Further results from the thimerosal-autism study

14 Sep

The recent study on thimerosal and autism was extensive. Much data and many results were included in two technical reports (nearly 400 pages total, volume 1 and volume 2). I haven’t had the time to read them thoroughly yet, but I did catch some interesting pieces of information.

The authors give the ASD prevalence (cases/1000) as a function of HMO and year of birth:

This is pretty flat. No huge increase seen over that 6 year time span. No evidence for an “epidemic”. The prevalence is about 1.1%. This is consistent with the current value quoted by the CDC.

There are remarkably a big variation by parents educational status (63% kids born to mothers who graduated from college). However, since the researchers are working with kids who are enrolled in an HMO, it seems likely this is due to some bias. I.e. the HMO participants could be better educated (and higher income) than the average.

There are indications that increasing parental age is related to increased autism risk. 36% of mothers were in the 30-34 age bracket, 35% were in the 35+ age bracket. So, about 70% of mothers were over 30 years of age. They list father’s age with different brackets, but 79% were 30 years old or older at the time of birth of their child. Again, could be some bias due to HMO membership, but a large fraction of the parents were older.

Some children (both ASD and controls) received no vaccines. Many received vaccines but no thimerosal–i.e. all their vaccines were thimerosal free.

The use of prenatal vitamins is given as having an increased risk of autism, but the odds ratio is not given.

Being a first-born or second-born child has a significant increased risk for autism (hazard ratios of about 1.6). They may discuss this, but I don’t know right now how much of this is due to parents of autistic kids deciding not to have larger families.

One of the stranger results–there is an increased risk of autism when mothers were using prenatal vitamins with folic acid. The hazard ratio was 2.3 with a p value of 0.0176

Pica and childhood lead exposures had very high hazard ratios: 3.7. This is a good case where it is worth asking if this is causal–does pica cause autism or, as is more likely, does autism cause pica and, with it, higher lead exposures.

Poverty was slightly protective for autism (hazard ratio of 0.92). Again, one has to question if this is real or whether poverty just results in a greater likelihood that a child’s autism will be misdiagnosed.

The authors list coexisting conditions for the autistic, ASD and control children:

Epilepsy is much higher at about 5%, compared to 1.6% for controls. Reports of the prevalence of epilepsy amongst autistics are often much higher, though.

Developmental delay (by parent report) is at about 18% for autistics, compared to about 0.66% in controls.

Gi disorder prevalence is about 2% amongst autistics. It is the same (or slightly higher) for controls. This is very interesting given the anecdotal reports of a high prevalence of GI disorders amongst autistics. I suspect this will form some of the complaints about this study–some will say they aren’t looking at the correct population and that a specific study on autism/regression/GI complaints needs to be done.

Cases (those with ASD) were more likely to get thimerosal free HepB and HIB vaccines.

Infants in this study do not get flu vaccines (near zero). Unless that habit has changed dramatically in the past few years–and that most doctors are giving infants flu vaccines with thimerosal–flu vaccines are not likely to be a reason for the continued climb in autism prevalence.

There is a lot more information there. If/when I get the chance to give the reports a more thorough read I’ll post what I find.

Misfolding neural proteins

14 Sep

Regular readers might recall me blogging about neural proteins awhile ago. If I may quote myself:

…when the authors blocked APC function, they found that levels of the proteins neuroligin and neurexin dropped. So what…? Well, without these two proteins at normal levels, synapses grew improperly. So what…? Turns out that scientists already know that mutuations in the genes for neuroligin and neurexin are associated with autism…

And now along comes a new study that builds on this science.

Palmer Taylor, associate vice-chancellor for Health Sciences at UC San Diego and dean of the Skaggs School of Pharmacy and Pharmaceutical Sciences, and colleagues report that misfolding of a protein called neuroligin-3, due to gene mutations, results in trafficking deficiencies that may lead to abnormal communications between neurons.

Source.

So here we have a situation where genetic mutations leads to a misfolding of a protein that results in affecting the growth of synapses which in turn affects the development of autism.

Taylor said identifying and describing the misfolded protein link advances understanding of the complex causes of certain autisms, including the influences of genes versus environment…

Thats an interesting statement. I will try to get in touch with Taylor to explain that further.

Questions and answers with the thimerosal-autism study author

13 Sep

It is a safe bet that there would be a lot of questions arising from the latest study, which shows no link between thimerosal exposure and autism. I thought there would be some interviews in the press covering most of the obvious questions, so I decided to ask some questions of my own of the study’s lead author, Cristofer Price of Abt associates.

I was very interested in the more complete discussion in their Techical Reports and data. I was also interested in how these results might apply to the idea that there are “too many” vaccines given “too soon”. Mostly I was interested in why this study took so long to get published give the CDC’s statements after the Thompson study of 2007–statements which indicated that this follow-on study should be available within about a year or so.

Below is the exchange:

First: you cite two Abt reports from 2009 on the subject:

Price C, Robertson A, Goodson B. Thimerosal
and Autism. Technical report. Vol I. Bethesda,
MD: Abt Associates Inc; 2009

I can’t find them on your site at this time. Are they there or will they be made available when the embargo is lifted?

[Response: The tech reports will be up on the CDC and Abt web sites on Monday. ]

Will the data be made available as was done with the Thomson(2007) study? If so, how would one access it?

[Response: Yes, the process for obtaining the data will be very much like the process that was in place for the Thompson(2007) study. Instructions for how to access the data and a data use agreement, etc. will be up on the CDC web site on Monday. The terms specified in the data use agreement are similar to those from the prior study. ]

As to the paper, I see that the results are the same for autism with and without regression. Are there any other issues of severity which were checked (e.g. level of intellectual disability, seizures) which were also monitored?

[Response: We did do a sub-analysis where AD cases with low cognitive functioning were excluded (see technical report on Monday for full details and results) Analysis of the subgroup of AD cases where children with low cognitive functioning were excluded was motivated by the following concern. Because children who are non-responsive during the assessment process are more difficult to assess, it can sometimes be difficult to determine whether children with severe developmental delay actually have autistic disorder. If the imprecision of the assessment process for such children resulted in inclusion of children without AD in the AD group, then we would expect that the estimate of the relationship of exposure to AD risk could be attenuated. Therefore, an outcome category for AD with low cognitive functioning excluded was created and its relationship to exposure was estimated. The results for this subgroup were very similar to those for the overall analysis.]

There are children (both case and control) who have 0 mercury exposure from vaccines in all categories. Are there children in all these categories who are unvaccinated?

[Response: I don’t have the answer to this handy. I know that there were a few kids in the sample that had zero vaccine receipts, but I don’t think they were in all of the categories because there were few of them. Most of the kids with 0 mercury exposure received at least some vaccines, but they were thimerosal free.]

To some extent, mercury exposure from vaccines could be used as a proxy variable for vaccine exposures. I.e. the amount of mercury would be somewhat proportional to the number of vaccines received. Are there any trends in just number of vaccines and autism? I.e. anything that would address the “too many, too soon” slogan? I do see that you discuss this somewhat on page 661

[Response: In the technical report (Volume II, Chapter 16) I show data on the the cumulative numbers of vaccines recieved as children aged. It shows that the cases and controls got the same numbers of vaccines. That chapter was not designed specifically to address your question about “too many too soon”, but it does show cases did not get more, sooner than controls.]

After Thomson(2007) came out, I recall that the CDC webpage suggested that your present study would be out in about a year. Why has this study taken so long to reach the public?

[Response: I’m not sure why the CDC web page had the overly optimistic suggestion that it would be out in about a year. To understand the timeline, I will need to explain some things about the phases of analysis, then the process of drafting the paper and getting it published. This is going to be a bit long winded, but part of it I am cutting and pasting from the technical report:

The study protocol was developed by a design group led by Abt Associates, Inc. working in close consultation with Principal Investigators from the
Centers for Disease Control and Prevention (CDC), Principal Investigators, Data Managers, and Study Managers from the each of the three HMOs, and with the study’s External Expert Consultants. Prior to recruitment and data collection, a detailed analysis plan was written for the study that specified the research questions, study design, eligibility criteria, sampling plan and target sample sizes, the form of the statistical models that would be used, the specific hypotheses to be tested, decision rules for categorizing outcome classifications, the coding of exposure variables,
the list of covariates to be used as statistical control variables, the coding of each of those variables, and decision rules for the retention or omission of each covariate in the final analysis models.

By agreement among the members of the design group, data analysis for the study was to be completed in two phases. In the first analysis phase, analysts at Abt Associates were to carry out as closely as possible the analyses specified in the plan and to do only the analyses specified in the plan. At the end of this phase, all members of the design group were invited to a meeting in Washington, DC where the first round, preliminary results were presented to the group. Prior to that meeting, the results of analyses linking exposures to outcomes had not been shared with anyone outside of Abt Associates. The second phase of analysis began with the meeting in Washington, DC. At that meeting, the design group considered the results and generated new hypotheses and questions that were to be pursued in the second phase. Over the ensuing months design team members provided written comments on the results of the preliminary analyses and made suggestions for additional analyses. The current report includes results from both phases.

The meeting in DC described in the paragraph above took place in May of 2008. We gave all of the members of the design group a couple of months to give feedback and suggestions on the analyses that they wanted in Phase II. There was a lot of back and forth there. The technical report includes results from both phases. We were well into 2009 before we (at Abt) had made it all the way through those second phase analyses. Then, drafts of the manuscript had contributions from a large number of authors (which takes a lot of time) and we sent drafts to our External Expert Consultants, made changes, replied to queries etc, then a draft had to go through CDC review which takes time, then we the publication process (getting a manuscript published in a peer-reviewed journal) takes a surprisingly long time. So, here we are in 2010.]

New thimerosal/autism paper – signal vs noise

13 Sep

The new thiomersal paper that Sully has blogged will be attacked by the antivaxxers in at least one key area. The area that will be attacked is – to those well schooled in the way good science operates – a standard way to improve the signal to noise ratio of the results. Or to put it another way, ensures ‘cleaner’ results.

From the paper:

…Children were excluded if they had the following medical conditions with known links to ASD traits: fragile X syndrome; tuberous sclerosis; Rett syndrome; congenital rubella syndrome; or Angelman syndrome…

So first of all why were children that fell within these groups excluded? As I said, the answer is to ensure better data. In order to get a cleaner signal, the more noise that can be eradicated the better.

In this instance, children who already have existing medical conditions known to be related to autism would produce noise. We already know what caused their autistic traits hence establishing a clear link to thiomersal would not be possible. In a very meaningful way, doing this does a large favour for antivax group. If these children were eradicated from the study and a clear link to thiomersal _had_ been established then denying the link would be very much more difficult.

However don’t expect the antivaxxers to see this. Or even if they _do_ see it, they will look away purposefully. They will use the fact that these children were excluded and say _”See? ‘They’ have to hide the autistic children!”_ .

When you see this tactic – and you will see it – see it for what it is. It’s simple noise generation to obscure the clear signal coming through. Thimerosal in vaccines doesn’t cause autism. And it never did.

Congenital Rubella Syndrome: a Novel Form of Mercury Poisoning?

13 Sep

I considered titling this: A peak into the upcoming book “Age of Autism?” as this seems to show us the sorts of arguments that will be made in that book.

One of the known environmental causes of autism is Congenital Rubella Syndrome, or CRS. This was discussed as part of a presentation to the IACC, What Causes Autism? The Case for an Environmental Contribution, by Dr. Philip Landrigan. (video is here, starting at about minute 79. Sorry it doesn’t embed).

In the question/answer session for that presentation on at about 114 minutes into the IACC meeting) Lyn Redwood of SafeMinds brought up a new argument–that CRS induced autism may be due to mercury. It turns out that in the 1950’s gamma globulin therapy was started as a means of preventing CRS. Gamma Globulin was injected into pregnant mothers who to prevent or reduce the rubella infections. This exposed the mother and fetus to mercury and should be considered the cause of the autism according to Ms. Redwood.

I must admit that when I heard this question I thought: “Well, here is one of the talking points we will hear from the upcoming book, ‘Age of Autism’, by Mark Blaxill and Dan Olmsted”. Their book appears to be an attempt to tie all of autism (and many other conditions) to mercury, including, I suspect now, CRS. There are other loose ends they will undoubtedly bring up and tie into the mercury hypothesis (like the existence of autistics who were born before thimerosal was invented. That will be interesting to read).

There is at least one big reason why CRS was possibly not linked to autism before Stella Chase’s work in the 1970’s. Congenital Rubella Syndrome causes major disability. Severe to profound mental retardation. There are big spikes in the California Department of Developmental Services data for severe and profound mental retardation corresponding to the CRS outbreaks of the 1960s. Why bring this up? Because for the first two decades after Kanner’s original paper, many people considered intellectual disability (mental retardation) and autism to be completely separate.

From Infantile autism reviewed: a decade of research, a review article written in 1981:

One of the chief problems has been how to handle the questions of mental retardation and organic brain disease, issues especially troublesome with regard to infantile autism. When Kanner (1943) first described the diagnostic features, he also remarked that the condition bore no resemblance to any known neurological condition and implied that autistic children had a basically normal intelligence. For over two decades afterwards, diagnosticians generally believed that the presence of mental retardation or neurologic signs ruled out the diagnosis of infantile autism in the Kannerian sense, even if the child met all behavioral criteria (Eisenberg 1966). Thus diagnosis was frequently one dimensional; a child was labeled as afflicted with either infantile autism or mental retardation, not both.

Or, to put it another way, what many people today call “Kanner’s Autism”, with intellectual disability and/or apraxia, is not what Kanner and most of the people of his time thought of as autism.

But, data, as they say, there’s a funny thing about evidence. Real data is worth more than all these blogger discussions. The paper out today from Pediatrics included immune globulins in their analysis and showed that mercury exposure prenatally and in infancy and found that these exposures did not increase the risk of autism.

Then again, the funny thing about evidence is that it is repeatable. Two previous papers showed no link between immune globulins and autism:

Maternal Rh D status, anti-D immune globulin exposure during pregnancy, and risk of autism spectrum disorders


Lack of association between Rh status, Rh immune globulin in pregnancy and autism.

So, if I am correct and “Age of Autism” the book claims immune globulins *are* a cause of autism, what can we say? We can say that the funny thing about evidence is that some people are not swayed by it. Some people will continue to push the mercury hypothesis forever.

Thimerosal in vaccines did not cause an autism epidemic

13 Sep

There have been two main theories linking vaccines to an “epidemic” of autism. Both theories have been studied. Both have been heard in the courts. Neither theory had a sound scientific basis and epidemiological data has shown that neither theories explained the increase in autism prevalence in the last 20 years.

First it was proposed that the MMR vaccine resulted in persistent measles infections that lodged in the intestines of children leading to “leaky guts” and that harmful substances were leaked into the blood, traveled to the brain and resulted in autism symptoms. This was proposed by Dr. Andrew Wakefield and has since been shown in epidemiological and other studies to be unsound. (This theory morphed for the Omnibus Autism Proceeding, the vaccine court. The argument there was that the measles virus itself traveled to the brain. Again, it is not supported by epidemiological data and is not scientifically sound).

The second theory was that mercury in vaccines from a compound called thimerosal caused autism. In that theory, it was proposed that autism symptoms were similar to mercury poisoning (autism was a “novel” form of mercury poisoning). This theory was not scientifically sound as autism symptoms are not like mercury poisoning. Previous epidemiological studies have also shown thimerosal was not behind the rising numbers of people diagnosed with autism.

In 2007 there was a study which looked at 1,000 kids aged 7-10 to see if various neurological symptoms were more prevalent in those who received higher exposures to thimerosal. Orac at Respectful Insolence blogged it and Kev posted that piece here on LeftBrainRightBrain as well. That study showed indications that in some measures children may perform more poorly with thimerosal exposure. It also showed that in some measures children may perform better with thimerosal exposure. This mixed result is (a) not very strong in either direction and (b) not very surprising when you look at a lot of different measures at the same time. Chance will result in some measures positive, some negative.

The 2007 study was published in the New England Journal of Medicine as Early Thimerosal Exposure and Neuropsychological Outcomes at 7 to 10 Years, by Thompson, et al.. (Thompson (2007))

What was missing in that report was a direct study of autism. Given the numbers of children (1,047) selected, there would only be about 10 kids with ASD expected in the group. This is too few for a strong conclusion on autism. At the time of that study it was noted that another study would follow concentrating on autism alone.

That study has just been published in the journal Pediatrics as Prenatal and Infant Exposure to Thimerosal From Vaccines and Immunoglobulins and Risk of Autism. They studied “256 children with ASD and 752 controls matched by birth year, gender, and [managed care organizations]”. I will give some details here. I expect the treatment on the Science Based Medicine and Steven Novela’s Neurologica blogs to cover the science thoroughly should you wish more detail.

Short answer: thimerosal exposure doesn’t cause an increased risk of autism. Neither thimerosal from vaccines given to the children nor thimerosal from products like Rhogam are behind the increase in autism prevalence we have seen.

It is worth noting that the authors looked at autism with and without regression.

Here is the abstract:

OBJECTIVE: Exposure to thimerosal, a mercury-containing preservative that is used in vaccines and immunoglobulin preparations, has been hypothesized to be associated with increased risk of autism spectrum disorder (ASD). This study was designed to examine relationships between prenatal and infant ethylmercury exposure from thimerosal containing vaccines and/or immunoglobulin preparations and ASD and 2 ASD subcategories: autistic disorder (AD) and ASD with regression.

METHODS: A case-control study was conducted in 3 managed care organizations (MCOs) of 256 children with ASD and 752 controls matched by birth year, gender, and MCO. ASD diagnoses were validated through standardized in-person evaluations. Exposure to thimerosal in vaccines and immunoglobulin preparations was determined from electronic immunization registries, medical charts, and parent interviews. Information on potential confounding factors was obtained from the interviews and medical charts. We used conditional logistic regression to assess associations between ASD, AD, and ASD with regression and exposure to ethylmercury during prenatal, birth-to-1 month, birthto-7-month, and birth-to-20-month periods.

RESULTS: There were no findings of increased risk for any of the 3 ASD outcomes. The adjusted odds ratios (95% confidence intervals) for ASD associated with a 2-SD increase in ethylmercury exposure were 1.12 (0.83–1.51) for prenatal exposure, 0.88 (0.62–1.26) for exposure from birth to 1 month, 0.60 (0.36–0.99) for exposure from birth to 7 months, and 0.60 (0.32– 0.97) for exposure from birth to 20 months.

CONCLUSIONS: In our study of MCO members, prenatal and early-life exposure to ethylmercury from thimerosal-containing vaccines and immunoglobulin preparations was not related to increased risk ASDs. Pediatrics 2010;126:656–664

My guess is that there will be much discussion of the methods on many websites. For now, here are the data from Table 2 and Table 3.

Table 2 (click to enlarge)

Table 3 (click to enlarge)

As with Thompson (2007) the authors will make longer reports available on their website and will allow access to the data.

This study is not the first of its kind. Here are a few of the large studies which have shown a lack of association between thimerosal exposure and autism in the past.

Thimerosal and the Occurrence of Autism: Negative Ecological Evidence From Danish Population-Based Data

Safety of Thimerosal-Containing Vaccines: A Two-Phased Study of Computerized Health Maintenance Organization Database

Thimerosal Exposure in Infants and Developmental Disorders: A Prospective Cohort Study in the United Kingdom Does Not Support a Causal Association

Autism and Thimerosal-Containing Vaccines Lack of Consistent Evidence for an Association

There are more.

One question is whether this will finally quiet those claiming an autism epidemic caused by mercury in vaccines. Unfortunately, I sincerely doubt it. This study included Sallie Bernard of SafeMinds in the acknowledgments. Ms. Bernard was also involved in the Thompson study of 2007. At that time she was listed as a “dissenting” member of the team. She submitted a letter to the NEJM discussing the reasons for her dissention, Perhaps the lack of the word “dissenting” this time is a good sign. I’ll wait and see.

The main question is how much impact this will have on the next generation of families with autistic children. I can’t but wonder that the age of the mercury hypothesis has seen its peak. Not only in research but in general acceptance.

Sharyl Attkisson blogs the Hannah Poling settlement

10 Sep

I had forgotten Sharyl Attkisson. She is a reporter for CBS news who has covered vaccines in the past, but has been silent on the issue for the past year or more.

Her recent piece shows exactly the sort of reporting that frustrated me in the past: Family to Receive $1.5M in First-Ever Vaccine-Autism Court Award

In that piece she links to her piece from 2008 on the Hannah Poling case: Vaccine Case: An Exception Or A Precedent?

Here’s a quote from that earlier piece:

While the Poling case is the first of its kind to become public, a CBS News investigation uncovered at least nine other cases as far back as 1990, where records show the court ordered the government compensated families whose children developed autism or autistic-like symptoms in children including toddlers who had been called “very smart” and “impressed” doctors with their “intelligence and curiosity” … until their vaccinations.

They were children just like Hannah Poling.

What’s still being debated is whether the Poling case is an exception … or a precedent.

So, which is it? Were there children “just like Hannah Poling” or is this the “First-Ever Vaccine-Autism Court Award”?

Actually, it is neither. This isn’t the first vaccine court award involving autism, and the other cases are not “just like Hannah Poling”.

For real information on the other nine cases, read Kathleen Seidel’s piece on Neurodiversity.com. Few, professional or amateur, can compare the the thoroughness of Kathleen Seidel. For example, one case (the first I read involving autism from the vaccine court) is Suel v. HHS. Young David Suel had tuberous sclerosis, a condition known to be associated with autism and epilepsy. Epilepsy occurs in about 60 to 90% of individuals with TS. Autism occurs in about 25-50%. David Suel’s case was declared to be a “table injury” wherein the seizures began within a set period after his DPT vaccination. What is notable about that is the table for DPT was later changed–when it was shown that DPT was not responsible for inducing seizure disorders. In other words, had David Suel been vaccinated, or just filed, after the change in the table, he likely would not have been awarded damages.

“They were children just like Hannah Poling”? Is tuberous sclerosis just like mitochondrial disease? (answer: not even close).

Shall we go on? In her recent piece, Ms. Attkisson states:

In 2002, Hannah’s parents filed an autism claim in federal vaccine court. Five years later, the government settled the case before trial and had it sealed

Not accurate. The court did not “settle” the case in 2007. They conceded the case, and they were in the process of completing the settlement when someone leaked the information to the press. The government did not “seal” the case–it is standard procedure to keep this information confidential until the settlement is completed.

But that doesn’t make a good story, does it?

Ms. Attkisson goes on:

In acknowledging Hannah’s injuries, the government said vaccines aggravated an unknown mitochondrial disorder Hannah had which didn’t “cause” her autism, but “resulted” in it. It’s unknown how many other children have similar undiagnosed mitochondrial disorder. All other autism “test cases” have been defeated at trial. Approximately 4,800 are awaiting disposition in federal vaccine court.

Mito-autism was a big thing for a while there. David Kirby took the story and ran with it–making a lot of mistakes along the way and propagating a lot of misinformation. It is unknown how many other children have similar disorders–but the researchers who studied cases like Hannah Poling have stated that cases such as hers are “rare”.

“All other autism “test cases” have been defeated at trial”.

What is conspicuous about the other “test cases” is that in none of them was it argued that the children were like Hannah Poling–i.e. the attorneys did not argue that a mechanism of autism through mitochondrial dysfunction aggravated by vaccines existed. In fact, one child named as a test case was pulled from that slot in order to argue that mitochondrial based case. The expert report filed for that child (since pulled from the Omnibus website) did not argue mitochondrial disorder or dysfunction at that time. In other words, the idea of a mitochondrial disorder being linked to autism was so alien from the cases being made by the attorneys for the families in the Omnibus that this child had to argue the case separately.

It is often pointed out that many autistics may have mitochondrial dysfunction. This is based largely on studies out of Portugal. It is left implied, and it is often believed that mitochondrial dysfunction means vaccine injury in these cases. This was the impression that David Kirby put forth and it was clearly wrong. First, mitochondrial disorders are a very broad spectrum. The type that Hannah Poling has is not the same as those detected in most autistics. Second, most reports of mitochondrial disorders and autism, including the Portugal studies, do not involve regression. Third, even amongst those children reported by the groups that identified Hannah Poling, regression was often idiopathic or followed fever clearly independent of vaccination.

I do not expect Ms. Attkisson to present the following (quality) information, so I will repeat it here:

Here are the answers to some questions posted to mitochondrial medicine experts and their answers:

When asked, to respond to the position: ‘‘I view the risk of vaccination in known metabolic disease patients to generally be outweighed by the risk of the infectious diseases being vaccinated against”

63.2% strongly agreed
31.1% agreed
0.9% disagreed
and 0.9% strongly disagreed.

Asked about the opinion that the risk of vaccination in metabolic disease was ‘‘greater than the risk of the infectious diseases being vaccinated against”

52.9% strongly disagreed
40% disagreed
3.5% agreed
and none strongly agreed

Mark Blaxill promotes bad science

8 Sep

[wags finger]…and don’t you ever forget it 😉

Basically, the story is that The Blax wrote a blog post in which he said:

Despite the relentless drumbeat of propaganda from the CDC, public health authorities and the thuggish on-line goons of the medical industry, there’s a funny thing going on. The evidence of a connection between mercury exposure and autism keeps growing.

It does? Really? Such as what science exactly?

Well The Blax has the answer to that in that he quotes from a study which according to The Blax:

They found that thimerosal at the same concentrations received in human infants had clearly measurable effects on opioid receptor development in the infant rats.

Huh. Well imagine my surprise when I read two blog posts, one from Emily in which she says:

Their starting dose is at least 3.2 times the relevant exposure of Hg. But they’re not finished. They don’t use that dose once. They use it four times, injecting the newborn rats on days 7, 9, 11, and 15 of life, each time with 3.2 times the actual relevant exposure of Hg, for a total of 48 mcg of Hg/kg in a little over a week. Indeed, even if 12 mcg were the relevant exposure, they’re dosing their animals with it four times within a week, give or take, giving us ~13 fold the relevant exposure.

and another from Orac in which _he_ says:

…the minimum dose received was 48 ?g Hg/kg, and the maximum dose received was a whopping 12,000 ?g Hg/kg, or 12 mg Hg/kg!

So when The Blax states that this paper is a like for like comparison between infant vaccines and their dosage, I think its clear to see that this is incorrect. What these researchers have in fact done, is massively overdose their test subjects.

And thats not the only problem with this paper that The Blax is so in love with. Geier, Haley, Bernard…recognise these names? Of course you do! They’re the names that this paper relies on to support its underlying ‘science’.

I think the only real question that needs answering here is – how in heck did this paper get past peer review??

Age of Autism – Amazon file wisely

8 Sep

We all know the new Age of Autism book is coming soon. Its stocked at Amazon for example where pre-orders for the book have placed the books ranking at the heady heights of the top 100,000.

However, whats most interesting is the cover art that Messers Blaxill and Olmsted have chosen for the Kindle edition of the book. In a refreshing turn of honesty, they selected the below (click for bigger) as the cover art.

You can also see it in situ at Amazon US store.

A brave and refreshingly intellectually honest move by Blaxill and Olmsted, I think you’ll agree.

Autism Science Foundation anounces pre and post doctoral training awards in autism research

7 Sep

The Autism Science Foundation has announced a new round of fellowships for grad students, medical students and post-doctoral fellows who will pursue autism research.

(September 7, 2010–New York, NY) The Autism Science Foundation invites applications for its Pre and Post Doctoral Training Awards from graduate students, medical students and post-doctoral fellows interested in pursuing careers in basic and clinical research relevant to autism spectrum disorders.

The proposed training must be scientifically linked to autism. ASF will consider for training purposes all areas of related basic and clinical research including but not limited to: human behavior across the lifespan (language, learning, communication, social function, epilepsy, sleep, repetitive disorders), neurobiology (anatomy, development, neuro-imaging), pharmacology, neuropathology, human genetics/genomics, immunology, molecular and cellular mechanisms, studies employing model organisms and systems, and studies of treatment and service delivery.

Applicants for the pre-doctoral awards must be students enrolled in a program in the United States leading to a research doctorate such as a Ph.D. or Sc.D., a combined degree such as an M.D./Ph.D., in an academic department at an accredited university or health/medical institution, or an M.D. at an accredited university medical school. Applicants for the post-doctoral awards must have completed their doctoral degree and have been accepted as a post doctoral fellow in good standing in a program in the United States. The selected awardee must spend 80% of his/her professional time engaged exclusively in autism research activities stipulated in the application for the duration of the award, and cannot simultaneously hold another named fellowship award during the support period.

Each applicant must apply with a mentor, who must hold a tenured or tenure-track faculty appointment (or equivalent) at an accredited institution of higher education or health/medical/research institution in the United States, and must be an established and active investigator in some aspect of autism research.
Each mentor may sponsor one pre-doctoral candidate and one post-doctoral candidate per year.

Learn more at www.autismsciencefoundation.org/ApplyForaGrant.html

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