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Thursday, March 31, 2016

The Enemy Within

From Spectrum News

By Lydia Denworth
March 9, 2016



Introduction

Judy Van de Water got into autism research precisely because she wasn’t an expert in autism. She is an immunologist, studying the strategies our bodies employ to defend us against pathogens, and the ways those strategies sometimes misbehave or overreact.

But about 15 years ago, the then-new MIND Institute, which sought to bring fresh eyes to understanding disorders of brain development and function, set up shop near her lab at the University of California, Davis. When the institute asked for grant proposals from specialists in fields outside brain development, Van de Water heeded the call.

Her proposal eventually led her to pursue an outsider idea: the possibility that immune responses in an expectant mother’s body, unleashed in the wrong place at the wrong time, can interfere with the development of the growing fetus’ brain. She now holds that this immune activity could be the cause of nearly one in four cases of autism.

In particular, Van de Water blames a certain set of antibodies, immune molecules designed to target invading infectious agents and destroy or neutralize them. She’s so sure she’s right that she refers to it confidently as ‘MAR,’ or ‘maternal-antibody-related autism.’

From the start, it was a provocative theory that ran counter to prevailing beliefs about both the immune system and autism, and in the early days Van de Water was one of its few proponents. “We’ve been swimming upstream — still are,” she says. Her peers criticized Van de Water’s work on the grounds that her results didn’t support her claims.


And, they were deeply upset when, in 2013, Van de Water formed a licensing partnership with a San Diego-based company called Pediatric Bioscience. That deal was aimed at developing a maternal antibody screen that might allow for early diagnosis of autism or, if performed prenatally, indicate the risk of having a child with autism. “This is very, very premature,” Yale University autism researcher George Anderson told Science at the time.

Still, despite the controversy, the basic idea underlying Van de Water’s work — that maternal immune activity can increase risk for some types of autism — is edging into the mainstream. Researchers from other labs are exploring the consequences of maternal immune activity. Some teams are investigating a second immune pathway, involving cytokines, signaling molecules that coordinate the response to infection.


Their results, showing that antibodies and cytokines are both capable of producing autism-like symptoms in mice, have been reported in the past year in prestigious journals and at high-profile conferences.

The implications of this idea could be a huge deal for families. It should be possible to offer a test that screens a woman for the antibodies that might trigger autism, just as Van de Water hopes to do. “Testing for the presence of a particular antibody is something that, in principle, we know how to do,” says Betty Diamond, an immunologist at the Feinstein Institute for Medical Research in Manhasset, New York, who is another leader in the new field. What’s still unclear is how accurately such a test in a woman would predict autism risk in her child.


Diamond is instead focusing her lab’s efforts on prevention. She envisions treating a woman who carries the harmful antibodies with a relatively benign medicine that would neutralize the antibodies. “We want to develop something that’s safe enough that if we give it to 10 times the number of people we need to in order to protect one fetus, we haven’t done any damage at all,” says Diamond.

Fragile Truce

The suspicion that there might be a connection between the immune system and autism first emerged in the 1980s, based mostly on anecdotal evidence. In a 2006 review of the nascent field, Van de Water’s team called the immune system “a new frontier” for autism research and laid out several relevant themes: Children with autism spectrum disorder often have problems with their immune systems — they are sick more often than typically developing children are — and show evidence of neurological abnormalities, such as aberrant brain structures.


What’s more, women with autoimmune diseases, in which the body attacks healthy cells as if they were invaders, are more likely to have children with neurological disorders than are their peers. (A 2015 paper later confirmed this, showing that women with the autoimmune condition lupus double their risk of having a child with autism, and women with rheumatoid arthritis or celiac disease are also at increased risk.)

In her review, Van de Water also noted that immune dysfunction and autoimmunity have been associated with other disorders of brain development, such as schizophrenia, Tourette syndrome and Alzheimer’s disease.

Since 2006, researchers pursuing these observations have generally followed one of two tracks: Some have focused on immune issues in children, and others have explored what might happen in utero when a woman’s immune system misfires, overreacts or is ill-timed.

During pregnancy, a woman’s immune system can be said to be conflicted. To defend her against invading pathogens and microbes, the system marshals a veritable army of weapons, ranging from B cells and T cells to antibodies, and deploys them in an impressive variety of ways to get the job done. Yet a growing fetus carries its father’s DNA as well as its mother’s, making it a half-foreign presence in her uterus.


In response to this built-in standoff, a pregnant woman’s body compromises. It lets down its defenses a little, suppressing the immune system of the mother in favor of the fetus. So what happens if the woman does get sick while pregnant? Or has an immune system that doesn’t work well to begin with?

From such questions, a theory emerged, first published in 1990, that perhaps the fragile truce between the maternal immune system and a developing fetus doesn’t always hold. When it fails, the hypothesis goes, the mother’s defense mechanisms are activated — or sometimes malfunction — and damage the fetus.

Resistance to investigating immune connections to autism, in either children or their parents, was strong. “People assumed that everything is genetic,” says Andrew Zimmerman, a pediatric neurologist at the University of Massachusetts Medical School and an early researcher of maternal immune antibodies. What’s more, it was long thought that the immune system and the nervous system don’t interact much because most pathogens and immune molecules cannot breach the blood-brain barrier. (That barrier acts as a moat to protect the brain from compounds or pathogens in the blood.)


Also, the idea that a woman’s immune system might cause problems in the fetus came to the fore as the autism community was trying to undo the damage from the now-discredited theory that vaccines can cause autism. The experience placed an additional burden on any research implicating the immune system in autism.

Forging Ahead

Undaunted by the headwinds, Van de Water’s lab initially pursued research in both children and mothers, but eventually, her former postdoctoral fellow, Paul Ashwood, took the lead in investigating children’s immune problems at his lab at the University of California, Davis, while Van de Water continued to think about the mothers. She pursued the idea that maternal antibodies attack the growing fetus’ brain, killing healthy cells and setting development off track in a way that might eventually result in autism.


“The maternal antibody story made sense on a biological level to me,” says Van de Water. She started by screening blood from women who have children with either autism or specific language impairment, looking for patterns that stood out when compared with the blood of mothers of typically developing children.


Support for the idea came from a 2003 case study of a 38-year-old woman who had one typically developing child, one with autism, and one with specific language impairment. A group of researchers at Oxford University in the U.K. found that her blood carried an antibody that bound to fetal brain tissue from mice, meaning that the antibody was specialized for a target, or antigen, in the mouse brain.

The scientists injected serum from that woman into pregnant mice. The pups from these mice were less likely to explore, and a little slower at a standard test of motor coordination, than pups born to mice injected with serum from controls.

In 2007, Zimmerman and his collaborators took the work further to show that antibodies in the serum from mothers of children with autism bind to targets in brains from only fetal rats, not adult rats.

Meanwhile, Van de Water’s hunt soon paid off. In 2008, her group reported that in 7 out of 61 mothers of children with autism, or 11.5 percent, they had found a common, characteristic set of antibodies in the women’s blood that bound to tissue from fetal, but not adult, human brains. The researchers could not say why some women produce these antibodies and others don’t or whether these antibodies persist in women for life or are transient — and they still don’t know.


It took four tries to get that paper published. Van de Water says one reviewer responded with just one line: “We don’t know that autism has anything to do with the immune system.” Shortly thereafter, her team joined with MIND Institute neuroscientist David Amaral and reported that four rhesus macaque monkeys exposed in utero to the human maternal antibodies showed behavioral abnormalities such as stereotypic pacing and hyperactivity.

Watching those young monkeys struggle, says Van de Water, was “the moment I knew the antibodies were doing something.”

In 2013, her group identified seven proteins, all involved in neural development, that apparently are targets of maternal antibodies. Of the 246 mothers of children with autism in this larger study, Van de Water’s team reported that 23 percent carried some combination of antibodies to the specified proteins, compared with only 1 percent of the 149 mothers of typically developing children.


(Others who have analyzed the data from that paper say 23 percent is too high because Van de Water’s team included various combinations of antibodies in that figure. Steven Goodman, a biostatistician at Stanford University, noted in Science that no single pattern was found in more than 7 percent of the mothers.)

Diamond, an expert in lupus, wondered whether these same women might have signs of autoimmune disease in their cells even if they showed no symptoms. That’s exactly what her research later found. “They weren’t hurt by it because of an intact blood-brain barrier, but their fetuses might be hurt by it,” she says.

It turns out that a developing brain might be more vulnerable to autoimmune activity because it is not yet fully protected by the blood-brain barrier. In 2014, Diamond and her colleagues found that in mice, the blood-brain barrier of a developing fetus becomes truly impenetrable only in the third trimester. If a similar window of vulnerability exists in people, the implications for brain development are significant.


The long-held belief that the brain is ‘immune privileged’ and that antibodies can’t reach it has had to evolve. “We were too limited by that,” says Lior Brimberg, a postdoctoral fellow in Diamond’s lab.

Diamond’s team tested sera from more than 2,400 mothers of children with autism for the antibodies that attack fetal brain tissue. They found that the women who have these antibodies are more likely to have an autoimmune disease than are women who do not have the antibodies. They also found that mothers of children with autism are four times more likely to harbor the antibodies than is a control group of women of childbearing age.

Most recently, Brimberg devised a way to identify at least one of the target neuronal proteins, CASPR2, in fetal brains. When she injected an antibody targeting CASPR2 into pregnant mice, she found that the pups later had structural abnormalities in their brains — their neurons had fewer branches — and behaviors reminiscent of autism, such as impaired sociability. If this protein is involved in autism, Diamond estimates that it could be responsible for up to 4 percent of cases.


Notably, CASPR2 is not on Van de Water’s list of seven proteins, which strongly suggests that more possible protein targets for maternal antibodies will be identified in the future.

Preventing Autism?

Another line of research traveling a different path through the immune system has arrived at a similar pattern of results. Some studies showed that a pregnant woman who has a viral infection has an increased risk of having a child with autism. These were retrospective, asking women sometimes years after the fact to report any illness during their pregnancy.


A 2014 Swedish study was more persuasive because it followed the outcomes of more than 2 million births, confirming that an infection requiring hospitalization during pregnancy increases the risk of having a child with autism by more than 35 percent — even though the overall risk is still quite small.

Viral infections such as the flu set off a surge of cell-signaling cytokines, and neurobiologist Paul Patterson at the California Institute of Technology in Pasadena, an early pioneer in this research, became curious about the connections between viral infections and brain development.


Working in mice, Patterson’s lab mimicked viral infection in pregnant animals, stimulating their immune systems and causing behavioral deficits in the pups. In studying these pups, Patterson zeroed in on a particular cytokine called interleukin-6 (IL-6) that he linked to their abnormal behavior.

Patterson died in 2014, and Dan Littman, a neuroimmunologist at New York University, picked up where Patterson left off. Littman’s team was already studying a type of T cell called T-helper 17 (Th17) that is one of several created in response to the surge in IL-6 during an immune response to infection. Th17 cells help preserve barrier surfaces such as skin and intestinal linings. In January, Littman’s team showed that a cytokine called IL-17A, made by Th17 cells in response to an infection, crosses the developing blood-brain barrier of the fetus, acts on receptors in the fetal brain, and causes a malformation in the one region of the developing brain.


The researchers also saw autism-like behaviors in mouse pups exposed in utero to IL-17A. “It’s probably changing the way that the circuitry of the neurons is laid out during development and that leads to the behavioral deficit,” says Littman. When he and his colleagues treated pregnant mice with an antibody that neutralizes IL-17A, their pups did not show any behavioral changes.

There is a major caveat to this work, says Littman: “Whether this occurs in humans, we have no idea.”

Still, there are grounds for optimism. Last year, the U.S. Food and Drug Administration approved an injectable drug that neutralizes a form of IL-17 to treat people with psoriasis; more than 80 percent of the people who received the drug have seen positive results. “It’s revolutionized the treatment of psoriasis,” says Littman.


In the past two decades, drug developers have become expert at inventing therapies that target cytokines: Drugs such as Humira, which is used to treat rheumatoid arthritis, Crohn’s disease and other autoimmune diseases, are a major pharmaceutical success story. So it might be possible one day to interfere with cytokines that target the developing brain.

However, cytokine-inhibiting drugs can have serious side effects. It’s also not clear how drug developers would be able to achieve Diamond’s vision of an antibody-blocking drug that can be taken safely by a woman who has these antibodies and is hoping to get pregnant. “That’s the fantasy,” she says. “I’m hoping it’s not that hard. We have our ideas of how to do it.”


The Test

Van de Water can take much of the credit for the growing acceptance of the role of the immune system in autism. “She has made an enormous contribution,” says Zimmerman. But clinicians are still wary of an antibody-screening test. They question what they would tell women based on the results of the potential Pediatric Bioscience test, which is not yet on the market. “Predictability is the key,” says Zimmerman.


It’s not enough, in other words, to say that a woman has some of the antibodies in question if you can’t also tell her what that means for her risk of having a child with autism. Those answers will come only with prospective studies, the kind that follow women before, during and after pregnancy and track the health of both mother and child. Several such studies, including two conducted by Van de Water’s lab, are underway.

“A fundamental issue has been the rapidity between raising a possibility and talking as though it’s fact,” says Emanuel DiCicco-Bloom, a pediatric neurologist at Rutgers Robert Wood Johnson Medical School in New Jersey.

“I worry about this because parents ask me whether they should be treating their kid with this or that, or shouldn’t get pregnant again. There are real-world consequences.”

Van de Water says many doctors and reporters misinterpreted the news of her relationship with Pediatric Bioscience. “You license early,” she says. “The issue that arose was the misunderstanding between academia and industry about what it takes to go to market with a test; it’s a long, slow process of validation and verification.”

She says the intention is for the test to be used initially as a postnatal screen for antibodies in women as an early warning sign that a child should be monitored closely, perhaps leading to earlier diagnosis and therapy.

Eventually, though, the test would be used to assist with family planning. Van de Water argues that families deserve as much information as scientists can give them. She points out that antibody screening would only suggest whether women are high- or low-risk for having a child with autism: “What it gives families is a tool to make what is quite often a very difficult decision.”

Parents desperate for answers are some of Van de Water’s biggest supporters. Having one child with autism raises the risk of having another by 20 percent, so many families welcome any way to get a clearer sense of the odds.

Steve White, of Hayward, California, decided to participate in Van de Water’s antibody study after his third child, Herbie, was diagnosed with autism, even though he and his wife weren’t planning to have any more children. His wife tested positive for two of Van de Water’s seven antibodies. “I can’t say it solved any problems we had, but we were very glad to have answers,” says White.


And a 30-year-old mother, Elise, who did not want to give her full name for privacy reasons, says that with a history of miscarriage and one son with autism, her negative results — she had none of the seven antibodies Van de Water has identified — helped her and her husband decide to try to have a second child. “We know it’s not a guarantee, but it’s nice to have one less thing to worry about,” she says.

Van de Water says she regularly gets emails from women asking when the antibody test will be ready. She knows of families who have one child with autism who have opted to use surrogates, for fear that a second child will also have the condition. Even women long past their childbearing years ask if they can be tested. “They just want to know,” she says.

Van de Water says her dream is that her work, combined with efforts to create drugs that protect against maternal antibodies, will one day make it possible to restore the fragile truce between a woman’s immune system and her growing fetus. “That would be amazing.”

High Anxiety Risk in Adolescence Linked to Single Gene

From LiveScience
via Fox News Health

By Bahar Gholipour
LiveScience

March 22, 2016



Anxiety disorders often emerge in adolescence, when the brain goes through massive changes and new genes are expressed. Now, researchers have found a gene that may be a factor in the general peak of anxiety during this time.

They also found that carrying a common version of this gene may protect people from anxiety.

"We were interested in why it's that anxiety peaks in adolescence, and in understanding the factors that might increase risk for anxiety to help target intervention and treatment," said study author Dylan Gee, an assistant professor of psychiatry at Weill Cornell Medicine in New York.

In the study, Gee and her colleagues focused on a genetic factor linked with anxiety that is also involved in a system called the endo-cannabinoid system. This system includes a number of signaling molecules — along with receptors and enzymes — that are involved in regulating appetite, pain and mood.


(It's also the system that responds to the psychoactive effects of cannabis.)

As a person enters adolescence, changes in gene expression increase the number of cannabinoid receptors in the brain. The levels of enzymes and signaling molecules fluctuate as well, altering the communication throughout this system. But exactly how the communication is altered depends on which version of certain genes a person has.

In the new study, the researchers focused on the gene that encodes a regulatory enzyme called FAAH. Most people carry the default version of the FAAH gene, but 20 percent carry a variant. Depending on which one a person carries, the levels of the FAAH enzyme could increase or decrease during adolescence, which affects brain development differently.

Using brain scans from 1,050 children and young adults ages 3 to 21, the researchers investigated the effects on the wiring of the brain of those people who carried default or variant FAAH.

Specifically, they looked at the neural tract that connects the brain's limbic structures, which are involved in emotions such as fear and anger, to frontal areas of the brain, which govern a diverse set of functions.

The results showed that the study participants who carried the gene variant had a stronger connection between their limbic and frontal brain areas, compared to those who carried the default gene. They also reported less anxiety.

The stronger connection between frontal and limbic areas might mean that in these people, the frontal areas are better at regulating fear responses in the limbic areas, effectively controlling anxiety levels, the researchers suggested.


Interestingly, however, this difference between the two groups was seen only in the participants who were older than 12. In other words, the difference appeared to emerge as people entered adolescence.

"We discovered that genetic variation in this endocannabinoid signaling emerges in adolescents, when anxiety peaks, but not in children," Gee said.

The researchers repeated these observations in mice genetically engineered to express human-like variants, according to the study, published today (March 21) in the journal Proceedings of the National Academy of Sciences.

The findings highlight just one factor among many that may contribute to the emergence of anxiety in adolescence. "We know there are so many different factors — biological, environmental, genetic — that all interact together," Gee said. "The new study helps to understand how genetic variation can emerge at different stages of development."

About 25 percent of people develop an anxiety disorder in their teen years, and 6 percent develop a severe form of an anxiety disorder during this time. Currently, the first, and gold-standard, treatment for anxiety is cognitive behavioral therapy, a method that aims to change a person's attitude in the face of problems and difficulties.

Sometimes, anti-anxiety medications as well as SSRI antidepressants are also used to treat anxiety.

The new findings are early, and need to be confirmed with further research. But if they hold true, they could help researchers fine-tune the biological targets that they look at when developing new medications for anxiety, and help optimize treatments that are better-tailored to developmental stages and individuals' genetic makeup, the researchers said.

Wednesday, March 30, 2016

A Brief History of Autism Research

From Spectrum
via The Atlantic

By Rachel Nuwer
March 15, 2016

Cautionary tales from researchers’ past mistakes.


The past six months saw the release of two bestselling books about autism: Steve Silberman’s Neurotribes, and John Donvan and Caren Zucker’s In a Different Key.

Both books chronicle the oftentimes dark history of autism while expressing hope for a better future for people with the condition. They focus on the good work of people—strong-willed parents and devoted advocates—who transformed a once-shameful diagnosis into a widely accepted condition. But they also highlight several missteps by scientists that derailed research and the lives of many people on the spectrum.

This history offers lessons for today’s scientists, ranging from the importance of purging presumptions about autism to the acute need for services that help people, especially adults, with the condition.

The books take the reader back to the infancy of autism research. In the late 1940s, psychiatrists declared that they had found autism’s cause: cold parents—particularly mothers—who did not love their children enough. Leo Kanner, one of the first psychiatrists to study the condition, abandoned his own theory that autism was innate in favor of what would later be called the “refrigerator mother” hypothesis.

“If Kanner had really stuck to his guns and gone with his instincts, it’s possible the whole refrigerator-mother theory never would have evolved the way it did,” Donvan says.

Instead, for the next two decades, many psychiatrists focused on treating what they believed were defective mothers and fathers. Research exploring other explanations for the condition stagnated.

Having a scientific orthodoxy can be a positive thing, but it can cause severe damage if it turns out to be inaccurate, Donvan says. “The history of autism has shown that, time and time again—particularly in the early days—researchers failed to examine their own assumptions and biases.”

* * * * *


Flawed assumptions also invade researchers’ attitudes toward people with autism, according to Silberman. He says scientists long viewed people with autism as less than human, rationalizing a range of “treatments” that were more akin to torture than therapy, including electric shocks and physical abuse such as hitting. Although contemporary practitioners have largely abandoned these methods, some continue to use punishment as a means of modifying behavior, he says.

“The first question that should be asked in any research project is, ‘Would you do this to a non-autistic person?’” he says, noting that asking adults with autism for their input is a crucial second step. “Autistic people should be seen as valuable collaborators in your work, rather than as passive subjects.”


Many researchers working in the field today are motivated by a deep desire to help people with autism, Donvan says. But scientists should still ask themselves, “Is there anything I’m doing now that I may regret 20 years from now?”

Some of the researchers who tested electroshock therapy or hallucinogenic drugs in children with autism back in the 1950s and ‘60s did so with the best of intentions, Donvan says. “In light of modern mores and best practices, those choices look bad today,” he says. “But that does not mean those researchers were motivated by cruelty or sadism.”

* * * * *

The 1990s saw a sea change in awareness of autism. People previously diagnosed with childhood schizophrenia or minimal brain damage were recognized as having autism all along. This new awareness sparked the notion of an ‘autism epidemic,’ which drew an influx of research dollars into a once underfunded and overlooked field. But unfortunately, little of this money went toward helping people with autism.

It went largely to uncovering autism’s cause, giving scientists insight into the workings of the brain. It also generated leads for drug targets. But for people with autism and their families, “the tangible benefits remain elusive,” Silberman says.

Researchers know “astonishingly little” about the lives of adults with autism, he adds, including how many of them there are, how other conditions associated with autism affect their lives and how best to translate their abilities into meaningful employment.

Likewise, little research focuses on how autism manifests itself in women, or on determining the prevalence of autism in minority communities with limited access to diagnostic services.

There is also little research into better drugs for controlling seizures—one of the leading causes of death among people with autism.

“These are not questions that can be answered by sequencing another set of genomes of people from multiplex families,” Silberman says. “That kind of work is still very much worth doing, but if we’re only doing that kind of long-range research, we’re not really meeting our responsibility as a society to help the autistic people who are all around us lead happier, healthier, more fulfilling and more secure lives.”

* * * * *


For those who are investigating treatments and services for people with autism, Zucker and Donvan warn that the work carries great responsibility. Parents are desperate for guidance about how to help their children, they say—especially in light of the emphasis put on early intervention.

As past examples ranging from vitamins to hugging therapy have shown, families will rush to adopt new methods that are prematurely presented as solutions.

“Researchers need to be very, very careful in how they present their findings, so as not to set off hope for a quick, silver-bullet-type solution,” says Donvan.

How researchers talk to the press can shape the public reaction to research. In 1987, for example, The New York Times reported on the work of Ivar Lovaas, a clinical psychologist and pioneer in applied behavior analysis. The story, titled Researcher Reports Progress Against Autism,” described children who were “transformed” into “apparently normal children.”

Although Lovaas never used the word ‘cure’ when talking to the Times, the story implied as much. The fact that his research was preliminary was largely overlooked. Parents frantically flew their children to his lab at the University of California, Los Angeles, even as he hopelessly tried to correct the false headlines.

Today’s scientists should take great care when describing their work and strive to communicate their findings in terms non-experts can understand, Donvan says. “Researchers need to understand that there’s a public that is hanging on their every word.”

Charter Schools are Suspending Kids More than Other Schools, and That’s a Problem

From the HuffPost Politics Blog

By Rebecca Klein
March 16, 2016

School suspensions contribute to the school-to-prison pipeline. 

Eva Moskowitz of Success Academy Charter Schools at a Harlem location.

Success Academy, a chain of high-performing charter schools, came under fire in October 2015 after revelations emerged that one of its principals had drawn up and distributed a “got to go” list of problematic students. Nine of the 16 students on the list eventually left the school after facing continuous suspensions and harsh punishments.

The incident sparked a federal complaint against the New York-based charter network, and fueled concerns from critics that it was pushing out its most vulnerable students.

Success Academy is just one example of a charter school network that has been dogged with controversies over methods of discipline. However, its practices raise questions about whether charter schools — institutions that are publicly funded but independently operated — punish students more harshly than traditional public schools.


A new report released Wednesday from the UCLA Civil Rights Project seeks to answer these questions.

Through analyzing public data submitted to the Office of Civil Rights in 2011-2012 from over 5,000 charter schools, UCLA researchers determined that charter schools punish students with out-of-school suspensions slightly more than traditional public schools. In many schools, these suspensions disproportionately target black students and students with disabilities.


Researchers recommend that charter schools — like regular public schools — work to reduce these numbers and instead embrace discipline methods that support students with behavioral issues.

During the 2011-2012 school year, charter schools suspended 7.8 percent of all of their students, whereas traditional public schools suspended 6.7 percent of all students enrolled. Since that time, the negative impact of school suspensions has become more widely publicized, with groups like the American Academy of Pediatrics recommending that schools reserve the practice for extreme circumstances.


A number of large school districts like Chicago and Denver have introduced policies designed to curb harsh discipline.

“The choice is not between chaos on the one hand and very strict discipline on the other,” said Daniel Losen, author of the report and director of the Center for Civil Rights Remedies, an initiative at the Civil Rights Project. “There are lots of things in between that teachers can learn.”

Some of the data submitted to the Office of Civil Rights is incomplete. A number of charter schools reported that they didn’t have any student suspensions, though state data proved otherwise. Law requires schools to report these numbers.

“This raises questions about whether charter schools may be violating civil rights law by not reporting the data on whom they exclude from school on disciplinary grounds,” noted researchers.

The news wasn’t all bad. Far more charter schools suspended low numbers of students than those that suspended many.

“One can reasonably infer that, like noncharter schools, there are likely many effective charter schools that reserve suspension as a measure of last resort,” notes the report.

On the other end of the spectrum, though, some schools clearly misuse the practice. Nearly 400 charter schools suspended a quarter of their student body at least once during 2011-2012.

Suspensions can have a devastating impact on students. Previous research has found that suspensions contribute to the school-to-prison pipeline, which pushes students out of school and makes them more likely to end up in the criminal justice system. Students who get suspended from school are more likely to drop out of high school later on.

And as states around the country gear up to implemented the Every Student Succeeds Act, the major federal law replacing the George W. Bush-era No Child Left Behind Act, Losen called on states to pay attention to these numbers. Under the new law, states are required to lower the number of schools overusing harsh discipline. Charter schools are also beholden to these requirements, unless a state specifically passes a law exempting them.

“There should be no exemptions or excuses for charter schools,” said the report.

Some groups have pushed back against the report’s data. The Center for Reinventing Public Education, a research center out of University of Washington, said the report “creates more confusion than clarity.” Comparisons between individual charter schools and public school districts are not necessarily representative, the group argues.

“Our expert panel agreed that comparisons must be apples to apples — among individual schools, not between schools and whole districts; among schools serving the same grade levels and demographic groups; and among schools in communities with similar rates of student attendance and school completion,” said a statement from CRPE director Robin Lake.


“Research must not simply compare averages, but analyze the relative contribution of school practices and other factors. It is misleading to make crude charter-district comparisons about discipline outcomes, just as it for achievement test scores.”

M. Karega Rausch, the vice president for research at charter school oversight group National Association of Charter School Authorizers, told The New York Times that it is important for parents to “have the ability to choose a school that best meets their children’s unique needs.”

“For some children, that may be a school with strict rules; for other children, that may be a school that is less strict,” he added.


........................................................................

Rebecca Klein covers the challenges faced in school discipline, segregation, and the achievement gap in K-12 education. In particular, she is drilling down into the programs and innovations that are trying to solve these problems. Tips: email Rebecca.Klein@huffingtonpost.com.

Tuesday, March 29, 2016

What Does it Mean to 'Look Autistic?'

From The Atlantic

By M. Nicole.R.Wildhood
March 24, 2016

A writer’s reflections on the pain of “passing” for neurotypical.


“But you don’t look autistic,” a new friend told me recently when I revealed my diagnosis. I could tell from his tone that he meant it as a compliment—his tone wasn’t accusatory so much as reassuring. It was as if he were trying to tell me that I could still find nourishing friendships “anyway,” or at least that our budding one wasn’t threatened.

Because this was not the first time I’d been told that I “don’t look autistic,” I had a response ready: “And what is it that you think autistic people look like?” He froze.

I am autistic: My official diagnosis is Asperger’s, or what is now Autism Spectrum Disorder (ASD). I actually prefer the phrasing he used: “But you don’t look autistic” uses “identity-first” language (“I am autistic”), as opposed to “person-first” language (“I am a person with autism/who has autism”).


So he had correctly identified me, even done it in the way I like to identify myself—and then told me I didn’t fit in with those I consider my people.

But ASD is not some oppressive overlay of my “real” personality. My diagnosis means that I fall outside certain bell curves for things like eye contact, needs for structure and routine, social engagement, rigid thinking patterns, and defaulting to literal interpretation, to name a few.

These traits are not always immediately visible to the observer, and others have said it—“You don’t look autistic”—with suspicion, as if I look too “well,” too “normal,” too not-autistic to actually be autistic. Somehow I need to prove, with my physical appearance or behavior, that I really am what I say I am.

Of course, I didn’t “look autistic” enough for anyone in my youth to catch on. Not even my mother, who taught special education for close to three decades, or the therapist who saw me regularly throughout my formative years. I “passed” as neurotypical until I was 28—long enough, in other words, to learn how to contort myself into someone who fit in.

On some level, though, it is difficult to fault the people whose care I was under for not noticing sooner: It’s a widely held belief that autism is much more common in boys than girls. This often translates to screening boys more carefully for autism than girls, and misdiagnosing girls with something else—obsessive-compulsive disorder, borderline personality disorder, depression, anxiety.I had to frantically learn to mimic how I saw others relating to one another.

By the time I got to high school, I was indeed depressed and anxious, unable to interact socially without sweaty, shaking hands. And high-school girls are especially unforgiving of what I came to think of as my relational “failings”—my inability to produce small talk, my struggle to maintain eye contact, my uncertainty about how many details to include when someone asks me how my day is.

Because I don’t naturally intuit cultural expectations for socially normative behavior, I had to frantically learn to mimic how I saw others relating to one another—which not only confused me, but likely made me seem robotic and stiff to the people I was trying to connect with. And those connections, even when they happened on a surface level, never felt real to me: It is impossible to metabolize the love people may genuinely be offering if the person they’re offering it to is actually a fa├žade.

I’ve hungered for deep, meaningful connection with other people for as long as I can remember. I’ve known I was different for almost as long. Being aware of the dissimilarities between me and my peers didn’t make things any easier—the awareness made me hyper-vigilant about appearing “normal,” and so all the more anxious.

By age 5, I had begun a high-level construction project, creating a new outward-facing version of myself to fit with the social norms I perceived. These contortions, as involuntary as they came to be, never felt natural. I always knew I was hiding, but did not know how obvious that was to others; I can only look out into the world autistically.

I didn’t know that what meticulously maintained masquerade was really about “not looking autistic.” Or that I would be so literally following the “therapeutic” advice of my childhood therapist: “Fake it till you make it.”

What qualifies as “making it,” though? If I don’t “look autistic” enough, people might think I’m a fraud, and I might not qualify for services designed to support me. My need for structure and routine might be seen as “controlling,” my meltdowns (not to be conflated with “tantrums”) merely the mark of immaturity.

If I do “look autistic,” though, would my anger be brushed off as “just the autism talking?” Would my meltdowns “allowed” the way a child’s acting-out would be—tolerated, but not engaged with? When I am so overcome with emotion that I cannot speak, it is called “selective mutism.” When I find joy in something seemingly incongruous with my age, gender or peer group, like trains or circuits, and get engrossed in it long enough to become a veritable expert, it’s called “restricted interests” or “fixations.”

The perspectives I have on people and the world I’ve interacted with thus far in my life are necessarily informed by my ASD, whether it looks like I’m an Aspie or not. Ultimately, when my friend told me I don’t look autistic, he was essentially affirming my constructed normalcy, my ability to fake it. In high school, I would have relished in this aptitude to appear “same,” and would have taken his remark as a compliment.

But I’ve come to realize that each attempts to somehow make myself more “acceptable” to someone else, more lovable, has left me with what is, in the end, a false connection. I don’t want to be judged based on my ASD alone, but nor do I want it to not matter. I may not “look autistic” from the outside, but if you see with my eyes, I do.

Standards, Grades And Tests Are Wildly Outdated, Argues 'The End Of Average'

From nprEd

By Anya Kamenetz
March 23, 2016

Todd Rose dropped out of high school with D- grades. At 21, he was trying to support a wife and two sons on welfare and minimum wage jobs.

Today he teaches educational neuroscience at the Harvard Graduate School of Education. He's also the co-founder of The Center for Individual Opportunity, a new organization devoted to "the science of the individual and its implications for education, the workforce, and society."


How We Succeed in a World
That Values Sameness
Hardcover, 246 pages
In other words, Todd Rose is not your average guy. But neither are you.

In fact, he argues, absolutely no one is precisely average. And that's a big problem, he tells NPR Ed:


"We've come to embrace a way of thinking about ourselves that was intentionally designed to ignore all individuality and force everything in reference to an average person."

Admissions offices, HR departments, banks and doctors make life-changing decisions based on averages. Rose says that "works really well to understand the system or the group, but it fails miserably when you need to understand the individual, which is what we need to do."

Rose talked with us about his new book: The End Of Average: How We Succeed in a World That Values Sameness.


The opening example you use in the book is that in the 1940s, when the Air Force designed cockpits based on the average measurements of the pilots, there were an unacceptable number of crashes. But when they went back and measured thousands of pilots, across 10 body dimensions, they found that zero of them even came close to the "average" on all 10. So they concluded that they had to redesign the seats and so forth to be adjustable to each person.

Body size is a very concrete example of what I call jaggedness. There is no average pilot. No medium-sized people. When you think of someone's size you think of large, medium, small. Our mass-produced approach to clothing reinforces that. But if that were true you wouldn't need dressing rooms.


So dimensions like height and weight and arm length and waist circumference ...

Yes, they're not nearly as correlated as you would think. Height is one-dimensional, but size isn't. People are jagged in size, in intelligence, everything we measure shows the same thing.

I'm going to quote a line from the book, said to psychologist Peter Molenaar, who is arguing for a greater focus on individual difference: "What you are proposing is anarchy!" How do you make decisions about people if you can't use statistics and cutoff scores and compare them to averages?

People feel like if you focus on individuality, everyone's a snowflake, and you can't build a science on snowflakes. But the opposite has been true.

It's not that you can't use statistics, it's just that you don't use group statistics. If I want to know something about my daily spending habits, one straightforward way would be to collect records of what I spend every day. To take an average for myself would be perfectly fine.

So you can generalize across time, but not across people?

We've got to let go of putting a group into a study and taking an average and thinking that's going to be close enough to universal insight.

Now we have something better. We have a natural science of individuality that gives us a surer foundation. We've gotten breakthrough insights in a whole range of research, from cancer to child development.

How does what you term "Averagerianism" impact our school system both historically and today?

It's so ubiquitous that it's hard to see.

We design textbooks to be age-appropriate, but that means, what does the average kid of this age know and can do? Textbooks that are designed for the average will be a pretty bad fit for most kids.

Then you think of things like the lockstep, grade-based organization of kids, and you end up sitting in a class for a fixed amount of time and get a one-dimensional rating in the form of a grade, and a one-dimensional standardized assessment. It's everything about the way we test and move kids forward.

With standardized tests, I often hear teachers talking about students being two months behind or ahead, as if there's a very fixed timeline for progress that all human beings should fit.

It feels comforting. But if you take the basic idea of jaggedness, if all kids are multidimensional in their talent, their aptitude, you can't reduce them to a single score. It gives us a false sense of precision and gives up on pretending to know anything about these kids.

So alongside jaggedness, two other principles of individual variation you look at are "context-dependence" and "pathways." Talk about those.

It's meaningless to talk about behavior and performance without context. Let's take assessment. Carnegie Mellon [University] had this work showing that changing the way a question is asked can fundamentally alter how a kid performs. So if the [math] problem is about football players instead of ballerinas, you can't standardize on the item. That systematically affects the kids' ability to demonstrate what they know.

But at a macro level, I think [context] introduces an attention to things like the impact of stress and trauma.

And what about pathways? This sounds a lot like the talk around personalizing learning using technology and allowing each student to learn at his or her own pace.

I think people who care about personalized learning talk about it as: If we just collect more data, we're going to have this personalization. And that's not clear to me at all.

I think when you look at the idea of pace, we are so convinced that slow means dumb and fast means smart. We feel justified in pegging the time to how fast the average person takes to finish.

But this is where, with a better understanding of this and realizing, "Oh, pace really has nothing to do with ability, people are fast at some things and slow with others," you would build a very different system than the one we have.

Do you think the school system acknowledges the need to treat students as individuals?

Two years ago I would have said no. But my colleague Paul Reville, who used to be secretary of education in Massachusetts, he's rethinking the architecture of school systems. In most states, people have put on the books goals about meeting every kid where they're at.


Even the "Every Student Succeeds" [ESSA, the new federal law] approach is based on the assumption that we're meeting each kid where they're at, to give them what they need to be successful.

But we haven't thought through the system design that needs to be in place to do that.

We're trying to have a system to do what it was never designed to do.

What about in higher education?

In higher ed we have a brutally standardized system. It doesn't matter what your interests are, what job you want, everyone takes the same courses in roughly the same time and at the end of the course you get ranked.

This is personal for me. I have two kids in college. The idea that someone is going to click a stopwatch, compare you to other kids in your class, and the kids with the best grades can get the best jobs, that's not a good deal. I want my two boys to figure out what they love and what they're good at and be exposed to things and be able to turn that into a job.

You talk about innovations that are starting to catch on, like competency-based education and credentialing — basically, accommodating different pathways and different balances of strengths and weakness.


There's plenty of ways we're making smaller units of learning to combine in ways that are useful to you. To me, competency based education is nonnegotiable. I don't think you can have fixed-time, grade-based learning anymore. I don't see how you justify diplomas.

It doesn't mean students can take forever, but allowing some flexibility in pace and only caring whether they master the material or not is a sound foundation for a higher ed system.

There are so many examples of a lot of really interesting universities trying these things.

Yes, reading this book it struck me that in some quarters, it seems like we've already moved forward to a focus on individuality, innovation, creativity. You talk about how companies like Google are finding that GPA or school prestige or even ranking employees against each other is not useful, and instead they need to create, essentially, performance-based assessments for doing tasks in context.

There are bright spots where you can see the principles of individuality at work.

So for me, it comes back to, well, wait a minute. So why is that not the mainstream?

What I think my contribution is, is to say: Our institutions are based on assumptions about human beings. Our education system is based on a 19th century idea of an average person and using 20th century statistics.

As long as people think you can understand people based on averages, or how they deviate from averages, it seems reasonable. It looks like accountability and fairness rather than absurdity.

And you're trying to show that there's an alternative?


If we don't get rid of this way of thinking about ourselves and the people around us, it's hard to get the public demand to create sustainable change. That's the role that I and my organization want to play. We're making a really big bet.

Monday, March 28, 2016

Why Are Our Kids So Miserable?

From Quartz

By Jenny Anderson
March 21, 2016

“Something in modern life is undermining mental health,” Jean Twenge, a professor of psychology at San Diego State University, wrote in a recent paper.

Specifically, something is undermining young people’s mental health, especially girls'.

In her paper, Twenge looks at four studies covering 7 million people, ranging from teens to adults in the US. Among her findings: high school students in the 2010s were twice as likely to see a professional for mental health issues than those in the 1980s; more teens struggled to remember things in 2010-2012 compared to the earlier period; and 73% more reported trouble sleeping compared to their peers in the 1980s. These so-called “somatic” or “of-the-body” symptoms strongly predict depression.

“It indicates a lot of suffering,” Twenge told Quartz.

It’s not just high school students. College students also feel more overwhelmed; student health centers are in higher demand for bad breakups or mediocre grades, issues that previously did not drive college kids to seek professional help. While the number of kids who reported feeling depressed spiked in the 1980s and 1990s, it started to fall after 2008. It has started rising again:


Kids are being diagnosed with higher levels of attention-deficit hyperactivity disorder (ADHD), and everyone aged 6-18 is seeking more mental health services, and more medication.


The trend is not a uniquely American phenomena: In the UK, the number of teenagers (15-16) with depression nearly doubled between the 1980s and the 2000s and a recent survey found British 15-year-olds were among the least happy teenagers in the world (those in Poland and Macedonia were the only ones who were more unhappy).

“We would like to think of history as progress, but if progress is measured in the mental health and happiness of young people, then we have been going backward at least since the early 1950s,” Peter Gray, a psychologist and professor at Boston College, wrote in Psychology Today.

What’s going on?

Researchers have a raft of explanations for why kids are so stressed out, from a breakdown in family and community relationships, to the rise of technology and increased academic stakes and competition. Inequality is rising and poverty is debilitating.

Twenge has observed a notable shift away from internal, or intrinsic goals, which one can control, toward extrinsic ones, which are set by the world, and which are increasingly unforgiving.

Gray has another theory: kids aren’t learning critical life-coping skills because they never get to play anymore.

“Children today are less free than they have ever been,” he told Quartz. And that lack of freedom has exacted a dramatic toll, he says.

“My hypothesis is that the generational increases in externality, extrinsic goals, anxiety, and depression are all caused largely by the decline, over that same period, in opportunities for free play and the increased time and weight given to schooling,” he wrote.

What’s so great about play?

If play seems trivial, it’s not. Play is brain-building for babies and young children. There is a sequence of how children develop, from the moral and emotional to the social and intellectual, says Dr. Ellen Littman, a clinical psychologist and co-author of Understanding Girls with AD/HD. Each phase requires building certain muscles, whether to do math, or make a friend.

“There is a developmental sequence and you can’t violate it all that much,” Littman told Quartz.

For example, circle time in preschool is not about learning the alphabet or mastering Old MacDonald as much as it is learning to be part of a group, mastering the art of taking turns, and starting to listen.

But preschool is increasingly about preparing kids for kindergarten, which itself used to be about play, but now operates more like first grade. Kids are expected to sit for longer and focus on more academic tasks, relegating play to recess. According to Daphna Bassok, an assistant professor of education and public policy at the University of Virginia, in 1998, 30% of teachers believed that children should learn to read while in kindergarten. In 2010, that figure was at 80%.

“They can do math in first grade, but they are not attuned to subtle social cues,” Littman says. “They are not developing the normal skills that come from interacting with play, including how to manage their emotions.”

Gray agrees. Playing—unstructured time, with rules set by the kids (no adults acting as referee)—is how kids learn independence, problem-solving, social cues, and bravery. Now, parents jump in to to solve the playground kerfuffle, spot with eagle eyes the dangers of tall trees and steep hills, and fail to let kids have any independence for fear they will be abducted or hit by a car.

“Where do children learn to control their own lives? When adults aren’t around to do it for you,” he said.

“If you don’t have the opportunity to experience life on your own, to deal with the stressors of life, to learn in this context of play where you are free to fail, the world is a scary place,” he says.

Beyond Play

Not everyone buys the play explanation. Twenge, whose latest book,Generation Me notes that it is impossible to scientifically test whether the lack of play causes these problems: we can observe correlation, but not causation.

She sees many potential factors contributing to the rise in symptoms and reported feelings of depression: a rise in broken relationships, such as divorce, a shift away from intrinsic to extrinsic goals, which can lead to a sense of not being able to control things, and higher expectations. The percentage of people who expect to get graduate and professional degrees, for example, has surged as have the number of people who aspire to secure a professional job. But the numbers of people getting these degrees and jobs has stayed flat.

“Expectations have risen, but reality has stayed the same,” she told Quartz.

She also refutes many popular explanations for why kids are increasingly stressed out. She does not believe the rise in anxiety and depression is due solely to more awareness about it. More kids are reporting huge increases in symptoms that predict depression, like inability to focus or trouble sleeping, without reporting an increase in feeling depressed.

“People don’t even know these symptoms indicate depression, but they are reporting more of them,” she said.

Many others blame technology for addling our brains. It is hard to imagine that it has not had some impact due to its pervasiveness and addictiveness. But Twenge says the data indicate anxiety and depression started rising long before SnapChat kidnapped our kids.

“These increases started long before cell phones were in common use,” she said.

Look in the Mirror

Parenting plays its part too. Some parents aren’t involved enough; others border on the obsessive. More work, meaning kids are in adult-led extra curricular activities, or home on the computer.

But psychologists say it’s not the absence of overworked parents that is causing the problem, but how we parent when we are home.

“We are enabling children to an extent to which they are almost helpless,” says Littman. “I have to stop parents from calling college professors to change their college grade,” she said.

Maybe driven by love, or perhaps a sense of paranoia, some parents are veering toward micro-managing our kids’ every mini-success (while extolling the virtues of failure).

We help with the science project, edit the college essay, advocate for the better grade, and apologize on the playground when little Lucy won’t share the way we grown-ups think she should share. We set lots of rules for our kids, and wonder why they can’t set their own.

Parents also play a critical role in setting those high expectations. At the upper end of the socioeconomic spectrum, we may be too evolved to push them toward the Ivy League, but we certainly want them to try their hardest—at everything: school, music, soccer, piano, judo, street dance. We say it’s not all about winning, but celebrate winning in spades.

We encourage kids to find a passion—maybe for them, maybe for the college application—and do anything to make sure they are not sitting at home on their phones, or—god forbid, feeling bored.

A New Way Forward

Gray says all is not lost. The first line of attack is to recognize there is a problem. “Parents and educators need to understand that free play is not optional,” he says. “It’s essential to their healthy development.”

He suggests ratcheting back organized, adult-led activities, and facilitating more open-ended ones where kids set the rules and parents play a less dominant role. One (lofty) idea: get schools to open in the afternoons with monitors, but not organized activities. He wants a shorter school year, which won’t go over well with those hell-bent on raising America’s weak academic standards, and a ban on homework for young kids. “All of this school is doing more harm than good,” he said.

Parents can of course try to set reasonable expectations. Many parents scramble for a tutor at the first sign that their child is struggling. But maybe that struggle is okay, and maybe not every kid is going to be good at every subject. Colleges are starting to take measures—albeit small ones—to de-escalate the college admissions arms race, which parents and educators should support (high schools tend to blame colleges, or parents, for why they push kids so hard; parents blame schools, and so on).

Like many things in life, intentionality is key. If we want our kids to play and have some freedom, we have to plan how to do it (yes, it has come to that). Facilitating time and space has to be a pre-meditated act, like signing up for soccer, or posting your daughter’s Girl Scout cookie sales target on Facebook.

It won’t be easy. But if we believe that our kids’ mental health is at stake, we should certainly give it a try.