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Steve Novella vs. Julian Whitaker on vaccines at FreedomFest

Steve Novella vs. Julian Whitaker on vaccines at FreedomFest

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454 thoughts on “Steve Novella vs. Julian Whitaker on vaccines at FreedomFest

  1. David Gorski says:

    Right from the beginning of this thread, you raised objections to Dr. Gorski’s style, his phases and his tone.

    That’s pretty much the only criticism Peter ever has of me. For some reason my style really, really irritates him. There was a time when I actually was concerned about his criticism of my “tone,” but that time is long past. Peter has utterly failed to persuade me, despite trying relentlessly for the last two or three years.

  2. daedalus2u says:

    The effect that papertrail mentions is common in many other knowledge domains. It is not surprising that it would show up in vaccine beliefs too. Dr Novella has written about something close to it, conspiracy theories

    http://theness.com/neurologicablog/index.php/category/conspiracy-theories/

    and the difference between skepticism and cynicism.

    http://theness.com/neurologicablog/index.php/skepticism-vs-cynicism/

    I think it is a natural consequence when you try to analyze reliability of what someone is saying in a field where you are ignorant based on your own unreliable beliefs. I think this also relates to crank magnetism.

    I suspect that it also relates to an uncanny valley type of information processing.

    https://en.wikipedia.org/wiki/Uncanny_valley

    Where the degree of similarity between existing beliefs and the world view being expressed by the other person corresponds to the X-axis. If the ideas are very similar (preaching to the choir), the ideas are accepted, it they are extremely divergent there isn’t enough intersection to matter and they are ignored. It is only when there is some overlap that revulsion and antipathy is triggered. In human interactions I think this is what triggers xenophobia, and I have blogged about it.

    This relates to a discussion that I had with Dr Atwood on how do positive anecdotes change the Bayesian prior plausibility of an intervention. My position is that positive anecdotes cannot reduce the prior plausibility of an idea, they an only increase it (but that increase may be very small and not quantifiable).

    In the limit, if the anecdote was completely made up, that is it is pure fiction, then it is equivalent to every other false idea and is completely unrelated to the validity of the idea in question. Something unrelated has no effect on the Bayesian analysis of plausibility.

    The plural of anecdote is not “data”, but it it also not “anti-data”. The anecdote might be correctly reported and might have a small but positive degree of reliability and so might provide small but positive support for the idea. If the anecdote was completely false it would have zero reliability and so has zero influence on the validity of the idea, that is zero influence positive or negative.

  3. pmoran says:

    Yes, daedalus2, we (meaning EBM/SBM) have never thought seriously about anecdote because we have always been able to dismiss it whenever it suits us to do so, without feeling we had to give any further explanation.

    That follows a rule-of-thumb convention that helps the proper and efficient functioning of medical science, but we need to delve deeper into the intricacies of anecdote if we are to communicate effectively with CAM, a “medical system” that relies almost totally upon anecdotal evidence.

    I suggest in the following commentary that the failure to understand this has helped the cause of cancer quacks.

    http://www.users.on.net/~pmoran/cancer/Brenneranecdote.htm

  4. daedalus2u says:

    PM, I have no qualms about discounting anecdotes to near zero. But positive anecdotes can never be discounted to below zero, that is used to reduce the prior plausibility below what the evidence in the absence of the positive anecdote would indicate.

    I get this all the time in my nitric oxide stuff. I present a theoretical argument, backed up with data from the literature, and people say it is plausible. I start talking about anecdotal results and it gets dismissed as quackery.

  5. pmoran says:

    D2: I get this all the time in my nitric oxide stuff. I present a theoretical argument, backed up with data from the literature, and people say it is plausible. I start talking about anecdotal results and it gets dismissed as quackery.

    The best definition of quackery is that Dr Barrett suggested, of “overblown medical claims” (implied ‘in relation to the available evidence”).

    I have been involved in those discussions with you, and I, too, thought that you can step over the line of reasonably supportable expectations concerning the medical implications and likely therapeutic applications of your work — for the simple reason that NO mediated processes may well be involved in many or most diseases and even in some placebo responses, but it is likely that other, overriding processes will be the usual main deteminant of symptoms and of outcomes.

    The poo-pooing of anecdote is an expected reflex response in this type of forum so recruting that will indeed tend to have a negative effect on attitudes towards your claims. I think anecdote is mainly of use when dealing with well-documented, replicated, and objective, otherwise unexplainable, outcomes.

  6. daedalus2u says:

    PM, I don’t base my claims on anecdotes, I base them on my understanding of nitric oxide physiology which I have gleaned from a deep reading of the literature. People who think my claims are overblown have not deeply read and then understood the literature as I have.

    The problem that most people have is that they are caught up in a number of wrong ideas about physiology. Most of these wrong ideas were not consciously adopted, they are the “conventional wisdom” that people understand physiology in. A few of these wrong ideas are:

    1. There is no such thing as homeostasis. There is nothing that physiology keeps “constant” as homeostasis posits.

    2. There is no teleology in physiology. Nothing just “happens”, things only happen because the control system of physiology causes them to happen (or failed to prevent them from happening) by mechanisms we do not understand.

    3. The most complicated physiological state is the state at rest when all physiological parameters are stable. The only reason those physiological parameters are stable is because the control system of physiology is maintaining them stable. Maintaining physiology stable is really really complicated and we have very little understanding of how that happens.

    4. All disorders are disorders of development. Either development led to a bad physiological state, or development did not lead away from a bad physiological state.

    I appreciate that essentially the opposite of these statements is the “conventional wisdom”, but there is no data to support that “conventional wisdom”. The “conventional wisdom” was adopted in the absence of data to support it, and unfortunately it has become the default, null hypothesis.

    It is unfortunate when people are unable to question their fundamental assumptions. I think this is mostly due to human hyperactive agency detection. Our pattern recognition is skewed to see false positives of agency even when it is not there. People want and need to see a top-down agent controlling things. There isn’t one.

  7. pmoran says:

    D2:It is unfortunate when people are unable to question their fundamental assumptions. I think this is mostly due to human hyperactive agency detection. Our pattern recognition is skewed to see false positives of agency even when it is not there. People want and need to see a top-down agent controlling things. There isn’t one.

    If you are saying that animal physiology is a ramshackle mess, cobbled together by evolutionary forces with whatever happened to be at hand, I would agree. Even the anatomy is crazy. Why have the urethra traversing the prostate gland, for God’s sake? The female genitourinary tract is also poorly arranged for medical purposes.
    An all-knowing being would have done better than this, even at His first go at designing a human being.

    But all this expedience also works against your wish to come up with your own simplifying principles. Might not some processes have complicated regulatory mechanisms involving higher level integration with other bodily activities including mental influences, and others have simple feed-back loops at the local level?
    .

  8. daedalus2u says:

    PM, I agree with you, but when you look at things the right way, there is a great deal of order that just falls right out. I am in the process of writing it up and I will email you a draft.

  9. pmoran says:

    David asks whether I have evidence for autism being connected with vaccines. The answer is no, I have no good evidence, but as anyone can see by going back through my posts I am more concerned about how we present our case to some sections of the public.

    Adding to Papertrail’s study regarding the quirks of personal belief, there is the following. Can the provision of the actual facts reinforce false beliefs?

    http://www.boston.com/bostonglobe/ideas/articles/2010/07/11/how_facts_backfire/?page=2

    I ask whether we on SBM are much better in our ability to re-examine our beliefs . Despite considerable contrary evidence, and extensive experience of the failure of that approach, just about every skeptic or healthfraud activist believes better education and confronting people with sound scientific information is the answer to that which we deem “quackery”.

    Providing information is indeed about all that we have to work with (other than fostering trust) , but it is also a trap. It becomes too easy, and self-reassuring, to attribute contrary thought to either stupidity or ill will — and worse, to let that show in our side of the dialogue, to the detriment of any small influence we may be striving for with the more reasonable elements among our “opponents”.

    This is why I cringe when, among other things, we start off public dialogue on vaccines by plunging into the epistemology of correlation and causation. Who the heck does not understand coincidence? This is talking down to people with quite reasonable concerns. It imparts no very relevant take-home message. It switches people off. It (and all other references to logical fallacies) is playing to our cliquey elite, potentially swamping debate with facile put-downs rather than precise, relevant rebuttal.

    If it is as difficult as it seems to modify personal belief, but we feel obliged to try, should we not be looking at better ways of providing the information?

    For a start, with regard to vaccines, we might try and look into people’s minds. This is what I think you will find there, and this is what our arguments need to be tuned to –. .

    Concerned parents will be asking themselves, what about these instances of the onset of regressive autism about the same time as vaccinations? I mean, what makes a two-year-old suddenly lose mental skills? How does science explain that? (Don’t bother telling me about the Special Masters cases — I have read them all — the question is how to present that to the public and what they really tell us.)

    What about indications that autism rates are increasing over the period of increasing vaccine exposure? It seems a lot of that increase can be shown to be spurious, but ALL of it? We need a clear answer to that if we are to support certain statements.

    We are told that autistics have physical changes in their brain so it must be a genetic or developmental disorder. Why so? How consistent is that evidence, and that for a genetic connection, or are these weak statistical correlations or ones which in no way exclude an environmental trigger?

    On top of this, they know that we would push hard for vaccines even at some small risk to some individuals. They also now know how scientific studies can be suspect if performed and interpreted against a background of bias, so why not here?

    They are aware that vaccines are not quite the same thing as a medical treatment, where immediate benefits may outweigh risks. Vaccines are given to healthy children who may never be exposed to the particular risk that is to be prevented. They have every right to expect the highest standard of evidence and they should not be required in their turn to mount a telling scientific case in support of their vague anxieties.

    In a way this is the other side of our differences with chiropractors about stroke from neck manipulation. Even if chiropractors think that this risk is not conclusively proven they should be taking precautions, since neck manipulation is rarely the only option available for any condition, and we do normally apply lower standards of proof to evidence of serious risk than we do for other matters in medicine.

    So we at least need to be seen to be taking this matter very seriously and keeping the question open to the degree that the quality of our evidence warrants. We should never, ever, ever hint at exasperation that people are not humbly bowing down under the weightiness of our medical authority and/or intellectual superiority. We should avoid any hint of exaggeration of our case. If we are asked for evidence we should provide it immediately.

    The truth is that we probably cannot persuade most people via the evidence, but we can gain (or lose) their trust through how we present our case. This is presumably why extravagant claims can have the opposite effect to that desired.

  10. Harriet Hall says:

    @pmoran,

    Quackery is not going to go away no matter what we do. If people distrust science or are already “true believers” we’re not likely to influence them. We are writing for people who have not yet irrevocably made up their minds. We’re hoping to reach the fence-sitters. It’s not one size fits all: different people will be receptive to different approaches from different writers. Some people want to hear all the quibbles, others want a clear yes or no answer. I’m sure you can remember patients in your own practice who listened to all the scientific pros and cons of the evidence for different treatment options and then wanted you to make the decision for them, asking “What would you do?”

    I wish you would stop repeating the same complaints about what we are doing wrong. You’ve made your point. It’s past time for you to SHOW us how you think we could do it right. Please give an example of how you would present the vaccine issue. I’m listening. I’m willing to learn. If you really have superior wisdom and insight into our audience’s minds, you can demonstrate it by stopping the preachy generalities and giving us something specific. Put up or shut up.

  11. David Gorski says:

    Indeed. Peter has become tiresomely repetitive in this thread. There is nothing in his most recent comment that I haven’t read at least two or three times already in just this comment thread alone. For instance:

    What about indications that autism rates are increasing over the period of increasing vaccine exposure? It seems a lot of that increase can be shown to be spurious, but ALL of it? We need a clear answer to that if we are to support certain statements.

    Jumpin’ Jesus on a pogo stick! This statement demonstrates some serious ignorance of the literature on autism, and it’s not for our lack of trying to educate our readers on the literature. Clearly, in your case, we have failed. We have written several posts explaining the concepts of broadening of the diagnostic criteria in the early 1990s, increased awareness, increased screening programs (you, of all people, a cancer surgeon, should know that the more you screen for a condition the more of that condition you will find), and the like. We’ve discussed the concepts of diagnostic substitution and cited studies applying today’s diagnostic criteria to adults and finding a prevalence similar to what we see today. Basically, there are several lines of evidence all converge on a conclusion that, controlling for changing definitions, autism prevalence has been fairly stable over the time period when there is claimed to be an “autism epidemic.” It’s possible that prevalence might have increased slightly (although that isn’t even sure), but what is certain is that the “true” prevalence of autism is not exploding as the prevalence figures seem to indicate.

    Seriously, Peter, at this point it was painful for me to read your most comment, and not because you were making points that made me wonder if I was wrong or that made me feel stupid. It was because I feel embarrassment for you.

  12. papertrail says:

    PMoran said: “Who the heck does not understand coincidence?”

    Those who ask, in spite of all the studies that have been done: “What about indications that autism rates are increasing over the period of increasing vaccine exposure?”

  13. papertrail says:

    The Boston Globe article you posted, Dr. Moran, seems to favor a more hammering approach when it comes to confronting sources of misinformation, which is what Dr. Gorski was doing in his article as he was expressing his disgruntled response to Whitaker, a source of vaccine misinformation (as opposed to addressing a parent with vaccination concerns).

    Here’s one of the concluding paragraphs of the Boston Globe article: “Nyhan ultimately recommends a supply-side approach. Instead of focusing on citizens and consumers of misinformation, he suggests looking at the sources. If you increase the “reputational costs” of peddling bad info, he suggests, you might discourage people from doing it so often. “So if you go on ‘Meet the Press’ and you get hammered for saying something misleading,” he says, “you’d think twice before you go and do it again.”

    Let me make this statement relevant to your dispute with Dr. Gorski’s approach in his article: So, if you go to a lecture and you get hammered by Dr. Novella and slammed by Dr. Gorski later on SBM for saying something misleading, you’d think twice before you do it again.

  14. RE: papertrail on 03 Aug 2012 at 4:30 am in reply to pmoran:

    Well played, sir.

  15. passionlessDrone says:

    Hello friends –

    Long thread. Mostly same discussion.

    Here are the problems from a standpoint of looking at the evidence.

    Studying thimerosal tells you about thimerosal. Studying the MMR tells you about the MMR. We have studied those things and the results are uniformly negative. Great!

    But These are distinctly different things that studying vaccination. Most everyone here knows that, in fact, but people don’t really want to admit it; instead they’ll say things like ‘there is no evidence that vaccination has caused autism’, which while technically true, ignores the exceedingly inconvenient fact that we haven’t really looked very hard. You’ll almost never get someone like Dr. Gorski to admit this; eventually he will fall back on the very problematic nature of a prospective study which is an end around way of admitting to the truth, our analysis is very, very weak in regards to the act of vaccination and autism. It just is. If this were not the case, he wouldn’t have been forced to make such blanket statements about thimersoal and the MMR; that’s the only bulletproof analysis we have.

    pD, why don’t our MMR studies help with this?

    They may, but the MMR is given very late in the vaccine schedule, between a year and eighteen months, long, long after the bulk of the vaccine schedule, which has inoculations for hib, DTP, polio, influenza (for some), pneumococcal, and hep-b at two, four, and six month appointments (in the US). I wonder, if Dr. Gorski has any particularly good reason to assume that time is an unimportant distinction in this type of discussion? I would argue that in a condition as complex as autism and the still very mysterious brain organizational efforts occurring in the brain during the first year of life that details matter.

    That being said, we can’t just say, ‘well things are complicated, and you haven’t studied it, so study this!’. There must be a biologically plausible mechanism by which vaccination could affect the developmental trajectory; else we have to study everything at every time frame, and that isn’t a very useful approach.

    Unfortunately, there is a mechanism by which vaccination could affect brain development in early life, and it just so happens, animal models of autism risk factors and immune observations from the autism cohort tell us that these intersect.

    There was a really neat paper by Patterson that came out a few weeks ago that is in a long line of maternal immune challenge studies in the animal realm that tell us roughly the same thing; gestational exposure to increased levels of immune activity are risk factors for behavioral and physiological changes consistent with autism. That study, Modeling an autism risk factor in mice leads to permanent immune dysregulation [PMID: 22802640] found that in utero exposure to immune challenge lead to persistence programming of the immune system, including decreased regulatory immune cells, and increased production of inflammatory cytokines. These changes were persitent through the lifetime of the animals.

    What this tells us is that a known risk factor for autism includes, as a byproduct, an altered immune profile that involves heightened inflammatory responses, and decreased regulatory capacities.

    It just so happens, this finding is consistent with a large swath of observations from children with autism. A lot of the time if you get someone like Dr. Gorski to acknowledge that there are immune findings in autism, it gets glossed over if ever mentioned; but the reality is that we have a lot of evidence of dysregulation, and in many cases point in the same direction, a state of increased inflammatory biomarkers. Here are some studies for anyone skeptical of this claim:

    Increased serum levels of high mobility group box 1 protein in patients with autistic disorder [PMID: 20302902]
    Elevated serum levels of interleukin-17A in children with autism [PMID: 22748016]
    Altered T cell responses in children with autism [PMID: 20833247]
    Macrophage migration inhibitory factor and autism spectrum disorders> [PMID: 18676531]
    The complementary role of high sensitivity C-reactive protein in the diagnosis and severity assessment of autism [not in pubmed for some reason]

    Now, here is the kicker; in each of those studies there was a positive relationship between the degree that inflammatory biomarkers were increased with autism severity; i.e., higher CRP == higher autism severity, higher MIF == higher autism severity, higher IL-17A, etc. If these studies are anamolies, they all found the same, wrong conclusion. Does anyone here think that is likely?

    “But, pD, ‘correlation is not causation!’”

    Another technically true statement, but one which is at odds with literally mountains of evidence that tells us that we can not longer decouple immune function with brain function. There are also similar numbers of studies that tell us that immune dysregulation occurs in depression, schizophrenia, OCD, tourettes, and just about everything else. [Interesting note, the Patterson paper above found that bone marrow replacements effectively 'cured' the autism mice of stereotypic behaviors.]

    “But, pD, that doesn’t mean vaccines caused the immune dysfunction. You can’t show that vaccines cause immune dysfunction.”

    True statement. But. It doesn’t matter.

    Let’s assume that vaccines cannot cause the persistent immune dysregulation observed by Patterson and observed in children with autism. Even though we haven’t studied it, for the sake of discussion, let us pretend that it has been studied, and that this immune profile can only be generated genetically or through insults that occur in-utereo. So what?

    That does not, absolutely does not mean that an interaction between a vaccination, or a real, live infection and that immune profile cannot occur. If a child was exposed to cigarette smoke in utero, we don’t pretend that there’s no reason not to cut out smoking in the home after birth because the damage has been done. The developmental origins of disease don’t magically stop at the exit of the birth canal.

    But, pD, just saying there is increased inflammatory profiles in autism and the fact that vaccines trigger an innate immune response isn’t a biologically plausible mechanism! You still are just pointing at things but can’t explain how one might lead to the other.”

    Fair enough.

    Has it ever occurred to anyone here that there seems to be a pretty big evolutionary disconnect between our infants susceptibility to infectious agents and their relative inability to mount an immune response early in life? We have hundreds of millions of years of evolution invested in our immune system, and yet, at our most vulnerable time, we rely on our mothers immune system for protection. Why?

    What if this isn’t a problem to be overcome, but rather, a feature that has been selected for through the cruicible of evolution? What if having a large immune response during infancy was so detrimental towards passing off genetic material, we were better off taking our chances during this critically vulnerable period?

    In the past few years, we have started to discover that the immune sentries of the CNS, the microglia, are doing a lot more than just responding to insults while ‘activated’ through injury or infection; it turns out, the microglia are performing critical optimization of the neural network during development; up to an including participating in the process of synaptic pruning. Here are some studies that demonstrate this:

    Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner [PMID: 22632727]
    Synaptic pruning by microglia is necessary for normal brain development [PMID: 21778362]
    A role for microglia in synaptic plasticity? [PMID: 21655446]
    Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals [PMID: 19339593]

    Or, for a terrifying review of these, glial priming, or many animal models of immune disturbances during development and associations with brain development, Microglia in the developing brain: a potential target with lifetime effects [PMID: 22322212]
    Perhaps our impaired immune capacity in early life is there for a reason, to keep our microglia from responding too vigorously when they are supposed to be paring our synaptic network down.

    Here is where the time component of ignoring all of the vaccines other than the MMR gets very, very problematic for people like Dr. Gorski. The first year of life is a busy, busy time inside the developing brain, and a lot of once in a lifetime optimization of the neural network is supposed to be happening. When we look at the autism brain, we see evidence that is consistent with impariments in synaptic pruning; i.e,. increased neuron counts and increased white matter tracks. [references available on request]. The microglia are supposed to be handling this for us; but their effect is highly time dependent on lots of other things that happen; including being in a non-activated state.

    But what if instead of performing maintenance on the neural network, our microglia were, instead, ‘activated’ with a different morphology and behavior set? That is what happens when we trigger the innate immune system! Fever is centrally mediated, peripheral immune markers trigger neuroimmunological changes in the brain, including morphological changes to the microglia. Our population of interest in this discussion, autism, just so happens to have abundant evidence of a heightened inflammatory response. If there was going to be a population of infants for which challenges to the innate immune system would have an exaggerated effect on microglial activation, it would be autism. Not only that, we have evidence of increased microglia numbers, and morphological changes (i.e., ‘activation’) in the autism brain. What a crazy set of coincidences!

    Does Dr. Gorski, or Stephen Novella, or anyone, have a good reason that we should ignore the possibility of time dependent effects on vaccination other than just chanting “Jenny McCarthy is a bimbo”? How would studying the MMR, administered at a year, give us insight into other vaccines given at two months, or four months? How does studying thimerosal help us understand this, at all? What reason?

    Vaccination doesn’t have to be causal in order to be participating. Dr. Gorski would be furious if someone were to try to tell us that cancer is dependent on one thing, happening once, and we get to ignore everything else that might be participating later on because there was “one” cause. It’s a lot messier than that. He’d be right. Why should a condition as complicated as autism be any different? Why?

    We can admit this while insisting that vaccines work (they do), that actual infection would have a similar effect (they would), and that our science on the thimerosal is rock solid (it is). But those are all different questions; this is supposed to be a site dedicated towards critical analysis, as such, our first goal should be the appropriate distinction of whether we can answer question B by looking at hypothesis A. Exclaiming that “there is no evidence that vaccination causes autism” is just a shell game for not wanting to admit we haven’t really looked. That would be fine and well if we didn’t have reasons to look. Unfortunately, we have those reasons, and pinning our hopes on the consistently unreliable findings of soft social scientists is a terrible, awful way to address the possiblity in a real change in the number of our children being changed.

    - pD

  16. daedalus2u says:

    PD, what hypothesis do you suggest should be looked at?

    What sample size would be necessary to look at that hypothesis with what degree of precision?

    How much would that research cost?

  17. Scott says:

    We know that the epidemiological studies haven’t picked up any correlation with vaccination in general, not just with MMR or thimerosal. We know that the people who continue to insist that there is a link won’t care what research is done.

    We also know that vaccines don’t constitute a meaningful fraction of the immune challenges infants face – no matter how young – and that any generically immune-mediated explanation doesn’t deserve a second look without concrete evidence behind it.

  18. BillyJoe says:

    passionlessDrone,

    It seems to me you are demanding 100% foolproof certainty before scientists can come to any conclusion about what the evidence says about anything. That’s a pretty high bar, and it would guarantee that no conclusions would ever be reached. Either that or you demanding that the conclusions be so loaded with qualifiers that the conclusion itself would be pretty well drowned out.

    The evidence is that vaccines do not cause autism. That evidence is so overwhelming that is unlikely that this conclusion will ever be overturned. Therefore the statement “vaccines do not cause autism” has attained the status of a scientific fact. That scientific fact, like any other fact in science, can be overturned, but it would require extraordinary evidence to do so. Unless and until this extraordinary evidence comes to light, scientists are indeed justified in saying that vaccines do not cause autism.

  19. passionlessDrone says:

    @Daedulus2u –

    PD, what hypothesis do you suggest should be looked at?

    Big Picture: Can the act of vaccination (or any immune challenge during infancy) affect the neurodevelopmental trajectory of infants within a susceptible subgroup? [A ways, ways down the road.]

    Smaller picture: What is the quality and quantity of the innate immune response in infants given the standard vaccine schedule? You might be surprised to find this information isn’t available; the idea that an innate immune response without pathogenic effects (i.e., just triggering the innate immune system) might have detrimental effects post dates increases to the vaccination schedule by many years. Despite being very highly studied, this component of vaccination, the innate immune response, just hasn’t been studied; especially in the infant cohort. If I am incorrect, it should be a simple statement to falsify.

    Smaller picture: Are the effects of vaccination (or infection) have different effects on infants with predisposition towards a state of inflammation, as the children in the autism population seem to have? What are the in-vivo immune marker profiles of such children compared to other children post vaccination?

    Smaller picture: Are changes to microglial population or morphology involved with any an immune challenge during infancy? Are there differences in those changes in subgroups that are predisposed towards a state of increased inflammatory cytokine production? Do those changes result in differences in neuroanatomy as a result of different patterns of synaptic pruning?

    Smaller picture: Are there different innate immune profile responses from broken apart vaccine schedules; i.e., a slowed down schedule, or a schedule based on one shot at a time?

    Smaller picture: What time dependent effects of innate immune response are associated with the vaccine schedule; i.e., is the immune response qualitatively or quantitatively different at one week, two, four, or six months of age? Is there a difference based on actual age, as opposed to exit from the womb age?

    Smaller picture: Are there differences in the length of alternate activation state and morphology of microglia in children vaccinated at early ages versus those that are not?

    Smaller picture: Getting smarter about the bazillion things we just learned and a bazillion other things.

    What sample size would be necessary to look at that hypothesis with what degree of precision?

    I don’t know. In any case, irrelevant towards the question towards biological plausibility.

    How much would that research cost?

    Irrelevant towards the question of biological plausibility.

    If someone were to ask you the cost of evaluating every degree by which NO is implicated in everything as a reason that it shouldn’t be studied, I doubt you’d find that to be a very convincing argument towards the plausibility of NO being involved in everything.

    I’m not advocating a vaccinated / unvaccinated study; it’s way to messy and we are way too dumb to sift through the data. I’m advocating being smarter in a targeted way about the state of the infant innate immune system and how tinkering with that system might interact with neurodevelopment. I’m not saying it’s easy, or in some cases, feasible with our existing toolset, but those are the types of questions we are going to need to ask in order to have confidence our actions aren’t having unintended consequences.

    Take Microglia in the developing brain: a potential target with lifetime effects for a spin; the animal models of immune disturbances are very robust and disturbances to microglial function is shown to have wide ranging effect on brain structure in ways with parallels to autism.

    @Scott –

    We know that the epidemiological studies haven’t picked up any correlation with vaccination in general, not just with MMR or thimerosal.

    Citation required. What the hell does “in general” even mean? You can be more specific than that, can’t you?

    We also know that vaccines don’t constitute a meaningful fraction of the immune challenges infants face – no matter how young – and that any generically immune-mediated explanation doesn’t deserve a second look without concrete evidence behind it.

    “Meaningful” in what way? Quality? Quantity? Details matter.

    Regarding quantity, my evidence is that vaccination very frequently generate fevers; up to 1/3 of the time depending on the vaccine. I don’t know if you’ve had children or not, but they do not have a fever one third of the days they are alive. Do you have any ideas on this paradox?

    How many fevers did your child have by the time they were two months old, or four months old? Lots? Any? [mine had zero] Yet, we are near 90% coverage with the vaccination schedule. Doesn’t this make vaccines qualitatively a meaningful fraction of immune challenges that infants face?

    We include adjuvants in bacterial vaccines because we need to overcome the noise of everyday immune function; the whole reason vaccines work is that they invoke a an immune response; that is why they work. If you think we don’t need a big kick to the immune system to achieve antibody recognition, why bother with adjuvants at all?

    If you can provide evidence of a non effect (i.e., no stimulation) of the innate immune response in infants following vaccination, that would do it. You can’t provide such evidence, and not only that, such evidence would mandate we rethink the entire organization of the immune system. Good luck with that. If you want to show me that it isn’t ‘meaningful’ whatever that means, you’ve got to be able to qualify your assertion with data instead of hyperbole and “in general”. You can’t.

    doesn’t deserve a second look without concrete evidence behind it

    You might be interested in knowing that hospitilization for infection during childhood is associated with an autism diagnosis; i.e.,

    Association of hospitalization for infection in childhood with diagnosis of autism spectrum disorders: a Danish cohort study [20439799]

    Similarly, infection during the first thirty days of life was associated with autism risk; i.e.,

    Infection in the first 2 years of life and autism spectrum disorders [17200260]

    - pD

    1. Harriet Hall says:

      @pD,
      “You might be interested in knowing that hospitilization for infection during childhood is associated with an autism diagnosis”

      So obviously we should vaccinate children to prevent those infections, right?

  20. daedalus2u says:

    The evidence that vaccines do not cause autism is really very strong, and it is not just the absence of a positive correlation. The major differences in neuroanatomy observed in autism compared to neurotypically developing individuals occur in utero. There is no mechanism other than magic by which the neuroanatomy of a typically developing infant could change to that of an infant with autism by any exposure to anything at age 12 months.

    It would be like suggesting that the number of toes a person has is determined by vaccines at age 12 months because the number of toes and the neuroanatomy of autism are both determined around the same time (in utero).

    There are differences in the immune systems of people with autism vs people who are neurotypical. Lets look at and understand those differences, not impute that they are due to vaccines (which both are exposed to).

    The vaccines cause autism idea is being pushed by people with an agenda. Their agenda is to get money from vaccine manufacturers or barring that, to destroy the vaccine industry. They are not honest brokers of information trying, in good faith, to figure out what causes autism. They don’t care what causes autism, they just want to get money. That was Wakefield’s motivation, that is why he committed fraud and published a fraudulent paper.

    The major change in infant immune system exposure from pre-industrial times is exposure to far fewer antigens and far fewer infections. Half of children don’t die by age 5 from some kind of infection any more the way they used to. Vaccination is a much milder immune system stimulation that having the disease. People who are unvaccinated still get autism. Vaccinated children don’t die of as many diseases as unvaccinated children do.

    If autism were caused by a specific vaccine containing a specific antigen, that would probably have shown up in the data. If the hypothesis is that autism is caused by a non-specific immune system activation, how do you propose to distinguish immune stimulation due to vaccines from immune stimulation due to a cold or any of the other zillions of infections that young children get? Put children in a germ-free environment? That would be even worse than not vaccinating because then the children would have no effective immune system even against non-pathogens (which are only non-pathogens because the normal body can easily mount a immune system response to them).

    If there is an immune system connection that triggers some symptoms of autism, it is triggered by immune system activation independent of vaccination. The neuroanatomy is generated in utero, if there is some “trigger” later, that “trigger” must have been “set” in utero, and that “trigger” can be activated by things other than vaccinations.

    The focus on vaccines and autism causation is misplaced. There is no science behind it, it is purely about people trying to get money from vaccine manufacturers. Unfortunately the people behind it are willing to lie in their efforts to scam money, and they don’t care who gets hurt by not being vaccinated. Unfortunately those people are willing to make threats against honest researchers who are trying to figure out what causes autism and how to make it better.

  21. daedalus2u says:

    PD, your hypotheses are hopelessly open ended. A subgroup? What does that mean? A subgroup of 1 per dozen, 1 per 100, 1 per 1000, 1 per 10,000? How big or small a subgroup do you mean? Do you define your subgroups post hoc?

    What kind of immune system changes? There are trillions of immune parameters. The antibody repertoire is ~10^15. Should we look at each one? Separately or in combination?

    What does a “predisposition to inflammation” mean? How does one measure it? At what point in time?

    How do you propose to measure changes in microglial morphology over time? Serial biopsies over time on individuals or single biopsy on different individuals at different times? Serial biopsies has the problem that the second biopsy would have to be in a different place than the first one. Which part of the brain would you biopsy first? The parts that are known to be essential for face processing? You do appreciate that those biopsies would cause the exact pathology you are trying to investigate?

    How many different vaccine schedules do you want to look at? If you have 20 different vaccines given with 20 different schedules with 5 different timings and use 100 children per test, that is 200,000 subjects. If you do $2000 worth of immunological testing on each, that is $400 million. Which immunological tests would you do?

    If you don’t know what it takes to determine “biological plausibility”, when will you know if you have found it (or not)?

    We know that children in the pre-modern era had more severe immune system stimulations than modern infants because many (if not most) of those children died from infectious diseases that they were unable to mount an effective response to.

    We know that vaccines are much milder immune system stimulations than what pre-modern infants were exposed to because infants only very rarely die from vaccinations.

  22. lilady says:

    @ pD

    “You might be interested in knowing that hospitilization for infection during childhood is associated with an autism diagnosis; i.e.,”

    Association of hospitalization for infection in childhood with diagnosis of autism spectrum disorders: a Danish cohort study [20439799]

    PMID:
    20439799
    [PubMed - indexed for MEDLINE]

    “A total of 7379 children were diagnosed as having ASDs. Children admitted to the hospital for any infectious
    disease displayed an increased rate of ASD diagnoses (HR, 1.38 [95% confidence interval, 1.31-1.45]). This association was found to be similar for infectious diseases of bacterial and viral origin. Furthermore, children admitted to the hospital for noninfectious disease also displayed an increased rate of ASD diagnoses (HR, 1.76 [95% confidence interval, 1.68-1.86]), and admissions for infection increased the rate of mental retardation (2.18 [2.06-2.31]).
    CONCLUSIONS:

    The association between hospitalization for infection and ASDs observed in this study does not suggest causality because a general association is observed across different infection groups. Also, the association is not specific for infection or for ASDs. We discuss a number of noncausal explanatory models.”

    “Similarly, infection during the first thirty days of life was associated with autism risk; i.e.,

    Infection in the first 2 years of life and autism spectrum disorders [17200260]”

    PMID:
    17200260
    [PubMed - indexed for MEDLINE]

    “Overall, infection diagnoses in the first 2 years of life were recorded slightly less often for children with autism than control children (95.0% vs 97.5%). Among specific diagnoses, upper respiratory infections were significantly less frequently diagnosed and genitourinary infections more frequently diagnosed in children with autism. In the first 30 days of life, the frequency of having an infection was slightly higher among children with autism (22.6% vs 18.7%).”
    CONCLUSIONS:

    Children with subsequent diagnoses of autism do not have more overall infections in the first 2 years of life than children without autism. Data suggest that children with autism may have modestly elevated rates of infection in the first 30 days and that, during the first 2 years, children with autism may be at higher risk for certain types of infections and lower risk for others. Additional studies that explore the associations between prenatal and early childhood infections and autism may help clarify the role of infection and the immune system in the etiology of autism

    Is that all you’ve got pD? These two abstracts really don’t support your very tenuous theory that stimulating the immune system through immunizations *triggers* autism.

  23. lilady says:

    Dr. Moran:

    Again, I am asking you, who appointed you as the sole arbiter of style, phraseology, tone and content on this blog?

    Dr. Gorski has his own style of blogging. He has a wide audience of readers on this blog and on his other blog. And, he has earned the respect of his readership and the respect of other science bloggers.

    I think at this point we all “get it”. You really do not understand the anti-vaccine climate in cyberspace. The quacks and assorted cranks bloggers who have an audience of fearful credulous parents, are vile and reprehensible…they will stop at nothing until they destroy our public health system. We cannot change the minds of those quacks or cranks…or the diehard anti-vaccine crowd…but we have had an impact on the fence sitters, who read the science blogs and have made the decision to immunize their children.

    You might be an expert on cancer and cancer quackery, but you are a naif when it comes to immunology, developmental disabilities, autism and the quackery associated with these subjects.

    Prove me wrong. Show us, by submitting a guest blog article about these subjects.

  24. passionlessDrone says:

    He Daedulus2u –

    The evidence that vaccines do not cause autism is really very strong, and it is not just the absence of a positive correlation.

    I wonder if there are any lurkers to this thread? Dr. Gorski posts a lot about autism and vaccines. All the time. No one who has read to this legnth of the comment thread would ever bother to deny this. And yet, with dozens (or hundreds) of posts here and at his psuedo-anonymous website, in his exchange with pmoran, he makes a very clear distinction about the state of our knowledge on thimersoal and the MMR, versus the practice of vaccination. Take his word for it.

    There is not a whiff of a hint of a link between the MMR vaccine and autism

    There is not a whiff of a hint of a link between thimerosal in vaccines and autism

    Both of these are pretty much bulletproof, as far as statements of scientific findings go.

    (On July 30, 6:23 pm.)

    Why bother make this distiction? I mean, let’s think about this clearly for a second; if Dr. Gorski didn’t have to make this distiction about the quality of our data, he wouldn’t. What he would have said is, this:

    There is not a whiff of a hint of a link between the process of vaccination and autism

    This is pretty much bulletproof, as far as statements of scientific findings go.

    Why wouldn’t he just say that? Think about that; a hundred (or many more?) posts about autism and vaccines through the blogosphere, and he won’t make this statement. What a crazy coincidence! I just cannot for the life of me figure out why!

    It is because he knows that this argument is not scientifically defendable. There is no other logical reason.

    If you have evidence that Dr. Gorski would like to understand that would enable him to make that kind of statement, why not just post it, instead of inferring it’s existence? For someone so interested in the degree of precision, I’m sure that the data you are about to post is going to be of high quality and addresses the act of vaccination.

    The major differences in neuroanatomy observed in autism compared to neurotypically developing individuals occur in utero.

    What is your definition of “major differences” in this regard?

    I am in full agreement that the in-utero environment is absolutely critical, but we don’t have a free pass once we are born. Important processes are still being performed.

    As evidence for this statement, and evidence that there are still major differences in neuroanatomy in autism that are being formed, after birth, I would submit the following:

    Neuron number and size in prefrontal cortex of children with autism [PMID: 22068992]

    Neat paper. Here is part of the discussion section;

    Apoptotic mechanisms during the third trimester and early postnatal life normally remove subplate neurons, which comprise about half the neurons produced in the second trimester.37 A failure of that key early developmental process could also create a pathological excess of cortical neurons. A failure of subplate apoptosis might additionally indicate abnormal development of the subplate itself. The subplate plays a critical role in the maturation of layer 4 inhibitory functioning as well as in the early stages of thalamocortical and corticocortical connectivity development.37 – 38 Reduced inhibitory functioning and defects of functional and structural connectivity are characteristic of autism, but the causes have remained elusive. The possibility of abnormal development of the subplate in autism merits investigation.

    This is actually a very nice example, it provides very recent, up to date literature that indicates important neuroanatomical differences are being formed after birth, and, is exactlywhat I am talking about.

    Do you think you could explain to us, here, with data, that Courchesne is wrong, that neuron removal does not occur postnatally? If he isn’t wrong, if neurons are still being removed postnatally, I wonder, could you explain to us why this isn’t a “major difference”. Do you have some reason to think that this effect is dependent on date of birth, as opposed to date of conception? If a full term, infant stops synaptic pruning four months into life, do you think a child conceived a month later, but born on the same day will be experiencing pruning five months after birth?

    My worldview is consistent with prenatal events being critical. The in-utero environment matters; but a blanket statement like “major differences” need to be clarified. It isn’t allowed to just be the things we want them to be, you. know. If a system is already messed up before birth, that doesn’t mean you can’t mess it up later on too.

    Even better, the mechanism of neuron removal are the immune sentries of the CNS; these cells are intimately tied to the immune system, and change function at immune challenge time. That is what I am talking about.

    They don’t care what causes autism, they just want to get money.

    Do you think that is why I am here?

    Half of children don’t die by age 5 from some kind of infection any more the way they used to.

    I agree.

    Vaccination is a much milder immune system stimulation that having the disease.

    How does this assessment take developmental timeframes into consideration? If our animal models show significant involvement of developmental timeframes. such that the effects of early life can have persistent effects, should this change our angle of thought regarding a series of immune challenges that occur very close to birth? Also, as you seem so keen on precision, maybe you could give us an idea of the quality of the innate immune response following vaccination (especially in infants). I asked Scott for some details in that regardd, but for some reason, he hasn’t responded with any data. Do you have any? Has it gotten to be so bad on this forum that “much milder” is taken as quality evidence.

    People who are unvaccinated still get autism. Vaccinated children don’t die of as many diseases as unvaccinated children do.

    I do not dispute either of these statements. I can’t, not dispute them any harder.

    If the hypothesis is that autism is caused by a non-specific immune system activation, how do you propose to distinguish immune stimulation due to vaccines from immune stimulation due to a cold or any of the other zillions of infections that young children get?

    Infants don’t get sick all of the time! Lots of infants, tons of them, don’t get colds in the first months of life. The bulk of our vaccine schedule is administered by six months of age, how hard is it to understand the difference between young child, and two month old? Do you understand this difference? In case you don’t understand this, there are some pretty significant differences between a two month old, and a four year old.

    Seriously. Do you think infants two motnths old get “zillions’ of infections?

    Also, people have succesfully detected immune stimulation due to vaccines, in vivoin adults, and in singularity.

    Effect of influenza vaccine on markers of inflammation and lipid profile [PMID: 15976761]

    Where pre and post blood samples were taken from recipients of influenza vaccine recipients. Increases in IL-6,CRP, and SAA were observed post vaccination. There are many other, similar studies, but all of them are in adults, and involve singular vaccines. Discerning innate immune response as a result of vaccination really isn’t that difficult; we just haven’t tried to do it in infants.

    Put children in a germ-free environment?

    Again, this assessment allows for no time dependent interactions. We don’t have to stop vaccinating. We may want to try to be more clever about vaccinating a lot, at the earliest stages of life. The animal models all tell us that there are developmental windows during which persistence of changes is possible.

    The neuroanatomy is generated in utero, if there is some “trigger” later, that “trigger” must have been “set” in utero, and that “trigger” can be activated by things other than vaccinations.

    Please see my concerns about regarding other neuroanatomical differences that are generated postnatally. In any case, as I’ve tried stating many times, just because something else can trigger the innate immune response doesn’t mean we should jump in head first without understanding the effects of our actions. Is that such a hard concept to understand? If a child is being raised in a house with smokers, does this mean we might as well let the workers at his daycare smoke too? Why shouldn’t we evaluate events we can control?

    What kind of immune system changes? There are trillions of immune parameters. What does a “predisposition to inflammation” mean? How does one measure it? At what point in time?

    If you were to take a look at some of the literautre I posted above, I seriously doo not understand why this is a difficult concept to grasp. For example:

    Macrophage Migration Inhibitory Factor and Autism Spectrum Disorders

    was published in Pediatrics. It was funded, in part, by the National Institute of Health. It involved genotyping, serum analysis, and behavioral diagnosis of over two hundred children. This was a very expensive and time consuming research effort. Here is the a snipet from the Introduction:

    Thus, the central hypothesis underlying this research was that a genetic predisposition to a particular level of MIF production may lead to a proinammatory proile of cell activation that, if present during a neurodevelopmentally sensitive period, might contribute to the etiopathogenesis of autism.

    What should we make of the apparent paradox wherein you do not understand a “predisposition to inflammation” means, but for some reason, the researchers, funders, peer reviewers, and editors of Pediatrics, all felt this was an appropriate wording? Are you suggesting that all of the entities I describe have it all wrong, but that you have it right? If you think that measuring a disposition towards a stateof inflammation isn’t possible, your problem isn’t with me, it is with the literature. Why not take up your concerns with the a letter to Pediatrics if you think this is such an impossible task to perform?

    Regarding your concerns over potential mechanisms to determine changes, I happen to be an optimist regarding human ingenuity, if not wisdom. We are approaching the realm of thousand dollar genome scans. The technology will get there, but we will have the courage to look?

    @Harriet Hall –

    So obviously we should vaccinate children to prevent those infections, right?

    I am not against vaccination. Your response implies a binary decision, vaccinate or not. We have a lot more options than that, I think you understand this, but I’m not sure.

    As I’ve stated many times, the animal models consistently show a time dependent effect. Do you understand what this means within a context of a vaccine schedule clustered in the first six months of life?

    @Lilady –

    I was using those studies to answer Scott’s statement that “generically immune-mediated explanation doesn’t deserve a second look without concrete evidence behind it.” Those studies provide evidence of such an association. If following that sequence of events was too difficult to follow, this conversation might not be appropriate discussion for you. Some of my reasoning on the potential for vaccination to participate in altering neurodevelopment is contained in my first post on this thread, 8/3/12 @ 11:12 am if you are interested.

    - pD

  25. Chris says:

    pD:

    Infants don’t get sick all of the time! Lots of infants, tons of them, don’t get colds in the first months of life. The bulk of our vaccine schedule is administered by six months of age, how hard is it to understand the difference between young child, and two month old?

    That is because we vaccinate. Infant mortality has decreased substantially because we do vaccinate for pertussis, tetanus, diphtheria, Hib, etc. In 1900 30% of children born died before their first birthday. This is what happened to one of my mother’s uncles, and the other died when he was six years old.

    If you have a better option to protect infants from those diseases, then do tell us what they are. Especially since pertussis is back to killing babies, last year babies were infected with measles and it will not be too long before diphtheria returns (which is what killed one of my mother’s uncles).

    If you are going to go on about inflammation, you need to compare it to the actual disease. What does cause more inflammation: the vaccine or the disease? Which is a corollary to my constant question to you: why does it have to be the vaccine?

  26. lilady says:

    @ Chris: Odd that you should mention invasive Hib disease and the immune response to the bacterium…

    http://www.cdc.gov/VACCINES/pubs/pinkbook/downloads/hib.pdf

    “In the prevaccine era, most children acquired immunity by
    5–6 years of age through asymptomatic infection by Hib
    bacteria. Since only a relatively small proportion of children
    carry Hib at any time, it has been postulated that exposure
    to organisms that share common antigenic structures with
    the capsule of Hib (so-called “cross-reacting organisms”) may
    also stimulate the development of anticapsular antibodies
    against Hib. Natural exposure to Hib also induces antibodies
    to outer membrane proteins, lipopolysaccharides, and other
    antigens on the surface of the bacterium.
    The genetic constitution of the host may also be important
    in susceptibility to infection with Hib. Risk for Hib disease
    has been associated with a number of genetic markers, but
    the mechanism of these associations is unknown. No single
    genetic relationship regulating susceptibility or immune
    responses to polysaccharide antigens has yet been convincingly demonstated”

    Have a look/see at these pictures of youngsters who were treated in hospital for invasive Hib disease. The picture of the infant with the gangrenous left arm is especially poignant…the baby’s lower arm was amputated just after that picture was taken.

    http://www.immunize.org/photos/hib-photos.asp

    Why has the incidence of invasive Hib disease in infants and children who received the Hib vaccine decreased by 99 % since the Hib vaccine became available?

    Just what do the two spurious links to autism do the two PubMed articles have to do with with vaccines? Those articles reference upper respiratory infections and strep infections that children with autism “may have” increased risk for….for which there are no vaccines available?

    @ pD

    “If following that sequence of events was too difficult to follow, this conversation might not be appropriate discussion for you.”

    Au contraire pD…I’m very much in tune with the appropriateness of this discussion…and very much aware of your fixation with vaccines, somehow, no matter how tenuous, being implicated in a diagnosis with autism.

  27. passionlessDrone says:

    @ Chris

    That is because we vaccinate

    The source you provide contraindicates your claim of causality rather directly.

    In 1900 in some U.S. cities, up to 30% of infants died before reaching their first birthday (1). Efforts to reduce infant mortality focused on improving environmental and living conditions in urban areas (1). Urban environmental interventions (e.g., sewage and refuse disposal and safe drinking water) played key roles in reducing infant mortality

    Next time, you might bother trying to read more than the first sentence of your source.

    Infant mortality has decreased substantially because we do vaccinate for pertussis, tetanus, diphtheria, Hib, etc

    Again, from your source:

    The reduction in vaccine-preventable diseases (e.g., diphtheria, tetanus, measles, poliomyelitis, and Haemophilus influenzae type b meningitis) has reduced infant morbidity and has had a modest effect on infant mortality (9)

    Do you know what modest means? It means the opposite of substantial. Listen, I know vaccines work. I know they keep infants from getting sick, and dying. I get it. I am not arguing against that; in fact, the thing that has me worried wouldn’t be an issue if they didn’t work.

    The part you aren’t getting, despite having it explained to you repeatedly, and despite it being an exceedingly simple concept, is the fact that very few children actually got hib, tetanus, measles, etc, in the first few months of life. Those that did, undoubtedly fared very poorly, and in many cases died. But no where close to 90+% of children got tetanus before they were sixty days out of the womb.

    Do you think 90% of children got measles by the time they were sixty days old? What about hib, do you think 90% of infants got hib when they were sixty days old? Do you think 100% of children got pertussis before they were four months old?

    Is the idea that there might be key differences in a two month old compared to a one year old, or four year old, really such a difficult concept to grasp? I am seriously flabbergasted at the number of times otherwise intelligent people fail to understand this.

    If you have a better option to protect infants from those diseases, then do tell us what they are.

    This is analogous to telling people concerned about global warming that they can’t point out the dangers of recklessly pumping carbon into the atmosphere unless they also are willing to explain how to power the world without using fossil fuels. A potential problem with the act of vaccination, and how to intelligently target such a problem are very different conversations.

    If you are going to go on about inflammation, you need to compare it to the actual disease. What does cause more inflammation: the vaccine or the disease

    It would help if someone like Scott, or Dr. Gorski, or you could point me in the direction of something that actually gives us empirical values on the innate immune response from the vaccine schedule in infants. I keep saying part of the problem is that we have not performed this analysis. If I’m saying it’s a problem that we don’t have that data available, I don’t think its fair for you to insist I produce it. I’d rather have someone that insists it is there produce it.

    The narrative goes that vaccines are the most studied of all medical interventions. Great. Then someone, somewhere, should be able to tell us the quality of the innate immune response they generate in the infants we are giving them to. Shouldn’t this be easy? How many times have you seen me make the same request? For some curious reason, no one ever responds. It is because there is no data. That’s what has me so worried, we have always assumed it to be an unimportant parameter.

    Dr. Gorski has decided not to engage me on this thread, maybe you should email him, and ask him to give you these studies, so you could finally, finally post the data and shut me up. If the data is available, this should be easy.

    In any case, my going “on about inflammation” also always includes the caveat of developmental timeframe. You can continue to not understand this as long as you’d like, but the only causality is your credibility.

    Which is a corollary to my constant question to you: why does it have to be the vaccine?

    I am not sure if you knew this beforehand or not, but this thread was about vaccination. Were you aware of that? If Dr. Gorski posted about the metabolic syndrome association with autism paper that came out a while ago, I’d post about that. I think it’s a neat study, albeit one that destroys the fairytale of a static rate of autism. Pretty much if he posted anything about autism, I’d post my thoughts. It just so happens, all of his posts about autism are also about vaccination. If all you want to read is the bobblehead sycophancy, just ignore my posts. I don’t know why my posts seem to bother you so much. Is it because I keep asking you to try to understand how time dependent effects should be an important consideration in the discussion?

    I’d also point out that I think you know that I am a regular contributor on LBRB on many posts that are not vaccination related.

    @lilady –

    I’m very much in tune with the appropriateness of this discussion

    If you understood the context with which I posted those studies to Scott, and the context of my previous post on this thread, why did you ask if that was “all I had”? That doesn’t make much sense.

    - pD

  28. lilady says:

    “If you understood the context with which I posted those studies to Scott, and the context of my previous post on this thread, why did you ask if that was “all I had”? That doesn’t make much sense.”

    It makes as much sense as the two articles that you cherry-picked and did not link to, each of which discuss early hospitalizations for URIs and other types of infections for children on the spectrum…not as a reaction to an immune reaction to a vaccine.

    It makes as much sense as this statement on your blog pD…

    “I am currently seeking self awarded degrees in immunology, neurobiology, gastroenterology, genetics, metabolism, epigenetics, and other areas to try to see how they all work together in the world of autism. Any commentators are welcomed to come along for the ride. Hopefully we can learn something from each other.”

  29. Chris says:

    Do you know what modest means? It means the opposite of substantial. Listen, I know vaccines work. I know they keep infants from getting sick, and dying. I get it. I am not arguing against that; in fact, the thing that has me worried wouldn’t be an issue if they didn’t work.

    So there is a number of children you are willing to sacrifice for your theory of “inflammation from vaccines cause autism” theory? Seriously? So a dozen children dying from pertussis does not bother you? Or how about the forty-one in Japan that prompted them to go back to vaccinating infants for pertussis: Impact of anti-vaccine movements on pertussis control: the untold story. You think that is an acceptable amount because it is “modest.”

    Do you think 90% of children got measles by the time they were sixty days old? What about hib, do you think 90% of infants got hib when they were sixty days old? Do you think 100% of children got pertussis before they were four months old?

    Strawman argument. I did not say that. I said those diseases affect infants. Babies who are loved by their parents and grieve at their loss. Babies that you are ignoring in your theory that inflammation from vaccines cause autism.

    Yet, you do not seem to understand that there is no real association between autism and vaccines, but the inflammation from actual diseases is even worse. But you seem to be okay with sacrificing infants to real diseases for you pet theory, because your cherry picked evidence says it is okay dokay.

    So the question is, pD, how many babies dying from pertussis and getting SSPE from measles infections is okay with you? Do you have a maximum number that are acceptable? Make sure that you tell this family, and definitely this other family. I’m sure they would be quite pleased that their children were in the “modest” category.

  30. papertrail says:

    Pd quoted this: “The reduction in vaccine-preventable diseases (e.g., diphtheria, tetanus, measles, poliomyelitis, and Haemophilus influenzae type b meningitis) has reduced infant morbidity and has had a modest effect on infant mortality (9)”

    Pd said: “Do you know what modest means? It means the opposite of substantial.”

    I was surprised to read that quote, but then it made sense that when infant mortality rates were so very high (10%) due to things like poor sanitation and malnutrition, the decrease in deaths attributable to vaccinations were moderate *in comparison*. Still, this moderate decrease could be regarded as a “substantial” number. Also, vaccinations aren’t expected to instantly induce 100% immunity against the diseases, but require a series and sometimes boosters, the idea being that you start early because a number of infants would be at least somewhat protected from morbidity and/or mortality (vaccination is not just about reducing deaths) even if not enough to “significantly” impact overall infact mortality rates. And, increasing herd immunity can be a benefit of immunizing infants.

    I know you made other points, Pd, but I just wanted to comment on that one thing, hoping it makes some sense; it’s 2 a.m..

  31. daedalus2u says:

    What is the criteria you are using when you say “infants don’t get sick all the time”. That infants don’t exhibit sickness behaviors to a degree that causes them to lie in bed? I can assure you that the infant immune system is working all the time, to varying degrees, which depend on how well it is working. When it is working really well, sickness behaviors are not needed to regulate allocation of substrates away from other activities so the immune system can use them.

    The only reason that infants are not “sick all the time” is because they mount a strong enough immune response to suppress the bacteria and viruses they are exposed to, and they are exposed to bacteria and viruses “all the time”, and if they were not mounting a strong enough immune response they wouldn’t just be sick all the time, they would be dead.

    The change from pre-industrial infants to now, is infants now are exposed to far fewer bacteria and viruses and far fewer antigens.

    As was pointed out, 30% of infants don’t die before their first birthday from infectious disease. If there is a “problem” with the immune system of modern infants it is not enough exposure to antigens.

    If anything, vaccinating infants results in a more “normal” immune system exposure than not vaccinating them. In pre-inustrial times, infants wouldn’t get vaccines, they would be exposed to the disease and would get the disease (and many die from it). Now they are just exposed to a weakened version of the antigen and merely have an effective immune response developed with very little risk of death or injury.

    If there is a problem due to exposure of the immune system, it is much more likely to be due to insufficient exposure. Maybe this is why that poorly done phone survey showed reduced autism in vaccinated children. Vaccination could be protective.

  32. passionlessDrone says:

    @Chris –

    A continued inability to decouple two distinct conversations presents a poor debating tactic; generally one in which you do not have substantive answers to one set of questions, so instead, you insist that your opponent answer another different set of questions. I know vaccines work. I know they save lives, and prevent sickness. I know that when people lose infants to disease, it must be a terrible, terrible thing. I really can’t even imagine it. How many times do I have to agree with you on this basic point?

    The appeal to emotion, as opposed to an analysis of the data is exactly what folks like Dr. Gorski jump on when someone posts pictures / storeis about children that are legitimately vaccine injured and attempts to use that as a deflection from the idea that vaccines work to prevent disease.

    Someone worried about global warming does not have to solve the energy crisis to be worried about global warming. I can be concerned about the increase in antibiotic resistant bacteria without wanting to abolish antibiotics. I can worry about how terrible the Republicans are while also understanding that the Democrats are almost as bad.

    We do not face binary decisions; we can be smarter about the choices we make. We can continue to craft our policies based on things we learn. If you don’t agree with that statement, I don’t know what else to tell you.

    @Lilady –

    I appreciate a lot of the work you have done in the past regarding people with disabilities and I do think you have the best interest of people like my son in your heart.

    This is supposedly a forum to openly discuss what our available data can tell us about the natural world. What the data tells me is that the resident immune cells of the CNS, the microglia, are responsible for critical maintenance of the brain during the developmental timeframes that include the bulk of our vaccination schedule. What the data tells me is that when we invoke the immune system outside the CNS, we also affect change inside the CNS; up to and including changing morphology and function of the same microglial cells. The data tells me that our population of interest, autism, has been shown repeatedly to have immune biomarkers consistent with impaired regulation of the immune response and increased production of substances known to be involved in the induction of fever, which is mediated centrally. The data tells me that our population of interest also has neuroanatomical features that are consistent with abberant function of the microglia at synapse maintenance time. The data tells me that people with autism have abnormal microglial populations and morphological structure when compared to people without autism, a set of features consistent with animal models of early life immune challenges resulting in persistent changes to adult physiology, neuroimmune characteristics, and behaviors. The data tells me that a dispassionate analysis of our data regarding the act of vaccination is extremely weak for a policy that touches nearly every single infant.

    I’m making a rule not to debate people that either cannot understand my arguments, or whom I do not truly feel are interested in an honest discussion. I’m not sure to which classification you belong, but I do think it is one of them. Perhaps I am wrong, show me wrong. Lets discuss the data. If you would like to discuss any of the data, or your different thoughts on the literature, then, fine. If, instead, your only contribution will be to quote my blogs ‘What is the all about’ page, you are free to do so, but the point you are making is that you are not interested in debate, only diversion. It speaks poorly towards either your mastery of the science, or, as I assert, the state of the science.

    @papertrail –

    You are, of course, correct in everything you said. I think I’ve stated this here, but for clarity, I would state that mortality prevention is not the only goal of vaccination, preventing sickness in itself is a worthy and valuable function of vaccines. I am sorry if I wasn’t clear on this. Furthermore, despite some accusations to the contrary, I harbor nothing but sadness for anyone who has had an infant catch any disease, vaccine preventable or not. Your comments make sense and I appreciate your tone.

    - pD

  33. passionlessDrone says:

    @daedulus2u –

    What is the criteria you are using when you say ‘infants don’t get sick all the time’.

    First you don’t understand what a predisposition to inflammation means, and now you don’t know what ‘getting sick’ means?

    That infants don’t exhibit sickness behaviors to a degree that causes them to lie in bed? I can assure you that the infant immune system is working all the time, to varying degrees, which depend on how well it is working.

    What are your thoughts on the paper I submitted above regarding empirical measurements of CRP, SAA, and IL-6 post vaccination? It looks to me as if there was a change, an increase in markers associated with inflammation post vaccination. If a car is idling all the time, and that doesn’t mean idling is the same thing as driving it one hundred miles an hour.

    When it is working really well, sickness behaviors are not needed to regulate allocation of substrates away from other activities so the immune system can use them.

    But sometimes sickness behaviors are observed post vaccination. Why? What are the chemical messengers that participate in this? If we were to take a population of infant with more CRP, more MIF, and more HMGB, can we make any prediction, at all, about the robustness of their immune response compared to an infant with decreased levels of those immune molecules?

    The only reason that infants are not ‘sick all the time’ is because they mount a strong enough immune response to suppress the bacteria and viruses they are exposed to, and they are exposed to bacteria and viruses ‘all the time’, and if they were not mounting a strong enough immune response they wouldn’t just be sick all the time, they would be dead.

    Then how do you explain our continued ability to detect fever in infants post vaccination? How do you explain the findings in the paper I provided above wherein post vaccination there were clear and consistent indicators of activation of the immune system? I know you have a very strong bias against the concept of homeostasis, but why are we able to detect changes in biomarkers post vaccination if the effect is so marginal compared to living in the big dirty world?

    Here is another example:

    HPV-16 L1 VLP vaccine elicits a broad-spectrum of cytokine responses in whole blood [PMID: 15855014]

    Here, we evaluated innate and adaptive immune system cytokine responses induced by HPV-16 L1 VLP in whole blood (WB) cultures from individuals receiving the vaccine (n=20) or placebo (n=4) before and after vaccination. 11 cytokines were measured: IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IFN-gamma, TNF-alpha, and GM-CSF using multiplex bead arrays. Cytokine profiles from WB samples clearly discriminated between vaccine and placebo recipients and between pre and post-vaccination responses. Significant increases in Th1, Th2 and inflammatory cytokines were observed in WB assays following vaccination

    So, even though everyones immune system was working all the time, researchers could still discern placebo/treatment groups by immune profiling. Do you have any explanation for why this might be the case? How were the researchers able to determine pre / post vaccination samples by evaluating cytokine profiles if the effect of the vaccine was not meaningful? My heart beats all day long too, but I seem to notice a difference when I hit the treadmill for thirty minutes. I think that there might be a difference between baseline operation and stimulated operation, but maybe that’s just me.

    The change from pre-industrial infants to now, is infants now are exposed to far fewer bacteria and viruses and far fewer antigens.

    There are other changes too, you know. What about antibiotics? What about sanitation? What about water treatment plants? Do you think there are any nutitional differences in children today compared to pre-industrialization?

    As was pointed out, 30% of infants don’t die before their first birthday from infectious disease.

    As I pointed out, most of the reduction in mortality was the result of things other that vaccination.

    If there is a ‘problem’ with the immune system of modern infants it is not enough exposure to antigens.

    I like the hygeine hypothesis more and more; I’d say that this one of the problems modern infants face.

    If anything, vaccinating infants results in a more ‘normal’ immune system exposure than not vaccinating them.

    Citation required! You are making bold but meaningless statements, ‘more normal’ when the nuances of the data tells us that things aren’t so simple. Want a real world example?

    Modulation of the infant immune responses by the first pertussis vaccine administrations

    Furthermore, the general cytokine profile of the Pa recipients was strongly Th2-skewed at 6 months, as indicated by the cytokines induced by the mitogen phytohaemagglutinin. 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

    What they found was that baseline cytokine profile of infants at six months was determined by which type of DTP/DTAP they got at 2,3, and 4 months of age. Can you tell me which immune profile is ‘normal’? Also, I think we can agree that the immune system of these infants was ‘working all the time’ in the hours between four months of age and six months of age; given that, do you have any ideas on how in the world researchers could discriminate which type of vaccine the infants got based on immune profile? All that ‘strong immune response’ to everyday viruses and bacteria, all day, every day, for two months, and it wasn’t sufficient to mask out the which type of vaccine the infants got.

    Can you explain this paradox? Can you do it with any data? This is a forum where you are expected to explain your resistance to published findings with something other than the vaguest “more normal”. Can you? If vaccines aren’t capable of affecting persistent change up and above recognition of antibodies, these results should be impossible.

    In pre-inustrial times, infants wouldn’t get vaccines, they would be exposed to the disease and would get the disease (and many die from it).

    No argument here.

    BTW – Have you had any thoughts as to why the Courchesne paper doesn’t describe major differences in neuroanatomy? Similarly, did you see Differences in White Matter Fiber Tract Development Present From 6 to 24 Months in Infants With Autism? I’m no expert, but I’m pretty sure that events starting at six months are after birth. What do you think? Do you have any reasons why we shouldn’t consider this a “major” neuroanatomical difference? [This paper also implicates improper axonal pruning as a potential mechanism of action. Go figure!]

    - pD

  34. Chris says:

    Daedelus2U:

    In pre-inustrial times, infants wouldn’t get vaccines, they would be exposed to the disease and would get the disease (and many die from it).

    The specific year, 1900, was not pre-industrial. In fact if we look at the CDC Pink Book Appendix G we see that in 1950 there were 120,718 cases and 1,118 deaths from pertussis. On that same line there were 5,796 cases and 410 deaths from diphtheria. I challenge anyone to tell me that was pre-industrial, and that sanitation systems were sub-par. And try the same for 2005 when there were 25,616 cases and 31 deaths from pertussis.

    Harriet Hall:

    So obviously we should vaccinate children to prevent those infections, right?

    pD replies:

    I am not against vaccination. Your response implies a binary decision, vaccinate or not. We have a lot more options than that, I think you understand this, but I’m not sure.

    Show us those options to prevent infant deaths from pertussis, Hib, etc. And then be very specific on exactly how DTaP is much more dangerous than diphtheria, tetanus and pertussis. Prove that if you are not against vaccination by explaining to why you insist on finding a way that autism can be caused by vaccination, when there is no real epidemiological evidence that vaccines can cause autism.

    Also, have you gotten your Tdap yet?

  35. daedalus2u says:

    pD Did you actually read the Courchesne paper you quoted from? Or is your distortion of what he says deliberate? From the abstract:

    “Results Children with autism had 67% more neurons in the PFC (mean, 1.94 billion; 95% CI, 1.57-2.31) compared with control children (1.16 billion; 95% CI, 0.90-1.42; P = .002), including 79% more in DL-PFC (1.57 billion; 95% CI, 1.20-1.94 in autism cases vs 0.88 billion; 95% CI, 0.66-1.10 in controls; P = .003) and 29% more in M-PFC (0.36 billion; 95% CI, 0.33-0.40 in autism cases vs 0.28 billion; 95% CI, 0.23-0.34 in controls; P = .009). Brain weight in the autistic cases differed from normative mean weight for age by a mean of 17.6% (95% CI, 10.2%-25.0%; P = .001), while brains in controls differed by a mean of 0.2% (95% CI, −8.7% to 9.1%; P = .96). Plots of counts by weight showed autistic children had both greater total prefrontal neuron counts and brain weight for age than control children.”

    “Conclusion In this small preliminary study, brain overgrowth in males with autism involved an abnormal excess number of neurons in the PFC.”

    Is 67% more neurons a “major difference”? Is “an abnormal excess number of neurons” a “major difference”?

    If you look at what he says in the paragraph just before the one you cited:

    “Because cortical neurons are not generated in postnatal life, this pathological increase in neuron numbers in autistic children indicates prenatal causes, including unchecked proliferation, reduced apoptosis, or both.23 ,29 – 33 Proliferation of cortical neurons is exponential between 10 and 20 weeks gestation and normally results in a net overabundance of neurons by as much as 100%.32 In animal models, dysregulation of genetic mechanisms are known that cause an even greater neuron overabundance and lead to increased head, brain, and cortical size,34 – 35 as is found in young children with autism.1 – 12 Functional analyses of genes located within copy number variation regions in autism also raise the possibility of dysregulation of proliferation during development.36”

    He is directly saying that neuronal proliferation occurs in utero, and only in utero and that there are genetic things that can increase that proliferation. You are cherry-picking what he says to impute that he is saying there is some post-natal exposure to something that is doing something that leads to what he is observing. That is not what the paper says. He observes higher than normal neuron numbers. The maximum number occurs in utero, but that maximum number can’t be measured because it would kill the infant. They happened to get to examine the brains of a few individuals that died, and so their brains could be examined in ways that the brains of living humans cannot be examined.

    When we know that there are teratogens that cause autism when there is exposure in utero during the time of neuronal proliferation (valproate and thalidomide) it is disingenuous to ignore that and focus on a hypothetical postnatal event and tie that hypothetical postnatal event to another postnatal event (vaccine exposure) when there is no data suggesting that there is a connection.

    The reason that infants today are exposed to far fewer bacteria and viruses is directly because of increased sanitation and modern water treatment and waste water disposal.

    Yes, the largest drop in mortality was due to better nutrition, clean water and better waste disposal. So what? Infants today have not been exposed to the antigen load that comes from having near-fatal infections. We know that 1/3 of infants had near-fatal infections because 1/3 of them had fatal infections and died before their first birthday. For what ever reason, infants today are not exposed to the immune response of near fatal infections. We know that because death from infection is pretty rare.

    If 1/3 of infants were exposed to fatal immune system stimulation and a tiny fraction of modern infants are exposed to fatal immune system stimulation, something that increases the exposure of modern infants to immune system stimulation makes their exposure “more normal”. We obviously don’t want to make that exposure so normal that 1/3 of them die, but vaccines don’t do that. Vaccines increase immune system stimulation without causing fatalities on the same scale as the diseases they are preventing.

    Yes, exposing infants to antigens causes their immune system to activate itself and this leads to measurable changes in various parameters of the immune system. That occurs if the antigens come from a vaccine, or if the antigens come from a mouthful of dirt, or from putting a toy that another infant has slobbered on in their mouth. The immune system activations observed today are not near-fatal immune responses.

    Why the concern with a handful of immune system activations from vaccines? Immune system activations that are mild compared to the near-death immune system activations that infants of earlier times experienced? What is the difference between immune system stimulation by vaccines and immune system stimulation by exposure to environmental antigens? The major difference is that vaccines are made under controlled conditions, have known amounts of known antigens, have been tested, and they are made by a large company with deep pockets which company can be sued and in the USA there is a chance of winning the legal lottery. So far, there is nothing special about vaccines other than that they are made by big companies with deep pockets that explains the hysteria there is about vaccines and autism.

  36. papertrail says:

    pD said:

    Similarly, did you see Differences in White Matter Fiber Tract Development Present From 6 to 24 Months in Infants With Autism? I’m no expert, but I’m pretty sure that events starting at six months are after birth. What do you think?

    pD, it’s like you have a travelling itch that no one here (or maybe anywhere, so far) is scratching. Perhaps this is not the best venue for the kind of analysis that you’re asking for, the end of a comment thread with few people participating. Still, I am finding it interesting. Personally, I think that every single vaccine critical hypothesis should be addressed and answered with facts and evidence and logic.

    Meanwhile, I’m not sure if I even know your hypothesis. I think you’re proposing, simply put, that newborn and very early infant vaccines are causing/evoking unique immune responses in infants (as revealed by the various studies you mentioned) that could conceivably lead to autism/neurological/CNS changes that ultimately reveal themselves later in the child’s life as regressive autism – either separately or in combination (“too many too soon”). Is that right? And, I guess you’d have to add that you believe the studies supporting the contention that “vaccines don’t cause autism” are missing detecting this relationship between vaccines and autism.

    I, for one, am a layperson and don’t understand all the big words being used by the studies you’re looking at, but I did decide to look at the abstract for the last one you mentioned. What I see is that their point is that their study suggests that the MMR vaccine does not cause autism, as crucial signs of brain changes occurred much earlier, like 6 mths. old. They used siblings of autistic children, assuming (apparently correctly) that they would be at high risk for autism themselves. Their choosing siblings indicates to me that your hypothesis wasn’t under study here, whether early vaccinations lead to the autism, but rather that autism has a *genetic* etiology and that the MMR jab couldn’t be the cause (and not that other vaccines could).

    As a layperson trying to understand scientific findings, one thing I picked up from sites like SBM is that studies should be designed with particular endpoints in mind and that it’s going to lead you astray if you try to extract other meaning (endpoints) after the data is in. (I am positive I just totally mutilated that point; I plead the layperson defense ;-)

    What I’m saying is that this study intended to identify if certain brain changes occur well before the onset of autism symptoms, which can be used as a marker to identify cases early, and they found that they did. They weren’t studying whether or not early vaccines lead to later autism symptoms, and so this study isn’t relevant to your hypothesis. On the contrary, they demonstrated that genetics plays a crucial role in predicting autism risk, and they put another nail in the MMR causes autism coffin.

  37. papertrail says:

    …And, I want to mention too, this study didn’t preclude that autism starts earlier than 6 months, perhaps even in the womb. They only looked at 6 mth olds, so far.

  38. papertrail says:

    correcting myself: I said “What I see is that their point is that their study suggests that the MMR vaccine does not cause autism,…”

    Actually, I don’t think that that was the point of the study. I was reading a commentary on that study, which pointed that out.

  39. lilady says:

    “I’m making a rule not to debate people that either cannot understand my arguments, or whom I do not truly feel are interested in an honest discussion. I’m not sure to which classification you belong, but I do think it is one of them. Perhaps I am wrong, show me wrong. Lets discuss the data. If you would like to discuss any of the data, or your different thoughts on the literature, then, fine. If, instead, your only contribution will be to quote my blogs ‘What is the all about’ page, you are free to do so, but the point you are making is that you are not interested in debate, only diversion. It speaks poorly towards either your mastery of the science, or, as I assert, the state of the science.”

    And I, should make a rule to never debate with you pD…because your arguments are indecipherable and lack a basic understanding of the immune response in infants or young children to vaccines and the immune response to antigens in the infant’s environment…as well as…antigens that cause vaccine-preventable diseases and the immune response to these antigens.

    http://www.cdc.gov/vaccinesafety/Vaccines/multiplevaccines.html

    “An infant’s immune system is more than ready to respond to the very small number of weakened and killed infectious agents (antigens) in vaccines. From the time they are born, babies are exposed to thousands of germs and other antigens in the environment and their immune systems are readily able to respond to these large numbers of antigenic stimuli. An infant’s immune system is more than ready to respond to the very small number of antigens in vaccines.”

    Again, what do those two studies that you cherry-picked and did not link to, about hospitalizations for URIs and other bacterial and viral illnesses, have to do with what you considered to be, a serious assault or over- stimulation of an infant’s immune system…in the form of vaccines…which minimally affect an infant’s immune system?

    Do you think that the voluminous posts on your blog, about cytokines and the stimulation of the immune system following vaccine administration, “qualify” you to be considered an expert in immunology? Excuse me pD…but your cherry-picking of other’s research…and your egesting of that research…combined with your spectacular lack of knowledge of immunology…do not qualify you as having *expertise* in immunology.

  40. passionlessDrone says:

    @daedulus2u –

    He is directly saying that neuronal proliferation occurs in utero, and only in utero and that there are genetic things that can increase that proliferation.

    This statement has been contradicted by later findings.

    Corridors of migrating neurons in the human brain and their decline during infancy [PMID: 21964341]

    Here we find that the infant human subventricular zone and RMS contain an extensive corridor of migrating immature neurons before 18 months of age but, contrary to previous reports, this germinal activity subsides in older children and is nearly extinct by adulthood. Surprisingly, during this limited window of neurogenesis, not all new neurons in the human subventricular zone are destined for the olfactory bulb–we describe a major migratory pathway that targets the prefrontal cortex in humans. Together, these findings reveal robust streams of tangentially migrating immature neurons in human early postnatal subventricular zone and cortex. These pathways represent potential targets of neurological injuries affecting neonates.

    If I understand correctly, the basis of applying the scientific method is to alter your model based on new information. Is that your understanding? Because of these new findings, we need to alter our model that all neurons are generated prenatally.

    This study was published after the Courchesne paper, and therefore, tells us that neurons are being generated postnatally. In any case, Courchesne states with some clarity that postnatal processes are invovled with neuron removal, and impairments in those processes could be responsible for the increase in neuron number.

    Is 67% more neurons a ‘major difference’? Is ‘an abnormal excess number of neurons’ a ‘major difference’?

    You are the one who is so stuck on using phrases like ‘major difference’ or ‘more normal’, not me. As such, it is up to you to tell us why this isn’t a meaningful finding. It was one of the keynote papers at IMFAR two years ago; I’ll let the readers determine if that merits any mention or not.

    That is not what the paper says.

    IT IS WHAT THE PAPER SAYS!

    Apoptotic mechanisms during the third trimester and early postnatal life normally remove subplate neurons, which comprise about half the neurons produced in the second trimester.37 A failure of that key early developmental process could also create a pathological excess of cortical neurons.

    “A failure of that key early developmental process could also create a pathological excess of cortical neurons”

    Are you going to deny that is what the text reads?

    My worldview is completely OK with prenatal exposures that you mentioned causing problems, I just haven’t seen any evidence that what happens after birth isn’t important too. Don’t you get that? Do you have any reason to believe that we can have a genetically mediated proliferation of neurons in-utero, but cannot also have an impaired removal process post natally? The system isn’t static after birth, it can still be affected.

    Yes, exposing infants to antigens causes their immune system to activate itself and this leads to measurable changes in various parameters of the immune system.

    Well, at least you aren’t claiming it is impossible to measure immune activation anymore!

    That occurs if the antigens come from a vaccine, or if the antigens come from a mouthful of dirt, or from putting a toy that another infant has slobbered on in their mouth

    Have you spent any time around a two month old, a baby that is literally sixty days from the womb? They don’t pick up toys that other infants have slobbered on. They don’t eat handfuls of dirt. They can’t even use their hands! Jesus Christ, what kind of households do you skeptics run, anyways? Please stop confusing neonates with children!

    Why the concern with a handful of immune system activations from vaccines

    Because we have changed our infants exposure at the earliest stages of life from a bell curve to a straight line at the top end of the percentage ratio.

    Immune system activations that are mild compared to the near-death immune system activations that infants of earlier times experienced?

    Just because something is mild compared to the past doesn’t mean it isn’t meaningful in the present.

    What is the difference between immune system stimulation by vaccines and immune system stimulation by exposure to environmental antigens?

    Good question! I wish someone could point me to a study that tried to answer that question; the fact that no one can is what has me really worried; we’ve become enamoured with the idea of a free lunch, but I don’t think nature works that way. What I can tell you is that there are good reasons to believe that stimulating multiple toll like receptors simultaneously is qualitatively and quantitatively different that just one at a time, and it seems likely that there are different qualitative immune profiles associated with endogenous versus exogenous based insults.

    Seriously, have you given any thought into the massive evolutionary failure involved in infants relative problems mounting an immune response early in life? Isn’t that a pretty severe chokepoint? Our immune system is pretty impressive, it can respond to whatever number you want to pick antigen patterns, has targeted receptors for a variety of pathogen classifications, and has a memory that lasts forever. And yet, when we are at our most vulnerable, it responds poorly. Has it never occurred to you that this might be a feature instead of a bug?

    So far, there is nothing special about vaccines other than that they are made by big companies with deep pockets that explains the hysteria there is about vaccines and autism.

    What about the developmental timeframe they are administered. That is what I am saying is so special!

    @papertrail –

    pD, it’s like you have a travelling itch that no one here (or maybe anywhere, so far) is scratching. Perhaps this is not the best venue for the kind of analysis that you’re asking for, the end of a comment thread with few people participating.

    I think you are correct. Mostly I got bored at work on a Friday and then just kept tugging on the string. I am getting bored, however. Same discussions and strawmen again and again.

    I think you’re proposing, simply put, that newborn and very early infant vaccines are causing/evoking unique immune responses in infants . . .

    I am proposing that this is biologically plausible in a specific subgroup of infants. I don’t know if it is happening or not.

    later in the child’s life as regressive autism

    Not necessarily. I don’t know if the possible changes I am proposing would manifest as regressive or not. (?) I’m really not worried about reports of drastic regression; I think it happens from time to time, but for the most part, observation of autism is a more gradual process.

    And, I guess you’d have to add that you believe the studies supporting the contention that ‘vaccines don’t cause autism’ are missing detecting this relationship between vaccines and autism.

    Don’t take my word for it, take Dr. Gorski’s word for it. The only classifications he is willing to give ‘bulletproof’ status is the MMR and thimerosal, as opposed to vaccination. Look up earlier in the thread where he got very precise in his wording. That wasn’t an accident. Why not ask yourself why Scott has refused to back up his claim that ‘vaccines in general’ are part of our evidence suite? Why not wonder why daedulus2u has refused to provide the “strong evidence” that vaccination is not associated with autism? I can’t prove a negative, but any of those people could prove me wrong; if they had any evidence. You’ll have to decide for yourself if they are intentionally holding back from releasing that evidence or not. Maybe they just like seeing me jump through hoops? Why not email Dr. Gorski and ask him if he can provide any more data?

    You are very subtly being sold a bait and switch here. Check out pmoran’s post on 7/24 @ 2:15 am where he quotes Dr. Novella as saying:

    the evidence did not support a link between vaccines in general

    and Dr. Gorski as saying:

    The bottom line, is that there is no scientific controversy over whether vaccines cause autism. The question has been asked multiple times and answered multiple times: No.

    When pmoran pushed, really pushed, Dr. Gorski on this, we got the distillation of what our data actually says; very good data on thimerosal, and good data on the MMR (“bulletproof”). The part Dr. Novella and Dr. Gorski are leaving out is that vaccines ‘in general’ haven’t really been studied very well at all. They are attempting to manipulate everyone who reads this text that the strength of our data is better than it is; that is why Dr. Gorski had to equivocate.

    What I see is that their point is that their study suggests that the MMR vaccine does not cause autism, as crucial signs of brain changes occurred much earlier, like 6 mths. old.

    You might be interested in looking at what the vaccine schedule is comprised of and more importantly, when those vaccines are administered. The overwhelming bulk of the vaccine schedule is given at two, four, and six month appointments. Those are the facts on the ground, though you will very rarely see that admitted to in this forum. I’ve harped again and again that the animal models consistently show a time dependent effect of early life immune challenges. I personally dont’ find that a difficult concept to understand, but it does seem to have problems sticking here for some reason. (?)

    Their choosing siblings indicates to me that your hypothesis wasn’t under study here, whether early vaccinations lead to the autism, but rather that autism has a *genetic* etiology and that the MMR jab couldn’t be the cause (and not that other vaccines could).

    My worldview is consistent with genetic participation. But again, that doesn’t mean you can’t still alter the trajectory of a system environmentally. Has anything you’ve read convinced you that a system defined by genetics can’t also be modified from outside the genome? My position is OK with two inputs, the position of nearly everyone else here allows only for one type of input (genetic) or one timeframe of input (prenatally). Which do you think more closely resembles reality?

    As a layperson trying to understand scientific findings, one thing I picked up from sites like SBM is that studies should be designed with particular endpoints in mind and that it’s going to lead you astray if you try to extract other meaning (endpoints) after the data is in.

    In that case, there is no reason that thimeosal or MMR studies should be used to validate ‘vaccines in general’, now, is there? And yet, you see people here, on this thread, trying to make the obfuscation.

    What I’m saying is that this study intended to identify if certain brain changes occur well before the onset of autism symptoms, which can be used as a marker to identify cases early, and they found that they did.

    I posted that study in order to illustrate the fact that there are important neuroanatomical features being developed after birth, and those features are abnormal in the autism population. This is in contrast of daedulus2u’s claim that all “major neuroanatomical” differences observed in autism are formed in utero.

    Also, you might want to peruse this blog posting by Stephen Novella (whose ‘debate’ initiated this thread)

    http://theness.com/neurologicablog/index.php/early-detection-of-autism/

    Where he discusses a study that indicates behavioral manifestations of autism may be detectable as early as six months.

    I’ve written several times regarding the new findings of microglial findings in autism and normal brain development on my blog. If you are really interested in what I’m saying, you might consider checking some of it out.

    I’m worried about our hubris. Think about it like this; we are now learning that being born by C-Section is associated with several adverse outcomes, such as asthma and obesity (and autism!). This is an intriguing finding, certainly very unexpected. We’ve been scheduling C-Sections for conveninence sake for a few decades now (more aggressively, recently); and now, we find that it is associated with things we had no clue could be a problem. Because we had no reason to believe that a C-section could cause this, we just never bothered to look. We barely understand the systems we are interacting with; while we can and do understand we are protecting infants, I’m not sure we should be so sure we aren’t also doing something else. When you really look at the what comprises our data, it isn’t as solid as you are being led to believe. If you don’t think so, why not email Dr. Gorski and Dr. Novella to send you a list of publications that evaluate the process of vaccination and autism and allow for us to discern differences “above the noise level of the epidemiological studies that have been done?” That is, after all, what has been claimed again and again by the posters on this blog. Let us know what the results of your query are!

    - pD

  41. Chris says:

    So, pD, have you helped prevent an infant getting pertussis by actually getting the Tdap yourself?

  42. papertrail says:

    pD said: “Think about it like this; we are now learning that being born by C-Section is associated with several adverse outcomes, such as asthma and obesity (and autism!). This is an intriguing finding, certainly very unexpected. …

    Interesting, but also a good example of how a preliminary finding of an “association” or correlation should not automatically make you leap to a conclusion about causation. There could easily be other reasons for this association. I know, I know, your point is that there are unknowns and unexpected finding and therefore vaccine-autism studies should continue. I have to say, finding that vaccines do cause autism would, at this point, be a very unexpected finding. You also may be very surprised one day to find out that you’ve been following the wrong path on this. Are you ready to eat hubris pie yourself?

    Looks to me like you found studies finding inflammatory activity after vaccination and some studies finding inflammatory activity among autistic children, but where are the (credible) studies connecting the two? Do you just want someone here to say this is plausible and should be studied further?

    The main hypotheses that were presented, MMR and/or thimerosal, have been sufficiently refuted, and you apparently agree. Then, some, like you, started to propose new hypothesis, which some disparagingly call “moving the goalpost” to: “too many” or “too soon” or “too many too soon”, and some argue there is “synergistic toxicity” occuring between vaccine ingredients and environmental chemicals. I think you raise a good point that these hypotheses haven’t been directly studied. The best argument I have heard against spending more millions or billions on such studies is that phase studies and post-licence surveillance haven’t shown such a connection, and the biological challenges of all vaccinations combined today are far less than before, when autism rates were much lower.

    I don’t know. It seems to me like you’re put something out there for debate, making points and counter-points to whatever comes your way, but it’s looking pretty messy. I recommend you put forth a clear statement of your hypothesis, do a careful reading of the studies that you claim to support your hypothesis to make sure they actually do, and suggest further studies. I don’t think you can say we’re at the point with these studies to do anything other than speculate about vaccines “causing” neurological impairment, which the evidence (on DPT whole cell too) doesn’t support.

  43. papertrail says:

    pD said: “What I’m saying is that this study intended to identify if certain brain changes occur well before the onset of autism symptoms, which can be used as a marker to identify cases early, and they found that they did.

    I posted that study in order to illustrate the fact that there are important neuroanatomical features being developed after birth, and those features are abnormal in the autism population. This is in contrast of daedulus2u’s claim that all “major neuroanatomical” differences observed in autism are formed in utero. ”

    Oh, okay. It became confusing because the study didn’t support what you were proposing either, about vaccines causing autism.

  44. daedalus2u says:

    pd, this does not contradict the other paper that says that most neuronal proliferation occurs in utero. It simply says that there is some migration and differentiation of neuronal stem cells, particularly along certain pathways. Science is cumulative and additive. This result doesn’t negate the findings that neuronal proliferation happens to a large degree in utero, it simply adds that some neuronal proliferation (which happens to be of a very different type), also happens post natal.

    A vaccine is a few antigens. Environmental exposures to organisms living in the wild are many orders of magnitude greater than exposure to vaccines. How often did infants growing up in Africa 50,000 years ago have their hands washed? When infants were carried, what did those infants hang onto or touch? How often did infant mothers bathe with soap and water? How often did infant mothers wash their hands and their breasts? How often were infant toys sterilized? How often did infants touch something non-sterile and then put their hands in their mouth? How often was the air that the infant inhaled sterile filtered? We know that there was none of that because soap, clean water, sterilizing facilities were not available. In many places in Africa they are still not available.

    Living in the “wild”, infants were exposed to gigantic quantities of antigens and microorganisms every second of every day. If you look at some of the microbiome work being done now, thousands of different organisms can be identified even on very small patches of skin. In humans there are more bacteria (by number) than there are human cells. If any of those bacteria could not be controlled by the immune system, a human would die from the infection. What basis is there for thinking exposures to bacteria were smaller when there was no water treatment, no soap, no municipal waste disposal, no refrigeration, no food preservation and flies and mosquitoes were buzzing around everything?

    You have a cartoonish idea of the complexity of the immune system. The immune system has a gigantic capacity to deal with trillions upon trillions of different antigens. The number of antigens in vaccines is tiny, less than a thousand. Infants are exposed to orders of magnitude more antigens every day. The only reason that special antigens are singled out to be put in vaccines is because those antigens come from replicating organisms that can cause diseases.

    So instead of exposing to infants to trillions of antigens from billions of different organisms in the “wild” in Africa, now we expose infants to billions of antigens from millions of organisms plus a hundred antigens from vaccines; and you think the “problem” comes from the vaccines?

    Where do you get this “one at a time”? How does the immune system tell if an antigen comes from 10^6 CFUs from a few drops of dirty sweat, from an infection, or from a vaccine?

    Every day of an infant’s life, that infant needs to do what all infants do the most of, eat, pee and poop. That has been true for as long as there have been humans. Every time an infant eats, the infant takes in nutrients, and if that nutrient mixture has not been sterilized, the infant will take in microorganisms. Every day, multiple times a day, all infants are exposed to microorganisms. We know this because every day, multiple times a day, infants put stuff in their mouth.

    What makes a day of vaccination special? Instead of only getting millions of new antigens from thousands of new bacteria, the infant also gets hundreds of antigens that have been specially prepared.

    What basis do you have for ignoring the normal everyday exposure that is completely unavoidable?

  45. papertrail says:

    pD said: “Seriously, have you given any thought into the massive evolutionary failure involved in infants relative problems mounting an immune response early in life? Isn’t that a pretty severe chokepoint? Our immune system is pretty impressive, it can respond to whatever number you want to pick antigen patterns, has targeted receptors for a variety of pathogen classifications, and has a memory that lasts forever. And yet, when we are at our most vulnerable, it responds poorly. Has it never occurred to you that this might be a feature instead of a bug?”

    So, you’re saying you think there must be an evolutionary advantage, a survival advantage, to infants having a poorer immune system than adults, implying that we shouldn’t mess with it by giving vaccines? If evolution worked like that, we’d all be “perfect” superhumans, and live forever, or heading there, at least. You seem to be saying that evolution created poorer immunity in infants for a reason. Hmm, sounds a bit religious.

    The way I imagine evolution working is that (again not an expert) our early ancestors who didn’t die from disease were those who did happen to have a good enough immune system to live long enough to procreate. Stronger immune system was passed on to offspring throughout the generations, while multitudes perished during the process of survival of the fittest (the strongest immunity, in this case). And now, babies do, in fact, have very good immune systems, and we evolved so that they get some additional immunity from the mother and through breastfeeding. Their fairly developed immune system is what enables early childhood vaccines to launch an immune response, although some brilliant engineering is done to make them work and work safely. But unlike an image of “god,” evolution doesn’t lead to perfection, and babies may be more vulnerable to harm from certain disease than adults (but perhaps not more than the elderly) due to a less developed immune system, or other factors. This would only matter in the evolutionary process if an infants’ somewhat less developed immune system impacted reproduction. I guess it didn’t, because we are here talking about it.

  46. daedalus2u says:

    What I said was:

    “There are lots of theoretical considerations as to why a connection would be highly implausible, foremost being the fact that neuroanatomy differences observed in autism occur before vaccines are given. A vaccine at 12 months, can’t change neuroanatomy that is fixed in the first trimester in utero.”

    I didn’t say the words that you put into my mouth:

    “I posted that study in order to illustrate the fact that there are important neuroanatomical features being developed after birth, and those features are abnormal in the autism population. This is in contrast of daedulus2u’s claim that all “major neuroanatomical” differences observed in autism are formed in utero. ”

    The major neuroanatomical difference I was thinking of when I said that was the number of minicolumns. That number is set in utero. That number is higher in people with autism. See

    Regulation of Cerebral Cortical Size And Neuron Number by Fibroblast Growth Factors: Implications For Autism
    Flora M. Vaccarino, Elena L. Grigorenko, Karen M. Smith, and Hanna Stevens.

    Disruption in the Inhibitory Architecture of the Cell Minicolumn: Implications for Autism
    MANUEL F. CASANOVA, DANIEL BUXHOEVEDEN, and JUAN GOMEZ

    There are also increased asymmetries:

    Brain asymmetries in autism and developmental language disorder: a nested whole-brain analysis
    Martha Herbert.

    Here is a nice very recent review that discusses some of the different factors involved, in utero.

    Above genetics: lessons from cerebral development in autism
    Emily L. Williams and Manuel F. Casanova

    There are major neuroanatomical differences observed between NT and ASDs, some of those differences occur in utero. For post natal exposure of something to “cause” autism, you would have to show how that hypothetical post-natal exposure can mimic the neuroanatomy differences that are known to happen in utero.

    pd, you are cherry-picking. You are taking statements by Dr Gorski that there is no hint that MMR causes autism and imputing that therefore some other vaccine might be causing autism when there is no data that any vaccine has any causal relationship to autism. You are playing wack-a-mole with the data, if a study shows that MMR is not associated with autism, then you say that leaves open the question of DPT causing autism. A study showing that DPT is not associated with autism leaves open the question of MMR.

    Now you want to add timing as another degree of freedom, that MMR according to one vaccine schedule doesn’t cause autism, but what about another schedule?

    The prior plausibility of vaccines being associated with autism is very low. The prodroma symptoms of autism are due to neural structures that are formed in utero. Some of these prodroma symptoms occur before vaccines are given. You have done nothing to address the timing of vaccines with the timing of when those neuroanatomical structures are formed. If there is timing sensitivity to immune system activation and neuroanatomy, that sensitivity has to be before the neuroanatomy forms.

    There is nothing unique about vaccines, except that they are produced by a company with deep pockets.

  47. pmoran says:

    David:“What about indications that autism rates are increasing over the period of increasing vaccine exposure? It seems a lot of that increase can be shown to be spurious, but ALL of it? We need a clear answer to that if we are to support certain statements.”

    Jumpin’ Jesus on a pogo stick! This statement demonstrates some serious ignorance of the literature on autism, and it’s not for our lack of trying to educate our readers on the literature. Clearly, in your case, we have failed. We have written several posts explaining the concepts of broadening of the diagnostic criteria in the early 1990s, increased awareness, increased screening programs (you, of all people, a cancer surgeon, should know that the more you screen for a condition the more of that condition you will find), and the like. We’ve discussed the concepts of diagnostic substitution and cited studies applying today’s diagnostic criteria to adults and finding a prevalence similar to what we see today. Basically, there are several lines of evidence all converge on a conclusion that, controlling for changing definitions, autism prevalence has been fairly stable over the time period when there is claimed to be an “autism epidemic.” It’s possible that prevalence might have increased slightly (although that isn’t even sure), but what is certain is that the “true” prevalence of autism is not exploding as the prevalence figures seem to indicate.

    Seriously, Peter, at this point it was painful for me to read your most comment, and not because you were making points that made me wonder if I was wrong or that made me feel stupid. It was because I feel embarrassment for you.

    Me, embarrassed? In this instance of creative quoting you extracted one out half a dozen statements that were explicitly stated as describing what is going on in the minds of many members of the public, You then even ignored some of its content. What else does “it seems a lot of that increase can be shown to be spurious” mean to you, other than an awareness of the factors you mention?

    My outlining of all the matters that may be affecting public perceptions was intended, in part, to alert you to the fact that we doctors can no longer expect “we have spoken on this matter” to have the force that it once had (or that we like to think it should have). I have given an example of how this may have been counterproductive in our response to cancer quackery.

  48. Harriet Hall says:

    @pmoran,

    “to alert you to the fact that we doctors can no longer expect “we have spoken on this matter” to have the force that it once had”

    As if you needed to alert him to that fact! How condescending!

    I’ve heard more than enough of your criticism. I ask you once more to try re-wording David’s explanations in a way that would satisfy all your objections. Stop telling us what we are doing wrong and show us an example of how you think we could have done it right.

    I’ve just read a new book about children’s medicines that devotes a chapter to answering parents’ questions about vaccines. It took a whole chapter and 24 pages to explain, and it didn’t even go into any background about the scientific method. I just don’t see how you expect us to present the issues with all their nuances in a brief statement in a blog post. Maybe there are some magic words that would briefly express the exact truth in a way you would find acceptable. If so, please tell us what those words are. What do you tell parents who ask about vaccines? Put up or shut up!

  49. @Harriet, do you mind sharing the main points the book made?

    1. Harriet Hall says:

      @SkepticalHealth,
      ” do you mind sharing the main points the book made?”

      It asks and answers a list of questions like “how do vaccines work?” “what concerns and fears do parents have about vaccines?” “how effective are vaccines?” “how is vaccine safety tested?” “how do we measure risk vs. benefit for vaccines?”
      It specifically asks “do vaccines cause autism?” and says “experts…have officially stated that there is no scientific proof that vaccines or thimerosal cause autism.” It refers to “several studies” but does not describe them. It references links where those studies are listed, warns against Internet misinformation, and lists reliable sources of vaccine information for readers who want to know more. It doesn’t bother to debunk all the details some parents might be concerned about like aluminum, adjuvants, fetal cells, etc. It mentions the concern about overloading the immune system by saying that vaccines use only a small part of the immune system’s ability to recognize and remember germs. It mentions delaying the vaccine schedule only to recommend against it.

      In a boxed highlight, it says “Vaccines and thimerosal do not cause autism. Many scientific studies have shown this. Most vaccines no longer contain thimerosal. Not giving vaccines to your child because of concerns about vaccines causing autism increases the risk of your child getting, and dying from, dangerous infectious diseases.”

      I think this is a reasonable approach, although it undoubtedly wouldn’t satisfy pmoran.

  50. papertrail says:

    “do you mind sharing the main points the book made?”

    In a nutshell: There isn’t a whiff of a hint of evidence that vaccines cause autism..

    Just kidding! Sorry, I couldn’t resist!

  51. Chris says:

    Patience, SkepticalHealth, a review of that book may be a future article by Dr. Hall!

  52. lilady says:

    Here we go again. Dr. Moran just what is your point about vaccines and the manner in which Dr. Gorski describes the anti-vaccination movement that permeates the internet? Do you even have a point…aside from your self-appointed role as the arbiter of the style, the phrases and the manner in which Dr. Gorski blogs on this site?

    Have you ever actually read the pseudoscience about vaccines that is out there? Have you ever provided information to young parents who are concerned about their child’s welfare and are confused because of the nonsense they read on the internet, or hear from other parents who have “opted out” of vaccines?

    I think it is time for you to back off with your commentary, which adds nothing to our discussion on this subject and only reveals your ignorance about vaccines.

    “My outlining of all the matters that may be affecting public perceptions was intended, in part, to alert you to the fact that we doctors can no longer expect “we have spoken on this matter” to have the force that it once had (or that we like to think it should have).”

    No Dr. Moran, you only *think* you have the knowledge and the experience to *alert us*. We are alerted to the realities of the anti-vaccine crowd and the impact it has on a child’s health and on public health. Unlike you, who still believes that a febrile seizure following a vaccination *might* been implicated in the onset of autism, we are attempting to restore parents’ confidence in themselves, and in their child’s health care provider.

    Do try to contain the animus that you have directed at Dr. Gorski and show us how you would write a vaccine blog…to show us how it should be “properly” done. Time to put up or shut up, Dr. Moran.

  53. papertrail says:

    “show us how it should be “properly” done. Time to put up or shut up, Dr. Moran.”

    I have to agree. Arguing back and forth like this is getting us nowhere.

  54. pmoran says:

    So now I am not to be permitted to respond to inappropriate use of my words? Shame on you, Harriet, and also for your own never acknowledged carelessness in that regard.

    You can all pretend as much as you like. It does not change the fact that David has claimed repeatedly to have specific epidemiological evidence that disposes once and for all of any small possibility that autism can be caused or triggered by vaccines but he has chosen to adopt a “dig it out yourself” attitude when asked to show it. This is at least the third time this has happened and if this is not reflecting the “I have spoken–” attitude I have implied he is relying upon, I don’t know what is.

    Yet if he could dispose of that association in the way he claims there is no need for your ” whole chapter and 24 pages” of text. We just need references to two or three good studies.

    There is method behind my madness, which this stonewalling, and indeed our whole approach prevents. Even if the data is not as conclusive as well-planned prospective randomized studies would be — and it’s not, Lilady, simply because it is not based upon those, and everyone here knows it but you, hence the need to keep on discrediting me with all the ad hominem — it might allow us to say correctly that “we find no good evidence that autism is connected to vaccines” but add “even if there were a connection it cannot be more than X per 100,000 vaccine episodes, which is very much less than the lifetime risks to any child of not vaccinating.”

    This has been in the back of my mind all along.

    PD demonstrates how vulnerable our case can be if it is based substantially upon plausibility and also when it pits us against those who also understand the weaknesses in our data. IIRC even Whitaker now knows what kind of data to demand of us if we claim there is absolutely no risk.

    This has always been about the accurate presentation of the science in the understanding that it is hypocritical of us to behave otherwise, even if in a good cause and even if it did not risk arousing damaging suspicions regarding our good faith.

    1. Harriet Hall says:

      @pmoran,
      “we find no good evidence that autism is connected to vaccines” but add “even if there were a connection it cannot be more than X per 100,000 vaccine episodes, which is very much less than the lifetime risks to any child of not vaccinating.”

      I asked you to put up or shut up. And this is your answer? Do you really think this will earn us credibility with parents, counteract all the anti-vaccine propaganda they have heard, and assuage all their fears? And what do you mean “no good evidence”? “No evidence” is more accurate. And don’t you think parents would be alarmed by the suggestion that there could be any number of X per 100,000? And won’t they argue that the lifetime risks to their child of catching these diseases is minuscule and don’t merit taking any risk?

      “Weaknesses of our data”? The data are strong. They show no association between autism and MMR or autism and thimerosal. There are no data showing any association between vaccines in general and autism; and there is no good reason to study that, since it has become increasingly clear from other data that autism is mainly due to genetic factors and is triggered before birth, not after. There is undoubtedly a correlation between the increased use of cell phones and the increase in autism diagnoses, and we can’t “absolutely” rule out the possibility that the mother’s use of cell phones during pregnancy might contribute to autism. We could come up with any number of hypotheses that would require large studies with thousands of subjects to investigate. We can’t throw research money at a hypothesis unless there is good reason to do so. And we can’t do controlled studies that deny children the proven benefits of vaccines.

      Scientists have considered the hypothesis of a link between vaccines and autism and have soundly rejected it for good science-based reasons. Explaining why would require far more than a sound bite.

      ” if we claim there is absolutely no risk”

      Nonsense! No one is saying “absolutely.” Very little in science is “absolute.” The absence of a whiff doesn’t imply absoluteness. The science says there is no evidence of risk of autism and no good reason to think there might be. And it says there are other risks of vaccination, but they pale beside the risks of not vaccinating.

      “Shame on you, Harriet”

      No, shame on you. You’ve had your say. You’ve made your point. Nuff said. Stop insulting us and trying to tell us what we should do. Go away and come back when you have something new to say.

  55. weing says:

    I think pmoran is correct. We must not overgeneralize from the given data. There is no proof that breathing does not cause and contribute to autism in the susceptible. And we know that those arguing otherwise are, above all, interested in the accurate presentation of the science.

  56. papertrail says:

    I know this is just one study, and it doesn’t address “all” or “every” (good luck finding that), but it’s relevant, maybe more to pD than pmoran’s issue:

    On-time Vaccine Receipt in the First Year Does Not Adversely Affect Neuropsychological Outcomes

    Michael J. Smith, MD, MSCE,
    Charles R. Woods, MD, MS

    http://pediatrics.aappublications.org/content/125/6/1134.abstract

  57. papertrail says:

    “For all intents and purposes, as far as science can tell, vaccines do not cause autism.”

    -Dr. Gorksi

  58. David Gorski says:

    And I stand by that statement. It is accurate. Or perhaps Peter can explain why it’s not.

    So I third Harriet and Lilady’s challenge, Peter: Put up or shut up. How, specifically, should it be done?

    Here are some examples for Peter to contemplate:

    http://vaccinesafety.ecbt.org/ecbt/website_documents/ExpertStatementChanges2.pdf

    Note that they do not sound a lot different from my way of doing it.

  59. David Gorski says:

    You can all pretend as much as you like. It does not change the fact that David has claimed repeatedly to have specific epidemiological evidence that disposes once and for all of any small possibility that autism can be caused or triggered by vaccines but he has chosen to adopt a “dig it out yourself” attitude when asked to show it. This is at least the third time this has happened and if this is not reflecting the “I have spoken–” attitude I have implied he is relying upon, I don’t know what is.

    And this is the at least the third time you’ve repeated this, even though I have referred you to a source listing some of the epidemiological evidence. Peter, here it is again:

    http://www.sciencebasedmedicine.org/reference/?p=1

    I could supplement it with a bunch of other papers, if I thought you would actually bother to read them. Your repetition several times now of the misinformation that I never delivered and instead told you to “go look it up yourself” makes it very clear to me that you don’t want to be educated on this issue.

    BTW, as I pointed out, Steve says much the same thing as I do. I don’t see Peter criticizing Steve. Just Harriet and me. As I pointed out, at the debate, he said the question had been answered and scientists have moved on. I agree.

  60. passionlessDrone says:

    @Dr. Gorski –

    And this is the at least the third time you’ve repeated this, even though I have referred you to sources of the epidemiological evidence, aggregated—on more than one occasion now. Peter, here it is again:

    I followed that link. It has dedicated sections towards: thimerosal and the MMR. I’m not sure if you are aware of this, but there is a difference between vaccination and thimerosal, and the MMR. Did you know that? Would you like me, or pmoran, to explain the difference to you?

    This is supposed to be a skeptical website, and yet, you can’t seem to understand that studying a vaccine ingredient, or a single vaccine given in toddlerhood is a different thing than studying the process of vaccination which primarily occurs in infancy. Based on your previous posts, many of which I enjoyed immensely, I am 99.99999% sure you are clever enough to understand these distinctions. Why keep pretending that you don’t?

    Understanding that you are not a pediatrician, are you aware that there are significant differences in a one week old neonate, or a two month old infant, and and eighteen month old toddler? Did you know that? What scientific reasons can you give us that the developmental age of infants should be ignored in our analysis? If you can’t give us any, and you cannot, then we must apply great skepticism towards assuming that studying the MMR is the same thing as studying the entire shot schedule.

    The animal models consistently, consistently tell us that there are significant time dependent interactions involved with persistent changes following early life immune challenges.

    Don’t take my word for it.

    A lifespan approach to neuroinflammatory and cognitive disorders: a critical role for glia [PMID: 21822589]

    Cognitive decline is a common problem of aging. Whereas multiple neural and glial mechanisms may account for these declines, microglial sensitization and/or dystrophy has emerged as a leading culprit in brain aging and dysfunction. However, glial activation is consistently observed in normal brain aging as well, independent of frank neuroinflammation or functional impairment. Such variability suggests the existence of additional vulnerability factors that can impact neuronal-glial interactions and thus overall brain and cognitive health. The goal of this review is to elucidate our working hypothesis that an individual’s risk or resilience to neuroinflammatory disorders and poor cognitive aging may critically depend on their early life experience, which can change immune reactivity within the brain for the remainder of the lifespan. For instance, early-life infection in rats can profoundly disrupt memory function in young adulthood, as well as accelerate age-related cognitive decline, both of which are linked to enduring changes in glial function that occur in response to the initial infection. We discuss these findings within the context of the growing literature on the role of immune molecules and neuroimmune crosstalk in normal brain development. We highlight the intrinsic factors (e.g., chemokines, hormones) that regulate microglial development and their colonization of the embryonic and postnatal brain, and the capacity for disruption or “re-programming” of this crucial process by external events (e.g., stress, infection). An impact on glia, which in turn alters neural development, has the capacity to profoundly impact cognitive and mental health function at all stages of life.

    There are literally dozens of studies in the animal realm that tell us that immune challenges early in life can have qualitatively different effects on the organism that persist through the lifetime. This is why time matters. This is why we cannot pretend that studying the MMR tells us about the rest of the vaccine schedule. Only a fool or a charlatten would continue pretending these are the same thing.

    Hey, do you want to talk abou the fact that post-mortem studies in the autism realm consistenly show a state of ongoing inflammation in the brain, even at an early age? Did you know that invoking the immune response outside the CNS results in changes to the neuroimmune environment, up to and including changes to form and function of microglia, the things that are supposed to be participating in synpatic pruning?

    I wonder, how do all of the studies that involve “vaccines in general” (but which aren’t available on the link you posted for some reason), take into consideration that the autism population has been shown to have immune biomarkers associated with increased inflammatory responses?

    Earlier in this thread you asked pmoran if he had an alnterantive explanation of something other than thimerosal or the MMR could be involved with autism. I am giving you that explanation. I will put up, if you have the guts to have an actual discussion.

    What are your thoughts on the early immune challenge literature? What are your thoughts on the entire realm of developmental programming, which tells us that the fetal and early postnatal periods can effectively program fundamental biological systems and increase risk for immune and metabolic disorders for life?

    Aren’t you tired of teeing off on naturopaths? Is there any challenge in that? Do you really get any satisfaction from showing us, again, how dumb Dr. Mercola is?

    And I stand by that statement. It is accurate. Or perhaps Peter can explain why it’s not.

    I can. It’s easy. The studies in your own link are about thimerosal and the MMR, which are different things than vaccination. Next time, try reading your own reference.

    Did anyone see the study that came out a few weeks ago about statins and increased risk of diabetes? This was a phase IV study, had a hard diagnosis available (very much in contrast to autism!), and still needed 18,000 participants to detect a relationship. 18,000! Since Dr. Gorski is so keen on harping about how strong our epidemiology is on vaccination, being able to detect any relationship over the range in one in a million, maybe we could ask him to post a study with sufficient numbers of participants to back up that claim, here, now. Why make everyone go hunting through your archives? If it exists, post it.

    What studies can you link to, here, in this thread, that allow us that degree of precision regarding autism and the process of vaccination? Thimerosal studies do not count. MMR studies do not count.

    I’m terrified of what is coming. Sooner or later we are going to have to find a way to study the act of immunization in much more nuanced ways than we have so far. I don’t know exactly how, but the critical mass of literature implicating the immune system in normal brain function and development is going to mandate that your charade be exposed. You’ve got a lot of sunk cost into defending the “vaccines in general” mantra, and you keep digging as hard as you can. The public isn’t going to be too happy when they find out that the “question has been asked and answered” thing is a total lie, and the result is going to make Wakefield’s effect on herd immunity look like a joke. The longer our time horizon before this inevitability occurs, however, will only make things worse. I am terrified.

    - pD

  61. David Gorski says:

    pD, we’ve been over this many times, both here and at my other blog. If you continue to be so condescending and use straw men (i.e., that I don’t know the difference between MMR and other vaccines or don’t understand how vaccines work), I see no point in engaging you, other than to point out some of the issues involved, as I did here:

    http://www.sciencebasedmedicine.org/index.php/the-perils-and-pitfalls-of-doing-a-vaccinated-versus-unvaccinated-study/

    And to answer a couple of questions:

    What are your thoughts on the early immune challenge literature? What are your thoughts on the entire realm of developmental programming, which tells us that the fetal and early postnatal periods can effectively program fundamental biological systems and increase risk for immune and metabolic disorders for life?

    Easy. That none of it supports a hypothesis that vaccines cause autism. Certainly, you’ve never shown that it does, which makes your next statement below,

    There are literally dozens of studies in the animal realm that tell us that immune challenges early in life can have qualitatively different effects on the organism that persist through the lifetime. This is why time matters. This is why we cannot pretend that studying the MMR tells us about the rest of the vaccine schedule. Only a fool or a charlatten would continue pretending these are the same thing.

    a nonsequitur and a straw man. A nonsequitur in that these studies do not tell us that the hypothesis that vaccines cause autism is biologically plausible (nor do they support the hypothesis) and a straw man because that is not the argument that is being made.

    Of course, antivaccinationists like to try to use an argument from ignorance, claiming that because we just don’t know every last variable then the autism-vaccine link must be not just plausible but that argument ignores the converging lines of evidence indicating that (1) autism prevalence has probably not changed appreciably in the last 30 or 40 years (no “autism epidemic,” no vaccine link; it’s quite simple); (2) autism has a large genetic component; (3) studies indicating that whatever causes autism largely occurs before birth; and (4) studies indicating that there are structural differences in autistic brains, including indications that autistic children have more neurons in the prefrontal cortex (more indication that the abnormalities associated with autism occur before birth).

    Add to that the persistent epidemiological evidence that fails to find a link between vaccines and autism, and the vaccine-autism hypothesis is about as dead as a hypothesis can be.

    But let’s ask two quick questions, given your comments on studies above:

    1. Do thimerosal-containing vaccines cause autism? I say the evidence is quite conclusive that they don’t, at least not detectably. Your comments seem to indicate that you accept the scientific literature concluding this; otherwise you would not harp on it.

    2. Does the MMR cause autism? Again, I say the evidence is quite conclusive that they don’t, at least not detectably. Your comments seem to indicate that you accept the scientific literature concluding this; otherwise you would not harp on it.

    If you accept that the answers to #1 and #2 are no (which they are; even Peter accepts this), if the”real” prevalence of autism and ASD has not been increasing over the last 30 years, the hypothesis that some other vaccine is causing autism is damned implausible. Not homeopathy-level implausible (but then few things are) but definitely extremely implausible.

  62. daedalus2u says:

    pd, there is nothing “special” about vaccination as an immune system stimulation other than it is a known antigen, in a known amount, administered in a standardized way, which has been tested and which has been prepared by a large company with deep pockets.

    MMR is a live virus vaccine. All vaccines that contained thimerosal are not live virus vaccines. That makes MMR and thimerosal containing vaccines very different. What reason is there to think that “vaccines” are a useful category of immune system stimulation to look at for autism causation?

    Every time an infant is exposed to an antigen, the same physiological processes as during vaccination occur. The antigen is taken up by antigen presenting cells, the antigen is digested and coupled to Major Histocompatibility Complexes and presented on the surface, other cells detect that and self modify to generate antibodies to the antigen.

    What about that process is different for “vaccines” as a class of antigen exposures that make them worthy of additional study beyond what has already been done and which continues to be done as part of the normal study of vaccine effects and side effects? Timing? Why isn’t the timing of exposure to each of the millions of other antigens important?

    Much more is known about exposure to vaccine antigens than is known about the millions of other antigens that infants are exposed to and which we know they mount a successful immune response to. We know if an infant has raised a successful immune response to environmental bacteria because that infant didn’t die of an infection.

  63. Chris says:

    pD, I noticed you have not answered how to protect babies in their first year from disease as an explanation for your statement:

    I am not against vaccination. Your response implies a binary decision, vaccinate or not. We have a lot more options than that, I think you understand this, but I’m not sure.

    Do tell us what those options are? It is obvious we don’t understand, so you need to clarify exactly what other ways than vaccines can protect infants from Hib, pertussis, tetanus, diphtheria, etc.

    And please tell us if you have been proactive in one other known way to protect infants from pertussis by getting a Tdap yourself to increase herd immunity in your local community. Our entire family has had a Tdap, and as benefit the two new babies on our little street are a wee bit safer.

  64. lilady says:

    @ P Moran:

    Is it any wonder that we have lost respect for you with these latest attacks on Dr. Gorski? What have you ever added to the discussion, that shows you are aware of the huge amount of disinformation that is deliberately being put out there, to instill fear uncertainty and doubt about vaccines?

    What about your moving of the goal post up thread, where you questioned whether a febrile seizure following an immunization *might* trigger the onset of autism? I provided you with a link to an NIH website about febrile seizures…which you totally dismissed as being “mildly reassuring”. We have to assume then, in spite of my requests for you to disavow your statement and in spite of papertrail’s link to a study that disproved your theory…that you still hold to that “belief”.

    I also provided a link to Dr. Whitaker’s blog that I posted on. Harriet Hall posted on his blog…but you didn’t. You prefer to confine your posts to Dr. Gorski’s blog and you prefer to restrict your comments that criticize Dr. Gorski’s style, phraseology and tone.

    If you ever decide to actually submit a guest blog about vaccines and combating the disinformation campaign, here’s an article for you to review, Dr. Moran:

    http://www.immunize.org/catg.d/p2070.pdf

    Oh, and here’s another 64 page publication written for parents who have questions about vaccines, their efficacy, the monitoring of their safety after licensing and the bogus vaccine-autism link:

    http://www.cdc.gov/vaccines/pubs/parents-guide/downloads/parents-guide-508.pdf

    So, when can we expect that you will submit a guest blog to SBM…to show us how it should be properly done, Dr. Moran?

  65. passionlessDrone says:

    @Dr Gorski –

    pD, we’ve been over this many times, both here and at my other blog. If you continue to be so condescending and use straw men (i.e., that I don’t know the difference between MMR and other vaccines or don’t understand how vaccines work), I see no point in engaging you, other than to point out some of the issues involved, as I did here:

    The guy that runs a blog called Respectful Insolence doesn’t like having condescending language used. Oh, the irony! Hey, at least I’m not censoring you like you complain so much about that AOA guys; that’s pretty rich, complain that you get censored in one place, threaten to run off and hide because I’m so mean to you when I come to your house and try to engage you. I have been trying very hard to refer to you as Dr. Gorski so as not to hurt your feelings.

    In any case, it is your arguments that force me to try to get you to admit if you understand that difference or not. If you do understand that difference, and you say you do, why do you keep on insisting that evaluating thimerosal or the MMR tells us anything except thimerosal or the MMR? Why? If you don’t want stupid questions asked of you, don’t keep on spouting out false equivalencies that infer that you don’t understand the difference between the MMR and vacciantion as a practice. It’s not that hard.

    That none of it supports a hypothesis that vaccines cause autism.

    Are you serious? Here is the hypothesis: Some infants who go on to develop autism are genetically or environmentally predisposed to react more vigorously to immune challenges than other infants. Within that subset of children, an innate immune response during infancy initiate (or propagate) a programming of the neuroimmune system such that behavioral and physiological manifestations of autism occur. A wide range of animal studies tell us that the effects of early life immune challenge can be qualitatively different than such an insult at a later timeframe. Because many of the observations from the autism realm have strong parallels to what has been observed in animal models, the underlying weaknesses in our existing vaccine/autism research suite should be addressed by more appropriately evaluating the process of vaccination in regards to future neurodevelopmental outcome.

    I can’t help but notice that instead of posting a link to the studies you insist exist, you tried to bait and switch thimerosal and MMR studies and jump to a ‘highly improbable’, meaningless qualifier. Instead of just inferring that there are a great number of animal studies that say what I claim, I’ll actually list some:

    Microglia and memory: modulation by early-life infection [PMID: 22031897]
    A lifespan approach to neuroinflammatory and cognitive disorders: a critical role for glia [PMID: 21822589]
    Enduring consequences of early-life infection on glial and neural cell genesis within cognitive regions of the brain
    Early-life programming of later-life brain and behavior: a critical role for the immune system [PMID: 19738918]
    Neonatal bacterial infection alters fever to live and simulated infections in adulthood [PMID: 19682802]
    Bacterial infection early in life protects against stressor-induced depressive-like symptoms in adult rats [PMID: 18164556]
    Early-life infection leads to altered BDNF and IL-1beta mRNA expression in rat hippocampus following learning in adulthood [PMID: 17997277]
    Neonatal infection induces memory impairments following an immune challenge in adulthood [PMID: 15727533]
    Neonatal infection-induced memory impairment after lipopolysaccharide in adulthood is prevented via caspase-1 inhibition
    Sex effects on neurodevelopmental outcomes of innate immune activation during prenatal and neonatal life [PMID: 22516179]
    Neonatal programming of innate immune function [PMID: 21045175]
    Early life activation of toll-like receptor 4 reprograms neural anti-inflammatory pathways [PMID: 20534845]
    Neonatal programming by neuroimmune challenge: effects on responses and tolerance to septic doses of lipopolysaccharide in adult male and female rats [PMID: 20136690]
    Postnatal programming of the innate immune response [PMID: 21665816]
    Early life exposure to lipopolysaccharide suppresses experimental autoimmune encephalomyelitis by promoting tolerogenic dendritic cells and regulatory T cells [PMID: 19542441]
    Postnatal inflammation increases seizure susceptibility in adult rats [PMID: 18596165]
    Neonatal programming of the rat neuroimmune response: stimulus specific changes elicited by bacterial and viral mimetics [PMID: 16423854]
    Early-life immune challenge: defining a critical window for effects on adult responses to immune challenge [PMID: 16395304]
    Long-term disorders of behavior in rats induced by administration of tumor necrosis factor during early postnatal ontogenesis [PMID: 19089635]
    Long-term alterations in neuroimmune responses after neonatal exposure to lipopolysaccharide [PMID: 15163684]
    Long term alterations in neuroimmune responses of female rats after neonatal exposure to lipopolysaccharide [PMID: 16226008]
    Peripheral immune challenge with viral mimic during early postnatal period robustly enhances anxiety-like behavior in young adult rats [PMID: 21643765]
    Adult brain and behavioral pathological markers of prenatal immune challenge during early/middle and late fetal development in mice [PMID: 18023140]
    Potential for early-life immune insult including developmental immunotoxicity in autism and autism spectrum disorders: focus on critical windows of immune vulnerability [PMID: 18821424]
    Neonatal lipopolysaccharide exposure alters central cytokine responses to stress in adulthood in Wistar rats [PMID: 20666652]
    Neonatal programming by immunological challenge: effects on ovarian function in the adult rat [PMID: 21084570]
    Inflammation during fetal and neonatal life: implications for neurologic and neuropsychiatric disease in children and adults [PMID: 22334391]

    The literature is absolutely unambiguous on this point: innate immune activation in early life can persistently change an organism in ways that the same challenge, later in life, does not. You don’t have to have a pathogen; the effect is from triggering the innate immune system. Vaccines trigger the same system. Those are facts. If you want to argue against that point, you’ve got a lot of work to do. I would encourage any reader to peruse any of these studies and then try to figure out if analyzing thimerosal or the MMR can tell us anything about them.

    What does early life mean? That’s tough to decide, I don’t know; animal models are crude instruments, but they are available. I do know that studying thimerosal does not illuminate the problem. Similarly, the MMR, which, as Dr. Gorski understands, occurs between a year and eighteen months, leaves the entire first year of life, at least, un-studied. I’ve asked Dr. Gorski, and others, again and again, if they have any particular reason we should ignore time in our analysis; his response was to quibble on my just asking for more and more detail. But the reality is that our analysis in the animal models tell us that time matters. That’s not quibbling, it’s just reporting the facts; you don’t get to ignore developmental timeframe on an animal if we want to know what is happening. It is simple and straightforward, and should be clear to anyone who views this website through a lens of fidelty to the data. If we want to know if our vaccine schedule is having unanticipated effects, we must include the dimension of time into our analysis. We haven’t.

    Note that every single one of those studies above, every one, was published after 2004, and most after 2008, which means that the people who crafted our current vaccine schedule did not have any capacity to incorporate these ideas into their analysis. How could they?

    What about autism? As I posted above, but will repost here with more detail, we have a ton of evidence of immune mediated participation in the autism world. As a first step, I would posit my evidence that children with autism are more likely to have an exaggerated innate immune response compared to chidren without autism.

    Increased serum levels of high mobility group box 1 protein in patients with autistic disorder [PMID: 20302902]
    Elevated serum levels of interleukin-17A in children with autism [PMID: 22748016]
    Altered T cell responses in children with autism [PMID: 20833247]
    Macrophage migration inhibitory factor and autism spectrum disorders> [PMID: 18676531]
    Decreased transforming growth factor beta1 in autism: a potential link between immune dysregulation and impairment in clinical behavioral outcomes [PMID: 18762342]
    The complementary role of high sensitivity C-reactive protein in the diagnosis and severity assessment of autism [not in pubmed for some reason]
    Differential monocyte responses to TLR ligands in children with autism spectrum disorders [PMID: 19666104]
    Preliminary evidence of the in vitro effects of BDE-47 on innate immune responses in children with autism spectrum disorders [PMID: 19211157]
    The role of immune dysfunction in the pathophysiology of autism [PMID: 21906670]
    Elevated cytokine levels in children with autism spectrum disorder [PMID: 16360218]
    Decreased serum levels of transforming growth factor-beta1 in patients with autism [PMID: 17030376]

    Note that the first six of these studies tell us that as autism severity increased, so too, did the degree of exaggerated immune response / ability to regulate immune response / inflammatory biomarker. I asked daedulus2u this question, but he decided not to respond:

    If we have an infant with increased MIF, increased CRP, increased IL-17A, and increased HBGB1, can we make any prediction, any at all, on the degree of their innate immune response compared to a child without such increased levels?

    My argument is that we can realistically say that the immune response would be more robust. The in vitro studies that I reference above show exactly that, increased production of inflammatory cytokines.

    If you want to argue against immune dysregulation in autism and a propensity for exaggerated innate immune responses, you are going to have to post more than a shell game about thimerosal/MMR, or point people to your archives and tell them to look for nonexistint literature. Can you? Can anyone?

    What about the CNS in autism? It just so happens, we have a similar number of observations that tell us that there is an ongoing immune response in the brain of people with autism. In parallel, we have observations of altered moprhology and population density of CNS immune cells. Here is a list for anyone who doubts this claim:

    Neuroglial activation and neuroinflammation in the brain of patients with autism [PMID: 15546155]
    Elevated immune response in the brain of autistic patients [PMID: 19157572]
    Immune transcriptome alterations in the temporal cortex of subjects with autism [PMID: 18378158]
    Transcriptomic analysis of autistic brain reveals convergent molecular pathology [PMID: 21614001]
    Glial fibrillary acidic protein is elevated in superior frontal, parietal and cerebellar cortices of autistic subjects.
    Abnormal microglial-neuronal spatial organization in the dorsolateral prefrontal cortex in autism [PMID: 22516109]
    Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism [PMID: 20674603]
    NF-?B signaling in the brain of autistic subjects [PMID: 22046080]

    And again, the evidence from a literature standpoint is clear; there is an altered neuroimmune environment in autism. If you would like to argue against that, you’ve got a lot of studies to rebut, and you are going to have to do better than a 2004 IOM report.

    Finally, the last piece of the puzzle, vaccines trigger the innate immune system. This is why vaccines work. It is how vaccines work. Not only that, but as has been painfully pointed out here again and again and again, they are designed to do so in such a way that a robust immune response is mounted.

    Earlier daedulus2u had some claptrap about antigens in a drop of sweat or whatever. The CDC says that the DTAP causes a fever in 1/3 doses. If our immune system treated a vaccine the same way it treats everyday exposure, this means that by the first time a child got the DTAP, sixty days out of the womb, that infant should have had a fever for 20 days of it’s life. Does anyone think this is realistic? Have any of you ever had a baby?

    So, here is the hypothesis again:

    Animal studies tell us repeatedly that innate immune challenges in early life can have persistent programming effects that include disturbances to the neuroimmune system and ultimately manifest as behavioral changes. These studies tell us repeatedly that the timeframes of early life are the most critical. The autism population has been shown to have a propensity for increased innate immune responses; this means that for the same insult, a child with autism will respond more vigorously and/or regulate the immune response less effectively; essentially making them a susceptible subgroup to changes as a result of early life insult. The autism population has also been shown to have altered neuroimmune characteristics, also consistent with the animal models. Because vaccines trigger the innate immune system as part of thier design, this is why we can learn about vaccination from the animal models. Because our existing autism / vaccine research is exclusively based on thimerosal, which does not measure whether or not the infant had an immune response or not, or the MMR, which does invoke an immune response, but which is given much later in time compared to the rest of the our vaccine schedule, our existing research is effectively blind to the possibility of changes as a result of our earliest vaccines. There is no mechanism by which our existing data could detect this relationship; the studies are inappropriately designed to identify it. That is experiment design 101; you can only answer the question that you ask.

    Is this really that difficult to understand? Does anyone here, honestly have trouble following any of that?

    (1) autism prevalence has probably not changed appreciably in the last 30 or 40 years (no ‘autism epidemic,’ no vaccine link; it’s quite simple)

    The epidemiology is a total joke and you know it; which is why you pepper your statement with impossible to quantify qualifiers like ‘probably’ and ‘appreciably’.

    What about the effect of older parents? How has your analysis taken this into consideration?

    What about the effect of mothers with metabolic syndrome? We’ve been getting fatter, a lot, and now we have evidence that having an obese mother increases the risk of autism diagnosis. Could you explain how this finding fits into your measurement of ‘appreciably’?

    Hey, did you know that having a mother with asthma increases your risk of being born with autism? It’s true! Crazy enough, asthma rates have also been rising. I wonder, could you explain to us how this fits into your value of ‘appreciably’?

    You are talking about literally the most important thing towards our species, whether or not our infants are being changed, and your argument hinges on meaningless adjectives. When Stephen Novella posted that ridiculous Korea study here, naming an astronomical 1 in 38 prevalance (!), nobody batted an eye. This was more than double the results from the adult “study” he trumpeted a year previously; autism rates are double in children what they are in adults, and nobody cares. What this should be telling everyone is that nobody actually trusts the autism epidmiology right now. You don’t get to decide that you like the epidemiology when it is expedient to your (already reached) conclusion, and not trust it when it isn’t. This is insanity.

    (2) autism has a large genetic component;

    OK. We might disagree on the degree of that component, but I won’t disagree. No dispassionate evaluation of the data allows for any other conclusion.

    (3) studies indicating that whatever causes autism largely occurs before birth;

    Some do, but some don’t, and again, you are applying a completely simplistic model to a very complicated condition. The developmental origin of disease do not end at the exit of the birth canal. If a mother smokes during pregnancy, that’s no reason for her to keep smoking in the nursery.

    (4) studies indicating that there are structural differences in autistic brains, including indications that autistic children have more neurons in the prefrontal cortex (more indication that the abnormalities associated with autism occur before birth).

    As I pointed out to daedulus2u, postnatal synaptic pruning is explicity mentioned in that paper as a potential participant. Similarly, the white matter tract paper I posted used only timeframes from 6 – 24 months, which I’m pretty sure is outside of the prenatal period.


    But let’s ask two quick questions, given your comments on studies above:
    1. Do thimerosal-containing vaccines cause autism? I say the evidence is quite conclusive that they don’t, at least not detectably. Your comments seem to indicate that you accept the scientific literature concluding this; otherwise you would not harp on it.
    2. Does the MMR cause autism? Again, I say the evidence is quite conclusive that they don’t, at least not detectably. Your comments seem to indicate that you accept the scientific literature concluding this; otherwise you would not harp on it.

    I agree with both points.

    Add to that the persistent epidemiological evidence that fails to find a link between vaccines and autism, and the vaccine-autism hypothesis is about as dead as a hypothesis can be.

    WHAT EVIDENCE? THE EVIDENCE YOU FAILED TO POST? This is exactly what pmoran is talking about, you go on and on about thimerosal and the MMR, and then try to spin it into a conversation about vaccination as a whole. Why? WITH WHAT EVIDENCE? If you don’t like having condescending questions asked, stop trying this kindergarden level bait and switch on everyone. It makes you look foolish. You are not fooling anyone over the age of 5.

    - pD

  66. David Gorski says:

    What about that process is different for “vaccines” as a class of antigen exposures that make them worthy of additional study beyond what has already been done and which continues to be done as part of the normal study of vaccine effects and side effects? Timing? Why isn’t the timing of exposure to each of the millions of other antigens important?

    Excellent questions, Daedulus, questions that neither pD nor any other believer in the vaccine-autism link has ever been able to answer for me in even a mildly convincing fashion, and it’s not for lack of their trying, as PD’s tsunami of verbiage demonstrates.

    In reality, it all seems to boil down to appeals to observations that there might be some sort of neuroinflammatory component to autism coupled with claims that vaccines don’t stimulate the immune system in a manner that antivaccinationists consider to be “natural”; so it must be the vaccines causing or contributing to autism rather than the thousands of other antigens babies and children encounter. In fact, pD’s most recent word deluge, boiled down to its essence, says something very similar to just that, with the added twist of saying that timing matters, all without anything other than speculation to link his perceived correlation to actual causation.

    At least he agreed that (1) the MMR vaccine doesn’t cause autism and (2) thimerosal-containing vaccines do not cause autism. That’s something, I suppose.

  67. Chris says:

    pD, it is obvious you don’t have “more options” than vaccines to protect infants from disease when you said “We have a lot more options than that.” So, can you at least answer if you have had the Tdap as part of the option to protect others (and yourself)?

  68. papertrail says:

    @pD You lost me at this: “studying a vaccine ingredient, or a single vaccine given in toddlerhood is a different thing than studying the process of vaccination which primarily occurs in infancy.”

    Who is studying just a single vaccine ingredient or just a single vaccine? My understanding is that vaccines are studied along with their ingredients as one product, and that new vaccines are studied on previously vaccinated subjects and in combination with other vaccinations. Reserachers are not telling subjects not to vaccinate for other VPDs while they’re testing a new vaccine for safety.

    Also, when we talk about thimerosal in vaccines having been shown to not cause autism, and it seems pD and pmoran both agree on that, we’re ruling out a connection to autism for several vaccines, the HIB, Hep B, DPT, at least. Now they don’t contain thimerosal anyway.

    I see Dr. Novella predicted that increases in autism rates will be found to be associated with unvaccinated children, not vaccinated. This seems to be coming to light. We can see that Utah has a very high autism rate and very low immunization rates. An association between higher educated parents and lower immunization is showing up, as well as an association between higher educated parents and higher autism rates. And there is no doubt that lower immunization is associated with higher disease outbreak rates.

    Spreading a sciency sounding argument that vaccines are causing autism is serious; it leads to lower immunization that leads to serious illness and death. If there is some emotion behind insisting that those who want to leave that door open without a truly compelling argument, you can see why. There is a body count involved in causing immunization rates to go down, especially considering that the concerns raised by pD are vague and weakly supported if at all and pmoran issue involves semantics more than anything else, as far as I can tell.

    I think that if someone has a hypothesis that vaccines are causing autism, do the studies yourself.

  69. papertrail says:

    continuing.. “I think that if someone has a hypothesis that vaccines are causing autism, do the studies yourself.”

    I say that because I believe the burden of proof currently rests with those making what could now be regarded as an extraordinary claim.

  70. papertrail says:

    pD shouted: “WHAT EVIDENCE? THE EVIDENCE YOU FAILED TO POST? This is exactly what pmoran is talking about, you go on and on about thimerosal and the MMR, and then try to spin it into a conversation about vaccination as a whole. Why? WITH WHAT EVIDENCE?”

    I agree that I see this happening, that Dr. G, H and O (as in Offit), and many, many other sources do cite the studies relating to MMR and thimerosal as the basis for stating that “vaccines” don’t cause autism.

    Personally, I translate that to mean:

    *there is no plausible reason to believe vaccines can lead to autism (that one will offend pD who believes he has come up with a concerning association between neonatal inflammation from vaccines and inflammation found among a subset of autistic kids), which includes a substantial number: measles, mumps, rubella, diphtheria, tetanus, pertussis, HIB, Hep B (and the other “old” thimerosal-containing vaccines that I’m too lazy to look up right now).
    *Manufacturer phase trials, often including a substantial Phase 4, and which include looking at the effects of concomitant vaccinations and the safety of adding a new vaccination to the existing schedule.
    *Post licensing surveillance.
    *A lack of substantial difference in the mechanism of action between the many vaccines that were already ruled out as having a connection to autism and the newer ones.

    Someone tell me if I’m wrong about this.

  71. papertrail says:

    Wait, I messed that up with cut and paste. Here’s a rewrite:

    pD shouted: “WHAT EVIDENCE? THE EVIDENCE YOU FAILED TO POST? This is exactly what pmoran is talking about, you go on and on about thimerosal and the MMR, and then try to spin it into a conversation about vaccination as a whole. Why? WITH WHAT EVIDENCE?”

    I agree that I see this happening, that Dr. G, H and O (as in Offit), and many, many other sources do cite the studies relating to MMR and thimerosal as the basis for stating that “vaccines” don’t cause autism.

    Personally, I translate that to mean:

    *there is no plausible reason to believe vaccines can lead to autism (that one will offend pD who believes he has come up with a concerning association between neonatal inflammation from vaccines and inflammation found among a subset of autistic kids), *Manufacturer phase trials, often including a substantial Phase 4, and which include looking at the effects of concomitant vaccinations and the safety of adding a new vaccination to the existing schedule.
    *Post licensing surveillance.
    *A lack of substantial difference in the mechanism of action between the many vaccines that were already “ruled out” as having a connection to autism and the newer ones, which includes a substantial number: measles, mumps, rubella, diphtheria, tetanus, pertussis, HIB, Hep B (and the other “old” thimerosal-containing vaccines that I’m too lazy to look up right now).

    Someone tell me if I’m wrong about this.

  72. lilady says:

    Well stated papertrail!

    Long before the proliferation of anti-vaccine bloggers and other assorted crank medicine bloggers, the CDC in cooperation with 10 regional all-inclusive HMOs set up the Vaccine Safety Datalink databank, which monitors every vaccine administered to their subscribers and their dependents. The Vaccine Safety Datalink also records, in next-to-real-time each and every doctors’ visit, each and every Emergency Room visit and each and every hospitalization within the HMO’s affiliate hospital for any and all (minor) side effects post vaccination…and each and every serious adverse effect of vaccinations, that require hospitalization.

    The Vaccine Safety Datalink database is far more reliable than the VAERS reports that are submitted by doctors, parents, and other parties who report some very *suspcious* instances of adverse events (i.e. drownings, deaths from impact injuries sustained in an automobile accident…months after receiving a HPV vaccine). One (in)famous VAERS report claimed that the recipient turned into the “Incredible Hulk” post vaccination. Didn’t Michele Bachmann, a Republican Presidential wannabe, claim to have spoken to a mom whose daughter received a HPV vaccine (and) “thereafter became mentally retarded”?

    http://www.who.int/docstore/bulletin/pdf/2000/issue2/bu0338.pdf

    Here’s an example of the value of real researchers and real statistician who monitor post marketing/post licensing of all vaccines through the VSD database. Read how quickly (13 months) the first rotavirus vaccine, Rotashield, was removed from the marketplace once analyses of adverse events determined there was a slight, but significant, uptick in intussusception, post immunization:

    http://www.cdc.gov/vaccinesafety/vaccines/rotateq_intussusception.html

    I do not wish to derail this thread, however, there is the matter of credulous parents who believe that their children are “vaccine damaged” and believe that they can cure (“recover” is the buzzword), their children’s autism. Some of the interventions are relatively benign (special diets and vitamin supplements). Other interventions are downright dangerous and downright abusive; Lupron chemical castration, IV chelations, “stem cell intrathecal infussions with G-d knows what substances and oral bleach and bleach enemas….topics that Dr. Gorski has extensively blogged about, as well.

    It’s past time that we contend we “Jaqing Off” remarks and other remarks that reek of tone trolling.

  73. passionlessDrone says:

    @Dr. Gorski & daedulus2u -

    What about that process is different for ‘vaccines’ as a class of antigen exposures that make them worthy of additional study beyond what has already been done and which continues to be done as part of the normal study of vaccine effects and side effects? Timing? Why isn’t the timing of exposure to each of the millions of other antigens important?

    Excellent questions, Daedulus, questions that neither pD nor any other believer in the vaccine-autism link has ever been able to answer for me in even a mildly convincing fashion, and it’s not for lack of their trying, as PD’s tsunami of verbiage demonstrates.

    Despite what some of you may think, I have been trying to apply a more critical eye towards my thought processes. One of the things that an application of this effot tells me is that if you have a model of how things work in your mind, you can see how well the model predicts your observations. If the model fails to predict your observations, there are two possibilities:

    1) Your model is wrong and needs to be adjusted.

    2) The observations are wrong, and your model is accurate.

    That being said, the model being proposed here by daedulus2u and advocated as an “excellent question” is essentially the “drop in the bucket” argument; the idea that because vaccines are such a small number of antigens, and our infants live in a world full of antigens, the effect of vaccination cannot be meaningful.

    Now, lets go back up to a post that daedulus2u posted earlier:

    What makes a day of vaccination special? Instead of only getting millions of new antigens from thousands of new bacteria, the infant also gets hundreds of antigens that have been specially prepared.

    The model proposed by daedulus2u, and echoed by Dr. Gorski is that, indeed, there is nothing “special” about a day of vaccination, that indeed, there are orders of magnitude of difference in the number of antigens a child is exposed to in vaccination versus everyday exposure. Impliccit in this model is the idea that antigen exposure, and their numbers, are the only meaningful measurement to understand the degree of innate immune system activation.

    The nice part is that this model should be able to make predictions, among them, that there is nothing special about a day of vaccinations. What are some observations we could use to try to determine if this model is correct?

    In the first place, we could look to CDC statistics regarding adverse reactions to vaccines (minor reactions). Fever is a very common one and is indicative of exactly my concern, an innate immune response. Here is a link to a table that displays this information for a lot of vaccines:

    http://www.cdc.gov/vaccines/vac-gen/side-effects.htm

    If we look to the DTaP vaccine, we can see that it is expected, by the CDC, to cause fever following a full one quarter of the doses.

    Fever (up to about 1 child in 4)

    Does this have any implications for the model proposed by daedulus2u? After all, the DTaP has a miniscule number of antigens in it, 7; lets say that daedulus2u is correct, and an infant gets ahold of a million antigens every single day.

    How does his model, the model that forms an “excellent question”, conform to our observations of an immune response in infants? To my eye, the model completely fails to predict what should happen post vaccination. We shouldn’t be able to detect any difference. There should be no way, no way in hell, we should detect an observation of increased fevers in these children if all we have to do is count up antigens. Can the fact that are observations being so at odds with the predictions of the model tell us anything about the quality of the model?

    If a measly 7 antigens can give a child a fever 1 out of 3 times, and children are exposed to millions of antigens every day, and all things are equal, shouldn’t an infant have a fever every day, all day and night long?

    Now, if 90% of children got diptheria, pertussis, or tetanus by the time they reached sixty days out of the womb, I would be an unabashed supporter of mass, nonstop vaccination. But that doesn’t happen, and even pre-vaccination, it didn’t happen. That is why the time dimension is of importance to us.

    Further, I have posted several clinical studies that attempt to qualify the immune response post vaccination already on this thread, at a high level they showed researchers capable of discerning pre/post vaccination and treatment/placebo groups by measuring cytokine levels. If there was ‘nothing special’ about a day of vaccinations, these results should be impossible to achieve, and yet, similar results are reported again and again. Again, we are forced to confront the fact that our observations are the opposite of a “nothing special about a day of vaccination” model would predict.

    Besides being an abject failure at predicting what happens after vaccination by both gross and fine leveled analysis, we could consider the components of vaccination and the components of natural antigen exposure to try to determine if there is a difference between them. The nice part about this approach is that it may inform us on our model seems to be so at odds with reality.

    For starters, we could note that the ‘millions’ of other antigens our infants are exposed to are not being delivered intramuscularly, directly bypassing the skin, saliva, gastric acid, and mucous that is there to prevent pathogens from entering our body. Perhaps Dr. Gorski and daedulus2u have different ideas on whether this is a difference or not; maybe they know something I don’t, and they know that all of the millions of antigens an infant is exposed to have identical mechanisms of entry into the body. I doubt it, but I am open to evidence. If we are looking to understand the discrpancy between our observations and the model, however, this might be an interesting point to consider.

    What about adjuvants, the aluminum salts used to insure that the immune response is sufficiently robust to confer immunity? Are the millions of antigens a child is exposed to daily also delivered alongside adjuvants? If not, I guess I’d wonder where this component of vaccination fits within the model proposed by daedulus2u, wherein we can simply count the antigens in a vaccine up.

    What if we wanted to actually look at things from a molecular standpoint? After all, ‘antigen’ is just a fancy word for a molecular fingerprint; but only a subset of the ones from the bacteria we are protecting oursevles from. In other words, bacteria have a lot of fingers with their own distinctive pattern, but we only choose a few, chop ‘em out, and use those as our epitopes. However, we are being very selective about which patterns we use during this process, we don’t just pick a random set of sugars from the bacterial wall, hope they are sufficient to provide an immunological memory and start cranking out vaccines. Instead, we selectively target specific patterns that both identify the pathogen, (hopefully) do not have parallels inside the body that could confuse the adaptive immune system, and help invoke an immune response. The molecular landscape of bacteria is a lot more complicated than ‘bacteria molecular pattern bad. initiate immune response’. Different bacteria have different molecular patterns, and when our immune systems detect those bacteria, they aren’t just finding the epitopes we have selected for vaccines; they select all kinds of things from all over the bacteria. What this means, according to our model, however, is yet another, layer of complexity; our bodies didn’t evolve fighting epitopes, they evolved running into entire bacteria. Presuming that the immune response from specific components of a bacteria would be the same as the entire bacteria seems incredibly naive, but maybe that’s just me.

    The simplicity on display here, the lack of curiosity, especially by someone who has literally done hundreds of posts about vaccination, ought to be opening some eyes.

    In reality, it all seems to boil down to appeals to observations that there might be some sort of neuroinflammatory component to autism coupled with claims that vaccines don’t stimulate the immune system in a manner that antivaccinationists consider to be “natural”; so it must be the vaccines causing or contributing to autism rather than the thousands of other antigens babies and children encounter.

    I’ve stated several times, including here on this thread, that a natural infection would have the same effect. The difference is, 90% of children aren’t infected their first week of life, or even the first two months. Or longer.

    The bad news for you regarding ‘some sort of neuroinflammatory component to autism’ is that there is a growing consensus among people paying attention that there is a neuroinflammatory component to almost all neurological disorders. Anyone with pubmed and the ability to type ‘depression’ ‘inflammation’ or ‘schizophrenia’ ‘cytokine’ can validate that. But only if you are curious about learning.

    There is a profound irony to this. One of the problems with debating cranks is that they can spew a lot of misinformation in a tiny amount of time; to rebut it, and rebut it effectively, you have to spend a lot of time. A verbiage-tsunami, so to speak. That is what is happening here.

    - pD

  74. Harriet Hall says:

    @pD,

    You have offered a tsunami of speculation, but no evidence that vaccines actually cause those hypothetical harmful effects.

  75. pmoran says:

    David: I see Dr. Novella predicted that increases in autism rates will be found to be associated with unvaccinated children, not vaccinated. This seems to be coming to light. We can see that Utah has a very high autism rate and very low immunization rates. An association between higher educated parents and lower immunization is showing up, as well as an association between higher educated parents and higher autism rates.

    Such evidence would be helpful, but why are you referring to this now and not the evidence that you claimed to have earlier i.e. “Multiple large, well-designed epidemiological studies comprising, taken together, many hundreds of thousand of children that fail to find a whiff of a hint of a wisp of a correlation between vaccination and autism prevalence or onset.”

    You could have simply ignored what I had to say and this would never have blown up into much. I even once offered you an easy “out”, by allowing that “we all make careless statements sometimes especially in more private discussion”.

    But no, instead you and Harriet felt that critical comment on these supposedly science-based pages had to be stifled or defused, so you consulted your own books of ad hominems and logical fallacies , quoted out of context, agreed to the pretence that this was all about “style” and “tone”, and even came up with the affectation that what I was saying was a great mystery to everyone so I should write a blog post to explain myself. (I admit that a perhaps confusing mixture of different matters emerged and that I can be unclear and clumsy in expression, but the main points cannot be THAT unclear after all these posts. Some people at least get the point about the evidence quality, and others may understand the importance of sticking to regular scientific process, and modes of expression.)

  76. passionlessDrone says:

    @papertrail -

    My understanding is that vaccines are studied along with their ingredients as one product, and that new vaccines are studied on previously vaccinated subjects and in combination with other vaccinations.

    If the measurement end points for these studies included autism, Dr. Gorski would just go ahead and post them? Why the subterfuge and the need for your translation?

    Reserachers are not telling subjects not to vaccinate for other VPDs while they’re testing a new vaccine for safety.

    There is a difference, a big one, between safety testing for acute reactions, and looking for unexpected outcomes that may manifest long after the fact. (see the C-section/obesity studies) This is why we performed repeated, retrospective analysis of the MMR for autism. The existing safety studies were not sufficiently designed to look for this association.

    concerns raised by pD are vague and weakly supported if at all

    If you feel my outline here has been insufficiently detailed, then I have failed. If you have read the animal studies and feel they are not compelling, I guess we see things differently.

    Personally, I translate that to mean:

    The language of science is supposed to be the opposite of requiring a translation. That is why so many of us appreciate science; it is exact, it is precise. There is an answer that is right. We can apply rules to our studies to tell us how likely our observations are the result of a real interaction. Above all, this editors of this site should be horrified that someone has had to make such a personal translation; they are supposed to be distributing facts, not editorials that people can take to mean whatever the please.

    How would you translate: “The question has been asked and answered”?

    - pD

  77. passionlessDrone says:

    @Harriet Hall –

    You have offered a tsunami of speculation, but no evidence that vaccines actually cause those hypothetical harmful effects.

    My entire concern is that we haven’t done the right analysis; I don’t think it is fair for you to insist that I go on to produce said analysis. If Dr. Gorski’s ‘the question has been asked and answered’ isn’t a load of horse manure, that’s his job to provide the analysis. He can’t.

    - pD

  78. Chris says:

    pD, have you had a Tdap vaccine? One option to protecting babies without vaccines is to make sure the diseases do not get transmitted. That transmission can be reduced by making more people immune, like all of the older children and adults being up to date with their Tdap and influenza vaccines. Have you done that?

  79. Harriet Hall says:

    @pD,

    ‘the question has been asked and answered’

    It has been asked and answered. You just don’t like the answers. You are demanding “the right analysis” but scientists and experts in those fields don’t see the need for the kind of analysis you want. Even if the analysis you want were done and were negative, you could go on to complain that a slightly different analysis might produce different results, and you could go on studying details forever. Scientific research is like Willie Sutton. It goes where the money is, and the consensus is that there’s not likely to be any money there.

  80. lilady says:

    @ P. Moran: You just don’t “get it” do you?

    Why not check the handy-dandy right column of this blog to see how many times and how many of the SBM bloggers have written about vaccines, the anti-vaccine movement and the many snake oil salesmen/saleswomen who endeavor to undermine public health initiatives to protect kids and adults from serious, oftentimes deadly, vaccine preventable diseases?

    http://www.sciencebasedmedicine.org/index.php/category/vaccines/

    Here, succinctly, IMHO, is your problem Dr. Moran.

    At one time you were the *go to guy/blogger* for advice on cancer treatment and for debunking bogus cancer treatments. Times change…and now Dr. Gorski is in his ascendency in cyberspace, for reliable information on cancer treatments and for debunking bogus cancer treatments. Dr. Gorski has also become well-versed in the science of immunology/vaccine development and the anti-vaccine culture….for which I am and most of his readership are grateful for. You, on the other hand, now see that your followers have dwindled. That is the nature of science, Dr. Moran. You, like me, see others who are more up-to-date with our specialties. Some of us…and I include myself…are delighted…that others have assumed the mantle of educating the public on science-based medicine. Others…perhaps you, Dr. Moran…have difficulty…ceding the roles of educators and bloggers…to Dr. Gorski and a slew of other science bloggers.

    That, is your problem, and that is what you must deal with, without hiding behind your tone trolling and your concern trolling.

  81. papertrail says:

    pD responded to me:

    “The language of science is supposed to be the opposite of requiring a translation. That is why so many of us appreciate science; it is exact, it is precise. There is an answer that is right. We can apply rules to our studies to tell us how likely our observations are the result of a real interaction. Above all, this editors of this site should be horrified that someone has had to make such a personal translation; they are supposed to be distributing facts, not editorials that people can take to mean whatever the please.

    How would you translate: “The question has been asked and answered”?

    First, I could just as easily say that I have to “translate” what you just said about science in order to answer. You said about science, “it is exact, it is precise. There is an answer that is right.” I translate what you are saying to mean that when a question of an association between two events is studied to discern if the relationship is causative, after conducting a number of studies of sufficient quality that confirm the association or lack thereof, we can safely conclude that this is the fact of the matter” (or something along those lines) – and this is only until new, compelling evidence comes along that overturns that conclusion.

    Scientific inquiry of the type we’re talking about is about discovering probabilities greater than chance, not exactitudes, no?

    So, when someone who is known for appreciating scientific inquiry and science based conclusions, like Dr. Gorski, says about vaccines and autism, “the question has been asked and answered,” I strongly suspect and “translate” that he is referring to the tests of the hypotheses that have been presented thus far (MMR and thimerosal) and to the lack of association between vaccinations and the rise in autism rates as indicated by the studies and surveillance to date.

    I hear in such expressions, also, a desire to simplify the matter to convey (1) that it’s time to move on to other, possibly more productive, hypotheses as to the causes of autism and (2) to tell those who continue to seek to capitalize on vaccine-autism fears to sell their brand of quackery better shut up or put up the evidence. Non-immunizations lead to suffering and deaths; this is indisputable.

    I want to add, though, what I have said before, that I personally prefer a less definitive expression of the matter. I don’t even like to say “vaccines are safe” because they aren’t risk free and no one can guarantee that any particular vaccination will be “safe” for an individual, and some might perceive this as distrustful statement. But I notice that those who do say “vaccines are safe” also tend to go on to mention the real but low risks of side effects, so obviously they don’t mean they are “perfectly safe.”

    And I appreciate that there aren’t big bullet-proof studies ruling out other vaccines causing autism like there were for MMR and the thimerosal ones. No one raised the question until the MMR and thimerosal hypotheses were basically overruled.

    There is a real fear among those who see the value of immunizations, which I share, that there will be no end to the hypotheses that vaccines are cause certain serious outcomes, and so I think it’s important to look at the credibility of the hypotheses in light of other, related studies (like those done with the MMR, all the thimerosal vaccines, as well as some large studies done in the past decade on the DPT (whole cell, which raised fears about encephalopathy).

    What I see you doing here, pD, is presenting hypotheses but perhaps not clearly enough, at least for me. I see you posting a lot of studies that suggest to you that there could be some connection between vaccines and autism, but none that actually do study this. I think you are striving to get people here, like Dr. Gorski, to recognize that your hypotheses are plausible enough to warrant their admission that the jury is still out regarding vaccines and autism. You think there is something wrong with their attitude, but is it possible that your arguments aren’t all that compelling, scientifically speaking?

    Again, I recommend you clearly state your hypotheses and then show evidence to support them.

    I think your hypotheses are: (1) neonatal and infant vaccinations, in particular the Hep B, HIB, and the first and second DPT, invoke an inflammatory response that is over and above the level that most infants would normally experience (that is to say: babies are very rarely exposed to the immune challenges of the vaccine targetting diseases while they are routinely exposed to the engineered versions of those diseases through vaccinations);
    (2) inflammatory reactions can cause neurological impairment in children, and
    (3) the Hep B, and/or HIB, and/or DPT vaccinations during infancy are causing inflammatory reactions that cause neurological impairment in children.

    Am I at least hearing your hypotheses accurately? Maybe everyone else here already got what you were hypothesizing, so I apologize in advance if I’m just a little dense about what you’ve been trying to say.

    If those are your hypotheses, do you have clear evidence for each one?

  82. weing says:

    “One of the problems with debating cranks is that they can spew a lot of misinformation in a tiny amount of time; to rebut it, and rebut it effectively, you have to spend a lot of time. A verbiage-tsunami, so to speak. That is what is happening here.”

    Well at least you are honest. I don’t have the time to rebut all your misinformation. That does not make you right. And even if anyone would take the time to effectively rebut your misinformation, what is going to stop you from spewing more?

  83. weing says:

    “If those are your hypotheses, do you have clear evidence for each one?” And how would you go about testing them?

  84. papertrail says:

    “If those are your hypotheses, do you have clear evidence for each one?” And how would you go about testing them?”

    … And if you can delineate all that, then go find some funding for your tests and conduct them.

  85. Chris says:

    weing:

    “If those are your hypotheses, do you have clear evidence for each one?” And how would you go about testing them?

    This is where we encourage pD to write up a test plan, get it approved by an IRB and go write a grant. He should then take that grant to SafeMinds, Generation Rescue, Autism Speaks, Autism Trust, etc to get the funding. And then do the tests.

  86. papertrail says:

    “take that grant to SafeMinds, Generation Rescue, Autism Speaks, Autism Trust, etc to get the funding”

    Except there’d be no hope of any quality or efforts to eliminate bias. Have you seen their (can’t recall which group sponsored it, one of the above) “study” comparing the health of vaccinated versus unvaccinated kids? Good heavens!

  87. Chris says:

    Not so fast, papertrail. SafeMinds has funded research in actual universities. Those researchers are bound by the same rules as anyone else in their institutions. Dr. Mady Hornig did a SafeMinds study (it was her autistic mice one), and later was the primary author of Lack of Association between Measles Virus Vaccine and Autism with Enteropathy: A Case-Control Study. Though, you would hope that pD would follow the rules, especially in regards to the Belmont Report.

  88. passionlessDrone says:

    Hi papertrail -

    I am intrigued.

    I translate what you are saying to mean that when a question of an association between two events is studied to discern if the relationship is causative, after conducting a number of studies of sufficient quality that confirm the association or lack thereof, we can safely conclude that this is the fact of the matter” (or something along those lines) – and this is only until new, compelling evidence comes along that overturns that conclusion.

    Yes. How many studies of ‘sufficient quality’ has Dr. Gorski decided to post here, despite having so much opportunity? On what studies is he basing those conclusions? There isn’t any science to overturn, just common sense and color by numbers immunology we’ve seen passed off here.

    So, when someone who is known for appreciating scientific inquiry and science based conclusions, like Dr. Gorski, says about vaccines and autism, ‘the question has been asked and answered,’ I strongly suspect and ‘translate’ that he is referring to the tests of the hypotheses that have been presented thus far (MMR and thimerosal) and to the lack of association between vaccinations and the rise in autism rates as indicated by the studies and surveillance to date.

    Sweet Jesus, you’ve drunk the Kool-Aid already! In one thread, you admit we have no studies, admit that Dr. Gorski didn’t mean there were actually any studies on vaccination, and then, try to make the same claim that he does!

    the lack of association between vaccinations and the rise in autism rates

    For someone so precise with language when, you seem to have had quite a slip up. Witness the subtle power of translations!

    Speaking more broadly towards the question of what Dr. Gorksi ‘referring to’, if you are a regular reader of this site, you’ll know that a common thread is the problem with public reporting and the relative lack of scientific rigor applied to the findings from scientific papers. Such translations, ‘I thought he was talking about one thing, even though he wasn’t, because he’s a smart fellow’, have been the genesis of many threads here. Imagine if every science reporter did that with what they saw on Oprah or whatever. What you are describing is an anathema to the editors of this site when it suits them, one seemingly minor mix up and suddenly the wrong thing is planted in peoples head.

    I seriously am wondering how someone can write this:

    “Scientific inquiry of the type we’re talking about is about discovering probabilities greater than chance, not exactitudes, no?”

    go on to defend how you figure that someone’s stature should allow us to translate their words from the findings of scientific research, to the findings that actually are. Do you think Dr. Gorski would try such creative substition, allowing his readers to ‘suspect and translate’ in one of his cancer posts? I thought we were supposed to be telling us the facts, not the facts they’d figure we’d come to the correct conclusion with.

    What I see you doing here, pD, is presenting hypotheses but perhaps not clearly enough, at least for me.

    Have you tried reading any of the animal studies I posted above? I identified about twenty of them. Earlier in this thread you professed a lack of understanding of the big words; but I get the feeling you are clever enough to understand a lot of the clear and plain text in those studies. Even more, I’d be interested in your thoughts regarding the detail you can see available for measurement in these studies versus the quality of argument I’ve been getting, here, in this thread (or elsewhere I’ve tried the same thing).

    By way of example,

    Microglia and Memory: Modulation by Early-life Infection

    Is a cool, cool paper. It is available in full, online. Here is the abstract:

    The pro-inflammatory cytokine interleukin (IL)-1ß is critical for normal hippocampus (HP)-dependent cognition, whereas high levels can disrupt memory and are implicated in neurodegeneration. However, the cellular source of IL-1ß during learning has not been shown, and little is known about the risk factors leading to cytokine dysregulation within the HP. We have reported that neonatal bacterial infection in rats leads to marked HP-dependent memory deficits in adulthood. However, deficits are only observed if unmasked by a subsequent immune challenge (lipopolysaccharide, LPS) around the time of learning. These data implicate a long-term change within the immune system that, upon activation with the “second hit”, LPS, acutely impacts the neural processes underlying memory. Indeed, inhibiting brain IL-1ß prior to the LPS challenge prevents memory impairment in neonatally-infected (NI) rats. We aimed to determine the cellular source of IL-1ß during normal learning, and thereby lend insight into the mechanism by which this cytokine is enduringly altered by early-life infection. We show for the first time that CD11b+ enriched cells are the source of IL-1ß during normal HP-dependent learning. CD11b+ cells from NI rats are functionally sensitized within the adult HP and produce exaggerated IL-1ß ex vivo compared to controls. However, an exaggerated IL-1ß response in vivo requires LPS prior to learning. Moreover, preventing microglial activation during learning prevents memory impairment in NI rats, even following an LPS challenge. Thus, early-life events can significantly modulate normal learning-dependent cytokine activity within the HP, via a specific, enduring impact on brain microglial function.

    And

    Importantly, they suggest an individual’s risk or resilience to neuroinflammatory disorders may critically depend on their early life experience, which can modulate normal cognition-dependent cytokine activity within the brain long after the initial insult.

    Doesn’t this sound similar to things I’ve been saying previously in this thread? This is part of the introduction:

    Importantly, they suggest an individual’s risk or resilience to neuroinflammatory disorders may critically depend on their early life experience, which can modulate normal cognition-dependent cytokine activity within the brain long after the initial insult.

    You are easily, easily clever enough to understand the above sentence and it’s relationship to the kind of thing I keep saying is plausible. This study was published in the Journal of Neuroscience, with a very high 7+ impact factor. This study was funded by an NIH grant.

    The question we have to ask ourselves is; why wouldn’t the editors, or peer reviewers of the Journal Of Neuroscience call the authors out as cranks for making the assertion that an individual’s risk or resilience to neuroinflammatory disorders may critically depend on their early life experience, which can modulate normal cognition-dependent cytokine activity within the brain long after the initial insult. If my ideas are as crazy as they sound to everyone here, why was this study published in a highly rated journal?

    Here is another one that has full free access:

    Neonatal programming of innate immune function

    The early life environment can be crucial in influencing the development of an animal’s long-term physiology. There is now much evidence to suggest that perinatal challenges to an animal’s immune system will result in changes in adult rat behavior, physiology, and molecular pathways following a single inflammatory event during development caused by the bacterial endotoxin lipopolysaccharide (LPS). In particular, it is now apparent that neonatal LPS administration can influence the adult neuroimmune response to a second LPS challenge through hypothalamic-pituitary-adrenal axis modifications, some of which are caused by alterations in peripheral prostaglandin synthesis. These pronounced changes are accompanied by a variety of alterations in a number of disparate aspects of endocrine physiology, with significant implications for the health and well-being of the adult animal. In this review, we discuss the newly elucidated mechanisms by which neonatal immune challenge can permanently alter an animal’s endocrine and metabolic physiology and the implications this has for various disease states.

    This paper was published in Endocrinology and Metabolism. Now check that out, for some reason, the peer reviewers, editors, all seemed exactly OK with the abstract reading: There is now much evidence to suggest that perinatal challenges to an animal’s immune system will result in changes in adult rat behavior, physiology, and molecular pathways following a single inflammatory event during development caused by the bacterial endotoxin lipopolysaccharide (LPS). Does this sound similar to what I’ve been trying to say? Try re-reading a few of my posts if you don’t think so; I’m not making stuff up, I am quoting the literature.

    Here is the conclusion:

    It is now abundantly clear that experiencing an immune challenge during the perinatal period can have far-reaching and long-term effects on many aspects of physiology. Current research has produced conflicting results regarding some of these aspects, but it is evident that there are critical windows during development when the animal is vulnerable to such challenges, and the outcomes may depend on the age, dose, type, and duration of the stimulus.

    I honestly do not believe for one second this is too vague for you to understand. If we replace the word ‘vaccine’ with ‘immune challenge’, your argument is directly with the literature, not with me.

    What’s more, the people that are performing these experiments are clever.

    Collectively, these results point to a collaborative TLR4- and COX-2-mediated mechanism by which early life exposure to LPS causes attenuated febrile responses to the same challenge in adulthood. Early exposure to LPS leads to greater expression of TLR4 in the liver and constitutive COX-2; thus, LPS acting on these more numerous TLR4, coupled with high peripheral levels of available liver COX-2, results in increased early PGE2 production, amplified early HPA axis activity, and subsequent downregulated cytokine production (Fig. 3).

    All of the studies I referenced above have the same broad foundation; early life matters in ways that we are just starting to comprehend. If you disagree with that, you are in disagreement with the literature, and in this case, the literature that can be referenced intead of inferred.

    Compare that level of detail with the responses you’ve seen to my ideas so far on this thread; infants eat dirt, you cannot measure a predisposition to inflammation, a day of vaccination is nothing compared to everyday exposure, and another adventure in utility free antigen counting.

    I think I’ve been very, very resopnsive to answering your questions. Try taking those papers for a read, then compare their methodology, the conciseness of their languge, to the substance of the arguments you’ve seen Dr. Gorski, Harriet Hall, deadulus2u are providing.

    The animal models tell us what is biologically plausible. The human studies tell us that people with autism have immunological profiles consistent with risk factors associated with early life immune insults. There are no studies, and there should be. I don’t have to know all the answers to be able to see the problem.

    Does that help any from a clarity standpoint? Ask me more questions; I’ll give you the best answer I can, as long as you promise to do the same.

    - pD

  89. papertrail says:

    pD responded to me, about pre license studies and post license surveillance:

    If the measurement end points for these studies included autism, Dr. Gorski would just go ahead and post them? Why the subterfuge…?

    …There is a difference, a big one, between safety testing for acute reactions, and looking for unexpected outcomes that may manifest long after the fact. (see the C-section/obesity studies) This is why we performed repeated, retrospective analysis of the MMR for autism. The existing safety studies were not sufficiently designed to look for this association.

    Dr. Gorski’s not posting these studies is dubious evidence that they don’t test for autism. The pre-licensure phase studies, as I understand it, require the manufacturer to note and examine *every* temporal adverse event following vaccination, even ones that seem to have nothing to do with vaccination, and these studies go on for several years so that neurological difficulties such as autism that reveals itself usually by 3 years old would be noted (although I don’t know if this was always the case or just with more recent vaccines, as regulations tightened up over the years). Every adverse event is analyzed as to possible or probable causation. Phase 4 studies involve very large samples of volunteers. The FDA then decides if the vaccine is efficacious and safe (safe enough; it’s a relative, risk-benefits decision), and if approved for licensing, the CDC and its advisory committees further evaluate the vaccines to decide if they should be distributed. Post distribution studies continue whenever there’s a compellling reason to suspect a serious problem, which includes VAERS and Vaccine Safety Datalink studies and academic studies. I do believe that any link between vaccines and autism, given that this is what many, many parents fear, is of paramount importance to the CDC and the WHO and advisory committees.

    I do believe that the CDC and other nations’ public health authorities pursued those repeated large studies on the MMR and thimerosal vaccines not because they had any evidence or belief that vaccines might cause autism but mostly because of rising public fear about methyl mercury (and lack of substantial studies on ethyl mercury used in vaccines) and due to studies like Wakefield’s MMR report (now known to be bogus). They needed to be able to respond to a growing number of vaccine injury court claims too and falling immunization rates. I believe the CDC requested a systematic analysis of the relevant studies from the Institute of Medicine so that they could respond more affirmatively to the claims that a very small subset of the population might be affected, undetected by smaller studies.

    I think the CDC is considering doing a large vax versus unvax study, but there are so few people who don’t vaccinate that I doubt the study would be large enough to satisfy those who believe vaccines cause autism.

    How many subjects would you need to satisfy your need to know if infant vaccines are causing autism? What kind of study would you accept?

  90. papertrail says:

    I wrote my last post before seeing your reply, just so you know. I might now have bothered.

    I am not qualified to go through all your listed studies and figure out if they actually support your hypotheses that vaccines cause inflammation and therefore they cause autism. It’s an interesting idea. It would take a systematic review from among experts.

    Take it to some credible immunologists and report back on their reactions. I’ll look forward to seeing their analysis. I don’t know you to be an expert on this. What is your background /qualifications?

    Write up a study proposal and submit it for funding. When it is peer reviewed, people will take greater notice.

    Meanwhile, your personal insults are flying wild here, showing you to be losing control. You are certainly not passionless, that’s for sure. Have you gotten any positive feedback on your hypotheses from anyone with expertise, and I’m not talking about biased anti-vax people? If you’re on to something, take the ball and run with it. Why waste your time here?

  91. Chris says:

    pD, have you protected yourself and others by getting a Tdap vaccine?

    Seriously, to others you say: “I think I’ve been very, very resopnsive to answering your questions.” But you have actually ignored my very simple questions. Why? I only asked about your statement:

    I am not against vaccination. Your response implies a binary decision, vaccinate or not. We have a lot more options than that, I think you understand this, but I’m not sure.

    I am not even asking about those other unknown options which you have never revealed, but a known one: the one that keeps infections away from infants. Yet, you do not answer. Why?

  92. papertrail says:

    Chris said: “Not so fast, papertrail. SafeMinds has funded research in actual universities. Those researchers are bound by the same rules as anyone else in their institutions.”

    I stand corrected, at least about SafeMinds, at least in that case. Thanks for pointing that out.

  93. papertrail says:

    @pD, have you read anything by Dr. Philip Landrigan? His bio says: “Dr. Landrigan has been a leader in developing the National Children’s Study, the largest study of children’s health and the environment ever launched in the United States.”

    He is committed to discovering causes of autism. He says, “there is substantial imbalance between the extensive and highly sophisticated information on the genetics of autism and the scarcity of investigation into potential environmental causes. This situation raises the possibility that still undiscovered environmental exposures also contribute to causation of autism perhaps acting in synergy with inherited genetic vulnerabilities.”

    Sounds like he’s not likely to rule out any viable possibility.

    He also says about vaccines:

    “There is no credible evidence that vaccines cause autism. To address the possibility of a connection between the MMR vaccine or thimerosal and autism, a dozen highly credible studies have been undertaken in the US, the UK, Europe, and Japan. None have found credible evidence for a connection between the MMR vaccine or thimerosal and autism. Most persuasive among these studies is an investigation in Yokohama, Japan. There, the MMR vaccination rate declined significantly between 1988 and 1992, and no MMR vaccine was administered in 1993 or thereafter. Despite declining immunizations, the cumulative incidence of ASD increased significantly each year from 1988 through 1996 and rose especially dramatically beginning in 1993. Overall incidence of autism nearly doubled in those years.”

    I think he’d be a good person for you to run your ideas past to see what he thinks and why he has discounted vaccine in general as a candidate for consideration while exploring environmental causes of autism, citing only those major MMR and thimerosal studies.

  94. pmoran says:

    Lilady:Here, succinctly, IMHO, is your problem Dr. Moran.
    At one time you were the *go to guy/blogger* for advice on cancer treatment and for debunking bogus cancer treatments. Times change…and now Dr. Gorski is in his ascendency in cyberspace, for reliable information on cancer treatments and for debunking bogus cancer treatments. Dr. Gorski has also become well-versed in the science of immunology/vaccine development and the anti-vaccine culture….for which I am and most of his readership are grateful for. You, on the other hand, now see that your followers have dwindled. That is the nature of science, Dr. Moran. You, like me, see others who are more up-to-date with our specialties. Some of us…and I include myself…are delighted…that others have assumed the mantle of educating the public on science-based medicine. Others…perhaps you, Dr. Moran…have difficulty…ceding the roles of educators and bloggers…to Dr. Gorski and a slew of other science bloggers.
    That, is your problem, and that is what you must deal with, without hiding behind your tone trolling and your concern trolling.

    I had sworn I would not prolong this further no matter what, but this is unacceptable on several grounds.

    Let’s overlook the ridiculous condescension and name-calling, and look at the hypothesis that I am driven by some weird personal vendetta against Dr Gorski.

    Would it shed any light on the matters that have been raised? Not in the least. It might make me more likely than other readers to pick up on his overstatements of the evidence, but their appropriateness within a science-based forum that also spends a lot of its time accusing others of sloppy science and logic (and none more so than Dr Gorski himself) will still have to be judged on other grounds, including its potential for supporting the common allegation that we apply inconsistent standards when looking at CAM..

    Is this even a valid hypothesis? Lilady, you may not have been here when I was one of the strongest critics of an Ob/Gyn commentator who is no longer here, because of her tendency to overstate the scientific case on certain matters. I have criticised other authors wherever I have observed poor use of science, for example, using the results of whole population studies to diminish the popularity and use of CAM, instead of the rather more meaningful gauge of use by those with various illnesses. I have been very vocal with other commenters on matters to with with placebo responses and what factors drive CAM. I have almost single-handedly reduced the level of juvenile name-calling on this supposedly science-based forum (or I had until you came along) and that concerned the writings of other principals as much as Dr Gorski.

  95. lilady says:

    Yes, Dr. Moran you have been posting here far longer than I have and won the respect of the bloggers and other posters alike. Recently you have used this platform to urge for more “tolerance” of alternative and complementary medicine and the placebo effect within science-based medicine. But, that is not the subject of this particular thread.

    Now you accuse me of “name calling” and bringing this thread down….while (you) ” have almost single-handedly reduced the level of juvenile name-calling on this supposedly science-based forum (or I had until you came along)…”

    I have read all your comments on this thread including the one about post vaccination febrile seizures *possibly* being linked to autism…which frankly is a new and rather unique hypothesis to me. I asked you for some studies that have linked febrile seizures from a vaccine to the onset of autism and you were exceedingly rude and dismissive…

    “Oh, and thanks, Lilady, for the link concerning febrile convulsions, which is mildly reassuring.”

    You then stated…

    “You misunderstand. I made a simple query, and found your link only mildly reassuring for the reasons that I mentioned. I am not saying that there is such a link. I do want to be prepared for that claim. There is no doubt that at some point this question will come up, if only because autistics are prone to epilepsy and presumably also to febrile convulsions after those vaccines that provoke fever. There is scope for another spurious causal theory.”

    No I didn’t misunderstand Dr. Moran. You made the statement and tried to blow me off…even after I provided links to the two studies of children whose parents claimed and were awarded damages for their children’s febrile seizures associated with the whole cell DTP vaccine. If you recall, these children underwent genetic testing and found to have Dravet Syndrome. Those cases, in particular, resulted in vaccine manufacturers shutting down their operations, thereby threatening the entire public health system for lack of drug companies willing to continue manufacturing vaccines.

    I’ve also asked you who appointed you as the sole arbiter of the content, the style, the tone and the phraseology that bloggers here use for their articles. You don’t seem to be able to answer that question Dr. Moran. Why not?

    It is your comments about the content, the style, the tone and phraseology that Dr. Gorski uses that have drawn the most comments here and they are not just from Dr. Gorski and Dr. Hall and me. I personally find your comments extremely offensive…they are the epitome of tone trolling and concern trolling.

    Perhaps you notice that I don’t comment on this blog about subjects I know nothing about…including many of Dr. Gorski’s blogs about cancer. I prefer to just read those blogs and read the comments from others who are far more educated and involved with cancer treatments. I do comment when the subjects are about infectious diseases, neurology, developmental disabilities and vaccinations…subjects that I am well-versed in and which were a large part of my work experience as a public health nurse/clinician. You would do well to consider not posting on subjects you know absolutely nothing about as well…instead of using this forum for tone trolling and concern trolling, directed at Dr. Gorski.

    Again, show us how you would deal with this topic, by submitting a guest blog for publication. I look forward to seeing it.

  96. passionlessDrone says:

    @papertrail –

    I am not qualified to go through all your listed studies and figure out if they actually support your hypotheses that vaccines cause inflammation and therefore they cause autism.

    I thought that you were having problems with my idea set being too vague; so I thought that I would try to show you the relatively clear language available in a lot of the literature I’ve been reading. I was just trying to present a less fuzzy picture of what I’ve been reading in regards to the animal literature; that is why the blindspot in our research bothers me so much; because the animal studies tell us it is possible. Despite your concerns about a relative lack of expertise for judgement, have I made my concerns any more clear?

    As pointed out previously by other here; I’m no expert and I don’t think I’ve ever claimed to be. That being said, the appeal to authority is generally considered a poor rebuttal in this forum. This site is about thinking about things critically and performing an unbiased evaluation of the data. Some others here may not think I’m doing that; hopefully you aren’t in that camp.

    I have heard of Landrigan and I share a lot of his concerns over the developmental toxicity of the ocean of synthetics our infants are developing in. Thanks though.

    Have you gotten any positive feedback on your hypotheses from anyone with expertise, and I’m not talking about biased anti-vax people?

    Funny that you should mention that. One of the big names in the autism / prenatal immune insult realm, Paul Patterson, actually stopped by my blog at random a while ago on a post I wrote about the connections between the brain and the immune system and how this is manifesting behaviorally. Take him for a spin in pubmed; he has a lot of animal models that utilize in vitro studies of immune challenges with outcomes similar to autism. [If you look to the first post I made here, Paul Patterson was an author on one of the studies I mentioned.]

    Anyways, here is a link to my blog posting:

    http://passionlessdrone.wordpress.com/2011/05/12/the-interconnectedness-of-the-brain-behavior-and-immunology-and-the-difficult-to-overstate-flaccidity-of-the-correlation-is-not-causation-argument/

    In any case, Mr. Patterson left several comments on my blog:

    Just came across this outstanding blog today. Really good coverage of the relevant literature in this area.

    Your topics are amazingly similar to those covered in my book that was just published by MIT Press: http://mitpress.mit.edu/catalog/item/default.asp?ttype=2&tid=12756

    And your blog and my new book blog also have some key overlaps: http://infectiousbehavior.wordpress.com/

    Keep up the good work!
    Cheers,
    PHP

    Later, after seeing some other comments on my blog specifically regarding vaccination, he left this message:

    Indeed, postnatal vaccinations would fit neatly into the scenario of immune disturbance in autism and its effect on behavior – if only the epidemiology supported a link, which it does not.

    Now here is the crazy part; when I took him to task on the fact that the epidemiology isn’t strong; he used as a reference the Dr. Offit “paper”, that uses exactly the same shell game Dr. Gorski uses here!

    In this instance, we have a well published researcher in the autism realm, specifically the immune disturbance component, who thinks that our epidemiology has studied postnatal vaccinations. He, apparently, didn’t put together from Dr. Offits paper to mean that ‘we should move on’ or ‘we’ve studied thimerosal and the MMR’. He thought the question had been asked or answered. [It must be said, it would appear that I have an apology to make to Dr. Gorski. Earlier I told him that his ploy of 'the question has been asked and answered' wouldn't fool anyone over five. In that regard, I appear to be incorrect.]

    Now, compare that with Dr. Gorski’s confusion over why vaccines should be special, or daeduls2u’s claim that antigen components from vaccines can’t be discriminated for versus everyday exposure.

    I apologize if I offended you in some way.

    - pD

  97. daedalus2u says:

    pd, I have met Dr Patterson, have heard him talk and have read a bunch of his papers. The immunological effects he is working with are non-specific. One of the models he uses is non-infective DNA, that is there is no “infection” to complicate things, there is just immune system stimulation.

    That non-specific immune system stimulation occurs with all infections and also with all vaccines, including MMR. If the epidemiology says that MMR does not cause autism, what the epidemiology is saying is that non-specific immune stimulation analogous to the non-specific immune stimulation of MMR does not cause autism. The non-specific immune stimulation effects of MMR are pretty strong, because MMR is live attenuated vaccine. If the non-specific immune stimulating effects of MMR are not associated with autism, then it is very unlikely that milder non-specific effects from killed vaccines would.

    That is why Dr Patterson is mostly looking at in utero stuff now regarding autism. He is sophisticated enough to understand the data and its implications, and he has moved on. The non-specific effects of post-natal immune system stimulation don’t cause autism. The data has spoken.

  98. passionlessDrone says:

    @daedulus2u –

    The immunological effects he is working with are non-specific. One of the models he uses is non-infective DNA, that is there is no “infection” to complicate things, there is just immune system stimulation.

    That’s the point; you don’t need an infection; just the immune stimulation. That’s the same thing as a vaccine.

    If the epidemiology says that MMR does not cause autism, what the epidemiology is saying is that non-specific immune stimulation analogous to the non-specific immune stimulation of MMR does not cause autism.

    I agree with your point. But the animal literature, some twenty study I listed above, all tell us that assuming that one timeframe, 12 – 18 months is the same as another timeframe, 2 months, is a flawed approach. It will lead you to an invalid conclusion. The data tells us again and again that ignoring the dimension of time in this analysis means that you ignore the critical factor.

    What, in the data, has led you to believe that we can and should equate things that happen at a year with things that happen at two months? My position is that we are not nearly sophisticated enough in our knowledge to make this equivalency.

    If I looked at a thousand people who have smoked for two days, can I learn anything about a relationship between smoking and cancer? If we looked at pregnant women who took thalidomide at nine months of pregnancy, should we assume it is safe during the entire pregnancy?

    Unless you can give me a reason, something with some literature support, on how you’ve reached the conclusion that the developmental timeframe of an insult is not meaningful, you’ve got to contend with a lot of literature that says it is critical. If you can do that, then post a link. Show it. I’ve showed the data indicating that time is an important dimension to the plausibility. If you want to disagree without providing any data, that is your choice, but it generally frowned upon here. If you want to disagree and provide data, then great! Where is the data?

    He is sophisticated enough to understand the data and its implications, and he has moved on.

    I think that we have enough evidence here, already, that assigning motives or knowledge to other people is fraught with problems.

    - pD

  99. passionlessDrone says:

    @Everyone –

    I feel like I keep on harping on the same thing, the criticality of incorporating developmental timeframe into our discussions. Yet, I’m not getting through.

    That being said, I’ve got a copy of Microglia in the developing brain: A potential target with lifetime effects [PMID: 22322212]

    It was authored by Harry Jean, with over 100 references in pubmed. Here are a few snipets from that paper which to my mind, make my point.

    Microglia are a heterogenous group of monocyte-derived cells serving multiple roles within the brain,many of which are associated with immune and macrophage like properties. These cells are known to serve a critical role during brain injury and to maintain homeostasis; yet, their defined roles during development have yet to be elucidated. Microglial actions appear to influence events associated with neuronal proliferation and differentiation during development, as well as, contribute to processes associated with the removal of dying neurons or cellular debris and management of synaptic connections. These long-lived cells display changes during injury and with aging that are critical to the maintenance of the neuronal environment over the lifespan of the organism. These processes may be altered by changes in the colonization of the brain or by inflammatory events during development. This review addresses the role of microglia during brain development, both structurally and functionally, as well as the inherent vulnerability of the developing nervous system. A framework is presented considering microglia as a critical nervous system-specific cell that can influence multiple aspects of brain development (e.g., vascularization, synaptogenesis, and myelination) and have a long term impact on the functional vulnerability of the nervous system to a subsequent insult, whether environmental, physical, age-related, or disease-related.

    It’s a difficult balance to keep from spamming everyone and (trying) to make my point, but I’ll try:

    Overall, the data suggest that microglial actions may be most critical during postnatal brain maturation rather than during embryonic stages of development.

    I assert that no one here, or anywhere, can adequately define what this postnatal brain maturation stages comprise. It might be over at birth. Maybe at twelve months. This paper was published in 2012; anyone telling you that they have a good reason to think they know, that ‘the data has spoken’, can’t back it up.

    What this data does demonstrate is that subtle changes in the neural environment, in the absence of a cell death response, can shift the morphology of developing microglia.

    And here, we have text that indicates that you don’t need big impacts to change the functionality of microglia. That’s important, they are (supposed to be) participating in synaptic pruning at the same time we are vaccinating.

    There is a significant amount of evidence regarding what is often termed ‘‘priming’’ and ‘‘preconditioning’’ events that serve to either exacerbate or provide neuroprotection from a secondary insult, respectively. In these states, the constitutive level of proinflammatory mediators would not be altered; however, upon subsequent challenge, an exaggerated response would be induced. The phenomena of priming represent a phenotypic shift of the cells toward a more sensitized state. Thus, primed microglia will respond to a secondary ‘‘triggering’’ stimulus more rapidly and to a greater degree than would be expected if non-primed. It has been considered that microglia in the aging brain exist in a primed state based upon the shift in morphology to fragmented processes and a elevation in basal levels of pro-inflammatory cytokines (Streit et al., 2004). Exactly how long this primed state will last has not been determined; however, data from microglia suggest that it can extend over an expanded period of time.

    Again, more evidence of the potential for long lived effects and the possibility that inflammatory events during development can perturb the trajectory of the microglia.

    These results again highlight this early postnatal period as a ‘‘critical window’’ of development vulnerable to long-lasting modification of microglia function by specific stimuli. Work by Bilbo and co-workers demonstrated LPS-induced deficits in fear conditioning and a water maze task following infection of PND 4 rats with Escherichia coli. In the young adult, an injection of LPS induced an exaggerated IL-1b response and memory deficits in rats neonatally exposed to infection (Bilbo et al., 2005). Consistent with the earlier work by Galic et al. (2008), an age dependency for vulnerability was detected with E. coli-induced infection at PND 30 not showing an increased sensitivity to LPS in later life (Bilbo et al., 2006).

    How have daedulus2u, Dr. Gorski, or anyone, defined what this ‘critical window’ looks like? How have they determined that it stops after birth? This review is new, published in 2012. Does anyone think that daedulus2u has data that Harry Jean doesn’t have?

    I keep getting complaints on this board that the things I’m asking for are just too darn complex. That isn’t me. It is the reality:

    One hypothesis for developmental sensitivity is the heterogenous roles for inflammatory factors and pro-inflammatory cytokines during development, including their timing-, region and situation-specific neurotrophic properties. Many of the proinflammatory cytokines are lower at birth with a subsequent rapid elevation occurring during the first few weeks of life.

    My insistence that we pay close attention to multiple parameters isn’t a function of me trying to craft ever difficult problems for you to solve, it is a mandated by an honest reading of the literature. If you don’t think we need to understand how cytokine exposure during development aren’t time, region and specific situation, your argument isn’t with me; it is with the research.

    We aren’t nearly as clever as we think we are, collectively. The systems we are interacting with are far, far too complicated to be understood by addition, or assuming that a year of age is the same thing as a week old, or two months old. If you don’t believe, try reading the literature.

    - pD

  100. Harriet Hall says:

    @pmoran,

    “I have almost single-handedly reduced the level of juvenile name-calling on this supposedly science-based forum”

    That’s not only hubris, it’s delusional.
    All you have contributed to this forum is criticism of our approach, and you have not backed it up with evidence that another approach would be more effective or even with a coherent example of what you think we “should” be doing. Please stop this useless, disruptive commenting and submit a guest post.

Comments are closed.