Autistic Disorder and Intellectual Disability: 70% Is Not a Coincidence, It Is a Vast Majority

                                  

The DSM-IV and popular media interpretation of the autism disorders (pervasive developmental disorders), have encouraged the world to see autism as shy or introverted personality and a different, sometimes superior, way of thinking and has obscured the very obvious and close connection between autistic disorder, the most severe form of autism, and intellectual disabilities.

Autism is described in a CHARGE Study article as follows (emphasis added, HLD):

"Autism is a serious neurodevelopmental disorder characterized by impairments in social interaction, abnormalities in verbal and nonverbal communication, and restricted, stereotyped interests and behaviors (American Psychiatric Association 1994). Although a large proportion of individuals with autism manifest abnormal development from birth, a subset of at least 20–30% experience a regression with onset between 18 and 24 months of age after a period of apparently normal development (Lainhart et al. 2002). Autistic disorder is the most severe form of autism spectrum disorders (ASDs), which include Asperger’s syndrome and pervasive developmental disorders (PDDs) not otherwise specified. Approximately 70% of individuals with autistic disorder have some degree of mental retardation, and about half are nonverbal or have very impaired speech.

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

CDC autism expert Dr. Marshalyn Yeargin-Allsopp has described those with intellectual disability as the "vast majority" of the original,  pre DSM-IV autism:

"But the autism umbrella has since widened to include milder forms, says Dr. Marshalyn Yeargin-Allsopp, a medical epidemiologist at the CDC. For example, it now includes Asperger syndrome, where the sufferer is socially impaired, but experiences typical language development.

Another difference between past and present autism diagnosis involves the presence of intellectual disabilities, adds Yeargin-Allsopp. During the 1960s and 1970s, the vast majority of those diagnosed with autism had an intellectual disability but today, only about 40% have one."

CDC Autism Expert Dr. Marshalyn Yeargin-Allsopp 

The attempt to hide the very strong and clear relationship between autistic disorder and intellectual disability is more than just wrong it is the last politically correct form of discrimination ... discrimination against those with intellectual disabilities.  It is also a huge step backwards in understanding the truth about autism, that autism is a form of intellectual disability, most evident in those with autistic disorder.  Studies of high functioning persons with autism and Asperger's are routinely reported as representing all persons with autism disorders even those with intellectual disability who are intentionally excluded from the studies.  

Autism's Compelling Question: What is Causing Spontaneous Mutations Linked to Autism?

"One compelling question is what is causing the mutations ... The obvious conclusion one has to reach is that something environmental may well be the cause of these [spontaneous] changes in DNA"

Irva Hertz-Picciotto, autism researcher and professor of public health science at UC Davis, commenting on studies led by Matthew W. State and  Michael Wigler, showing hundreds of spontaneous mutations linked to autism, LA Times, June 9, 2011 

The gene environment interaction (GEI)  model of autism causation has been emerging over the past half dozen years. Even this humble layperson has noted the GEI model on several occasions on this blog. The "it's gotta be genetic" (IGBG) model was noted over a decade ago by Teresa Binstock. The GEI model has developed despite, or perhaps more accurately because of, the almost exclusive dedication of research dollars to  the  "it's gotta be genetic" (IGBG) model of autism causation. 

It is the failure of the pure genetic research to identify a specific genetic basis for  autism that only now is beginning to cause its adherents to doubt their faith.  It is the failure of the pure genetic model to explain autism causation beyond the existence of hundreds of spontaneous mutations that must finally make even the most determined of the IGBG school of autism causation ask ... could environmental factors be involved?  Spontaneous mutation is giving rise to spontaneous combustion as the purely genetic model of autism causation burns in the flames of failure.

Autism's most compelling question, as stated by Hertz-Picciotto: What is causing the spontaneous mutations?

Michael Szpir: Tracing the Origins of Autism: A Spectrum of Studies

Michael Szpir's article Tracing the Origins of Autism: A Spectrum of New Studies is full open access  [Copyright This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose] at Environmental Health Perspectives. Given it's lack of restrictions on use and reproduction I have reprinted it here in its entirety. Notwithstanding it was published in 2006 I recommend it for anyone interested in the autism paradigm shift currently underway, albeit slowly, from the faith like,  "it's gotta be genetic", 100% genetic model, which has simply and totally failed to explain what is happening with autism disorders to a more rational, gene environment interaction model. Szpir reviews some of the important studies and includes commentary from gene environment focused autism researchers including Dr. Irva Hertz-Picciotto, a leading light in the shift to a gene environment model of autism.

The etiology of a medical condition might seem an unlikely subject to arouse intense feelings. Yet few medical disorders have stirred up as much passion and divisiveness among scientists and the general public as autism has in recent years. The heat of the controversy has even attracted attention from periodicals such as The Wall Street Journal, the Columbia Journalism Review, and Wired magazine—seemingly improbable forums for a medical debate. Why all the furor?

At the eye of the storm is the startling climb in the numbers of children who have been diagnosed with one of the autism spectrum disorders (ASDs). The most severe ASD is autistic disorder (which often is called simply “autism”); other forms include Asperger syndrome and the much rarer childhood disintegrative disorder. In the United States, the diagnosis of ASDs increased roughly 10-fold over the course of a decade, from 4–5 children per 10,000 in the 1980s to 30–60 children per 10,000 in the 1990s, according to a report in the August 2003 Journal of Autism and Developmental Disorders. The 5 May 2006 issue of Morbidity and Mortality Weekly Report describes the results of two parent surveys from 2003 and 2004, which suggested that 55–57 children per 10,000 had autism (however, an editorial note points out that, due to the nature of the surveys, parents of children with other ASDs may have reported their children as having autistic disorder).

Some scientists believe that much of the upsurge is the result of increased awareness of ASDs or changes in diagnostic criteria, which would suggest that the true prevalence of the disorders has been stable over time. Others disagree. “It is premature to state that there is no increase in prevalence,” says W. Ian Lipkin, a professor of neurology, anatomy, and neurobiology at Columbia University. “None of the studies to date has been designed to definitively address the issue.”

The prevalence of ASDs plays into the fundamental question of what causes these disorders. If the number of cases is truly on the rise, then it would seem likely that some change in the environment is driving up the total. That’s partly what has divided scientists into opposing camps—they cannot agree on the relative importance of genetic and environmental factors in the disorders’ etiology.

Alas, answering the prevalence question might not end that debate. “Even if the prevalence of autism were stable,” says Lipkin, “you would not be able to rule out the possibility of an environmental trigger.” That’s because very little is known about the mechanisms that cause autism, be they environmental or genetic.

“The study of autism was, until recently, largely dominated by the field of psychology, where characterizing the behaviors and developing reliable instruments for diagnosis have been major areas of research over the past few decades,” says Irva Hertz-Picciotto, an epidemiologist at the University of California, Davis.

Indeed, the core symptoms of ASDs—social disinterest, repetitive and overly focused behavior, and problems in communication, usually appearing before 3 years of age—have been well described. Much less research has focused on the causes of these symptoms.

Several investigations dating back to the 1970s indicate that identical twins have a much higher concordance rate of ASDs than fraternal twins, according to a report in the Spring 1998 issue of Mental Retardation and Developmental Disabilities Research Reviews. Those studies provide some of the best evidence that these disorders have a strong genetic component. But the identity of the genes involved, much less how they produce ASDs, has not been established. Moreover, the concordance rate for identical twins is not 100%, which suggests that at least some cases must be associated with environmental or epigenetic factors.

A few cases of ASDs have been clearly linked to environmental insults. These include prenatal exposure to chemical agents such as thalidomide and valproic acid, as well as to infectious agents such as the rubella and influenza viruses. Here again, the concordance rate is not 100%, which suggests that a genetic predisposition is necessary for chemical and microbial factors to act as triggers.

Tantalizing clues like these are prompting scientists to reconsider the research agenda for ASDs. Martha Herbert, a pediatric neurologist at Harvard Medical School, and her colleagues have been applying the methods of genomics to identify environmentally responsive genes that might be important in these disorders.

“When you realize that the widespread changes we’re seeing in autistic brains may occur in parallel with or even downstream from widespread changes in the body—such as in the immune system—and that these changes may be environmentally triggered, you start looking for ways to think more broadly about genetic vulnerability. It can’t be just about ‘brain genes,’” Herbert says.

Some new epidemiological studies also are looking for gene–environment interactions. According to Diana Schendel, an epidemiologist and project officer for autism research at the CDC, which funds one of the projects, these initiatives will be able to examine many possible causal pathways to ASDs, including both genetic and environmental causes that may lead to the development of the disorders in different subgroups of children.

Some of these projects are already under way, whereas others will begin soon. All of the scientists involved, however, believe their research will finally provide some of the answers that everyone has been looking for.

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CHARGE

The Childhood Autism Risks from Genetics and the Environment (CHARGE) project is unique among the large ASD epidemiological studies. It focuses solely on autistic disorder, and it emphasizes a search for environmental factors—including a broad array of chemicals in food, consumer products, and ambient air, as well as infectious and medical exposures—that might be linked to the disorder. The study is funded by the NIH.

CHARGE is a case–control study in which a group of autistic children aged 2 to 5 years is compared to a group of age-matched controls in a population-based study. “Because of the California Department of Developmental Services’ system of Regional Centers [nonprofit corporations that coordinate health care services and support for citizens with developmental disabilities], we have a handle on enumerating a high proportion of the children newly diagnosed with autism in our defined area over a specific time period,” says Hertz-Picciotto, the principal investigator of the CHARGE study. “Similarly, we can enumerate the children in the same area and time period who are not cases. We then sample from both.”

The project was initiated in 2002 with the goal of recruiting 1,000 to 2,000 children. Half of the children will be autistic. The other half will make up two control groups: one group of children with developmental delays (but not an ASD) and a second group of children selected from the general population without regard to developmental characteristics.

The advantage of the case–control design is that scientists can acquire large numbers of children with the disorder. By comparison, in a cohort design researchers would need a very large sample size, given the prevalence of autism, to acquire the same number of cases.

Hertz-Picciotto expects to have enrolled nearly 700 children by August 2006, the end of the first funding period. “I’ve applied for another five-year grant,” she says, “and I hope to be funded to enroll nine hundred in that round, which would bring us to sixteen hundred children.”

The CHARGE team is looking at possible exposures during the prenatal period and early childhood. Some of the data will be gathered through comprehensive interviews with parents, but Hertz-Picciotto admits that this is not the best way to look for exposures. “You ask people questions, and their answers may be colored by the fact that they know they have a child with a condition,” she says. “They may spend a lot of time thinking about what they might have done or what might have gone wrong, and they may have preconceived ideas about what caused [the disorder]. They might not be as objective.” Such problems with postdiagnosis interview information are recognized as a weakness of retrospective studies.

The scientists are getting around this issue by examining each child’s medical records and those of the mother during pregnancy and delivery—nonsubjective data gathered in the course of routine obstetric care. They are also collecting blood, urine, and hair specimens that will be analyzed in the laboratory.

The study has already provided some intriguing leads. “We’re finding that the immune system seems to function at a lower level in autism,” says Hertz-Picciotto. “That’s an important clue. It could mean that whatever causes autism also disrupts the immune system, or it could be that the immune system disrupts neural development so that something goes awry in laying down brain circuitry prenatally or in the early postnatal period.” [For more information on the CHARGE study, see p. 1119, this issue.]

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ABC

The Autism Birth Cohort (ABC) Study, now under way in Norway, is a large prospective design that is expected to gather information on 100,000 babies. The work is being led by scientists at the Mailman School of Public Health at Columbia University, who are collaborating with colleagues at the Norwegian Institute of Public Health, with funding from the U.S. National Institute of Neurological Disorders and Stroke.

“When you want to know why some people are more at risk than others in a population, then that’s best answered using a cohort design,” says Ezra Susser, an epidemiologist at Columbia University and a co-investigator on the ABC project. “When we think about environmental causes of [ASDs], we’re probably interested in phenomena that occur prior to birth or perhaps shortly after birth. So you want to collect prospective data from people as early as possible in pregnancy.” Because ASDs are not common, the study will need large numbers of children to have enough statistical power, according to Susser.

So far the ABC team has recruited 75,000 pregnant Norwegian mothers, but Susser is hoping for more. “We’ve got enough to look for an environmental risk factor, but you need larger numbers for studying gene–environment interactions, which could turn out to be important,” he says. It’s possible the team could acquire greater numbers by collaborating with other studies. One candidate for collaboration is the Avon Longitudinal Study of Parents and Children in the United Kingdom, which is looking at the complex ways in which environmental features may relate to optimal development and health in children. But there’s been no agreement yet, Susser says.

Even so, the ABC scientists are optimistic about their study. “Little is known about the natural history of [ASDs],” says Lipkin, who is the principal investigator of the project. “By starting prenatally, we’re collecting detailed, critical information about environmental exposures in an unbiased fashion.”

The scientists are also collecting plasma, serum, RNA, and DNA. “We have extraordinary biological materials,” says Lipkin. “We can pursue biomarkers as well as exposure to toxicants and infection. We also have maternal DNA, paternal DNA, and the child’s DNA [so-called trio data]; thus we can look for the appearance of novel mutations,” he adds.

The ABC researchers will follow the children through time, with parents answering questionnaires about the health and social interactions of their children as they reach 6, 18, and 36 months of age. “It may be that the developmental trajectory tells us much more than a single time point can ever tell us about the pathogenesis of [ASDs],” says Mady Hornig, a physician-scientist at Columbia University who participates in the project.

Despite their enthusiasm for the project’s potential, the ABC scientists feel they could accomplish much more if they only had the funding. “The pity of it is we have no money to do the biological work,” says Lipkin. “We can collect the samples and do the questionnaires, but we’ve been unable to get funding to look for any of the environmental factors. We’re collecting blood, but we won’t know whether there’s a biomarker until we do a biomarker analysis. We have funds to collect RNA, but in order to do the transcript profiling we need approximately four hundred dollars per sample,” he says.

Lipkin adds that there’s only so much that one can do with questionnaire data. “We do ask about infection and diet, but that’s not the same as having a lab value that can validate what was reported, and then look at a direct correlation with the outcome,” he says.

Lipkin believes that part of the problem is that searching for environmental factors goes against the current research paradigm in ASDs. “The focus is on genetic factors,” he says. “Infectious diseases, toxicology, and immunology receive short shrift. The ABC is clearly the right opportunity to pursue these other leads because we have the ideal samples to survey prenatally and postnatally,” he says.

The scientists are just now receiving the responses to the 36-month questionnaire. “It’ll probably be another two years before we have our first report,” Hornig says. Funds are now in place to study the children at 36 months; however, the team hopes to follow them for a lifetime, according to Hornig.

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CADDRE

In response to the Children’s Health Act of 2000, the CDC established and funds six Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) to investigate potential risk factors for ASDs. The multisite approach offers a study group that is geographically and demographically more representative of the general U.S. population than a smaller regional study could provide, according to Craig Newschaffer, an epidemiologist and principal investigator at the Johns Hopkins Bloomberg School of Public Health CADDRE site.

According to Newschaffer, the CADDRE sites will use a case cohort design in which the exposure patterns of the ASD cases are compared to a random sample of children living in the same geographic area. A third study group, consisting of neurodevelopmentally impaired children who do not have an ASD, will round out the sample populations. The investigators hope to enroll a total of 650 to 900 children, aged 3 to 5 years, in each study group across all the sites, making CADDRE the largest study of its kind in the United States, says Newschaffer. A uniform protocol across the sites will allow the scientists to pool their data.

CADDRE will collect and archive blood, cheek cell, and hair samples from the children in order to investigate a broad range of potential risk factors. “We’re not focused on the environment as much as CHARGE is,” says Newschaffer, “but we are collecting data on questionnaires and reviewing medical records on exposure, in addition to the biosampling for exposures.”

The scientists should have sufficient numbers to look at gene–environment interactions. “We are collecting DNA from the parents and the kids from each of the groups. We’ll have trio data in each of the three groups, a potentially powerful design,” says Newschaffer.

CADDRE scientists will also characterize the behavior of the children, as well as describe any comorbid medical conditions and atypical physical features. The goal is to sort out different etiologic subgroups within the autism spectrum. As Newschaffer explains, “There are a lot of possible reasons why we’ve had a hard time coming up with genetic and nongenetic risk factors. One of them is that autism is likely a heterogeneous condition, with different etiologies producing kids with what appear to be similar phenotypic profiles. If you don’t separate out the different etiologic groups, it’s going to be very hard to find an association with a gene or an exposure. If we limit our analyses to kids that have a certain profile, we’re going to be able to make some informed guesses about what profiles might allow risk factors to emerge,” he says. The CADDRE sites will begin recruiting children into the study in the fall of 2006.

More Studies, More Acronyms

There are several other smaller epidemiological studies in the works. In California, scientists are tapping into specimen banks that have stored blood samples taken from mothers during pregnancy and from their children at birth. The Early Markers for Autism (EMA) study employs a case–control design, with about 100 children with an ASD (primarily autism), 100 who are developmentally delayed, and 200 from the general population. “We can correlate what’s happening in the mom and the baby, which is really exciting,” says Lisa Croen, a perinatal epidemiologist at the Kaiser Permanente Division of Research in California and the project’s principal investigator.

EMA is a multidisciplinary collaboration with epidemiologists, geneticists, immunologists, neurovirologists, and endocrinologists, according to Croen. “Because autism is so complex, it’s important for all these researchers to communicate with each other. I think EMA is a model for how to do research in autism,” she says. EMA is unique, according to Croen, because the study will be looking for biological markers of ASDs very early in development, during gestation, and at birth. “This allows us to focus on mechanisms that may be leading to autism rather than mechanisms that are consequences of having autism,” she says.

The EMA scientists are investigating genetic and nongenetic factors, with a focus on the immune dysregulation hypothesis of ASDs. “We’re measuring different kinds of immune markers, including immunoglobulin levels and antibodies to specific infectious agents, cytokines, and autoantibodies,” says Croen. “We’re looking for things that distinguish kids who are subsequently diagnosed with autism from those who aren’t. This will help us understand the pathobiology of autism—the mechanisms that are leading to the dysregulation in development.”

The three-year EMA is currently in its last year. “We still have lots of analyses to do,” says Croen, “but we’re beginning to write some papers. We’re finding differences between the children in levels of certain proteins measured in the circulating blood collected from mothers during pregnancy. I think the study has much to contribute to our understanding of the biology of what might be going wrong.”

Croen is also an investigator on the California Autism Twin Study (CATS), which expects to recruit 300 identical and fraternal twin pairs born between 1987 and 1999 in which at least one of the twins has an ASD. Comparing the twin pairs will allow the scientists to estimate the heritability of ASDs—the relative genetic and environmental contributions to the disorder. “Knowing the behavioral and developmental differences between the twins might help us understand the effects of gene expression, the in utero environment, and environmental triggers,” Croen says.

Hertz-Picciotto is also excited about a five-year study that she and her colleagues hope to begin soon. Unlike CHARGE, the new effort, called MARBLES (Markers for Autism Risk in Babies—Learning Early Signs), will be a prospective study in which data will be gathered before the children are diagnosed. Pregnant women who already have at least one child with autism will be enrolled right at the beginning of pregnancy. The mothers will keep diaries about their symptoms and health-related events, and the researchers will collect cord blood samples and placentas.

Based on previous research, Hertz-Picciotto expects that about 1 in 10 siblings of the autistic children will also have the disorder, and perhaps 1 in 4 or 5 will be “on spectrum” with a related but less severe condition such as Asperger syndrome, or with some symptoms of the broad behavioral phenotype, such as language delays and atypical social skills. “This work is complementary to the case–control approach, and should provide us with a lot of information that will build on what we find in CHARGE. It should be a phenomenal resource,” she says.

You Say You Want a Revolution

In April 2004, the U.S. DHHS issued a publication, Congressional Appropriations Committee Report on the State of Autism Research, describing recommendations made by a panel of expert scientists convened by the Interagency Autism Coordinating Committee (IACC). The IACC panel suggested an ambitious agenda, which included the goal of identifying environmental risk factors and their associated developmental windows within a four- to six-year period, as well as identifying genetic and nongenetic causes of ASDs and their interactions within seven to ten years.

Hertz-Picciotto, a member of the IACC panel, thinks these goals should be taken with a grain of salt. “I’m optimistic that we will have identified some environmental risk factors, and may have excluded a few others, between 2008 and 2010—but by no means will we have the final word. The genetics and the gene–environment interactions may be even tougher. Unfortunately, I don’t see enough groups working on the environmental contribution to autism, so it may be slower than projected,” she says.

Mark Blaxill, vice president of SafeMinds, a parent-led advocacy group, also believes that environmental risk factors don’t receive enough consideration. “The CDC has not addressed the crisis in autism responsibly,” he says. “They should be raising the alarm, and they have failed to do so. They should be asking why so many children are sick. Instead, they’ve tried to suggest a degree of doubt about the increases, and that diverts attention and funding from environmental causes.”

Schendel responds, “It is clear that more children than ever before are being classified as having an ASD. It is important that we treat common developmental disorders, and especially the ASDs, as conditions of urgent public health concern. The CDC’s efforts in addressing this public health concern include funding for ASD monitoring programs to understand ASD trends, funding for research into the genetic and environmental causes of ASDs, and education and outreach programs to promote early identification and timely intervention for all children with developmental problems.”

Despite the promise of the new epidemiological studies, some researchers are still dismayed, as one scientist put it, that “geneticists are running the show, and ignoring the environmental aspects.” What would it take for things to change? Blaxill invokes the ideas of philosopher Thomas Kuhn, who suggested that scientific revolutions occur when an old paradigm is replaced by a new one. “I believe we’re in the middle of a paradigm shift,” Blaxill says. “The dramatic explosion of autism rates does not fit the genetic model. It’s an anomaly that will kill the old paradigm.”

Autism Speaks & CDC Autism Prevalence Increase Workshop Timely: Autism is Rising & Environmental Factors Likely Involved

"Based on the above mentioned research, approximately 53% percent of the increase in autism prevalence over time may be explained by changes in diagnosis (26%), greater awareness (16%), and an increase in parental age (11%). While this research is beginning to help us understand the increase in autism prevalence, half of the increase is still unexplained and not due to better diagnosis, greater awareness, and social factors alone. Environmental factors, and their interactions with genetic susceptibilities, are likely contributors to increase in prevalence and are the subject of numerous research projects currently supported by Autism Speaks.

The increase in autism prevalence is real and the public health crisis is growing. More families are affected by autism today then ever before."

Autism Speaks Official Blog, October 22, 2010

The above statement by Autism Speaks was based on several published sources and CDC information. including articles by authors Bearman and King, who have indicated that approximately 50% (47%) of autism prevalence increases are based on factors other than social factors. Now Autism Speaks and the Centers for Disease Control and Prevention (CDC) are co-sponsoring a workshop  on February 1, 2011 to investigate the changes in autism prevalence over time in the United State:

"The purpose of this workshop is to identify promising directions, priorities, and needs for better understanding ASD prevalence trends. The workshop will include presentations on what has been done to understand reasons for ASD prevalence changes, examples of understanding prevalence change from other conditions, and panel breakout sessions to allow for further discussions.


This meeting is open to the public with pre-registration required by January 24, 2011 for US citizens and January 13 for non-US citizens."

Autism Speaks Official Blog, January 5, 2011

While Autism Speaks has been puzzling at times in its efforts to "speak" about autism disorders, promoting the careers of purported autism spokespersons who question the very existence of autism as a  medical  disorder,  the importance of the above initiative can not be overstated.  For far too long the "it's gotta be genetic" mindset has held sway and prevented substantial scientific exploration of possible environmental causes or triggers of autism. Hopefully the recent US Senate hearings, official statements by the IACC acknowledging the emergence of a gene environment interaction paradigm, the CHARGE study, work by Dr. Irva Hertz-Picciotto and UN Davis M.I.N.D. researchers,  and efforts like the Autism Speaks/CDC prevalence workshop will lead to further environmental autism research; research which should have been commenced  years ago.

Facing Autism in New Brunswick Thanks the Canadian Weblog Awards

 

Thank you to Canadian Weblog Awards for having nominated Facing Autism in New Brunswick for a 2010 CWA  and a big thank you to the jurors in two rounds of voting who selected Facing Autism as the First Place Winner in the Health & Wellness category and Third Place Winner in the Ecology & Social Justice category. I encourage readers to visit the CWA site and check out all the excellent winning and nominated blogs.

I also encourage our Canadian federal government to begin implementing a REAL National Autism Strategy.  The current National Autism Strategy is a very bad joke. Canadians with autism disorders and their families deserve much better than the patch work quilt of services that exists across Canada.  This is not a partisan issue. As yet no Canadian federal party has used the power of government to help autistic Canadians in any meaningful way. Canadians with autism disorders are Canadians too. They deserve recognition and real help from our federal government. 

I also encourage researchers, particularly in the United States, where most significant autism research is done, to continue efforts to finding causes, treatments and ... someday ... cures for autism disorders.  Autism is not just a different personality, a life style or a culture.  It is a medical disorder that restricts the lives of most affected by it.  I also encourage autism researchers in the US to contribute more funding towards environmentally focused autism research. Autism has not even remotely been explained by the total dedication of funding dollars towards genetic autism research.  The emerging paradigm recognizes autism as resulting from gene environment interaction. So it might be a very good idea to recognize the fine work done by Dr. Irva Hertz-Picciotto and her colleagues who have done so much to bring attention to the environmental side of the autism equation.

I encourage everyone .. researchers, doctors, government leaders, media "journalists", bloggers and citizens of all countries to recognize that autism is not just a childhood disorder, that autistic children grow up to become autistic adults. Many will require services in all areas of life including residential care and treatment which accommodates the challenges presented by their autism disorders.

In 2010 the Gene Environment Interaction Model of Autism CHARGEd to the Fore

"Uncovering environmental causes of autism

CHARGE (Childhood Autism Risks from Genetics and the Environment) was launched in 2003 as a study of 1,000 to 2,000 children with differing patterns of development. The goal is to better understand the causes and contributing factors for autism or developmental delay. Three groups of children are being enrolled in the CHARGE study: children with autism, children with developmental delay who do not have autism and children from the general population. All of them are evaluated for a broad array of exposures and susceptibilities.

Refining our understanding of environment-gene interactions

Little is known about what causes autism or developmental delay. We will learn how genes and the environment interact to change children’s behaviors and skills. By studying a large number of children, we will discover which particular genes and/or environmental exposures might result in non-typical patterns of development and special subtypes of autism or developmental delay."

2010 could be known as the year that serious autism research arising from the genetic-environmental interaction model CHARGE'd to the fore with two major genetic-environmental focused autism research studies being published and receiving widespread attention.   2010 could also come to be known as  the year that  the "it's gotta be genetic" model of autism causation began its retreat from the battlefield in our attempt to understand autism causes  and seek autism cures.  Nothing can be done to retroactively counter the  time, financial resources,  attention and energies lost promoting the ill conceived notion that all autism disorders are 100% genetically based but there are now clear signs we are moving forward in our efforts to understand what causes autism disorders and real progress is being made.

Researchers involved with the recent mitochondrial dysfunction study and the proximity to proximity to highways (and air borne pollutants) study used data from the CHARGE program.  In each case the study authors are careful to report the limitations of their studies and to indicate that their studies indicate associations but do not, as yet,  identify specific causes of autism disorders. The studies  are exploratory and provide the foundation for further research.  Such studies are long overdue and are very welcome. 

A solid foundation for serious autism research has been established.  The autism research paradigm shift whispered about over  the last 3 years is now fully emerging and we are seriously studying the interaction of genetic and environmental research.  The gene environment model of autism is strongest in  California where researchers like  Dr. Irva Hertz-Picciotto, principal investigator on the CHARGE study, Dr.  Heather E. Volk  and Dr. Cecelia Giulvi use data from the CHARGE program as the basis for their research. 

The gene environment model of autism was also featured prominently at the  US Senate Committee on Environment and Public Works, Subcommittee on Children’s Health hearing entitled, "State of Research on Potential Environmental Health Factors with Autism and Related Neurodevelopment Disorders"   in August 2010. One of those who made written submission to the hearing was Dr. Isaac N. Pessah, Director UC Davis Center for Children’s Environmental Health and Disease Prevention Professor of Toxicology and a Co-Investigator with the CHARGE study.

There are signs Canada has also  begun to embrace the gene environment model of autism causation.  The York Alliance Autism Research Group includes  Dr. Dorothy Crawford,  focusing on gene environment interaction as causes of autism disorders in her research. Even the US IACC (Interagency Autism Coordinating Committee) has acknowledged, albeit somewhat timidly, the emergence of the gene environment model in understanding autism causation:

"As with many complex disorders, causation is generally thought to involve some forms of genetic risk interacting with some forms of non-genetic environmental exposure. ... In addition, a number of other environmental factors are being explored through research because they are known or suspected to influence early development of the brain and nervous system. Recent studies suggest factors such as parental age, exposure to infections, toxins, and other biological agents may confer environmental risk. ... Progress in identifying environmental factors which increase autism risk has been made recently (Eskenazi et al., 2007; Palmer et al., 2006; Palmer, Blanchard,; Wood, 2009; Rauh et al., 2006; Roberts et al., 2007; Windham et al., 2006), although this area of research has received less scientific attention and far fewer research dollars than genetic risk factors"

I have bold highlighted the last quoted statement from the IACC because it confirms exactly what has been said about autism research funding by autism researches from Dr. Teresa Binstock to Dr. Irva Hertz-Picciotto. Funding dollars have gone overwhelmingly toward genetic based autism research at the expense of environment autism research and that imbalance must be corrected.  Hopefully, as the gene environment model continues to gain ground amongst scientists involved in autism research that imbalance will also be corrected by funding authorities from government agencies to Autism Speaks.

It is time to CHARGE ahead with the gene environment interaction model of understanding and researching autism disorders. 

Autism Speaks Role in Exploring the Environmental Causes of Autism and Other Learning Disabilities

Autism Speaks has been open to legitimate criticism on several aspects of its autism advocacy of late including promoting the views of those who do not view autism disorders as medical disorders and do not think that autism disorders should be cured.  AS even promotes the views of Alex Plank, a very high functioning young man, with no obvious or apparent autism deficits, who runs a forum which, amongst other disreputable behavior, actually permitted posters to cheer the passing of Dr. Ivar Lovaas.  On its official blog site though Autism Speaks has just given notice  that it can still engage in some  genuine, and much needed, autism advocacy with its sponsorship of, and reporting on, the Mount Sinai Children's Environmental Health Center's workshop "Exploring the Environmental Causes of Autism and Other Learning Disabilities".     , 

In Feeling exposed? Insights from a new meeting on environmental impacts in autism Autism Speaks board member, and co-founder and Executive Director of Safe Minds, Sallie Bernard provides an overview of “Exploring the Environmental Causes of Autism and Learning Disabilities” a conference  organized  by the Children’s Center for Environmental Health at the Mount Sinai School of Medicine in New York City run by Dr. Phil Landrigan.

Dr. Landrigan is no vaccine patent holder or industrial  or  pharmaceutical company apologist. His credibility on children's health areas is well summarized on Wikipedia.

"Landrigan's reputation rests largely on his role as a highly credible evidence-based advocate for public health, specifically in his focus on reducing the level of children's exposure to lead and pesticides and for his participation in the World Health Organization's global campaign to eradicate smallpox. 


He was also a central figure in developing the National Children's Study[1][3] and in the medical and epidemiological studies that followed the destruction of the World Trade Center on September 11, 2001.[4] Additionally, from 1995 to 1997, Landrigan served on the Presidential Advisory Committee on Gulf War Veteran’s Illnesses,[5] and, in 1997 and 1998, served as Senior Advisor on Children's Health to the Administrator of the U.S. Environmental Protection Agency, where he helped establish the Office of Children's Health Protection.


He has been awarded the Meritorious Service Medal of the US Public Health Service[6] and is a frequent consultant to the World Health Organization, which called Landrigan's work "instrumental in passing the Food Quality Protection Act of 1996."


In 2005, Landrigan, along with Drs. Ramon Murphy and David Muller, founded the Global Health Center, a division of the Mount Sinai Medical Center dedicated to finding evidence-based solutions to global health problems.[7]"

The Autism Speaks summary of the conference points out that the primary purpose of the conference was to highlight the fact that environmental autism science should now be considered mainstream.  Hopefully if this message permeates the consciousness of mainstream media decision makers it will  lead to fewer personal attacks on those who advance environmental theories of autism causation and more serious investigation of all possible environmental causes of autism disorders.  Some of the key points as reported by Autism Speaks:

"A few interesting bits of information came out of the conference. One was the definition of “environment” that the insiders use. It covers synthetic chemicals like pesticides, flame retardants and plasticizers; heavy metals like arsenic, lead and mercury; combustion and industrial by-products; diet and nutrients; medications, medical interventions, and substance abuse; infections; the microbiome; heat and radiation; and lifestyle factors. Some may be harmful; others protective. They may operate before conception, during pregnancy or in early life, and some may alter gene expression through epigenetic modifications to chemicals surrounding our genes. Craig Newshaffer, who runs the EARLI study to look at environmental factors among younger autism siblings, referred to the concept of the “exposome”, that is, everything we are exposed to and its effects on health. Dr. Birnbaum’ made the point that health does not equal medicine, and prevention through reduction in chemical exposures is of equal importance to health. Colleen Boyle from the CDC stated that the next prevalence report will be issued in April 2011. We will see if the 1 in 110 number from last year’s report has changed. New research from Korea was unable to confirm increased risk of autism due to parental age or low birth weight, which have been identified as risk factors in Western studies.


The most informative talk was by Dr. Irva Hertz-Picciotto from UC-Davis. She explained how changes in diagnosis do not account for most of the increase in autism rates, and how recent research by their group on mercury and flame retardant blood levels do not address whether these substances are causative for autism because the blood samples were taken years after the autism diagnosis. A paper out this week from UC-Davis found that proximity to traffic air pollution during pregnancy almost doubles the risk of autism. Another paper just accepted by a journal has found higher antibodies to cerebellar tissue in children with autism relative to controls, highlighting the immune component in autism.

Other than these interesting items, the conference covered minimal new ground as far as the science goes. Rather, the points of the meeting seemed to be to make the case that environmental factors research in autism must now be considered mainstream science and to showcase the work being done or about to be done to investigate the issue. Dr. Landrigan made the case for an environmental role by noting that the rate of autism has increased too much to be solely genetic, and that at most, genetics alone will end up explaining 40% of autism cases with the likely percentage much lower."

I appreciate Autism Speaks and Sallie Bernard's  reporting on this conference. I depart from Ms Bernard's description slightly in referring to the information as being just "interesting" points.  In my view it is critically important that the mainstream media, dependent as it is on advertising dollars from business interests, to hear directly from such credible sources as Dr. Landrigan that genetics alone does not explain the incredible increases in autism diagnoses, that environmental factors play a role.  It is also very important for people to understand that the environment can impact child neurological development in many different ways at different developmental times.  The specific reports by Dr. Hertz-Piccotto, herself a leading figure in environmental autism research, are worthy of substantial mainstream media attention.

Autism Speaks has stepped up to the plate with its support for this important conference and by reporting it on their official blog site.  But Autism Speaks can, and should, do more. No one can question the demonstrated ability of Autism Speaks to raise media attention for autism disorders.  Autism Speaks should use its ability to  break through the fog of mainstream media understanding of autism disorders and convince institutions like CNN, CBC, NY Times, Newseek, and all the major television networks to start understanding the environmental component of autism.

The Offit Offensive, with its focus on personally discrediting anyone who questions possible vaccine autism connections,  has dominated mainstream media discussion of any environmental component of autism.  That offensive has not worked and may have been counter productive. Regardless, the vaccine issue is only one component of possible environmental contributors to autism disorder increases as the conference highlights.  It is time that mainstream media began to demonstrate awareness of this reality. No one is better able to help the mainstream media understand the full scope of environmental issues and autism disorders  than Autism Speaks.  I hope  Autism Speaks dedicates more of its impressive resources to doing exactly that. 

Autism Speaks Supports More Environmental Research? Terrific! Now Please Help Even Out the Funding

Right now, about 10 to 20 times more research dollars are spent on studies of the genetic causes of autism than on environmental ones.

We need to even out the funding.

Dr. Irva Hertz-Picciotto, UC Davis M.I.N.D. Institute


I have been a  supporter of Autism Speaks over the course of its brief existence. I appreciate the media savvy and political skills of its leadership. The World Autism Awareness Day that it assisted in bringing into existence is, in my humble opinion, a great accomplishment in itself.  The connections and skills of Autism Speaks leadership have been very impressive in bringing in people and events who, by themselves command attention, from NASCAR to Jerry Seinfeld, people and events that are seen and heard focusing on autism.  Well done, very well done.

I have though been concerned, rightly or wrongly, about  what I thought was a  subscription by Autism Speaks to the "it's gotta be genetic" mindset which has dominated autism research  and hindered  progress in understanding autism disorders and developing treatments and cures.   I was pleasantly surprised when I received from Jane Rubenstein of Rubenstein Communications Inc. the Autism Speaks statement  "HEARING ON STATE OF RESEARCH ON POTENTIAL ENVIRONMENTAL HEALTH FACTORS WITH AUTISM AND RELATED NEURODEVELOPMENT DISORDERS U.S. Senate Committee on Environment & Public Works, Subcommittee on Children’s Health".   In the statement Autism Speaks Chief Science Officer Dr. Geri Dawson states unequivocally Autism Speaks endorsement on the need for more environmentally based autism research:

(NEW YORK, N.Y., August 4, 2010) – Autism Speaks’ Chief Science Officer Geraldine Dawson, Ph.D. emphasized the importance of research on environmental risk factors for autism spectrum disorders as the U.S. Senate Committee on Environment & Public Works, Subcommittee on Children’s Health convened a special hearing yesterday on potential environmental health factors associated with autism spectrum disorders (ASD) and related neurodevelopmental disorders. The hearing examined the latest research on potential environmental factors that may increase the risk for autism spectrum disorders.

As this hearing reviewed studies funded by the Environmental Protection Agency and the National Institute of Environmental Health Sciences on environmental factors associated with autism, including toxins and other factors that can influence brain development, Dr. Dawson reiterated that it is important to remember that, “Although genetic factors clearly contribute to the causes of autism, we also need to understand environmental factors and their interactions with genetic susceptibility.”

Dr. Dawson's statement  includes examples of  what appear to be impressive  initiatives undertaken by Autism Speaks in support of environmental autism research.  The links to review these initiatives can be found on the Autism Speaks web site, science section.  What isn't clear is the level of financial commitment to environmental autism research compared to genetic research.  Does, or will, Autism Speaks commit to balanced funding of environmental and genetic autism research as called for by Dr. Irva Hertz-Picciotto of the UC David MIND Institute?

If I have wronged Autism Speaks with my perception of an imbalance on its part in favor of genetic over environmental autism research I would genuinely appreciate being notified of my error. If that is the case then I will apologize but would humbly and respectfully ask Autism Speaks to use its proven and impressive communication skills to convince public health funding authorities to follow the approach recommended by Dr. Hertz-Picciotto. 

Much valuable time has been lost with the autism is genetic obsession.

Balanced funding of environmental and genetic autism research is needed now, not tomorrow.

Dr. Philip J. Landrigan Calls for Expanded Research Into Environmental Causes of Autism

Dr. Philip J. Landrigan  has published, in the April 201 edition of Current Opinion in Pediatrics,   an article  titled  What causes autism? Exploring the environmental contribution in which the he calls for expanded research into environmental causes of autism.  As set out in the abstract summary:

"Expanded research is needed into environmental causation of autism. Children today are surrounded by thousands of synthetic chemicals. Two hundred of them are neurotoxic in adult humans, and 1000 more in laboratory models. Yet fewer than 20% of high-volume chemicals have been tested for neurodevelopmental toxicity. I propose a targeted discovery strategy focused on suspect chemicals, which combines expanded toxicological screening, neurobiological research and prospective epidemiological studies."

Dr. Landrigan notes that genetic factors are implicated in causing autism but only in a very small number of cases and they do not explain key clinical and epidemiological features. He suggests as a hypotheses that early environmental factors could contribute.  Dr. Landrigan notes two important indirect sources of support for the hypothesis: "studies demonstrating the sensitivity of the developing brain to external exposures such as lead, ethyl alcohol and methyl mercury" and, more importantly, "studies specifically linking autism to exposures in early pregnancy – thalidomide, misoprostol, and valproic acid; maternal rubella infection; and the organophosphate insecticide, chlorpyrifos."

In December 2009 I  wrote a blog comment on this very subject Autism and Human Exposure to Environmental Chemicals: Time to Put a Stake Through the Heart of the "It's Gotta Be Genetic" Model of Autism Research. My comment was based on the CDC Fourth National Report on Human Exposure to Environmental Chemicals, which:

"measured 212 chemicals in people's blood or urine—75 of which have never before been measured in the U.S. population. The new chemicals include acrylamide, arsenic, environmental phenols, including bisphenol A and triclosan, and perchlorate"

I noted that this alarming report had been released just days before Christmas when it would attract little public attention. But I am not a scientist and even worse, I am a parent of an autistic child, which means that my opinion about the realities of autism disorders,  is generally worth less than nothing in public health authority circles.  I am very pleased that someone as distinguished as Dr. Landrigan has in fact been paying attention to the possible role played by untested synthetic chemicals in causing autism in children. For those who do not know who Dr. Philp J. Landrigan is I am citing, in full his bio,  as listed on the Environmental Health Perspectives site:

"Philip J. Landrigan, MD
Center for Children's Health and the Environment
Department of Community &  Preventive Medicine
Mount Sinai School of Medicine

Philip J. Landrigan, a pediatrician, is the Ethel H. Wise Professor and chair of the Department of Community and Preventive Medicine at the Mount Sinai School of Medicine. He also holds a professorship in pediatrics at Mount Sinai. He directs the Mount Sinai Center for Children's Health and the Environment. Landrigan is a member of the Institute of Medicine of the National Academy of Sciences (NAS) and is currently editor-in-chief of the American Journal of Industrial Medicine. He has served in many other capacities, including editor of Environmental Research and committee chair at the NAS on Environmental Neurotoxicology (NAS 1992) and on Pesticides in the Diets of Infants and Children (NAS 1993).

The report of the NAS committee that Landrigan chaired on pesticides and children's health was instrumental in securing passage of the Food Quality Protection Act of 1996, the major federal pesticide law in the United States. In New York City, he served on the Mayor's Advisory Committee to Prevent Childhood Lead Paint Poisoning and on the Childhood Immunization Advisory Committee. He is chair of the New York State Advisory Council on Lead Poisoning Prevention. From 1995 to 1997, Landrigan served on the Presidential Advisory Committee on Gulf War Veteran's Illnesses. In 1997 and 1998, he served as senior advisor on children's health to the administrator of the U.S. Environmental Protection Agency (EPA). He was responsible at the U.S. EPA for helping to establish a new Office of Children's Health Protection."

Hopefully Dr. Insel and the IACC will take seriously the warning sounded by Dr. Landrigan. With his qualifications and experience his is a voice that should be heeded if we are to ever find out what is happening to our children, what is causing them to develop so many neurodevelomental disorders in such alarming numbers.  Rooting endlessly through the genetic family histories of autistic children has not  helped.  Fudging the facts, distorting the picture by periodic DSM changes will not help our children. It is time the IACC and other public health authorities joined respected voices like Dr. Landrigan, Dr. Irva Hertz-Picciotto, Dr. Jon Poling and others who have called for research into the environmental causes of autism disorders.  

Autism is rising. It is time to quit the genetic stalling game and find out why.

Does Wakefield Decision Prove Vaccines Never Cause or Trigger Autism Disorders?

Does Wakefield Decision Prove Vaccines Never Cause or Trigger Autism Disorders? No it does not.

The UK General Medical Council found that Dr. Andrew Wakefield had engaged in several instances of unprofessional conduct. The decision has little, if any, bearing on the science involved in vaccine autism issues.

Several prominent health authorities and researchers have stated that there is a need for stronger science on autism vaccine issues including Dr. Bernadine Healy, Dr. Julie Gerberding and Dr. Irva Hertz-Picciotto..

Environmental Factors Contributing To Autism By Irva Hertz-Picciotto

Autism researcher Dr. Irva Hertz-Picciotto has published an excellent commentary on the Environmental Factors Contributing to Autism at scientificblogging. This is a must read for anyone with a serious interest in autism disorders and ALL of the possible contributing factors to autism.

This comment is, fittingly, posted on the scientificblogging Autism Awareness page.

It is a valuable contribution to real autism awareness.

The Time is Now to Redress the Autism Research Imbalance

As with many complex disorders, causation is generally thought to involve some forms of genetic risk interacting with some forms of non-genetic environmental exposure. The balance of genetic risk and environmental exposure likely varies across the spectrum of ASD.  ..........  Researchers are working to better understand the interaction of genetic vulnerability with developmental experiences, such as a specific environmental exposure. While gene-environment interactions have been hypothesized to play a role in many medical disorders, these interactions have been difficult to prove or disprove beyond statistical tests showing that some genetic subgroups have a greater response to some environmental factor. ............ Progress in identifying environmental factors which increase autism risk has been made recently (Eskenazi et al., 2007; Palmer et al., 2006; Palmer, Blanchard, & Wood, 2009; Rauh et al., 2006; Roberts et al., 2007; Windham et al., 2006), although this area of research has received less scientific attention and far fewer research dollars than genetic risk factors. Environmental factors may be pertinent not only to brain development but also to chronic systemic features of at least some subgroups of ASD.

- The 2010 Interagency Autism Coordinating Committee Strategic Plan for Autism Spectrum Disorder Research - January 19, 2010, Question 3: What Caused This To Happen and Can It Be Prevented?

The 2010 IACC Strategic Plan  statement  that environmentally focused autism research has been under funded and largely ignored could properly be characterized as a long overdue confession by the autism research establishment.  Autism research has been  focused overwhelmingly on genetic causes of autism to the near exclusion of environmentally focused research. for well over a decade with potentially serious consequences for our current understanding of possible autism causes and treatments.   Given that imbalance it is perfectly understandable that few potential environmental causes of autism have been identified or confirmed through research.  If we don't open our eyes and look, if we don't do the research, then we will not find environmental causes of autism.

The overwhelming imbalance in favor of genetically based autism research was identified over a decade ago by  researcher Teresa Binstock in her 1999 description of the  "It's gotta be genetic" autism research paradigm.  Binstock  pointed to the culprit -  the old guard network that insisted that autism research be genetically focused in order to have any hope of receiving public funded research dollars:

My own hunch is that the NIH and NIMH will not change from within; the senior practitioners of the "it's gotta be genetic" model have too much influence. Just as Semmelweiss and his data were suppressed, so too will the NIH/NIMH autism-research insiders continue to act against the the growing body of new data in autism; the NIH's pro-genetic old-timers will cling to their paradigm and its funding. As a result, change within the NIH and NIMH will have to be initiated from outside those tax-supported corporations.

-Teresa Binstock, 1999, IGNAZ SEMMELWEISS and AUTISM: when prevailing paradigms resist change

The imbalance in favor of genetic over environmental focused autism research has resulted in a call for more balance from many sources and hopefully that call will result in more than lip service.  There have been signs of an autism research paradigm shift over the past few years from the purely genetic model of autism to one which looks at autism as the result of a genetic and environmental interaction but the pace of change has been far slower than first hoped as pointed out by the 2010 IACC Strategic Plan above , by Dr. Irva Hertz-Picciotto and by Dr. Jon Poling.

Too much time has been wasted on the irrational insistence that autism research must be genetically focused.  We have lost the knowledge that years of more balanced autism research, with greater attention to potential environmental factors, might have given us. We must find that balance as we move  forward or more knowledge, and possibly treatments and cures, will continue to be lost.

Environmentally focused autism research must receive more attention and funding. Even the IACC has recognized the imbalance in favor of genetic over environmentally focused research. 

It is now time to redress the imbalance. 

autism

Autism and Human Exposure to Environmental Chemicals: Time to Put a Stake Through the Heart of the "It's Gotta Be Genetic" Model of Autism Research

"My own hunch is that the NIH and NIMH will not change from within; the senior practitioners of the "it's gotta be genetic" model have too much influence. Just as Semmelweiss and his data were suppressed, so too will the NIH/NIMH autism-research insiders continue to act against the the growing body of new data in autism; the NIH's pro-genetic old-timers will cling to their paradigm and its funding. As a result, change within the NIH and NIMH will have to be initiated from outside those tax-supported corporations."

 

Teresa Binstock, 1999,  IGNAZ SEMMELWEISS and AUTISM: when prevailing paradigms resist change

"Right now, about 10 to 20 times more research dollars are spent on studies of the genetic causes of autism than on environmental ones.

We need to even out the funding."

 

Dr. Irva Hertz-Picciotto, 2009, UC Davis M.I.N.D. Institute Researcher

The CDC has issued its Fourth National Report on Human Exposure to Environmental Chemicals which is available for downloading along with an executive summary and a list of the 212 chemicals present in humans measured by the CDC:

The Fourth National Report on Human Exposure to Environmental Chemicals is the most comprehensive assessment to date of the exposure of the U.S. population to chemicals in our environment. CDC has measured 212 chemicals in people's blood or urine—75 of which have never before been measured in the U.S. population. The new chemicals include acrylamide, arsenic, environmental phenols, including bisphenol A and triclosan, and perchlorate.

The blood and urine samples were collected from participants in CDC's National Health and Nutrition Examination Survey (NHANES), which is an ongoing survey that samples the U.S. population every two years. Each two year sample consists of about 2,400 persons. The Fourth Report includes findings from national samples for 1999–2000, 2001–2002, and 2003–2004. The data are analyzed separately by age, sex and race/ethnicity groups.

I do not want to be accused of quackery or woo or some other such  insult used to  bully people into submission who disagree with the scientific and medical orthodoxy of the day.  Therefore  I am not saying that because the CDC has issued another report measuring the presence of hundreds of toxic  chemicals in human beings that it  means that autism, or any  other neurological or developmental disorder, is environmentally caused or triggered by these substances. The CDC site (FAQ section) makes it clear that:

The National Exposure Report does not provide health or toxicity information, state- or community-specific data, specific product or environmentally related information, or regulatory guidelines or recommendations.

I also fully acknowledge that I have only begun to read this report and that reading it and understanding the report will take this humble layperson some time. The report itself though is further confirmation of the presence of many toxic, dangerous substances in human bodies, including the bodies of young children and pregnant women.  My suspicions aside, I recognize that further research is necessary to indicate what role is played by these substances in causing or triggering autism and other disorders in our children.

There is no dispute that autism diagnoses have risen dramatically and that some of the increase is accounted for by diagnostic definition changes, increased awareness and other social factors.  But no one can credibly say that the toxic substances described in  the CDC's latest report on human exposure to environmental chemicals are NOT linked to the increases in neurological disorders in children, including autism.

Tomorrow, Friday, December 18, 2009 the CDC is expected to release a study confirming that 1 in 100 persons have autism spectrum disorders.   Given the increasing numbers of  persons with autism disorders and the presence of so many environmental chemicals, including mercury, lead and arsenic, in the bodies of our children, it is time to do the environmentally based research to determine what impact these chemicals are having on the development of our children.

Amongst other research on the effects of these chemicals, it is time to emphasize environmentally oriented autism research.

It is time to put a stake through the heart of the "it's gotta be genetic model"  of autism research.

autism