Confusing and Fascinating Findings – Gestational Age at Delivery and Special Educational Need
Posted on: June 11, 2010
Hello friends –
I ran across this one on accident the other day (why wasn’t it in one of my pubmed alerts?):
Background
Previous studies have demonstrated an association between preterm delivery and increased risk of special educational need (SEN). The aim of our study was to examine the risk of SEN across the full range of gestation.
Methods and Findings
We conducted a population-based, retrospective study by linking school census data on the 407,503 eligible school-aged children resident in 19 Scottish Local Authority areas (total population 3.8 million) to their routine birth data. SEN was recorded in 17,784 (4.9%) children; 1,565 (8.4%) of those born preterm and 16,219 (4.7%) of those born at term. The risk of SEN increased across the whole range of gestation from 40 to 24 wk: 37–39 wk adjusted odds ratio (OR) 1.16, 95% confidence interval (CI) 1.12–1.20; 33–36 wk adjusted OR 1.53, 95% CI 1.43–1.63; 28–32 wk adjusted OR 2.66, 95% CI 2.38–2.97; 24–27 wk adjusted OR 6.92, 95% CI 5.58–8.58. There was no interaction between elective versus spontaneous delivery. Overall, gestation at delivery accounted for 10% of the adjusted population attributable fraction of SEN. Because of their high frequency, early term deliveries (37–39 wk) accounted for 5.5% of cases of SEN compared with preterm deliveries (<37 wk), which accounted for only 3.6% of cases.
Conclusions
Gestation at delivery had a strong, dose-dependent relationship with SEN that was apparent across the whole range of gestation. Because early term delivery is more common than preterm delivery, the former accounts for a higher percentage of SEN cases. Our findings have important implications for clinical practice in relation to the timing of elective delivery
[Full paper from link. Emphasis is mine]
Essentially the authors evaluated gestational lengths with a fine tooth comb to discern if ‘early’, though not technically ‘pre-term’ delivery was associated with a ‘special education need’ (SEN), which in this case embodies a range of developmental problems including dyslexia, autism, or even physical problems like deafness or vision problems.
What the authors found was that there were subtle, but real effects in the likelyhood of having a special education need for non full term births that was dose dependent, but even included children that would not necessarily be considered early by existing standards.
Our study demonstrated a strong trend of decreasing risk of SEN with advancing gestational age at birth. The key finding of the present analysis is that this trend continued across gestational ages classified as term. Although the risk of SEN was highest among infants who were delivered preterm (<37 wk gestation), these accounted for only 5.1% of deliveries. Therefore, only a relatively small proportion of SEN (3.5%) could be attributed to preterm delivery. By contrast, 39.6% of infants were delivered between 37 and 39 wk gestation. Therefore, whilst these early term infants had only a moderately increased risk, 5.3% of SEN cases could be attributed to early term delivery.
The authors claim that the finding of effects at early, but not pre-term gestational lengths is one that is largely missing from existing studies, which have not taken these date ranges into consideration, or the ones that did, were not studying for cognitive problems, and indeed, excluded children with these criteria. Curiously, they also report an increase in SEN in children who had extra gestational periods, i.e., > 41 weeks in some studies.
The authors make absolutely no speculation as to what might be driving increased special education needs as the result of premature or early birth.
Looking at their results, one of the most striking things is that the impact did not alter if elective (i.e. C-Section) versus non-elective births were used as a variable. But this has deep ramifications for the autism storyline, which holds that if there are environmental factors that can contribute to autism, they are prenatal, and indeed, are often thought to involve insults very early in the prenatal period. In this case, we know that a genetic or environmental force isn’t contributing to the early birth, because it didn’t matter if the birth was spontaneous or not. The only area for an effect is postnatal. That is a big, big difference in the narrative.
Is this a matter of some just in time epigenetic programming happening in the womb that doesn’t get a chance to finish up in early births? Alternatively it could be that early birth allows for environmental exposures that the infant is not quite prepared to deal with. Or it could be both, or neither, or an illusory finding, but if these findings can be replicated, it raises a lot of questions about the sacred line between prenatal and postnatal environmental influences.
Unfortunately, the raw data for this project doesn’t seem to be available online; it might be really nice to see if there were patterns to be observed had particular salience to our population of interest.
– pD
20 Responses to "Confusing and Fascinating Findings – Gestational Age at Delivery and Special Educational Need"
June 18, 2010 at 2:11 am
Would you like this blog added under the hodge-podge of autism blogs on the Autism Blogs Directory? 🙂
June 18, 2010 at 12:59 pm
Hi Kwombles –
I would like that very much. Thank you for the opportunity!
– pD
June 21, 2010 at 3:14 pm
I wonder if the higher rate of autism among early births holds true for unvaccinated babies. Many parents have reported their tiny newborns receiving regular HepB vax on date of birth, for example, even though the baby was so small, and then the baby went on to receive the regular vaccine schedule based on age calculated from birth date rather than from due date. Perhaps preterm birth is a risk factor for adverse effects from vaccines, e.g. immune system and GI system thrown off kilter, neuroinflammation, biochemical changes, or other forms of developmental changes.
June 21, 2010 at 4:17 pm
Hi Twla –
What you describe may be possible. Some animal models of early life immune activation and consequent outcomes show relatively narrow timeframes of sensitivity.
But, itcould be lots of environmental factors out there that might be having this impact. Or it could be the result of not getting some last minute help from the mother in ways that we don’t yet understand. The effect still seems to be relatively small, at least compared to what is generally considered a pre-term birth, the longer timeframes of which seem to predispose to a variety of developmental problems.
I think the big take home message from this study should be that our knowledge is only as good as the detail of our analysis; it has been well known for decades that very early births are at risk for developmental problems. The common knowledge, that ‘mostly’ to term births was not associated with adverse outcomes was based on very course grained study; every time we apply a finer filter, we learn more. We can’t study everything, so the question becomes, how do we determine which areas get a closer examination, and which high level assumptions are we willing to live with?
– pD
June 22, 2010 at 5:28 am
I agree that there may be other factors besides vaccines. Yet, I also agree that “our knowledge is only as good as the detail of our analysis” and “We can’t study everything, so the question becomes, how do we determine which areas get a closer examination.” With so many people reporting an autism-vaccine link, one would think that vaccines would be studied in many ways, and considered as a factor in many studies. It puzzles me that so many look at this issue as “asked and answered” (which is not a quote from you of course) and/or untouchable.
June 28, 2010 at 9:03 pm
“We can’t study everything, so the question becomes, how do we determine which areas get a closer examination.” With so many people reporting an autism-vaccine link, one would think that vaccines would be studied in many ways, and considered as a factor in many studies. It puzzles me that so many look at this issue as “asked and answered” (which is not a quote from you of course) and/or untouchable.
First, there isn’t ‘so many people reporting an autism-vaccine link’ twyla; that is your determination from existing in an echo chamber. Since it is unlikely that vaccines are a contributing factor to the rise in ASD diagnoses, albeit possible that they can exacerbate pre-existing conditions in a small subset of children, it seems rather ironic that you would be so opposed to the genetic studies that are under way and currently being published. You see, that is the fastest and most precise way to identify children that may have particular environmental sensitivities whether an in utero or post-natal origin.
July 2, 2010 at 6:01 am
There are thousands of people reporting vaccine reactions causing autism, including the thousands who have actually filed claims with the vaccine court. To me, that is “so many”. I’m not so opposed to genetic studies, but I am opposed to vaccines not being studied. Vaccines need to be fully studied, and vaccine injured children need to be studied. A few limited biased epidemiological studies is far from adequate. See Pd’s post https://passionlessdrone.wordpress.com/2009/05/13/a-brief-overview-on-early-life-immune-challenges-and-why-they-might-matter/
July 2, 2010 at 3:36 pm
There are thousands of people reporting vaccine reactions causing autism, including the thousands who have actually filed claims with the vaccine court. To me, that is “so many”.
The operative word being ‘reported’, this is not evidence of causality. Additionally, what was the scientific reporting and consensus that arose during the OAP? The actual decision isn’t as compelling for me as the quality of evidence presented by the respective experts.
I’m not so opposed to genetic studies, but I am opposed to vaccines not being studied.
You don’t frequently complain about the amount of autism research being directed towards genetics? You don’t complain about genetics being the only interest of researchers (even though that is patently false)?
Vaccines need to be fully studied, and vaccine injured children need to be studied.
First, define what you mean by ‘vaccines need to be fully studied’. It is a rather general and empty statement as it stands. There is a disparity in what you consider to be ‘vaccine injured children’ with reality. You are convinced that most, if not all ASDs are vaccine injuries but you provide no evidence of this. So can you also refine your definition of ‘vaccine injured children’?
A few limited biased epidemiological studies is far from adequate.
What studies are you referring to and what are their biases? Please don’t refer me to the ‘fourteen studies’ website; it’s been roundly discredited by others and I concur upon reading it myself. Also, how aware are you of ongoing research into the immunological aspect of autism development?
July 3, 2010 at 11:56 pm
Science Mom –
Pd replied to most of your comment – and did so better than I could have.
Regarding vaccine injured children, I am talking about children whose parents reported vaccine injuries, including those whose injuries were paid by vaccine court. CBS has written about this:
CBS News has learned the government has paid more than 1,300 brain injury claims in vaccine court since 1988, but is not studying those cases or tracking how many of them resulted in autism.
The branch of the government that handles vaccine court told CBS News: “Some children who have been compensated for vaccine injuries…may ultimately end up with autism or autistic symptoms, but we do not track cases on this basis.”
“What we’re seeing in the bulk of the population: vaccines are safe,” said Healy. “But there may be this susceptible group. The fact that there is concern, that you don’t want to know that susceptible group is a real disappointment to me. If you know that susceptible group, you can save those children. If you turn your back on the notion that there is a susceptible group… what can I say?”
Government officials would not respond directly to Healy’s views… but reiterated, vaccines are safe.
http://www.cbsnews.com/stories/2008/05/12/cbsnews_investigates/main4086809.shtml
According to Healy, when she began researching autism and vaccines she found credible published, peer-reviewed scientific studies that support the idea of an association. That seemed to counter what many of her colleagues had been saying for years. She dug a little deeper and was surprised to find that the government has not embarked upon some of the most basic research that could help answer the question of a link.
The more she dug, she says, the more she came to believe the government and medical establishment were intentionally avoiding the question because they were afraid of the answer.
Why? Healy says some in the government make the mistake of treating vaccines as an all-or-nothing proposition. The argument goes something like this: everybody gets vaccinated at the same time with the same vaccines or nobody will get vaccinated and long-gone deadly diseases will re-emerge. (When I asked about cases of brain damage resulting in autism that have been quietly compensated by the government in vaccine court over the years, one government official recently told me that “it’s still better overall to get vaccinated than not to get vaccinated.”)
Healy says the argument need not be framed in those terms (vaccinate or don’t vaccinate). Instead, she says, we should vaccinate, but work to do it in the safest manner possible based on what we know and what we can find out.
That’s what the parents of autistic children have told me as well. If we can screen children to see which ones might be more susceptible to vaccine side effects, and vaccinate them on a more personalized schedule that is safer for them, why wouldn’t we? If it’s safer for all children to have their vaccinations spread out, why wouldn’t we? Healy says it’s called “personalized medicine” and is being done in virtually all areas of medicine today with the exception of vaccines. Yet the government continues to frame the conversation in all-or-nothing, “one-size-fits-all” terms.
Lastly, Healy says the government has a long way to go to even do basic research that could get at the heart of what she believes is an open question. For example: why in the past decade hasn’t the government compared the autism/ADD rate of unvaccinated children with that of vaccinated children? If the rate is the same, it tends to point away from vaccines. If the rate is markedly lower in unvaccinated children, it tends to point toward vaccines.
The government has a dataset of unvaccinated children available. It has published more than one survey of parents of undervaccinated and unvaccinated children (to find out why the parents are choosing not to vaccinate). It would seem simple to use those same families to measure their rate of autism/ADD. Also, why hasn’t the government used vaccine court as a resource to ask the autism/vaccine question. There, nearly 5,000 families have self-selected as believing their children’s autism was caused by vaccines. Many have expressed willingness to let their children’s medical records be released and studied; but nobody in the government has been interested.
http://www.cbsnews.com/8301-500803_162-4090144-500803.html
Shouldn’t the CDC be interested in gaining a better understanding of vaccine injures? ‘Vaccines need to be fully studied’ is a general statement, but not an empty one.
July 4, 2010 at 2:54 pm
Science Mom –
Pd replied to most of your comment – and did so better than I could have.Regarding vaccine injured children, I am talking about children whose parents reported vaccine injuries, including those whose injuries were paid by vaccine court. CBS has written about this:
Of course pD could answer better than you. While I don’t always agree with him, he puts thought into his posts and statements; looks at the original literature. I asked you questions to provoke some thought about what you were actually saying and instead, give me regurgitations from Attkisson and Healy. I’m disappointed.
I’m sorry but where did Healy’s name ever appear on the expert list for the OAP or in association with autism research? She is a politician, not a scientist and ironically, outspoken against evidence-based medicine and in favour of tobacco companies. There hasn’t been ‘quiet’ compensation of vaccine injuries either; it’s been ‘hiding out in the open’ for years: http://neurodiversity.com/weblog/article/148/
That’s what the parents of autistic children have told me as well. If we can screen children to see which ones might be more susceptible to vaccine side effects, and vaccinate them on a more personalized schedule that is safer for them, why wouldn’t we?
These are the vapid statements I am talking about that you are merely parroting. Screen for what? You have to know what you are looking for in order to screen for something.
As for Attkisson, a tired, agendised talking head who doesn’t bother speaking to actual experts but cherry-picks those that support her story. And what has she done for you lately?
July 4, 2010 at 9:07 pm
@ Science Mom’s comments 7/4 2:54 p.m. 7/2 3:36 p.m.
“You are convinced that most, if not all ASDs are vaccine injuries…” I am quite sure that some autism is caused by vaccines. And I believe that vaccines are the primary factor in the tremendous increase in autism over the past thirty years. But as I have often stated, I also believe vaccines are not the only cause of autism. Autism is a broad spectrum which is defined by behaviors, not etiology. There may well be some cases of autism which are purely genetic, some which are caused by chemicals in our food, air, water, furniture, plastics etc., or by other factors we don’t even suspect yet.
But there is a whole lot of evidence of vaccine causation that is being dismissed as “coincidence” with no investigation, including what parents have witnessed in their children who react to vaccines.
Regarding Dr. Bernadine Healy, you said that “She is a politician, not a scientist”. Actually, she is a doctor, former head of the NIH, and currently works as a journalist. From her bio at http://www.nlm.nih.gov/changingthefaceofmedicine/physicians/biography_145.html :
“Healy graduated first in her class at Hunter, went on to Vassar where she graduated summa cum laude, earned her M.D. at Harvard Medical School, and completed her training in internal medicine and cardiology at Johns Hopkins University School of Medicine.
“After completing her internship and residency at Johns Hopkins Hospital in Baltimore, Dr. Healy spent two years at the National Heart, Lung, and Blood Institute at the National Institutes of Health before returning to Hopkins in 1976, where she became a professor of medicine. She earned a reputation as a skilled cardiovascular researcher specializing in the pathology of heart attacks.”
She has served as deputy director of the White House Office of Science and Policy, chairman of the Research Institute at the Cleveland Clinic Foundation where she directed the research programs of nine departments, and director of the National Institutes of Health.
“In addition to her various administrative positions, Dr. Healy has continued to treat patients during much of her career. Her research has led to deeper understanding of the pathology and treatment of heart attacks, especially in women. An author as well as a policymaker and manager, Dr. Healy has written or co-authored more than 220 peer-reviewed manuscripts on cardiovascular research and health and science policy.”
Of course it’s your right to disagree with her, but to dismiss her opinions because she is just “a politician” is inaccurate as well as lame.
Nothing you said contradicts Sheryl Attkisson’s statement that “CBS News has learned the government has paid more than 1,300 brain injury claims in vaccine court since 1988, but is not studying those cases or tracking how many of them resulted in autism. The branch of the government that handles vaccine court told CBS News: ‘Some children who have been compensated for vaccine injuries…may ultimately end up with autism or autistic symptoms, but we do not track cases on this basis.’” Do you have any information to contradict that statement? Or is your only response to malign Ms. Attkisson?
In response to Attkisson’s statement “That’s what the parents of autistic children have told me as well. If we can screen children to see which ones might be more susceptible to vaccine side effects, and vaccinate them on a more personalized schedule that is safer for them, why wouldn’t we?” you said, “Screen for what? You have to know what you are looking for in order to screen for something.” Exactly! For the most part, they don’t know what to look for! This is the kind of thing that agencies such as the CDC should be studying. What are susceptibility factors? Of those children who have had severe reactions to vaccines, are there certain lab results they have in common, or something in their health history? Do they have family history of auto-immunity or immunodeficiency? Did they have prior reactions to vaccines?
Barbara Loe Fisher said, “NVIC has been calling for basic science research into the biological mechanisms of vaccine injury and death for more than two decades. Without understanding how and why vaccines can cause brain and immune system dysfunction, there will be no way to develop pathological profiles to help scientifically confirm whether or not an individual has been injured or died from vaccination.” http://www.nvic.org/NVIC-Vaccine-News/November-2008/Thursday,-November-20,-2008-Vaccine-Injury-Compens.aspx
When vaccine reactions occur, it is usually dismissed as coincidence by mainstream doctors and agencies. Rather than just dismissing thousands (yes, thousands) of parental reports, and not even studying those cases that have been conceded in vaccine court, our agencies should be researching these adverse reactions, studying these children. Instead of just defending the vaccine program by denying the negatives and talking about how terrible diseases are, agencies such as the CDC and FDA should be understanding the negatives and working to make our vaccine program as safe as possible.
And yes, my statements are general. I am not a scientist. But you seem to expect us parents to prove something before it should be studied. I am not able to prove anything. I can only say what I have observed and read. And there are a whole lot of parents (some of whom are PhDs and MDs), as well as some doctors and scientists (some of whom are also parents) who are clamoring for more research on vaccines in relation to autism, seizure disorders, ADHD, auto-immune disorders, allergies, and more.
If scientists only studied what has already been proven they would never learn anything new. When people clamor for more research, it doesn’t make sense to tell them to first offer proof.
July 3, 2010 at 11:58 am
Hi ScienceMom –
Thanks for stopping by my blog.
The operative word being ‘reported’, this is not evidence of causality.
You are shifting your goalposts a bit, as you originally stated that there were not many people reporting such events.
First, there isn’t ‘so many people reporting an autism-vaccine link’ twyla; that is your determination from existing in an echo chamber.
Ascertaining a causal relationship is very difficult with a condition as complicated as autism.
First, define what you mean by ‘vaccines need to be fully studied’. It is a rather general and empty statement as it stands.
Well, I don’t want to speak for Twyla, but I share what I think are similar feelings; namely that we should attempt to gain a fuller understanding of the potential for vaccination to have effects up and above protection from pathogens. I think you are likely aware of my theories and what makes autistics a potentially susceptible subgroup for unintended effects from vaccination. I would be happy to be more specific if you would like.
To be more specific in what I think we could try to learn concerning vaccination the following would be good starting points:
1) Short, medium and long term effects on the innate immune system after vaccination. When I waded into this discussion, I was shocked to find that there is almost no research whatsoever concerning the innate immune response in the pediatric vaccine schedule. What little I did find was not reassuring, especially considering the narrative that is being distributed.
For example, this paper: Modulation of the infant immune responses by the first pertussis vaccine administrations
Which startlingly found very different immune profiles between infants who received the DTAP versus the DTP.
These data demonstrate that the cytokine profile of 6-month-old infants is influenced by the type of formulation of the pertussis vaccine they received at 2, 3 and 4 months of life. Large prospective studies would be warranted to evaluate the possible long-term consequences of this early modulation of the cytokine responses in infants.
I don’t believe for a single second that there is anyone out there that understands the implications of making such a change in a generation of infants. Perhaps you would like to share some references that could guide us in understanding how such a change to the cytokine profile during infancy will, or won’t affect a child? The underlying assumption of the vaccination program has been that the only end point immunological measurement of interest is antibody recognition; which is why this type of study was only performed nearly a decade after the DTAP was licensed.
2) The potential for our earliest vaccinations to alter systems such as the HPA-Axis or areas like seizure susceptibility. There are several animal models of neonatal exposure to endotoxin or Poly:IC that seem to observe long term programming of the neuroendocrine systems or neural excitability. I’m working on a couple of posts in this area that aren’t ready yet, but when they do come out, I would be interested in your thoughts on them.
Disregarding for now the feasibility and / or shortccomings of a vaccinated / unvaccinated study, do you think gaining this type of knowledge would be a worthwhile area for research?
What studies are you referring to and what are their biases?
Well, to my mind, the biggest problem is that our existing research suite doesn’t really speak towards vaccination, but rather, only towards thimerosal or the MMR, which is but one vaccine given much later in life than the remainder of our shot schedule. This isn’t so much a bias; but the reality of the scientific method is that you only learn about what you study, and we haven’t studied vaccination all that well.
Also, how aware are you of ongoing research into the immunological aspect of autism development?
I would like to think that I know a little about the subject. On this blog I’ve written some posts on some nice ones (well, I think they’re nice), including:
Differential Monocyte Responses to TLR Ligands in Children With Autism
and
Immune Transcriptome Alterations In The Temporal Cortex of Subjects With Autism
The second having mentioned you by name, as a matter of fact. I would love to hear your comments on either of those studies. Are there any other studies in the immunological area of autism you would like to discuss? Which ones?
– pD
July 4, 2010 at 2:47 am
The operative word being ‘reported’, this is not evidence of causality.
You are shifting your goalposts a bit, as you originally stated that there were not many people reporting such events.
Yes, it does appear that way so I should have been more precise. First, there isn’t ‘so many’ reporting an autism-vaccine link, the ~5000 involved with the OAP and a subset of those participating on forums is very small in relation to the number of autistics in the population. My response ended up more closely addressing her second charge of causality, which has been roundly discredited during the OAP.
Ascertaining a causal relationship is very difficult with a condition as complicated as autism.
Yes, it is difficult which is why concluding ‘it must be the vaccines’ is so spurious and also why we need to let the research commence in the multi-faceted directions that it is going in.
Well, I don’t want to speak for Twyla, but I share what I think are similar feelings; namely that we should attempt to gain a fuller understanding of the potential for vaccination to have effects up and above protection from pathogens. I think you are likely aware of my theories and what makes autistics a potentially susceptible subgroup for unintended effects from vaccination. I would be happy to be more specific if you would like.
I agree with your first statement. Your second however, is merely a variation of ‘vaccinesdidit’ without persuasive biological plausibility to support it. In the interest of accepted nomenclature, yours are not theories, but rather theoretic or un-tested hypotheses.
For example, this paper: Modulation of the infant immune responses by the first pertussis vaccine administrations
Which startlingly found very different immune profiles between infants who received the DTAP versus the DTP.
First of all, not very startling and secondly, the findings of this study need to be considered within the larger frame work of numerous other factors that contribute to infant immune modulation. I’m surprised that you aren’t more interested in the hygiene hypothesis.
I don’t believe for a single second that there is anyone out there that understands the implications of making such a change in a generation of infants. Perhaps you would like to share some references that could guide us in understanding how such a change to the cytokine profile during infancy will, or won’t affect a child? The underlying assumption of the vaccination program has been that the only end point immunological measurement of interest is antibody recognition; which is why this type of study was only performed nearly a decade after the DTAP was licensed.
I can’t really argue here as there are scant data to specifically address this. Although you are operating within the vacuum of the U.S. vaccine schedule and the temporal relationship to autism, rather than considering what this relationship looks like in other countries. For example Sweden, a much lighter vaccine schedule, no birth doses of anything (save at-risk infants) and their ASD prevalence surpassed 1% a full decade before that of the U.S.
2) The potential for our earliest vaccinations to alter systems such as the HPA-Axis or areas like seizure susceptibility. There are several animal models of neonatal exposure to endotoxin or Poly:IC that seem to observe long term programming of the neuroendocrine systems or neural excitability. I’m working on a couple of posts in this area that aren’t ready yet, but when they do come out, I would be interested in your thoughts on them.
I will be happy to comment on those when I see them. But I do caution that you don’t fall into confirmation bias. I have gleaned some of what you have written on the topic thus far and in general, I don’t fully agree with your interpretations and applications of the literature. I guess I would have to comment in depth on your actual posts to be really meaningful but let’s just say, for now, that you are ignoring the much more fertile ground of in utero exposures to many potential teratogens.
Disregarding for now the feasibility and / or shortccomings of a vaccinated / unvaccinated study, do you think gaining this type of knowledge would be a worthwhile area for research?
It’s rather difficult to divorce feasibility and shortcomings of a vax/unvaxed study so I’m not sure how to answer. What are the questions you wish to answer? I don’t think a general vaxed/unvaxed study would add much to the literature since it would have to be very longitudinal and very large to be even remotely informative and even then, would probably be very confounded.
Well, to my mind, the biggest problem is that our existing research suite doesn’t really speak towards vaccination, but rather, only towards thimerosal or the MMR, which is but one vaccine given much later in life than the remainder of our shot schedule. This isn’t so much a bias; but the reality of the scientific method is that you only learn about what you study, and we haven’t studied vaccination all that well.
It’s not a reality of the scientific method but rather a response to what was deemed viable biological questions. To a degree, although not as robust as a dedicated study certainly, thimerosal studies are a proxy for the number of vaccinations. This approximation was related by the most recent study of vaccines and neurological outcomes: http://pediatrics.aappublications.org/cgi/content/abstract/125/6/1134
I am aware of the limitations of this study, namely using study groups that received vaccines between 1993-1997, however, there should have been a dose-dependent effect if the ‘too many too soon’ claim was valid.I would be interested in longitudinal prospective (if possible) studies examining immunomodulation and also microbial ecology as they relate to mass vaccination but probably not for the same reasons as you pD. If an agency, institution or organisation wants to examine autism from a vaccines standpoint, that’s fine but I doubt it will ever be to the satisfaction of the vaccines cause autism crowd.
I would like to think that I know a little about the subject. On this blog I’ve written some posts on some nice ones (well, I think they’re nice), including:
Differential Monocyte Responses to TLR Ligands in Children With Autism
and
Immune Transcriptome Alterations In The Temporal Cortex of Subjects With Autism
The second having mentioned you by name, as a matter of fact. I would love to hear your comments on either of those studies. Are there any other studies in the immunological area of autism you would like to discuss? Which ones?
I will take a look at those and comment directly to those posts; I’ve probably de-railed enough here already.
July 4, 2010 at 1:06 pm
Hi ScienceMom –
Your second however, is merely a variation of ‘vaccinesdidit’ without persuasive biological plausibility to support it. In the interest of accepted nomenclature, yours are not theories, but rather theoretic or un-tested hypotheses.
I’d agree with our second statement, though not with your first. Considering that further down the post you admit that you haven’t looked into my theoretics too deeply, I find your gross over simplification of my position intellectually lazy, though not unsurprising.
Any unbiased reading of the available studies regarding early life immune challenges and subsequent alterations of a variety of physiological systems including seizure susceptibility, neuroimmune function, stress response and ultimately behaviors reaches the unavoidable conclusion that there are developmental timeframes during which stimulation of the innate immune response can have difficult to predict outcomes. Furthermore, we have a wealth of research telling us that the immune system likely playing a critical role in the pathogenesis of autism, and the specifics of immune dysfunction in autism point towards a propensity towards an exaggerated innate immune response and difficulties attenuating an immune response; properties that would speak directly towards a subgroup of individuals most likely to be affected in ways similar to what has been observed in animal studies.
But the specifics are important. I’d be interested in having a more detailed understanding of where you feel my untested hypothesis fails the test of biological plausibility. Do you have any thoughts you would be willing to share?
First of all, not very startling and secondly, the findings of this study need to be considered within the larger frame work of numerous other factors that contribute to infant immune modulation. I’m surprised that you aren’t more interested in the hygiene hypothesis.
Well, I’m startled Asthma, dermatitis, thyroid disease, schizophrenia, and mania are all conditions associated with altered TH1/TH2 balances, among many others. Do you think that if it was found that Papmers modulated TH1 / TH2 balance in infants, but Huggies did not, there would be no response from our regulatory agencies? We shouldn’t be shuffling our infants immune system like a deck of cards and assuming everything will come out in the wash because to do otherwise forces us to acknowledge the limitations of our knowledge.
Regarding the hygiene hypothesis, I’m plenty interested in that; there have been a few studies lately showing that the method of delivery has a large impact on the resultant microflora of the infant, something I don’t believe we understand the implications of very well yet; though it does illustrate how the line between the in utero environment and postnatal environment is not always as strong an indicator as we might have previously though. (Indeed, the overall topic of the OP) I will note with some amusement that while you think other immunomodulating factors are important, you seem unconcerned that they seemed unable to disturb the profile set in place by the type of vaccine received by these infants. If other factors are contributing to immunomodulation, do you have any thoughts as to why their effects were unable to mask the effect of three vaccination events in the different groups in this study?
I can’t really argue here as there are scant data to specifically address this. Although you are operating within the vacuum of the U.S. vaccine schedule and the temporal relationship to autism, rather than considering what this relationship looks like in other countries. For example Sweden, a much lighter vaccine schedule, no birth doses of anything (save at-risk infants) and their ASD prevalence surpassed 1% a full decade before that of the U.S.
If there is no data regarding the effect on children, but there is voluminous data towards evidence of TH1 / TH2 cytokine profile involvement in a variety of pathologies, I’m curious as to how you arrived at your unstartled stance? Earlier you accused Twyla of rather general and empty statement; given your desire for preciseness, could you refine your position on why you don’t find distinct immunomodulatory properties of vaccine types of concern?
Regarding Sweden, I am curious as to your thoughts on this study from Stockholm, which found rates at 60 per 10,000 for ASDs. Do you have a compelling reason we should put complete faith into your prevalence value, other than expediency to your favored conclusion?
I have gleaned some of what you have written on the topic thus far and in general, I don’t fully agree with your interpretations and applications of the literature. I guess I would have to comment in depth on your actual posts to be really meaningful but let’s just say, for now, that you are ignoring the much more fertile ground of in utero exposures to many potential teratogens.
Fair enough. I would warn the opposite confirmation bias may exist in your analysis; that you are viewing the problem solely through an in utero lens. I have a great interest in such teratogens; for example, I feel the likelyhood is very great that endocrine disrupting agents capable of interferring with thyroid metabolism are very likely capable of causing autism. I even blogged about it a few times. Please avoid the temptation to pigeonhole my position as vaccine autism causation only; it is more of a position that regards a non trivial increase in incidence is probable, and secondarily, our available evidence on vaccines woefully inadequate.
It’s not a reality of the scientific method but rather a response to what was deemed viable biological questions. To a degree, although not as robust as a dedicated study certainly, thimerosal studies are a proxy for the number of vaccinations. This approximation was related by the most recent study of vaccines and neurological outcomes:
The fact that twenty five years after aggressively increasing the childhood vaccine schedule, a proxy study of one thousand children who suffer from massive self selection bias is the hole card in the question has been answered debate illustrates the pathetic state of our knowledge better than I ever could.
I would be interested in longitudinal prospective (if possible) studies examining immunomodulation and also microbial ecology as they relate to mass vaccination but probably not for the same reasons as you pD.
OK. What are your reasons? I am genuinely interested.
I will take a look at those and comment directly to those posts; I’ve probably de-railed enough here already
I welcome your thoughts.
– pD
July 6, 2010 at 4:58 pm
I’d agree with our second statement, though not with your first. Considering that further down the post you admit that you haven’t looked into my theoretics too deeply, I find your gross over simplification of my position intellectually lazy, though not unsurprising.
Intellectually busy is more like it. pD, I read copious amounts of literature, blogs, etc. in addition to my experience as a bench and field scientist and I have become rather adept at critically evaluating data and subsequent interpretations. I go to the original literature, which I had done for a couple of your studies that you were evaluating and it didn’t take me long to spot some overreaching conclusions on your part. If my intent was to pick apart your entire post, I would have done so with a thorough critique of what I considered to be your errors. Don’t get me wrong though, you have an interesting approach and some very thought-provoking posts.
Any unbiased reading of the available studies regarding early life immune challenges and subsequent alterations of a variety of physiological systems including seizure susceptibility, neuroimmune function, stress response and ultimately behaviors reaches the unavoidable conclusion that there are developmental timeframes during which stimulation of the innate immune response can have difficult to predict outcomes.
I agree although again, it is prudent to follow the evidence, rather than draw conclusions.
Furthermore, we have a wealth of research telling us that the immune system likely playing a critical role in the pathogenesis of autism, and the specifics of immune dysfunction in autism point towards a propensity towards an exaggerated innate immune response and difficulties attenuating an immune response; properties that would speak directly towards a subgroup of individuals most likely to be affected in ways similar to what has been observed in animal studies.
This is where I have difficulty with your slant. You are making overreaching conclusions with regards to sequence of events, exposure period, exposure and pathogenesis. I am not dismissive, it is just that these studies are peripheral and/or preliminary to your hypothesis.
Well, I’m startled Asthma, dermatitis, thyroid disease, schizophrenia, and mania are all conditions associated with altered TH1/TH2 balances, among many others. Do you think that if it was found that Papmers modulated TH1 / TH2 balance in infants, but Huggies did not, there would be no response from our regulatory agencies? We shouldn’t be shuffling our infants immune system like a deck of cards and assuming everything will come out in the wash because to do otherwise forces us to acknowledge the limitations of our knowledge.
It’s not that simple now is it? Infants are born with a suppression of Th1 responses that balance out by ~2 years old so you need to consider if vaccination is permanently altering this as well as the plethora of other factors that would influence immunomodulation to the detriment of the system.
I will note with some amusement that while you think other immunomodulating factors are important, you seem unconcerned that they seemed unable to disturb the profile set in place by the type of vaccine received by these infants. If other factors are contributing to immunomodulation, do you have any thoughts as to why their effects were unable to mask the effect of three vaccination events in the different groups in this study?
You are misinterpreting my statements. I’m not unconcerned; I’m cautious. If you are referring to the Mascart et al. (2007) study, they didn’t follow the infants past 6 months so how can you draw any conclusions as to what these infants immune profiles looked like at 12 or 24 months. Even the authors state that any ‘defect’ (i.e. Th2 skew) can be overcome by acute infection with bordatella pertussis, although this holds true for other Th1 stimulating pathogens as well.
If there is no data regarding the effect on children, but there is voluminous data towards evidence of TH1 / TH2 cytokine profile involvement in a variety of pathologies, I’m curious as to how you arrived at your unstartled stance? Earlier you accused Twyla of rather general and empty statement; given your desire for preciseness, could you refine your position on why you don’t find distinct immunomodulatory properties of vaccine types of concern?
You seem to be conflating different statements of mine. I’m not surprised that the authors found what they did given what I know about immunomodulation of pathogens and even non-pathogenic antigens, what vaccines are comprised of and mounds of data regarding vaccine mode of action. Again, not unconcerned; I just don’t choose to leap to conclusions that aren’t well-grounded in evidence.
Regarding Sweden, I am curious as to your thoughts on this study from Stockholm, which found rates at 60 per 10,000 for ASDs. Do you have a compelling reason we should put complete faith into your prevalence value, other than expediency to your favored conclusion?
Actually, that study took place in Göteborg , the prevalence found for any registered ASD in the last 6 year bin surveyed was 0.8% (children born 1989-1994) and Aspergers was underestimated due to the cut-off date of the study. The U.S. prevalence for 8 year olds in 2002 was 0.66%: http://www.ncbi.nlm.nih.gov/pubmed/17287715 Additionally, the Swedish study found that 1.23% of boys and 0.23% of girls in Göteborg were registered at the neuropsychiatry clinic for an ASD at the end of 2001. So what was your point?
Fair enough. I would warn the opposite confirmation bias may exist in your analysis; that you are viewing the problem solely through an in utero lens. I have a great interest in such teratogens; for example, I feel the likelyhood is very great that endocrine disrupting agents capable of interferring with thyroid metabolism are very likely capable of causing autism. I even blogged about it a few times. Please avoid the temptation to pigeonhole my position as vaccine autism causation only; it is more of a position that regards a non trivial increase in incidence is probable, and secondarily, our available evidence on vaccines woefully inadequate.
I’m afraid that you have pigeon-holed my position, which incidentally, is constantly in flux on the issue of aetiology, as I follow the evidence. I have merely cautioned you not to get too wedded to a particular belief at the expense of more plausible explanations.
The fact that twenty five years after aggressively increasing the childhood vaccine schedule, a proxy study of one thousand children who suffer from massive self selection bias is the hole card in the question has been answered debate illustrates the pathetic state of our knowledge better than I ever could.
Massive self-selection bias? Could you provide evidence of such? No one said this was the lynch pin for absolute safety of a vaccine schedule; it is just more evidence that there is little validity to the vaccine-autism claim.
OK. What are your reasons? I am genuinely interested.
I am interested in the apparent protective factors that have facilitated optimal immune function and the influences that contemporary lifestyle, environmental and medical changes have had on alterations of that system. I am also interested in the changes that some vaccines have and will have upon host microbial ecology and epidemiology of pathogens due to poly-microbial serotype replacement.
July 8, 2010 at 11:27 am
Hi ScienceMom –
Intellectually busy is more like it. pD, I read copious amounts of literature, blogs, etc. in addition to my experience as a bench and field scientist and I have become rather adept at critically evaluating data and subsequent interpretations. I go to the original literature, which I had done for a couple of your studies that you were evaluating and it didn’t take me long to spot some overreaching conclusions on your part. If my intent was to pick apart your entire post, I would have done so with a thorough critique of what I considered to be your errors.
My apologies. You might be surprised to learn that one reason you’ve seen me in many of the more skeptical areas is that I want a critical eye cast towards my ideas; if they can’t stand up to critical analysis, they aren’t thoughts worth having.
I agree although again, it is prudent to follow the evidence, rather than draw conclusions.
OK. Perhaps my posts are not worded cautiously enough.
This is where I have difficulty with your slant. You are making overreaching conclusions with regards to sequence of events, exposure period, exposure and pathogenesis. I am not dismissive, it is just that these studies are peripheral and/or preliminary to your hypothesis.
OK. That’s a big topic to dig deeper into, but I would welcome your thoughts on any of my posts if you felt like it.
It’s not that simple now is it? Infants are born with a suppression of Th1 responses that balance out by ~2 years old so you need to consider if vaccination is permanently altering this as well as the plethora of other factors that would influence immunomodulation to the detriment of the system.
Well, I should have been more clear (again), that I’m not trying to make causation claims here, and the claim of oversimplication stings. Permenance is a good question relating to Mascart, but tangential to my primary concerns; that we are tinkering around with a system with only a primitive understanding of the ramifications up and above pathogen memory. That might be one thing if we didn’t appear to be observing a remarkable rise in a variety of autoimmune disorders, or in the case of autism, disorders with possible immune components. Mascart says it quite clearly:
However, little is known about the general immune modulation induced by early vaccination
That’s a lot different than the narrative we are being sold. My fear is that the great success of vaccination, and the very real problems associated with a return of disease has made this topic impervious to dispassionate analysis.
You are misinterpreting my statements. I’m not unconcerned; I’m cautious. If you are referring to the Mascart et al. (2007) study, they didn’t follow the infants past 6 months so how can you draw any conclusions as to what these infants immune profiles looked like at 12 or 24 months. Even the authors state that any ‘defect’ (i.e. Th2 skew) can be overcome by acute infection with bordatella pertussis, although this holds true for other Th1 stimulating pathogens as well.
My apologies. However, I don’t get the feeling that the regulatory agencies feel any such cautiousness regarding our vaccination program regarding the possiblity of ‘general immune modulation induced by early vaccinaton’. Perhaps you feel differently? In any case, infancy is a critical time for brain development and there is a ton of evidence of neuro-immune crosstalk that has nothing to do with the animal studies I’ve posted in other locations. I don’t want to misinterpret you again, but my version of cautious is that the assumption of no harm based on a lack of quality analysis is a bad foundation for a national health policy that touches four million infants a year. We may have different ideas on this.
You seem to be conflating different statements of mine. I’m not surprised that the authors found what they did given what I know about immunomodulation of pathogens and even non-pathogenic antigens, what vaccines are comprised of and mounds of data regarding vaccine mode of action. Again, not unconcerned; I just don’t choose to leap to conclusions that aren’t well-grounded in evidence.
I must apologize again. Regarding not being surprised, could you give me a little more insight into why you feel the accelular version of the vaccine would have transient (?) effects on TH1 / TH2 balance? My admittedly primitive understanding was that the move to the DTAP involved changing epitopes to more commonly shared protein structures, thereby reducing the number of distinct antigens required for immune memory. Presumably there were more subtle changes to the vaccine which I am not aware of. Do you have any references regarding the different vaccine modes of action between these two vaccines that might help me? It may, in fact, disuade me from some of my concerns. (?)
Actually, that study took place in Göteborg , the prevalence found for any registered ASD in the last 6 year bin surveyed was 0.8% (children born 1989-1994) and Aspergers was underestimated due to the cut-off date of the study. The U.S. prevalence for 8 year olds in 2002 was 0.66%: http://www.ncbi.nlm.nih.gov/pubmed/17287715 Additionally, the Swedish study found that 1.23% of boys and 0.23% of girls in Göteborg were registered at the neuropsychiatry clinic for an ASD at the end of 2001. So what was your point?
Where did I get Stockholm? In any case, my point is that in order for us to reference US / Sweden vaccine \ prevelance rates to get to any type of valid conclusion, we have to have confidence in the prevelance numbers. The Goteborg study tells us that our ducks may not be in order sufficiently for us to declare that the incidence in Sweden raced well past 1% over a decade ago. The entire argument of a genetically mediated condition that is not experiencing a real increase absolutely relies on the inherent flaws in our prevelance studies of the past.
For example, the Faroes study interviewed every child in school, and found a prevelance rate below 60 per 10,000. http://www.ncbi.nlm.nih.gov/pubmed/17029020
This was an assessment of every child in school using DSM-IV criteria. Of course, they might have missed kids that didn’t goto school, but to get anywhere close to over 1%, as we seem to see in some Sweden studies, we need to conclude that over half of the cases of autism in the Faroes are very severe kids. This is highly discordant with the idea that the bulk of additions to the spectrum are less severe kids, kids that would have been quirky a generation ago.
What is to keep me from using the Faroes as a baseline to the current US prevelance numbers and declaring there must be some environmental diffference that is causing (or preventing) so much autism?
For someone who doesn’t want to jump to conclusions without quality evidence, I can’t figure out why you’ve decided that two very specific prevelance studies, current US and a decade old Sweden, are the two we should use for any type of equivalency analysis between vaccine schedules. What has given you confidence that either of these studies are accurate when so many of our other studies show such different results? If we have no such confidence, how can we draw conclusions using them as measurement points?
I’m afraid that you have pigeon-holed my position, which incidentally, is constantly in flux on the issue of aetiology, as I follow the evidence. I have merely cautioned you not to get too wedded to a particular belief at the expense of more plausible explanations.
Shame on me!
Massive self-selection bias? Could you provide evidence of such? No one said this was the lynch pin for absolute safety of a vaccine schedule; it is just more evidence that there is little validity to the vaccine-autism claim.
The original cohort on which this study was based was drawn from parents who had the time to have their child participate in a series of IQ and other tests; around two thirds of the parents contacted declined to participate. I don’t know if you have a child on the spectrum or not, but I can tell you that mine is getting ABA, speech, or OT six days a week. Time to participate in studies is preciously sparse, though we did attempt one a few years ago that we considered a failure. Furthermore, at age seven, my son still struggles with concepts such as yes or no, or orange and green; it isn’t that he has a low IQ (he might), it’s that he doesn’t understand the types of requests that would are being made of him. [pretty much what happened a few years ago].
This study didn’t take autism into consideration, and everyone seems to admit that this is the first, and currently only study, even attempting a look at the entire vaccination schedule; as such, I think that ‘just more’ could easily be replaced with ‘only’.
I am interested in the apparent protective factors that have facilitated optimal immune function and the influences that contemporary lifestyle, environmental and medical changes have had on alterations of that system. I am also interested in the changes that some vaccines have and will have upon host microbial ecology and epidemiology of pathogens due to poly-microbial serotype replacement
Did you see this? http://blogs.discovermagazine.com/notrocketscience/2010/06/29/does-national-iq-depend-on-parasite-infections-er/
Check out some of the links from comment 12.
– pD
July 11, 2010 at 3:09 pm
Twyla:
@ Science Mom’s comments 7/4 2:54 p.m. 7/2 3:36 p.m.
“You are convinced that most, if not all ASDs are vaccine injuries…” I am quite sure that some autism is caused by vaccines. And I believe that vaccines are the primary factor in the tremendous increase in autism over the past thirty years. But as I have often stated, I also believe vaccines are not the only cause of autism. Autism is a broad spectrum which is defined by behaviors, not etiology. There may well be some cases of autism which are purely genetic, some which are caused by chemicals in our food, air, water, furniture, plastics etc., or by other factors we don’t even suspect yet.
I noticed that you left off diagnostic expansion and substitution. Why is that? Doing so doesn’t lend any validity to what are very flaccid statement of causation. How are vaccines the primary contributing factor to the increase in ASDs? How does it magically become concluded that if a child with autism is vaccinated that it is the vaccines but when a child with autism isn’t vaccinated, it’s some ambiguous environmental factor or even more ridiculously, vaccines that previous generations had? Don’t you realise that no one is going to lend you any credibility when the goal-posts get shifted at such a dizzying pace?
But there is a whole lot of evidence of vaccine causation that is being dismissed as “coincidence” with no investigation, including what parents have witnessed in their children who react to vaccines.
Evidence? How are a collection of anecdotes evidence? I would think that parents of autistic children would have a better understanding of how autism progresses and their own limitations and biases. I wonder how many of you actually read the OAP transcripts or just relied upon the heavily biased reporting by second and third parties.
Regarding Dr. Bernadine Healy, you said that “She is a politician, not a scientist”. Actually, she is a doctor, former head of the NIH, and currently works as a journalist. From her bio at http://www.nlm.nih.gov/changingthefaceofmedicine/physicians/biography_145.html :
Of course it’s your right to disagree with her, but to dismiss her opinions because she is just “a politician” is inaccurate as well as lame.
I am dismissive of her opinion because she is a politician and administrator, and failed ones at that. You don’t mention her contentious and short tenures at the Red Cross and NIH. Now she did make some very hard and good decisions while at both those posts, but ultimately, her politics (which were responsible for getting her those posts to begin with) were more important than navigating those waters and being the voice for sound scientific reasoning. I don’t care what her educational credentials are, you can’t rest on such laurels as evidenced by scientists such as Linus Pauling and Peter Duesberg; off to brilliant starts and even a Nobel prize for the former but they took the fast lane to crazytown.
You aren’t considering the totality of Healy’s deeds; she has some impressive letters after her name and says what you want to hear. She rejects evidence-based medicine and from the way she criticises it, I don’t think she even knows what it is. Her most recent blunder being the criticism of the U.S Preventative Services Task Force on Mammograms and pulling her own recommendation from her bum. She clearly hasn’t consulted the global literature on the subject. Her role as an advisor to TASSC: http://en.wikipedia.org/wiki/The_Advancement_of_Sound_Science_Coalition should leave someone like you reeling with disgust, but yet you continue to defend her. Not me, anyone who would be involved with such dealings is a no-brainer to disregard. She is now a journalist for a rag that caters to the lowest common denominator; even that incompetent bureaucrat Julie Gerberding managed to land herself a cushy post at Merck after plunging the CDC into the ground.
Nothing you said contradicts Sheryl Attkisson’s statement that “CBS News has learned the government has paid more than 1,300 brain injury claims in vaccine court since 1988, but is not studying those cases or tracking how many of them resulted in autism. The branch of the government that handles vaccine court told CBS News: ‘Some children who have been compensated for vaccine injuries…may ultimately end up with autism or autistic symptoms, but we do not track cases on this basis.’” Do you have any information to contradict that statement? Or is your only response to malign Ms. Attkisson?
Of course I have information to contradict Attkisson’s woefully amateur reporting. Her piece on Dr. Offit was rife with conjecture and errors, had she bothered to use reliable sources for that, she would have seen that. Instead, she relied upon her own agenda and biases to create a story that she wanted to hear. Likewise, you like what she says so you don’t bother to critically evaluate the accuracy. Also, where was she when Wakefield was struck-off the GMC? Why didn’t she interview him or any of your AoA overlords when this happened? Follow up on his claim that 5 different countries replicated his so-called research?
The HHS does not track vaccine injuries compensated through NVICP because that is not within their purview to do so; Ms. Attkisson should know that and that information is easily ascertained but it doesn’t fit with her slant. Also, injuries compensated by NVICP are not conclusive for causality, rather they are found to be ‘more likely than not’. Furthermore, these cases don’t have anything to do with the OAP now do they? What she also neglects to explain are the differences in those children compensated; they all suffered a physical disability following their vaccinations. If this was the case with the OAP petitioners’ cases, then why didn’t they hitch their wagons to the existing table injuries rather than go for a de novo vaccine injury of autism spectrum disorders? I know the answer to this but do you?
In response to Attkisson’s statement “That’s what the parents of autistic children have told me as well. If we can screen children to see which ones might be more susceptible to vaccine side effects, and vaccinate them on a more personalized schedule that is safer for them, why wouldn’t we?” you said, “Screen for what? You have to know what you are looking for in order to screen for something.” Exactly! For the most part, they don’t know what to look for! This is the kind of thing that agencies such as the CDC should be studying. What are susceptibility factors? Of those children who have had severe reactions to vaccines, are there certain lab results they have in common, or something in their health history? Do they have family history of auto-immunity or immunodeficiency? Did they have prior reactions to vaccines?
I see you don’t understand how you could proceed with such an association; you don’t just ‘study’ children that have had adverse reactions for what would you ‘study’? Entire genome sequencing? Full immunology panels? Infectious disease panels? MRIs? CATscans? You want scientists to take a shotgun approach and this can simply not be done. But please feel free to explain how this is viable; I’m listening. As for no one studying vaccine reactions, how do you account for these:
http://www.iom.edu/Reports.aspx?topic1=BA4CD870-F567-46E3-88DE-20E50AD7ED3E&series=6F4ACEDB-41C5-4AC5-BBDE-39D9A343A8D3
Or how about this undertaking: http://www.scientificamerican.com/article.cfm?id=vaccinomics-personal-vaccine
Not only does this tech specifically identify vaccine reactions but also the areas of the genome that may be responsible or contributory to them and individualised vaccines made.
Pay attention to the references used to generate those reports. The claim that those experience vaccine reactions aren’t being studied is bollocks. When a pattern emerges via surveillance, then there is something to go on. There is no discerning pattern for your claims in spite of parental reporting. I would like you to conduct a little mental exercise in hopes that you can appreciate the scientific method. Design a study for what you propose. State your hypothesis, your study group(s), inclusion/exclusion criteria, methods for testing your hypothesis and sample size required for adequate statistical power. Go!
Barbara Loe Fisher said, “NVIC has been calling for basic science research into the biological mechanisms of vaccine injury and death for more than two decades. Without understanding how and why vaccines can cause brain and immune system dysfunction, there will be no way to develop pathological profiles to help scientifically confirm whether or not an individual has been injured or died from vaccination.” http://www.nvic.org/NVIC-Vaccine-News/November-2008/Thursday,-November-20,-2008-Vaccine-Injury-Compens.aspx
When vaccine reactions occur, it is usually dismissed as coincidence by mainstream doctors and agencies. Rather than just dismissing thousands (yes, thousands) of parental reports, and not even studying those cases that have been conceded in vaccine court, our agencies should be researching these adverse reactions, studying these children. Instead of just defending the vaccine program by denying the negatives and talking about how terrible diseases are, agencies such as the CDC and FDA should be understanding the negatives and working to make our vaccine program as safe as possible.
See links above. The problem is, is that you are convinced that vaccines cause autism, i.e. ‘brain injury’ and don’t approve of the way medical-scientific research is conducted to determine mechanisms of action. As for dismissing parental reports of ‘my baby was vaccinated and is now autistic’, it goes to credibility and plausibility and these claims are neither. Again I think you should read all 6 OAP test cases to get an idea of the science and how absurd these claims are. Now I do think that some bona fide vaccine injury cases do fall through the cracks and that is very unfortunate which is why I think that all claims should be reported and let follow-up by the CDC determine association, even if they have to deal with ludicrous claim.
And yes, my statements are general. I am not a scientist. But you seem to expect us parents to prove something before it should be studied. I am not able to prove anything. I can only say what I have observed and read. And there are a whole lot of parents (some of whom are PhDs and MDs), as well as some doctors and scientists (some of whom are also parents) who are clamoring for more research on vaccines in relation to autism, seizure disorders, ADHD, auto-immune disorders, allergies, and more.
If scientists only studied what has already been proven they would never learn anything new. When people clamor for more research, it doesn’t make sense to tell them to first offer proof.
If you are not a scientist and/or physician then what makes you think you are qualified to dictate how and what research should ensue? Have you been onto PubMed and searched the literature for ‘autism’? Every aspect of autism is being examined from brain structure to genomics to immune/endocrine function to co-morbid or contributory disorders. That is how we find the answers and they aren’t going to be found immediately either. As for saying what you have read or observed, well what does that mean? That your anecdotes are worth more than carefully conducted clinical and/or epidemiological studies? Your appeal to authority is merit-less also since I have seen what most of your ‘experts’ have to say and they aren’t credible and in fact, are taking advantage of parents like you.
And yes, since your group is making the claim of a vaccine causation of autism, don’t approve of the current direction of ASD research (which will actually address your concerns) and dismiss numerous studies that fail to find associations between certain vaccines and constituents with autism, then yes, the onus is upon you to substantiate your claims vis de vie your own studies. Isn’t Generation Rescue funding a study that examines unvaccinated and vaccinated cohorts? Why don’t we wait for those results then?
passionless Droning about autism 
June 17, 2010 at 2:12 am
i also wonder if there might be a strong correlation between pre-term birth and other factors that we might be less surprised to see associated with SEN (i.e. socioeconomic status, nutrition, etc.)
June 18, 2010 at 1:02 pm
Hi Eleanor –
Maybe, but I would have thought that the lack of a difference between elective and spontaneous births in this study would argue against these types of factors; in general, I’m thinking that lower SES, for example would have a lower elective C-Section rate. I may be way off base here though. Good question.
– pD