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The Next Vaccine-Autism Newsmaker…5 years later

6 Feb

Years back, much focus in online autism parent community discussions focused on the Omnibus Autism Proceeding (OAP). This was the large “vaccine court” proceeding to explore if people could be compensated for autism as a vaccine injury. Those hearings were held in 2008, and the decisions went against the families.

A year ago I wrote (The Omnibus Autism Proceeding: effectively over), and while, yes, as an “Omnibus” it is effectively over, there is still activity for those who filed claims and were included in the Omnibus Autism Proceeding. Statistics as of today show there were 5,635 claims included in the Omnibus, and 4,564 have been dismissed. 2 claimants have been compensated, with the caveat given that “**HHS has never concluded in any case that autism was caused by vaccination.” This leaves 1,069 cases still pending. A relatively small fraction of the original Omnibus, but a large number nonetheless.

Another way to look at this is the Omnibus proceedings are over, the docket hasn’t been updated for quite some time but there are still individual cases to be decided. Including one case that was rather prominent in the Omnibus: that of A. Krakow. He was intended to be one of the test cases for the thimerosal but was pulled out to pursue another argument: that metabolic dysfunction is involved. David Kirby referred to him as “The Next Vaccine-Autism Newsmaker”, following the supposed game-changer of Hannah Poling.

That was in 2008. As it’s been nearly 5 years, I checked the status of the case. It turns out the first hearing was held in December (a hearing on fact) and a second hearing is set for expert witnesses to testify in April of this year. One way to explore the arguments the family may be taking is to review the experts that are testifying. For example, the family has chosen Richard Deth as an expert. His work has not focused on mitochondria. On the other hand, Yuval Shafir is also listed as an expert and has listed many articles on mitochondria with his report. Richard Frye’s CV was submitted (he also has some work on mitochondria and autism), but I don’t see that an expert report from him has been submitted.

Other experts date from 2008 (from when he was going to be an Omnibus test case) include: Elizabeth A. Mumper, Robert S. Rust, Richard Deth and Sander Greenland.

(edit to add, I see a report in the docket from Marcel Kinsbourne in 2010).

So, is this going ahead as a “mitochondrial autism” case? The “Next Hannah Poling” as David Kirby claimed in Spectrum Magazine? Well, even Hannah Poling wasn’t the game-changer some people predicted. Probably the most we can say is that is 10 years old, with a docket 16 pages long, will finally be heard.

edit to add: For the curious, here is the docket.

By Matt Carey

The Omnibus Autism Proceeding: effectively over

21 Jan

The Omnibus Autism Proceeding (OAP) was held in the U.S. Court of Federal Claims to group the large number of claims filed involving autism and vaccines. The Docket was opened on July 3, 2002, nearly 10 years ago. The last entry was placed 1 year ago. Since then many cases have been dismissed. About half the cases are left to hear, but the fact that the two causation theories presented (that the MMR vaccine causes autism and that Thimerosal causes autism) were both found to have no merit (“not even close” one special master put it) and no new theory is proposed by the Petitioners’ Steering Committee (the attorneys who presented the case for the petitioners) makes it clear that the group claim, the omnibus, is effectively over.

That is not to say that other claims are not proceeding through the court, or that new cases will not be presented. There is at least one case pursuing the idea of mitochondrial dysfunction and autism, as with the Hannah Poling case. ([edit to add–the case ongoing, which was briefly closed, is not the Hannah Poling case. See the comments below). The case was actually dismissed for lack of action by the petitioners but the special master allowed it to continue again).

Looking back, the Omnibus peaked in 2003 when 2,437 cases were filed (close to 1/2 of the total that would eventually be filed).

Reassessing the role of mitochondrial DNA mutations in autism spectrum disorder.

12 Apr

Autism and mitochondrial medicine have become a very hot topic in recent years. What the connections are between autism and mitochondrial disorders has yet to be clarified. Mitochondria are little structures within cells that produce much of the energy required. Mitochondria have their own DNA (mtDNA) in addition to the nuclear DNA (nDNA) of the cell. nDNA is what most people think of when we hear “genes” or DNA. Given the focus on mitochondrial dysfunction and autism, it is natural to consider the question: are there mutations in the mtDNA which increase the risk of autism?

A new paper takes a look at the question. They studied 148 patients with ASD and found, well, no support for a link to mtDNA mutations. Here is the abstract:

BMC Med Genet. 2011 Apr 6;12(1):50. [Epub ahead of print]
Reassessing the role of mitochondrial DNA mutations in autism spectrum disorder.
Alvarez-Iglesias V, Mosquera-Miguel A, Cusco I, Carracedo A, Perez-Jurado LA, Salas A.
Abstract
ABSTRACT:
BACKGROUND: There is increasing evidence that impairment of mitochondrial energy metabolism plays an important role in the pathophysiology of autism spectrum disorders (ASD; OMIM number: 209850). A significant proportion of ASD cases display biochemical alterations suggestive of mitochondrial dysfunction and several studies have reported that mutations in the mitochondrial DNA (mtDNA) molecule could be involved in the disease phenotype.

METHODS: We analysed a cohort of 148 patients with idiopathic ASD for a number of mutations proposed in the literature as pathogenic in ASD. We also carried out a case control association study for the most common European haplogroups (hgs) and their diagnostic single nucleotide polymorphisms (SNPs) by comparing cases with 753 healthy and ethnically matched controls.

RESULTS: We did not find statistical support for an association between mtDNA mutations or polymorphisms and ASD.

CONCLUSIONS: Our results are compatible with the idea that mtDNA mutations are not a relevant cause of ASD and the frequent observation of concomitant mitochondrial dysfunction and ASD could be due to nuclear factors influencing mitochondrion functions or to a more complex interplay between the nucleus and the mitochondrion/mtDNA.

PMID: 21470425 [PubMed – as supplied by publisher]Free Article

This is consistent with previous studies, as noted in a recent review article which was itself summarized at The Thinking Person’s Guide to Autism by Emily Willingham as Mitochondrial Disease and Autism: Linked?

Ms. Willingham noted there:

Thus, tracking down mitochondrial dysfunction in the context of ASD to a specific mutation has remained an elusive goal. Two scenarios are likely for this lack of mutational findings: (1) there are mutations, but we just haven’t found them yet; or (2) the environment is largely responsible for any mitochondrial dysfunction that abnormal marker levels might indicate.

This paper is available as a free manuscript online. Here is the

Although it is widely accepted that some forms of ASD appear concomitantly with the impairment of mitochondrial energy metabolism, there are reasons to believe that the cause of these mitochondrial disorders does not systematically rest on mutations or variants in the mtDNA molecule. Pathogenic mtDNA mutations have been reported in ASD patients, but this seems to be the exception rather than the rule. It is more likely that the real causes of mitochondrial deficiencies in some ASD cases are due to the intervention of several nuclear factors acting alone (additively or epistatically) or through a complex interplay with mtDNA variants. For the time being, while the cause for mitochondrion dysfunction in ASD remains unclear, there is no reason to indicate systematic screening for mtDNA mutations in ASD patients unless a mitochondrion disorder is suggested by a clear phenotype.

What is also interesting to me is the table of characteristics of the study subjects. In particular, there is a big difference in the percentage with epilepsy and dimorphism between adults and children:

Mitochondrial dysfunction is listed as mild and somewhat infrequent (about 10%). Not the very high prevalences of mitochondrial dysfunction that some have suggested are present in autitics. This does beg the question: should this genetic study be performed on those with some measure of mitochondrial dysfunction?

This doesn’t mean that mitochondrial dysfunction isn’t an important area for autism research, or that a genetic study such as this shouldn’t be done on a larger group with some measure of mitochondrial dysfunction.

Of course it would be great to hear that there is something definitive in this study. As in, “this is it!” rather than “this probably isn’t it”. Mitochondrial DNA mutations “probably isn’t it” when it comes to the etiology of ASD in most people.

Proton Magnetic Resonance Spectroscopy and MRI Reveal No Evidence for Brain Mitochondrial Dysfunction in Children with Autism Spectrum Disorder.

16 Mar

A study published today looks for mitochondrial dysfunction in autistic children. In specific, the researchers are looking directly at the brains of autistic children. The team, from the University of Washington, used both MRI (Magnetic Resonance Imaging) and proton magnetic resonance spectroscropic imaging (HRMS). MRI gives structural information on soft tissues. HMRS is a “spectroscopic” techinque: it gives chemical information on
Here’s a good reference with a discussion of HMRS on brain tissue (as a spectroscopy, not an imaging technique): Quantitative neuropathology by high resolution magic angle spinning proton magnetic resonance spectroscopy

With that background in hand, here is the abstract from the recent study on autism:

Proton Magnetic Resonance Spectroscopy and MRI Reveal No Evidence for Brain Mitochondrial Dysfunction in Children with Autism Spectrum Disorder.

Corrigan NM, Shaw DW, Richards TL, Estes AM, Friedman SD, Petropoulos H, Artru AA, Dager SR.

Department of Radiology, University of Washington, Seattle, WA, USA.
Abstract

Brain mitochondrial dysfunction has been proposed as an etiologic factor in autism spectrum disorder (ASD). Proton magnetic resonance spectroscopic imaging ((1)HMRS) and MRI were used to assess for evidence of brain mitochondrial dysfunction in longitudinal samples of children with ASD or developmental delay (DD), and cross-sectionally in typically developing (TD) children at 3-4, 6-7 and 9-10 years-of-age. A total of 239 studies from 130 unique participants (54ASD, 22DD, 54TD) were acquired. (1)HMRS and MRI revealed no evidence for brain mitochondrial dysfunction in the children with ASD. Findings do not support a substantive role for brain mitochondrial abnormalities in the etiology or symptom expression of ASD, nor the widespread use of hyperbaric oxygen treatment that has been advocated on the basis of this proposed relationship.

Does this mean that mitochondrial dysfunction never occurs in autistics? No. But it makes it very unlikely that more than a fraction of autistics have mitochondrial dysfunction in their brains.

Beyond that, the use of spectroscopic imaging is very impressive to me. MRI structural data is quite valuable on its own, but adding chemical information is very powerful.

Mitochondrial Disease and Autism: Linked?

11 Mar

Mitochondrial disease and autism. I don’t read about it as much as during the peak of the Hannah Poling story, but it is a big topic. Emily Willingham at
Thinking Person’s Guide to Autism has put together an excellent post on the subject. Here’s the first paragraph:

Hannah Poling’s family entered the national spotlight when they revealed that Hannah’s autism-like symptoms may have been linked to a reaction to several childhood vaccines at once in combination with her mitochondrial dysfunction. Her case was not the first revelation of a possible mitochondrial disorder (MD)-autism spectrum disorder (ASD) link, but because of her ultimately successful vaccine injury suit, she became the avatar of the vaccines-cause-harm movement — which almost eclipsed the real scientific and therapeutic feature of her case: the mitochondria.

I’d love to do a wholesale copy of the post, but that’s hardly fair now, is it? So, I’ll send you all to the Thinking Person’s Guide to Autism and Mitochondrial Disease and Autism: Linked?

Mitochondrial Dysfunction in Autism

22 Dec

A recent paper from the MIND Institute, published in the Journal of the American Medical Association (JAMA) entitled Mitochondrial Dysfunction in Autism caused a bit of a stir. One which is far beyond what is supported by the paper’s conclusions or data, I will add.

The study is very small: 10 autistic children and 10 controls. The authors used a very nonstandard methodology. Perhaps the best summary of this study so far can be found on the Simons Foundation blog SFARI (Defects in mitochondria linked to autism). Deborah Rudacille discusses the methodology and brings in quotes from the study’s lead author (Cecilia Giulivi) as well as established experts in the field of mitochondrial disease and autism such as Jay Gargas.

Before I get too far ahead of myself, here is the abstract:

Context Impaired mitochondrial function may influence processes highly dependent on energy, such as neurodevelopment, and contribute to autism. No studies have evaluated mitochondrial dysfunction and mitochondrial DNA (mtDNA) abnormalities in a well-defined population of children with autism.

Objective To evaluate mitochondrial defects in children with autism.

Design, Setting, and Patients Observational study using data collected from patients aged 2 to 5 years who were a subset of children participating in the Childhood Autism Risk From Genes and Environment study in California, which is a population-based, case-control investigation with confirmed autism cases and age-matched, genetically unrelated, typically developing controls, that was launched in 2003 and is still ongoing. Mitochondrial dysfunction and mtDNA abnormalities were evaluated in lymphocytes from 10 children with autism and 10 controls.

Main Outcome Measures Oxidative phosphorylation capacity, mtDNA copy number and deletions, mitochondrial rate of hydrogen peroxide production, and plasma lactate and pyruvate.

Results The reduced nicotinamide adenine dinucleotide (NADH) oxidase activity (normalized to citrate synthase activity) in lymphocytic mitochondria from children with autism was significantly lower compared with controls (mean, 4.4 [95% confidence interval {CI}, 2.8-6.0] vs 12 [95% CI, 8-16], respectively; P = .001). The majority of children with autism (6 of 10) had complex I activity below control range values. Higher plasma pyruvate levels were found in children with autism compared with controls (0.23 mM [95% CI, 0.15-0.31 mM] vs 0.08 mM [95% CI, 0.04-0.12 mM], respectively; P = .02). Eight of 10 cases had higher pyruvate levels but only 2 cases had higher lactate levels compared with controls. These results were consistent with the lower pyruvate dehydrogenase activity observed in children with autism compared with controls (1.0 [95% CI, 0.6-1.4] nmol × [min × mg protein]?1 vs 2.3 [95% CI, 1.7-2.9] nmol × [min × mg protein]?1, respectively; P = .01). Children with autism had higher mitochondrial rates of hydrogen peroxide production compared with controls (0.34 [95% CI, 0.26-0.42] nmol × [min × mg of protein]?1 vs 0.16 [95% CI, 0.12-0.20] nmol × [min × mg protein]?1 by complex III; P = .02). Mitochondrial DNA overreplication was found in 5 cases (mean ratio of mtDNA to nuclear DNA: 239 [95% CI, 217-239] vs 179 [95% CI, 165-193] in controls; P = 10?4). Deletions at the segment of cytochrome b were observed in 2 cases (ratio of cytochrome b to ND1: 0.80 [95% CI, 0.68-0.92] vs 0.99 [95% CI, 0.93-1.05] for controls; P = .01).

Conclusion In this exploratory study, children with autism were more likely to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA deletions than typically developing children.

As the abstract states, the MIND Institute study methodology involved: “Mitochondrial dysfunction and mtDNA abnormalities were evaluated in lymphocytes from 10 children with autism and 10 controls”. Lymphocytes (a type of white blood cell). Children were concecutively recruited and genetically unrelated. Mitochondrial function was tested first, and given the results seen, children were brought back for a second blood draw where mitochondrial DNA (mDNA) and nuclear DNA (nDNA) were examined.

As shown in the figure below, they found that the autistic children had different mitochondrial activity levels than their controls. Note that “low” activity is not referenced to any standardized norms, but to the 10 control children.

They also performed genetic testing. Table 3 from the paper is reproduced below:

They show that, by their methodology, 7 of their 10 autistic kids have some form of genetic signature for mitochondrial dysfunction. 2 of 10 of their controls meet their criteria as well.

The Simons blog quotes the study author, Prof. Giulivi on this choice:

“Lymphocytes do not rely as heavily on mitochondria as the brain does,” she says, “so if this is happening in cells that don’t use mitochondria as much, it’s likely to be happening in cells that rely more heavily on mitochondria, like neurons.”

They also quote Dr. Fernando Scaglia, of the Baylor Clinic:

However, the unconventional decision to use lymphocytes should have been validated, says Fernando Scaglia, associate professor of molecular and human genetics at Baylor College of Medicine in Houston. “I’m not saying that studies done in lymphocytes are useless,” says Scaglia, an expert in inherited metabolic disease. “But they should be validated in other tissue.”

and Prof. Gargas of the University of California at Irvine:

“Lymphocytes are fine to study chromosomal DNA, but they are a horrible source for studying mitochondrial DNA,” he says.

Cells have hundreds of mitochondria, each with multiple copies of the DNA. In people with mitochondrial disease, some cells have healthy DNA and others have the mutated copies, he notes. In a blood sample, defective lymphoctyes tend to get lost among rapidly proliferating healthy cells.

“The best source for studying mitochondria are post-mitotic cells such as muscle,” he says. “That way you are sampling the set of cells the child was born with.”

In the end, if we stick to the idea that this is a very preliminary report and relies on a new unproven methodology at that, we can consider the study as posing interesting questions. Is mitochondrial dysfunction more prevalent in autistics than the general population? Are there ways to test this in a faster, less intrusive manner than is often used? If we take this study in context, there may be some value. Unfortunately as Seth Mnookin has already pointed out, this study has already been used to promote ideas that are clearly outside of the study and conclusions. This is the unfortunate world of autism research: it is hard for people to push the boundaries and risk being wrong. Not because it may cause the researchers some embarrassment, but because there are a multitude of people waiting to misuse information and mislead.

Commentary on Mitochondrial Dysfunction in Autism

22 Dec

I recently wrote about the paper Mitochondrial Dysfunction in Autism by the MIND Institute. It is difficult to write about the topic of mitochondrial dysfunction and mitochondrial disorders and autism without discussing vaccines. Even the Simons Foundation blog mentioned vaccines in their treatment of the paper, even though the paper makes no comments about vaccines.

Why? Because the case of Hannah Poling and, especially, the way David Kirby presented it to the public has linked autism–mitochondrial dysfunction–vaccines into one neat package. With posts like “NEW STUDY – “Mitochondrial Autism” is Real; Vaccine Triggers Cannot Be Ruled Out” and “The Vaccine-Autism Story: Trust Your Government, or Be a Patriot and Get on Google”. In the latter post he wrote:

“Google “autism and mitochondria,” (96,900 hits) and then Google “mercury and mitochondria,” (169,000 hits) and draw your own, informed conclusions. “

It was very much in David Kirby’s style. Don’t come out and say something directly (like, “mercury is the cause of mitochondrial disease”) but lead the reader along with a series of, well, leading statements.

A more responsible approach would be that one needn’t trust the government nor seek advice on google. A more responsible approach for Mr. Kirby would be to suggest that perhaps, just perhaps, parents of autistic kids should seek out the advice of experts in mitochondrial medicine. Mr. Kirby clearly had an agenda, and it wasn’t the well being of autistics. He was promoting the idea that vaccines caused an autism epidemic.

Mr. Kirby thankfully appears to have moved on from focusing his attention on promoting the vaccine-autism hypotheses. And yet, there is obviously a hunger amongst his old readers for this discussion. This can be seen in Mark Hyman’s blog post at the Huffington Post, “Autism Research: Breakthrough Discovery on the Causes of Autism” which has nearly 1,900 comments. Where David Kirby was promoting himself and the interests of groups like SafeMinds and Generation Rescue, Dr. Hyman uses the MIND Institute paper to promote himself and his own business.

What is worse is the way he goes about doing this. Dr. Hyman is even less capable of covering his obvious mistakes than was David Kirby.

Dr. Hyman writes:

While we don’t have all the answers, and more research is needed to identify and validate the causes and treatment of autism, there are new signs of hope. A study just published in The Journal of the American Medical Association by researchers from the University of California, Davis called “Mitochondrial Dysfunction in Autism” (i) discovered a profound and serious biological underpinning of autism — an acquired loss of the ability to produce energy in the cells, damage to mitochondria (the energy factories in your cells), and an increase in oxidative stress (the same chemical reaction that causes cars to rust, apples to turn brown, fat to become rancid, and skin to wrinkle). These disturbances in energy metabolism were not due to genetic mutations, which is often seen in mitochondrial problems, but a condition the children studied acquired in utero or after birth.

The statement is amazing. Not in a good way. It is amazing that someone could write such an irresponsible paragraph and attribute it to a paper which clearly doesn’t make or support these claims.

The very title of Dr. Hyman’s post (Autism Research: Breakthrough Discovery on the Causes of Autism) is in error. The study makes no claims about the causes of autism. Dr. Hyman didn’t have to look any farther than the paper itself which clearly states as one of the limitations:

Sixth, inferences about a cause and effect association between mitochondrial dysfunction and typical autism cannot be made in a cross-sectional study.

Given this, we can also throw out Dr. Hyman’s wild claim that the study’s authors “discovered a profound and serious biological underpinning of autism”.

Since it is already clear that Dr. Hyman is using the paper to promote his own ideas, regardless of the facts in the paper, I won’t posit as to why he claims that the mitochondrial dysfunction is “acquired”, or that this is due to “damage” to mitochondria. The paper does not support either of these conclusions as fact.

He makes the claim that “These disturbances in energy metabolism were not due to genetic mutations, which is often seen in mitochondrial problems, but a condition the children studied acquired in utero or after birth.”

I am unsure how Dr. Hyman reached this conclusion. The paper notes differences in the mtDNA of many of the children studied. It does not provide evidence as to when or how these genetic differences arose.

Table 3 clearly shows the genetic measures the MIND Institute researchers used. Question the method as you may (or some experts have), there are differences in the mtDNA. The methodology doesn’t allow one to state if these difference were present at birth or not.

The MIND Institute hosts an interview with Prof. Giulivi
At about 3:30 into Prof. Giulivi’s interview, she states clearly that they can not conclude if the mitochondrial dysfunction they claim causes autism or is a result of it.

It is hard for me to decide if Dr. Hyman is more irresponsible than David Kirby or if it is the other way around. David Kirby was certainly doing some self promotion, but his impact was largely as a publicist for the autism-as-vaccine-injury groups like SafeMinds and Generation Rescue. Dr. Hyman is clearly focused on promoting his own services as a practitioner of alternative medicine.

The problem is that in the end, rather than being a leader in treatment, as Dr. Hyman presents himself, such irresponsible actions hinder advancement.

The Huffington Post: Featuring bad science, facile reasoning since 2005

14 Dec

That’s the title of a new blog post by Seth Mnookin, author of “The Panic Virus“. The title is spot on (and could be the the title of a book in its own right): The Huffington Post: Featuring bad science, facile reasoning since 2005.

Seth Mnookin took a look at unscientific thinking that can lead to dangerous results. Not surprisingly, he found that the anti-vaccine movement and the autism-vaccine discussion in particular made an excellent core for his book. In his first blog piece related to Panic Virus, Mr. Mnookin takes a look at how the Huffington Post reported a recent study on mitochondrial dysfunction and autism. The Huffington Post piece, authored by Mark Hyman, made claims well beyond those supported by the paper itself.

A brief quote by Mr. Mnookin:

If you’re confused as to why The Huffington Post would run Hyman’s piece — well, I have my theories, but suffice it to say that the site arguably features more scientific quackery than any other mainstream media outlet.

Is the end of the Omnibus Autism Proceeding near?

2 Oct

The Omnibus Autism Proceeding (OAP or omnibus) is the way the Court of Federal Claims (vaccine court) has been handling the now 5,000+ claims submitted for autism as a vaccine injury. The Omnibus started officially in July of 2002 with Autism General Order #1. Along the way it was decided that the best way to handle the large number of claims was using “test cases”. Three test cases were heard for each of two “causation theories”. The idea was that “general causation” arguments could be made once, and very thoroughly, and the other cases could be decided on the outcome.

The first causation theory was that the MMR vaccine in combination with thimerosal could result in autism. The test cases for this theory were those of Michelle Cedillo, William Yates Hazelhurst and Colten Snyder. Attorneys for the families presented evidence for a mechanism where thimerosal was proposed to reduce the immune response and the MMR vaccine led to a persistent measles infection which, again as proposed, led to symptoms of autism. In all three cases the special masters (judges) ruled against the petitioner families. They found that the evidence did not support the mechanism proposed.

The second causation theory held that thimerosal in vaccines could result in autism. Three test cases were presented, again with individual and general causation evidence. The test cases, Jordan King and William Meade, and Colin Dwyer were heard. Their attorneys argued that mercury from the thimerosal in the vaccines accumulated in the brains and resulted in neuroinflammation which, in turn, resulted in autism. As with the MMR case, the special masters ruled against the petitioner families.

To put it simply: all the data and all the experts that could be put together to support the idea that vaccines cause autism weren’t persuasive. They came up with two stories (MMR and thimerosal) and neither story made a case that was even close (the special master’s word).

Some of the petioners appealed. Some appealed to multiple levels. The appeals were denied.

The Court recently issued an update letter. I quote part of it below:

As described above in part I of this Update, all of the court rulings in the six test cases described above have found no causal link between autism and MMR vaccines and/or thimerosal containing vaccines. Further, the PSC has informed the special masters that no additional OAP test cases are contemplated.

Therefore, the Office of Special Masters has begun discussions with members of the petitioners’ bar and respondent’s counsel about how best to conclude the approximately 4,700 autism cases remaining open on the court’s docket. To aid in that process, some petitioners’ counsel have contacted all of their OAP clients to advise them of the results in the test cases and to recommend a course of action with regard to their claims. Additionally, all petitioners who are not represented by counsel have been ordered to inform the court either that they wish to dismiss their claim or that they intend to proceed with their case. For petitioners who wish to continue with their claim, orders to identify a theory of causation, produce an expert report, and file additional evidence will follow. Petitioners’ counsel who have not yet done so are encouraged to contact their clients and determine how their clients wish to proceed.

The issue of attorneys’ fees and costs for petitioners’ counsel is part of the discussion about how to conclude proceedings on the OAP petitions. Mediation efforts are underway to develop methods to resolve the fees and costs issues, and a report on the progress in these talks is expected at the October judicial conference.

The special masters are assuming that no one will go forward with the MMR and thimerosal theories. Since those theories don’t hold up in court, it seems a good assumption.

Petitioners can still go forward as individual cases, as in any non-omnibus case. They will need to submit records and a theory of causation and support that theory in hearing.

The PSC (petitioner’s steering committee, a group of lawyers which has managed the Omnibus from petitioner’s side) has decided that no additional OAP (Omnibus) test cases are planned.

This is very important. They have no other theories to present. They don’t plan to present “too many too soon”. They don’t plan to present a Wakefield-like theory of persistent measles infections leading to “leaky guts”. They don’t plan to present a “mitochondrial autism” theory.

This last bit is very important. The Hannah Poling case made a lot of news when it was leaked that the government had conceded her case as a table-injury MMR encephalopathy. She was supposed to be one of the three thimerosal test cases. At the time of the concession and since, it was asserted that her case was “not rare” and that the attorneys were prepared to go ahead with the mitochondrial disorder story. It would appear that there are not many (if any) other “Hannah Poling” cases out there. There is at least one family pursuing a variation of the mitochondrial disorder theory. Alexander Krakow was scheduled to be a test case for the thimerosal theory and his family pulled out of the Omnibus to pursue the mitochondrial theory.

While there may be a case or two that we hear about from here on out, it appears that the Omnibus, the “class action” type phase, is over.

Hannah Poling and the Pediatrics thimerosal study: two “big” stories with little press response

18 Sep

Two stories which are “big” news in some segments of the online autism community are the settlement amount for Hannah Poling and the recent study showing no link between autism and thimerosal in vaccines. While these have caused a fair amount of discussion on blogs (like this one), they didn’t generate that much press coverage.

We broke the Hannah Poling award story here on LeftBrainRightBrain on September 3. The story was ignored, even by such pro autism-as-vaccine-injury blogs as the Age of Autism until September 9th, when Sharyl Attkisson (who has some connection to the people at the Age of Autism blog) wrote about it for CBS.

There are a couple of dozen entries in Google News on Hannah Poling. Few major outlets. One that did carry it is the Atlanta Journal Constitution, the home town newspaper for the Poling family. In Settlement reached in autism-vaccine case the AJC quoted Dr. John Shoffner:

Dr. John Shoffner, a neurologist and national expert who has conducted research on autism and its causes, said researchers have found no link between vaccines and autism. And he said he strongly favors vaccination.

“The preponderance of data shows that vaccines are important and safe for children to prevent preventable and sometimes life-threatening infectious diseases,” Shoffner said. “I certainly am in favor and support the CDC’s as well as the American Academy of Pediatrics’ recommendation of vaccination.”

Shoffner is a co-author of a journal article that describes Poling’s case without naming her.

Edited to add: I forgot to include this quote from the Atlanta Journal Constitution:

“It’s critical to remember that the government has never compensated, nor has it ever been ordered to compensate, any case based on a determination that autism was actually caused by vaccines,” said Martin Kramer, communications director for the Health Resources and Services Administration. The National Vaccine Injury Compensation Program is part of the administration. The U.S. Court of Federal Claims decides who will be paid damages for injuries that result from vaccines, under a 1988 law that created a program.

Another so-called “big” story from the last few weeks is the study on autism and thimerosal in Pediatrics, Prenatal and Infant Exposure to Thimerosal From Vaccines and Immunoglobulins and Risk of Autism. Sometimes when an important paper comes out (that I am aware of) I watch Google News as the embargo is lifted. I did so with this paper. Nothing happened. OK, I think Disability Scoop had a story out right at midnight (this one, if I recall correctly). Heck, it wasn’t until Friday that the CDC added the study to their website (it isn’t mentioned on the main cdc.gov webpage). Even SafeMinds (who are, in cases like this SafeBet–as in, it is a safe bet they will put out a critique of the paper) didn’t respond for days.

Sure, I was interested. And, yes, these stories sparked some of the most active conversations on this blog in a while. But I am still left with the basic conclusion: the general public has already absorbed these stories. The government conceded the Hannah Poling case 2 years ago. It isn’t new. The idea that mercury in vaccines cause autism–no longer part of the front line public discussion.

I’m not the only one to make this comment. The Washington Post had this to say four days after the paper was made public:

But when the journal Pediatrics published on Monday a study that found no increased risk of autism among more than 1,000 babies who’d been exposed prenatally or in the first 20 months of life to ethylmercury from vaccines, it was met with a general shrug. Neither The Washington Post nor The New York Times even reported on it, though the Los Angeles Times did, in its Booster Shots blog.

Sure, these stories will never completely go away. The vaccine/autism story will never go completely away. But the heyday is over.