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Saturday, March 30, 2013

Mindfulness from Meditation Associated with Lower Stress Hormone

From University of California Davis News

March 27, 2013

Focusing on the present rather than letting the mind drift may help to lower levels of the stress hormone cortisol, suggests new research from the Shamatha Project at the University of California, Davis.

The ability to focus mental resources on immediate experience is an aspect of mindfulness, which can be improved by meditation training.

"This is the first study to show a direct relation between resting cortisol and scores on any type of mindfulness scale," said Tonya Jacobs, a postdoctoral researcher at the U.C. Davis Center for Mind and Brain, and first author of a paper describing the work, published this week in the journal Health Psychology.

High levels of cortisol, a hormone produced by the adrenal gland, are associated with physical or emotional stress. Prolonged release of the hormone contributes to wide-ranging, adverse effects on a number of physiological systems.

The new findings are the latest from the Shamatha Project, a comprehensive long-term, control-group study of the effects of meditation training on mind and body.

Led by Clifford Saron, associate research scientist at the U.C. Davis Center for Mind and Brain, the Shamatha Project has drawn the attention of both scientists and Buddhist scholars including the Dalai Lama, who has endorsed the project.

In the new study, Jacobs, Saron and their colleagues used a questionnaire to measure aspects of mindfulness among a group of volunteers before and after an intensive, three-month meditation retreat. They also measured cortisol in volunteers’ saliva.

During the retreat, Buddhist scholar and teacher B. Alan Wallace of the Santa Barbara Institute for Consciousness Studies trained participants in such attentional skills as mindfulness of breathing, observing mental events, and observing the nature of consciousness. Participants also practiced cultivating benevolent mental states, including loving kindness, compassion, empathic joy and equanimity.

At an individual level, there was a correlation between a high score for mindfulness and a low score in cortisol both before and after the retreat. Individuals whose mindfulness score increased after the retreat showed a decrease in cortisol.

"The more a person reported directing their cognitive resources to immediate sensory experience and the task at hand, the lower their resting cortisol," Jacobs said.

The research did not show a direct cause and effect, Jacobs emphasized. Indeed, she noted that the effect could run either way — reduced levels of cortisol could lead to improved mindfulness, rather than the other way around.

Scores on the mindfulness questionnaire increased from pre- to post-retreat, while levels of cortisol did not change overall.

According to Jacobs, training the mind to focus on immediate experience may reduce the propensity to ruminate about the past or worry about the future, thought processes that have been linked to cortisol release.

"The idea that we can train our minds in a way that fosters healthy mental habits, and that these habits may be reflected in mind-body relations is not new; it's been around for thousands of years across various cultures and ideologies," Jacobs said. "However, this idea is just beginning to be integrated into Western medicine as objective evidence accumulates. Hopefully, studies like this one will contribute to that effort."

Saron noted that in this study, the authors used the term "mindfulness" to refer to behaviors that are reflected in a particular mindfulness scale, which was the measure used in the study.

"The scale measured the participants’ propensity to let go of distressing thoughts and attend to different sensory domains, daily tasks, and the current contents of their minds. However, this scale may only reflect a subset of qualities that comprise the greater quality of mindfulness, as it is conceived across various contemplative traditions," he said.

Previous studies from the Shamatha Project have shown that the meditation retreat had positive effects on visual perception, sustained attention, socio-emotional well-being, resting brain activity and on the activity of telomerase, an enzyme important for the long-term health of body cells.

The U.C. Davis Center for Mind and Brain

The Center for Mind and Brain is one of three overlapping research centers at U.C. Davis that bring together researchers from the School of Medicine, College of Biological Sciences, and College of Letters and Science to work on the function of the brain. Founded in 2002, the Center for Mind and Brain studies cognition, vision, language, meditation and music.

The Center for Neuroscience, established in 1990, investigates brain structure, memory, and the genes and molecules involved in conditions such as schizophrenia and depression. The MIND Institute was founded in 1998 with the support of six local families, five of whom have children with autism. It works with autistic children and their families, and on fragile X syndrome, Tourette's Syndrome and other neurodevelopmental disorders.

Autism Speaks Launches Employment Tool Kit

From Autism Speaks Family Services

March 28, 2013

"We have created this Employment Tool Kit, written directly to adults with autism, to help them research, find and keep employment in the current, competitive labor market."

Autism Speaks would like to help adults with autism with their employment search by giving them tools and tips while they look for a job.

Adults on the autism spectrum have strengths and abilities that employers are just beginning to understand. We have created this Employment Tool Kit, written directly to adults with autism, to help them research, find and keep employment in the current, competitive labor market.

Stories, tips and resources were developed by a collaboration of people, including adults with autism, dedicated to increasing employment of adults on the spectrum.

Although this Employment Tool Kit is geared towards adults on the spectrum, we know that families, transition coordinators, vocational rehabilitation staff, business leaders and anyone who is helping someone with autism find and keep employment will also find this resource helpful!

Immune Cells Regulate Brain Development

From NIH (National Institutes of Health) - Research Matters

By Meghan Mott, Ph.D.
March 25, 2013

Scientists discovered a new role for immune cells called microglia in the developing brain. The finding may reveal insights into neurodevelopmental disorders like autism and schizophrenia.

Microglia serve as a primary defense against infection and disease in the central nervous system. In the adult brain, microglia survey the environment, hunting for infectious agents or injured cells. When they detect damage or pathogens, microglia become activated and change shape in order to engulf and eat their targets. They rapidly clear away dying cells and repair tissue damage.

Microglia (green) contact and envelop
neural precursor cells (red) in the
developing brain. Image courtesy of
Journal of Neuroscience.
Microglial cells are also found in the brain’s cerebral cortex during prenatal development, but their role wasn’t well understood.

To investigate, a research team led by Dr. Stephen Noctor at the University of California Davis, studied microglia in the developing brain tissue of fetal rats, monkeys and humans. The work, funded in part by NIH’s National Institute of Mental Health (NIMH), appeared in the March 6, 2013, issue of the Journal of Neuroscience.

During prenatal development, neural precursor cells—cells with the ability to generate neurons—are rapidly produced in well-defined regions of the brain called proliferative zones. By labeling neural precursor cells and microglia with specific antibodies and other markers, Noctor and his colleagues were able to track them using confocal microscopy.

To their surprise, the scientists found that microglia were engulfing healthy precursor cells in developing brain tissue. Microglia were colonizing proliferative zones and the vast majority of them (over 95%) were activated. Time-lapse images showed microglia contacting healthy neural precursor cells and eating them within a few hours.

The researchers speculated that microglial activity during brain development might affect the number of neural precursor cells. To explore this idea, they used bacterial lipopolysaccharide (LPS)—a toxin that activates microglia—and the antibiotic doxycycline (Dox), which inhibits microglial activation.

The brain tissue of LPS-treated rat pups showed reductions in the number of neural precursor cells of up to 40% compared to untreated rats. The tissue of Dox-treated pups, on the other hand, showed an increase of 20% compared to controls.

Finally, the researchers tested a chemical that selectively kills microglia to see what effect it would have on neural precursor cells. The treatment removed 90% of microglia from the developing brain and significantly increased the neural precursor cell population.

Noctor proposes that the reason microglia feast on neural precursor cells may be to prune brain size during development. “It’s kind of like putting breaks on the system; it’s as if the brain is saying we have enough cells, we don’t need any more and the microglia come in and wipe up the remaining precursor cells,” he says.

Past studies have linked infections and immune activation during pregnancy with neurodevelopmental disorders such as schizophrenia and autism. Future research will explore whether the process this study uncovered could play a role.

Related Links


  • J Neurosci. 2013 Mar 6;33(10):4216-33. doi: 10.1523/JNEUROSCI.3441-12.2013. PMID: 23467340.

Antisocial Personality Disorder: The Hidden Epidemic

From OUPblog- Oxford University Press's Academic Insights for the Thinking World

By Donald W. Black, M.D.
March 22nd, 2013

It's hard to believe, but one of the most common and problematic mental disorders is ignored by the public and media alike.

People — and reporters — breathlessly talk about depression, substance abuse and autism, but no one ever talks about antisocial personality disorder. Why?

Though better known as sociopathy, Antisocial Personality Disorder, or ASP, affects up to 8½ million Americans and there is no cure, nor are there any good treatments.

Psychiatrists like me who are interested in this disorder tend to be ignored, and our concerns marginalized. The patients themselves can be difficult, and even unpleasant, and that limits interest. It is hard for people to be sympathetic toward those who tend not to arouse our concern. There are no poster children to point to.

Few mental health professionals are interested in the disorder, and some run when a colleague tries to refer an antisocial patient to them. ASP is rarely discussed in medical schools, and few researchers take it on as a cause. Most telling, the National Institutes of Health (NIH), the government’s premier medical research organization, funds a grand total of two projects in which the term “antisocial” appears in the title.

By contrast, the NIH funds hundreds if not thousands of studies on more conventional mental health topics such as schizophrenia, depression, anxiety disorders, and autism. How are we — as mental health professionals — to make headway in treating and preventing this disorder when the government does not lead the way?

First, let us consider what ASP is. Briefly, it is a disorder of chronic or serial misbehavior that begins in childhood and continues into adulthood, persisting throughout a person’s life. These individuals are the rule breakers who see fit to violate society’s conventions.

As children they fight with others, lie to their parents, and steal from the corner store. As adults, they abuse their partners or spouses, are irresponsible toward their children, and some are criminal. In the worst cases, some commit heinous acts of violence. Few of its sufferers are women, as it is predominately a man’s disorder.

"...most antisocial persons do not “suffer” in the usual sense since they rarely believe anything is wrong. Their behavior is not the problem; society and its tiresome rules are the problem."

And sufferer is not the right word, because most antisocial persons do not “suffer” in the usual sense since they rarely believe anything is wrong. Their behavior is not the problem; society and its tiresome rules are the problem.

How did we arrive at this point? First, there is the lack of visibility. ASP is not on the public’s radar screen. While known to psychiatrists and psychologists for nearly 200 years in one form or another, few mental health professionals bother to make the diagnosis or to even make referrals for its evaluation or treatment.

The public misunderstands the term antisocial, believing the disorder to relate to shyness, when it really relates to bad behavior directed against society. Finally, researchers tend to go where the money is. Since the NIH directs few funds to investigate ASP, why would an investigator study it?

Take autism as an example. The amount of research exploded within the last decade when it became clear that the government was interested in the disorder. That could happen with ASP if the NIH changed its tune. Despite this deliberate indifference, over the past 50 years researchers have — mostly on their own time and money — consistently shown it to be one of the most heritable of disorders and to have a clear neurobiological basis.

Why should I and others care? Though under the radar, ASP isn’t going anywhere. It will continue — over time — to cost us billions and billions though its direct and indirect costs associated with law enforcement and criminal justice. Nearly all of us are victims of an antisocial person’s misdeeds; we fear them and even grapple with the disorder in our families.

Now more than ever, psychiatry and society have the means to explore why some people turn bad, but progress will continue to accrue slowly until we begin to see ASP more clearly and commit ourselves to doing something about it.

Understanding the scope of ASP and coming to grips with it requires time and money. The NIH and other agencies must change their tune about funding ASP research and its many facets, particularly crime and violence. Priorities should include wide-reaching projects to explore its origins and search for methods to change its course.

Geneticists must continue to investigate genes that might predispose individuals to ASP and determine how they function. Neuroscientists should work to pinpoint brain regions linked to antisocial behavior, while identifying the neurophysiological pathways that influence its expression. Mental health professionals must overcome their own resistance to working with antisocial persons to develop new treatments.

Last, we must focus attention on the group at highest risk of developing ASP: children with antisocial behavior. Improved understanding of their home life and social environment may lead to more effective interventions that may prevent ASP from developing. By treating and possibly preventing ASP, we can have a broad impact that ripples through society, thereby helping to reduce spousal abuse, family violence, and criminal behavior.

About Dr. Donald Black

Donald W. Black, M.D., is the author of Bad Boys, Bad Men: Confronting Antisocial Personality Disorder (Sociopathy), Revised and Updated Edition. He is a Professor of Psychiatry at the University of Iowa's Roy J. and Lucille A. Carver College of Medicine in Iowa City. A graduate of Stanford University and the University of Utah School of Medicine, he has received numerous awards for teaching, research, and patient care, and is listed in “Best Doctors in America.” He serves as a consultant to the Iowa Department of Corrections. He writes extensively for professional audiences and his work has been featured in television and print media worldwide.

Prekindergarten Program Boosts Children's Skills

From Science Daily

March 28, 2013

Boston Public Schools' pre-kindergarten program is substantially improving children's readiness to start kindergarten, according to a new study of more than 2,000 children enrolled there.

The program uses research-based curricula and coaching of teachers, is taught primarily by masters-level teachers, and is open to any child regardless of income.

The study, out of Harvard University, appears in the journal Child Development. Some of the study's findings on the effects of the program are the largest found to date in evaluations of large-scale public prekindergarten programs.

Researchers found that the program substantially improved children's language, literacy, math, executive function (the ability to regulate, control, and manage one's thinking and actions), and emotional development skills citywide.

Children in the program were 4 and 5 years old and from racially, linguistically, and socioeconomically diverse backgrounds. While all students who participated benefited, the improvements were especially strong for Latino children.

Preschool has been shown to help prepare children for kindergarten and is an increasing priority among federal, state, and local policymakers. But many preschool programs struggle to attain good instructional quality.

"We can draw several important lessons from our findings about factors that support quality in prekindergarten," notes Christina Weiland, assistant professor at the Univ. of Michigan's School of Education, who was at Harvard when she led the study.

First, the combination of explicit, evidence-based curricula (in language/literacy and math), and in-classroom coaching of teachers as part of professional development, likely played a major role in improving student outcomes.

Investing in such quality supports for prekindergarten teachers may lead to gains in students' school readiness, the study found.

"...implementing consistent math, language, and literacy curricula might build children's executive function skills. Curricula in these areas may also improve such domains as executive functioning, even without directly targeting them."

Second, implementing consistent math, language, and literacy curricula might build children's executive function skills. "Our results suggest that curricula in these areas may also improve such domains as executive functioning, even without directly targeting them," according to Weiland.

"Interestingly, research shows that these kinds of skills -- which reflect early brain development, the ability to focus, and behavior -- are critical to children's success down the road."

Third, students in the program also may have benefited from having more mixed-income peers than is typical in most public prekindergarten programs, which are means tested and therefore tend to include mostly low-income students.

"Given the particularly large impacts for Latinos, a group that tends to be underenrolled in preschool programs, efforts to increase the enrollment of Latino children in high-quality prekindergarten programs such as the one studied here may be beneficial," Weiland adds.

Journal Reference
  • Christina Weiland, Hirokazu Yoshikawa. Impacts of a Prekindergarten Program on Children's Mathematics, Language, Literacy, Executive Function, and Emotional Skills. Child Development, 2013; DOI:10.1111/cdev.12099

Autism Prevalence is Now at 1 In 50 Children

From Forbe's Magazine - Pharma & Healthcare

By Emily Willingham
March 20, 2013

"CDC: These findings suggest that the increase in prevalence of parent-reported ASD resulted from improved ascertainment of ASD by doctors and other health care professionals in recent years, especially when the symptoms are mild."

The US Centers for Disease Control and Prevention (CDC) has released new figures for autism prevalence in the United States. They now give a prevalence of 1 in 50, but this story, like most autism-related stories, goes deeper than the numbers.

First, this prevalence estimate doesn’t focus only on 8-year-olds, the population used for deriving the 1 in 88 number reported in 2012. Instead, it encompasses the number of diagnosed autistic people walking around in 2011 and 2012 who were ages 6 to 17.

The 2007 percentage of the population fitting that description was 1.16%. These new numbers put that value for 2011-2012 at 2%.

From the CDC’s report [PDF]:

"The magnitude of the increase was greatest for boys and for adolescents aged 14–17. Cohort analyses revealed consistent estimates of both the prevalence of parent-reported ASD (autism spectrum disorder) and autism severity ratings over time. Children who were first diagnosed in or after 2008 accounted for much of the observed prevalence increase among school-aged children (those aged 6–17).

School-aged children diagnosed in or after 2008 were more likely to have milder ASD and less likely to have severe ASD than those diagnosed in or before 2007."

According to the CDC, hidden within these numbers, is the finding that most of the increase from 2007 to now occurred in school-aged children. In other words, given that it’s possible to diagnose autism as early as age 18 months and usually by age 5, many of these new autism diagnoses were in children who received them relatively later. Children who were, therefore, walking around for quite a few years with autism that went unrecognized … and uncounted.

That fits with the idea that a lot of the increase in autism we’ve seen in the last decade has much to do with greater awareness and identification.

The CDC’s information comes from parent reports, acquired by random telephone surveys. Parents answered questions about the ASD diagnosis and severity, and the age and year the child was diagnosed.

When the CDC did this study in 2007, the results relied on information for 63,967 children; for 2011-2012, that number was slightly higher at 65,556.

From 2007 to 2013, parent-reported autism prevalence increased significantly in all age groups in the 6-17 range, and increased for boys from 1.8% to 3.23%. Girls also showed an increase, but not as dramatic, from 0.49% to 0.70%. Autism among children ages 14 to 17 was up more than 1%, compared to children in the youngest, 6 to 9 age group (0.5%). In 2007, this older group, born in the 1990s, was less likely to have ASD than younger children.

Autism severity ratings (or, as a friend of mine analogizes, octane ratings) also were revealing. Children ages 2 to 13 in 2007 and diagnosed by that year — and who were thus 6 to 17 in 2011-2012 — showed no changes in ASD severity across years.

However, children in the 6 to 17 bracket diagnosed after 2007 were more likely to be rated as having “mild” ASD (6.9% for 2011-2012 versus 16.9% for 2007), suggesting that greater awareness and diagnostic capture explain the ASD increase in this group.

The CDC authors observe that the 14% of children ages 14 to 17 who were diagnosed at age 7 or later received their diagnosis “well beyond” the time when autism signs and symptoms become clear. In addition, more than half these children were classified as having “mild” ASD, according to their parents. The CDC authors say,

"Together, these findings suggest that the increase in prevalence of parent-reported ASD may have resulted from improved ascertainment of ASD by doctors and other health care professionals in recent years, especially when the symptoms are mild.

Changes in the ascertainment of ASD could occur because of changes in ASD awareness among parents or health care professionals, increased access to diagnostic services, changes in how screening tests or diagnostic criteria are used, or increased special education placements in the community." 

The report concludes:

"Increases in the prevalence of parent-reported ASD continued through 2011–2012, and much of the recent increase—especially for children aged 6–13—was the result of diagnoses of children with previously unrecognized ASD."

You will see a lot of headlines about the 1 in 50. Some organizations might even try to use those numbers to scare people, to talk about an “epidemic” or a “tsunami.”

But if you look at the numbers and the report itself, you’ll see that overall, the numbers of people born with autism aren’t necessarily increasing dramatically. It’s just that we’re getting better and better at counting them.

The next step is getting better at accepting autistic people, seeing their potential, and ensuring the supports and resources they need to fulfill that potential.

Friday, March 29, 2013

Support the Autism Special Education Center Tuesday, April 9th!

A MAC Program - Massachusetts Advocates for Children

OSEP on FAPE: Education of a Child with a Disability Must Also Address Non-Academic Needs

From MAC - Masssachusetts Advocates for Children

The following document interprets a February 29, 2012 letter from the federal Department of Education's OSEP (Office of Special Education Programs), clarifying that FAPE applies to all children with IEP's, and that that the educational needs of a child with a disability include nonacademic as well as academic areas.

"The Department's position that "the IDEA and its regulations do provide protections for students with high cognition and disabilities who require special education and related services to address their individual needs." Therefore, students with high cognition and disabilities such as Asperger's Syndrome or Autism Spectrum Disorder " could be considered under the disability category of autism and the individualized evaluation would address the special education and related services needs in the affective areas--social skills and classroom behavior--as appropriate." See Letter to Anonymous, (1/13/10).

A public agency cannot rely on any single procedure as the sole criterion for determining whether a child is a child with a disability and for determining an appropriate educational program for the child. 34 CFR § 300.304(b)(2). In conducting the evaluation of a child suspected of having a disability, including a child with high cognition, a public agency must use a variety of assessment tools and strategies to gather relevant functional, developmental, and academic information, including information provided by the parent, about the child that may assist in determining whether the child is a child with a disability and the educational needs of the child. 34 CFR § 300.304(b)(1).

As you referenced, it has been the Department's longstanding position that the educational needs of a child with a disability "include nonacademic as well as academig areas." The term "educational performance" as used in the IDEA "means more than academic standards as determined by standardized measures." See Letter to Lybarger, (September 14, 1990).

A public agency must provide an eligible child with a disability special education and related services. Under 34 CFR § 300.39(a), special education means specially designed instruction, at no cost to the parents, to meet the unique needs of a child with a disability. Specially designed instruction means adapting, as appropriate, to the needs of an eligible child under this part, the content, methodology, or delivery of instruction: (1) to address the unique needs of the child that result from the child's disability; and (2) to ensure access of the child to the general curriculum, so that the child can meet the educational standards within the jurisdiction of the public agency that apply to all children. See 34 CFR § 300.39(b)(3). 

Therefore, regardless of their level of cognition, when children with disabilities have been determined eligible for special education, specially designed instruction must be provided at no cost to the parents. Specially designed instruction must address both the unique needs of the child that result from the child's disability, which could include classroom behavior and social skills, and ensure access to the general curriculum. The school district's obligation under the IDEA to provide special education is not altered by the adoption of statewide academic achievement standards.

Based on section 607(e) of the IDEA, we are informing you that our response is provided as informal guidance and is not legally binding, but represents an interpretation by the U.S. Department of Education of the IDEA in the context of the specific facts presented.

If you have further questions, please do not hesitate to contact Dr. Deborah Morrow, of my staff, at 202-245-7456 or by email at"

Regulations Cited
  • 34 CFR 300.1(a)
  • 34 CFR 300.101(a)
  • 34 CFR 300.101(c)
  • 34 CFR 300.39(b)(3)
  • 34 CFR 300.304(b)(1)
Case Cited
  • 55 IDELR 172

Can Nutritional Supplements Help Treat Some Cases of Autism?

From SFARI - The Simons Foundation Autism Research Initiative

By Emily Singer
March 21, 2013

Pill potential: There is little hard evidence on the benefit of different nutritional supplements for autism.

The mention of nutritional supplements to treat autism might make some scientists wary. Little rigorous research has been done on their effects, and what research exists is often inconclusive.

In the past year, however, researchers have found specific genetic problems that point toward a metabolic deficiency in some cases of autism. These studies open up the possibility that supplements such as carnitine or certain amino acids may help treat autism.

The findings are exciting, because they suggest that some forms of autism may be preventable. But scientists don't yet have data on whether supplementing the diet in these cases can prevent the disorder or improve symptoms. Nor do they know whether the potential benefits will be limited to those with specific genetic deficiencies or be effective more broadly.

Some teams are looking more rigorously at the benefit of supplements across a larger population.

In January, a large-scale study from Norway showed that women who take folic acid supplements during early pregnancy reduce their risk of having a child with autism1. And a small, placebo-controlled trial of N-acetylcysteine (NAC), an antioxidant used to treat acetaminophen overdose, found that the supplement improves irritability in children with autism2.

Despite the promise, scientists say it's important to tread carefully and keep expectations in check.

Joseph Gleeson, professor of neurosciences at the University of California San Diego, published a study in September on a rare metabolic deficiency that may be treatable with certain amino acids. After the publication, he cautioned parents not to give it to their children until there was evidence of if and when it worked.

"We had people tell us, 'I know you said don't start this, but we did,'" he says.

Following the Genes

Last May, Arthur Beaudet and his collaborators showed that a small deletion in a gene called trimethyllysine hydroxylase, epsilon (TMLHE), involved in synthesizing carnitine, raises autism risk. (Carnitine helps transport fatty acids into the mitochondria, the cell's energy producer, which has also been implicated in autism.)

The study looked specifically at TMLHE, but Beaudet says that common variations in a number of genes have been shown to influence carnitine levels in the blood. He says environmental factors, such as diet, illness or even the microbes living in the gut, may also alter carnitine and, potentially, the risk of autism.

Beaudet's team is studying children with severe carnitine deficiency, a rare condition, and trying to get carnitine testing implemented on a wider scale.

It's not yet clear how broadly applicable the findings will be. "We already have a lot of patients who take carnitine and don't see striking behavioral effects," says Gleeson, who is not involved in the carnitine study. "Whether it will have a striking effect when used at optimal dosage, I don't know."

Beaudet says he hopes to work with researchers studying infants at high risk of autism — those who have an older sibling with the disorder and a 20-fold higher risk of developing the disorder than does the general population.

"I would like to see if nutritional supplementation from birth can push down this rate," says Beaudet. "But I don't know if I can convince anyone to buy into a trial like this."

It's not yet clear how lack of carnitine affects the brain, but Beaudet's team aims to answer that question by studying animal models — including worms, fruit flies and mice — with abnormal carnitine metabolism.

In September, Gleeson's team published a study identifying rare mutations in a gene called branched-chain ketoacid dehydrogenase kinase (BCKDK) in a pair of siblings with autism. BCKDK is involved in the breakdown of branched-chain amino acids, a set of molecules that are essential for building proteins.

Gleeson says he doesn't yet have enough people with the mutation to start a clinical trial of supplements. His team has shown, however, that giving the amino acids to mice lacking the enzyme helps restore their brain levels of them to normal.

To test whether the treatment might work for other forms of autism, his team is testing the amino acids in other mouse models of autism.

Diet Dilemma

These new studies aren't the first to link metabolic problems and autism3. Some children with untreated phenylketonuria, an inherited metabolic condition, or other rare inherited metabolic disorders also show symptoms of autism.

It's unclear how common these disorders are among people with autism. A 2011 study found that only 2 of 274 children with autism tested positive for a metabolic disorder. But Beaudet and Gleeson's studies, as well as ongoing sequencing studies of autism, may expand the number of disorders that fall into this category.

Other researchers are looking at whether supplements can lower autism risk or symptoms generally.

A study of more than 800 children, published in July, found that mothers who take 600 micrograms of folate during the first month of pregnancy are less likely to have a child with autism4.

The effect is strongest in women with a mutation in an enzyme called methylenetetrahydrofolate reductase (MTHFR), which is involved in a chemical reaction involving folic acid. MTHFR mutations have been weakly linked to autism.

A second, much larger study, published in January, provides further support that folic acid early in pregnancy can reduce the child's risk of autism by about 40 percent1.

The antioxidant NAC has also shown preliminary promise. A study published in June of 31 people with autism, half taking the supplement and half on a placebo, found that those taking the drug improved on a test of irritability. (The only two drugs approved by the U.S. Food and Drug Administration for autism both treat irritability.)

Antonio Hardan, who led the NAC study, says he was inspired to study the supplement in part because parents were already using it, despite little evidence of its benefit. But he says he was also interested in its antioxidant properties.

"There is some evidence to suggest oxidative stress is abnormal in individuals with autism," says Hardan, associate professor of child and adolescent psychiatry at Stanford University School of Medicine in California. NAC also targets a signaling chemical in the brain called glutamate, which has also been implicated in autism.

The fact that nutritional supplements are available over the counter has both benefits and drawbacks for clinical research. It's often easier to get approval to study these molecules in people. But because they are more loosely monitored than traditional drugs, the quality can vary widely, and researchers often need to do quality control tests themselves.

"We had huge issues over how and where to get NAC, and the quality," says Hardan.

It's also more difficult to find funding for these types of trials, because pharmaceutical companies aren't interested. The NAC study was funded by a private, parent-run foundation. With the promise of the pilot trial under his belt, Hardan is applying for funding for a larger trial from the National Institutes of Health.

  1. Surén P. et al. JAMA 309, 570-577 (2013) PubMed
  2. Hardan A.Y et al. Biol. Psychiatry 71, 956-961 (2012) PubMed
  3. Zecavati N. and S.J. Spence Curr. Neurol. Neurosci. Rep. 9, 129-136 (2009) PubMed
  4. Schmidt R.J. et al. Am. J. Clin. Nutr. 96, 80-89 (2012) PubMed

Thursday, March 28, 2013

Important Ruling: OSEP "Letter to Ramirez" on School Discipline and Special Education

From MAC - Massachusetts Advocates for Children

March 26, 2013

An OSEP letter regarding the purview of IDEA hearing officers will cause more parents to appeal the discipline decisions of school districts, attorneys and administrators fear.

Key points:
  • OSEP's Letter to Ramirez sparks concern among attorneys, administrators;
  • Agency says IDEA permits hearing officers to analyze school rules;
  • Sources fear letter opens door for more due process hearings over discipline.
When assessing disciplinary changes of placement under the IDEA, hearing officers can determine whether a student's action violated school rules, the agency said in Letter to Ramirez, 60 IDELR 230 (OSEP 2012).

"The IDEA and its implementing regulations neither preclude nor require that a hearing officer determine whether a certain action by a student with a disability amounts to a violation of the school district's Student Code of Conduct," OSEP Director Melody Musgrove wrote.

Traditionally, however, hearing officers have not examined local disciplinary findings or school policies in such discipline challenges, focusing instead on procedural compliance with IDEA stay-put and manifestation determination rules. Yet, sources say this letter now opens the door for parent challenges at the due process stage over whether students truly violated, or even knew about, their schools' codes of conduct.

What's more, sources question whether it's appropriate or even feasible for hearing officers to investigate local student conduct policies, and they advise you to work with general education staff to shore up the language contained in them.

Assessing IDEA's Intent

"I find the letter disturbing and confusing," said Jose Martín, a school attorney at Richards, Lindsay & Martín LLP in Austin, Texas. "What this letter is saying is hearing officers can look into the guilt and innocence of the student, and that's significant," he said. "Hearing officers have never been previously authorized to second-guess that sort of fact-finding, which involves interpreting local codes of conduct and making determinations of student behavior."

Yet, because the hearing officer's authority includes determining whether a child with a disability who violates school rules should be removed from his current placement, Musgrove wrote, "there may be instances where a hearing officer, in his discretion, would address whether such a violation has occurred."

Regardless, Martín said, the letter "confuses the longstanding understanding of the division of decision-making authority in IDEA discipline matters. ... The IDEA's mere reference to 'a child with a disability who violates a code of student conduct' doesn't mean Congress intended to create a second independent due process avenue to challenge local discipline fact-findings made under state and local DP systems, and it has never been interpreted in that way before."

In fact, Martín said, Congress sought to reduce litigation over discipline during IDEA '04 reauthorization by amending MDR and stay-put language. "This letter works against that policy and threatens to provide a new and significant incentive to discipline litigation before the IDEA IHOs."

On Alert for Costly Consequences

Questions about IDEA's intent notwithstanding, expanding hearing officers' purview in this manner raises concerns for schools that due process may become more costly and time-consuming, according to Christina Sepiol, an attorney and assistant director of the Southwest Cook County (Ill.) Cooperative Association for Special Education.

"The Letter to Ramirez could very likely have the effect of expanding the scope of a due process hearing," said Sepiol, who has served as a hearing officer in Indiana. "This translates into both time and additional witnesses in an already lengthy process."

Costs will rise if IHOs increasingly and more thoroughly review if and how the student behavior in question violated school policies, she said.

"Districts should be alerted that language used in their codes of conduct may be scrutinized, as well as their administrative implementation of them and students' understanding of the code."

"Districts should be alerted that the language used in their codes of conduct may be scrutinized, as well as their administrative implementation of such codes and students' understanding of the code," Sepiol said. "These are future areas of in-servicing and [staff] training."

For IHOs who are inclined to fully participate in the due process hearing, or who are cognizant of being overturned on appeal, this letter "offers an invitation for them to start at the beginning of the story," she said.

Due Process Discretion Advised

However, OSEP's opinion should be read "very narrowly," according to Deusdedi Merced, chief hearing officer to the IDEA hearing system in the District of Columbia and a trainer to IDEA hearing officers in the states of Illinois and New York.

That is, Merced said he would not suggest that hearing officers' jurisdiction has been expanded to include review of a student code of conduct violation that is unrelated to the hearing officers' subject matter jurisdiction found in 34 CFR 300.507.

Such a review may be necessary, he said, "to the extent that the IHO's inquiry ... informs his IDEA-centered appraisal of the student's provision of a FAPE or the appropriateness of the educational placement."

And, in truth, parent attorneys likely will seek relief at due process from detentions, suspensions and the like only in cases where a questionable or minor behavioral offense has occurred, Sepiol said. This could include when a student with a disability is alleged to have engaged in minor incidents involving fighting or aggression, hazing, or harassment, she said. It wouldn't include when principals or school boards react strongly to drug or weapon offenses.

Still, in the former cases, "parent attorneys have nothing to lose by asking an IHO to 'start from the beginning' by looking at the code of conduct and second-guessing the actions of general and special education administrators," she said.

Martín agrees.

"Parents would definitely prefer a special ed hearing officer to hear this as opposed to a local principal," he said. "If you open this door a hair, you're going to get parents appealing this stuff to hearing officers."

In the end, will hearing officers take this guidance to heart?

"Well," Martín said, "they're going to be asked to."

Where Does Anxiety Reside in the Brain?

From Machines Like Us

By Susan Lampert Smith
March 27, 2013

New findings from nonhuman primates suggest that an overactive core circuit in the brain, and its interaction with other specialized circuits, accounts for the variability in symptoms shown by patients with severe anxiety.

In a brain-imaging study published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the University of Wisconsin School of Medicine and Public Health describe work that for the first time provides an understanding of the root causes of clinical variability in anxiety disorders.


An abstract  of this study is available HERE.


Using a well-established nonhuman primate model of childhood anxiety, the scientists identified a core circuit that is chronically over-active in all anxious individuals, regardless of their particular pattern of symptoms. They also identified a set of more specialized circuits that are over- or under-active in individuals prone to particular symptoms, such as chronically high levels of the stress-hormone cortisol.

“These are important new insights into altered brain functioning that explains why people with anxiety have such different symptoms and clinical presentations, and it also gives us new ideas, based on an understanding of altered brain function, for helping people with different types of anxiety,’’ says Ned Kalin, senior author, chair of Psychiatry and director of the Health Emotions Research Institute.

“There is a large need for new treatment strategies, because our current treatments don’t work well for many anxious adults and children who come to us for help.”

In the study, key anxiety-related symptoms were measured in 238 young rhesus monkeys using behavioral and hormonal measurement procedures similar to those routinely used to assess extreme shyness in children. Young monkeys are ideally suited for these studies because of their similarities in brain development and social behavior, Kalin notes. Variation in brain activity was quantified in the monkeys using positron emission tomography (PET) imaging, a method that is also used in humans.

Combining behavioral measures of shyness, physiological measures of the stress-hormone cortisol, and brain metabolic imaging, co-lead authors Alexander Shackman, Andrew Fox and their collaborators showed that a core neural system marked by elevated activity in the central nucleus of the amygdala was a consistent brain signature shared by young monkeys with chronically high levels of anxiety.

This was true despite striking differences across monkeys in the predominance of particular anxiety-related symptoms.

The Wisconsin researchers also showed that young monkeys with particular anxiety profiles, such as high levels of shyness, showed changes in symptom-specific brain circuits. Finally, Shackman, Fox and colleagues uncovered evidence that the two kinds of brain circuits, one shared by all anxious individuals, the other specific to those with particular symptoms, work together to produce different presentations of pathological anxiety.

The new study builds upon earlier work by the Kalin laboratory demonstrating that activity in the amygdala is strongly shaped by early-life experiences, such as parenting and social interactions. They hypothesize that extreme anxiety stems from problems with the normal maturation of brain systems involved in emotional learning, which suggests that anxious children have difficulty learning to effectively regulate brain anxiety circuits. Taken together, this line of research sets the stage for improved strategies for preventing extreme childhood anxiety from blossoming into full-blown anxiety disorders.

“This means the amygdala is an extremely attractive target for new, broad-spectrum treatments,’’ says Shackman. “The central nucleus of the amygdala is a uniquely malleable substrate for anxiety, one that can trigger a wide range of symptoms.”

The work also suggests more specific brain targets for different symptom profiles. Such therapies could range from new, more selectively targeted medications to intensive therapies that seek to re-train the amygdala, ranging from conventional cognitive-behavioral therapies to training in mindfulness and other techniques, Shackman noted. To further understand the clinical significance of these observations, the laboratory is conducting a parallel study in young children suffering from anxiety disorders.

Other members of the research team include Jonathan Oler, Steven Shelton and Richard Davidson, all of the University of Wisconsin-Madison. Shackman is in the process of moving to the University of Maryland as an assistant professor.

Study Finds No link between Autism and Gut Microbes

From SFARI - Simons Foundation Autism Research Initiative

By Emily Anthes
November 5, 2012

Contradicting a popular hypothesis, a new study from Australia has found no connection between autism and bacteria in the gut.

The analysis, published 20 September in the journal Autism Research, reports that the gastrointestinal (GI) systems of children with autism harbor the same bacteria as those of their typically developing siblings1.

Bacterial controversy: Some studies have found
certain bacterial species in children with autism
and not in controls, but a new study says
there are no differences between the groups.

“Our conclusion was there’s no single organism that we can pinpoint as being always involved in autism,” says
Enzo Palombo, associate professor of microbiology at the Swinburne University of Technology in Melbourne, Australia, who is one of the investigators.

Based on 51 children with autism and 53 unaffected siblings, the study is larger than most studies of the microbiome — the collection of microbes in the body — in children with autism. Because siblings share genes and environment, this approach reduces ‘noise’ in the data from factors unrelated to autism, the researchers say.

However, critics argue that because children in the same family tend to have similar microbiomes, comparing children who have autism with their unaffected siblings may also make it more difficult to pick out subtle abnormalities associated with autism.

For years, scientists have
suspected that something is amiss in the guts of children with autism. Multiple studies have shown, for instance, that these children suffer from GI problems at rates far higher than other children do2 3 4.

Analysis of gut bacteria in children with the disorder has revealed some provocative findings. For instance, a 2005 study found that children on the autism spectrum have elevated levels of Clostridia, a class of bacteria that can produce neurotoxins, in their guts
5. And in a study this year, researchers found a class of bacteria known as Sutterella in children who have both autism and GI problems, but not in typically developing controls.

Some researchers have gone so far as to suggest that these atypical microbial populations may actively contribute to autism symptoms. For example, research last year showed that the fatty acids produced by gut bacteria can
alter the brain and behavior6 7.

Murky Link

That’s a controversial proposition, especially because the connection between autism and gut microbes remains murky. So far, studies have been small and their results inconsistent, implicating different kinds of bacteria.

In the new study, the researchers sequenced DNA extracted from the stool of 51 children with autism and 53 of their unaffected siblings, all between the ages of 2 and 12. The researchers then matched the sequences against a database of bacterial genomes to identify the microbes in each sample.

There are no significant differences in the types of bacteria or in their levels between children with autism and their typically developing siblings, the researchers found. Nor did they find differences between the gut microbes of children with autism who have GI symptoms and those who do not, or between children with severe forms of autism and those with mild forms of the disorder.

“We are showing that the link between specific bacteria in the gut and autistic symptoms and behavior is not definite,” says Palombo.

Still, other researchers say it’s too early to reject the idea that intestinal bacteria play a role in autism.

“In general, I think it’s a well-run study,” says
Sydney Finegold, emeritus professor of medicine at the University of California, Los Angeles. Finegold compliments the Australian researchers in particular for their large sample size, and for including children both with and without GI problems. But, he adds, “I disagree with their conclusion that there’s no relationship between intestinal bacteria and GI dysfunction and autism.”

For one thing, Finegold says, the results of the study may be confounded by antibiotic use. Palombo and his colleagues excluded children from their study who had taken antibiotics in the previous 15 days, but Finegold says he believes that that criterion is not stringent enough.

“We know that the impact of antibiotics on intestinal bacteria lasts for months, and some would say for years,” he says. He says these studies should preferably exclude children who have taken antibiotics anytime in the previous several months.

For his part, Palombo says, “I agree that a longer abstinence period would have been ideal, but we may not have had as many study participants.”

Subtle Differences

Palombo agrees that it’s too early to rule out a connection between intestinal bacteria and autism. A handful of the children with autism have various bacterial abnormalities, such as an elevated level of one species or another, he says, indicating that a subset of children with the disorder may show differences.

Some experts say comparing the gut microbes of children who have autism with those of their unaffected siblings, rather than with unrelated controls, may make it more difficult to detect subtle differences.

“Autism is a complex etiology,” says
Catherine Lozupone, a postdoctoral fellow in Rob Knight’s lab at the University of Colorado at Boulder. “There’s a genetic basis to it and there’s an environmental basis to it.”

Siblings share many genes and environmental exposures, would be expected to have similar microbiomes. In fact, some research has shown that whereas the gut microbes of children with autism are significantly different from those of unrelated controls, siblings have microbial populations that fall somewhere in the middle
5 8.

The Australian team next plans to look for differences in viral populations among these groups, as well as to study whether the bacteria in children with autism produce different metabolites than those in typically developing children.

Overall, the conflicting results of these studies may result from the fact that there’s not yet a single standard way to conduct this research, Lozupone says.

In addition to using different kinds of control populations, researchers can collect microbial DNA from fecal samples or, occasionally, directly biopsy the intestines. Some scientists compare the presence of specific species or genera, and others look for differences in families or classes of bacteria, which may obscure subtle differences at the finer, species level.

“It’s really hard to interpret microbiome results,” Lozupone says. “It’s a new field — we’re still trying to figure out how to analyze data.”


1: Gondalia S.V. et al. Autism Res. Epub ahead of print (2012)

2: Valicenti-McDermott M. et al. J. Dev. Behav. Pediatr. 27, S128-S136 (2006) PubMed

3: Gilger M.A. and C.A. Redel Pediatrics 124, 796-798 (2009) PubMed

4: Horvath K. and J.A. Perman Curr. Opin. Pediatr. 14, 583-587 (2002) PubMed

5: Parracho H.M. et al. J. Med. Microbiol. 54, 987-991 (2005) PubMed

6: MacFabe D.F. et al. Behav. Brain Res. 176, 149-169 (2007) PubMed

7: Shultz S.R. et al. Neuropharmacology 54, 901-911 (2008) PubMed

8: Finegold S.M. et al. Anaerobe 16, 444-453 (2010) PubMed

Wednesday, March 27, 2013

Must-See BBC Video: Through My Eyes - Rosie's Story

From the BBC's "Inside Out"

February 19, 2012

A BBC Documentary Looking at Autism
Airing April 2, 2013

Choosing Safe Children’s Toys and Products: Are They Phthalates-Free?

Excerpted from KidCompanions - For Kids that Love to Fidget & Chew

March 21, 2013

"...there is a potential for phthalates to impact birth outcomes, including gestational age and birth weight, fertility (lower sperm production), and anatomical abnormalities related to the male genitalia. Studies are now looking at the relationship between phthalates and asthma, and examining whether phthalates influence the timing of puberty or the risk for childhood obesity.”

Why are the chemical additives called phthalates banned in toys and products for children? Are you sure your children’s toys and products are phthalates-free?

Does your child, like most children, mouth items around the house that do not fall under the safety guidelines for kids’ products?

While researching to write this post on safe children’s toys and products. I learned a lot, and I was shocked at what dangers are lurking in toy boxes, cupboards and many other places in our homes!

What are phthalates?
  • Phthalates (pronounced “thah-lates”) are chemicals most commonly used to make a type of plastic called PVC (polyvinyl chloride).
  • These chemical plasticizers have been widely used since the 1950s.
  • They increase flexibility in plastic products, allowing them to bend without breaking.

Where are phthalates found?
  • Phthalates are in many household products, including adhesives, plastic wrap, plastic containers, flooring, furniture, wallpaper, shower curtains, window blinds, paint, and other things made of vinyl or PVC.
  • They are in personal care items like soap, deodorants, perfumes, lotions, creams, and powders.
  • These chemical additives are found in baby lotions, creams, and powders.
  • They help lotions penetrate and soften the skin, and help fragrances last longer.
  • Phthalates are in nail polish to prevent chipping and hair spray to prevent stiffness.
  • They are in some soft plastic toys, teethers, bath books, polymer clays, baby bottles, etc.
  • They are used to make soft plastic medical equipment, like bags for blood and intravenous fluids, catheters, tubing –even the ones used in the NICU and other baby and child care areas.
  • Phthalates can be breathed in from dust or fumes from any products that contain vinyl, such as vinyl flooring, vinyl seating found in cars, and some diaper-changing mats.
  • The production of fumes by these products is called off-gassing.
  • Phthalates can cross the placenta, so they can be passed to a baby during pregnancy when the mother is exposed. 

How do phthalates enter the body?

Phthalates generally enter the body via inhalation or absorption. Health Canada says while the phthalates in most PVC does not constitute a health risk, phthalates can leach out of soft vinyl when the products are sucked or chewed, migrating into the body through the saliva and creating a health risk. When items containing phthalates are subjected to heat, like microwave ovens or from the sun, or as these items get older it accelerates their escape from the plastics.

The reason phthalates are continuously released into the air, food, or liquids is that they are not chemically bound to the plastics. Have you seen brittle, hardened plastics? Most likely the phthalates have leached out, leaving behind plastic that breaks as you try to pick it up. 

Phthalates are also lipophilic, or attracted to fats. Fat present in blood can actually draw them out of IV bags, for example, and carry them into the body.

“Children are uniquely vulnerable to phthalate exposures given their hand-to-mouth behaviors, floor play, and developing nervous and reproductive systems,” says Sheela Sathyanarayana, an acting assistant professor in the Department of Pediatrics at the University of Washington.

Why ban phthalates in toys and children’s products?
  • Phthalates are linked to various health problems.
  • Phthalates are not chemically bound to the plastics they’re added to, they’re continuously released into the air or food or liquid.
  • They are linked to genital and urinary malformations in boys.
  • They may be the cause of some prostate cancers.

Studies have been made: “The animal studies suggest there is a potential for phthalates to impact birth outcomes, including gestational age and birth weight, fertility (lower sperm production), and anatomical abnormalities related to the male genitalia,” says Maida Galvez, a pediatrician and director of the Mount Sinai Pediatric Environmental Health Specialty Unit in New York City.

Galvez adds: “Human studies are now looking at the relationship between phthalates and asthma. There are also studies examining whether phthalates influence the timing of puberty or the risk for childhood obesity.”

Health Canada’s new restrictions on the use of six phthalates in children’s toys and products used in the care of children came into force on June 10, 2011. “These new regulations will ensure products that are imported, sold or advertised in Canada do not present a risk of phthalate exposure to children and infants,” Health Minister Leona Aglukkaq said in a statement.

Rick Smith, the executive director of Environmental Defence Canada, added: “Canada’s phthalates regulations are now aligned with measures taken in the United States and the European Union and will ensure our children receive the same high level of protection.”

How to protect my family from phthalates?

  • Choose products that are phthalate-free.
  • Check that the product’s container is phthalate-free.
  • To be sure use glass and stainless steel instead of plastic for water bottles, storage containers, and baby bottles…
  • Don’t microwave food in plastic, and don’t put plastic containers in the dishwasher.
  • Check the bottom of containers and choose those labeled #1, 2, 4, or 5, which are generally considered safer.
  • Buy only plastics made of polyethylene or polypropylene plastics rather than vinyl or PVC.
  • Be wary of hand-me-downs made of plastic because most will contain phthalates.

Here’s a list of the most common phthalates:
  • DBP (dibutyl phthalate)
  • DNOP (di-n-octyl phthalate)
  • DiNP (diisononyl phthalate)
  • DEP (diethyl phthalate)
  • BBzP (benzyl butyl phthalate)
  • DEHP (di 2-ethylhexl phthalate)
  • DiDP (diisodecyl phthalate)
  • DnHP (di-n-hexyl phthalate)
  • DMP (dimethyl phthalate)
  • DnOP (di-n-octylphthalate)

Parents and other care givers must stay informed about safe children’s toys and products. Arm yourself with knowledge about unsafe baby products.

Be vigilant because imported goods often do not pass US and Canadian standards, but find their way into our homes, day cares and unfortunately, into our children.