…there’s still no link.
‘Neuropsychological Performance 10 Years After Immunization in Infancy With Thimerosal-Containing Vaccines‘ is a new study from Italy.
Nearly 70% of the invited subjects participated in the neuropsychological assessment (N = 1403). Among the 24 neuropsychological outcomes that were evaluated, only 2 were significantly associated with thimerosal exposure. Girls with higher thimerosal intake had lower mean scores in the finger-tapping test with the dominant hand and in the Boston Naming Test.
And here’s the conclusion from the penultimate page of the paper (excluding references):
No study conducted to date has been able to provide conclusive evidence of an effect of thimerosal on neuropsychological development. Final judgments regarding this association must rely on the entire body of results from studies conducted in different settings and with different levels of validity and on the coherence of results. The lack of consistency among the results of our study and other available studies suggests that an association between thimerosal exposure through vaccination in infancy and neuropsychological deficits is unlikely or clinically negligible. Additional data from populations with wider ranges of
exposure to thimerosal and additional neuropsychological assessments at older ages may help to clarify the issue of potential associations between thimerosal and neurodevelopmental outcomes.
Oh, and for the conspiracy theorists:
The authors have indicated they have no financial relationships relevant to this article to disclose.
I’m not an epidemiologist so I’m not going to attempt to go through the nuts and bolts of this paper. Hopefully those who have more expertise can go through yet again why this shows that thimerosal in vaccines seems to be about as dangerous as the average housefly. I can’t imagine they really want to. God knows I don’t. But the stupidniks will no doubt need the finer points hammered home again.
Can you sense I’m getting bored with this yet?
Left Brain Right Brain 
No Silly Billy! It was the Aluminum all along….
Just a comment on the “significant” associations in this study:
Following standard practice, the authors set the significance level at 5%, meaning that they accept that the results of 1 in 20 tests will seem “statistically significant” if there is in fact no difference between the tested groups.
If you do enough tests, you’ll find something that seems significant, due to chance alone. Tozzi et al. noted: “Because we did not correct for multiple comparisons in the statistical analyses, we expected to find . . . significant associations . . . as effects of chance.” Finger tapping speed might or might not be associated with thimerosal exposure, but tests of 78 parameters in this study should turn up about 4 findings that seem “significant” due to chance alone.
You might think of this in the context of the Wakefield “vaccine schedule” study with macaques: Perhaps Wakefield might not think of “color discrimination” as the first thing to test for in an autism-related study of primates, but he reported that exposure to vaccines was associated with a significant difference in that paramenter—although apparently many other tested parameters did not produce results that seemed significant. If you do enough tests, you’ll get a result that may seem “significant”. Or not.
BTW, here’s a direct link to the original article, which is currently freely available from Pediatrics:
http://pediatrics.aappublications.org/cgi/reprint/123/2/475
I believe that was pointed out in Orac’s take-down of that paper (conference abstract rather). Is it already published anywhere, BTW? It would be of interest to see how many tests were made.
The same type of result was obtained by Thompson et al. (2007), a much bigger thimerosal study. They made something like 370 measures, of which they found 19 in the range of significance. It was almost exactly what you’d expect by chance.
What an amazing study, comparing two groups who were exposed to thimerosal, each with different levels of thimerosal exposure, instead of comparing a group with no thimerosal exposure to a group with some thimerosal exposure. So reminiscent to me of those studies that claimed smoking doesn’t cause cancer, by comparing smokers who smoked different amounts of cigarettes a day.
Who cares who authored the study, when the CDC, who participated in the thimerosal cover up with their numerous conflicts of interest, actually funded this study, and that the study was published in Pediatrics-official journal of the American Academy of Pediatrics, which is funded by pharmaceutical companies.
Billy, billy, billy. If the study can be replicated, its independent. Do you understand why?
And I thought the anti-vaxxers liked to claim that _no_ amount of thimerosal was safe? Are you suggesting that we now have an established safe minimum amount?
@Billy: 2001 called; it wants its thimerosal hypothesis back.
The fact that you’re an anti-vaxer puts your other statements in perspective, you know.
I’m going to call bullshit on this one. Show me.
Epidemiological studies generally did show a connection between smoking and lung cancer. There obviously must be a dose-response relationship there.
“If the study can be replicated, its independent.” Kev, that doesn’t make any sense. If a faulty study is replicated, it’s still trash, no matter who comes up with it. There is no safe amount of thimerosal established, and there is no way you could think I claimed that from what I said.
Joseph, I’m not an anti-vaxer, I’m against mercury and other toxic substances. “Epidemiological studies generally did show a connection between smoking and lung cancer” Duh. I bet they didn’t do that without using a non-smoking control group.
The difference in thimerosal effects between low and high exposure levels, may not be as large as between a some exposure level and a no exposure level. No matter how many times the half-truths are told and no matter how long the distortions goes on, it doesn’t yield truth.
I didn’t find it when I searched online for that paper today, Joseph. Like you, I’m interested in the range of the parameters they examined.
Also BTW, some of the “significant” results (naming, finger-tapping) in the Thompson paper you mentioned happened to skew the other way: For example, higher exposure to thimerosal in early postnatal life improved finger tapping performance in boys!
So, Billy, did you find that citation about the studies on smoking?
No. If you look at some such studies you will see they are not simply comparisons of smokers and non-smokers. Some studies look at smokers only.
Trying to determine dose-reponse is a perfectly valid methodology, especially if there is really no way to find a matching control group that was completely unexposed.
That would be an observation of interest if this had been the first thimerosal study ever. There are much bigger individual-level studies that look at a wider range of exposures.
More importantly, about 180 micrograms of thimerosal were removed from the vaccine schedule and nothing happened. Seriously, how divorced with reality do you have to be to continue to give credence to the thimerosal hypothesis in this day and age?
Joseph, don’t be denying that there were phony studies to falsely disprove the smoking-cancer link. This study was not a dose-response study. Even the lead author of the study Dr. Tozzi said that comparing to children with no thimerosal exposure could have improved the study. I think there should also be consideration for the specific ages at which the doses of thimerosal were administered, and for how spaced out in time the doses were, instead of just the total thimerosal exposure that was attained at a certain age.
What about the thimerosal still in flu-vaccines that are even administered to pregnant women, and the mercury throughout the environment? What makes you think nothing happened? There’s no reliable evidence that any neurodevelopmental disorder decreased in prevalence after the removal of thimerosal from the vaccine schedule.
I don’t doubt that there might have been some studies that could not reject the null hypothesis. Strangely, even though this is a point the anti-vaxers always push, I haven’t seen the citations.
I would suggest it’s mostly an urban myth by the anti-vaxers that smoking studies were generally pointing toward the null hypothesis. My understanding is that epidemiology was always clear about a link, but animal studies were not. The Tobacco companies obviously preferred the animal studies.
There’s not as much thimerosal in available flu vaccines as you might have been led to believe, BTW.
Regardless, the fact remains that about 180 micrograms were removed from the childhood vaccination schedule. Do you dispute this? Either thimerosal in childhood vaccines does something or it doesn’t. It’s nonsensical to propose that thimerosal in childhood in vaccines is significant, but its removal is not, because some other effect (also made up) happened to mask it just so. We’re getting into the realm of magical thinking here.
Only the fact that I’ve looked at the data up and down. Formalization of what everyone can see in California data can be found in Schechter & Grether (2008).
You can also use common sense. If something had happened, it would’ve been noticed.
Why is there such frequent citation of California data? Why has nobody done a reliable updated study to determine recent autism rates, instead of just using that unreliable CDDS data? There’s no reliable evidence that rates are still increasing or that they haven’t decreased.
By saying that California data is unreliable, you create a catch-22 for yourself. Without California data and special education data, there wouldn’t be a thimerosal hypothesis, and there wouldn’t be any claims of an “autism epidemic.”
The anti-vaxers only started using this argument after the caseload failed to drop.
Additionally, it doesn’t matter if California undercounts autism, which it obviously does. The way undercounting works, you should still see an impact of thimerosal removal in the trend. Saying “California data is unreliable” is nothing but a quick excuse that is completely unconvincing and demonstrates lack of understanding of the problem.
California is not undercounting a whole lot these days either. Prevalence in the 3-5 cohort is already at 40 in 10,000, despite restrictions in California DDS admissions. This can only be taken as a lower bound. If we can tell anything from the data it’s that autism didn’t go away, obviously.
Finally, there are recent epidemiological studies of autism. Autism didn’t go away or decline or any nonsense of the sort. This should be obvious to anyone who doesn’t have their fingers in their ears.
“Saying “California data is unreliable” is nothing but a quick excuse that is completely unconvincing and demonstrates lack of understanding of the problem.”
Some would probably also call it “jumping on the Neurodiversity bandwagon” since, that argument was put forth by “the ND movement” years ago.
It’s true that “California data is unreliable” has been used as a quick excuse by both sides at one time or another. Note, however, that Autism Diva inquired about the data and was trying to understand it there. Trying to explain why the data is what it is is very different to just dismissing it with “it’s unreliable.”
I don’t think CDDS data should be used either to show an epidemic or a continuing rise in rates. Why should such bureaucratically controlled administrative data, which wasn’t designed to look for prevalence of something in the population, be used to answer the crucial question of whether autism rates went down or not after thimerosal removal?
I don’t think that all of the time varying things about this data set can be dealt with reliably, like changing guidelines for enrollment, changing practices in reporting cases in their records, and changing practices in removing inactive cases from their records.
How can the reported increasing prevalence shown among 3-5 year olds over time be trusted as accurate, considering that over time, the age of diagnosis may decline and the proportion of autistics in that age range who have a diagnosis can consequently go up?
I’m Italian, my english is very poor, but I hope you will understand me.
My son was vaccinated (in postmarketing phase) with the thimerosal containing vaccine of the mentioned pertussis clinical trial (Phase III) in the ’90, and now he suffers from an autistic disorder.
Just a comment on this study:
1- “‘Some limitations should be considered in the interpretation of our results […] Our analysis included only healthy children who were selected during enrollment in the original trial, and some families might have declined to participate in the present study because their children had cognitive developmental problems.”
If you exclude the sick children (or their familes do it themselves), only the healthy children remain.
2- “The authors have indicated they have no financial relationships relevant to this article to disclose.”
Tozzi, that is working now at Bambin Gesù Hospital, in the ’90 worked at Istituto Superiore di Sanità, with Stefania Salmaso (another author of the Pediatric’s publication).
Both were member of ‘Progetto Pertosse Working Group’, the working group of the mentioned DTaP clinical trial: they administered (not materially) the vaccines more than ten years ago. And to do that have received funds from
US NIAID and from vaccine manufacturers, and now they have received funds from CDC.
Today should tell us that the vaccines were not safe?
Who does control the controllers?
It’s very simple Billy. The thimerosal hypothesis is based on the assumption that the data is accurate. It is. Therefore, to falsify the hypothesis, you assume the data is accurate.
Of course these issues exist in the data, and I’d be the first to tell you that. This doesn’t mean the data doesn’t tell you anything. That’s nonsense. In fact, it’s very good data compared to that of other databases that are used all the time.
The data gives an approximate lower bound of ASD cases in California. Do you dispute this, and if so, why?
You are claiming that 40 in 10,000 kids in the 3-5 cohort of California DDS is not important to the thimerosal hypothesis. That’s absolutely ridiculous and shows you’re just making up excuses.
Why are any databases used? What does it matter if it shows a lower bound, when such lower bounds in previous recording periods may have been lower only due to other reasons other than actual lower prevalence rates? The data is either reliable or it’s not. I don’t think the data can accurately show prevalence patterns over time. My side of the debate isn’t the only one to have criticized this data. You can’t repudiate the data at one time, and at another time say it’s satisfactory when it shows what you want it to show. The analysis of this data doesn’t disprove the thimerosal hypothesis.
Seriously? So you’d invalidate all studies that use, say, psychiatric registries, hospital records, school records, special education records, annual surveys, etc.
Why keep records at all if they are useless according to Billy?
Let’s take the famous CDC phone survey on the prevalence of autism, which is widely cited. Do you think this has great strengths compared to California DDS ascertainment? I can think of a couple. But it mostly has weaknesses.
It matters because the lower bound is 40 in 10,000, which is high for a population that is below 5 and one that is not supposed to include Asperger’s and PDD-NOS. In other words, if this (minimum) prevalence is supposed to signify the existence of an autism epidemic, it’s clear that removal of thimerosal did nothing to reverse said epidemic.
Don’t come here pretending that it doesn’t matter. We’re not stupid.
Well, no. Data can be reliable for some things and not for others. This is the part that you either don’t get or pretend not to get as an excuse for a failed hypothesis.
For example, does the data tell me accurately how many people are receiving services from California DDS? It tells me this with full accuracy. Does it tell me how many autistic people total there are in California at different times? No, it does not have the power to tell me this. Does it give me a lower bound? Approximately, yes.
You mean like in my latest post where I “criticize the data” ? Except I don’t do that. I criticize the interpretation of the data. That’s very different. I’d argue that data in itself is not good or bad. The conclusions from the data, given its limitations, can be good or bad. From my very first analysis of California DDS I never criticized the data, though I’ve criticized lack of understanding and misuse of the data.
Geeez Joseph. I just read through this column of back-and-forths. What a mess. You’ve got a lot of patience.
Hey Billy. Has it ever occurred in this exchange that maybe, just maybe, you might be wrong, or don’t know what you’re talking about? Is that totally off the table in your mind? You are so sure you’ve got a grasp of the basic, remedial, fundamental concepts in this area that you feel you are fully qualified to discuss it? Because from an outside perspective, it looks to me that you are lacking in some basic understanding, on this topic, basic science, and how studies are designed/executed. But, hey, that’s just me.
If I was going back and forth with Joseph for this long on an issue, I’d take a break and do some research on my own….WAIT! Scratch that. You’ll probably go to your usual supply of ‘knowledge’ on the internet. Hey, here’s a tip…visit an academic library sometime and read up on these topics. I know…you have to go to a library (booo! Not fun like the computer.) But hey, the information is credible.
Just a friendly suggestion.
http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/docketDetail.jsp
Hit the ‘views’ to read the .pdf on this issue.
When are people going to get it? This horse is dead, decayed, buried…gone! It’s over. Move on!
Joseph, I doubt that the CDC phone survey could be any worse. That 40 in 10000 number hasn’t been reliably compared to previous numbers. No, the data’s interpretation is not reliable. Therefore if your side has previously repudiated the interpretation of the data for determining prevalence, you should not use it for the same type of interpretation unless you’re being deceptive. Period.
“For example, does the data tell me accurately how many people are receiving services from California DDS? It tells me this with full accuracy.” No way, it doesn’t even do that reliably. Who knows how many inactive cases of theirs haven’t been removed from their records at different times. Think about the differences in the numbers from different reporting years, due to changes in the reporting system, and not from changes in enrollment.
RJ, what does it matter? The data wasn’t designed by scientists. Since when are administrators qualified? Why can’t any decent epidemiological studies be done to determine prevalence, instead of relying on CDDS? I don’t think the CDDS study takes enough things into account, and shouldn’t overlook its limitations. Since Joseph is qualified enough to do an analysis, and admits the limitations of making interpretations from the data, why shouldn’t I make an assertion based on those same limitations? What makes you so right?
“What makes you so right?”
I was not claiming to be right and have not discussed the particulars of the topic…at all.
I was asking if you have considered the fact that your position may be lacking in credence and if you, in fact, truly understand the issues relevant to the discussion, because from what I’ve been reading, it seems not to be the case.
Sorry about the error. I copied this from Josephius at the Huffington Post RFK jr / Kirby rant:
http://www.regulations.gov/fdmspublic/component/fdmsSearchResult/fdms_docket_detail?d=FDA-2007-P-0232&docType=fdms_docket&returnUrl=http%3A%2F%2Fwww.regulations.gov%2Fsearch%2Fsearch_results.jsp
And selecting the .pdf relating to FDA-2007-P-0232-0004
“I was asking if you have considered the fact that your position may be lacking in credence”
RJ, maybe, because I’m not that knowledgeable about these things.
Fair enough. And that’s a respectable position, because we’re all at there at one point.
Asking good questions is a great way to become more knowledgeable.
Well, I can appreciate that Billy is not familiar with the history of the argument; otherwise, I could only presume that he’s being disingenuous.
I’m saying that because if things had turned out as David Kirby, JB Handley, Mark Blaxill, Ginger Taylor and the rest hoped, Billy would not be here saying that California DDS data is unreliable and should therefore be ignored. If there had been a clear drop in the 3-5 caseload, we would’ve had to accept that removal of thimerosal was the likely cause. David Kirby, Blaxill and the others would now be seen as visionaries of sorts (instead of cranks).
That’s a key point. The main proponents of the hypothesis always relied on the California DDS data. They proposed ways to falsify the hypothesis based on this data, which we accepted.
“Well, I can appreciate that Billy is not familiar with the history of the argument; otherwise, I could only presume that he’s being disingenuous.”
He IS being disigenuous.
As you’ll see in his ‘work’ on your blog.
David, what would you know about being sincere?
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