Archive | September, 2010

Autism researchers want your input: Autism and the Internet at UCLA

18 Sep

Researchers at UCLA are interested in your input on a survey of Autism and the Internet. The study has IRB approval and the description from their site is below:

You are asked by Dr. Patricia Greenfield, of the Department of Psychology at the University of California, Los Angeles, if you would like to participate in this anonymous internet survey comparing how people with and without autism use the internet. Your participation in this study is voluntary and you may stop doing the survey at any point in time.

Purpose of the Research: The goal of this study is to see if the internet helps autistic and non-autistic people make friends and/or learn about their hobbies. We would also like to know if different ways of seeing the world, regardless of diagnosis, relate to different ways of using the internet.

Outline of Procedures: If you would like to participate in this study, please select the box at the end of this consent form titled “I consent to participate in the survey Autism and the Internet”. If you would not like to participate, select the box titled “I do not consent to participate in the survey Autism and the Internet.” If you consent to participate, the survey will appear on your computer screen. If you ever decide that you no longer want to complete the survey, you are free to stop taking the survey at any point in time. Your responses to the survey will remain anonymous. The survey will take between 15 minutes and one hour to complete.

Foreseeable Discomforts: Your may feel uncomfortable emotions when thinking about questions on the survey. If the survey questions make you feel uncomfortable, you are free to stop taking the survey at any point in time. The questions are designed to be as clear as possible so it is likely that you will not experience emotional discomfort as a result of the survey.

Potential Benefit to Participants and Society: Possible benefits of the study to society are that the knowledge gained may help people evaluate whether the internet helps autistic and non-autistic people to form connections and learn about their passions. This information may be useful in designing treatments to help autistic people communicate more effectively or in recognizing when such treatments are unnecessary because the autistic people are already satisfied with how they use the internet to communicate and learn.

Your participation would be anonymous and greatly appreciated. If you have the time and inclination, consider offering your experience to help out these researchers. The survey can be found here.

Autism researchers want your input: Autism Life Histories at Columbia

17 Sep

Prof. Peter Bearman’s group at Columbia has done and is still doing much in the way of autism epidemiology research. We have discussed many of his group’s papers here on LeftBrainRightBrain. Prof. Bearman’s group now has a website up, Understanding Autism.

As a part of their continuing research into autism, the Bearman team has launched a new project, AutismLifeHistories.org. This is essentially a survey to collect information from parents about their child’s

edit to add–here is how I intended that sentence to read
This is essentially a survey to collect information from parents about their child’s history, but nothing prevents a self-advocate from submitting information on him/her self.

The full description is below, but here is a shorter version from page 1 of the survey:

The purpose of this online survey is to learn about how you recognized your child’s autism, sought professional help and navigated the system of services. We hope that these stories help us arrive at a better understanding of the difficulties of the road to diagnosis and service provision.

While we do not believe that the content and the nature of the questions presented in this survey will cause you any discomfort, your participation is absolutely voluntary throughout the survey. This means that you are free to leave this survey at any time you wish. We will only read your responses if you complete and submit your responses.

It took me about 10 minutes. One could easily spend less.

Here is the longer description of the project:

Autism Life Histories
Dear Parent,

We are researchers at Columbia University’s Institute for Social and Economic Research and Policy studying autism. We are currently collecting life stories from parents about their experiences in recognizing their child’s autism, seeking professional help and navigating the system of services.

The goal of this project is to gain a better understanding of the road to diagnosis. Parents have different experiences and observations of their child’s development and they have different personal resources with which they access care and services. Parents also differ in the type and extent of their support networks and social relations. And finally parents make different decisions in their quest for obtaining the right diagnosis and care for their child. We are eager to hear about how these factors affected your experience and your child’s experience with autism.

We invite you to tell your story by completing a semi-structured survey in which your identity will remain confidential. In fact, this task is less of a survey and more of a conversation between you and us. There are three main sections to this conversation. The first section is set up to learn about you; we ask you a series of short questions. The second section is designed to learn about your child; we ask a series of short questions about his/her age, birth year and place and interaction with other children. The third section provides you with unlimited space to write about your story in recognizing your child’s autism. We hope you will decide to talk with us.

We thank you in advance for taking the time to read through this invitation and look forward to getting to know you. Please feel free to contact us via e-mail at understandingautism@columbia.edu with any questions that you may have. Please be assured that we will not share your story with anyone other than authorized members of our research team. No one else will have access to it.

To share your story, please click on the following link talk-to-us to the online survey.

Sincerely,

Peter Bearman, Principal Investigator
Cole Professor of the Social Sciences

Why are autistic people mainly male?

17 Sep

Excluding the ever humorous ideas of the Geier’s and more serious ideas of Simon Baron-Cohen regarding testosterone, the reasons as to why there are (or seem to be) many more autistic males than females have not been adequately explained. However that might be about to change.

A new study gives the first starting point as to why this situation might come about.

As we all know, males have an X and a Y chromosome whereas females have two X’s. This new study postulatesthat this fact plays an important role.

If a boy’s X-chromosome is missing the PTCHD1 gene or other nearby DNA sequences, they will be at high risk of developing ASD or intellectual disability. Girls are different in that, even if they are missing one PTCHD1 gene, by nature they always carry a second X-chromosome, shielding them from ASD…

The PTCHD1 gene is responsible for determining the development of human embryo’s and is already associated with autism. Because males only have 1 X chromosome, if this is defective then they – obviously – don’t carry that secondary level of shielding that females – with 2 X chromosomes – do.

However, this is very much preliminary. It should be noted that:

The researchers found that about one percent of boys with ASD had mutations in the patched domain containing 1 (PTCHD1) gene on the X-chromosome.

1% is not a very high number but as LBRB interviewee Stephen Scherer says:

The male gender bias in autism has intrigued us for years and now we have an indicator that starts to explain why this may be…

In other words, no one is saying this is a done deal – merely that its a strong possibility with some decent science behind it.

Autism causation and the Hepatitis B vaccine: no link

16 Sep

One of the primary subjects for those promoting vaccines as a primary cause of autism is the Hepatitis B vaccine. This vaccine is given at birth and represents a child’s first exposure outside the womb to a vaccine and, in the old days, to thimerosal. David Kirby attempted to link the rise in autism prevalence to the introduction of the HepB vaccine. Others have claimed that the rates of special education placements are 9 times higher amongst children given the HepB vaccine at birth. Here is the abstract for (Hepatitis B triple series vaccine and developmental disability in US children aged 1–9 years rel=”nofollow”)

This study investigated the association between vaccination with the Hepatitis B triple series vaccine prior to 2000 and developmental disability in children aged 1– 9 years (n¼1824), proxied by parental report that their child receives early intervention or special education services (EIS). National Health and Nutrition Examination Survey 1999–2000 data were analyzed and adjusted for survey design by Taylor Linearization using SAS version 9.1 software, with SAS callable SUDAAN version 9.0.1. The odds of receiving EIS were approximately nine times as great for vaccinated boys (n¼46) as for unvaccinated boys (n¼7), after adjustment for confounders. This study found statistically significant evidence to suggest that boys in United States who were vaccinated with the triple series Hepatitis B vaccine, during the time period in which vaccines were manufactured with thimerosal, were more susceptible to developmental disability than were unvaccinated boys.

The recent study on thimerosal and autism gives us a look at how the Hepatitis B vaccine might (or might not) be linked to autism. Exhibit 16.1 on page 82 of volume 2 of the technical report is a graph of HepB vaccine uptake among autistic children (AD) and non-autistic children (controls)

Here is that exhibit, showing the total number of vaccines (count) and amount of thimerosal (amt) for all vaccines and for HepB alone:

Price-HepBGraphs1-copy[1]

The top right graph shows the number of HepB vaccines for autistic kids (solid line) and non-autistic kids (dotted line). They are, to all intents and purposes, the same.

Take a look at the birth dose. Not every kid got it. Maybe about 1/2 got the birth dose at birth, and about 2/3 got it within the first few days.

If the birth dose of HepB caused autism to any significant degree, I would expect to see a higher percentage of autistic kids than non-autistic kids getting that shot. It just didn’t happen. Take a closer look at that graph:

Price-HepBGraphs2[1]

The same percentage of got the HepB shots–all 3 of them– as non-autistic kids.

Still wondering about that birth dose? Let’s zoom in on the graph:

Price-HepBGraphs3[1]

Those lines are right on top of each other.

The HepB hypothesis won’t go away. Just like the thimerosal hypothesis or the MMR hypothesis. Just today, Mark Blaxill and Dan Olmsted put out a very long post at the Age of Autism blog pushing the idea. They use the bad and worse studies from Thoughtful House on infant macaques to bolster their arguments.

The funny thing about evidence is, some people never accept it.

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.

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