angelman syndrome.

As a cancer drug, topotecan works by gumming up cell division to halt tumor growth. It does this by inhibiting enzymes called topoisomerases, which keep DNA from becoming knotted up.

In our cells, DNA is typically tightly wound in packages for efficient storage. But DNA must be unwound during two crucial processes: cell division and gene expression. Topoisomerases make this unwinding possible. Zylka calls the enzymes “scissors and glue,” saying, “They cut the DNA, uncoil it, and stick it back together very, very fast.”

In the case of Angelman syndrome, Philpot was interested not in cell division but in gene expression – the process by which genes do their biological jobs, whether specifying eye color or telling a cell to become a neuron.

The ‘Eureka’ Moment

Philpot, Zylka and their colleagues treated human cells with topotecan and ran the samples through the Next Generation machine, a high-throughput gene sequencer. “It’s incredibly powerful,” Zylka says of the machine, which he and Philpot acquired in March. “You can put a chemical on a cell and see how it affects every single gene in your genome. And it’s fast – the machine takes 24 hours to run.”

The data from the experiment came out on an enormous spreadsheet. The genes were listed in order, with those at the bottom being the least expressed – that is, they were less capable than usual of doing their biological jobs.

Zylka remembers his eureka moment: “I was sitting a computer one evening and I was looking at the genes at the bottom of list and I saw this gene called dystrophin that’s associated with Duchenne muscular dystrophy.” The gene was familiar to him because it was discovered by one of his professors at Harvard. “I remember him telling us this is one of the biggest genes in the human genome, and it was sitting at the bottom of list. I looked at a few other genes and had a sense they might be big.”

A bit more work proved his insight to be correct: Genes at the bottom of the list were all long genes, meaning that topotecan had the most negative impact on long genes.

The ‘Long Gene’ Factor

Zylka noticed something else about the genes at the bottom of the spreadsheet. Other researchers have identified around 300 genes that are associated with autism, and Zylka realized that a fair number of those genes were at the bottom of the list.

“These two unexpected observations centered on gene length: Topoisomerases regulate really long genes, and autism genes are really long,” he said. This led to the insight that inhibiting topoisomerases, as topotecan does, might increase the risk of autism.

Most of the affected genes are related to brain development and do their most important work during times of rapid brain development before birth and in early childhood. That means timing is crucial: Exposure to topotecan during those sensitive times could lead to lifelong effects even after the exposure ended.

Presumably, not many women take topotecan while they are pregnant, but there are other drugs currently on the market that also inhibit topoisomerase enzymes, including some antibiotics and antifungals.

“We want to try to find as many additional chemicals as we can that inhibit long genes, so that we can start to inform the public,” Zylka said. “We aren’t going to be able to prove that any of these things cause autism; ultimately you need epidemiological studies to nail that. But we hope it’s the beginning of a broader base of knowledge that will help people down the road.”

Andy Shih, the senior vice president of scientific affairs at Autism Speaks, calls the results of Zylka and Philpot’s work exciting, and said, “What’s important about this study is that it reveals another potential mechanism by which autism risk could be affected.”

Shih also said the study could inspire ideas for autism treatments: “If we know that topoisomerase is not functioning optimally, you can imagine that a compound or drug that compensates for that change or restores the function of the topoisomerase could have a positive impact on those individuals whose autism is tied to that.”

Research Continues

Back in the lab, Zylka is investigating the impact of other topoisomerase-inhibiting drugs on gene expression. He works with a sense of urgency, fueled on a personal level by questions about how everyday chemicals could be affecting his two young children, and on a societal level by the knowledge that autism rates are continuing to rise in the United States. The Centers for Disease Control estimated in March that 1 in 50 children has an autism spectrum disorder.

“It’s an area of neuroscience where you have the potential to impact a large number of people in a positive way,” Zylka said. “I always try to keep that in mind. It’s easy to get focused on research and not realize the broader context. The public funds us and I try to do the best we can to move fast and make big discoveries that are going to help people.”


Zylka and Philpot’s study was funded by the National Institute of Mental Health, an arm of the NIH.

Read more here:

Friday, October 25, 2013

Reflections on Citizenship, #DigitalCitizenship, and Parenting for #DigCitWk

From the Blog

By Chris Thinnes
October 24, 2013

As a junior high school administrator 10 years ago, it was easy to separate children’s lives at school from the lives they led at home, and the relationships they developed in ‘real life’ from the relationships they developed ‘online.’ Five years ago, it was clearer to all of us that behaviors off-campus were affecting relationships on campus, and vice-versa, both for well and for ill — and that social interactions rooted in the ‘virtual world’ grew branches, stems, and leaves in the community of students on campus.

Nowadays, it would be foolish for a teacher or a school leader to suggest that ‘virtual’ interactions are any less ‘real’ to children than the friendships we see flourish or, occasionally, wither inside or outside our classrooms. At the end of the day, ‘citizenship’ and ‘digital citizenship’ are organically and inextricably intertwined in the experience of our school-aged children — and it is only those of us, as educators and/or as parents who are old enough to have had to ‘adapt,’ who think of our own social lives otherwise.

Over time, parents — myself included — have never really had inhibitions about starting or sustaining open, clear, and purposeful conversations with their children about their expectations for their children’s behavior in the classroom, on the playground, at a friend’s house, or at the dinner table. But they have never been as comfortable or confident — even now — fostering those conversations about their children’s interactions online.

Sometimes this is because parents don’t fully understand the nature, variety, depth, or implications of those interactions; sometimes this is because parents don’t recognize the very healthy learning opportunities available to children in those interactions; and sometimes this is simply because of their own limited proficiency with technology.

In every case, though, this discomfort follows from the fact that we haven’t had the experience of growing up as a child in a digital world. In the difference between our own and our children’s childhoods lies our discomfort with some of the most important conversations we need to have with our children.

I find the rampant misconception baffling (among educators, among parents, and sometimes in my own attitudes as well) that in order to be helpful to children, we need to be ‘experts’ in a subject matter, or to have had an identical experience. The goal of these conversations about digital citizenship is not to ‘front’ as a video gamer or software designer; you don’t need a degree in Computer Engineering, or the slightest interest in subscribing to Wired.

The goal of these conversations is to help your child to identify and to make good decisions. You do that every day in their ‘real’ lives — and these matters are no less ‘real’ than any others for them.

In our recent ‘Town Halls for Parents and Guardians,’ we explored two prompts in the contexts of a ‘Question Formulation Technique’ exercise, and a follow-up conversation to develop shared criteria and strategies to make better decisions as parents. These prompts were:

A. Parents create an environment and climate that supports learning at home;

B. Parents strive to balance structure/order with independence/resilience at home.

Though each of these was meant to represent a balance that parents are trying to sustain with reference both to our children’s learning, and their lives (if there is any such distinction to be made), I think these also serve as great focal points for our decisions about how to support our children’s ‘digital citizenship’ with intentional conversations, clear expectations, and open dialogue at home.

I don’t get to wear a sash as ‘Model Parent’ in this particular pageant — my son was raised more on South Park and Family Guy than on Sesame Street and Reading Rainbow; need I say more? — but I can share with you the most valuable tips I’ve inherited from other parents who have successfully framed these kinds of conversations at home.

Each of these I’ve tried to follow (to the best of my ability, but not always successfully) as a fellow traveler on this learning journey as the parent of a digital citizen:

1. Social Interactions in Social Spaces

Under no circumstance should 12-and-unders be allowed or encouraged to interact online in the privacy of their rooms: all connected devices should be used in ‘public’ spaces. This includes computers, tablets, and phones. In face-to-face interactions with their peers, children can rely on tone, context, body language, and other nonverbal indicators of a classmate’s intent. Behind a closed door, children this age should not be expected fully to understand or to filter some of their own or their friends’ comments.

Though their screen’s visibility to you serves as a crude substitute, your own proximity to your children can help them resist certain impulses, or invite a conversation about a decision with which they might be wrestling. Ideally you should establish this dynamic before a device is introduced: the happy accident of my wife’s clear thinking when my son was an infant, has normalized this condition for a 15 year old who now doesn’t even ask to take his computer into his room.

2. Support Versus Surveillance

Children need coaches and role models, not wardens or secret agents, to learn how to make better decisions. Our goal is not to ‘catch’ a bad decision, but to ‘coach’ a good one. The playing field needs clear boundaries, and clear rules, in order for children to play freely — but not every foul should get a player ejected from the game.

Many parents install Safe Eyes or some other such filtering and security software, but relatively few parents openly discuss this with their children. When my son was younger, that conversation about what I was installing, and why, was one of the most powerful conversations about digital citizenship we’ve ever had. We explored every one of the software’s settings together, and had a thorough conversation about what he thought he was ready to do without supervision, ‘where’ he thought he was ready to ‘go,’ and who he thought he was ready to join in his online travels. I got to listen, to learn, and in a few cases strongly to push back — with the shared goal of trying to decide together, through open dialogue, how we could set goals for his developing independence in the months to come.

3. You Bought It; You Own It

One of the great strategic suggestions I’ve ever heard — at which I have sometimes failed, and with which I wish you better luck — is to establish a very clear understanding in the home about who owns the device, and who’s borrowing it. What are the terms of the agreement? What is acceptable use? The value of this dynamic is particularly evident when something goes wrong. (By the way: something will go ‘wrong.’ It should. That, like every learning opportunity, is a good thing.) In such cases, it is much simpler and more effective to withhold the privilege of borrowing a device, than to ‘repossess’ a device a child thinks s/he ‘owns.’

4. Not Every Feeling is a Fact

Valuable learning experiences are always attended by some measure of discomfort: it should never be so slight as to be completely comfortable, nor so overwhelming as to paralyze. In the sphere of social networking, this is often hard to gauge. To the point: when a child experiences a hurt feeling, it does not necessarily mean s/he has been ‘cyberbullied.’
Sometimes s/he has simply been disappointed or misunderstood.

Your child will also say things, on the playground or online, that have a hurtful impact well beyond her or his intent. These are coincidental but wondrous opportunities to foster conversations about intent, impact, respect, and inclusion that are every bit as valuable — and perhaps more valuable because of their relationship to an authentic experience in your child’s life — than more abstract conversations children experience as ‘lectures.’

I am certain, for example, that the most impactful conversations I’ve had with my son in the last year — about race, class, privilege, and cultural competence — have followed directly on the heels of ill-considered comments he and his classmates have posted on Facebook, and which he has confided in me.

I could go on and on — maybe I already have? — but I’m just as eager to learn from your experience and wisdom as I am to share my own impressions. What are some of the obstacles and opportunities you’ve discovered at home as you support your children’s digital citizenship? What are some of the goals you’ve set? What does an effective and open conversation with your child look like, and sound like? To what resources, other than those Jason Moore and I have compiled below, have you turned for insight or support on parenting digital citizens?


A Failed Hypothesis: Mercury in Vaccines as a Cause of Autism and Autism Spectrum Disorders (ASDs)

From Science-Based Medicine

By David Gorski
January 7, 2008

One of the most pernicious medical myths of recent years has been the claim, promulgated by a subgroup of parents of autistic children and facilitated by scientists of dubious repute, that somehow the mercury in the thimerosal (ethyl mercury) preservative used in common childhood vaccines in the U.S. until early 2002 causes autism.

Although it had been percolating under the radar of most parents and scientists for several years before, this belief invaded the national zeitgeist in a big way in 2005, beginning with the publication of a book by journalist David Kirby entitled Evidence of Harm: Mercury in Vaccines and the Autism Epidemic: A Medical Controversy.

The fires of hysteria were stoked even higher by Robert F. Kennedy, Jr., who published a truly twisted and misleading piece of pseudojournalism and pseudoscience simultaneously in Rolling Stone and on entitled Deadly Immunity.

Relying primarily on quote-mining of the transcripts of both a conference held Atlanta by the CDC to discuss the question of whether autism is related to thimerosal in vaccines, and an Institute of Medicine report on vaccines while simultaneously misrepresenting the results of two studies by Verstaeten et al to paint a false picture of a government coverup, RFK Jr. almost single-handedly managed to stoke fears that vaccines were causing an “epidemic of autism.”

I say “almost” single-handedly, because, unfortunately, he had help. Relying on the dubious research of a variety of investigators, such as the
father-and-son team of Dr. Mark Geier and David Geier, whose prodigious output of badly designed studies emanating from a lab in their home in suburban Maryland, done using a rubberstamp institutional review board stacked with friends and cronies to approve the studies, and published for the most part in non-peer-reviewed journals, activists loudly insisted that mercury in vaccines was the cause of most autism.

Others claiming to demonstrate this link include Boyd Haley, a chemist from the University of Kentucky, and a few other vocal scientists and advocates, who claim that autism is, in essence, mercury poisoning. Facilitating the dissemination of this message were reporters such as David Kirby, activists such as Robert F. Kennedy, Jr., and media personalities such as Don Imus. Indeed, some activists claimed that some vaccines were “poisoning” our children, even going so far as show photos of autistic children with the label “mercury-poisoned“ underneath them on placards held aloft at protest rallies. They made quite a splash then, and still do to a lesser extent even today. There’s just one problem.

The scientific data, taken in totality, do not support a link between mercury in vaccines and autism. Today yet another important study, by Robert Schechter and Judith Grether, was published in the Archives of General Psychiatry, entitled Continuing Increases in Autism Reported to California’s Developmental Services System: Mercury in Retrograde (
1), that utterly failed to support the hypothesis that mercury in vaccines is an etiological factor in autism. It is yet another nail in the coffin of the medical myth that mercury in vaccines causes autism.

Before I discuss this new study in more detail, a bit of background is in order. In response to the FDA Modernization Act of 1997, prior to the hypothesis that thimerosal might cause autism the U.S. Food and Drug Administration (FDA) compiled a list of vaccines and how much thimerosal they contained. Thimerosal had been commonly used to prevent microbial contamination of vaccines, particularly multidose vials, since the 1930s. It could be reasonably argued that, given the more lax standards of the time, thimerosal had not been adequately tested before use in humans, but decades of use after that had, as far as could be discerned, revealed only occasional skin hypersensitivity reactions due to this component.

By 1999, under the recommended schedule of childhood vaccines at the time, concern was expressed that infants, before six months of age, were potentially being exposed to cumulative doses of ethyl mercury that may have exceeded safety standards. It should be noted that these safety standards were based on an indirect surrogate of ethyl mercury, namely methyl mercury, and largely in the absence of any real data. In July, 1999, the American Academy of Pediatrics and the U.S. Public Health Service decided, as a precaution, to recommend that thimerosal be removed as soon as possible from childhood vaccines.

It did not take long for this recommendation to be implemented. By March, 2001, all vaccines in the recommended infant vaccination schedule were available in forms that had at most traces of thimerosal left over from the manufacturing process. The last lots of childhood vaccines with thimerosal had expiration dates in 2002. Indeed, as Arthur Allen documented in his recent book
Vaccine: The Controversial Story of Medicine’s Greatest Lifesaver, a survey of several hundred medical offices in February, 2002 conducted by the CDC found that, of the three pediatric vaccines that contained thimerosal in the 1990s, only 2% of vaccine stock still contained thimerosal.

Since then, with the exception of the flu vaccine, no childhood vaccine in the U.S. has contained more than trace amounts of thimerosal. There has been considerable debate over whether the decision to remove thimerosal was undertaken too quickly. True, at the time it seemed like a prudent, cautious step. However, the decision had unintended consequences. One was that it resulted in a temporary shortage of childhood vaccines. More importantly, though, it fed the fears of activists that the mercury in vaccines must really be harmful. After all, if it weren’t harmful, why would the AAP and PHS recommend its removal?

Why indeed? The use of this precautionary measure, which to health officials seemed prudent at that time, as justification for attacking the safety of vaccines is as good an example of how no good deed goes unpunished as I’ve ever seen. Many parents, faced with the enormous challenge of raising autistic children, not unreasonably wondered whether there was something wrong with vaccines in the first place.

The second bit of background information that you need to know is that, over the last couple of decades, the incidence of autism and autism spectrum disorder (ASD) has increased markedly to an estimated 1 in 150 children. Robert F. Kennedy, Jr. and others who believe that mercury in vaccines somehow cause autism have referred to this increase as an “autism epidemic” (or, more offensively, as an “
autism tsunami“) and frequently claim that there must be an environmental factor that has led to this increase.

Because the symptoms of autism, such as cognitive delay and withdrawal from interaction with parents, often manifest themselves between one and three years of age and because this is the age when children receive the bulk of their vaccines, there is a correlation. However, correlation does not necessarily equal causation. It may, but often it does not. Often the correlation is spurious, unrelated, or related to a common factor. More investigation is always required to determine if an apparent correlation is or is not due to causation.

In the case of autism, there is good evidence, most recently published by Paul Shattuck (2), that increased awareness and diagnostic substitution since the criteria for a diagnosis of ASD were broadened in 1994 account for the apparent increase in diagnoses of autism, as pointed out by Arthur Allen and Roy Grinker.

Regarding the question of vaccines and autism, for ethical reasons we cannot do a double-blind, randomized, control trial of vaccines with and without thimerosal. However, we can do the next best thing, and, indeed, we now have several good studies since 1999 that do just that. Some of these studies are epidemiological; some are ecological. What allows us to use them to reject the hypothesis that mercury in vaccines is an etiological agent that is either associated with or causes autism is a very simple but powerful prediction that the hypothesis makes.

Quite simply, if the hypothesis is true and thimerosal-containing vaccines (TCVs) cause autism (or are even merely a significant contributing factor), we would expect that the removal of thimerosal from vaccines would lead to a rapid decrease in autism incidence and prevalence within 2-5 years.

There have now been several studies that examined this very hypothesis in countries that removed thimerosal from their vaccines before the U.S. did. For example Hviid et al (
3) reported that autism prevalence in Denmark increased from 1991 to 1996 despite the removal of thimerosal from vaccines, while Madsen et al (4) looked at the time period from 1971 to 2000 and concluded that autism diagnoses continued to increase after thimerosal was removed from vaccines. Neither study supported a causal link between TCVs and autism, and they were a prominent part of the dataset that was used by the Institute of Medicine to conclude in 2004 that there was no good evidence to support a link between TCVs and autism.

A more recent study by Eric Fombonne (5) in Montreal examined 27,749 children born from 1987 to 1998 attending 55 different schools. Cumulative thimerosal exposure by age 2 years was calculated for the 1987-1998 birth cohorts. This exposure ranged from 100-125 μg from 1987 to 1991, 200-225 μg from 1992 to 1995, and then none after 1996, which was when thimerosal was completely removed from vaccines in Canada. The result was that autism, ASD, and pervasive developmental disorder diagnoses continued to increase in all periods, demonstrating no relationship between TCVs and autism or ASDs.

Even more recently, a large study (6) failed to support a relationship between thimerosal and adverse neurodevelopmental outcomes, a result that led one of the investigators in the study, Sallie Bernard, a proponent of the thimerosal hypothesis, to disavow the study in a case of sour grapes, because it did not show what she had hoped that it would show.

We are now nearly six years out from the near-complete removal of thimerosal from vaccines. Other than the flu vaccine, there is no more than trace thimerosal in any childhood vaccine; overall mercury exposure due to vaccines has not been this low in decades. Consequently this hypothesis can now be tested in the United States.

In a deliciously ironic twist, Schechter and Grether chose to use a source of data that has frequently been abused by advocates claiming a link between TCVs and autism to try to show one where there isn’t one, as though the conclusions were foreordained. Although it is probably not, it has even been referred to as the “gold standard” of autism epidemiology by none other than David Kirby. Indeed, this is the very same database in which David Kirby predicted that there should be a noticeable decrease in new diagnoses of autism by 2007 if the thimerosal hypothesis is true, and then later shifted the goalposts to 2011 when it became apparent that there has been no decrease.

This source is the California Department of Developmental Services (CDDS) database. The CDDS administers a statewide system of regional centers and developmental centers designed to serve people who are substantially disabled because of autism, mental retardation, or other developmental disabilities. It maintains an archive file of client developmental evaluation reports on clients enrolled in the system. Among the strengths of the system are that it is a population-based system representing the most populous state in the U.S. Moreover, the client reporting form was consistent throughout the study period, preventing confounders due to changes in reporting.

The weaknesses of the CDDS is that its data is derived from an administrative system that was designed to track enrollment and fiscal data and is not as well suited to measuring the occurrence of developmental disabilities in the population. However, with proper statistical analysis, considerable information can still be gleaned from this data for specific birth cohorts.

In order to ask the question of whether autism rates had declined, Schechter and Grether examined data for clients with active status reported from January 1, 1995 to March 31, 2007. Using careful statistical analyses, they used two approaches to measure the occurrence of ASD during this period. The second approach, in which ASD prevalence was determined in the 3 to 5 year old cohort, is perhaps the most informative. It shows a continuing increase in autism prevalence without even a blip or decrease in the rate of increase after 2002.

Indeed, showing the skill of some bloggers to analyze the same data, the money figure in the paper (Figure 3) looks almost exactly the same as the graph prepared in early 2007, a continually increasing curve since 1995. This result is not only consistent with multiple other published and unpublished studies, including the aforementioned Danish and Canadian studies (7), but it is about as unambiguous evidence as can be obtained from a database like the CDDS database. Indeed, despite the limitations of the use of this database, it is an excellent example of proponents of a “mercury injury” hypothesis of autism being “hoisted by their own petard,” so to speak. Indeed, Eric Fombonne, in a blistering editorial (8) that accompanies this study, agrees:

"The particular significance of the study by Schechter and Grether is that it relies on the California Department of Developmental Services database, which has been systematically used by proponents of the thimerosal hypothesis to argue that the rising number of children accessing these services— or the “epidemic” of autism— was linked to the increasing exposure to ethylmercury of US children occurring in the 1990s through the changes in the immunization schedule. To the contrary, the data analyzed by Schechter and Grether9 provide a clear and unambiguous test that shows that the expected decline in autism rates following discontinuation of thimerosal in US vaccines did not occur."

Noting that, “with the exception of studies conducted by a single pair of authors” (with uncharacteristic restraint Fombonne does not name whom he obviously meant, namely Mark and David Geier), all studies done have thus far failed to find a link between TCVs and autism, Fombonne continues:

"Despite the accumulation of scientific evidence rejecting these 2 hypotheses linking autism to various components of childhood vaccines, these theories and the practices that accompany them have not faded away. Why? How many more negative study results are required for the belief to go away, and how much more spending of public funds on this issue could even be justified?"

He then postulates an explanation that I happen to agree with:

"Outside academic circles, powerful advocacy groups developed and started to lobby decision makers to influence decisions about which autism research to fund and even how to conduct it. Unaware of scientific studies, or worse, doubtful of their results, bestselling writers, journalists, and politicians were drawn to embrace conspiracy theories that portrayed vaccine manufacturers and the Centers for Disease Control and Prevention as public enemies. Fifteen law firms saw an opportunity to obtain large financial compensations from the U.S. Vaccine Injury Compensation Court or before local federal courts, the viscous U.S. legal process allowing for fermentation of misconceptions.

Exploiting further families’ beliefs and their understandable desire to try everything possible to help their children, charlatans developed alternative (and lucrative) “treatments” for autism, which included chelation therapy, use of a hyperbaric oxygen chamber, and testosterone suppression. All are of unproven efficacy, and many are dangerous."

In other words, it’s all about obtaining compensation for nonexistent “vaccine injury” and “biomedical treatments” for this injury. Never mind that these “treatments” are neither scientifically plausible nor have convincing evidence in the form of well-designed clinical trials to support their efficacy in ameliorating the cognitive delays observed in autistic children. Unfortunately, parents who love their autistic children and desperately want to do something to “make them better” are fertile ground for the blandishments of proponents of these implausible and unproven “therapies.”

Some of these treatments, such as chelation therapy, which, it is claimed, will remove the mercury that, according to proponents of the thimerosal hypothesis, is the root cause of autism, have developed into veritable cottage industries that prey on desperate parents. It has even progressed to the point where the Geiers can convince some parents that most autistic children exhibit signs of “precocious puberty” and that the elevated testosterone in such children forms “sheets” that bind mercury and prevent it from being chelated properly. As hard as it is to believe, they then use that claim as a justification for using powerful anti-androgenic drugs such as Lupron on autistic children to treat their autism.

Vaccination is arguably the most effective single public health intervention ever developed. As recently as 50 years ago, for example, our parents and grandparents lived in deathly fear of diseases like polio, which is virtually a thing of the past. Because they are preventative in nature and administered to a very large population of healthy people, vaccines have a very high hurdle to jump as far as safety is concerned, because when an intervention is performed on millions of otherwise healthy people, even a low rate of complications can result in large numbers of injured people. Modern vaccines have achieved that level of safety.

Are they completely safe? Nothing in medicine is absolutely, 100% safe. In comparison to the risk of the diseases they prevent and by any reasonable standard, the risks due modern vaccines are extremely low. Moreover, the claims of proponents of an increasingly untenable hypothesis to the contrary, there is no convincing evidence that thimerosal-containing vaccines, or vaccines in general, have anything to do with the etiology of autism. Whatever tiny risk there may be from childhood vaccines, autism and ASDs are not among them.

Indeed, even before this study by Schechter and Grether, under the onslaught of studies that all fail to find a link between thimerosal and autism, even David Kirby and those more zealous than him were starting to back away from the hypothesis, invoking hand-waving and vague “environmental toxins” or even going so far as to blame mercury from pollution wafting over from China or, even more ludicrously, mercury from the cremation of bodies with mercury amalgam dental fillings.

Meanwhile, in the wake of this study, Mark Blaxill is retreating to saying that “the epidemiological analysis doesn’t prove that thimerosal exposure cannot cause individual cases of autism” and blaming vaccines in general for autism (while also not being able to wait for the embargo to try to put his spin on the matter, by the way).

This study is clearly but one more nail in the coffin of this dying hypothesis. Unfortunately, like Jason in the Friday the 13th movies, the hypothesis that mercury in vaccines is a major cause of autism just refuses to die, no matter how many studies fail to find even a wisp of a link between the two. Just when you think it’s finally, really dead, it has an unpleasant way of being resurrected. That’s why it is not difficult to predict that the usual suspects will refuse to believe it, just as they have refused to believe the studies preceding it.


1.) Schechter R and JK Grether (2008). Continuing Increases in Autism Reported to California’s Developmental Services System. Arch. Gen. Psychiatry 65: 19-24.

2.) Shattuck P (2006). The Contribution of Diagnostic Substitution to the Growing Administrative Prevalence of Autism in US Special Education. Pediatrics 117:1028-1037.

3.) Hviid A, M Stellfeld, J. Wohlfahrt, and M Melbye (2003). Association between thimerosal-containing vaccines and autism. JAMA 290:1763-1766.

4.) Madsen KM, MB Lauritsen, CB Pedersen, P Thorsen, AM Plesner, PH Andersen, PB Mortensen (2003). Thimerosal and the Occurrence of Autism: Negative Ecological Evidence From Danish Population-Based Data. Pediatrics 112:604-6.

5.) Fombonne E, R Zakarian, A Bennett, L Meng, D. McLean-Heywood (2006). Pervasive Developmental Disorders in Montreal, Quebec, Canada: Prevalence and Links With Immunizations. Pediatrics 118:e139-50.

6.) Thompson WW, C Price, B Goodson, DK Shay, P Benson, VL Hinrichsen, E Lewis, E Eriksen, P Ray, SM Marcy, J Dunn, LA Jackson, TA Lieu, S Black, G Stewart, ES Weintraub, RL Davis, F DeStefano; Vaccine Safety Datalink Team (2007). Early Thimerosal Exposure and Neuropsychological Outcomes at 7 to 10 Years. NEJM 357:1281-1292.

7.) Parker SK, B Schwartz, J Todd, and LKPickering (2004). Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data. Pediatrics 114:793-804.

8.) Fombonne E (2008). Thimerosal disappears but autism remains. Arch. Gen. Psychiatry 65: 15-6.