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Comment on: Maternal autoantibodies are associated with abnormal brain enlargement in a subgroup of children with autism spectrum disorder

14 Feb Antibodies figure

In 2008 a paper opened up a new area of research in autism risk factors: Autism: maternally derived antibodies specific for fetal brain proteins. The researchers at the U.C. Davis MIND Institute found that for a subset of autistic kids, they could find antibodies in the mothers’ sera that reacted to human fetal brain tissue. Other teams have found similar results, and the MIND researchers have continued to explore this topic.

In the present study, the researchers studied 131 ASD kids and 50 non-ASD controls. 10 of the ASD kids were born to mothers with the brain specific autoantibodies detected in their serum. Autism severity, by their measure, was the same for the two ASD groups. The rate of develpmental regression is the same for the two groups, but strikes me as rather high at 40-50% . Previous studies by this team and others indicated a higher rate of regression in the ASD kids in the maternal-autoantibody group.

Brain volumes were measured via MRI. Most children were tested during sleep. 10 children (all ASD) were tested under anesthesia. Scans were corrected for instrument distortions before volumes were measured. Brain volumes were higher for the ASD kids than the typical kids, consistent with previous results. However, the kids in the maternal autoantibody group had brain volumes even higher than the rest of the ASD kids. The kids in the maternal autoantibody group had brains 12% larger on average than the non ASD kids, while the rest of the ASD group had about 4.4% larger volumes.

The volume differences were not the same over the entire brain:

Furthermore, the frontal lobe was selectively enlarged in the ASD-IgG children relative to other ASD children, and both gray and white matter were similarly affected.

Previous work by the authors indicate the possibility that the autoantibodies themselves might cause brain differences resulting in autism. Their animal model was rhesus monkeys, whose mothers were injected with the autoantibodies.

The authors note there are a number of open questions:

Obviously, several questions remain: What are the brain antigens recognized by the 37/73 kDa maternal IgG autoantibodies, and what is their role normal neurodevelopment? What induces the production of these antibodies in some women but not in others? What is the mechanism by which these maternal autoantibodies alter brain development? Are there processes that could be implemented to block the deleterious effects of the antibodies? Studies are currently underway to address each of these issues and they will undoubtedly shed more light on the role that maternal
autoantibodies may play in ASD and abnormal brain enlargement in ASD.

Another open question they raise has to do with siblings of the autoantibody ASD kids. In specific, since these autoantibodies can persist in the mother’s serum for many years, it is likely that younger siblings are exposed to them as well. If these children do not develop ASD, what is the reason?

The brain volume differences are shown in summarized in this figure:

Antibodies figure

There is a large spread for the brain volumes for the non-autoantibody ASD kids. While on average they are larger, a number are comparable to the average for non-ASD kids. Also, there is a large overlap between the ASD groups from parents positive for the autoantibodies and without the autoantibodies. The kids in the autoantibody group are almost all at the high end of the distribution for the non-ASD kids.

The main thing this paper adds to the autoantibody story is evidence that this may represent a separate group within the ASD population. The work is being performed on members of the Autism Phenome Project. If this is a separate group, so far the evidence is only in brain volume. The authors note: “There were no differences in age, height, autism severity, or DQ between the two ASD groups. Furthermore, the two groups did not differ in the rate of parent reported history of regression.” So on other physical measures, and on autism-based measures, there are no differences. Obviously it would be valuable to see diffrences in autism-specific measures so we could back track how those measures are related to etiology and brain structure. But it is also interesting that this group does not have differences as it could indicate multiple pathways are not always distinct in the end result in autism development.

Nordahl, C., Braunschweig, D., Iosif, A., Lee, A., Rogers, S., Ashwood, P., Amaral, D., & Van de Water, J. (2013). Maternal autoantibodies are associated with abnormal brain enlargement in a subgroup of children with autism spectrum disorder Brain, Behavior, and Immunity DOI: 10.1016/j.bbi.2013.01.084

ResearchBlogging.org


By Matt Carey

Autism Phenome Project announces first results at the Asia Pacific Autism Conference

8 Sep

The Asia Pacific Autism Conference is ongoing in Perth Australia. Prof. David Amaral of the Mind Institute at U.C. Davis (California) will speak and present the first results from the Autism Phenome Project. This is a study to separate autism into various groups, or phenomes.

Here is a blurb from the press announcement for the conference:

The announcement of the first results of the Autism Phenome Project, the largest and most comprehensive assessment of children with Autism ever attempted. The project started in 2006 and is being conducted at the MIND Institute at the University of California, Davis (UC Davis). It is headed by Dr David Amaral and involves 52 scientists across eight fields. Dr Amaral is the President of the International Society of Autism Research. He is Distinguished Professor of Psychiatry and Behavioural Sciences at the Centre for Neuroscience at UC Davis. He is also Research Director and Beneto Foundation Chair of the MIND Institute. Dr Amaral will announce the results.

An Australian news outlet carried the story as US researchers’ discovery promises answers on autism.

Researchers from the University of California Davis’s MIND Institute in Sacramento began the Autism Phenome Project in 2006. They have been studying the brain growth, environmental exposure and genetic make-up of 350 children aged between 2 and 3 1/2 years, and have so far found two biologically distinct subtypes of autistic brain development.

One group of children – all boys – had enlarged brains and most had regressed into autism after 18 months of age; another group appeared to have immune systems that were not functioning properly.

Prof. Amaral’s slides have been made available.

They show, amongst other findings

Total cerebral volume is highly variable in ASD, but appears to be on average higher in ASD boys than controls.

There are various onset types: early onset, plateau, and regression.

Those who exhibit loss of skills have enlarged brains. But, interestingly, the head circumferences start to diverge at about 4-6 months. I.e. there are signs even before the regression occurs.

However, he has a talk “Neurobiological and neuro-immune features of Autism” with the following abstract:

The slides do not appear to discuss the immune phenotype mentioned in the press. However, Autism now affects 1:110 children in the United States. It is a complex disorder that likely has many variants and various etiologies. The first half of this presentation evaluates the hypothesis that the amygdala plays an important role in the pathophysiology of autism. First, MRI studies of the amygdala in children with autism are presented. Then, postmortem data on the morphology of the amygdala in autism are described. Observations are presented both on neurons and glia in the amygdala. Taken together these data confirm that the amygdala is clearly pathological in autism. Given that the amygdala is pathological, what might this pathology contribute to the behavioural impairments of autism? To address this issue, research on the nonhuman primate is discussed. These studies highlight a role for the amygdala in fear regulation and perhaps in mediating the co?morbid anxiety in autism. In the second part of the talk, data demonstrating abnormalities of the immune system of children with autism and a subset of mothers of children with autism are discussed. I also review findings of a nonhuman primate model of autism based on a neuroimmune intervention.

Autism Baby Siblings Study: recurrence risk 19%

15 Aug

Results of the MIND Institute’s baby sibling study have been published in the journal Pediatrics. The study puts the recurrence risk of autism at 19%. In other words, a family with one autistic child has, on average, a 19% chance that a subsequent child will be autistic. The study authors stress that the risk may be higher in some families and lower in others.

More discussion can be found in various news outlets carrying the story, including

http://m.heraldextra.com/news/science/health-med-fit/article_a90c6549-3444-5b6a-800a-85aba7234914.html

Onset patterns in autism: correspondence between home video and parent report

27 Jul

Regression is a major topic in autism. Children who lose abilities at a very young age. In Onset patterns in autism: correspondence between home video and parent report, Sally Ozonoff, Ph.D. and a team of researchers at the U.C. Davis MIND Institute looked at the developmental trajectories of children, autistic and non autistic. They reviewed home videos of the children to map those trajectories. They monitored social communication as a function of time.

What they found was even more complex than expected. Instead of finding that some children show low levels of social communication from very early in life. A second group has early high levels of social communication, followed by significant decreases over time (regression). But, there was a third group: a group which was more typical in development followed by not regression, but a plateau in progress in social communication.

The numbers of children in the study are small (53 autistic children), making it unlikely to get a precise idea of what fraction of the children follow each trajectory. According to the IMFAR abstract for this study:

Bayesian Information Criteria were used to select the number of trajectories that best fit the data. There was strong support from coded home video for 3 onset trajectories. The first “early onset” trajectory (n = 20) displayed low rates of social-communication behavior at all ages. The second “regression” trajectory (n = 20) displayed high levels of social-communication behavior early in life and significantly declined over time. The third “plateau” trajectory (n = 12) was similar to the typical children early in life but did not progress as expected. There was no support for a mixed (early signs + regression) trajectory.

Here is the abstract for the published paper:

OBJECTIVE:
The onset of autism is usually conceptualized as occurring in one of two patterns, early onset or regressive. This study examined the number and shape of trajectories of symptom onset evident in coded home movies of children with autism and examined their correspondence with parent report of onset.

METHOD:
Four social-communicative behaviors were coded from the home video of children with autism (n = 52) or typical development (n = 23). All home videos from 6 through 24 months of age were coded (3199 segments). Latent class modeling was used to characterize trajectories and determine the optimal number needed to describe the coded home video. These trajectories were then compared with parent reports of onset patterns, as defined by the Autism Diagnostic Interview-Revised.

RESULTS:
A three-trajectory model best fit the data from the participants with autism. One trajectory displayed low levels of social-communication across time. A second trajectory displayed high levels of social-communication early in life, followed by a significant decrease over time. A third trajectory displayed initial levels of behavior that were similar to the typically developing group but little progress in social-communication with age. There was poor correspondence between home video-based trajectories and parent report of onset.

CONCLUSIONS:
More than two onset categories may be needed to describe the ways in which symptoms emerge in children with autism. There is low agreement between parent report and home video, suggesting that methods for improving parent report of early development must be developed.

The last statement in the results is obviously intriguing. “There was poor correspondence between home video-based trajectories and parent report of onset.”

Here is the segment of the IMFAR abstract:

There was poor correspondence between parent report and home video classifications (kappa = .11, p = .30). Only 9 of 20 participants whose home video displayed clear evidence of a major decline in social-communication behavior were reported to have had a regression by parents. Only 8 of 20 participants with evidence of early delays in social-communication on video were reported to demonstrate an early onset pattern by parents. Of the 10 whose parents described a plateau, only 3 had home video consistent with this pattern.

So, none of the three groups were able to correctly recall the trajectory. Not the parents of kids who regressed. Not the parents of kids who plateaued. Not the parents of kids who had early onset autism.

As parents we’d like to see ourselves as the experts of our children. And, frankly, we are. No one else knows them like we do. But that doesn’t make us infallible.

The study was presented at IMFAR and Shannon Rosa wrote about it for The Thinking Person’s Guide to Autism.

So what do parents really think causes autism?

12 May

According to the MIND institute, presenting at IMFAR:

The two most common causes of autism cited among all parents was an environmental cause (51%) and/or a genetic cause (51%). Vaccines (22%) were the third most commonly believed etiological factor, followed by 20% of parents who did not know or have a guess as to what may cause autism.

This is an interesting set of results to me. I’m frequently told that the overwhelming majority of parents believe vaccines cause autism. Turns out less than a quarter do.

Also of interest was the following statement:

Vaccines are commonly cited as a cause by parents in all ethnic groups despite a clear lack of scientific evidence demonstrating a relationship between autism and either the measles, mumps, rubella (MMR) vaccine, or thimerosal containing vaccines

Wasn’t that long ago that autism anti-vaxxer supermo Rick Rollens was basically in charge of MIND. How times have changed.

Detection of Plasma Autoantibodies to Brain Tissue in Young Children with and without Autism Spectrum Disorders

25 Mar

Researchers at the MIND Institute published studies in the past few years correlating antibodies to brain tissue and autism. The first study of this sort (that I recall) studied whether the mother had antibodies to fetal brain tissue: Autism: maternally derived antibodies specific for fetal brain proteins. Other studies have looked at autoantibodies within the plasma of the autistics themselves: Detection of autoantibodies to neural cells of the cerebellum in the plasma of subjects with autism spectrum disorders.

The idea is fairly simple. If the mother or the autistic has antibodies against brain tissue, this might lead to an increased risk of autism.

There are even patent applications in for use of these methods to For example, a 2011 patent application US20110038872A1: METHODS OF DIAGNOSING AND TREATING AUTISM:

Determining a risk of an offspring for developing an autism spectrum disorder comprises identifying in a biological sample from the mother of the offspring in the presence of maternal antibodies that bind to the biomarkers

This past week, another paper from the MIND group came out:

Detection of Plasma Autoantibodies to Brain Tissue in Young Children with and without Autism Spectrum Disorders

In this study they looked for autoantibodies and compared autistics and non-autistics. They found no differences between the groups in frequency of autoantibodies.

Abstract
Autism spectrum disorders (ASDs) are characterized by impaired language and social skills, often with restricted interests and stereotyped behaviors. A previous investigation of blood plasma from children with ASDs (mean age = 5½ years) demonstrated that 21% of samples contained autoantibodies that reacted intensely with GABAergic Golgi neurons of the cerebellum while no samples from non-sibling, typically developing children showed similar staining (Wills et al., 2009). In order to characterize the clinical features of children positive for these autoantibodies, we analyzed plasma samples from children enrolled in the Autism Phenome Project, a multidisciplinary project aimed at identifying subtypes of ASD. Plasma from male and female children (mean age = 3.2 years) was analyzed immunohistochemically for the presence of autoantibodies using histological sections of macaque monkey brain. Immunoreactivity to cerebellar Golgi neurons and other presumed interneurons was observed for some samples but there was no difference in the rate of occurrence of these autoantibodies between children with ASD and their typically developing peers. Staining of neurons, punctate profiles in the molecular layer of the dentate gyrus, and neuronal nuclei were also observed. Taken together, 42% of controls and subjects with ASD demonstrated immunoreactivity to some neural element. Interestingly, children whose plasma reacted to brain tissue had scores on the Child Behavior Checklist (CBCL) that indicated increased behavioral and emotional problems. Children whose plasma was immunoreactive with neuronal cell bodies scored higher on multiple CBCL scales. These studies indicate that additional research into the genesis and prevalence of brain-directed autoantibodies is warranted.

” Immunoreactivity to cerebellar Golgi neurons and other presumed interneurons was observed for some samples but there was no difference in the rate of occurrence of these autoantibodies between children with ASD and their typically developing peers.”

Autism Clusters Found: areas with high incidence of autistic children

1 Jan

Researchers at the U.C. Davis MIND Institute has discovered regions in the state of California that have notably higher autism incidence. But the story is more complicated, and more sad, than one might think at first. Instead of indications of an “autism epidemic”, these clusters point to the fact that minority and poor children are much less likely to receive autism diagnoses.

I don’t have the paper yet (I’m still trying to find the abstract), but articles in the Woodland Daily Democrat and the San Diego Union-Tribune are reporting the story.

The clusters do not appear to point to environmental causes. Instead…well, read for yourself:

Researchers said that in this investigation the clusters probably are not correlated with specific environmental pollutants or other “exposures.” Rather, they correlate to areas where residents are more educated.

Children with autism diagnoses in these clusters are more likely to be White and have parents with high education levels. Again, a quote:

“In the U.S., the children of older, white and highly educated parents are more likely to receive a diagnosis of autism or autism spectrum disorder. For this reason, the clusters we found are probably not a result of a common environmental exposure. Instead, the differences in education, age and ethnicity of parents comparing births in the cluster versus those outside the cluster were striking enough to explain the clusters of autism cases,” said senior author Irva Hertz-Picciotto.

Kids in the “clusters” are about twice a likely to be diagnosed autistic and kids in nearby areas.

Twice as high.

To the many of us armchair epidemiologists who who have looked closely at the California Department of Developmental Services (CDDS) data, this comes as no surprise.

For me, the most memorable discussion of the autism clusters came from Autism Diva, in her post from July 1997, Malibu and Compton: Compare and Contrast.

Here is a graph from that post:

The South Central Regional Center, in a predominantly non-White, poor area of the Los Angeles basin, had an administrative prevalence of 33 per 10,000. Compare that to Westside Regional Center with a prevelance of 84. Westside is a much more affluent are with a higher proportion of White families.

From the San Diego Union-Tribune:

“There is mounting evidence that at least some of this clustering results from the greater access and utilization of services by those with more years of schooling,” the UC Davis researchers wrote.

Yes, there is a certain “I told you so” moment here. This blog, Autism Diva, Autism Natural Variation, Autism Street and others have been pointing out the apparent autism clusters in the raw CDDS data for years. Long before I started blogging. But the real story isn’t the effect such clusters have on the idea of the “autism epidemic”. Rather, this is a clear indication that we are underserving the disabled in our minority and poor communities. This is just plain wrong.

It is long past time for real autism advocacy organizations to work on increasing awareness and access to services in underserved areas. The autism “clusters” are probably not real. From where I sit, what is real are the “anti–clusters” of undiagnosed autistics, minorities, the poor, and, yes, adults.

Fallout of the vaccine-autism scare: Measles in Wales

24 Apr

Jim Carrey, Jenny McCarthy, Andrew Wakefield…what do these people have in common? They have all helped promote fear of vaccines–especially the Measles/MumpsRubella (MMR) vaccine–by claiming there is evidence vaccines cause autism.

To be fair, Jim Carrey and Jenny McCarthy relatively new to the scene, unlike Dr. Wakefield, whose flawed research really fueled the fear. Perhaps the actors could learn from the doctor’s lesson: you claim MMR causes autism, that reduces the number of people getting immunized and people get sick. Pretty simple logic.

Measles was considered basically wiped out in the UK until a few years ago when it returned, sickening thousands and killing a few. Last year, measles returned to the US, and it’s back this year. Now we see that the UK isn’t being spared int he 2008-09 season: Wales has approximately 60 cases of measles suspected or confirmed.

Nineteen cases are in Llanelli–that’s in the lower left corner of this map:

Map showing location of recent measles outbreak in Wales

Map showing location of recent measles outbreak in Wales

That’s a short ride from Swansea, Cardiff, Bristol…lots of high density population centers. Any reasonable person would find that scary.

We in the autism communities need to stand up against misinformation that leads to people being sickened and, in some cases, killed. The MMR-Autism link never had good evidence, and now there is good evidence that MMR does not cause autism Even people like the autism-is-vaccine-injury proponent Rick Rollens admitted it’s time to look beyond MMR (and here).

Jim Carrey seems to understand at least on some level that it is wrong to dissuade people from vaccination. He claimed (incorrectly):

We have never argued that people shouldn’t be immunized for the most serious threats including measles and polio…

Maybe there is some Clintonian logic about the words “We” and “argued”. But, on Larry King Live, Jenny McCarthy stated:

You need to find a doctor that can find an alternate schedule. Generationrescue.org has three of them on there.

Generation Rescue, aka “Jenny McCarthy and Jim Carrey’s Autism Organization” has alternate schedules on their website. The “favorite” of the three alternate vaccine schedules states, very clearly,

One should avoid vaccines that contain live viruses. This includes the combined measles mumps and rubella vaccines…

You’ve talked the talk, time to walk the walk, Jim. Pull that schedule off your website. Get your organization to make a clear statement about the value of vaccinating against measles.

I realize that I have concentrated a lot on Jim Carrey in this piece. But, there is a man who can make a difference in the future. That future will see people in the US and the UK sickened by measles. The question is how many. What Jim Carrey says could make that number larger or smaller, it all depends on whether he makes good on his sentiment that measles is a serious disease worth immunizing against.

Oldstone letter in the Omnibus docket

25 Mar

When I found that the Autism Omnibus Proceeding expert reports were public, the first one that caught my eye was by Andrew Zimmerman. Obviously, it caught Kev’s attention too :)

But, I have only a brief time available today, so I will start with this letter by Dr. Michael Oldstone. It is brief enough that I have copied the body in its entirety below.

To summarize, Rick Rollens asked Dr. Oldstone to consider collaborating with Dr. O’Leary and Dr. Wakefield on the Autism/MMR question. It was a good move on Mr. Rollens’ part, as Dr. Odlstone is one of the preeminent researchers in viral pathogenesis. Has been for decades.

Before agreeing to collaborate, Dr. Oldstone wanted to check on the quality of the results coming out of the O’Leary laboratory. Dr. Oldstone sent tissue samples to Dr. O’Leary’s laboratory, some with measles virus, some without. Dr. O’Leary tested them–and got the wrong answer 20% of the time. Dr. Oldstone sent another batch of samples, some duplicates from the first batch. Not only did Dr. O’Leary’s laboratory get 20% wrong again but, in Dr. Oldstone’s words:

Most troublesome, some samples, when tested twice under different code numbers ‘switched’ from positive to negative or from negative to positive. On this basis of inaccuracies of their PCR test, I declined from further working with either Drs. Wakefield or O’Leary.

This goes directly towards the question of the quality of the data coming from Dr. O’Leary’s laboratory. This is a big question. The Hornig study came out last year, an attempt to replicate Dr. Wakefield’s research. In one of the strangest moves I have ever seen by a researcher, Dr. Wakefield claimed that this study actually supported his research by demonstrating that Dr. O’Leary’s lab is capable of making accurate PCR measurements. Dr. Wakefield neglected the obvious point–being accurate today doesn’t mean one was accurate yesterday. He also neglected the suggestion (made by Dr. O’Leary himself at the press conference for the Hornig study) that Dr. Wakefield’s samples could have been contaminated.

Well, here is a good example that Dr. O’Leary’s laboratory was not making accurate measurements. This was iin the “early 2000′s”. Note that the Uhlman paper (Dr. Wakefield’s team’s paper supposedly finding measles virus in gut tissue) came out in 2002–the same time period.

Below is the letter, dated Oct. 12, 2007, from Dr. Oldstone to Dr. Brian Ward.

Dear Dr. Ward:

I recently became aware that my work in the field of viral persistence is being quoted in support of the hypothesis that the measles virus component of the measles-mumps-rubella (MMR) vaccine is supposedly associated with the development of autistic spectrum disorder (ASD).

Measles virus has been a focus of my laboratory for many years so this autismlmeasles link has been of interest to me. Further, I should state up front that I see at present no evidence whatsoever for such a link.

In the early 2000s I was asked by Rick Rollens to consider a collaborative grant between my laboratory and that of Drs. Wakefield and O’Leary. Prior to making a decision, I decided to assess the performance of Dr. O’Leary’s PCR-based assays targeting measles virus. My laboratory generated samples from tissue culture cells infected with MV as well as tissue samples from our transgenic mouse model of MV infection (including gut and brain tissues), which were coded and sent to the O’Leary laboratory. Samples had varying titers of measles virus as well as appropriate negative control and measles virus positive samples. The arrangement was informal in that the samples were only sent to Dr. O’Leary for testing. After receiving Dr. O’Leary’s results, the code was broken and I discovered that approximately 20% of the samples were incorrect as to the
presence or absence of measles virus. I reviewed the results with Dr. O’Leary as well as his protocols for preparing his assay, which I found to be sound and decided that perhaps there may have been some unknown error and a second set of samples should be sent. This second set was again coded anew and contained both new samples and several original samples. The results of the second round were no better with again approximately 20% of the samples misidentified by Dr. O’Leary’s laboratory. Most troublesome, some samples, when tested twice under different code numbers ‘switched’ from positive to negative or from negative to positive. On this basis of inaccuracies of their PCR test, I declined from further working with either Drs. Wakefield or O’Leary.

Sincerely,
Michael B.A. Oldstone, M.D.
Head, Viral-lmmunobiology Laboratory

Why is David Kirby grasping at straws?

9 Jan

Once more for the record, I like David. I tried very hard to get to see him in London last time he was over and we’d arranged to meet up for a drink but due to my family situation it wasn’t to be. However, I cannot let that stop me from recalling that we have very differing views on a wide range of things to do with autism and vaccines.

I have noticed of late a tendency for David’s HuffPo blog posts to be more than usually full of ‘if’ ‘maybe’ ‘might’ etc. However his skill as a writer buries these ambiguities and makes them appear certainties. I’m not even sure its a concious thing for David. His need to write well sometimes (I think) obscures a clinical need for precision in such delicate areas as he and I write in.

With that in mind, I recalled a post of his from November 2008 entitled ‘Tom Daschle: Friend to Many Autism Families’ in which he describes Mr Daschle thusly:

By nominating Tom Daschle to head up the Department, President Elect Obama has selected a man who has demonstrated an unflinching willingness to question vaccine safety, and to fight for the rights of those people who believe they have been, or may be, seriously injured by certain vaccinations.

I think David might’ve been trying to insinuate that Tom Daschle’s nomination was good for the autism/antivaccine community. Certainly however, as with the autism/antivaccine’s belief that RFK Jr would be appointed by Obama, this nomination might not be quite what that community is expecting. As blogged by Orac today, Daschle’s true feelings on vaccinations were spelt out by the man himself:

Immunization is probably as — as sound an investment as we can make in good health. I can’t imagine that we could do any better than ensure that every — every child is immunized, and that we understand the importance of — of broad-based immunization and the tremendous good health that can come from it.

Following that, David made a fairly innocuous presentation from a US Army scientist look much more sinister than it actually was. He claimed that the army listed autism as a possible ‘health effect’ of mercury/thiomersal. It turned out that that was not actually the case.

Dr. Centeno’s presentation, entititled ‘Mercury Poisoning: A Clinical and Toxicological Perspective,’ did mention Thimerosal. However, its inclusion was specifically intended to point out that although there has been some speculation about a potential association between Thimerosal and Autism, currently there is no data or science to support such a claim. Neither the AFIP nor Dr. Centeno have been involved in or conducted research on Autism.

After that was the recent debacle when David mixed up Change.org and Change.gov – the latter being a website of Obama. The former a privately owned enterprise for at least the last 2 years. David thought (and committed to a blog post) that Obama had hired pro-neurodiversity bloggers and he imagined a conversation Obama might have with an autism parent:

It is hard to imagine the President one day saying…“I do not think we should devote resources to finding out what happened to your [autistic child]. I do not believe there is anything we can do to help him, and it is not desirable to even try.

This post made me sad and angry. I thought better of David than that. To say that any of us who do not believe vaccines cause autism do not think it is desirable to help our autistic children is massively insulting. I hope someday David can maybe spend a bit of time with parents who don’t think vaccines caused their child’s autism and see for himself how we help our kids. And maybe an apology might be forthcoming also.

David’s latest faux pas is regarding the latest MIND institute study. In a post entitled ‘UC Davis Study: Autism is Environmental (Can We Move On Now?)’ David says:

Autism is predominantly an environmentally acquired disease, the study seems to conclude. Its meteoric rise, at least in California, cannot possibly be attributed to that shopworn mantra we still hear everyday, incredibly, from far too many public health officials: It’s due to better diagnosing and counting.

The autism epidemic is real, and it is not caused by genes alone: You cannot have a genetic epidemic. It really is time that we, as a society, accept that cold, hard truth.

Here’s the full conclusion:

Autism incidence in California shows no sign yet of plateauing. Younger ages at diagnosis, differential migration, changes
in diagnostic criteria, and inclusion of milder cases do not fully explain the observed increases. Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.

Lets look at that last again:

…the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.

And yet David seems to to think its crystal clear. The paper itself also contains some direct and fairly easy-to-check errors. For example:

The inclusion of milder cases has been suggested as an explanation for the increase in autism. Neither Asperger’s
syndrome nor “pervasive developmental disorders not otherwise specified” qualify under the category of autism in the DDS system.

Here is what DDS passed on to me in Summer of 2007. I promised not to attribute the quote to an individual so I won’t, but you can email DDS yourselves and ask them.

The current CDER was written in 1978 and updated in 1986, which is why the language is so out of date ( e.g., Residual Autism). California has clinicians in the field who are, of course, using modern criteria in their assessments but then they have to go backwards and try to fit those kids into the 1986 CDER. So you are going to have Aspergers kids, PDD-NOS kids in both categories 1 and 2. Categories 1 and 2 are called ‘Autism.’ But because there are so many clinicians, using lots of different techniques for evaluation, there is a lot of inconsistency and enrollment figures should not be misused as epidemiological data.

Hertz-Picciotto might also be interested in a quote from Rita Eagle PhD of the California Dept. of Developmental Services (DDS) to Journal of Autism and Developmental Disorders, Vol. 34, No. 1, February 2004:

To many clinicians, it appears that more and more children who, in the past, would never have been referred to the regional centers for example, bright but anxious and slightly socially inept kids with average or better IQs and children who, in the past, had been or would have been diagnosed as ADHD, OCD, ODD, anxiety disorder, learning disabilities, psychotic, and so forth are now being diagnosed wit high-functioning autism and/or Asperger syndrome and referred to the regional centers for services.

Truth is that a lot of Hertz-Picciotto 2009 is simply wrong. For an extensive overview of why, please read Joseph’s technical takedown from which I’ll quote his conclusion:

H-P et al. is a surprisingly poor paper. It does not produce any new data in order to support its two main results. It makes an apples-to-oranges comparison between a Finnish epidemiological study and California DDS ascertainment over time. It tells us the obvious about “milder” cases. In the end, I don’t think this is an improvement over the 2002 MIND Institute report to the California Legislature. In fact, it could very well be worse.

The way H-P et al. have gone about trying to show there’s a real rise in autism incidence over time is not a very good way to go about doing things, in my view. There are other ways. For example, I’ve suggested trying to replicate Lotter (1967) in detail. This would not be as easily challenged.

David closes his latest error prone piece with:

But the sooner our best minds in science and medicine come to grips with the fact that these poor, hapless kids have been exposed to the wrong environmental toxins and/or infectious agents at the wrong time, the sooner we can find out how to best treat what really ails them.

This is a prime example of bad science leading the media. David has reported on a paper that has made fairly bad errors and taken them at their word. Sadly, this sort of thing will only continue as long as institutions like MIND (controlled by a man who is dedicated to proving vaccines cause autism) churn out error strewn papers.

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