I normally am someone who doesn't like to post email correspondence. Usually, if someone takes the time to email me, it is of a personal matter or private matter, which the individual doesn't want aired out all over the interwebz. However, when that email constitutes a legal threat, even one as laughable as this one, then it's fair game to post it on my blog. So, here it is, ladies and gentlemen; my first legal threat from someone who really has no idea what Libel is.
I have been removed as an LBRB contributor after Olmsted made a completely vacuous legal threat:“Remove accusations of hoax by aoa and apologize within 24 hours or I will pursue all available remedies.” I wish to sue Dan Olmsted for libel for said threat, on the following grounds:
1. The reference to a “hoax by AoA” is itself a false accusation. I stated my opinion that AoA was reporting a story based on a forged document. I did not allege that any member of the AoA organization was responsible for a forgery. In fact, I suggested that the document’s creator was “an English-speaking author from the UK rather than the US”, which to my knowledge was not true of any of AoA’s core members. When some misunderstood the article as a direct allegation against AoA, I promptly made revisions and comments to clarify my position.
2. My efforts included 2 comments posted at Olmsted’s own article. The first stated in part that “I do not suspect you or anyone within your organization”. The second, in response to a comment by Craig Willoughby, stated in full: “I proposed that the document was a forgery. I never speculated on the identity of the forger, beyond proposing that it was someone from the UK. To claim that I ever accused anyone within AoA of forgery is LIBEL against me.” By AoA’s stated policies, Olmsted is “moderator” of his own articles and had sole discretion to allow my comment to appear, or at least to make a statement of his own acknowledging its substance. These comments never appeared. This will serve to establish that, where Olmsted may be said to have begun with legitimate cause for complaint, he refused to acknowledge and when given the opportunity actively obstructed my efforts to resolve the issue in “good faith” and in a timely manner. (MySocratesNote: I never said it was David Brown, aka Evil Possum who made the allegation. Here is the actual comment in it's entirety, along with a link to the article:
"I think it is hysterical how some of the Oraccolytes are clinging to the idea that this is some elaborate hoax that AoA has concocted in order to discredit this poor man. I've even seen them go as far as accusing AoA of faking the original document.The pathetic! It Burns!!")
3. Olmsted made his original threat without presenting any argument against my conclusions, offering any evidence or argument for the document’s authenticity, or even stating that he sincerely believed it to be authentic. He thus offered no reasonable grounds for me or LBRB to issue a correction, let alone “remove” the article from public view. Furthermore, his failure to comment directly on the issue of authenticity raises the question whether even he had full confidence in the “source” for his story.
4. A key article, written by Katherine Burgemeister and reposted at AoA under Olmsted’s own byline, made so many allegations clearly contradicted by the disputed document and/or independent records (most notably that ““Thorsen vanished in March 2009”, where the document said only that he “resigned his faculty position at Aarhus University” at that time, and even though I and others easily located ample documentation of his activities after that time) that it could credibly be argued to be a “hoax” (by its broadest usages including unintentional deception and self-deception, as in “`War of the Worlds’ hoax”) even if the document itself is accepted at face value.
5. Olmsted’s failure to correct or qualify a single one of Burgemeister’s unsubstantiated or clearly erroneous claims proves that at best he had not studied the document in any detail, and therefore was unqualified to make any comment on its authenticity. The only alternative is that he chose to repost Burgemeister’s article uncritically, despite full knowledge that it contained many errors, and therefore is guilty (conceivably even more than Burgemeister) of knowingly promoting falsehood.
(MySoctatesNote: The previous statements are grounds for Libel? And, I do believe the story was corroberated by the CDC and several different news sources, wasn't it? Ah, but only David Brown has his story correct.)
6. Olmsted had personal motive to use a heavy-handed response to this article as a means to seek to limit the circulation of other works by me, including an LBRB post in which I showed that Olmsted exaggerated a vaccine inventor’s income from a patent by 500% based mainly on documents which were clearly dated before that patent existed. Since my removal as an LBRB contributor, this work and others making well-substantiated complaints and criticisms against AoA have no longer been visible there, giving Olmsted something he had reason to desire but was in no position to achieve by honest and direct argument. (MySocratesNote: Oh, the horror!! Everyone is out to get him! Dan is teh bad ebil person who is trying to prevent the troof from coming out!!)
7. Writing is my sole source of actual and potential income. Making free contributions to others’ sites is my sole means of promoting works from which I can receive income. By causing or contributing to my removal as a contributor to Left Brain/ Right Brain, Olmsted’s substantially false complaint has significantly damaged my potential to support myself, and thus satisfies the definition of “libel”. (MySocratesNote: And yet, he offers no real evidence of how Dan's complaint is false. He has failed to really offer any valid reason for libel. And if this is his sole means of income? Well, I'm sorry, but he needs to find a real job)
8. Olmsted and other AoA staff have on many previous occasions censored my comments, referenced my work inaccurately and without “credit”, and referred to me pejoratively. I consider some of these prior instances sufficient to justify legal action in and of themselves, if the resources had been available. This will serve to establish that this complaint is only my most serious against Olmsted and his organization. Furthermore, I offer this as evidence that I cannot disregard Olmsted and his allies as a threat to my future livelihood: If I do not take action now to establish as a matter of undisputed, public record that Olmsted’s complaint against me was spurious and that what he reported was in fact false on many levels, said complaint could be reused against me at a future time. (MySocratesNote: *Sniffle Sniffle* They're making fun of poor wittle David? Waaaaaaahhh!!!! Notice how he offers no evidence of said pejorative comments.)
At the present time, I have no fiscal resources to pursue such an action. I request donations and/or other assistance that others can offer this matter. I will freely forego such an action now or in the future if Age of Autism publishes a post making the following admissions:
i. Statements by Olmsted, Craig Willoughby and others to the effect that I had accused AoA of creating a forgery were in error. (MySocratesNote: Be specific now, David....where did I accuse you of making the claim that AoA made a forgery? Lawyers and judges like specifics)
ii. As of end March 2010, representatives of Aarhus University had neither confirmed nor denied the authenticity of the disputed document. (MySocratesNote: In the case of a criminal investigation, that is entirely in their right and best interests)
iii. The statement that Aarhus “appears only to have been made available today to the media” was unsubstantiated, as the full contents of the document were not carried by mainstream media prior to its distribution by the anti-vaccine movement. (MySocratesNote: Except from the Copenhagen Press....which is a media outlet)
iv. Statements that Thorsen “disappeared” on March 2009 or at any other time were in error, as the document stated only that he “resigned his faculty position at Aarhus University” at that time, and his regular appearances and communications (if not his exact, current place(s) of residence) can be documented from public information up to at least March 16, 2010. (MySocratesNote: No, they said he resigned his position at Aarhus University in March of 2009 (link here))
v. The initial identification of Thorsen as a suspect, prior to a confirming statement on March 10 from the US CDC, was based on descriptions of an unidentified suspect in the Danish media. Those who identified Thorsen on these grounds, without qualifying that the suspect was unnamed in primary sources, acted inappropriately. (MySocratesNote: How so? The statement was true, was it not?)
vi. The statement that Aarhus “`expressly prohibited' Dr Poul Thorsen from working for a second university, Emory” was unsubstantiated, as the relevant passage in the document refers to “double Full-time employment “ as the subject of a dispute. It is reasonably clear that it is not being claimed that Thorsen was forbidden from being employed at all by Emory. It was also highly improbable, given that simultaneous employment at multiple institutions as “adjunct faculty” is a pervasive practice, and Aarhus openly records current employment of others such as Albert Gjedde, Martin Kussman and Henrik J. Andersen as “adjunct faculty”. (MySocratesNote: Evidence?)
vii. The statement that “(t)he double role of Thorsen came to light after the university detected a shortfall in funding” was unsubstantiated and probably in error, as the document makes no statement to this effect. (MySocratesNote: So, the document was their only source of information about this? Wow)
viii. The statement that “(t)he revelation that Thorsen had a second secret job will raise fears of a hidden bias in the studies and undermine the scientific case for thiomersal" was in error. His employment at Emory was not secret, as he was openly listed among Emory faculty, and the Aarhus document makes no statement to the effect that his employment there was ever wholly unknown to the university. It did not constitute a “conflict of interest” related to vaccination, because Emory University does not manufacture vaccines. It was irrelevant to his paper on thimerosal, because that paper was published 5 years before he became an emory employee. (MySocratesNote: The Danish publication Politiken reported [in translation]: “'He is no longer employed at Emory. He was part time occupied at the department of epidemiological research from 2003 and from April 2008 to June 2009 as full time research professor' informs assistant vice director at Emory University Sarah E. Goodwin." When was the Thimerosal study done again? 2003?)
ix. The statement that Thorsen “continued to pass himself off as the head of the international project” is unsubstantiated, as the document only states that he “has continued to act in such a manner as to create the impression that he still retains a connection to Aarhus University after the termination of his employment by the university”. The document’s allegation appears to be itself in error (at least for the document’s given date), as Thorsen’s biography as of January 22, 2010 indicates that his employment at Aarhus ended in 2008.
x. The statement that Thorsen “was an author along with Kreesten Madsen of a key study that used data from Danish children to show that there was no link between mercury” was in error. This study was published in 2003, and had five additional coauthors. (MySocratesNote: Is AN AUTHOR. Doesn't that make him a co-author? So, how is this in error again?)
xi. Statements that Thorsen “absconded with $2 million” are unsubstantiated and probably in error, as the relevant document mentions only “advances” of an unspecified amount on grants for that total amount, makes no allegation that Thorsen took or spent any amount of money for his personal use, and makes no reference to a discrepancy between the money given and recorded spending on research that would justify such an allegation. (MySocratesNote: This claim by David is unsubstatiated. The CDC has confirmed the missing $2 million)
xii. The statement that data in an email by Dianne Simpson showed “a clear, linear relationship between the increase in vaccination rates (from 50.9% to 75.7%) and the number of autism cases per year (from 176 to 1182, a 6.7x increase) between 1980-1994...” These data actually show an exponential rise in autism diagnoses, compared to fluctuations and some linear increase in vaccination rates. The data also show the trend in autism diagnoses continuing if not accelerating in ca. 1990, as low-thimerosal or thimerosal-free DTaP vaccines became increasingly available. (MySocratesNote: Heh.....heh heh...BWAHHAHAHHAHAHA!!!!! Oh my....oh my goodness...stomach hurts!)
Now, I understand that, allegedly, David has Asperger's Syndrome (likely self diagnosed). Some of you may think that my criticism of this letter is cruel because of this. No, I am treating this letter with all of the scorn and derision it deserves because this is nothing but the petty foot stomping of a spoiled child. If he thinks that some of the things said about him by Olmsted and Handley were cruel, then he needs to pony up and offer examples.
Wednesday, April 7, 2010
Monday, April 5, 2010
Novella Gets it Wrong Big Time, part deux
Again, I would like to take the time to thank our guest blogger, Schwartz, for his time and effort in taking down Novella's shameful display of ignorance. Schwartz, I do hope to see more of your writing here. Thank you again! -MySocratesNote
In Part I of this series, we examined an interaction between Dr. Novella, and Mr. JB Handley regarding a new study on Autism. You can re-read the exchange here, here and here
The study being discussed is A Prospective Study of the Emergence of Early Behavioral Signs of Autism.
In the first segment we went through Dr. Novella’s last post and examined in detail his arguments. A close examination reveals almost all of them to be light in evidence and logic, and heavy in biased or erroneous opinion.
In this second segment, we’re going to drill in a lot deeper into the cornerstone of Novella’s primary argument and the unsupported assumptions his arguments all hinge on.
Let’s start with looking back at Novella’s key point in his final conclusion:
In the end, all that matters is the science, which clearly shows that there is no association between vaccines and autism. This one study has minimal implications for an alleged connection, except that it clears the most often implicated vaccine – MMR. It also supports other evidence that the onset of autism is earlier than many parents observe and much earlier than formal diagnosis, which calls into question any casual observations about the timing of onset to any potential triggers.
All of these conclusions rest primarily on one key assumption which is repeated by Novella throughout his opinion pieces.
As we now know, from multiple studies, true clinical onset (biological onset is likely earlier) is between 6 and 12 months.
I noted in the first segment that this assertion was unreferenced by Novella. This is certainly true in the second segment of the series which we looked at. When we look through the whole series, Novella’s hypothesis changes a bit over time and he discusses it in more detail in prior postings. Let’s review some segments from his first piece:
Retrospective studies, largely involving review of home movies, have suggested that autism can be diagnosed as early as 6-12 months,…
...
But what these results indicate is that clear signs of autism emerge between 6 and 12 months of age.
In this segment, he provides some references which we’ll go through a bit later.
Prior studies using home movies have shown that signs of autism can be detected between 8-12 months. A study looking at head circumference found statistical differences prior to 12 months. And one study looking at movements found differences between 4-6 months. So it seems the consensus of current evidence is that objective and detectable signs of autism emerge between 6-12 months. This study does not support detection prior to 6 months, but other studies do suggest this might be possible.
...
The true onset of autism in most ASD children likely began a year or two prior to the vaccines that are blamed as the cause.
...
The current study adds nicely to the growing consensus that the true clinical onset of ASD is between 6 and 12 months of age.
This shows an interesting progression:
* He starts out with suggesting that autism can be diagnosed as early as 6 months.
* Then we have clear signs emerging between 6-12 months.
* a couple more studies later (which we’ll examine in more detail later) and suddenly we have a consensus that detectable signs of Autism emerge between 6-12 months
* all of a sudden true clinical onset is most likely in the first year of life
* now we have a growing consensus that the true clinical onset is between 6-12 months
In the second segment we see:
As we now know, from multiple studies, true clinical onset (biological onset is likely earlier) is between 6 and 12 months.
...
Now we know the age of clinical onset is between 6 and 12 months…
He has now progressed to definitive onset being known without any further evidence: “The true clinical onset is known to be between 6-12 months.”
I’m going to point out and list the assumptions inherent in Novella’s assertion. Our astute readers will already realize Novella’s assertion is really a hypothesis, and infers the following assumptions:
1. There is a consensus about the age of the clinical onset of Autism
2. The “consensus” has changed from some earlier consensus or lack of consensus
3. The clinical onset of autism is consistent within a narrow range of 6-12 months
4. The onset is early and uniform, consistent with genetic causes
Keep these in mind as we review the evidence that Novella is using and ignoring to form his opinion.
After the current study under question, Novella’s first reference is his own opinion piece here.
Once you stop laughing, I’ve done the work for everyone and linked and summarized a couple of the studies his older opinion piece references.
Rate of Head Circumference Growth as a Function of Autism Diagnosis and History of Autistic Regression.
Summary of study findings:
* retrospective study of 28 boys with ASD and 8 with developmental delay
* measured the rate of growth of head circumference and compared to reference population data published by CDC
* in 60% of the autistic boys, they had accelerated growth prior to the onset of the symptoms of autism (7-10 months old)
* in the children who’s parents reported regression the results were similar – unknown if the sample size here was large enough to allow those results to be considered significant
This small study noted that in children that were ultimately diagnosed with ASD, there were biological differences from the general population at 7-10 months of age. However, these differences were not coincident with the onset of Autism as described by the studies authors in the conclusion:
Findings from this study suggest that the aberrant growth is present in the first year of life and precedes the onset and diagnosis in children with autism spectrum disorder with and without a history of autistic regression.
Summary of conclusions:
* identifies possible predictors of future onset of ASD
* does not suggest the onset of autism is coincident with accelerated head growth
* does not suggest an onset of Autism prior to 12 months of age
* suggests that head growth is similar in regressive vs non-regressive Autism
* despite significant differences, the results were not overly consistent or homogenous (60% with a small sample size)
Novella is implying that observed correlation of increased head circumference growth is coincident with the onset of Autism and thus it supports his assertion that the “true onset” of Autism is earlier than the reported onset of actual ASD symptoms. This study in no way suggests that increased head circumference growth causes or is equivalent to the onset of Autism.
Novella refers to some studies that looked at home videos and found some possible signs of autism as early as 12 months, but the link is broken. At any rate from his own description, these do not support a “true onset” from between 6-12 months of age.
The next study is from Philip Teitelbaum:
Movement analysis in infancy may be useful for early diagnosis of autism
Summary of study findings:
* retrospective study of 17 children diagnosed with Autism
* they found detectable movement disorders in all of the children including some issues visible at birth
* a wide range of different movement issues occurring at different ages were discussed
* based on 17 cases, the authors suggest that their diagnostics procedures could be used to provide an earlier diagnosis of autism
This is a very interesting study as they research a number of infant movements is explicit detail and find problems in each of their test cases and in some of the cases, very early ages. Here as well, we find a leap of assumption by the study authors similar to that of Novella:
Furthermore, because these movement disorders always could be detected with our methods as early as 4–6 months of age and sometimes as early as the first few days after birth, we suggest that the study of movement disorders in infancy may serve as an earlier indicator than presently available methods for diagnosing autism in children.
That wording is pretty bold as they state it can be used to diagnose Autism at such a young age. However, when we read on, it is tempered by a later discussion (emphasis mine):
The fact that such early diagnosis is possible now highlights the need for the development of earlier therapies that will be effective in the treatment of potentially autistic children. Because diagnosis was not generally possible so early, no systematic methods are currently available for the treatment of infants at risk for autism. Our findings should provide the impetus for systematic search for such treatment methods.
Yet another quote:
By combining movement analysis in infancy with MRI analysis, it may be possible eventually to diagnose differential areas of brain involvement in different subtypes of autism.
Novella has clearly focused on the text that supports what he seems to desperately want to believe: biological onset of autism occurs in the first months of life and pre-determined by genetics. Although Teitelbaum suggests this in one section, the bulk of the discussion appropriately limits the scope of his conclusions.
This study was published in 1998 and there was a single follow-up in 2004:
Eshkol-Wachman movement notation in diagnosis: The early detection of Asperger’s syndrome.
In this study, they find similar results as the first.
In the present article, using Eshkol–Wachman movement notation, we present evidence that abnormal movement patterns can be detected in AS in infancy. This finding suggests that AS can be diagnosed very early, independent of the presence of language. As shown earlier by us, almost all of the movement disturbances in autism can be interpreted as infantile reflexes “gone astray”; i.e., some reflexes are not inhibited at the appropriate age in development, whereas others fail to appear when they should. This phenomenon appears to apply to AS as well. Based on preliminary results, a simple test using one such reflex is proposed for the early detection of a subgroup of children with AS or autism.
Again, we get some strong but ultimately conflicting language. A few more observations come to mind here. This research is quite old, and yet, there has been no follow-up to validate these findings in a prospective, or larger study. I’ll also note that these studies were published in PNAS. Although it is peer-reviewed, they allow member authors to select their own referees and manage the referee process. This may explain the conflicting and sometimes overreaching statements. I also found it interesting to note that the members of second study group were recruited personally by the authors at conferences, the internet, and through advertisements.
Study Conclusions:
* the authors find a correlation between autistic children and detectable movement disorders in some cases at an early age
* sample size is very small – 17 children
* the results do not support a uniform or consistent onset of symptoms
* the use of these finding as a diagnostic tool is untested despite the results being quite old
Unfortunately, the sample size is very small, so leaping to any conclusions regarding the “true onset” of autism is clearly premature.
In this opinion piece Novella makes the following statement based on the first two studies we just looked at:
Taken together there is copious evidence that autism is a primarily genetic disorder that is present at birth, with subtle but increasing signs that separate ASD children from non-ASD children as they age.
I’ll just note quickly, that in the comments on Novellas blog we see a familiar pattern: Novella hasn’t even read the original study. In fact, he doesn’t even link to it, he just links a press release. I’m curious how anyone – let alone a scientist – can consider two retrospective investigations of a total of 45 children copious amounts of evidence of anything.
(A side note: it is not lost on me that the original Wakefield Lancet study was a retrospective case study with a small number of cases and a key criticism is that the cases were recruited by the doctors…)
I’m also unclear what evidence is presented here to indicate that Autism is genetic in nature or that the onset actually occurs when some of these early signs are present. The only way to draw a genetic conclusion based on these studies is to assume that the early biological signs and movement disorders found in the first months of life are caused primarily by genetic defects. His assumption of early onset of Autism implies that the biological cause of autism is present and also causing the early signs observed in these two studies.
There is no evidence in either of these studies to support that hypothesis as they are only noting a correlation in a very small retrospective sample. Without a prospective study of a larger size, that conclusion is a giant leap of faith, unless you assume that the cause is genetic. Of course in that case, Novellas argument now looks circular because he uses these assumptions to state that the “true onset” of Autism is uniform and in the early years of life consistent with genetic disorders.
Early and fairly uniform onset is consistent with genetic causes of ASD, rather than environmental causes.
These studies do not provide any evidence of uniformity in timing or signs and symptoms.
Let’s get back to the study that started the whole series.
A Prospective Study of the Emergence of Early Behavioral Signs of Autism
In an editorial in the same journal (Journal of the American Academy of Child & Adolescent Psychiatry), Tony Charman, PhD discusses the study:
To date, less than a handful of studies have reported in terms of early signs that predict autism outcomes. The study by Ozonoff and colleagues [1] is the first to do so on a sample as large as 25 siblings who went on to receive an autism spectrum (ASD) diagnosis at 36 months.
On one side we’ve got Novella throwing around “copious” amounts of evidence and from the expert we have a handful of small retrospective studies.
From the study itself (Ozonoff et al) we see they talk about conflicting evidence from different patterns of the onset of autism:
Recently, the adequacy of a dichotomous classification of onset has been questioned,17 based on emerging results from studies that provide evidence of other onset patterns. Some parents report that their child displayed neither early signs of autism nor regression, a phenomenon that has been called developmental plateau17,18 or stagnation.19 Other studies have found evidence of both early signs of ASD and regression simultaneously present in the retrospective histories of children with ASD.9,11,12,20
The introduction of this study discusses the various onset patterns in autism and references no less than 20 different studies. Apparently Novella must have skipped or missed this part of the study because it’s pretty clear right from the introduction that there is no consensus on the question of onset of Autism(s), let alone “true clinical onset”. In fact, many of the different Autisms are classified by the differing timings of actual onset. There is certainly no evidence of uniformity. The authors confirm this in the discussion section and even diverge from the traditional classifications of the Autisms:
The present findings suggest that existing definitions of onset patterns will need to undergo further development. One possibility is that we need to expand the number of categories used to describe onset. For example, perhaps there are four rather than two categories of onset, including groups characterized by developmental plateaus and by mixed features of early symptoms plus later regression, as we have suggested elsewhere. 17 The prospective data acquired in the present investigation suggest another possibility, however. We hypothesize that symptom emergence may better be considered dimensionally, as a continuum characterized by the amount and timing of regression.
They are not describing consensus at all. In fact there is little consensus in the prevailing classifications and these authors are suggesting yet another point of view. However, this point of view is not consistent with Novella’s assumption of uniformity of onset. That is clear in the following quote:
In this conceptualization, at one end of the continuum lie children who display loss of social interest so early that the regression is difficult to see and symptoms appear to have always been present. At the other end of the continuum lie children who experience losses of social interest and communication skills so late that the regression appears quite dramatic.
So this study has already torpedoed two of Novella’s key assumptions, let’s tackle the “true clinical onset” at 6-12 months assumption. Looking at the abstract we see the following in the results:
Group differences were significant by 12 months of age on most variables.
The fact that significant differences were noticed at 12 months does not imply uniformity and is not evidence that the “true clinical onset” is uniform and occurs between 6 and 12 months. Reading the conclusions from the abstract:
These results suggest that behavioral signs of autism are not present at birth, as once suggested by Kanner, but emerge over time through a process of diminishment of key social communication behaviors.
The authors specifically avoid listing a timeline and that is consistent with the discussion we reviewed above. It appears that Novella might have gotten one assumption right: that the old consensus – genetic disorder present at birth as per Kanner – is no longer considered valid. If we go back to Tony Charman we see he also makes another important note when it comes to old preconceptions:
Ozonoff et al. suggest that regression might be the norm and not the exception in autism. A similar suggestion was recently made by Pickles et al.8 based on retrospective parental report. They found not only that regression was very specific to autism, as it was almost never found in children with language impairment without autism, but also a strong association between age of first words and likelihood of undergoing regression. That is, frank loss of language skills was associated with switching from the most advanced early language to being among the slowest (in terms of eventual onset of phrase speech).
He implies that Autism is unique compared to other developmental disorders involving language impairment. At first blush, that doesn’t seem consistent with uniform genetic disorders. He goes on:
We do not know what the nature and causes are of the neurodevelopmental perturbations that underlie regression but the existence of such “high-risk” prospective studies offers an opportunity to investigate these questions.
This pretty much puts the nail in the coffin of Novellas hypothesis masquerading as fact. Without knowing the causes or the nature of the neurodevelopment signs we’re seeing at a young age in some children, we can’t know whether they are genetically caused or whether they’re predictive of an autism diagnosis later in life.
Dr. Charman closes with this statement:
Ten years ago, the prospective study of the emergence of early or even prodromal signs of autism would not have been considered possible or practicable. These two studies exemplify the new science of “autism in infancy.”
The real Autism scientists are talking about small new groundbreaking Autism science in it’s “infancy” and the “scientist” Novella is spewing opinion about copious amounts of evidence and a conclusive understanding of the “true” clinical onset from genetic causes.
Conclusion:
In this segment, we investigate in detail the cornerstone of Novella’s argument against vaccine causation and for the genetic causation of Autism. Not surprisingly, we find it completely unsupported by the evidence he provides. Even worse, most of his implicit assumptions contradict the evidence he references.
Walking through his arguments which move from a “suggestion of early signs” to a conclusive statement of “true clinical onset” of autism reveals that his interpretation of the evidence and application of logical arguments is seriously compromised. It is bordering on nonsensical. It appears he makes his definitive statements based on a few select lines from study abstracts and press releases. From this “selective hearing” – my apologies to Alan Golding and his video about Brian Deer – he makes giant leaps of assumption and produces what he and Gorski consider “scientific reference” material for doctors.
It certainly doesn’t take a degree in Neurology to understand the scope of these small case studies. If Novella makes so many errors of interpretation and leaps of assumption in these simple cases, it makes me question what he and Gorski are doing when they look into the far more complex epidemiology studies that form the basis of his vaccine safety arguments.
I can’t decide which of his bias’ he is so desperately trying to protect: the quickly dying idea that Autism is purely genetic or the idea that vaccines have no part in the autistic regression of many children. Perhaps if he declared his conflicts of interest, we would gain some insight into the true source of his bias?
I found a lot of details that have interesting implications when reading these studies. They point to a large variance in onset and early signs and symptoms which leads us farther away from a pure genetic cause and explains why there is a growing consensus that environmental influences have a key role to play in the causation of Autism. This new information certainly does not exonerate vaccines or MMR.
Perhaps I’ll write a third segment pointing some of my observations of the science.
Potential Conflicts of Interest: None
In Part I of this series, we examined an interaction between Dr. Novella, and Mr. JB Handley regarding a new study on Autism. You can re-read the exchange here, here and here
The study being discussed is A Prospective Study of the Emergence of Early Behavioral Signs of Autism.
In the first segment we went through Dr. Novella’s last post and examined in detail his arguments. A close examination reveals almost all of them to be light in evidence and logic, and heavy in biased or erroneous opinion.
In this second segment, we’re going to drill in a lot deeper into the cornerstone of Novella’s primary argument and the unsupported assumptions his arguments all hinge on.
Let’s start with looking back at Novella’s key point in his final conclusion:
In the end, all that matters is the science, which clearly shows that there is no association between vaccines and autism. This one study has minimal implications for an alleged connection, except that it clears the most often implicated vaccine – MMR. It also supports other evidence that the onset of autism is earlier than many parents observe and much earlier than formal diagnosis, which calls into question any casual observations about the timing of onset to any potential triggers.
All of these conclusions rest primarily on one key assumption which is repeated by Novella throughout his opinion pieces.
As we now know, from multiple studies, true clinical onset (biological onset is likely earlier) is between 6 and 12 months.
I noted in the first segment that this assertion was unreferenced by Novella. This is certainly true in the second segment of the series which we looked at. When we look through the whole series, Novella’s hypothesis changes a bit over time and he discusses it in more detail in prior postings. Let’s review some segments from his first piece:
Retrospective studies, largely involving review of home movies, have suggested that autism can be diagnosed as early as 6-12 months,…
...
But what these results indicate is that clear signs of autism emerge between 6 and 12 months of age.
In this segment, he provides some references which we’ll go through a bit later.
Prior studies using home movies have shown that signs of autism can be detected between 8-12 months. A study looking at head circumference found statistical differences prior to 12 months. And one study looking at movements found differences between 4-6 months. So it seems the consensus of current evidence is that objective and detectable signs of autism emerge between 6-12 months. This study does not support detection prior to 6 months, but other studies do suggest this might be possible.
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The true onset of autism in most ASD children likely began a year or two prior to the vaccines that are blamed as the cause.
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The current study adds nicely to the growing consensus that the true clinical onset of ASD is between 6 and 12 months of age.
This shows an interesting progression:
* He starts out with suggesting that autism can be diagnosed as early as 6 months.
* Then we have clear signs emerging between 6-12 months.
* a couple more studies later (which we’ll examine in more detail later) and suddenly we have a consensus that detectable signs of Autism emerge between 6-12 months
* all of a sudden true clinical onset is most likely in the first year of life
* now we have a growing consensus that the true clinical onset is between 6-12 months
In the second segment we see:
As we now know, from multiple studies, true clinical onset (biological onset is likely earlier) is between 6 and 12 months.
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Now we know the age of clinical onset is between 6 and 12 months…
He has now progressed to definitive onset being known without any further evidence: “The true clinical onset is known to be between 6-12 months.”
I’m going to point out and list the assumptions inherent in Novella’s assertion. Our astute readers will already realize Novella’s assertion is really a hypothesis, and infers the following assumptions:
1. There is a consensus about the age of the clinical onset of Autism
2. The “consensus” has changed from some earlier consensus or lack of consensus
3. The clinical onset of autism is consistent within a narrow range of 6-12 months
4. The onset is early and uniform, consistent with genetic causes
Keep these in mind as we review the evidence that Novella is using and ignoring to form his opinion.
After the current study under question, Novella’s first reference is his own opinion piece here.
Once you stop laughing, I’ve done the work for everyone and linked and summarized a couple of the studies his older opinion piece references.
Rate of Head Circumference Growth as a Function of Autism Diagnosis and History of Autistic Regression.
Summary of study findings:
* retrospective study of 28 boys with ASD and 8 with developmental delay
* measured the rate of growth of head circumference and compared to reference population data published by CDC
* in 60% of the autistic boys, they had accelerated growth prior to the onset of the symptoms of autism (7-10 months old)
* in the children who’s parents reported regression the results were similar – unknown if the sample size here was large enough to allow those results to be considered significant
This small study noted that in children that were ultimately diagnosed with ASD, there were biological differences from the general population at 7-10 months of age. However, these differences were not coincident with the onset of Autism as described by the studies authors in the conclusion:
Findings from this study suggest that the aberrant growth is present in the first year of life and precedes the onset and diagnosis in children with autism spectrum disorder with and without a history of autistic regression.
Summary of conclusions:
* identifies possible predictors of future onset of ASD
* does not suggest the onset of autism is coincident with accelerated head growth
* does not suggest an onset of Autism prior to 12 months of age
* suggests that head growth is similar in regressive vs non-regressive Autism
* despite significant differences, the results were not overly consistent or homogenous (60% with a small sample size)
Novella is implying that observed correlation of increased head circumference growth is coincident with the onset of Autism and thus it supports his assertion that the “true onset” of Autism is earlier than the reported onset of actual ASD symptoms. This study in no way suggests that increased head circumference growth causes or is equivalent to the onset of Autism.
Novella refers to some studies that looked at home videos and found some possible signs of autism as early as 12 months, but the link is broken. At any rate from his own description, these do not support a “true onset” from between 6-12 months of age.
The next study is from Philip Teitelbaum:
Movement analysis in infancy may be useful for early diagnosis of autism
Summary of study findings:
* retrospective study of 17 children diagnosed with Autism
* they found detectable movement disorders in all of the children including some issues visible at birth
* a wide range of different movement issues occurring at different ages were discussed
* based on 17 cases, the authors suggest that their diagnostics procedures could be used to provide an earlier diagnosis of autism
This is a very interesting study as they research a number of infant movements is explicit detail and find problems in each of their test cases and in some of the cases, very early ages. Here as well, we find a leap of assumption by the study authors similar to that of Novella:
Furthermore, because these movement disorders always could be detected with our methods as early as 4–6 months of age and sometimes as early as the first few days after birth, we suggest that the study of movement disorders in infancy may serve as an earlier indicator than presently available methods for diagnosing autism in children.
That wording is pretty bold as they state it can be used to diagnose Autism at such a young age. However, when we read on, it is tempered by a later discussion (emphasis mine):
The fact that such early diagnosis is possible now highlights the need for the development of earlier therapies that will be effective in the treatment of potentially autistic children. Because diagnosis was not generally possible so early, no systematic methods are currently available for the treatment of infants at risk for autism. Our findings should provide the impetus for systematic search for such treatment methods.
Yet another quote:
By combining movement analysis in infancy with MRI analysis, it may be possible eventually to diagnose differential areas of brain involvement in different subtypes of autism.
Novella has clearly focused on the text that supports what he seems to desperately want to believe: biological onset of autism occurs in the first months of life and pre-determined by genetics. Although Teitelbaum suggests this in one section, the bulk of the discussion appropriately limits the scope of his conclusions.
This study was published in 1998 and there was a single follow-up in 2004:
Eshkol-Wachman movement notation in diagnosis: The early detection of Asperger’s syndrome.
In this study, they find similar results as the first.
In the present article, using Eshkol–Wachman movement notation, we present evidence that abnormal movement patterns can be detected in AS in infancy. This finding suggests that AS can be diagnosed very early, independent of the presence of language. As shown earlier by us, almost all of the movement disturbances in autism can be interpreted as infantile reflexes “gone astray”; i.e., some reflexes are not inhibited at the appropriate age in development, whereas others fail to appear when they should. This phenomenon appears to apply to AS as well. Based on preliminary results, a simple test using one such reflex is proposed for the early detection of a subgroup of children with AS or autism.
Again, we get some strong but ultimately conflicting language. A few more observations come to mind here. This research is quite old, and yet, there has been no follow-up to validate these findings in a prospective, or larger study. I’ll also note that these studies were published in PNAS. Although it is peer-reviewed, they allow member authors to select their own referees and manage the referee process. This may explain the conflicting and sometimes overreaching statements. I also found it interesting to note that the members of second study group were recruited personally by the authors at conferences, the internet, and through advertisements.
Study Conclusions:
* the authors find a correlation between autistic children and detectable movement disorders in some cases at an early age
* sample size is very small – 17 children
* the results do not support a uniform or consistent onset of symptoms
* the use of these finding as a diagnostic tool is untested despite the results being quite old
Unfortunately, the sample size is very small, so leaping to any conclusions regarding the “true onset” of autism is clearly premature.
In this opinion piece Novella makes the following statement based on the first two studies we just looked at:
Taken together there is copious evidence that autism is a primarily genetic disorder that is present at birth, with subtle but increasing signs that separate ASD children from non-ASD children as they age.
I’ll just note quickly, that in the comments on Novellas blog we see a familiar pattern: Novella hasn’t even read the original study. In fact, he doesn’t even link to it, he just links a press release. I’m curious how anyone – let alone a scientist – can consider two retrospective investigations of a total of 45 children copious amounts of evidence of anything.
(A side note: it is not lost on me that the original Wakefield Lancet study was a retrospective case study with a small number of cases and a key criticism is that the cases were recruited by the doctors…)
I’m also unclear what evidence is presented here to indicate that Autism is genetic in nature or that the onset actually occurs when some of these early signs are present. The only way to draw a genetic conclusion based on these studies is to assume that the early biological signs and movement disorders found in the first months of life are caused primarily by genetic defects. His assumption of early onset of Autism implies that the biological cause of autism is present and also causing the early signs observed in these two studies.
There is no evidence in either of these studies to support that hypothesis as they are only noting a correlation in a very small retrospective sample. Without a prospective study of a larger size, that conclusion is a giant leap of faith, unless you assume that the cause is genetic. Of course in that case, Novellas argument now looks circular because he uses these assumptions to state that the “true onset” of Autism is uniform and in the early years of life consistent with genetic disorders.
Early and fairly uniform onset is consistent with genetic causes of ASD, rather than environmental causes.
These studies do not provide any evidence of uniformity in timing or signs and symptoms.
Let’s get back to the study that started the whole series.
A Prospective Study of the Emergence of Early Behavioral Signs of Autism
In an editorial in the same journal (Journal of the American Academy of Child & Adolescent Psychiatry), Tony Charman, PhD discusses the study:
To date, less than a handful of studies have reported in terms of early signs that predict autism outcomes. The study by Ozonoff and colleagues [1] is the first to do so on a sample as large as 25 siblings who went on to receive an autism spectrum (ASD) diagnosis at 36 months.
On one side we’ve got Novella throwing around “copious” amounts of evidence and from the expert we have a handful of small retrospective studies.
From the study itself (Ozonoff et al) we see they talk about conflicting evidence from different patterns of the onset of autism:
Recently, the adequacy of a dichotomous classification of onset has been questioned,17 based on emerging results from studies that provide evidence of other onset patterns. Some parents report that their child displayed neither early signs of autism nor regression, a phenomenon that has been called developmental plateau17,18 or stagnation.19 Other studies have found evidence of both early signs of ASD and regression simultaneously present in the retrospective histories of children with ASD.9,11,12,20
The introduction of this study discusses the various onset patterns in autism and references no less than 20 different studies. Apparently Novella must have skipped or missed this part of the study because it’s pretty clear right from the introduction that there is no consensus on the question of onset of Autism(s), let alone “true clinical onset”. In fact, many of the different Autisms are classified by the differing timings of actual onset. There is certainly no evidence of uniformity. The authors confirm this in the discussion section and even diverge from the traditional classifications of the Autisms:
The present findings suggest that existing definitions of onset patterns will need to undergo further development. One possibility is that we need to expand the number of categories used to describe onset. For example, perhaps there are four rather than two categories of onset, including groups characterized by developmental plateaus and by mixed features of early symptoms plus later regression, as we have suggested elsewhere. 17 The prospective data acquired in the present investigation suggest another possibility, however. We hypothesize that symptom emergence may better be considered dimensionally, as a continuum characterized by the amount and timing of regression.
They are not describing consensus at all. In fact there is little consensus in the prevailing classifications and these authors are suggesting yet another point of view. However, this point of view is not consistent with Novella’s assumption of uniformity of onset. That is clear in the following quote:
In this conceptualization, at one end of the continuum lie children who display loss of social interest so early that the regression is difficult to see and symptoms appear to have always been present. At the other end of the continuum lie children who experience losses of social interest and communication skills so late that the regression appears quite dramatic.
So this study has already torpedoed two of Novella’s key assumptions, let’s tackle the “true clinical onset” at 6-12 months assumption. Looking at the abstract we see the following in the results:
Group differences were significant by 12 months of age on most variables.
The fact that significant differences were noticed at 12 months does not imply uniformity and is not evidence that the “true clinical onset” is uniform and occurs between 6 and 12 months. Reading the conclusions from the abstract:
These results suggest that behavioral signs of autism are not present at birth, as once suggested by Kanner, but emerge over time through a process of diminishment of key social communication behaviors.
The authors specifically avoid listing a timeline and that is consistent with the discussion we reviewed above. It appears that Novella might have gotten one assumption right: that the old consensus – genetic disorder present at birth as per Kanner – is no longer considered valid. If we go back to Tony Charman we see he also makes another important note when it comes to old preconceptions:
Ozonoff et al. suggest that regression might be the norm and not the exception in autism. A similar suggestion was recently made by Pickles et al.8 based on retrospective parental report. They found not only that regression was very specific to autism, as it was almost never found in children with language impairment without autism, but also a strong association between age of first words and likelihood of undergoing regression. That is, frank loss of language skills was associated with switching from the most advanced early language to being among the slowest (in terms of eventual onset of phrase speech).
He implies that Autism is unique compared to other developmental disorders involving language impairment. At first blush, that doesn’t seem consistent with uniform genetic disorders. He goes on:
We do not know what the nature and causes are of the neurodevelopmental perturbations that underlie regression but the existence of such “high-risk” prospective studies offers an opportunity to investigate these questions.
This pretty much puts the nail in the coffin of Novellas hypothesis masquerading as fact. Without knowing the causes or the nature of the neurodevelopment signs we’re seeing at a young age in some children, we can’t know whether they are genetically caused or whether they’re predictive of an autism diagnosis later in life.
Dr. Charman closes with this statement:
Ten years ago, the prospective study of the emergence of early or even prodromal signs of autism would not have been considered possible or practicable. These two studies exemplify the new science of “autism in infancy.”
The real Autism scientists are talking about small new groundbreaking Autism science in it’s “infancy” and the “scientist” Novella is spewing opinion about copious amounts of evidence and a conclusive understanding of the “true” clinical onset from genetic causes.
Conclusion:
In this segment, we investigate in detail the cornerstone of Novella’s argument against vaccine causation and for the genetic causation of Autism. Not surprisingly, we find it completely unsupported by the evidence he provides. Even worse, most of his implicit assumptions contradict the evidence he references.
Walking through his arguments which move from a “suggestion of early signs” to a conclusive statement of “true clinical onset” of autism reveals that his interpretation of the evidence and application of logical arguments is seriously compromised. It is bordering on nonsensical. It appears he makes his definitive statements based on a few select lines from study abstracts and press releases. From this “selective hearing” – my apologies to Alan Golding and his video about Brian Deer – he makes giant leaps of assumption and produces what he and Gorski consider “scientific reference” material for doctors.
It certainly doesn’t take a degree in Neurology to understand the scope of these small case studies. If Novella makes so many errors of interpretation and leaps of assumption in these simple cases, it makes me question what he and Gorski are doing when they look into the far more complex epidemiology studies that form the basis of his vaccine safety arguments.
I can’t decide which of his bias’ he is so desperately trying to protect: the quickly dying idea that Autism is purely genetic or the idea that vaccines have no part in the autistic regression of many children. Perhaps if he declared his conflicts of interest, we would gain some insight into the true source of his bias?
I found a lot of details that have interesting implications when reading these studies. They point to a large variance in onset and early signs and symptoms which leads us farther away from a pure genetic cause and explains why there is a growing consensus that environmental influences have a key role to play in the causation of Autism. This new information certainly does not exonerate vaccines or MMR.
Perhaps I’ll write a third segment pointing some of my observations of the science.
Potential Conflicts of Interest: None
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