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Monday, April 30, 2012

Experimental Drug Reduces Autism Symptoms in Mice, Government Study Shows

From www.TheAutismNews.com

April 27, 2012

"These findings offer encouragement that research focused on developing medicines for core symptoms of autism are gaining momentum," said study co-author Robert Ring, vice president for translational research for Autism Speaks, an autism research and advocacy organization."

(CBS News) Autism affects one out of every 88 American children, and while there are available treatments for early intervention, there is no cure. A new government-funded study has found an experimental treatment is effective at reversing symptoms of autism in mice.

For the study, published in the April 25 issue of Science and Translational Medicine, researchers from the National Institutes of Health bred a strain of mice to display autism-like behaviors.

Just as children with autism have social deficits and engage in repetitive behaviors, these mice did not interact and communicate with each other and spent an inordinate amount of time engaging in repetitive behavior – in this case self-grooming.

Autism-like behaviors in mice have been reduced, using an experimental agent being tested in patients for a related disorder. Here, a mouse is absorbed in repetitive self-grooming. The agent reduced this repetitive behavior in a strain of mice that is prone to it, and almost stopped repetitive vertical jumping in another strain of mice.

Cue the experimental drug called GRN-529. The drug was designed to inhibit a type of brain cell receptor that receives the neurotransmitter glutamate. Glutamate is typically involved in learning and memory processes and stimulates other areas of the brain and nervous system.

When mice with the autism-like behaviors were injected with the experimental compound, they reduced the frequency of their repetitive self-grooming and spent more time around strange mice, even sniffing them nose to nose. When tested on a different strain of mice, the experimental compound stopped all repetitive jumping behavior.

“These new results in mice support NIMH-funded research in humans to create treatments for the core symptoms,” Dr. Thomas R. Insel, director of the National Institute of Mental Health, said in a statement. “While autism has been often considered only as a disability in need of rehabilitation, we can now address it as a disorder responding to biomedical treatments.”

Autism-like behaviors in mice have been reduced, using an experimental agent being tested in patients for a related disorder. Here, a mouse pays a social visit to a strange animal. The agent increased such sociability, which is impaired in autism.

Sunday, April 29, 2012

Meditation Helps Children with ADHD, Focus and Memory

From www.http://anmolmehta.com Blog

"Meditation helps children who suffer from ADD (Attention Deficit Disorder) and ADHD (Attention Deficit Hyperactivity Disorder), by helping them develop calmness, presence, focus and control over their reactions to external stimuli."

Frustrated parents and educators have long sought alternatives to medication when helping children deal with Attention Deficit Disorder and Attention Deficit Hyperactivity Disorder. Who knew that ancient Buddhists have long held a valuable tool in reaching that goal? Only recently are we realizing the tremendous benefits that meditation can bring as a very viable course of action in aiding the 5.2 million children diagnosed in America with ADD or ADHD, according to the Center for Disease Control.

The art of mindfulness, or focusing the thoughts, has been a practiced meditation technique for thousands of years. Scientists and medical professionals are now discovering that meditation can be a huge factor in teaching ADD/ADHD children to increase focus, improve overall memory, reduce anxiety levels and calm a hyperactive mind and body.

“One recent study found evidence that the daily practice of meditation thickened the parts of the brain’s cerebral cortex responsible for decision making, attention and memory”, claims a study from Mass. General Hospital. According to a study published in Time Magazine, scientists discovered that those who meditated just 40 few minutes a day reaped huge benefits for many aspects of the brain development.

Teaching children how to meditate in school can increase student’s ability to successfully perform as it heightens awareness and increases attention sustainability. Additionally, schools specializing in educating learning-disabled students are incorporating meditation into their school-wide curriculum and noticing a huge increase in the ability of ADHD students to perform.

Teaching a child to meditate at home, when ADD/ADHD children are now able to ‘let off the steam’ built up in trying to focus at school, gives kids an additional outlet to take a few moments of calm and center themselves to handle homework or retain calm for their other activities after school. Parents have reported happier homes once they incorporated daily meditation into their routines.

Sara, a mother of 4, reported that her son Gabe has been dealing with ADHD since the age of 5. His hyperactivity really reduced the amount of play dates he was offered as he was not able to understand boundaries and he often overwhelmed the other children in school. When Sara first discovered meditation for her herself, she realized the soothing affect it had on her entire day.

She decided to teach Gabe some of the techniques she had learned during her sessions. Within days, she realized that Gabe was generally less anxious and overall easier to handle at home. Three years later, daily meditations have taught Gabe to focus and calm the mind and better hyperactivity management. Meditation has been a life-changer for their family and Gabe’s functioning both in school and at home.

Meditation practice teaches children how to learn to control their thoughts and in turn their reactions, to outside distractions. One of the main components that ADD/ADHD children struggle with is the inability to control themselves, their thoughts and their reaction to stimuli. Through practice of meditation children can learn to calm the mind, focus on the purpose of restructuring the thoughts back to the deliberate and intentional spot or focal point. Meditation can also provide a much needed break in routine that allows children dealing with attention disorders to come back and refocus on the task refreshed and renewed.

Parents, educators and medical professionals have been looking to incorporate alternative methods for years. Meditation practice is a proven effective, healthy and holistic way to improve the overall anxiety levels, focus levels and functioning levels of the 8.4 % of children dealing with ADD/ADHD all over the country.


NOTE: NESCA Yoga Therapist Hannah Gould, RYT incorporates elements of mindfulness practice and meditation into her work, which addresses many specific areas of need, including self-regulation, sensory integration, relaxation, motor-planning, self-awareness and self-esteem.

What is Epigenetics, and What Does It Have to Do with Autism?

From www.AutismSpeaks.org Blog

This week’s “Got Questions?” answer comes from Alycia Halladay, Ph.D., Autism Speaks director of research for environmental sciences.

If you’ve been following autism research in recent years, you have probably read—many times—that familial, or inherited, risk is seldom the whole picture. A few inherited genes are sufficient by themselves to cause autism. But most so-called “autism genes” only increase the risk that an infant will go on to develop this developmental disorder. As is the case in many complex diseases, it appears that autism often results from a combination of genetic susceptibility and environmental triggers.

This is where epigenetics comes in. Epigenetics is the study of the factors that control gene expression, and this control is mediated by chemicals that surround a gene’s DNA. Environmental epigenetics looks at how outside influences modify these epigenetic chemicals, or “markers,” and so affect genetic activity.

It is important to remember that scientists use the term “environment” to refer to much more than pollutants and other chemical exposures. Researchers use this term to refer to pretty much any influence beyond genetic mutation. Parental age at time of conception, for example, is an environmental influence associated with increased risk of autism, as are birth complications that involve oxygen deprivation to an infant’s brain.

Because epigenetics gives us a way to look at the interaction between genes and environment, it holds great potential for identifying ways to prevent or reduce the risk of autism. It may also help us develop medicines and other interventions that can target disabling symptoms. We have written about epigenetics previously on this blog (here and here). So in this answer, I’d like to focus on the progress reported at a recent meeting hosted by Autism Speaks.

The Environmental Epigenetics of Autism Spectrum Disorders symposium, held in Washington, D.C. on Dec. 8, was the first of its kind. The meeting brought together more than 30 leaders in autism neurobiology, genetics and epidemiology with investigators in the epigenetics of other complex disorders to promote cross-disciplinary collaborations and identify opportunities for future studies.

Rob Waterland, of Baylor College of Medicine in Texas, described epidemiological studies and animal research that suggested how maternal nutrition during pregnancy can affect epigenetic markers in the brain cells of offspring.

Julie Herbstman, of Columbia University, described research that associated epigenetic changes in umbilical cord blood with a mother’s exposure to air pollutants known as polycyclic aromatic hydrocarbons (PAHs). PAHs are already infamous for their association with cancer and heart disease.

Rosanna Weksberg, of the Hospital for Sick Kids in Toronto, discussed findings that suggest how assisted reproductive technology may lead to changes in epigenetically regulated gene expression. This was of particular interest because assisted reproduction has been associated with ASD. Taking this one step further, Michael Skinner, of Washington State University, discussed “transgenerational epigenetic disease” and described research suggesting that exposures during pregnancy produce epigenetic changes that are then inherited through subsequent generations.

Arthur Beaudet, of Baylor College of Medicine, discussed a gene mutation that controls availability of the amino acid carnitine. This genetic mutation has been found to be more prevalent among children with ASD than among non-affected children, suggesting that it might be related to some subtypes of autism. Further study is needed to follow up on the suggestion that dietary supplementation of carnitine might help individuals with ASD who have this mutation. Caution is needed, however. As Laura Schaevitz, of Tufts University in Massachusetts, pointed out, studies with animal models of autism suggest that dietary supplementation may produce only temporary improvements in symptoms of neurodevelopmental disorders.

So what does this all mean for research that aims to help those currently struggling with autism? The meeting participants agreed that the role of epigenetics in ASD holds great promise but remains understudied and insufficiently understood. For clearer answers, they called for more research examining epigenetic changes in brain tissues. This type of research depends on bequeathed postmortem brain tissue, and Autism Speaks Autism Tissue Program is one of the field’s most important repositories. (Find more information on becoming an ATP family here).

The field also needs large epidemiological studies looking at epigenetic markers in blood samples taken over the course of a lifetime. One such study is the Early Autism Risk Longitudinal Investigation (EARLI). More information on participating in EARLI can be found here.

Autism Speaks remains committed to supporting and guiding environmental epigenetics as a highly important area of research. We look forward to reporting further results in the coming year and years.

Got more questions? Send them to gotquestions@autismspeaks.org.

Read more autism research news and perspective on the science page.

Saturday, April 28, 2012

Changing The Brain to Enhance Well-Being, Happiness

From www.PsychCentral.com News

By Rick Nauert, Ph.D., Senior News Editor
Reviewed by John M. Grohol, Psy.D. on April 19, 2012

A provocative new paper suggests people can take advantage of the brain’s neuroplasticity to train it to be more empathetic, appreciative and compassionate.

Practices like physical exercise, certain forms of psychological counseling and meditation can all change brains for the better, according to the authors of an online review in Nature Neuroscience. Moreover, given advances in neuroscience, these changes can now be measured. The study reflects a major transition in the focus of neuroscience from disease to well-being, said the study’s lead author Dr. Richard Davidson, professor of psychology at University of Wisconsin-Madison.

The brain is constantly changing in response to environmental factors, he said, and the article “reflects one of the first efforts to apply this conceptual framework to techniques to enhance qualities that we have not thought of as skills, like well-being.

“Modern neuroscience research leads to the inevitable conclusion that we can actually enhance well-being by training that induces neuroplastic changes in the brain.”

“Neuroplastic” changes affect the number, function and interconnections of cells in the brain, usually due to external factors.

Although the positive practices reviewed in the article were not designed using the tools and theories of modern neuroscience, “these are practices which cultivate new connections in the brain and enhance the function of neural networks that support aspects of pro-social behavior, including empathy, altruism, kindness,” said Davidson.

The review, co-written with Dr. Bruce McEwen of Rockefeller University, begins by considering how social stressors can harm the brain. As an example, the massive neglect of children in orphanages in Romania did not just have psychological impacts; it created measurable changes in their brains, Davidson said.

“Such studies provide an important foundation for understanding the opposite effects of interventions designed to promote well-being.”

Davidson said his work has been shaped by his association with the Dalai Lama, who asked him in the 1990s, “Why can’t we use the same rigorous tools of neuroscience to investigate kindness, compassion and well-being?”

Davidson has explored the neurological benefits of meditation and said “meditation is one of many different techniques, and not necessarily the best for all people.

“Cognitive therapy, developed in modern psychology, is one of most empirically validated treatments for depression and counteracting the effects of stress.”

Overall, he said, the goal is “to use what we know about the brain to fine-tune interventions that will improve well-being, kindness, altruism. Perhaps we can develop more targeted, focused interventions that take advantage of the mechanisms of neuroplasticity to induce specific changes in specific brain circuits.”

Brains change all the time, Davidson emphasized. “You cannot learn or retain information without a change in the brain. We all know implicitly that in order to develop expertise in any complex domain, to become an accomplished musician or athlete, requires practice, and that causes new connections to form in the brain. In extreme cases, specific parts of the brain enlarge or contract in response to our experience.”

Davidson believes brain training will expand in a similar fashion as has occurred for physical exercise.

“If you go back to the 1950s, the majority of middle-class citizens in Western countries did not regularly engage in physical exercise. It was because of scientific research that established the importance of physical exercise in promoting health and well-being that more people now engage in regular physical exercise. I think mental exercise will be regarded in a similar way 20 years from now.

“Rather than think of the brain as a static organ, or one that just degenerates with age, it’s better understood as an organ that is constantly reshaping itself, is being continuously influenced, wittingly or not, by the forces around us,” said Davidson.

“We can take responsibility for our own brains. They are not pawns to external influences; we can be more proactive in shaping the positive influences on the brain.”

Brain Drain: Could Environmental Chemicals Cause Autism?

From the Natural Resources Defense Council (NRDC) Blog Smarter Living: Family Health

"We've created a situation where we are exposing our children and grandchildren every day to new chemicals that didn't exist [until recently]," says Landrigan. "We've never tested them, and we don't have a clue what these chemicals do to early development."

There are few new parents today who haven't considered the possibility that autism might affect their child. And many parents are wondering if chemicals in our air, food, and water are to blame for what has been called the "autism epidemic."

The number of children with autism spectrum disorders (ASDs) has been rising steadily, and the Centers for Disease Control and Prevention (CDC) now estimate that ASD affects about 1 in 110 children in the U.S. 40 percent of these children have intellectual disabilities, and all suffer from impairments in social interactions. Some also have problems with communication and behavior.

The cause of this rise in autism, which many studies have shown cannot be explained by changes in diagnosis methods, is still unknown. Although a few percent of ASD cases can be traced to inherited genes, our genes don't change dramatically over the span of just a few decades.

One thing that has changed dramatically over the last several decades is human exposure to toxic chemicals and metals in the environment. Many of these chemicals and metals are known to affect the developing fetal brain. These include lead, methylmercury, polychlorinated biphenyls (PCBs), arsenic, cadmium, and manganese.

The developing brain is highly sensitive during the first three months of growth. In children who are susceptible, exposure to a neurotoxic metal or chemical during this window could confer a lasting change in brain structure and function.

The chemicals known to cause harm to the developing fetal and infant brain are part of a larger family of 200 chemicals known from workplace studies to cause neurological harm in humans, according to a review article by Dr. Philip J. Landrigan of the Children's Environmental Health Center at the Mount Sinai School of Medicine published in the January, 2010 issue of Current Opinion in Pediatrics. Children are exposed to roughly 3,000 chemicals in personal care products, building materials, cleaning products and motor vehicle fuels, yet fewer than 20 percent of these chemicals have been tested thoroughly to see if they harm the developing brain. "We've created a situation where we are exposing our children and grandchildren every day to new chemicals that didn't exist [until recently]," says Landrigan. "We've never tested them, and we don't have a clue what these chemicals do to early development."

When it comes to environmental exposures, much of the public focus has been on finding links between vaccines and autism. Landrigan argues, however, that it is time to move on. "There have been a dozen well-conducted epidemiological studies that have failed to detect a connection between vaccines and autism," Landrigan says, "so I think as a matter of research priority it is time to look at other hazards."

Chemicals suspected of harming the developing brain include phthalates (found in personal care products), bisphenol A (BPA), found in the linings of food cans), brominated flame retardants (found in old computers, television sets and foam padding), chlorinated solvents used in industry, the now-banned organochlorine pesticide DDT, and organophosphate pesticides. Although these chemicals have not been directly linked to ASD, the fact that they can cause learning and behavioral problems supports the idea that chemicals in the environment could cause ASD.

A further line of evidence for a link between environmental chemicals and ASD comes from a handful of known examples where chemicals taken during pregnancy appear to have caused the disorder. These chemicals include the drug thalidomide, the anti-seizure medication valproic acid, and the drug misoprostol, says Landrigan. A link has also been found between prenatal exposure to the organophosphate pesticide chlorpyrifos and increased risk of pervasive developmental disorder, a form of autism. Rubella infection during pregnancy also appears to increase the risk of ASD. "That series of observations raises the question in my mind, could there be other environmental causes, other chemicals or other environmental factors that cause autism?" says Landrigan.

How might environmental chemicals contribute to the risk of developing autism? One possibility is that these chemicals trigger ASD in children who inherited genes that make them susceptible to autism. These genes could be "turned on" or activated by an exposure in the womb, during childbirth, in early life, or during the toddler years.

Another possibility is that chemicals in the environment cause spontaneous gene alterations, called "de novo" mutations because they arise anew rather than being inherited. Mutations are fairly common but normally our DNA-repair mechanisms keep them from causing disease. When DNA-repair mechanisms fail, these mutations can lead to diseases such as cancer. Several de novo mutations have been detected in children with ASD. Some of these mutations are in genes related to brain development.

Environmental chemicals also could cause de novo mutations in the one or both of the parents. If these mutations occurred in egg or sperm cells, they could be passed on to the next generation. This could help explain why older fathers and mothers are more likely to give birth to a child with ASD.

It may be that multiple factors contribute to the range of conditions we call ASD. Many researchers now view ASD as an array of related disorders with similar symptoms but potentially with different causes.

More research is needed to explore the environmental aspects that contribute to the risk of developing ASD. Over a lifetime, the cost of care is estimated to reach $3.2 million per individual. Autism's costs are felt not just by the parents of children with ASD but also by society as a whole.

Parents who already have a child with autism should consider genetic consultation, recommends Landrigan. "If they have one child with autism, it is wise to check to see if they have one of the known genetic risk factors for autism," he says.

What You Can Do

To reduce the risk of giving birth to a child with learning or behavioral problems, says Landrigan, adults who plan to become parents should try to live as healthily as possible. This includes eating a healthy diet, getting adequate sleep and exercise, and limiting your exposure to known and suspected neurotoxic chemicals. Here are some tips:
  • Have your home or apartment tested for lead paint before beginning any sanding or other renovations (lead exposures have been declining over the years so lead is unlikely to be a cause of autism, but it is linked to lasting harm to the brain and can result in lower performance on tests and behavioral problems)
  • Avoid fish high in PCBs and methylmercury (see NRDC's Consumer Guide to Mercury in Fish.)
  • Minimize exposure to pesticides by eating organic foods and not using pesticides around the home and yard
  • Even though the evidence is not definitive, people should reduce their exposure to phthalates in personal care products and avoid canned foods because the can linings contain BPA.
Learn More

For a good overview see, CDC's Autism Spectrum Disorder page (with stats and definition of autism)

For 1 in 110 children developing autism, see "Prevalence of Autism Spectrum Disorders --- Autism and Developmental Disabilities Monitoring Network, United States, 2006." The authors note that, "Although improved ascertainment accounts for some of the prevalence increases documented in the ADDM sites, a true increase in the risk for children to develop ASD symptoms cannot be ruled out."

For Landrigan's literature survey on environmental chemicals and metal related to learning disorders and the possible links between environmental contaminants and autism, see Landrigan, P.J. "What causes autism? Exploring the environmental contribution." Curr Opin Pediatr. 2010 Jan 16.

For flame retardants as a potential risk factor, see: Messer A. "Mini-review: Polybrominated diphenyl ether (PBDE) flame retardants as potential autism risk factors." Physiol Behav. 2010 Jan 25. [Epub ahead of print]

For solvents such as trichloroethylene, and vinyl chloride, see: Windham GC, Zhang L, Gunier R, Croen LA, Grether JK. "Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco Bay area." Environ Health Perspect2006;114(9):1438–44.

For organophosphates, see the following three studies:

Eskenazi B, Rosas LG, Marks AR, et al. "Pesticide toxicity and the developing brain."Basic Clin Pharmacol Toxicol 2008; 102:228–236.

Roberts EM, English PB, Grether JK, Windham GC, Somburg L, Wolff C. "Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley." Environ Health Perspect 2007;115(10):1482–9.

Rauh VA, Garfinkel R, Perera FP, et al. "Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children." Pediatrics 2006; 118:e1845–e1859.

The Childhood Autism Risks from Genetics and Environment study has a goal of addressing a wide spectrum of chemical and biologic exposures, susceptibility factors and their interactions with regard to ASDs. This older paper provides a good overview of the potential genetic and environmental causes and the interaction of the two:

Hertz-Picciotto et al. "The CHARGE Study: An Epidemiologic Investigation of Genetic and Environmental Factors Contributing to Autism"

For a discussion of "de novo" mutations caused by environmental mutagens see: "Environmental risk factors for autism: Do they help cause de novo genetic mutations that contribute to the disorder?" Dennis K. Kinney et al. Medical Hypotheses 74 (2010) 102–106

For parental age as risk factor, see: Shelton JF, Tancredi DJ, Hertz-Picciotto I. "Independent and dependent contributions of advanced maternal and paternal ages to autism risk." Autism Res. 2010 Feb;3(1):30-9.

Copy number variations are mutations resulting in extra or decreased numbers of genes. For an association between copy number variations and autism, see the following two studies:
Sebat J. et al. "Strong Association of De Novo Copy Number Mutations with Autism."Science 20 April 2007: Vol. 316. no. 5823, pp. 445 - 449

Glessner JT et al. "Autism genome-wide copy number variation reveals ubiquitin and neuronal genes." Nature. 2009 May 28;459(7246):569-73. Epub 2009 Apr 28.

Tuesday, April 24, 2012

Rescue, Recovery or Cure? A Very Revealing Iceberg View of Autism

From the Psychology Today Blog Making Sense of Autistic Spectrum Disorders: A Critical Review of Fact, Fiction, and Speculation in the Field of Autism

By James Coplan, M.D.
Published on August 9, 2010

Everywhere you turn, you hear about "rescue," "recovery," and "cures" for ASD. There are lots of heartwarming testimonials, and lots of snake-oil vendors eager to sell you their products, but there are no randomized controlled studies of anything, to show that ASD is curable, or to show that the long-term outcome is different from what would have happened via natural history alone.

The most intense features, such as flapping and spinning, echolalia, and panic in response to changes in routine or sensory overload, gradually fade, with or without intervention. Leo Kanner first documented this in 1943. The higher the IQ, the faster and more completely the symptoms fade; this has been summarized in my own research. In order to establish that a given therapy alters long-term outcome, one would need to show that the child is more improved than would have been the case just by passage of time.

Nobody has ever done that, for any therapy. Wouldn't that kind of research be unethical? A good question. On the other hand, what are the ethics of promising a cure without proof, and billing a family tens of thousands of dollars? We wouldn't need to have a "no treatment" group. We could compare treatments "A" and "B," or 20 hours per week of "A" versus 30 or 40, and so forth. But it's never been done.

Alas, there is another, deeper problem with claims of cure: Adolescents and adults who have "outgrown" ASD diagnoses are still plagued by a host of non-ASD neuropsychological disorders: anxiety, depression, bipolar disorder and a susceptibility to alcoholism. This is not "cure."

The figures show what I'm talking about. You saw the first of these figures in Post 16: a neurodevelopmental "iceberg," with ASD at the tip. These are the children who come to see me in the office, for initial diagnosis. When I look in the family history, I usually find that one or both parents have some combination of the issues that are "below the water line" of that first iceberg; anxiety, depression, or some other mental health issue.

The second figure is based on long-term outcome studies of adults with a childhood diagnosis of ASD, and shows the same disorders. The "tip" of the iceberg (ASD) has been worn away, but all the issues that lie beneath the waterline remain.

References for both of these figures are listed in my book.

About Dr. James Coplan

Dr. James Coplan is board-certified in general pediatrics, neurodevelopmental disabilities and developmental-behavioral pediatrics. He is also the sibling of an individual with special needs. Dr. Coplan has published extensively in the medical literature on early speech and language development, and has written a book for parents of children on the autistic spectrum: Making Sense of Autistic Spectrum Disorders: Create the Brightest Future for Your Child with the Best Treatment Options (Bantam-Dell, 2010). He is in private practice in Rosemont, PA, teaches in the Medical and Nursing Schools at the University of Pennsylvania and is a public speaker on the subject of early child development and autistic spectrum disorder.

And in the Same Vein... "Do Autistic Symptoms Persist Across Time?"

Evidence of Substantial Change in Symptomatology Over a 3-year Period in Cognitively Able Children With Autism

From the American Journal of Intellectual and Developmental Disabilities

By Elizabeth Pellicano
March, 2012

According to a new paper by researchers led by Elizabeth Pellicano of the Centre for Research in Autism and Education in  London and colleagues from the University of Western Australia in Perth, the symptoms of autism in thirty-seven children studied over a 3-year period decreased significantly in response to intervention. Specifically, their social communications improved, and the frequency of repetitive behaviors declined.

The authors state, "Children showing diagnostic discontinuity (relief of symptoms)) were distinguishable from those who fulfilled ADOS-G criteria only in terms of the age at which they began receiving intervention. The presence of a significant proportion of children showing considerable progress over the 3-year period challenges assumptions of diagnostic continuity and highlights the potential long-term benefits of early intervention."

You can read an abstract or order the entire paper HERE.

Monday, April 23, 2012

Study: ADHD Linked to Pesticide Exposure

From the CNN.com Special Report - Toxic America

By Sarah Klein
May 17, 2010

Is enough being done to protect us from chemicals that could harm us?

Children exposed to higher levels of a type of pesticide found in trace amounts on commercially grown fruit and vegetables are more likely to have attention deficit hyperactivity disorder than children with less exposure.

Researchers measured the levels of pesticide byproducts in the urine of 1,139 children from across the United States. Children with above-average levels of one common byproduct had roughly twice the odds of getting a diagnosis of ADHD, according to the study, which appears in the journal Pediatrics.

Exposure to the pesticides, known as organophosphates, has been linked to behavioral and cognitive problems in children in the past, but previous studies have focused on communities of farm workers and other high-risk populations. This study is the first to examine the effects of exposure in the population at large.

Organophosphates are "designed" to have toxic effects on the nervous system, says the lead author of the study, Maryse Bouchard, Ph.D., a researcher in the department of environmental and occupational health at the University of Montreal. "That's how they kill pests."

The pesticides act on a set of brain chemicals closely related to those involved in ADHD, Bouchard explains, "so it seems plausible that exposure to organophosphates could be associated with ADHD-like symptoms."

Environmental Protection Agency regulations have eliminated most residential uses for the pesticides (including lawn care and termite extermination), so the largest source of exposure for children is believed to be food, especially commercially grown produce. Adults are exposed to the pesticides as well, but young children appear to be especially sensitive to them, the researchers say.

Detectable levels of pesticides are present in a large number of fruits and vegetables sold in the U.S., according to a 2008 report from the U.S. Department of Agriculture cited in the study. In a representative sample of produce tested by the agency, 28 percent of frozen blueberries, 20 percent of celery, and 25 percent of strawberries contained traces of one type of organophosphate. Other types of organophosphates were found in 27 percent of green beans, 17 percent of peaches, and 8 percent of broccoli.

Although kids should not stop eating fruits and vegetables, buying organic or local produce whenever possible is a good idea, says Bouchard.

"Organic fruits and vegetables contain much less pesticides, so I would certainly advise getting those for children," she says. "National surveys have also shown that fruits and vegetables from farmers' markets contain less pesticides even if they're not organic. If you can buy local and from farmers' markets, that's a good way to go."

A direct cause-and-effect link between pesticides and ADHD "is really hard to establish," says Dana Boyd Barr, Ph.D., a professor of environmental and occupational health at Emory University. However, she says, "There appears to be some relation between organophosphate pesticide exposure and the development of ADHD."

This is the largest study of its kind to date, according to Barr, who researched pesticides for more than 20 years in her previous job with the Centers for Disease Control and Prevention but was not involved in the study.

Bouchard and her colleagues analyzed urine samples from children ages 8 to 15. The samples were collected during an annual, nationwide survey conducted by the CDC, known as the National Health and Nutrition Examination Survey.

The researchers tested the samples for six chemical byproducts (known as metabolites) that result when the body breaks down more than 28 different pesticides. Nearly 95 percent of the children had at least one byproduct detected in their urine.

Just over 10 percent of the children in the study were diagnosed with ADHD. The kids were judged to have ADHD if their symptoms (as reported by parents) met established criteria for the disorder, or if they had taken ADHD medication regularly in the previous year.

One group of pesticide byproducts was associated with a substantially increased risk of ADHD. Compared with kids who had the lowest levels, the kids whose levels were 10 times higher were 55 percent more likely to have ADHD. (Another group of byproducts did not appear to be linked to the disorder.)

In addition, children with higher-than-average levels of the most commonly detected byproduct -- found in roughly 6 in 10 kids -- were nearly twice as likely to have ADHD.

"It's not a small effect," says Bouchard. "This is 100 percent more risk."

To isolate the effect of the pesticide exposure on ADHD symptoms, the researchers controlled for a variety of health and demographic factors that could have skewed the results.

Still, the study had some limitations and is not definitive, Bouchard says. Most notably, she and her colleagues measured only one urine sample for each child, and therefore weren't able to track whether the levels of pesticide byproducts were constant, or whether the association between exposure and ADHD changed over time.

Long-term studies including multiple urine samples from the same children are needed, Bouchard says. She suspects such studies would show an even stronger link between pesticide byproducts and ADHD.

EPA spokesman Dale Kemery said in a statement that the agency routinely reviews the safety of all pesticides, including organophosphates. "We are currently developing a framework to incorporate data from studies similar to this one into our risk assessment," Kemery said. "We will look at this study and use the framework to decide how it fits into our overall risk assessment."

Kemery recommended that parents try other pest-control tactics before resorting to pesticide use in the home or garden. Washing and peeling fruits and vegetables and eating "a varied diet" will also help reduce potential exposure to pesticides, he said.

"I would hope that this study raises awareness as to the risk associated with pesticide exposure," Bouchard says. "There's really only a handful of studies on this subject out there, so there's room for more awareness."

Download a PDF of the full report from the journal Pediatrics HERE.

Sunday, April 22, 2012

New Numbers On Autism As A Disorder Of The Whole Body

From WBUR 90.9 FM's CommonHealth Blog

By Carey Goldberg
April 18, 2012

“I have come to believe that just as autism is not simply a genetics problem, it is not simply a brain problem, either. Autism involves the whole body. As a physician, I’ve seen so many autistic children with similar medical problems that I can’t believe it’s just a coincidence…At this point, I think there is enough evidence to say that while autism certainly involves the brain, it is really a problem of the whole body, including the brain, from molecules to cells, from organs to metabolism, from immune to digestive systems.”

That passage comes from “The Autism Revolution,” by Harvard neurologist Dr. Martha Herbert and CommonHealth contributor Karen Weintraub, a new book that we excerpted just last month. Now, just out in the journal PLOS One, is a Harvard paper that mined Boston hospital electronic health records of more than 14,000 young people and produced the striking illustration above of just how whole-body a condition autism can be.

Particularly of note in the chart: the high prevalence of bowel disorders in those with autism, a topic that has been somewhat controversial; and the high levels of schizophrenia and auto-immune disorders. I interpret the study’s conclusions, below, as saying, “Kids with ASD — Autism Spectrum Disorders — don’t just have brain problems, they may have many physical problems and we’d better all keep that in mind.”

From PLOS One, The Co-Morbidity Burden of Children and Young Adults with Autism Spectrum Disorders

The comorbidities of ASD encompass disease states that are significantly overrepresented in ASD with respect to even the patient populations of tertiary health centers. This burden of comorbidities goes well beyond those routinely managed in developmental medicine centers and requires broad multidisciplinary management that payors and providers will have to plan for.

Dr. Herbert was not involved in the study, and I asked her for her take on it.

“We already knew that a lot of these conditions exist in autism,” she said, though “many people thought that they were not any more common in autism than in the generally population. But this study shows that many of these conditions occur more frequently in autism, although there still remains some uncertainty.”

“What we don’t know yet,” she said, “is, how do we translate these correlations into clues that lead us to underlying biology? Because once we’re dealing with these kinds of medical issues, we’re not just talking about broken genes in the brain, we’re talking about conditions that we might be able to help medically.”

Read the full PLOS One paper here.

How Exercise Could Lead to a Better Brain

From NYTimes.com

NOTE: Running makes mice smarter; it probably works for people, too. At NESCA, our clinicians routinely recommend exercise as part of their treatment plans for anxiety and learning disorders, ADHD and depression. Parents might consider reading Spark: The Revolutionary Science of Exercise and the Brain by Psychiatrist John Ratey, which we featured HERE in January, 2010. 

By Gretchen Reynolds
Published: April 18, 2012 

The value of mental-training games may be speculative, as Dan Hurley writes in his article on the quest to make ourselves smarter, but there is another, easy-to-achieve, scientifically proven way to make yourself smarter. Go for a walk or a swim.

For more than a decade, neuroscientists and physiologists have been gathering evidence of the beneficial relationship between exercise and brainpower. But the newest findings make it clear that this isn’t just a relationship; it is the relationship.

Using sophisticated technologies to examine the workings of individual neurons — and the makeup of brain matter itself — scientists in just the past few months have discovered that exercise appears to build a brain that resists physical shrinkage and enhance cognitive flexibility. Exercise, the latest neuroscience suggests, does more to bolster thinking than thinking does.

The most persuasive evidence comes from several new studies of lab animals living in busy, exciting cages. It has long been known that so-called “enriched” environments — homes filled with toys and engaging, novel tasks — lead to improvements in the brainpower of lab animals. In most instances, such environmental enrichment also includes a running wheel, because mice and rats generally enjoy running. Until recently, there was little research done to tease out the particular effects of running versus those of playing with new toys or engaging the mind in other ways that don’t increase the heart rate.

So, last year a team of researchers led by Justin S. Rhodes, a psychology professor at the Beckman Institute for Advanced Science and Technology at the University of Illinois, gathered four groups of mice and set them into four distinct living arrangements. One group lived in a world of sensual and gustatory plenty, dining on nuts, fruits and cheeses, their food occasionally dusted with cinnamon, all of it washed down with variously flavored waters. Their “beds” were colorful plastic igloos occupying one corner of the cage. Neon-hued balls, plastic tunnels, nibble-able blocks, mirrors and seesaws filled other parts of the cage. Group 2 had access to all of these pleasures, plus they had small disc-shaped running wheels in their cages. A third group’s cages held no embellishments, and they received standard, dull kibble. And the fourth group’s homes contained the running wheels but no other toys or treats.

All the animals completed a series of cognitive tests at the start of the study and were injected with a substance that allows scientists to track changes in their brain structures. Then they ran, played or, if their environment was unenriched, lolled about in their cages for several months.

Afterward, Rhodes’s team put the mice through the same cognitive tests and examined brain tissues. It turned out that the toys and tastes, no matter how stimulating, had not improved the animals’ brains.

“Only one thing had mattered,” Rhodes says, “and that’s whether they had a running wheel.” Animals that exercised, whether or not they had any other enrichments in their cages, had healthier brains and performed significantly better on cognitive tests than the other mice. Animals that didn’t run, no matter how enriched their world was otherwise, did not improve their brainpower in the complex, lasting ways that Rhodes’s team was studying. “They loved the toys,” Rhodes says, and the mice rarely ventured into the empty, quieter portions of their cages. But unless they also exercised, they did not become smarter.

Why would exercise build brainpower in ways that thinking might not? The brain, like all muscles and organs, is a tissue, and its function declines with underuse and age. Beginning in our late 20s, most of us will lose about 1 percent annually of the volume of the hippocampus, a key portion of the brain related to memory and certain types of learning.

Exercise though seems to slow or reverse the brain’s physical decay, much as it does with muscles. Although scientists thought until recently that humans were born with a certain number of brain cells and would never generate more, they now know better.

In the 1990s, using a technique that marks newborn cells, researchers determined during autopsies that adult human brains contained quite a few new neurons. Fresh cells were especially prevalent in the hippocampus, indicating that neurogenesis — or the creation of new brain cells — was primarily occurring there. Even more heartening, scientists found that exercise jump-starts neurogenesis. Mice and rats that ran for a few weeks had about twice as many new neurons in their hippocampi as sedentary animals. Their brains, like other muscles, were bulking up.

But it was the ineffable effect that exercise had on the functioning of the newly formed neurons that was most startling. Brain cells can improve intellect only if they join the existing neural network, and many do not, instead rattling aimlessly around in the brain for a while before dying.

One way to pull neurons into the network, however, is to learn something. In a 2007 study, new brain cells in mice became looped into the animals’ neural networks if the mice learned to navigate a water maze, a task that is cognitively but not physically taxing. But these brain cells were very limited in what they could do. When the researchers studied brain activity afterward, they found that the newly wired cells fired only when the animals navigated the maze again, not when they practiced other cognitive tasks. The learning encoded in those cells did not transfer to other types of rodent thinking.

Exercise, on the other hand, seems to make neurons nimble. When researchers in a separate study had mice run, the animals’ brains readily wired many new neurons into the neural network. But those neurons didn’t fire later only during running. They also lighted up when the animals practiced cognitive skills, like exploring unfamiliar environments. In the mice, running, unlike learning, had created brain cells that could multitask.

Just how exercise remakes minds on a molecular level is not yet fully understood, but research suggests that exercise prompts increases in something called brain-derived neurotrophic factor, or B.D.N.F., a substance that strengthens cells and axons, fortifies the connections among neurons and sparks neurogenesis. Scientists can’t directly study similar effects in human brains, but they have found that after workouts, most people display higher B.D.N.F. levels in their bloodstreams.

Few if any researchers think that more B.D.N.F. explains all of the brain changes associated with exercise. The full process almost certainly involves multiple complex biochemical and genetic cascades. A recent study of the brains of elderly mice, for instance, found 117 genes that were expressed differently in the brains of animals that began a program of running, compared with those that remained sedentary, and the scientists were looking at only a small portion of the many genes that might be expressed differently in the brain by exercise.

Whether any type of exercise will produce these desirable effects is another unanswered and intriguing issue. “It’s not clear if the activity has to be endurance exercise,” says the psychologist and neuroscientist Dr. Arthur F. Kramer, director of the Beckman Institute at the University of Illinois and a pre-eminent expert on exercise and the brain. A limited number of studies in the past several years have found cognitive benefits among older people who lifted weights for a year and did not otherwise exercise. But most studies to date, and all animal experiments, have involved running or other aerobic activities.

Whatever the activity, though, an emerging message from the most recent science is that exercise needn’t be exhausting to be effective for the brain. When a group of 120 older men and women were assigned to walking or stretching programs for a major 2011 study, the walkers wound up with larger hippocampi after a year. Meanwhile, the stretchers lost volume to normal atrophy. The walkers also displayed higher levels of B.D.N.F. in their bloodstreams than the stretching group and performed better on cognitive tests.

In effect, the researchers concluded, the walkers had regained two years or more of hippocampal youth. Sixty-five-year-olds had achieved the brains of 63-year-olds simply by walking, which is encouraging news for anyone worried that what we’re all facing as we move into our later years is a life of slow (or not so slow) mental decline.

Gretchen Reynolds writes the Phys Ed column for The Times’s Well blog. Her book, ‘‘The First 20 Minutes,’’ about the science of exercise, will be published this month.

Saturday, April 21, 2012

CDC: Why Are Autism Spectrum Disorders Increasing?

The CDC estimates 1 in 88 children has been identified with an autism spectrum disorder (ASD). Why is the number of children with ASDs on the rise?

Find out what CDC has learned.

The Centers for Disease Control and Prevention (CDC) estimates that about 1 in 88 children has been identified with an autism spectrum disorder (ASD). This data comes from the Autism and Developmental Disabilities Monitoring (ADDM) Network, which estimated the number of 8-year-old children with ASDs living in 14 communities throughout the United States in 2008. This new estimate marks a 23% increase since our last report in 2009, and a 78% increase since our first report in 2007.

At CDC, we know that people want answers to what is causing this increase, and so do we. The reasons for the increase in the identified prevalence of ASDs are not understood completely. Some of the increase is due to the way children are identified, diagnosed, and served in their local communities, although exactly how much is due to these factors is unknown. Also, it is likely that reported increases are explained partly by greater awareness by doctors, teachers, and parents. To understand more, CDC will keep guiding and conducting research into what is putting our children at risk.

However, the data tell us one thing with certainty—more children are being identified as having ASDs than ever before and these children and their families need help.

Pregnancy and Birth Factors

CDC researchers developed a model to estimate how changes in six pregnancy and birth factors might have contributed to the increase in ASD prevalence:
  • Preterm and very preterm delivery
  • Low and very low birthweight
  • Multiple birth
  • Cesarean delivery
  • Breech presentation
  • In vitro fertilization or other assisted reproductive technologies (ARTs)
The study found that it is very unlikely that any of the pregnancy and birth factors included in the study could have been responsible for such a large increase in ASDs from 2002 through 2006.
However, the model developed for this study will be useful for future research and can be used to assess other risk factor scenarios.
Evaluation Workshop
To provide a forum for sharing the latest information on ASD prevalence changes, CDC and Autism Speaks co-hosted the "Workshop on U.S. Data to Evaluate Changes in the Prevalence of Autism Spectrum Disorders." The workshop brought together scientists and stakeholders from the autism community to increase knowledge about ASD prevalence, to learn from other conditions, and to share ideas on how to move forward to better understand ASD trends.

Thursday, April 19, 2012

Dr. Martha Herbert on Autism: Risk vs. Cause

From Autism Speaks' Blog: Got Questions?
Wednesday, April 18, 2012

What’s the difference between something causing autism versus increasing risk for autism?

Today’s “Got Questions?” answer comes from Martha Herbert, Ph.D., M.D., a pediatric neurologist and neuroscientist at the Massachusetts General Hospital, Harvard Medical School, a member of the Autism Speaks Scientific Advisory Committee and the author of the recently published The Autism Revolution: Whole Body Strategies for Making Life All It Can Be.

The search for the causes of autism is challenging because many things are risk factors – and yet when examined by themselves no one of them has the power to be labeled the sole “culprit.” Asking the question a different way might help. I think we need to ask, “How is autism caused?” I want to propose that genes and environment lead to autism by an accumulation of “Total Load” – a pile-up of risk factors to the point of overflow.

A case in point is the recent information implicating maternal obesity and diabetes as risk factors for having a child with autism. Clearly many or even most mothers of children with autism were not obese or diabetic during pregnancy. So this is obviously not the sole cause of autism. But that does not erase the finding. For women with these conditions, the study suggests that the diabetes or obesity might have had something to do with the autism that their child developed.

So let’s ask the “how” question: How could diabetes or obesity contribute to autism? The study’s title – “Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders” – points in an important direction. To understand why this choice of words is important, we need to understand what “metabolism” is and what happens when it gets into trouble.

Everything in our bodies involves biochemistry and physiology. Every microsecond, each of our cells is buzzing with innumerable chemical reactions and processes – building things up, breaking things down and sending messages. This is “metabolism.” Any glitches can make the operation get clumsy.

Genes can cause glitches in metabolism, and so can “environment.” Toxins can change metabolism – by blocking it, by revving it up, by confusing it. Sometimes the impact is subtle – but our bodies are dealing with lots of impacts all at the same time. The sum total of all environmental impacts – subtle and not so subtle – can be called “total load.” By “environment,” we scientists mean non-genetic influences, which can include such factors as maternal health during pregnancy and birth complications, not just toxic chemicals.

Think of it this way. We each have our own barrel that slowly fills up with noxious environmental exposures. Genes shape how much it can hold and how strong its walls are. So does the food we eat. A big barrel with strong walls can tolerate a lot, but a small barrel with thin, rusty walls is going to overflow and leak much more easily.

“Total Load” offers a good explanation of how people get diabetes or obesity – and these days so many people have both at once that it’s simpler to say “diabesity.” Diabesity is a metabolic condition, but when you dig below the surface, there’s a lot more to it than “a problem with insulin” or “too much fat.” From a “systems biology” viewpoint, diabesity can be understood as the end result of a long process of metabolic deterioration caused by an ever bigger “total load.”

Years of storing toxic exposures in our bodies gums up our metabolism. And years of nutrient-depleted processed food can produce deficiencies in the vital antioxidants and minerals we need to protect ourselves. By the time someone develops diabesity, it’s way more than eating too much. The whole metabolism handles calories differently.

In some people, “diabesity” is what happens when the Total Load overflows the barrel. In others it is autoimmune disease and in still others it is cancer. How it turns out for each of us probably depends on our genes, the toxins to which we’ve been exposed – and our diets, exercise and other lifestyle factors.

But underneath there are some commonalities. Indeed, many chronic conditions share underlying “metabolic” problems such as impaired energy production in the mitochondria, oxidative stress and inflammation. (You can read a variety of relevant research studies here.)

There is by now a large literature implicating these inflammatory, oxidative stress and mitochondrial metabolic problems in autism. This, too, implicates environment as well as genes.

The problem with metabolic compromises is that the more things go wrong, the easier it is for them to get worse. You slide downhill for a while but then you hit a tipping point, where your system gets stuck in a place we call “disease,” and it’s really hard to extricate yourself. It turns into a vicious circle. This may be what happens when someone slips from “insulin resistance” into “diabetes.”

It may also be what happens when a small child regresses into autism.

Which brings us back to the How question – How is autism caused? In The Autism Revolution: Whole Body Strategies for Making Life All It Can Be, I explain this in more detail through the stories of people with autism who got worse and then got better. But in brief, you can make a working model of autism as a different way of brain functioning that emerges when the Total Load exceeds the brain and body’s capacity to compensate.

Even better, this “Total Load” model can point you toward practical, everyday ways of reducing this Total Load now, while we wait for more detailed science to develop.

So then, how might diabetes or obesity contribute to a baby developing autism? Perhaps by accelerating the baby’s accumulation of Total Load. A mother with diabetes or obesity is short on antioxidants and has too many inflammatory factors – and these problems get passed on to the fetus. This does not in itself cause autism – but it may prime the baby for future trouble by making it more reactive to further stresses, and by failing to prepare it for these challenges with a good store of protective nutrients. The baby’s barrel is small, and its walls are thin.

If you look at it like this, diabetes and obesity are among the many ways that environment can create autism risk for a baby.

Risks don’t “cause” autism. But they may very well lay the groundwork for the tipping point when the Total Load becomes too much and the barrel starts to overflow and leak. The metabolic disturbance that started in adolescence or adulthood for the mother might start in infancy or even before birth for the baby.

Obviously this is a model. It strings together a lot of different observations into an interpretation, or story, that science can only test piece by piece. But there is no escaping models – we all use them whether we know it or not – and a big advantage of this Total Load model is that right now you can reduce the Total Load of your child by making their barrel stronger through eating a a high nutrient density unprocessed plant-based diet, getting regular sleep and exercise, and eliminating as many noxious exposures as possible. You can do this for yourself too, before your next pregnancy. This won’t be a quick fix for autism, but it’s certainly a foundation for making life as good as it can get under the circumstances.

Friday, April 13, 2012

Study Links Autism with Industrial Food, Environment

New Research Models Real-World Exposures to Environmental Causes of Autism

The Institute of Agriculture and Trade Policy

By Katie Rojas-Jahn, Renee Dufault, FIHRI
Published April 11, 2012

Minneapolis — The epidemic of autism in children in the United States may be linked to the typical American diet according to a new study published online in the journal Clinical Epigenetics by Renee Dufault, et. al. The study explores how mineral deficiencies—affected by dietary factors like high fructose corn syrup (HFCS)—could impact how the human body rids itself of common toxic chemicals like mercury and pesticides.

The release comes on the heels of a report by the Centers for Disease Control and Prevention (CDC) that estimates the average rate of autism spectrum disorder (ASD) among eight year olds is now 1 in 88, representing a 78 percent increase between 2002 and 2008. Among boys, the rate is nearly five times the prevalence found in girls.

“To better address the explosion of autism, it’s critical we consider how unhealthy diets interfere with the body’s ability to eliminate toxic chemicals, and ultimately our risk for developing long-term health problems like autism.” said Dr. David Wallinga, a study co-author and physician at the Institute for Agriculture and Trade Policy (IATP).

Commander (ret.) Renee Dufault (U.S. Public Health Service), the study’s lead author and a former Food and Drug Administration (FDA) toxicologist, developed an innovative scientific approach to describe the subtle side effects of HFCS consumption and other dietary factors on the human body and how they relate to chronic disorders. The model, called “macroepigenetics,” allows researchers to consider how factors of nutrition, environment and genetic makeup interact and contribute to the eventual development of a particular health outcome.

“With autism rates skyrocketing, our public educational system is under extreme stress,” said Dufault, who is also a licensed special education teacher and founder of the Food Ingredient and Health Research Institute (FIHRI). As part of the current study, the authors found a 91 percent increase in the number of children with autism receiving special educational services in the U.S. between 2005 and 2010.

Key Findings
Autism and related disorders affect brain development. The current study sought to determine how environmental and dietary factors, like HFCS consumption, might combine to contribute to the disorder.
  • Consumption of HFCS, for example, is linked to the dietary loss of zinc, which interferes with the elimination of heavy metals from the body. Many heavy metals like mercury, arsenic and cadmium are potent toxins with adverse effects on brain development in the young.
  • HFCS consumption can also impact levels of other beneficial minerals, including calcium. Loss of calcium further exacerbates the detrimental effects of exposure to lead on brain development in fetuses and children.
  • Inadequate levels of calcium in the body can also impair its ability to expel organophosphates, a class of pesticides long recognized by the EPA and independent scientists as especially toxic to the young developing brain.
“Rather than being independent sources of risk, factors like nutrition and exposure to toxic chemicals are cumulative and synergistic in their potential to disrupt normal development,” said Dr. Richard Deth, a professor of Pharmacology at Northeastern University and a co-author of the study. “These epigenetic effects can also be transmitted across generations. As autism rates continue to climb it is imperative to incorporate this new epigenetic perspective into prevention, diagnosis and treatment strategies.”

The picture of how and why a child develops autism is a complicated one influenced by many different factors. The authors of this study have given insight into the complex interplay between several of the factors that may lead to the development of this debilitating neurodevelopmental disorder.

In order to curb the epidemic of autism in the U. S., continued analysis of the impact of the industrialized food system and exposure to environmental toxins on ASD must be key areas of research moving forward.

The Institute for Agriculture and Trade Policy works locally and globally at the intersection of policy and practice to ensure fair and sustainable food, farm and trade systems.

The Food Ingredient and Health Research Institute (FIHRI) is a non-profit organization devoted entirely to food ingredient safety, education, and research. foodingredient.info

Wednesday, April 11, 2012

Insights from New Research into Autism

From The Diane Rehm Show
Guest Host: Susan Page
Wednesday, April 11, 2012

A new report from the Center for Disease Control shows the incidence of autism in American children has dramatically increased over the last decade. A debate is raging over why. Some experts say better detection is the reason. Others say it reflects the broadening definition of autism. At the same time, medical breakthroughs have given doctors and researchers hope that they may soon be better able to identify what causes autism -- and how to treat it. What does this new research mean?

On today's Diane Rehm Show on NPR, Guest Host Susan Page, Washington Bureau Chief of USA Today, interviewed four impressive guests on the new autism prevalence statistics and related topics. You can listen to the entire hour HERE, or order a CD of the show HERE.

Her Guests

Amy Harmon, national correspondent with the New York Times. She has written extensively on autism

Jennifer Walsh, parent of a child with autism

Lauren Kenworthy, director, Center for Autism Spectrum Disorders, Children's National Medical Center

Sunday, April 8, 2012

Outgrowing Autism? Study Looks at Why Some Kids "Bloom"

From VITALS on msnbc.com

By Linda Carroll

About 10 percent of children who are severely affected by autism at age 3 seem to have “bloomed” by age 8, leaving behind many of the condition’s crippling deficits, a new study shows.

Karen Melville remembers when her son Danny was diagnosed with autism so severe that his doctor feared he might never even talk, much less go to school. “It was like a freight train hit,” said Melville, a 39-year-old mother of two who lives in Brunswick, Ohio.

Five years of intensive therapy have paid off. Danny, now age 7, is OK’d to go to school next year in a mostly mainstream class that will have a total of three “high functioning” kids with autism. “Now when he finds something he thinks is really cool on the computer -- like a humpback whale swimming -- he wants to show me,” Melville said.

Danny may be one of what researchers are now calling “bloomers” – kids who start out as severely affected but who manage to grow beyond most of their symptoms.

About 10 percent of children who are severely affected by autism at age 3 seem to have “bloomed” by age 8, leaving behind many of the condition’s crippling deficits, a new study shows. And while these “bloomers” still retain some of autism’s symptoms, like the tendency to rock back and forth when stressed or to repeat the same behavior over and over, they become what experts dub, “high functioning,” according to the study published today in Pediatrics. That means their social skills and their ability to communicate have vastly improved.

A child at the low end of the communication scale might not be able to talk, or even to make any sounds, explained the study’s lead author Christine Fountain, a postdoctoral fellow at Columbia University. Those at the other end of the scale “would have a broad vocabulary, understand the meaning of words and use them in appropriate contexts, understand the meaning of story plot and carry on complex conversations,” she explained.

Similarly, a child with a low score on the social scale would have problems interacting with others and would not be able to make friends or socialize. At the high end of the scale, is a child who “would initiate one-on-one interactions with both peers and others in familiar and unfamiliar settings, initiate and maintain friendships, and not need encouragement to participate in social activities,” Fountain said.

"Bloomers” are edging up towards the upper half of both those scales."

Fountain and her colleagues didn’t expect to see kids jump from the low end to the high end in just a few short years. “It was a surprise to see how much improvement they showed – and how quickly,” Fountain said. “That’s kind of hopeful message.”

Hopeful, because "the odds of such big improvements might rise if more kids got the right kind of therapy early in life," Fountain said. 

The researchers studied the records of 6,975 California children who had been diagnosed with autism. They found that many of the children showed improvements between ages 3 and 8, but some, the bloomers, showed startling progress, moving from the most severely affected to some of the highest functioning.

Kids who are older can continue to make progress, but more slowly, experts say. While many of their symptoms fade, they still retain the autism diagnosis.

Fountain and her colleagues suspect, after scrutinizing the differences between children who bloomed and those who didn’t, that it likely comes down to which kids were able to get early, intensive therapy since the children who improved the most had parents with more education and financial wherewithal. Researchers say that it’s possible there might be something inherently different about the children themselves who are “bloomers,” but they don’t know that for sure.

As they delved into the bloomers backgrounds, the researchers found that these children were more likely than others to have mothers with at least a high school education and to come from a higher socio-economic class. (They didn’t have information on the fathers.) Bloomers also tended not to have any intellectual disabilities.

The findings don’t surprise autism expert Tamar Apelian.

“Most children need about 30 to 40 hours a week of intervention,” said Apelian, a staff psychologist at the autism evaluation clinic at the University of California, Los Angeles. “What’s tricky is being able to navigate the system to get the therapy, especially with the state budget crisis. The parents who do this seem to have more means and they can hire an advocate or a lawyer.”

And that’s where parents’ backgrounds come in to play.

After absorbing Danny’s diagnosis at 25 months, Karen asked his doctor about the future. “I said, ‘OK, what can we do about it?’ The doctor said, ‘How much money do you have?’”

The Melville’s weren’t independently wealthy. They were comfortably middle class – but that certainly doesn’t pay for therapy that can cost upwards of $70,000 per year. So that meant the Melvilles had to be creative to get Danny what he needed.

While Danny waited for his turn to come up on program waiting lists the Melvilles found a student to work with him. In the meantime, Danny’s dad, Michael, went back to school to get certified as a pharmacy tech so he could get a job at a university that came with benefits including a break on Danny’s therapy.

The family scraped together money from a variety of sources and finally managed to get Danny into an intensive program that offered one-on-one help.

“When I think back, I think about how I sat and watched for hours waiting for him to make that first sound,” Karen said. “I think about how grim things looked. I can’t stress enough that people determine what it is their children need and then get on those waiting lists. Keep digging and fighting to find someone to start with. It doesn’t matter if it’s a student while you’re on the waiting list. It’s just so important to get help early."


Watch below as Autism Speaks founders Bob and Suzanne Wright join Morning Joe to discuss autism research, having an autistic child in their family, and the costs of caring for a child with autism.