Picking up one’s marbles and going home

One of the greatest gifts anyone can give is to donate his body to science after death. Such anatomic gifts contribute to the training of medical students, residents, and other medical professionals as well as being used for research that can contribute to the advancement of medical science. One of the things that makes an anatomic gift such a profound gift is that the donor usually has little control over what their body or body parts will be used for. There is, thus, more than a little trust in medical science involved in these gifts. When the deceased is a child, the donation of a child’s body or part of a child’s body to medical research is an even more amazingly generous gift. Such donations are precious gifts that are difficult enough to persuade people to give. It doesn’t take much to turn a “yes” answer into a “no.”

That’s why an article by Katie Wright at the anti-vaccine crank blog entitled Courchesne Brain Study Not Worth Sacrificing our Children Further really irritated me. Basically, Wright is saying that she used to think she would donate her child’s body to science if he were ever to die but, because she doesn’t like the result of a study that studied the brains of deceased autistic children and compared them to neurotypical controls, she’s now changed her mind:

If Christian’s deceased body could meaningfully contribute to innovative causation research, it would be very, very hard, but I would say yes and donate his body. If his brain were used to accelerate true progress I think it would be a great tribute to his spirit. I am sure most ASD parents feel the same way.

However the recent Courchesne Study made me change my mind about donating Christian’s brain to science. This study represents my nightmare, the worst-case scenario. Children’s brains have been used for politically driven poor quality science. I would rather Christian be buried with his brain intact than used for such abysmal research.


Why is the research so “abysmal”? Wright, who has no qualifications in science, proclaims it so because the results do not fit with her preconceived belief that vaccines cause autism and that her son Christian’s autism is due to “vaccine injury.” It is, in fact, a study that some of my readers sent to me when it first came out a couple of weeks ago. It just so happened to be around the time I was out of town giving a talk; so somehow it slipped through the cracks, as so many other worthy blogging topics often do because I just can’t blog about everything that is of interest to me. On the other hand, sometimes I’m given a chance to revisit one of these topics when someone like Katie Wright decides to go all full mental jacket on it.

This study was described in news articles that appeared around the time of its release, but, as always, I’ll go to the source, an article in JAMA entitled Neuron Number and Size in Prefrontal Cortex of Children With Autism. The study came out of UCSD and presents some provocative findings. It’s a preliminary study, given that it only examined the brains of 13 children, seven autistic boys and six control boys, but its results are fascinating and, best of all, hypothesis-generating. In brief, the authors obtained these brains from the National Institute of Child Health and Human Development (NICHD), University of Maryland Brain and Tissue Bank, the Autism Tissue Program at the Harvard Brain Tissue Resource Center, and the New York State Institute for Basic Research in Developmental Disabilities. As you might expect, young postmortem cases are scarce and difficult to come by for research, again, pointing to the importance of anatomical donations that Wright characterizes in this case as “sacrificing our children further” over.

Contrary to the way Wright portrays the study, which, if you believe her, was barely different from Young Frankenstein using the brain from Abby Normal, investigators were very careful to try to quantify the number of neurons in the prefrontal cortex (PFC) in both autistic and normal brains. The brains were analyzed by expert anatomists who were blinded to the group from which the brain came. The findings were simple:

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.

Leading the authors to conclude:

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

Again, this was a preliminary study with small numbers, which makes it even more surprising that a significant difference in neuronal counts was found. Considering normal variation among humans and the fact that, given the scarcity of postmortem tissue from children, it’s amazing that the investigators found anything at all. Could it be a spurious result? Sure. That’s why it needs to be confirmed with a bigger study; that is, if a bigger study can even be done. It’s also consistent with other lines of evidence implicating brain overgrowth in certain anatomic structures as being somehow related to the development of autism. What this tells us about the pathophysiology of autism remains to be seen, but it’s an intriguing observation that is likely to spur more research into the neurobiology of autism and autism spectrum disorders.

So what does Wright say about it? She doesn’t like it. Because it isn’t consistent with vaccines as a cause of autism (it being very difficult to imagine a mechanism by which vaccines could increase the number of neurons in such a manner, she’s very, very unhappy and assumes that it must be crap science:

What Couchesne’s study actually tells us is that 6 ASD children had more prefrontal cortex neurons than 7 typical children. There were no aged matched controls! 2 of the 7 “ASD” children did not even have an official ASD diagnosis! 5 of the 7 ASD kids were on anti-psychotic drugs. We have idea how these drugs affect developing brain tissue. 1 of the control children had been taking Concerta and klonopin. Another control had had an organ transplant and was on immunosuppressive drugs for lengthy periods of time. There are only 5 controls not, as far as we know, on various prescription drugs. The fact that this study was actually published only proves how low the bar is for ASD genetic and brain research. There are not enough hours this day to list all the incredible, innovative environmental research studies regularly rejected by autism research journals. A 7-person biomedical study would NEVER be published by JAMA, I promise you.

I’m not sure where Wright got the idea that two of the seven children didn’t have an ASD diagnosis. If I missed it somehow even though I read the whole paper and the online supplement, I’m sure someone will point out my mistake in the comments. The autistic cases were chosen primarily for having a diagnosis of autism, and in the text it reads:

No autism case had a diagnosis of Asperger syndrome or pervasive development disorder-not otherwise specified.

As for the rest of the obfuscation that Wright throws out about antipsychotic drugs is just that: Obfuscation. There is a table in the paper that lists all the cases and controls and describes a bit about their medical background; several of the autistic children were on psychotropic medications, which is not uncommon in children with autism. I rather suspect that when Wright wrote “We have idea how these drugs affect developing brain tissue” that she in fact meant “We have no idea how these drugs affect developing brain tissue.” Assuming that’s what she meant, she’s wrong, of course. We actually have a pretty good idea how many of these drugs affect developing brain tissue. At the very least, as the authors point out, none of these drugs are known to affect the number of neurons in the PFC. In essence, Wright’s complaints are all smoke and mirrors, whines designed to cast doubt on the study. In fact, the only points she makes that are semi-reasonable is that this was a small study (which the authors concede multiple times in the paper, pointing out that it is a preliminary study) and that maybe the criticism that including the child who had had cancer and a multiorgan transplant in the control group might not have been the best choice, given the chemotherapy treatment and immunosuppressive medications the child was on.

Not surprisingly, Wright doesn’t know what she’s talking about. It’s the perfect example of the Dunning-Kruger effect, the arrogance of ignorance, at work. It’s not as though the investigators in this study didn’t go to great lengths to try to control for the other confounding factors that she complains about, namely the lack of age-matched controls. Did she not pay attention to the part of the paper that points out how scarce postmortem brains from children that can be used for this sort of research are? Scientists make due with what they have. Wright is, in essence, intentionally making the perfect the enemy of the good and treating this study as though it were more than a preliminary study. She’s basically criticizing it because it is a preliminary study, even though, once again, the authors say right in the article that it’s a preliminary study.

Perhaps one of the most important implications of this study is mentioned in the discussion, and it’s obvious that this is the real reason Wright hates this study:

Also, prefrontal neuron counts in controls did not vary with age, which is concordant with literature that cortical neurons are generated prenatally, not postnatally.

Or, as this news report quotes Dr. Max Wiznitzer:

But since the excess neurons were found in a part of the brain that develops before a child is born, it points to a prenatal problem playing a role in autism.

“This is not consistent with that claims that heavy metals [from vaccines for example] cause the death of brain cells,” says Wiznitzer, because there are too many brain cells not less.

And that’s exactly why Wright is so upset. This study suggests that, whatever causes autism, it probably happens before birth, not after. If true, that rules out vaccines as a cause. Of course, we already have abundant scientific, clinical, and epidemiological evidence that fails to implicate vaccines as a cause of autism. It’s not as though scientists haven’t looked, either. Multiple large, well-designed studies have failed to find a correlation between vaccine and autism. As hypotheses go, the vaccine-autism hypothesis is as dead as dead can be, at least as dead as the famous parrot in a famous Monty Python sketch. Truly, it’s “pinin’ for the fjords.”

But, of course, to Wright, it’s all a huge conspiracy. Note how she writes that a study this small would never have been published in JAMA. Of course, the wag in me can’t help but note that this study is basically the same size as the infamous 1998 Lancet study published by Andrew Wakefield. One wonders whether Katie thinks that study should ever have been published in The Lancet, which is at least as high an impact a journal as JAMA. After all, the studies were basically the same size; so presumably she thinks that Wakefield’s study was no good either. But wait! I spoke too soon. Wright loves Andrew Wakefield because his “research” (such as it is) supports her pseudoscientific belief that vaccines cause autism. She even called the British General Medical Council investigation that led to Andrew Wakefield having his medical license stripped from him a “crime against humanity.” In other words, if a study with 12 or 13 subjects supports her belief that vaccines cause autism, she has no concern about the number of subjects, even when there is no control group.

I’ll take a moment to educate Wright why this study passed muster for JAMA and a study of “biomedical interventions” with only 13 subjects wouldn’t. It’s because it was incredibly difficult to obtain 13 suitable brains from children to study in this manner. Given the difficulties involved, this study was actually rather large. In the case of “biomedical” treatments, scientists would be looking at living children, meaning that there would be no barrier equivalent to what Courchesne et al faced in doing their study to recruiting a more statistically robust number of subjects.

Never mind that, though. According to Wright, this conspiracy is so pervasive that it prevents any scientist from doing anything other than gene-based research:

Families are frequenting told there isn’t enough research money available to address these issues. But guess what there is plenty of money for? Brain and gene research! These “Autism Centers for Excellence” centers blow almost $17 million a year on redundant brain and gene research. It is estimated that 50% of the ACE budgets go to overheard. There is no consumer oversight or public accountability for the money they spend. The NIH doles of autism research money behind closed dollars and without consumer input (they are under no obligation to follow the IACC recommendations), and guess what they love to fund the most? Brain and gene research.

Maybe, just maybe, the reason that the NIH funds brain and gene research is because that is the sort of research that is most likely to illuminate the biological mechanisms that lead to autism and thus point the way to treatments. The “biomedical” treatments that Wright is so enamored of are, by and large, pure quackery with no randomized clinical trial evidence to support their efficacy, much less even a modicum of biological plausibility.

Much like the notion that vaccines cause autism.

None of this stops commenters from dropping bombs of ignorance like:

The deceptive part of the report was the speculation that the increase in pre-frontal cortex neurons happened in utero. This could only be speculative and was probably intended to absolve post utero toxic exposures (e.g., mercury, which can cause abnormal cell growth in the CNS).

Uh, no. It’s not “speculation.” It’s a conclusion based on the known biology of brain development. The prefrontal cortex is already known to develop before birth. The authors even point out that the number of neurons in the prefrontal cortex was independent of age, consistent with completion of its development before birth. Seriously, these people need to learn a bit of neurobiology and actually think.

Even worse than the unrelenting ignorance on display in the article and in the comments, in the end Wright writes that “this Courchesne study has changed my mind” about donating her son’s brain to science. Because a single study doesn’t show what she wants it to show, she’s changed her mind. As if we’re supposed to be impressed. After all, fortunately the deaths of children are uncommon. Fortunately for both her and her son, it’s highly unlikely that wright will ever be called upon to donate her son’s brain to research, and that’s a good thing. No one wants to see a child die. Even though it’s an empty threat, though, Wright’s attitude is very much akin to that of a child who, if he doesn’t get her way, threatens to take all his marbles and go home. The study didn’t show what she wanted it to show; so Wright “changes her mind” about tissue donation. Even if the study to which she objects were crap, her reaction would be akin to tearing up your organ donation card because an alcoholic got a liver, after which he went back to drinking and destroyed the new liver or because Steve Jobs got a liver for a somewhat dicey indication to treat his cancer and his cancer recurred a year and a half later.

One can only hope that she doesn’t persuade other parents.

Comments

  1. #1 Professor Blackheart
    December 6, 2011

    pD

    “The fact of the matter is that the animal studies tell us that immune disturbances early in life have the capacity to persistently dysregulate immune function, the neuroimmune environment, and utlimately, behavior.”

    This is the complexity of the matter at hand and we have just a small window into this world provided by researchers like Peter Aaby. Where the sequencing of various vaccine and other health initiatives like micronutrients effect immune systems that are currently poorly understood.

  2. #2 lurker
    December 6, 2011

    @Justin
    Bravo, well said!
    @pD
    Thanks again!

  3. #3 T-reg
    December 6, 2011

    @pD:
    The articles that you cite do indeed hint that there is an abnormal immunological activity associated with autism.
    But why do you think that “association is not necessarily causation” is a weak argument here?

    None of the studies you cite firmly establishes that immunological phenomena cause autism.
    Sure, it IS one possibility that autism could be an auto-immune phenomenon.
    But the other possibility is that the signalling pathways which appear to be aberrant maybe normally responsible for both, neuro-development as well as immunological signalling. Thus an aberration in these pathways could be responsible for both, aberrant neuro-development as well as aberrant immunological activity. They could be two parallel phenomena, not necessarily cause and effect.

    Secondly, assuming that autism is an auto-immune disease why do you think that “vaccine related antigens are responsible” is the only possibility?
    It could be one possibility (let’s ignore the epidemiological evidence for the time being).
    The other possibilities are –
    1) Exposure of sequestered CNS antigens leading to an auto-immune response.
    2) Emergence of aberrant epitopes on proteins normally exposed to the CNS, leading to an auto-immune response.

    There’s also the question of why you believe the exposure to the antigens on the pathogenic strains of the disease cannot cause autism but the same antigens when exposed through vaccination cause autism?

    Also, your assertion that early activation of the immune system is responsible for aberrant neuro-develpoment: do you have any studies to prove that neonates recovering from neonatal sepsis or other neonatal infections have a greater risk of developing autism than those who have not experienced such antigenic challenge at such a young age?

    There are too many unknowns yet and epidemiological data doesn’t seem to support your assertions. Just because there exists a theoretical possibility (that too one that is very weak, going by current knowledge and epidemiological evidence) it isn’t enough to change established protocols.

  4. #4 Krebiozen
    December 6, 2011

    Justin,

    We are exposed to millions and millions of antigens upon entry into the world and every waking second thereafter. Of course it varies from person to person and his/her particular environment, but the large majority of these antigens are non-immunogenic (do not stimulate immune response), which is good because otherwise we would be dead within a short while from septic shock if all antigens we encountered stimulate the immune response.

    Just how many pathogens or other immunogenic proteins are we exposed to daily? How many pathogens is a baby exposed to during its first years? How many are transferred to them by their parents, and other people coughing and sneezing near them, touching them, and their mother sticking possibly contaminated nipples, teats or pacifiers in their mouths?

    I don’t know the answers to these questions, but I would make an educated guess that it is a lot. Potentially pathogenic viruses, such as rhinoviruses, Epstein Barr, HHV-6, Coxsackie B, cytomegalovirus, parvovirus B19 are very common. Potential pathogenic fungi such as candida and aspergillus are ubiquitous. Then there are very common but potentially pathogenic species of bacteria; streptococcus, staphyloccus, E. coli, pseudomonas to name but a few, and before vaccination the common childhood diseases, varicella, measles, rubella, pertussis were also ubiquitous.

    We know that people with immunodeficiency are vulnerable to all these diseases – even brewer’s yeast has been known to cause infection – so the immune systems of immunocompetent people must surely have at some time developed an adaptive response to these pathogens, presumably when they were first exposed, in childhood. Mustn’t they?

    If so, is there a qualitative or quantitative difference between the immune response to these pathogens, and that to vaccinations?

  5. #5 Chris
    December 6, 2011

    A couple of things Justin (and others for whom the answer always has to be “vaccines cause autism!):

    Before you can figure out how vaccines cause autism, you must determine if there is an epidemiological relationship. Well, there have been several of those studies done in several countries including Japan, Finland, Denmark, UK and USA… with others in Italy, etc. There does not seem to be a correlation.

    And then, you have to ask yourself: If vaccines are only a few antigens of either dead or attenuated pathogens (or just a protein from some other microbe), how can they cause more of a response than the fully alive and active pathogen? How exactly does a protein from a yeast cause more harm than a real active hepatitis b virus? It does not make any sense.

    It is seriously like trying to find out how sitting in an easy chair watching television causes drowning.

    But for you guys it will always be the vaccines. As discussed with new Orac essay on the anti-vaccine fantasy.

    For the rest of us in the real world:

    The science has been done, the link between vaccines and autism does not exist. It is a dead link… “It’s not pinin’! ‘It’s passed on! This link is no more! It has ceased to be! It’s expired and gone to meet its maker! It’s a stiff! Bereft of life, it rests in peace! If you hadn’t nailed it to the perch it’d be pushing up the daisies! Its metabolic processes are now ‘istory! It’s off the twig! It’s kicked the bucket, it’s shuffled off its mortal coil, run down the curtain and joined the bleedin’ choir invisible!! THIS IS AN EX-LINK!! ” (hat-tip to Monty Python and the dead parrot sketch)

  6. #6 passionlessDrone
    December 6, 2011

    Hi T-reg –

    The articles that you cite do indeed hint that there is an abnormal immunological activity associated with autism.

    We are in complete agreement.

    But why do you think that “association is not necessarily causation” is a weak argument here?

    Because it is a last ditch effort to misdirect attention after the ridiculous notion that there is no association between immune dysregulation and autism has been discarded. Because of the animal studies that tell us that immune dysfunction in early life can drive behavior differences into adulthood. Because we are learning that a host of neurological disorders, such as bipolar, schizophrenia, and depression also have immune components, and therapies involving immunomodulation are showing efficacy. Because of we don’t know what causes autism in almost any case. My position is OK with uncertainty; the opposite position, the one taken by Anteaus, that ‘there are no known links between the immune system and autism’ cannot withstand these findings. There seems to be an amazingly persistent ability to assign certainty towards the noisiest of science (thimerosal/MMR epidemiology) and great uncertainty towards fine grained knowledge. I don’t get it.

    Also, because I was a little bored, I only bothered to present data that showed evidence of an ongoing immune response in the CNS. If we look in the periphery, we’ve got a lot more data points to evaluate, and a bunch of them have a curious profile; namely that as indices of the immune response increase so too, does autism severity.

    For example. Macrophage migration inhibitory factor and autism spectrum disorders. found that as circulating levels of MIF increased, so too did the severity of the disease; i.e.,

    There were genetic associations between known functional polymorphisms in the promoter for MIF and autism spectrum disorder-related behaviors. Also, probands with autism spectrum disorder exhibited higher circulating MIF levels than did their unaffected siblings, and plasma MIF concentrations correlated with the severity of multiple autism spectrum disorder symptoms.

    Now, sure, this could a coincidence, bogus data, or as you say, associated data points. (If asked, I could provide four or five other papers that associated increased innate immune response biomarkers with autism severity.) But, we also have data that indicates that as the ability to attenuate the immune response decreases, autism severity increases.

    Decreased transforming growth factor beta1 in autism: a potential link between immune dysregulation and impairment in clinical behavioral outcomes

    Children with ASD had significantly lower plasma TGF beta 1 levels compared with typically developing controls (p=0.0017) and compared with children with developmental disabilities other than ASD (p=0.0037), after adjusting for age and gender. In addition, there were significant correlations between psychological measures and TGF beta 1 levels, such that lower TGF beta 1 levels were associated with lower adaptive behaviors and worse behavioral symptoms. The data suggest that immune responses in autism may be inappropriately regulated due to reductions in TGF beta 1

    This is a tricky one. We have data that tells us that modifications to either end of the immune resopnse, initiation or regulation, are associated with behavioral severity, but both associations point in the same direction; over overzealous, or under regulated immune response, is associated with worse behavior. If you want to argue for dual purpose, that’s fine, but we need to find a mechanism by which we can coincidentally correlate behaviors and both ends of the immune response. While such a thing is possible, the fact that coincidences happen every day doesn’t mean that everything is a coincidence.

    None of the studies you cite firmly establishes that immunological phenomena cause autism.

    OK. But again, the animal studies I present, do show behavioral changes as a result of immune disturbances. There aren’t very many studies that firmly establish anything as a cause of autism.

    But the other possibility is that the signalling pathways which appear to be aberrant maybe normally responsible for both, neuro-development as well as immunological signalling. Thus an aberration in these pathways could be responsible for both, aberrant neuro-development as well as aberrant immunological activity. They could be two parallel phenomena, not necessarily cause and effect.

    I don’t believe that an argument hinging on the pleiotropic nature of of cytokines is very damaging to my position; but it is very problematic for the idea that what happens in the immune system doesn’t affect the brain, and ultimately, behaviors. These very interactions, immune crosstalk with the brain are very new concepts in a relative sense. If there is an underlying genetic, epigenetic, or environmetnally mediated difference in these pathways before birth, that doesn’t mean we can interferre with these pathways further without affecting change.

    Secondly, assuming that autism is an auto-immune disease why do you think that “vaccine related antigens are responsible” is the only possibility?

    In the first case, I’m not hung up on ‘antigens’ in vaccines, that’s the purvey of some of the other respondents here. I’m curious, where in my postings, as opposed to someone else’s paraphrasing, have led you to believe this is my position? I am genuinely curious how you came to this conclusion.\

    Secondarily, I would suggest you re-read my response to you in #493, where I addressed this concern specifically:

    Sure. Please check out my response to Dangerous Bacon above, in post #383 , where I showed two studies that seemed to indicate increased risk of autism in infants with hospitilizations for infection during the first year, and reports of increased risk for infants with infections during the first month of life.

    I’m open to lots of things.

    It could be one possibility (let’s ignore the epidemiological evidence for the time being).

    What epidemiological evidence? As I’ve stated again and again, the epidemiological data is on:

    1) thimerosal
    2) the MMR

    Nothing else. Just saying there is more data than this doesn’t make it so.

    Exposure of sequestered CNS antigens leading to an auto-immune response.

    OK. But that doesn’t explain the repeated studies in animals that tell us the maleability of the immune response can manifest as behaviors.

    Emergence of aberrant epitopes on proteins normally exposed to the CNS, leading to an auto-immune response.

    I particularly like a lot of the studies on antibodies to fetal brain proteins from the MIND guys in California, where approximately 10% of mothers with autism show reactivity to very specific fetal brain proteins. Immunoglobulin transfer from human mothers positive for antibodies to pregnant rhesus monkeys resulted in extreme behavioral differences in the treatment group offspring. You might find that data of interest. My idea set is not tied to vaccines, or immunology, or away from genes, or anything other than an honest evaluation of what we know and what we don’t know.

    There’s also the question of why you believe the exposure to the antigens on the pathogenic strains of the disease cannot cause autism but the same antigens when exposed through vaccination cause autism?

    Please see my response to DB #383, and my response to you at #493 for why this is an inaccurate understanding of my position.

    Regarding sepsis, this study speaks somewhat towards your question, though the inclusion of preterm infants is very problematic, as this in off itself is a risk factor for autism and/or developmental delay.

    Adverse neurodevelopmental outcome in preterm infants: risk factor profiles for different gestational ages

    which found associations between sepsis and developmental delay. The preterm data point is problematic, as this in off itself is a risk factor for autism/developmental delay, but it is better than no data at all.

    Just because there exists a theoretical possibility (that too one that is very weak, going by current knowledge and epidemiological evidence) it isn’t enough to change established protocols.

    I do not believe that I have advocated changing any established protocols, just an honest discussion. See my response to DB on #506 for more on this.

    – pD

  7. #7 passionlessDrone
    December 6, 2011

    Hi Krezbiozen –

    If so, is there a qualitative or quantitative difference between the immune response to these pathogens, and that to vaccinations?

    Great question! One that actually leads me not to be bored. And, coincidentally, one that I’ve been asking someone, anyone to provide some evidence of. Dangerous Bacon keeps on insisting we have data to this point, but just can’t bring himself to post it, for some reason. My continued assertion is that we do not have any information to speak to this (i.e., innate immune response following vaccination in a pediatric cohort), and until we have measurements of the infant immune response to the vaccine schedule, we cannot begin to answer this question. You may be able to find some studies I’ve been unable to find, but please remember that as shown by Corbett above, the infant immune response is qualitatively different than that of the adult, so we should avoid using adults as proxies for this.

    That being said, we do have some good reasons to think that there may be qualitative differences between normal infection, and vaccination immune response. Unfortunately, as we have no measurements in the infant innate immune response post vacciation, what we have left is largely speculative.

    Here is a neat study that came out a few months ago that speaks tangentially towards this point:

    LPS elicits a much larger and broader inflammatory response than Escherichia coli infection within the hippocampus of neonatal rats (Neuroscience Letters Volume 497, Issue 2, 22 June 2011, Pages 110-115)

    An immune challenge during the neonatal period can significantly affect the development of the nervous and immune systems, such that long-term abnormalities in immune function and behavior persist into adulthood. Given that immune activation and individual cytokines have been linked to the etiology of many developmental neuropsychiatric disorders, a complete characterization of the neonatal immune response within the brain is warranted. In this study, rats were treated peripherally on postnatal day (P) 4 with either a live Escherichia coli (E. coli) infection or lipopolysaccharide (LPS), two common models of neonatal immune activation. Inflammatory gene expression was measured within the hippocampus 2 and 24h later. We determined that E. coli and LPS produce very distinct inflammatory profiles within the brain. Infection with E. coli produced a robust, yet relatively IL-1 pathway focused activation of the neonatal immune system within the brain, while LPS produced a very broad and robust immune response within the brain. This analysis also identified common inflammatory genes up-regulated by both E. coli and LPS treatment.

    So, what we can see here is that just giving an animal something to provoke an immune resopnse (i.e., LPS), generates a different profile of neuroinflammation than infecting them with e-coli. The authors speak towards what might be driving this in the discussion section.

    The differences in the immuneresponse produced by E. coli and LPS may also be due to differences in the concentration of LPS molecules available for recognition by peripheral immune cells and/or CNS microglia.If true,then the differences in gene expression between LPS and E. coli may involvea critical difference in mechanism downstream of antigen presentation.Moreover, E.coli infection may recruit multiple microglial pattern recognition receptors and pathogen-associated molecular patterns involved in phagocytosis and the inflammatory response beyond just LPS and TLR4 alone(e.g.TLR9,CR3,MHCII,andFc (Fcg) immunoglobulin receptors Fcgr1 adFcgr3a) [41]. These questions remain to be explored in further studies.

    Clearly, LPS and vaccination are different things, but at the heart, this experiment bears much resemblance to your question; the immune response from a pathogen versus an intentional provocation of the immune system without the pathogenic effects of an organism. In vaccines for bacterial pathogens, we are not including the entire organism, just pieces of it, the pieces we want our immune system to remember. But the immune system is highly conserved evolutionarially, we evolved responding to bacterial organisms, not just specific pieces parts of them. Regulation of the immune response is just as important as turning it on, but this requires a chemical cascade that is still largely mysterious to us. Here the authors speculate that actual infection ‘may recruit multiple pattern recognition receptors and pathogen-associated molecular patterns involved in phagocytosis and the inflammatory response beyond LPS and TLR4 alone’. So, while the exact mechanisms as to why there appears to be a qualitative difference in the immune response following LPS or e-coli infection, it does seem clear there is a difference. I’d also like to point out, that in this case, the animals were infected / challenged peripherally, with subcutaneous injections, and subsequent inflammatory responses were observed in the hippocampus. The fact that external immune activation results in CNS immune activation is a relatively new realization.

    Secondarily speaking towards your question, you have to remember that vaccines also come with adjuvants to insure the immune resopnse is sufficiently robust to insure protection. The only approved adjuvant in the US is an aluminum salt, alum, and without this alum, vaccines have a decreased success rate (when success is defined as subsequent antibody generation). If we want to believe that there are no qualitative differences between vaccination and infection, we’d need to think that somehow, our bodies immune system has evolved to generate an immunological response to aluminum in the same way that it evolved to respond to e-coli, or pertussis, or any other pathogen. Does that sound like a plausible scenario to you? Of course, if we had any data, it would help us in this discussion. I can’t prove that the observations don’t exist, but anyone with the desire, and data, could prove that the studies do exist.

    We know that people with immunodeficiency are vulnerable to all these diseases – even brewer’s yeast has been known to cause infection – so the immune systems of immunocompetent people must surely have at some time developed an adaptive response to these pathogens, presumably when they were first exposed, in childhood.

    We should try not to confuse childhood, with infancy. They are very different timeframes, and the animal studies tell us that time dependent effects are an important metric to incorporate.

    – pD

  8. #8 Professor Blackheart
    December 7, 2011

    Trends Immunol. 2009 Mar;30(3):109-16. Epub 2009 Feb 21.

    Linking allergy to autoimmune disease.
    Valenta R, Mittermann I, Werfel T, Garn H, Renz H.
    Source

    Division of Immunopathology, Department of Pathophysiology, Center for Physiology and Pathophysiology, Medical University of Vienna, A-1090 Vienna, Austria. rudolf.valenta@meduniwien.ac.at
    Abstract

    Type I allergy is a classical Th2-driven hypersensitivity disease based on IgE recognition of environmental allergens. Exposure of allergic individuals to exogenous allergens leads to immediate type inflammation caused by degranulation of mast cells via IgE-allergen immune complexes and the release of inflammatory mediators, proteases and pro-inflammatory cytokines.

    However, allergic inflammation can occur and persist in the absence of exposure to exogenous allergens and might paradoxically resemble a Th1-mediated chronic inflammatory reaction.

    We summarize evidence supporting the view that autoimmune mechanisms might contribute to these processes.

    IgE recognition of autoantigens might augment allergic inflammation in the absence of exogenous allergen exposure. Moreover, autoantigens that activate Th1-immune responses could contribute to chronic inflammation in allergy, thus linking allergy to autoimmunity.

  9. #9 Krebiozen
    December 7, 2011

    pD,
    In the absence of any solid evidence that there is a qualitative or quantitative difference between the immune system’s response to pathogens and vaccines in humans, this is really just speculation, isn’t it? The possibility that our immune systems react differently to single antigens than to a whole organism is intriguing, but that’s about it, as far I’m concerned anyway. Evidence of elevated cytokines in autistic brains suggest an ongoing inflammatory process, perhaps an autoimmune response, lasting for years or decades, and I find it hard to see how vaccination could cause this. I enjoy a bit of speculation beyond the data as much as the next person, but it’s important not to lose sight of what it is.

    You point out that there is data linking immune dysfunction with autism, but there is no evidence, as far as I am aware, that vaccination causes immune dysfunction. The close links between the immune system and the nervous system (which I first became aware of from the other end – psychoneuroimmunology) suggest that the behavioral and immune phenomena associated with autism are likely to have a common cause. Of course it is possible that immune dysfunction plus vaccination can sometimes lead to autism, but that brings us back to a difference in response to pathogens and vaccines. What does vaccination do today that a series of infections with childhood diseases didn’t do a few decades ago, assuming that the underlying immune dysfunction existed then?

    If we want to believe that there are no qualitative differences between vaccination and infection, we’d need to think that somehow, our bodies immune system has evolved to generate an immunological response to aluminum in the same way that it evolved to respond to e-coli, or pertussis, or any other pathogen. Does that sound like a plausible scenario to you?

    Yes, well, sort of. Soil is very rich in aluminum salts, so any wound that is contaminated with soil will have its own aluminum adjuvant added to it. An exaggerated immune response to soil, which contains many potential pathogens, might well bring a survival advantage. Speculation I know, but it is plausible.

  10. #10 Professor Blackheart
    December 8, 2011

    Proinflammatory and regulatory cytokine production associated with innate and adaptive immune responses in children with autism spectrum disorders and developmental regression

    We determined innate and adaptive immune responses in children with developmental regression and autism spectrum disorders (ASD, N=71), developmentally normal siblings (N=23), and controls (N=17).

    With lipopolysaccharide (LPS), a stimulant for innate immunity, peripheral blood mononuclear cells (PBMCs) from 59/71 (83.1%)

    ASD patients produced >2 SD above the control mean (CM) values of TNF-α, IL-1β, and/or IL-6 produced by control PBMCs. ASD PBMCs produced higher levels of proinflammatory/counter-regulatory cytokines without stimuli than controls. With stimulants of phytohemagglutinin (PHA), tetanus, IL-12p70, and IL-18, PBMCs from 47.9% to 60% of ASD patients produced >2 SD above the CM values of TNF-α depending on stimulants.

    Our results indicate excessive innate immune responses in a number of ASD children that may be most evident in TNF-α production.

  11. #11 blackheart
    December 8, 2011

    Selected Quotes

    “epidemiological data doesn’t seem to support your assertions”

    Epidemiological data doesn’t support any aetiology of vaccine.

    “In the absence of any solid evidence that there is a qualitative or quantitative difference between the immune system’s response to pathogens and vaccines in humans, this is really just speculation, isn’t it?”

    Randomized trials show that measles vaccine has strong nonspecific effects. So does DTaP.

    Evidence of elevated cytokines in autistic brains suggest an ongoing inflammatory process, perhaps an autoimmune response, lasting for years or decades, and I find it hard to see how vaccination could cause this.

    Epigenetics

    You point out that there is data linking immune dysfunction with autism, but there is no evidence, as far as I am aware, that vaccination causes immune dysfunction.

    “worrying evidence that whole-cell diphtheria-tetanus-pertussis vaccine (DTP) may increase mortality from infections other than diphtheria, tetanus, or pertussis in high-mortality areas”

    If vaccines are only a few antigens of either dead or attenuated pathogens (or just a protein from some other microbe), how can they cause more of a response than the fully alive and active pathogen?

    “When DTP was first introduced into Guinea-Bissau, despite the absence of herd immunity, mortality was 5.1 deaths per 100 person-years among children who did not receive DTP but 11.3 deaths per 100 person-years among children who did receive DTP”

  12. #12 Beamup
    December 8, 2011

    Epidemiological data doesn’t support any aetiology of vaccine.

    Not relevant to the point for which you are offering it as a response.

    Randomized trials show that measles vaccine has strong nonspecific effects. So does DTaP.

    If you read carefully (or at all) you might notice that the key word was DIFFERENCE. That there is a response to vaccination, certainly. They wouldn’t work otherwise. That does not establish that there is a DIFFERENT response than that to the actual pathogens, much less that said difference is harmful.

    Epigenetics

    Throwing out a buzzword does not a mechanism make.

    As to the other two, [citation needed].

  13. #13 Professor Blackheart
    December 8, 2011

    Beamup

    Not relevant to the point for which you are offering it as a response.

    Not relevant to you but it shows that the use of epidemiology in explaining complex disease processes is of little value particularly as you are having difficulty in defining the disease.

    If you read carefully (or at all) you might notice that the key word was DIFFERENCE.

    No DIFFERENCE between a child that dies and one that doesn’t ? That’s a peculiar definition of “difference” you have.

    Throwing out a buzzword does not a mechanism make.

    Buzzword it is a major field of medical research that is unlocking many disease processes including autism.

  14. #14 Krebiozen
    December 8, 2011

    Blackheart,

    Randomized trials show that measles vaccine has strong nonspecific effects. So does DTaP.

    So does measles – it causes immunosuppression in the short term but in the long term also seems to reduce mortality from other causes in those who survive it, in developing countries that is.

    Epigenetics

    Like Beamup, I find it hard to deduce what you are suggesting. That vaccines somehow cause a permanent change in gene expression that natural infections do not? Any evidence for that at all?

    “worrying evidence that whole-cell diphtheria-tetanus-pertussis vaccine (DTP) may increase mortality from infections other than diphtheria, tetanus, or pertussis in high-mortality areas”

    Have you seen Peter Aaby’s latest paper on this? “An early two dose measles vaccination strategy was associated with a non-significant 22% reduction in all cause mortality between 4.5 and 36 months of age in children who had received all doses of DTP vaccine before enrolment.” There may (or may not) be something interesting going on here, but I seriously doubt it has any connection to autism, to epigenetics or to permanent immune dysfunction.

  15. #15 blackheart
    December 9, 2011

    Krebiozen

    So does measles – it causes immunosuppression in the short term but in the long term also seems to reduce mortality from other causes in those who survive it, in developing countries that is.

    You have a point to make ?

    Like Beamup, I find it hard to deduce what you are suggesting.

    That’s no surprise at all.

    “NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcriptionDNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. of

    NF-κB plays a key role in regulating the immune response to infection (kappa light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.

    Known inducers of NF-κB activity are highly variable and include reactive oxygen species (ROS), tumor necrosis factor alpha (TNFα), interleukin 1-beta (IL-1β), bacterial lipopolysaccharides (LPS), isoproterenol, cocaine, and ionizing radiation.[18]

    NF-κB is a major transcription factor that regulates genes responsible for both the innate and adaptive immune response.

    NF-κB has been demonstrated to have diverse functions in the nervous system including roles in plasticity, learning, and memory.

    Because NF-κB controls many genes involved in inflammation, it is not surprising that NF-κB is found to be chronically active in many inflammatory diseases, such as inflammatory bowel disease, arthritis, sepsis, gastritis, asthma, among others. It is important to note that the key regulators of NF-κB are associated with elevated mortality, especially from cardiovascular diseases.[51][52] Elevated NF-κB has also been associated with schizophrenia”

    Have you seen Peter Aaby’s latest paper on this?

    2010 paper …Yes.

    There may (or may not) be something interesting going on here

    There’s a lot of interesting ‘stuff’ going on here … this is a complete overturn of ‘vaccine speficity’ theory.

    The unlocking of these types of questions could save millions of more lives through safe and efficacious administration of targetted vaccines.

    Already 500,000 premature female child deaths have been averted. Licky for us there are advicates like myself and researchers like Aaby that have an unprejudiced look at vaccines.

    but I seriously doubt it has any connection to autism, to epigenetics or to permanent immune dysfunction

    I suppose it would depend on if you also looked at the current immunological research surrounding autism and couple that with understandings of known gene expresssions (Epigenetics) in autism and how they are work through the signalling pathways such as NFkB.

    Aberrant NF-KappaB Expression in Autism Spectrum Condition: A Mechanism for Neuroinflammation 2011

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3098713/

    NF-κB is aberrantly expressed in the orbitofrontal cortex as indicated by measurements on post-mortem tissue from ASC patients, and particularly in highly activated microglia. This region is a locus of abnormal function in ASC that underlies the abnormal development of social and cognitive skills (Sabbagh, 2004).

    This is the first discovery of its kind that identifies a potential mechanism for neuroinflammation in ASC through increased expression of this pro-inflammatory molecule and the significant involvement of resident immune cells. The connection of this result to changes in intracellular acidity indicates an investigation of pH across the entire brain parenchyma in living patients.

    NF-kB: a crucial transcription factor for glial and neuronal cell function

    http://www.cell.com/trends/neurosciences/…/S0166-2236(96)01035-1

    NF-kB is one of the best-characterized transcription factors. It is expressed ubiquitously and regulates the expression of many genes, most of which encode proteins that play an important and often determining role in the processes of immunity and inflammation. Apart from its role in these events, evidence has begun to accumulate that NF-kB is involved in brain function, particularly following injury and in neurodegenerative conditions such as Alzheimer’s disease. NF-kB might also be important for viral replication in the CNS. An involvement of NF-kB in neuronal development is suggested from studies that demonstrate its activation in neurones in certain regions of the brain during neurogenesis. Brain-specific activators of NF-kB include glutamate (via both AMPA/KA and NMDA receptors) and neurotrophins, pointing to an involvement in synaptic plasticity. NF-kB can therefore be considered as one of the most important transcription factors characterized in brain to date and it might be as crucial for neuronal and glial cell function as it is for immune cells.

    Expression Profiling of Autism Candidate Genes during Human Brain Development Implicates
    Central Immune Signaling Pathways

    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0024691

    By implementing a biologically relevant approach, we identified a subset of highly expressed ASD-candidate genes from which interactome networks were derived. Strikingly, immune signaling through NFκB, Tnf, and Jnk was central to ASD networks at multiple levels of our analysis, and cell-type specific expression suggested glia—in addition to neurons—deserve consideration.

    This work provides integrated genomic evidence that ASD-implicated genes may converge on central cytokine signaling pathways.

    Shown at Table 3 Gene ontology enrichment of the 32 highly expressed Autism genes revealed four new GO categories representing two significant processes—immune system regulation and apoptosis

    GO: 0002682 Regulation of Immune System Process

    GO: 0006915 Apoptosis (cell death)

    GO: 0012501 Programmed cell death

    GO: 0031347 Regulation of defense response – (Any process that modulates the frequency, rate or extent of a defense response.)

    Interestingly, there is also mounting evidence at the cellular and tissue levels that more in depth investigation of an immune component is warranted in ASD [46]. For instance, multiple studies have demonstrated altered cytokine profiles in ASD patients [47], [48], and altered TGF-B concentration in serum and CSF correlates with disease severity [49].

    This considerable attention to the immune response in previous ASD research has resulted in two prevailing theories:

    1. one suggests exogenous factor(s) stimulate neuro-inflammation during development,

    2. while the other postulates autoimmune activation causes ASD pathology

    —————————–

    NF-kB can be activated by exposure of cells to LPS (Lipopolysaccharides) or inflammatory cytokines such as TNF (Tumour Necrosis Factor) or IL-1 (Interleukin-1), growth factors, lymphokines, oxidant-free radicals, inhaled particles, viral infection or expression of certain viral or bacterial gene products, UV irradiation, B or T-Cell activation, and by other physiological and non physiological stimuli.

    “The recognition of bacterial and viral products by Toll-like receptors on cells of the innate immune system also results in NF-kB induction, leading to the production of proinflammatory cytokines”

    ———————-

    Cytokines – Pieces of the Autism Puzzle

    http://www.rndsystems.com/cb_detail_objectname_SP02_Cytokines.aspx

    A subacute, chronic tetanus infection in the intestinal tract can promote the symptoms of autism as well.9 Tetanus toxins may be transported to the brain through the vagus nerve disrupting the release of neurotransmitters. In addition, maternal/fetal immune interactions may result in autism. Some mothers of autistic children express antibodies that are reactive to both lymphocytes from their autistic children as well as lymphocytes from their husbands.10

    In light of the many potential causes, immune system abnormalities and cytokines are repeatedly implicated in ASD (see reference 12 for a review). Detection of elevated IL-2 serum levels in autistic subjects suggests that activation of a T cell subpopulation may be important in autism.

    Measles Virus Activates NF-κB and STAT Transcription Factors and Production of IFN-α/β and IL-6 in the Human Lung Epithelial Cell Line A549

    http://www.sciencedirect.com/science/article/pii/S0042682201911742

    NF-κB activation was rapid and it was not inhibited by the protein synthesis inhibitor cycloheximide, suggesting that MV directly activates NF-κB.

    In conclusion, the results suggest that MV infection activates transcription factors involved in the initiation of innate immune responses in epithelial cells by two different mechanisms: directly by leading to NF-κB activation and indirectly via IFN-α/β leading to STAT activation.

    Associations between SNPs in toll-like receptors and related intracellular signaling molecules and immune responses to measles vaccine: Preliminary results

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292110/ ( Mayo Clinic / Dr Poland)

    Tanabe et al [9] reported that laboratory adapted and vaccine strains of measles virus, including Edmonston, up-regulate the expression of TLR3 in human dendritic cells via enhanced IFN-β secretion. The 500bp region upstream of exon 1 is characterized as a measles virus-responsive segment in the TLR3 gene. This region contains the NF-κB and STAT (family of eukaryotic transcription factors that mediate the response to a large number of cytokines and growth factors) binding sites.

    J Virol. 2011 Apr;85(7):3162-71. Epub 2011 Jan 26.
    The measles virus V protein binds to p65 (RelA) to suppress NF-kappaB activity.

    Measles virus-induced modulation of host-cell gene expression
    http://jgv.sgmjournals.org/content/83/5/1157.short

    In the present study, a total of 17 genes was found to be upregulated by MV infection.

    The Edmonston strain grew better in the PBMC cultures than the wild-type MV, and the Edmonston strain was a stronger inducer of the upregulated host cell genes than the wild-type virus.

    The anti-apoptotic B cell lymphoma 3 (Bcl-3) protein and the transcription factor NF-κB p52 subunit were upregulated in infected PBMCs both at the mRNA and at the protein level.

    PLoS One. 2008;3(11):e3825. Epub 2008 Nov 27.
    Modulation of the NF-kappaB pathway by Bordetella pertussis filamentous hemagglutinin.

    These results reveal a complex temporal dynamic, and suggest that despite short term effects to the contrary, longer exposures of host cells to this secreted adhesin may block NF-kappaB activation, and perhaps lead to a compromised immune response to this bacterial pathogen.

    Infect Immun. 2001 Apr;69(4):2650-8.
    Proinflammatory and proapoptotic activities associated with Bordetella pertussis filamentous hemagglutinin.

    Virology. 1999 Jun 20;259(1):74-84.
    Involvement of a p53-dependent pathway in rubella virus-induced apoptosis.

    The expanding realm of heterologous immunity: friend or foe?

    http://onlinelibrary.wiley.com/doi/10.1111/j.1462-5822.2005.00653.x/full

    Polarization of immune responses by vaccination may influence the outcome of future infections. Epidemiologic studies have shown that immunization with live attenuated vaccines that elicit predominantly type 1 immune responses, such as M. bovismeasles vaccine had a non-specific beneficial effect on childhood survival. In contrast, diphtheria-pertussis-toxoid (DPT) vaccine, which primarily elicits type 2 immune responses, had the opposite effect

    Heterologous immunity between viruses.
    http://www.ncbi.nlm.nih.gov/pubmed/20536568

    Immune memory responses to previously encountered pathogens can sometimes alter the immune response to and the course of infection of an unrelated pathogen by a process known as heterologous immunity. This response can lead to enhanced or diminished protective immunity and altered immunopathology.

    Here, we discuss the nature of T-cell cross-reactivity and describe matrices of epitopes from different viruses eliciting cross-reactive CD8(+) T-cell responses. We examine the parameters of heterologous immunity mediated by these cross-reactive T cells during viral infections in mice and humans. We show that heterologous immunity can disrupt T-cell memory pools, alter the complexity of the T-cell repertoire, change patterns of T-cell immunodominance, lead to the selection of viral epitope-escape variants, alter the pathogenesis of viral infections, and, by virtue of the private specificity of T-cell repertoires within individuals, contribute to dramatic variations in viral disease.

    We propose that heterologous immunity is an important factor in resistance to and variations of human viral infections and that issues of heterologous immunity should be considered in the design of vaccines.

    Physiology over epidemiology. I think there are a number of very good reasons to continue the investigation of vaccines / immune system dysfunction and neurodevelopmental and other neurological conditions

    Autism May Be Caused By An Immune System Response To A Virus
    http://www.sciencedaily.com/releases/1998/10/981031181106.htm

    Brain’s Immune System Triggered In Autism
    http://www.sciencedaily.com/releases/2004/11/041117004123.htm

    The immune response in autism: a new frontier for autism research
    http://www.jleukbio.org/content/80/1/1.full

    Autism: It’s Not Just in the Head
    discovermagazine.com/2007/apr/autism-it2019s-not-just-in-the-head

    Immune Response Offers Possible Insight to Schizophrenia, Autismhttp://psychcentral.com/news/2010/10/20/immune-response-offers-possible-insight-to-schizophrenia-autism/19690.html

  16. #16 blackheart
    December 9, 2011

    Transcriptomic analysis of autistic brain reveals convergent molecular pathology

    http://www.nature.com/nature/journal/v474/n7351/full/nature10110.html

    Our system-level analysis of the ASD brain transcriptome demonstrates the existence of convergent molecular abnormalities in ASD for the first time, providing a molecular neuropathological basis for the disease, whose genetic, epigenetic, or environmental aetiologies can now be directly explored. The genome-wide analysis performed here significantly extends previous findings implicating synaptic dysfunction, as well as microglial and immune dysregulation in ASD by providing an unbiased systematic assessment of transcriptional alterations and their genetic basis.

    We show that the transcriptome changes observed in ASD brain converge with GWAS data in supporting the genetic basis of synaptic and neuronal signalling dysfunction in ASD, whereas immune changes have a less pronounced genetic component and thus are most likely either secondary phenomena or caused by environmental factors.

    There’s still that 88% regression in ASD children to be factored in ?

  17. #17 Professor Blackheart
    December 9, 2011

    Seems there is some ‘censorship’ past comments are not getting through moderation ?

    Technical glitches ?

  18. #18 Professor Blackheart
    December 10, 2011

    Apologies to Orac … posts are up.

    Krebiozen …over to you.

  19. #19 Agashem
    December 11, 2011

    “These data suggest that typical regional differences, many of which are observed during fetal development10, are attenuated in frontal and temporal lobe in autism brain, pointing to abnormal developmental patterning as a potential pathophysiological driver in ASD. This is especially interesting in light of a recent anatomical study of five cases with adult autism which demonstrated a reduction in typical ultrastructural differences between three frontal cortical regions in autism11. Together, these independent studies provide both molecular and structural evidence suggesting a relative diminution of cortical regional identity in autism.”
    From the study you quoted, Blackscum, note the line which states “observed during fetal development”. Now I am not qualified to look at the entirety of this article and criticize it, but that part seems to be at odds with what you have said. I also don’t see in the abstract any mention of the environment. Perhaps you could point it out.

  20. #20 Denice Walter
    December 11, 2011

    @ Blackheart:

    Best to cut to the chase: anti-vaccination advocates often use research about the “environment” to implicate vaccines whereas much of the research cited is about a *much earlier* environment, the pre-natal one, where neuro-development begins.

    For comparison: in schizophrenia, a genetic cause is discussed ( see Schizophrenia.com; causes) as well as environmental ones that include: place and time of birth ( urban and winter are higher risk), infection ( e.g. rubella), pre-natal variables ( what the *mother* experienced prior to giving birth- e.g. bereavement, famine), obstetrical difficulties( time of birth). The relative risks of these variables are illustrated pictorially relative to “family history”.

    Autism may follow a roughly similar path. There is already data about pre-natal PFC differences/ other physiological measures present at birth ( facial proportions, head size) and very early indicators ( e.g. gaze patterns) in young infants. I expect that there will be more.

  21. #21 Chris
    December 11, 2011

    Is blacky still here?

  22. #22 Miltant Agnostic
    December 11, 2011

    Agashem @622 & Denice Walter @623

    Processor Blackscum takes the correlation = causation fallacy a step further into the land of the loons by claiming that if B precedes A then A causes B. Presumable faster than light neutrinos are involved in this along with a heaping helping of “quantum”.

  23. #23 Denice Walter
    December 11, 2011

    @ Militant Agnostic:

    Right. Those neutrinos are a b-tch! Always were.
    Be that as it may. Perhaps he has been meandering around the land of “oceanic feelings”** where one is “at one” with all- I am of course speaking of that font of dreams, visions, and myths: the unconscious mind**. In primary process** thought opposites co-exist,objects transform into each other, words can mean their converse, day is night and black is white, timelessness reigns; time’s arrow may point backwards and forwards. At once. Scary place, I don’t want to go there.

    ** read my Freud and Jung.

  24. #24 Chris
    December 11, 2011

    Denice, that is pretty much a description of Htrae (yes, I admit to reading Superman comics as a kid).

  25. #25 Johnny
    December 11, 2011

    Processor Blackscum takes the correlation = causation fallacy a step further into the land of the loons by claiming that if B precedes A then A causes B. Presumable faster than light neutrinos are involved in this along with a heaping helping of “quantum”.

    People assume that time is a strict progression of cause to effect, but *actually* from a non-linear, non-subjective viewpoint – it’s more like a big ball of wibbly wobbly… time-y wimey… stuff.

  26. #26 Militant Agnostic
    December 11, 2011

    Deinice – would that land of “oceanic feelings” be multilayered?

  27. #27 Denice Walter
    December 11, 2011

    @ Chris:

    We catch a glimpse of what Freud was talking about if we look at *lapses* in rational thought: errors, jokes, symptoms of SMI, thought while intoxicated, dreams, fantasy, art, and literature. Oh, and there are great examples- I am so not a Freudian or Jungian- and don’t believe in the unconscious as portrayed- but both F & J had important things to say if you want to understand people. Blackie hinted at his inclination by talking about Mr Joyce.( OMFG, he actually compared me to JJ**! My Irish friends/ cousins will be so jealous).

    ** Yeah right. But I do take it as a compliment, others may not.

  28. #28 lurker2
    December 11, 2011

    There is some serious denial going on here.
    Happy to read Blackheart’s links- neuroscience had progressed in research and
    more questions have been raised in the past decade about vaccines effects
    on the brain. Research along these lines should be continued.

  29. #29 Edith Prickly
    December 11, 2011

    People assume that time is a strict progression of cause to effect, but *actually* from a non-linear, non-subjective viewpoint – it’s more like a big ball of wibbly wobbly… time-y wimey… stuff.

    Fantastic!! One of my favourite Tenth Doctor quotes from one of the best episodes. 🙂

  30. #30 Chris
    December 11, 2011

    There is some serious denial going on here.

    Exactly. The Wakefield fanboys like Blackie cannot seem to get past the fact that he committed fraud. Plus, even without the fraud there was no real evidence in his “research” that any form of the MMR vaccine used in the UK between 1988 and 1997 have any connection to autism or gastrointestinal disorders.

  31. #31 lurker2
    December 11, 2011

    @Chris,
    I don’t think that’s relevant- I don’t see him harping on Poul Thorsen’s research.

  32. #32 Chris
    December 11, 2011

    Oh, so you missed all the links he did trying to justify the now retracted Lancet paper? Oh, and what Thorsen research? I see no paper with him as either a first or second author.

  33. #33 Chris
    December 11, 2011

    You might want to read the article above, it is about research done by Courchesne, and it actually has to do with neuroscience.

  34. #34 LW
    December 11, 2011

    #625:

    Processor Blackscum takes the correlation = causation fallacy a step further into the land of the loons by claiming that if B precedes A then A causes B. Presumable faster than light neutrinos are involved in this along with a heaping helping of “quantum”.

    We’ve already learned from dear Professor Blackheart that certain ASD phenotypes feature reversal of cause/effect temporal sequence: 

    15. “If MMR is causally related to either GI disturbances or AUT it should precede their onset.”

    This is not a logical statement, particularly in regards to what we now know about ASD phenotypes.

  35. #35 Denice Walter
    December 11, 2011

    @ Militant Agnostic:

    Multi-layered, nested, and twirled about like a Mobius ring.

    But seriously, this is what you get when you matriculate at the U of Goggle.( Normal higher ed courses provide a systematic over-view and ways of accessing the important questions and history of a subject, as well as surveying meaningful research that will generate additional questions). Instead, they chip away at tiny details while the panoramic view escapes them, remaining out of sight -and out of mind. Read any of the autism hypotheses displayed @ AoA and you’ll catch a glimpse of this fractured approach: non-experts guiding novices who teach the un-tutored. Fits right in with Woo-cademic studies.

  36. #36 The Very Reverend Battleaxe of Knowledge
    December 11, 2011

    The black-hearted “Professor” at 618:

    Already 500,000 premature female child deaths have been averted. Licky [sic] for us there are advicates [sic] like myself and researchers like Aaby that have an unprejudiced look at vaccines.

    I don’t know how many times it’s been explained to you, in words of one syllable, that this “500,000” figure is an estimate of increased mortality if a less effective vaccine had been used in place of a more effective one? It is NOT a comparison of vaccine vs. no vaccine!

    Since you continue FVCK!NG LYING about this over and over and over and over again, why should anyone pay any attention to the mishmash of irrelevant, undigested abstracts of articles you’ve never read and wouldn’t understand if you did? Help me out here—what do you hope to accomplish by these Gish Gallops of irrelevancy? Wakefield is a proven fraud. Douche-niak is an idiot and/or lunatic. Why are you wasting your time defending these punks with these wall-o-text braindumps? Take some Kaopectate and leave us alone.

  37. #37 Krebiozen
    December 11, 2011

    “Krebiozen …over to you.”
    Sorry, been busy. I still don’t see anything in the material you have regurgitated that suggests vaccination has a different and more damaging effect on neurodevelopment as compared to exposure to natural pathogens. Considering the quantities of antigens involved and the effects of vaccine preventable diseases as compared to vaccines, you would expect infection to have a far greater effect. All the evidence you have come up with is consistent with the theory that inflammation, elevated cytokines, immune dysfunction and developmental delay in autism, if they are connected, have a common, probably prenatal and largely genetic, cause.

    Oh, and pretty much anything stimulates NF-κB so that doesn’t support your ideas, unless any stress at all (including sunlight) causes autism which would, of course, include the infections that vaccines prevent.

    Do you have any bright ideas for effective vaccines that would not, in your view, cause autism?

  38. #38 Professor Blackheart
    December 12, 2011

    Krebiozen

    Sorry, been busy.

    That’s OK we all lead busy lives.

    I still don’t see anything in the material you have regurgitated that suggests vaccination has a different and more damaging effect on neurodevelopment as compared to exposure to natural pathogens.

    Vaccines are specifically designed in the lab to have an immunostimulatory effect greater than natural pathogens.

    Considering the quantities of antigens involved and the effects of vaccine preventable diseases as compared to vaccines, you would expect infection to have a far greater effect.

    I don’t see the reasoning behind this. Once again it is the design of the vaccine to produce an immunostimulatory response that needs to be considered.

    All the evidence you have come up with is consistent with the theory that inflammation, elevated cytokines, immune dysfunction and developmental delay in autism, if they are connected, have a common, probably prenatal and largely genetic, cause.

    Actually they are consistent with both genetics and environment and are not limited to a prenatal condition. Though one suspects that there are genetic susceptabilities that are indeed in play.

    This would then enable us to understand the differing pathology pathways and phenotypes that seem to be emerging in ASD aetiology.

    Oh, and pretty much anything stimulates NF-κB so that doesn’t support your ideas

    It is aberrant expression that is the key – for example.

    “NF-κB is aberrantly expressed in the orbitofrontal cortex…” which in turn “This region is a locus of abnormal function in ASC that underlies the abnormal development of social and cognitive skills”

  39. #39 Professor Blackheart
    December 12, 2011

    The Very Reverend Battleaxe of Knowledge

    It is your misconception that needs to be cleared up.

    “It is NOT a comparison of vaccine vs. no vaccine!”

    Correct

    I am comparing the implementation of one vaccine against another. Simple as that.

    Standard Titre was safe High Titre Measles Vaccines unsafe invoked an unknown mechanism in conjunction with DTaP.

    Are vaccines therefore safe … in some cases … No

    If I wanted to do a vaccine vs. no vaccine I’d show this …

    When DTP was first introduced into Guinea-Bissau, despite the absence of herd immunity, mortality was 5.1 deaths per 100 person-years among children who did not receive DTP but 11.3 deaths per 100 person-years among children who did receive DTP (risk ratio, 2.03; 95% CI, 1.17–3.52

    ———————————–

    But being a safe / efficacious vaccine advocate

    I’m not only interested in harm minimisation but also wider positive implications of this type of research.

    Calmette-Guérin vaccine (BCG) reduces mortality from infections other than tuberculosis and that measles vaccine reduces mortality from infections other than measles

    Particularly the effects of BCG in reducing mortality other than it’s targetted disease TB. (45% truly spectacular)

    I’m also interested that measles vaccine (MV)of the right type and in the right schedule reduces mortality from other infections. (By as much as 45%)

    Apparently saving several million lives per annum by unlocking the implications of this research is not yet on the skeptik radar

    I am as always your humble servant. (Though smarter obviously)

  40. #40 Professor Blackheart
    December 12, 2011

    Agashem

    “observed during fetal development”.

    Correct

    You did realise there are differing pathways involved in ASD aetiology and pathology ? No

    You did know that research shows a 55% / 45 % split in favour of environmental factors ? No

    You did know that there are differing phenotypes of ASD ? No

    I filled in the blanks …

  41. #41 Professor Blackheart
    December 12, 2011

    Johnny

    B precedes A then A causes B.

    Although a fuller explanation is given here … post #71
    …the simple version seems more appropriate here for obvious reasons…

    If you can’t define B then you can’t have a logical statement.

    It ain’t rocket science.

  42. #42 LW
    December 12, 2011

    15. “If MMR is causally related to either GI disturbances or AUT it should precede their onset.”

    This is not a logical statement, particularly in regards to what we now know about ASD phenotypes.

    B precedes A then A causes B.

    [babble]
    If you can’t define B then you can’t have a logical statement.

    Hmm, I would have thought the MMR was pretty well defined, really, but then I don’t pretend to be a professor.  

  43. #43 Guidance Counsellor Blackheart
    December 12, 2011

    LW

    There’s always time for a new career path, if it isn’t the hallowed halls of academia, may I suggest

    First Internet Clown School. Academy of Performing Arts in Clowning

    Citation

    http://www.clownschool.net/

    You are a natural.

  44. #44 Th1Th2
    December 12, 2011

    When DTP was first introduced into Guinea-Bissau, despite the absence of herd immunity, mortality was 5.1 deaths per 100 person-years among children who did not receive DTP but 11.3 deaths per 100 person-years among children who did receive DTP (risk ratio, 2.03; 95% CI, 1.17–3.52

    Interesting. So there must be some 95 reasons why getting unvaccinated is not after all like a “city being burned to the ground”. This, despite the absence of the so-called herd immunity in a third world country. I can only imagine Gray’s disappointment.

  45. #45 Gray Falcon
    December 12, 2011

    Th1Th2, Chris’ offer is #399 also extends to you. Now tell me, where are all the polio victims hiding?

  46. #46 Krebiozen
    December 12, 2011

    There is disagreement about whether the DTP really does lead to an increase in mortality, or if this is an artefact of the way data is collected. There is also disagreement about the significance of non-specific effects of vaccines.

    Much of the evidence for these so-called ‘non-specific effects’ has been accrued in Guinea Bissau, a country whose child health characteristics are far from typical.

    The same article concludes:

    The hypothesis that non-specific effects may be greater in females and are dependent upon prior infections or vaccines deserves further exploration, by independent groups of scientists, in different settings. Importantly, discussion of these effects should not blind us to the enormous gains in health which have been achieved through our immunisation programmes. Basic immunisation programmes must keep evolving with the times, in terms of the vaccines and services they provide and their precise schedules.

    I don’t think many people would disagree with that. I certainly would not.

  47. #47 Th1Th2
    December 12, 2011

    Th1Th2, Chris’ offer is #399 also extends to you.

    So if there is an evidence that demonstrates a particular vaccine did not save lives, then all Chris has to do is to simply move the goalpost. I see.

    Now tell me, where are all the polio victims hiding?

    AFP

  48. #48 Gray Falcon
    December 12, 2011

    For those who are wondering, Th1Th2 believes that polio is still around, going around as “AFP”, even though the term existed long before the vaccine was developed and is still defined as a symptom of polio. As far as I can tell, Th1Th2 doesn’t really understand how “honesty” works.

  49. #49 lilady
    December 12, 2011

    Please do not feed delusional, disease-promoting, uneducated, health care professional wannabe troll…it needs “terminal disinfection.”

    Heartless: I note with amusement your various incarnations as pretend barrister, sensei, professor, doctor and real Wakefield apologist. Why doesn’t Wakefield return to the U.K. and appeal the decision of the GMC and re-institute his lawsuit against Brian Deer? You really need a new schtick.

  50. #50 Th1Th2
    December 12, 2011

    Gray Falcon,

    For those who are wondering, Th1Th2 believes that polio is still around, going around as “AFP”, even though the term existed long before the vaccine was developed and is still defined as a symptom of polio. As far as I can tell, Th1Th2 doesn’t really understand how “honesty” works.

    There are 91,752 cases of AFP this year alone. More than quadruple the number of paralytic cases in 1952. Do you have a better explanation for there punk?

  51. #51 Chris
    December 12, 2011

    Please move to Guinea Bissau, and just live on the economy with only enough money to match the average income of the general population. Then tell us if it is comparable to the health standards of the USA and UK.

  52. #52 Gray Falcon
    December 12, 2011

    Th1Th2, do you have a source for your numbers? You have this tendency to omit any information that disagrees with you/

  53. #53 Th1Th2
    December 12, 2011

    Th1Th2, do you have a source for your numbers? You have this tendency to omit any information that disagrees with you/

    h_ttp://apps.who.int/immunization_monitoring/en/diseases/poliomyelitis/afpextract.cfm

    Updated on: 12-Dec-2011

  54. #54 lilady
    December 12, 2011

    “There are 91,752 cases of AFP this year alone. More than quadruple the number of paralytic cases in 1952. Do you have a better explanation for there (sic) punk?”

    According to the Global Polio Eradication Initiative… there are 560 confirmed cases of polio YTD (December 6, 2011).

    Please do not feed delusional, disease-promoting, uneducated, health care professional wannabe punk troll…it needs “terminal disinfection.”

  55. #55 Th1Th2
    December 12, 2011

    Chris,

    Please move to Guinea Bissau, and just live on the economy with only enough money to match the average income of the general population. Then tell us if it is comparable to the health standards of the USA and UK.

    You’ve committed a serious logical fallacy by moving the goalpost. Thank you, come again.

  56. #56 Th1Th2
    December 12, 2011

    According to the Global Polio Eradication Initiative… there are 560 confirmed cases of polio YTD (December 6, 2011).

    So according to ill-lady, 91,752 paralysis YTD are better than 560. Nice.

  57. #57 Gray Falcon
    December 12, 2011

    I read that document: Not every case of AFP turned out to be polio. Of course, for Th1Th2, if something applies to one item a set, it must apply to all of them. She still has yet to understand the flaws in her logic.

  58. #58 lilady
    December 12, 2011

    Thingy, you don’t get to define what constitutes a case of polio. Why don’t you write up your definition/differential diagnostic criteria and send it to the CDC and the WHO…I’m certain the scientists and researchers would be very interested in your “germ theory”.

  59. #59 LW
    December 12, 2011

    #646: “First Internet Clown School. Academy of Performing Arts in Clowning”

    Oh, is *that* where you learned it? You are a credit to your alma mater.

  60. #60 Th1Th2
    December 12, 2011

    I read that document: Not every case of AFP turned out to be polio.

    Then show me any incidence rates of AFP before 1955. Any AFP surveillance before 1996? Well? Good luck with that.

  61. #61 Th1Th2
    December 12, 2011

    Thingy, you don’t get to define what constitutes a case of polio.

    That’s why I have to stick with the original definition of paralytic poliomyelitis as defined by WHO prior to 1955 (no *AFP screening*, no lab studies, diagnosis is made by clinical assessment)

    * Geez, they didn’t even have a case definition of AFP to define.

  62. #62 lilady
    December 12, 2011

    “Then show me any incidence rates of AFP before 1955. Any AFP surveillance before 1996? Well? Good luck with that.”

    Then show me any incidence rates of ***Thingism before 1955. Any ***Thingism surveillance before 1996. Well? Good luck with that.

    ***Thingism Case Definition: Delusionary, Uneducated, promotes disease, health-care-professional wannabism, trollish behaviors.

    -FTFY

  63. #63 Th1Th2
    December 12, 2011

    Of course, for Th1Th2, if something applies to one item a set, it must apply to all of them. She still has yet to understand the flaws in her logic.

    Well the thing is AFP surveillance is virtually nonexistent in the pre-OPV unless you have the evidence on the contrary. You only learned about AFP since 1996 at least that’s according to WHO.

  64. #64 Gray Falcon
    December 12, 2011

    Note that Th1Th2 believes that if she pretends the column marked “confirmed polio cases” doesn’t exist, we won’t notice it there.

  65. #65 Th1Th2
    December 12, 2011

    Note that Th1Th2 believes that if she pretends the column marked “confirmed polio cases” doesn’t exist, we won’t notice it there.

    1. FYI, the original WHO definition of paralytic poliomyelitis before 1955 did not include confirmation by lab nor stool exam is a must.

    2. Poliomyelitis has been redefined several times. Had the current method of diagnosing polio (by exclusion) been applied before the advent of OPV, there would be AFP cases right? Where’s the statistics?

    3. So just how do you confirm a polio case? Tell me about it.

  66. #66 Gray Falcon
    December 12, 2011

    Also, Th1Th2 thinks she can just make an accusation and we have to prove her wrong.

  67. #67 lilady
    December 12, 2011

    “So just how do you confirm a polio case? Tell me about it. ”

    So just how do you confirm a ***Thingism case? Tell me about it.

    ***Thingism Case Definition: Delusionary, Uneducated, promotes disease, health-care-professional wannabism, trollish behaviors.

    -FTFY

  68. #68 Th1Th2
    December 12, 2011

    Also, Th1Th2 thinks she can just make an accusation and we have to prove her wrong.

    Now you’re being silly. Isn’t it you’re the one who claimed that AFP “existed long before the vaccine was developed and is still defined as a symptom of polio.”? Where’s your evidence? Show me the stats.

  69. #69 The Very Reverend Battleaxe of Knowledge
    December 12, 2011

    So in Thingyland symptom = disease? We already knew that any pollution of one’s Precious Bodily Fluids™ = infection.

    So, thingy: One of the symptoms of smallpox is fever. People still get fevers. I guess that means smallpox is still around, it’s just been “relabeled”, right?

  70. #70 The Very Reverend Battleaxe of Knowledge
    December 12, 2011

    So in Thingyland symptom = disease? We already knew that any pollution of one’s Precious Bodily Fluids™ = infection.

    So, thingy: One of the symptoms of smallpox is fever. People still get fevers. I guess that means smallpox is still around, it’s just been “relabeled”, right?

  71. #71 The Very Reverend Battleaxe of Knowledge
    December 12, 2011

    Sorry, foks—I waited a long time and then refreshed the page. My comment wasn’t there and the text was still in the box. That’s a first.

  72. #72 Th1Th2
    December 12, 2011

    So, thingy: One of the symptoms of smallpox is fever. People still get fevers. I guess that means smallpox is still around, it’s just been “relabeled”, right?

    Why it can’t be smallpox, you tell me.

  73. #73 Renate
    December 12, 2011

    Perhaps because the other symptoms of smallpox are missing?

  74. #74 lilady
    December 12, 2011

    “Why it can’t be smallpox, you tell me.”

    Why it can’t be ***Thingism, you tell me

    The absence of delusions, having a real education, promoting science-based medicine, actual employment as a real health care provider and rational thought processes is part of the differential diagnosis of Thingism.

    -FTFY

  75. #75 Th1Th2bot
    December 12, 2011

    Had the current method of diagnosing polio (by exclusion) been applied before the advent of OPV, there would be AFP cases right? Where’s the statistics?

    Shut up the concept body in the doctors. By live vaccine AFP in Gangta’s paradise do you even before an animal, that and with deliberate disinformation; consider yourself from the used when is essential to straw man unless of infection promoting.

  76. #76 lilady
    December 12, 2011

    @ Th1Th2bot: Thank you again for your superb Thinglish to English translation…remember to always “terminally disinfect” your computer screen.

  77. #77 Prometheus
    December 12, 2011

    Thing1Thing2 (#668):

    “2. Poliomyelitis has been redefined several times. Had the current method of diagnosing polio (by exclusion) been applied before the advent of OPV, there would be AFP cases right? Where’s the statistics?”

    I realise that there is no hope of convincing “Th1Th2” of anything, but this statement seemed to suggest a root of the confusion within his/her/its brain.

    AFP (acute flaccid paralysis) was and is a “surveillance marker” for polio outbreaks in much the same way that “influenza-like illness” is used as a surveillance marker for influenza.

    In a population without widespread immunity to polio, a sudden rise in cases of AFP are most likely to signal a polio outbreak, whereas the same AFP rise in a largely immune population (like the US) is more likely due to one of the other viruses that can cause AFP, such as other picornaviruses (e.g. enteroviruses, echoviruses) and adenoviruses.

    I hope that helps some people – I know it won’t help “Th1Th2”.

    Prometheus

  78. #78 W. Kevin Vicklund
    December 12, 2011

    There are 91,752 cases of AFP this year alone. More than quadruple the number of paralytic cases in 1952. Do you have a better explanation for there punk?

    Let’s see. In 2011, there will have been about 92,000 cases of AFP world-wide, not including the United States. In 1952, there were 21,000 cases of paralytic polio, not including the rest of the world. These two numbers can not be meaningfully compared.

  79. #79 Gray Falcon
    December 12, 2011

    @681. Thank you, now I have a perfect reason to ignore Th1Th2. Did she really think that was an honest comparison?

  80. #80 lilady
    December 12, 2011

    Regarding the differential diagnostic criteria for AFP…

    Acute Flaccid Paralysis

    Differential Diagnosis: A neuroanatomical approach

    1. Muscle (acute myopathies):

    – Inflammatory myopathy (polymyositis, dermatomyositis)

    – Rhabdomyolysis (extreme exertion, drugs, viral myositis, crush injury etc.)

    – Acute alcoholic necrotizing myopathy

    – Periodic paralyses (hypokalemic, hyperkalemic)

    – Metabolic derangements (hypophosphatemia, hypokalemia, hypermagnesemia)

    – Thyroid or steroid myopathy

    2. Neuromuscular Junction:

    – Myasthenia Gravis

    – Botulism

    – Tick paralysis

    – Other biotoxins (tetradotoxin, ciguatoxin)

    – Organophosphate toxicity (can also cause neuropathy)

    – Lambert-Eaton Myasthenic Syndrome (LEMS)

    3. Nerve (acute neuropathies):

    – Diphtheria

    – Porphyria

    – Drugs & Toxins (arsenic, thallium, lead, gold, chemotherapy – cisplatin / vincristine)

    – Vasculitis (incl. lupus, polyarteritis)

    – Paraneoplastic and Paraproteinemias

    – Multifocal motor neuropathy

    4. Nerve Roots (acute polyradiculopathies):

    – Guillain-Barre Syndrome

    – Lyme disease

    – Sarcoidosis

    – HIV

    – other viruses (CMV, VZV, West Nile)

    – Cauda equina syndrome (lumbar disc, tumour, etc.)

    – Plexus lesions (brachial plexitis, lumbosacral plexopathy)

    5. Anterior Horn Cell (motor neuron diseases):

    – Amyotrophic lateral sclerosis (ALS) – with UMN findings

    – Poliomyelitis

    – Kennedy’s disease (spinobulbar atrophy / androgen receptor gene)

    – other spinomuscular atrophies (inherited)

    – Anterior spinal artery syndrome (with grey matter infarction)

    6. Spinal Cord (corticospinal tract diseases):

    – Inflammatory (Transverse myelitis)

    – Subacute combined degeneration (B12 deficiency)

    – Spinal cord infarction

    – other myelopathies (spondylosis, epidural abscess or hematoma)

    7. Brain

    – Pontine lesions (eg. central pontine myelinolysis, basis pontis infarct or bleed)

    – Multifocal lesions (multiple metastases, dissemination encephalomyelitis [ADEM], multiple infarcts or hemorrhages – eg. DIC, TTP, bacterial endocarditis)

    (Source: Neurological Medical Pocketbook-2003)

  81. #81 lilady
    December 12, 2011

    I have a comment stuck in moderation about AFP-differential diagnosis.

    See also:

    CDC VPD Surveillance Manual 3rd Edition 2002 Chapter 10, Poliomyelitis 10-1

  82. #82 Th1Th2
    December 12, 2011

    Let’s see. In 2011, there will have been about 92,000 cases of AFP world-wide, not including the United States. In 1952, there were 21,000 cases of paralytic polio, not including the rest of the world. These two numbers can not be meaningfully compared.

    Oh yeah let’s take a look shall we? Oh wait I don’t see any incidence rates of AFP since they started recording paralytic poliomyelitis in 1937, do you? The hell with that? So to which are you comparing paralytic poliomyelitis with in 1952 you tell me.

    BTW, that 2011 figure is a global total, understood?

  83. #83 lilady
    December 12, 2011

    The references I cited to differential diagnoses of AFP are in English, not Thinglish.

    Delusional, disease-promoting, uneducated, health care professional wannabe troll needs “terminal disinfection.”

  84. #84 Lawrence
    December 12, 2011

    LOL – troll still can’t read!

  85. #85 Narad
    December 12, 2011

    Thank you, now I have a perfect reason to ignore Th1Th2.

    I’ve long thought that its obvious discomfiture at being ignored was a pretty good reason in and of itself. This rehashing of its AFP script seems merely to be a reboot meant to dilute the memory of its truly mortifying, protracted Dryvax blunder from last week.

  86. #86 Th1Th2
    December 12, 2011

    AFP (acute flaccid paralysis) was and is a “surveillance marker” for polio outbreaks in much the same way that “influenza-like illness” is used as a surveillance marker for influenza.

    AFP surveillance began only in 1996 whereas recorded incidence rates of paralytic poliomyelitis could be traced as far back in 1937. You sure know what you’re talking about.

    In a population without widespread immunity to polio, a sudden rise in cases of AFP are most likely to signal a polio outbreak, whereas the same AFP rise in a largely immune population (like the US) is more likely due to one of the other viruses that can cause AFP, such as other picornaviruses (e.g. enteroviruses, echoviruses) and adenoviruses.

    As I said where did you find AFP cases in the pre-vaccine era? Where’s your evidence that there had been such a surveillance before there was OPV?

  87. #87 lilady
    December 12, 2011

    LOL – troll still can’t read!…or write, or think coherently, or get an education, or leave the dole, or get a life-ROTF-LMAO.

  88. #88 Th1Th2
    December 12, 2011

    This rehashing of its AFP script seems merely to be a reboot meant to dilute the memory of its truly mortifying, protracted Dryvax blunder from last week.

    So you’re resurrecting Offit’s infamous and now deader than dead Children-are-Exposed-to-Fewer-Antigens-in-Vaccines-Today-Than-in-the-Past- gambit huh? When will you ever learn?

  89. #89 lilady
    December 12, 2011

    “As I said where did you find AFP cases in the pre-vaccine era? Where’s your evidence that there had been such a surveillance before there was OPV?”

    As I said where did you find delusional cases in the pre-Thingy era? Where’s your evidence that there had been such a surveillance before there was Delusional Thingitis?

    -FTFY

  90. #90 Narad
    December 12, 2011

    So you’re resurrecting Offit’s infamous and now deader than dead Children-are-Exposed-to-Fewer-Antigens-in-Vaccines-Today-Than-in-the-Past- gambit huh? When will you ever learn?

    I’ve explained this concept to you before: I was talking about you, not to you. Mind your place.

  91. #91 Th1Th2
    December 12, 2011

    I have a comment stuck in moderation about AFP-differential diagnosis.

    Great. Now find a single case of AFP before 1955.

  92. #92 lilady
    December 12, 2011

    “Great. Now find a single case of AFP before 1955.”

    Great. Now find a single case of Delusional Thingitis before 1955.

    FTFY

  93. #93 The Very Reverend Battleaxe of Knowledge
    December 12, 2011

    Great. Now find a single case of AFP before 1955.

    There can never be a “case” of AFP, you imbecile, because it’s a symptom, not a disease. It was one of the symptoms of polio before the vaccine era and after the vaccine era. It’s a symptom of several other diseases as well, and now that polio is almost gone, this particular symptom is very unlikely to be caused by polio.

    I really didn’t think you’d bite on the smallpox/fever thing. Somebody should be chasing you with a butterfly net—I’m serious.

  94. #94 Th1Th2
    December 12, 2011

    There can never be a “case” of AFP, you imbecile,

    There have been 91,752 cases of AFP so far this year, you moron! Do you think the reason they started AFP surveillance in 1996 is due to other diseases? Just think about it bozo.

  95. #95 lilady
    December 12, 2011

    @ The Very Reverend Battleaxe of Knowledge: On the planet Htrae where the inhabitants are delusional, uneducated, have imaginary lives, are earth-germ phobic and where the inhabitants speak Thinglish…symptoms such as fever and AFP…are always endemic infectious diseases.

    Time to “terminally disinfect” the Thing.

  96. #96 Lawrence
    December 12, 2011

    A pretty good presentation on the polio eradication campaign (along with the definition of AFP survelliance).

    http://www.slideshare.net/avinash15/afp-surveillance

    It is too bad they missed the benchmarks due to the spreading of false information.

  97. #97 Stu
    December 12, 2011

    Holy crap, Thingy is well and truly off the sidewalk now.

    Should we get it a shammy to wipe the spittle of its screen?

  98. #98 lilady
    December 12, 2011

    Dumber than Dumb, sh** for brains Troll is running on empty now. Shammy cloths do not work on computer screens…it needs “terminal disinfection.”

  99. #99 evilDoug
    December 12, 2011

    Anti-vax idiot writes book
    http://freethoughtblogs.com/butterfliesandwheels/2011/12/hey-kids-want-to-get-dead/

    Sane people, take your barf bucket.

  100. #100 Agashem
    December 12, 2011

    Lilady, I love your ‘redesigning’ of the thing-dong’s writing. It is perfection!

  101. #101 lilady
    December 12, 2011

    @ Thingy: My comment # 683 is out of moderation now…for your perusal. Why not do a Copy & Paste job at Google Translate.com for the English to Thinglish translation…or consult your “Immunology for Idiots” textbook?

    @ evilDoug: The author of that children’s book is an anti-vax mommy from Australia who “claims” her child died from the cumulative effects of vaccines. On her blog she refers people to the NVIC and whale.to websites

    @ Agashem: There are times when the Th1Th2bot needs a rest…it is an honor to sub for the bot.

  102. #102 Blackheart
    December 12, 2011

    Krebiozen

    There is disagreement about whether the DTP really does lead to an increase in mortality, or if this is an artefact of the way data is collected.

    I have no problem that other researchers find the many and varied data sets coming from multiple study areas challenging to the theory of specificity. Thats what good science debate is about.

    There is also disagreement about the significance of non-specific effects of vaccines.

    In what way ? The very positive effects that could change the very nature of disease mortality and burden in Africa and other developing areas. Or the fact that there are very real negative outcomes on mortality.

    Are you really going to pick and choose which data you believe ?

    Much of the evidence for these so-called ‘non-specific effects’ has been accrued in Guinea Bissau…

    I think this is adequately covered in the original authors reply to the Fine and Elliman (Perspective)

    “I presented evidence from 11 randomised trials suggesting that BCG and measles vaccines reduce mortality from diseases other than tuberculosis and measles—and only two of the 11 trials were performed in Guinea-Bissau.”

    “The evidence for non-specific effects is therefore very strong indeed, and most of it comes from outside Guinea-Bissau ” Shann BMJ

    a country whose child health characteristics are far from typical

    What child health characteristics do they mean ? How does that relate to the variety of differing vaccines trialled and researched ?

    The hypothesis that non-specific effects may be greater in females and are dependent upon prior infections or vaccines deserves further exploration, by independent groups of scientists, in different settings. Importantly, discussion of these effects should not blind us to the enormous gains in health which have been achieved through our immunisation programmes. Basic immunisation programmes must keep evolving with the times, in terms of the vaccines and services they provide and their precise schedules.

    I don’t think many people would disagree with that. I certainly would not.

    There you go … I knew you’d come around to a common sense legitimate investigation of all aspects of vaccine safety.

    Congratulations Krebiozen perhaps you could convince a few more of the minions to also acknowledge the very real positive and unfortunately negative aspects of vaccine administration and safety.

  103. #103 T-reg
    December 13, 2011

    Is it me or has thingy just slipped a notch lower on its mental competence levels? I didn’t even think it was possible!

    With all due respect, but why are we entertaining it again?

  104. #104 Krebiozen
    December 13, 2011

    Blackheart,

    Are you really going to pick and choose which data you believe ?

    Like you do, you mean? No, we should treat data with caution, especially it is contradictory. When trials give opposite results depending on how data is gathered, when there is highly variable mortality in the trials conducted, and when relatively small numbers of subjects are involved you have to be very careful not to jump to conclusions that can have serious effects on people’s lives. We need properly controlled studies done by an independent group to find out what is really going on, not just these crossover studies that are vulnerable to all sorts of confounding factors.

    Remember, these results are from developing countries with high background mortality. Aaby’s group found no effects in areas with low mortality, so even if independently replicated these results do not apply to developed countries like the USA and the UK, and certainly have no direct relevance to discussions about vaccines causing autism.

    You are fond of referring to Aaby’s claim that withdrawing the high titer measles vaccine saved 500,000 girls’ lives. Are you aware that was extrapolated from fewer than 30 actual excess deaths in areas with background mortality that varied from 0% to 23%? The highest mortality was seen in the medium titer group, by the way.

    perhaps you could convince a few more of the minions to also acknowledge the very real positive and unfortunately negative aspects of vaccine administration and safety

    I don’t think anyone here has ever suggested otherwise. The positive aspects of vaccination are regularly mentioned here. I don’t think anyone would dispute the possible importance of Aaby’s results where vaccine administration in areas of high mortality is concerned.

    What some of us keep patiently repeating is that the negative effects of modern vaccines in developed countries are far, far less common than the adverse effects of the diseases they help to prevent. In many cases adverse events due to vaccinations are so rare as to undetectable even in trials with very large numbers of subjects, and we are not even sure they occur at all. As I have pointed out many times, even the Urabe mumps vaccine which was withdrawn because it sometimes caused aseptic meningitis had far less serious effects than mumps itself.

    Like other “safer vaccine advocates” you make a lot of noise about the possible negative effects of vaccines, though you have to look to Africa to find anything that remotely supports your case, and you don’t have any solutions.

    There are two real options:

    The first is to carry on with the current schedule, and continue research into vaccination, the immune system, autism and related areas, which is what is actually happening. There are more than 44,000 papers on PubMed with “vaccine” in the title, more than 8000 with “autism” in the title, and nearly 80,000 with “immune” in the title, published this year alone. How much more research do we need?

    For many diseases if vaccine coverage is great enough for long enough the diseases can be eliminated globally, and vaccination could eventually be stopped altogether. Wouldn’t anyone truly concerned about vaccine safety support a measure that could lead to an end to vaccination for most diseases?

    The other option is to stop vaccinating until we have vaccines that are proven to be 100% safe, which is impossible without testing them on very large numbers of people. Stopping vaccination would result in a rapid return of vaccine preventable diseases and a huge increase in child morbidity and mortality. No one wants to see that.

    Which of these are advocating?

  105. #105 Krebiozen
    December 13, 2011

    ‘!$%s!!! typos – should read:
    “especially if it is contradictory” and
    “Which of these are you advocating?”

  106. #106 Denice Walter
    December 13, 2011

    @ Blackheart:

    Although I can’t speak for the other minions, I absolutely acknowledge that I believe that there are risks associated with vaccines. *However* (and it’s a big “however”)I don’t think that my information about risk is in any way remotely related to what many who – at heart really oppose vaccines and would like to see their usage greatly diminished- are talking about.

    They argue( and there are articles with titles that revolve upon this idea)that vaccines are not 100% safe and effective. They speak about extremely rare events, conditions reported to occur around the time of vaccination ( but which could not be feasibly connected in any manner except via imagination- e.g. a girl in the UK gets a jab and dies soon afterward of an undiagnosed cancer or another who dies in a car accident), *or* speak about autism as being a consequence of vaccination ( not supported by data). These ideas are presented in an emotional fashion, often with numerical estimates left out. All of this engenders distrust of vaccines, medical personnel, and governments.

    So I acknowledge “risk” and imperfection in vaccines which have many *benefits* that greatly outweigh the possible risks. Opponents of vaccines over-stress the risks and underplay the benefits, thus distorting and slanting the whole story. Now why would anyone do this?

    It seems that those who eternally cry, “Conflict of interest!” have COIs of their own: which can be monetary ( selling alt med products, books) or emotional ( seeking out fame or having reasons to think away a child’s autism). They won’t tell you this: I just did. And -btw-, my own COIs are minuscule in comparison to those of many anti-vaxxers ( my work doesn’t involve meds of any sort and I only own Pharma shares through a mutual I inherited).

    I see many of those who oppose vaccines *professionally*( as their *metier* or claim to fame) as manipulators of information and people. I feel that those of us who are fortunate enough to have gotten a good education *owe* others our service in this area.

  107. #107 Th1Th2
    December 13, 2011

    Lawrence,

    A pretty good presentation on the polio eradication campaign (along with the definition of AFP survelliance).

    Let’s a look at some interesting slides, shall we?

    33. WHAT IS PULSE POLIO ?
    TO IMMUNIZE ALL THE KIDS (younger than) 5YRS NATION WIDE ON A SINGLE DAY IN THE SHORTEST POSSIBLE TIME WITH OPV & THAT THE ENVIRONMENT WILL GET SATURATED WITH THE VACCINE VIRUS SO THAT IT WILL REPLACE THE WILD VIRUS AND THUS INTERUPT THE TRANSMISSION OF WILD VIRUS .

    India’s AFP case since getting drunk with OPV.

    1997 3047
    1998 9465
    1999 9587
    2000 8103
    2001 7470
    2002 9705
    2003 8508
    2004 13274
    2005 27049
    2006 32194
    2007 41524
    2008 45582
    2009 50405
    2010 55785
    2011 53994

    Source: h_ttp://apps.who.int/immunization_monitoring/en/diseases/poliomyelitis/afpextract.cfm

    37. WHY AFP SURVEILLANCE INSTEAD OF POLIO SURVEILLANCE?
    SURVEILLANCE OF A POLIO CASE ALONE IS NOT SUFFICIENT BECAUSE IT IS IMPOSSIBLEE[sic] TO PRECISELY IDENTIFY ALL CASES OF POLIO CLINICALLY DUE TO CONFUSING AND AMBIGUOUS CLINICAL SIGNS AND VARIABLE CLINICAL KNOWLEDGE & SKILLS OF DOCTOR.
    CLINICALLY POLIO IN ACUTE STAGE, IS DIFFICULT TO DISTINGUISH FROM OTHER CAUSES OF ACUTE ONSET OF FLACCID PARALYSIS.—–

    Trans: This is how we were able to hide polio from the public eye.

  108. #108 The Very Reverend Battleaxe of Knowledge
    December 13, 2011

    CLINICALLY POLIO IN ACUTE STAGE, IS DIFFICULT TO DISTINGUISH FROM OTHER CAUSES OF ACUTE ONSET OF FLACCID PARALYSIS.—–

    Seriously, nobody can be this dense. “Other causes” up there—it’s in your own quote! There are plenty of other causes, some of them obviously increasing, as shown by your figures. Polio would be one you could have crossed off, since it should have been eradicated by now. Unfortunately, due to idiots like you, India is one of the places it’s hanging on. When someone presents with the SYMPTOM AFP, they have to make damn sure the DISEASE that’s causing it isn’t polio. It’s like talking to a freakin’ stump.

  109. #109 Anton P. Nym
    December 13, 2011

    It’s like talking to a freakin’ stump.

    I, sir, take offense at this gross calumny against the intellectual capacities of deceased arboreal entities. At least they’re smart enough not to use citations that undermine their own arguments.

    — Steve

  110. #110 Narad
    December 13, 2011

    Trans: This is how we were able to hide polio from the public eye.

    This doesn’t even make any sense. Take the 2010 data: 83% of the 55785 AFP cases had two stool samples within 14 days, and 97% had some sample for analysis. The breakdown?

    Culture positive for poliovirus: 2796
    Culture positive for poliovirus and NPEV: 465
    NPEV: 14174
    No poliovirus or NPEV: 36546

    AFP surveillance casts a wider net. The only thing that seems to be conspicuously missing from the public eye is your reading comprehension (*koff*Dryvax*koff*).

  111. #111 Th1Th2
    December 13, 2011

    Seriously, nobody can be this dense. “Other causes” up there—it’s in your own quote! There are plenty of other causes, some of them obviously increasing, as shown by your figures. Polio would be one you could have crossed off, since it should have been eradicated by now.

    You do realize, don’t you that AFP surveillance is primarily a monitoring tool in identifying cases of paralytic poliomyelitis and NOT for some other diseases? Read,

    35. AIM OF AFP SURVEILLANCE
    TO DETECT POLIO TRANSMISSION & INTERRUPTION OF TRANSMISSION

    And there are three scenarios wherein poliovirus can be transmitted and cause poliomyelitis and therefore can be detected on a population.

    1. WT poliovirus
    2. OPV
    3. VDPV

    So it’s obviously impossible to for you to just “cross off” poliovirus from the list and to blame something else since India is still highly “saturated” with vaccine poliovirus. If nothing else, India needs a convincing exit strategy plan since poliovirus eradication is impossible when OPV vaccinators become polio promoters themselves.

    Unfortunately, due to idiots like you, India is one of the places it’s hanging on. When someone presents with the SYMPTOM AFP, they have to make damn sure the DISEASE that’s causing it isn’t polio. It’s like talking to a freakin’ stump.

    As I said, it’s easy to manipulate polio cases when substitution has always been the name of the game.

  112. #112 Th1Th2
    December 13, 2011

    Narad,

    They don’t have that screening tool as a requirement to diagnose polio before the vaccine was introduced. In short, they don’t look at your nasty stool; they look for paralysis. So mind your stool please.

  113. #113 Narad
    December 13, 2011

    So it’s obviously impossible to for you to just “cross off” poliovirus from the list and to blame something else since India is still highly “saturated” with vaccine poliovirus.

    Oh, look, that’s broken out as well. Of the 3261 positive cultures for poliovirus in the 2010 AFP surveillance, what do we have?

    Wild type 1: 18
    Wild type 2: 0
    Wild type 3: 23
    OPV1: 882
    OPV2: 445
    OPV3: 1177
    OPV mixed: 643
    VDPV 1: 0
    VDPV 2: 5
    VDPV 3: 0
    NPEV by PCR: 50
    Non-EV: 13
    Negative: 5

    So, let’s see….

    If nothing else, India needs a convincing exit strategy plan since poliovirus eradication is impossible when OPV vaccinators become polio promoters themselves.

    Now, how many asymptomatic carriers is one likely to have on one’s hands for every detected case of paralytic wild-type poliomyelitis? This might just give one a hint as to an “exit strategy.”

  114. #114 Narad
    December 13, 2011

    They don’t have that screening tool as a requirement to diagnose polio before the vaccine was introduced.

    That’s because, for all intents and purposes, “they don’t have that screening tool” at all before the vaccine was introduced. So what?

  115. #115 Th1Th2
    December 13, 2011

    Narad,

    That’s because, for all intents and purposes, “they don’t have that screening tool” at all before the vaccine was introduced. So what?

    It’s because poliomyelitis is a clinical diagnosis and a straightforward diagnosis. There wasn’t any AFP screening before. All these AFP cases this year could have been a diagnostic case of paralytic poliomyelitis back then. Before the Cutter Incident in 1955, the only known causative agent for paralytic poliomyelitis was the transmissible WT poliovirus. But after that horrible incident, stool exam had since been required to detect WT from VT poliovirus. But we know it didn’t stop there. Currently, we have three etiologic sources of poliovirus; adding VDPV to the list.

    Now you know why they require stool samples- to detect transmission.

  116. #116 Lawrence
    December 13, 2011

    The only stool here is what continues to come out of Insane Troll’s mouth….

  117. #117 Gray Falcon
    December 13, 2011

    Th1Th2, you realize your pathological hatred of doctors doesn’t count as evidence.

  118. #118 Th1Th2
    December 13, 2011

    Narad,

    Oh, look, that’s broken out as well. Of the 3261 positive cultures for poliovirus in the 2010 AFP surveillance, what do we have?

    Like I said, stool cultures are done to detect transmissibility of the poliovirus, whatever strain that is. It will not rule out infectivity since all who had received OPV essentially have been primarily infected. They don’t want the people to know that they’ve been infected deliberately that’s why they never used serologic testing as a preliminary diagnostic tool.

    Now, how many asymptomatic carriers is one likely to have on one’s hands for every detected case of paralytic wild-type poliomyelitis? This might just give one a hint as to an “exit strategy.”

    Like ill-lady, you seem to think that 91,752 AFP cases are better than 560 paralytic poliomyelitis. Oh and like India, you too need a better “exit strategy”.

  119. #119 Stu
    December 13, 2011

    Yessss, nassssty stool! All they had to do was stay on the sidewalk!

  120. #120 Narad
    December 13, 2011

    They don’t have that screening tool as a requirement to diagnose polio before the vaccine was introduced.

    That’s because, for all intents and purposes, “they don’t have that screening tool” at all before the vaccine was introduced. So what?

    It’s because poliomyelitis is a clinical diagnosis and a straightforward diagnosis.

    What in G-d’s name are you yammering about? This isn’t 1955. Polio was a clinical diagnosis because the ability to culture the virus went hand in hand with the development of the vaccine.

    Before the Cutter Incident in 1955, the only known causative agent for paralytic poliomyelitis was the transmissible WT poliovirus. But after that horrible incident, stool exam had since been required to detect WT from VT poliovirus.

    Did you see the part of the text you quoted with the curly line above a dot? (<–Looks like this.) Try addressing that part. The Cutter Incident isn’t even apropos of the “diagnostic substitution” argument that you are apparently having to travel back and forth in time to try to prop up.

    Now you know why they require stool samples- to detect transmission.

    This diversionary psychohistorical tale doesn’t make a whit of difference in any event. You would like to simultaneously downplay polio as having been inflated in the past as a purely clinical diagnosis while also dramatizing it in the present. It’s no big deal unless it has something to do with a vaccine. Simple. It would have just gone away if people had only had Th1Th2 around to explain Pure Livin’. Why bother with the song and dance? This is all you have.

  121. #121 lilady
    December 13, 2011

    “So it’s obviously impossible to for you to just “cross off” poliovirus from the list and to blame something else since India is still highly “saturated” with vaccine poliovirus. If nothing else, India needs a convincing exit strategy plan since poliovirus eradication is impossible when OPV vaccinators become polio promoters themselves.”

    So it’s obviously impossible to for you to just “cross off” “INSANITY from the list and to blame something else since “SH** FOR BRAINS TROLL” is still highly “saturated” with “SH**”. If nothing else, “RESPECTFUL INSOLENCE” needs a convincing exit strategy plan since “INSANITY” eradication is impossible when “SH** FOR BRAINS TROLL” becomes a polio promoter ITSELF.

    -FTFY, SFB TROLL

  122. #122 Narad
    December 13, 2011

    Like I said, stool cultures are done to detect transmissibility of the poliovirus, whatever strain that is. It will not rule out infectivity since all who had received OPV essentially have been primarily infected. They don’t want the people to know that they’ve been infected deliberately that’s why they never used serologic testing as a preliminary diagnostic tool.

    Yah. Unfortunately, this paranoiac trip requires that “They” and “the people” from whom this has somehow been kept a big secret for 55 years give a rat’s ass about Th1Th2’s pureed semantics and purity routine, which is to say, didn’t want poliovirus antibodies in the first place.

    Like ill-lady, you seem to think that 91,752 AFP cases are better than 560 paralytic poliomyelitis. Oh and like India, you too need a better “exit strategy”.

    You keep asserting this connection, but you have failed to explain why a cursory examination of the Indian numbers you yourself invoked point to the overwhelming number of AFP cases having, you know, no isolatable poliovirus.

  123. #123 Th1Th2
    December 13, 2011

    Narad,

    What in G-d’s name are you yammering about? This isn’t 1955. Polio was a clinical diagnosis because the ability to culture the virus went hand in hand with the development of the vaccine.

    If this is 1955 and knowing what they know now that there have been 91,752 AFP this year, they’ll be up on their a$$ “yammering” for a novel vaccine. It seems though that they were culturing the wrong specimen since 1996 or they have given up looking for the inevitable exit strategy.

    Global Total AFP

    1996 13857
    1997 17365
    1998 24664
    1999 29924
    2000 30625
    2001 33519
    2002 36832
    2003 34915
    2004 42511
    2005 62434
    2006 68519
    2007 77395
    2008 85404
    2009 90227
    2010 98788
    2011 91752

    Source: h_ttp://apps.who.int/immunization_monitoring/en/diseases/poliomyelitis/afpextract.cfm

    Did you see the part of the text you quoted with the curly line above a dot? (< --Looks like this.) Try addressing that part.

    This?

    CLINICALLY POLIO IN ACUTE STAGE, IS DIFFICULT TO DISTINGUISH FROM OTHER CAUSES OF ACUTE ONSET OF FLACCID PARALYSIS.—–

    I did. And my response to this particular statement is: “This isn’t 1955.”

    The Cutter Incident isn’t even apropos of the “diagnostic substitution” argument that you are apparently having to travel back and forth in time to try to prop up.

    The Cutter Incident was a revelation of the covert infection-promoting agenda of polio vaccination. If this disaster had not happened, poliomyelitis would still remain a monocausal diagnosis.

    This diversionary psychohistorical tale doesn’t make a whit of difference in any event. You would like to simultaneously downplay polio as having been inflated in the past as a purely clinical diagnosis while also dramatizing it in the present. It’s no big deal unless it has something to do with a vaccine. Simple. It would have just gone away if people had only had Th1Th2 around to explain Pure Livin’. Why bother with the song and dance? This is all you have.

    It has everything to do with the poliovirus-containing vaccine. Causation is very well established.

  124. #124 lilady
    December 13, 2011

    Please do not feed delusional, uneducated, disease promoting. health-care-professional wannabe, sh** for brains troll. It needs “terminal disinfection”.

  125. #125 Narad
    December 13, 2011

    It has everything to do with the poliovirus-containing vaccine. Causation is very well established.

    Once again, I commend to you the notion of reading comprehension. Aside from the fact that you appear to have totally failed to grasp seized upon the bit of text that you think is easiest to misinterpret and most amenable to recycling, when it is in fact a characterization of your own position, it’s still upon you to demonstrate that AFP that has no isolatable poliovirus of any stripe is somehow due to OPV.

  126. #126 Narad
    December 13, 2011

    Oh, and…

    Did you see the part of the text you quoted with the curly line above a dot? (

    This?

    CLINICALLY POLIO IN ACUTE STAGE, IS DIFFICULT TO DISTINGUISH FROM OTHER CAUSES OF ACUTE ONSET OF FLACCID PARALYSIS.—–

    No, not “this.” Wie sagt man “no loitering allowed”?

  127. #127 Th1Th2
    December 13, 2011

    Narad,

    Yah. Unfortunately, this paranoiac trip requires that “They” and “the people” from whom this has somehow been kept a big secret for 55 years give a rat’s ass about Th1Th2’s pureed semantics and purity routine, which is to say, didn’t want poliovirus antibodies in the first place.

    You’re terribly misinformed. They are NOT acquiring poliovirus antibodies through vaccination. Vaccine-induced infection always precedes antibody production. You should know; you’re an infection promoter.

    You keep asserting this connection, but you have failed to explain why a cursory examination of the Indian numbers you yourself invoked point to the overwhelming number of AFP cases having, you know, no isolatable poliovirus.

    Stool exam is NOT the GOLD STANDARD in diagnosing poliomyelitis. People don’t get paralyzed because they were poliovirus in their feces. That’s laughable. You know what I’m talking about, don’t you? Check their every goddamn tissues, blood and if they died, brain! But why they don’t do that? Because they know exactly what to expect.

    OK rant over.

  128. #128 lilady
    December 13, 2011

    “OK rant over.” Thingy keeps promising to stay away and then always comes back with another rant. Now it is fixated on its own brain matter…”Stool exam is NOT the GOLD STANDARD in diagnosing poliomyelitis.”

    Please do not feed delusional, uneducated, disease promoting. health-care-professional wannabe, sh** for brains troll. It needs “terminal disinfection”.

  129. #129 Th1Th2
    December 13, 2011

    Narad,

    Once again, I commend to you the notion of reading comprehension. Aside from the fact that you appear to have totally failed to grasp seized upon the bit of text that you think is easiest to misinterpret and most amenable to recycling, when it is in fact a characterization of your own position, it’s still upon you to demonstrate that AFP that has no isolatable poliovirus of any stripe is somehow due to OPV.

    They are not checking it properly. And that is exactly how it’s supposed to be in order for them to conceal the virus and to claim that OPV works. Obviously, they just can’t hide paralysis.

  130. #130 Narad
    December 13, 2011

    You’re terribly misinformed. They are NOT acquiring poliovirus antibodies through vaccination. Vaccine-induced infection always precedes antibody production.

    Jesus Christ, do I have to tell you what your talking points are now, or do you just need a refresher on what “always” means?

    OK rant over.

    Promises, promises, Norberg.

  131. #131 lilady
    December 14, 2011

    “They are not checking it properly. And that is exactly how it’s supposed to be in order for them to conceal the virus and to claim that OPV works. Obviously, they just can’t hide paralysis”.

    They are not checking “SFB Thingy Troll” properly. And that is exactly how it’s supposed to be in order for “Its Keepers” to conceal the “Delusions” and to claim that “Thingy is Sane”. Obviously, they just can’t hide “The Insanity”.

    -FTFY

  132. #132 Narad
    December 14, 2011

    It is cute that this has finally turned into rank conspiracy theory, if you ask me.

  133. #133 TBruce
    December 14, 2011

    Still boring, stupid and insane, I see.

  134. #134 The Very Reverend Battleaxe of Knowledge
    December 14, 2011

    Still boring, stupid and insane, I see.

    Oh, it’s progressively getting crazier and crazier. Before, anything defiling your precious bodily fluids was an “infection”, but at least she was talking about something connected with an actual infectious agent. Synthetic chemicals resembling parts of the measles virus’ capsule was a “measles infection”. Insane, but there was some connecting thread.

    Now, any instance of paralysis, even if they find some other virus is causing it, is actually polio, because, well, because…well, it just is, dammit! All that polio didn’t just disappear! Vaccination couldn’t have prevented it! No, it’s hiding somewhere! Somebody took those strawberries!

  135. #135 Narad
    December 14, 2011

    Synthetic chemicals resembling parts of the measles virus’ capsule was a “measles infection”. Insane, but there was some connecting thread.

    The connecting thread is embodied in the babbling about serology. The smoking antibodies, as it were. I wouldn’t be surprised if it recognized the “mapping” of this bottomless causal swamp as a promising new direction from which attention might be garnered with free labor.

  136. #136 Th1Th2
    December 14, 2011

    The Very Reverend,

    Synthetic chemicals resembling parts of the measles virus’ capsule was a “measles infection”.

    Insane, but there was some connecting thread.

  137. #137 T-reg
    December 14, 2011

    Uh, I hate to interrupt, but for all the cases of AFP, we had only 1 confirmed case of polio in the whole country.

    And, yes, there is an exit strategy to stop OPV (due to the risk of it causing polio, a risk FAR smaller than the risk of WT polio virus causing polio). Once we have no confirmed cases of polio for 5 years, with full OPV coverage, we will be switching over to IPV.

    AFP is a useful surveillance method because it doesn’t make sense to go and check the excrement of all the 1.2 bn residents (plus the illegal immigrants from our extremely porous border in the east). AFP hints at who may have polio which eventually has to be confirmed.

    Also, AFP surveillance is highly sensitive, easy and cost effective to perform. However, it has low specificity and so is not a useful diagnostic tool.

  138. #138 T-reg
    December 14, 2011

    Also, as far as conspiracies are concerned, the politicians in my country are more likely to bottle water in the OPV vials and have it distributed as OPV in order to pocket large parts of the allocated funds.
    It’s cheaper than buying OPV and so a larger part of the funds would be available for them to pocket. Besides, they don’t have to share their profits with some Pharma company as they can easily have some back-alley workshops (or the like) to bottle the water in small vials at a fraction of the cost.

  139. #139 LW
    December 14, 2011

    T-reg, thank you for your on-the-spot observations. Perhaps you know: did the campaign to report cases of AFP to try to identify any cases of polio perchance *start* in 1995 and take a while to get properly set up nationwide? I imagine that would take a lot of training of reporters and setting up reporting mechanisms, which would explain the ramp-up in numbers.

  140. #140 lilady
    December 14, 2011

    @ T-reg: Thank you for the clarification of the situation in India with AFP surveillance as an effective methodology to finally have a polio-free India. It’s nice to have a physician from India actually posting here and I love your description of AFP as a “high sensitivity-low specificity” screening tool.

    Try to ignore the troll…it is a disease-promoter who in its delusional deranged state, sees conspiracies all over the world. It still needs “terminal disinfection”.

  141. #141 Th1Th2
    December 14, 2011

    Perhaps you know: did the campaign to report cases of AFP to try to identify any cases of polio perchance *start* in 1995 and take a while to get properly set up nationwide? I imagine that would take a lot of training of reporters and setting up reporting mechanisms, which would explain the ramp-up in numbers.

    **All polio cases reported before 1997 were confirmed by attending physicians with no standard case definition.

    h_ttp://www.who.int/bulletin/archives/78(3)321.pdf

    Ouch!

    Again, “this wasn’t 1955”, right Narad?

  142. #142 Gray Falcon
    December 14, 2011

    Th1Th2, what evidence do you have that every single case of AFP is, in fact, polio?

  143. #143 lilady
    December 14, 2011

    Try to ignore the troll…it is a disease-promoter who in its delusional deranged state, sees conspiracies all over the world. It still needs “terminal disinfection”.

  144. #144 Narad
    December 14, 2011

    Ouch!

    Again, “this wasn’t 1955”, right Narad?

    You really seem to be having a lot of trouble answering the question “so what?” You’re upset that someone would decide to try to eradicate polio without your input and iron-fisted guidance, that’s understood. This is why you’re an infection promoter. There’s no point being an evasive infection promoter on top of it.

  145. #145 Th1Th2
    December 14, 2011

    Gray Falcon,

    Th1Th2, what evidence do you have that every single case of AFP is, in fact, polio?

    Simple. Paralysis.

  146. #146 Th1Th2
    December 14, 2011

    Narad,

    You really seem to be having a lot of trouble answering the question “so what?” You’re upset that someone would decide to try to eradicate polio without your input and iron-fisted guidance, that’s understood.

    They’ve been doing that S#!++y OPV in India since 1979 and look what they got this year—53,994 paralysis.

    This is why you’re an infection promoter. There’s no point being an evasive infection promoter on top of it.

    I don’t have the qualification. Sorry but you’re barking up the wrong tree.

  147. #147 Th1Th2
    December 14, 2011

    Treg,

    And, yes, there is an exit strategy to stop OPV (due to the risk of it causing polio, a risk FAR smaller than the risk of WT polio virus causing polio). Once we have no confirmed cases of polio for 5 years, with full OPV coverage, we will be switching over to IPV.

    Forget it. Your country had simply given up after that embarrassing promise bragging that polio would have been eradicated back in 2000.

  148. #148 Narad
    December 14, 2011

    They’ve been doing that S#!++y OPV in India since 1979 and look what they got this year—53,994 paralysis.

    The overwhelming number of which have no isolatable poliovirus, remember? The part where you have no evidence whatever for your claim?

    And anyway, what quantifiable results have your efforts at Better Disease Eradication through Bubble Living had, other than the obvious mixture of being promptly ignored or heaped with ridicule?

  149. #149 Th1Th2
    December 14, 2011

    Narad,

    The overwhelming number of which have no isolatable poliovirus, remember? The part where you have no evidence whatever for your claim?

    The fact is these people were paralyzed and they’re ONLY going to check the stool for poliovirus and to discard them if they were unable to excrete the virus? That’s it? Do you think poliovirus is solely an enterotropic virus with no neurotropism. Where’s your science going forward?

    If this happened to be a case of a paralyzed unvaccinated child , you’ll be “yammering” on CSF, serum neutralization assay and whatever goddamn tests that are available here on Earth. But why settle on stool?

  150. #150 Narad
    December 14, 2011

    If this happened to be a case of a paralyzed unvaccinated child , you’ll be “yammering” on CSF, serum neutralization assay and whatever goddamn tests that are available here on Earth.

    Ah, whatever you say, Carnac.

    But why settle on stool?

    Do you think it maht mebbe haz ta doo with availability and specificity? Naturally, it’s time to demand tens of thousands of lumbar punctures because, goshdurnit, noted expert Th1Th2 says AFP is polio and that’s that! Brilliant.

  151. #151 Professor Blackheart
    December 15, 2011

    Krebiozen

    Like you do, you mean?

    How do you mean. My narrative is a lot more balanced than yours.

    No, we should treat data with caution, especially it is contradictory.

    Hmmm …. that data has been around since 1996 has been replicated in random controlled trial at multiple times and multiple locations. Has been extended to other vaccines and other health initiatives.

    I’m unsurprised by your sloth like approach to safety.

    Remember, these results are from developing countries with high background mortality.

    Yes I think I’m able to recall that fact from the multiple studies and the multiple geographic areas.

    Aaby’s group found no effects in areas with low mortality

    They haven’t are you sure …this what Peter Aaby’s group says.

    These observations question many assumptions
    underlying the current program of interventions
    for children in low-income countries. Taking
    these observations into consideration in planning
    the intervention programs may have major
    impact on child survival.

    Low income not low mortality.

    so even if independently replicated these results do not apply to developed countries like the USA and the UK

    Why not ? You need to explain your reasoning there are population cohorts within the United States and the UK that may very well reflect the same factors found in low income populations. This is assuming form your response you understand the mechanism behind the findings of Aaby’s research.

    certainly have no direct relevance to discussions about vaccines causing autism.

    I think research groups such the Patterson Lab at California Institute of Technology may be interested particularly in regards to immune system dysfunction and infection.

    You are fond of referring …

    I am fond of using direct robust evidence of harm … apparently you are not.

    I don’t think anyone here has ever suggested otherwise.

    Here’s one skeptik response – Since you continue FVCK!NG LYING about this over and over and over and over again

    Very objective , well thought out and balanced. Using all the critical thinking on display.

    What some of us keep patiently repeating is that the negative effects of modern vaccines in developed countries are far, far less common than the adverse effects of the diseases they help to prevent.

    That’s the argument. Then I’m thoroughly underwhelmed especially when you the underlying mechanism is unknown. Therefore effect is unknown and cannot be calculated.

    So tell me the cost / benefit ratio you’d like to operate under ?

    In many cases adverse events due to vaccinations are so rare as to undetectable even in trials with very large numbers of subjects

    That is generally acknowledged through standard research that revolves around the theory of specificity. But vaccine have non specific effects and act differently in regards to gender and in regards to how they are schedules. Where’s the evidence that says vaccines have been examined in developed nations that addresses these issues and factors ?

    As I have pointed out many times, even the Urabe mumps vaccine which was withdrawn because it sometimes caused aseptic meningitis had far less serious effects than mumps itself.

    I think you are beginning to confuse even yourself on what position you are taking.

    Like other “safer vaccine advocates”

    That’s supposed to be a dirty word is it ? Challenging the skeptik POV ?

    you make a lot of noise about the possible negative effects of vaccines

    Well duh (excuse the language) … that’s the whole point of being an advocate on safety in medicines.

    But it was I who pointed the very real positive benefits that could save additional millions of lives .

    Didn’t see that from ‘skeptiks’.

    you have to look to Africa to find anything that remotely supports your case

    Is that important ? 500,000 lives seems more important .

    you don’t have any solutions

    I don’t …of course I have.

    There are two real options:

    There are …you are a very black and white type of thinker.

    How much more research do we need?

    Focused research – show me the pubmed results for non specific effects of vaccines in the UK population ? Any ?

    Sex differentials effects in vaccine efficacy in the US ?

    Wouldn’t anyone truly concerned about vaccine safety support a measure that could lead to an end to vaccination for most diseases?

    That’s the theory…I’d like to see the pragmatics and the cost.

    You have a plan for the eradication of tetanus ? Differing pertussis strains ? I’m interested.

    You’ve calculated the effect of eliminating one virus and effects on other viruses and systems ?

    The other option is to stop vaccinating

    So you obviously disagree with those that took HTMV off the shelves ?

    You have little to no interest that DTaP has been show to be highly dangerous in developing countries ?

    Which of these are advocating?

    Neither. Now there’s a surprise.

  152. #152 Th1Th2
    December 15, 2011

    Narad,

    Do you think it maht mebbe haz ta doo with availability and specificity?

    Only if the brain normally herniates to the bowels, then stool exam has a point.

    Naturally, it’s time to demand tens of thousands of lumbar punctures because, goshdurnit, noted expert Th1Th2 says AFP is polio and that’s that! Brilliant.

    If they want to properly diagnose paralytic poliomyelitis then yes since neurotropic viruses such as poliovirus are capable of attacking the CNS thereby causing paralysis.

  153. #153 dedicated lurker
    December 15, 2011

    Simple. Paralysis.

    Christopher Reeve had polio? And Stephen Hawking still has it?

  154. #154 Th1Th2
    December 15, 2011

    Christopher Reeve had polio? And Stephen Hawking still has it?

    Good night.

  155. #155 lilady
    December 15, 2011

    @ dedicated lurker: Hmmm, don’t you recall that Aristotle Onassis was misdiagnosed with myasthenia gravis…he really had polio. And, all the people who were paralyzed by West Nile Fever…also had polio.

    Thingy has “special connections” with every hospital in the world. It gets to “consult” with every emergency room and it actually performs all the lumber punctures. It also has its own virology and bacteriology labs.

    It also has “special dispensation” and exemptions from receiving vaccines, when it sees patients in the neuro ICU or consults with other physicians.

    We should feel privileged that this internationally-acclaimed infectious diseases specialist deigns to come to this blog to inform us…and to spread its brain droppings.

  156. #156 lilady
    December 15, 2011

    Oh..and another point about West Nile Virus. I recall my County health department setting up chicken coops with “sentinel chickens” which we tested for the presence of WNV, when the County was at the epicenter of the WNV outbreak.

    I suggest that we build some Thingy coops, cage the troll and test its brain droppings weekly, for the presence of the WNV and for polio virus.

  157. #157 Agashem
    December 15, 2011

    I’m with you Lilady, “thing coop” has a nice ring to it. Also, I guess the 3 year old I was recently involved with had polio rather than spinal muscular atrophy – those silly doctors. Or the 4 year old who had tranverse myelitis must have had polio. Paralysis = polio! Great, now we can stop diagnosing these other issues and just quarantine all these children (and their families, and many of the kids they go to school with and their families and the teachers and their families……)

  158. #158 Professor Blackheart
    December 15, 2011

    Denice Walter

    Nice vaccine apologist polemic and diversion but what is needed is some frank self reflection. Pull up a couch…

    See I can look at any aspect of vaccination positive / negative and not lose any perspective. I’m fascinated by the science unfolding before us … here’s another example.

    A number of case-control studies from high-income countriessuggest that smallpox vaccination protect againstdiverse chronic conditions and cancers.

    In a European study of people with malignant melanoma,
    smallpox vaccination reduced the risk of developing malignant melanoma and smallpox vaccination improved survival among malignant melanoma patients who had been smallpox-vaccinated several years prior to diagnosis.

    Considering these observations and our findings
    from Guinea-Bissau, we wanted to study whether smallpox vaccine and BCG also had non-specific effects in a European setting.

    Atopy, allergic rhinitis and asthma From an
    ecological perspective, the termination of smallpox
    vaccination in high-income countries coincided with an increased incidence of asthma.

    We examined the occurrence of atopy, allergic rhinitis,
    and asthma among Danish women within a
    national birth cohort study.

    Among the 1960 women for whom sera were available, 552 (28%) were classified as atopic; among the 1927 women
    with information on allergic rhinitis and asthma,
    263 (14%) had allergic rhinitis, and 165 (9%)
    were cases of asthma.

    Overall, smallpox vaccination was not associated with risk of atopy or allergic rhinitis compared to unvaccinated women.

    However, smallpox vaccination was associated with an OR of asthma of 0.55 (0.30 to 1.00) adjusting for birth cohort, sibship size, age of the women’s mother at birth, and social class.

    Hence, women who had received smallpox vaccination
    were less likely to have asthma, an association previously not described (9).

    Now that was interesting.

    Infectious disease hospitalisations

    Through linking of the CSHRR to the Danish registry of hospitalisations we were able to determine
    infectious disease hospitalisation (N=765) for the 2039 individuals for whom we had determined vaccination
    status.

    Preliminary analysis shows that BCG is associated with a lower risk of all-cause infectious disease hospitalization among women and a tendency
    towards smallpox-vaccinated subjects having a lower risk of all-cause infectious disease hospitalisation than subjects not vaccinated with these vaccines.

    Smallpox-vaccinated subjects were less likely to have skin infections and BCG vaccinated subjects less likely to be hospitalised for sexually transmitted
    infections (STI) than unvaccinated individuals.

    These observations are being pursued with studies of specific STIs including HIV-1.

    The preliminary indications are that BCG protects women against HIV-1 infection (hazard ratio (HR) 0.30 (0.12-0.77)) whereas the effect for smallpox vaccine was smaller (HR=0.81 (0.24-2.73)).

    …and so was that. Vaccines so many enigmatic results who’d have thought.

    ps apologies about the formatting differing documents

  159. #159 LW
    December 15, 2011

    “You have a plan for the eradication of tetanus ?”

    Ah, now I understand the reasoning of the aptly-named blackheart. Tetanus cannot be eradicated by vaccination, so therefore no one should be protected against a painful death from it. Death rates from tetanus in Africa are high and they should stay high.

    Got it.

  160. #160 lilady
    December 15, 2011

    @ Agashem: I happen to like chickens which are unaffected by infection with the WNV…and think it would be a good idea to put the humanoid Thingy in a large coop as bait for infected mosquitoes.

    Gee, when my son had an episode of post ictal Todd’s paralysis 30 years ago and my friend also had post ictal Todd’s paralysis 6 weeks ago, they were hospitalized…and Thingy was not consulted. Because Thingy was not “on their cases”, their stool wasn’t tested, they didn’t undergo LPs and were not put in “isolation”.

  161. #161 Narad
    December 15, 2011
    Naturally, it’s time to demand tens of thousands of lumbar punctures because, goshdurnit, noted expert Th1Th2 says AFP is polio and that’s that! Brilliant.

    If they want to properly diagnose paralytic poliomyelitis then yes since neurotropic viruses such as poliovirus are capable of attacking the CNS thereby causing paralysis.

    Uh-huh. Let’s have some numbers then for (1) CSF cultures showing the presence of poliovirus in the face of a negative stool culture and (2) the other way around.

  162. #162 Krebiozen
    December 15, 2011

    Blackheart,
    You seem to have a social scientist’s approach to natural science, and I don’t think it does you any favors. In the social sciences this may make you a “deep thinker” but in the natural sciences it means you see connections and patterns where there are none, and habitually speculate far beyond the data. Since you value a “balanced narrative” you may find it useful to read this and this if you want to understand my “sloth like approach to safety”.

    The issue of non-specific effects of vaccines is complicated in many ways, in terms of data collection, analysis, interpretation, biological mechanism and programmatic implication. It is essential that care is taken at each step of investigations and full details are provided in publications, in order that the scientific and public health communities can interpret critically and respond appropriately.

    And:

    The study of complex interactions between vaccines and gender involves subdividing cohorts into several groups, some of which may in consequence be small, or contain few deaths. In such circumstances, results can lack robustness owing to observations whose omission or inclusion in the analysis produce widely different results. Analyses should be scrutinized for such observations, their impact assessed, and relevant data on numerators and denominators reported.

    Oh, by the way:

    Aaby’s group found no effects in areas with low mortality

    They haven’t are you sure …

    I can’t find any studies Aaby or anyone else has done that found these effects in an area with low infant mortality. From Aaby’s ‘Child Mortality Following Standard, Medium or High Titre Measles Immunization in West Africa’:

    The results from Guinea-Bissau, Senegal and Haiti,all with high background child mortality, showed an association between high dose measles vaccines and decreased survival, especially among females, while studies from The Gambia and Mexico, where there was low background infant mortality, displayed no difference in mortality.

    Infant mortality in Guinea-Bissau is 126, in Senegal 60, Haiti 70, in The Gambia 80 and in Mexico 22 per 1000 live births. Infant mortality in the USA and UK is 7 and 5 per 1000 live births respectively. Aaby considers areas with infant mortality much higher than the USA and UK as areas with low infant mortality. Yet you stated that:

    there are population cohorts within the United States and the UK that may very well reflect the same factors found in low income populations.

    There are population cohorts in the USA and UK that have lower income and higher mortality than Gambia and Mexico? Where would those be?

  163. #163 Professor Blackheart
    December 16, 2011

    You seem to have a social scientist’s approach to natural science

    You say science speaks … show me the evidence that refutes these multiple findings non specific effects , gender differences , scheduling differences …. over multiple geographical areas over multiple times and multiple vaccines.

    Since you value a “balanced narrative” you may find it useful to read this and this if you want to understand my “sloth like approach to safety”.

    Apply all this to vaccine / autism epidemiological studies. Seems you can accept weak evidence there but not robust evidence here … interesting point of view.

    Your positions are always confusing … why is that ?

    The issue of non-specific effects of vaccines is complicated in many ways …

    Yes it is and so are other issues regarding vaccines.But you haven’t shown any scientific evidence that refutes these various findings..

    The study of complex interactions between vaccines and neurological effect involves subdividing cohorts into several groups, some of which may in consequence be small, or contain few deaths.

    In such circumstances, results can lack robustness owing to observations whose omission or inclusion in the analysis produce widely different results. Analyses should be scrutinized for such observations, their impact assessed, and relevant data on numerators and denominators reported.

    Differing arguments for differing occasions. Interesting.

    I can’t find any studies Aaby or anyone else has done that found these effects in an area with low infant mortality.

    Low income krebiozen.

    Yet you stated that

    Yes I did …

    there are population cohorts within the United States and the UK that may very well reflect the same factors found in low income populations.

    There are population cohorts in the USA and UK that have lower income and higher mortality

    Nice try … not interested.

    There are population cohorts in the USA and UK that have low income and high mortality

  164. #164 Agashem
    December 20, 2011

    Hate to leave a troll the last word. FWIW, reason’s greetings to all on RI…..

  165. #165 Narad
    December 20, 2011

    Why you sleepin’ wit ya eyes closed, Th1Th2?

    Let’s have some numbers then for (1) CSF cultures showing the presence of poliovirus in the face of a negative stool culture and (2) the other way around.

    Coochy-coo.

  166. #166 Krebiozen
    December 20, 2011

    Blackheart,
    I forgot about this thread…

    You say science speaks … show me the evidence that refutes these multiple findings non specific effects , gender differences , scheduling differences …. over multiple geographical areas over multiple times and multiple vaccines.

    Show me the controlled independent studies that support these multiple findings.

    Seems you can accept weak evidence there but not robust evidence here … interesting point of view.

    You are the one providing weak evidence Blackheart, not me, that’s the problem.

    Your positions are always confusing … why is that ?

    Strange, no one else seems to find my position confusing, yet many people have been left puzzled by yours. I have stated and restated my position in plain English many times. Until Aaby’s studies are replicated by other researchers using more robust methodology his results should be treated with caution. Is that clear enough for you?

    The issue of non-specific effects of vaccines is complicated in many ways …

    Yes it is and so are other issues regarding vaccines.But you haven’t shown any scientific evidence that refutes these various findings..

    Science doesn’t work like that. You don’t believe every piece of research that comes along until it is refuted, you treat results with caution until they have been independently replicated. I have linked above to evidence that the results of the studies on DTP vary wildly depending on how data is collected. I have pointed out the varying mortality and small sample sizes Aaby has used and the unreliability of his methodology. His group wouldn’t be the first to be fooled by noisy data or methodological artifacts. There may be something interesting there, or there may not.

    Differing arguments for differing occasions. Interesting.

    Not at all. When you are looking at very noisy data, with small numbers, as we are in these studies where mortality is high but highly variable, it is difficult to be sure you are looking at a real effect. That is true in any area of science.

    I can’t find any studies Aaby or anyone else has done that found these effects in an area with low infant mortality.

    Low income krebiozen.

    That doesn’t help. Where are Aaby’s studies on low mortality groups that find these effects? I can only find his studies on (relatively) low mortality groups in low income countries that find no such effects. Let me remind you what Aaby found, “studies from The Gambia and Mexico, where there was low background infant mortality, displayed no difference in mortality”.

    Nice try … not interested.

    You either miss my point or you are being deliberately obtuse. Aaby’s studies, that have not been replicated independently with controlled studies, found non-specific effects of vaccines in areas of high mortality, but none at all in areas of low mortality, yet you want to apply these unconfirmed results to populations with much lower mortality. Surely you see the problem with that.

    There are population cohorts in the USA and UK that have low income and high mortality

    Aaby found no non-specific effects on mortality in The Gambia (infant mortality 80 per 1000) or in Mexico (infant mortality 22 per 1000 live births), no difference in mortality. Please tell me, in which population cohorts in the UK or the USA does infant mortality even approach 22 per 1000, much less 80?

  167. #167 Blackheart
    December 20, 2011

    krebiozen

    Show me the controlled independent studies that support these multiple findings.

    I already have and you know that very well.

    Aaby, Bukh et al. 1986; Smedman, Gunnlaugsson et al. 1988; Whittle, Hanlon et al. 1988; Aaby, Hansen et al. 1988; Aaby, Jensen et al. 1988; Aaby and Clements 1989; Aaby, Pedersen et al. 1989; Aaby, Knudsen et al. 1990; Aaby, Samb et al. 1991; Burstrom, Aaby et al. 1992; Burstrom, Aaby et al. 1993; Samb, Aaby et al. 1993; Aaby, Andersen et al. 1993; Aaby, Knudsen et al. 1993; Aaby, Samb et al. 1993; Bennett, Aaby et al. 1994; Jensen, Whittle et al. 1994; Lisse, Aaby et al. 1994; Aaby, Andersen et al. 1994; Aaby, Knudsen et al. 1994; Aaby, Lisse et al. 1994; Aaby, Samb et al. 1994; Burstrom, Aaby et al. 1995; Samb, Aaby et al. 1995; Aaby 1995; Aaby, Samb et al. 1995; Knudsen, Aaby et al. 1996; Shaheen, Aaby et al. 1996; Aaby, Samb et al. 1996; Aaby, Samb et al. 1996; Atabani, Obeid et al. 1997; Benn, Aaby et al. 1997; Bennett, Whittle et al. 1999; Cisse, Aaby et al. 1999; Garly, Martins et al. 1999; Marchant, Goetghebuer et al. 1999; Seng, Samb et al. 1999; Whittle, Aaby et al. 1999; Whittle, Aaby et al. 1999; Aaby, Cisse et al. 1999; Benn, Lisse et al. 2000; Kristensen, Aaby et al. 2000; Shann 2000; Aaby, Shaheen et al. 2000; Garly, Bale et al. 2001; Garly, Bale et al. 2001; Schim van der Loeff, Aaby et al. 2001; Benn, Balde et al. 2002; Fischer, Valentiner-Branth et al. 2002; Ota, Vekemans et al. 2002; Steinsland, Valentiner-Branth et al. 2002; Aaby and Jensen 2002; Aaby, Jensen et al. 2002; Benn, Bale et al. 2003; Fine 2003; Garly, Martins et al. 2003; Garly and Aaby 2003; Steinsland, Valentiner-Branth et al. 2003; Aaby, Bhuiya et al. 2003; Aaby, Garly et al. 2003; Aaby, Jensen et al. 2003; Aaby, Jensen et al. 2003; Aaby, Jensen et al. 2003; Garly, Jensen et al. 2004; Hall 2004; Newport, Goetghebuer et al. 2004; Steinsland, Valentiner-Branth et al. 2004; Steinsland, Valentiner-Branth et al. 2004; Aaby 2004; Aaby, Jensen et al. 2004; Aaby, Jensen et al. 2004; Aaby, Rodrigues et al. 2004; Benn, Martins et al. 2005; Broutin, Mantilla-Beniers et al. 2005; Hull 2005; Nielsen, Eugen-Olsen et al. 2005; Roth, Sodemann et al. 2005; Shann 2005; Veirum, Sodemann et al. 2005; Aaby, Hedegaard et al. 2005; Aaby and Jensen 2005; Aaby, Rodrigues et al. 2005; Fine and Smith 2006; Rodrigues, Fischer et al. 2006; Roth, Garly et al. 2006; Roth, Sodemann et al. 2006; Roth, Stensballe et al. 2006; Aaby, Gustafson et al. 2006; Aaby, Ibrahim et al. 2006; Aaby, Jensen et al. 2006; Aaby, Vessari et al. 2006; Benn, Fisker et al. 2007; Diness, Fisker et al. 2007; Fisker, Lisse et al. 2007; Rodrigues, Schellenberg et al. 2007; Valentiner-Branth, Perch et al. 2007; Aaby, Benn et al. 2007; Aaby, Biai et al. 2007; Aaby, Garly et al. 2007; Benn, Diness et al. 2008; Shea, Benn et al. 2008; Benn, Lund et al. 2009; Benn, Martins et al. 2009; Benn, Rodrigues et al. 2009; Farrington, Firth et al. 2009; Fine, Williams et al. 2009; Stephensen and Livingston 2009; Villumsen, Sorup et al. 2009; Aaby, Martins et al. 2009; Aaby, Ravn et al. 2009; Agergaard, Lemvik et al. 2010; Bawah, Phillips et al. 2010; Benn, Fisker et al. 2010; Diness, Christoffersen et al. 2010; Elliman 2010; Fine and Elliman 2010; Hein-Kristensen, Jørgensen et al. 2010; Sartono, Lisse et al. 2010; Shann 2010; Shann 2010; Shann, Nohynek et al. 2010; Whittle and Aaby 2010; Aaby 2010; Aaby, Martins et al. 2010; Agergaard, Nante et al. 2011; Flanagan, Klein et al. 2011; Aaby and Benn 2011

    Yeah yeah I get it … you have a small statement in one Aaby study back in 1996 that says they found no non-specific effects on mortality in the Gambia or Mexico.

    I also get that there are some criticisms of best methodology…which may I say came out on Aaby’s side of the argument, though of course I can see skeptiks wishing to pursue random controlled studies where certain individuals are given “placebos” … but I’m sure it won’t get past the ethics boards.

    I also get it …that you don’t want to ‘lose’ another argument. Well get over it.

    That doesn’t help. Where are Aaby’s studies on low mortality groups that find these effects?

    Have you not undertaken any independent research yourself …. other than that 1996 study ?

    Go check Post #761

    A number of case-control studies from high-income countriessuggest that smallpox vaccination protect againstdiverse chronic conditions and cancers.

    In a European study of people with malignant melanoma,
    smallpox vaccination reduced the risk of developing malignant melanoma and smallpox vaccination improved survival among malignant melanoma patients who had been smallpox-vaccinated several years prior to diagnosis.

    Considering these observations and our findings
    from Guinea-Bissau, we wanted to study whether smallpox vaccine and BCG also had non-specific effects in a European setting.

    Atopy, allergic rhinitis and asthma From an
    ecological perspective, the termination of smallpox
    vaccination in high-income countries coincided with an increased incidence of asthma.

    We examined the occurrence of atopy, allergic rhinitis,
    and asthma among Danish women within a
    national birth cohort study.

    Among the 1960 women for whom sera were available, 552 (28%) were classified as atopic; among the 1927 women
    with information on allergic rhinitis and asthma,
    263 (14%) had allergic rhinitis, and 165 (9%)
    were cases of asthma.

    Overall, smallpox vaccination was not associated with risk of atopy or allergic rhinitis compared to unvaccinated women.

    However, smallpox vaccination was associated with an OR of asthma of 0.55 (0.30 to 1.00) adjusting for birth cohort, sibship size, age of the women’s mother at birth, and social class.

    Hence, women who had received smallpox vaccination
    were less likely to have asthma, an association previously not described (9).

    Now that was interesting.

    Infectious disease hospitalisations

    Through linking of the CSHRR to the Danish registry of hospitalisations we were able to determine
    infectious disease hospitalisation (N=765) for the 2039 individuals for whom we had determined vaccination
    status.

    Preliminary analysis shows that BCG is associated with a lower risk of all-cause infectious disease hospitalization among women and a tendency
    towards smallpox-vaccinated subjects having a lower risk of all-cause infectious disease hospitalisation than subjects not vaccinated with these vaccines.

    Smallpox-vaccinated subjects were less likely to have skin infections and BCG vaccinated subjects less likely to be hospitalised for sexually transmitted
    infections (STI) than unvaccinated individuals.

    These observations are being pursued with studies of specific STIs including HIV-1.

    The preliminary indications are that BCG protects women against HIV-1 infection (hazard ratio (HR) 0.30 (0.12-0.77)) whereas the effect for smallpox vaccine was smaller (HR=0.81 (0.24-2.73)).

    Please tell me, in which population cohorts in the UK or the USA does infant mortality even approach 22 per 1000, much less 80?

    I just showed you non specific effects in high income / very low mortality. Wasn’t that interesting.

    I suppose if I wanted to find a population with high infant mortality in the US / UK I’d be looking at the Indian Nations population , perhaps Traveller communities, migrant populations, infants born with disabilities and infants born with immune system dysfunction / chronic diseases as particularly high risk groups …

    But then it’s not all about mortality … it’s also about disease prevention / burden.

    Several million lives free from disease burden and hopefully premature death by safe , efficacious use of vaccines that have been researched to align with this new knowledge. Who could argue against that …

    Guess who.

  168. #168 Agashem
    December 21, 2011

    Honestly, there must be a simpler way to make a point. So you are saying, blackscum, that you are against saving millions from premature deaths?
    OK :/

  169. #169 Chris
    December 21, 2011

    Well, he obviously does not understand the difference between countries like the USA and UK compared to countries like Guinea Bissau.

  170. #170 TBruce
    December 22, 2011

    blackheart@770:

    Did you really read all those citations?

    Or did you just find every Google reference with Aaby’s name and vomit it all over the page?

    You really should clean up after yourself.

  171. #171 Blackheart
    December 22, 2011

    TBruce and other minions

    Run out of intellectual arguments ?

    Did you really read all those citations?

    The more important question is have you ?

    Sort of very casual attitude to medical safety and the lives of Africans and other people of the developing world.

    But hey …there’s always time for change.

    The references are self contained within a Statens Institute / Bandim Health publication that gives an overview of all the research, including criticism.

    There’s some 42 pages in this Vaccines appendix outlining the various studies / abstracts and notations.

    56 pages on measles

    13 pages on Vitamin supplementation

    43 pages on HIV

    In fact a 262 page Annotated Bibliography outlining all the differing aspects of the research taken by this eminent team of researchers

    Look it’s hard changing your mind set about these types of issues. If you can’t … well you can’t.

    If you want to make silly , immature responses …knock yourself out… real science moves on.

  172. #172 Blackheart
    December 22, 2011

    Krebiozen

    Merry Christmas and all that .. one day I’ll buy you a beer. Your responses always made me think and that’s the important part.

    Hey I am stubborn and all that. But someone’s got to challenge the world view. Otherwise how would you know you the truth .

    Whatever that is ?

  173. #173 Narad
    January 6, 2012

    There’s a “John Smith” commenting on a Nature.com thread and on Austisticland.blogspot.com, both on Nov. 4th; and an “Open Opinion”, on a Childhealthsafety.wordpress.com thread, way back on September 4th (almost a monthly cycle).

    And lest there be any doubt, “John Richard Smith” is regurgitating the NF-κB routine in the comments to Mnookin’s recen HuffPo article.

  174. #174 lilady
    January 6, 2012

    @ Narad: John Richard Smith’s fixation and comments on the Mnookin blog have been mostly ignored…sort of a collective ho-hum yawn.

    “Jened” has been posting there in reply to my comments…and I am handling this troll…rather expeditiously.

  175. #175 Krebiozen
    January 14, 2012

    Blackheart,

    I neglected this thread, sorry about that.

    I haven’t read all the 120+ citations you listed but I have read some and I have looked through all of them. I can’t see any independent studies supporting Aaby’s findings of adverse non-specific effects of vaccines. They are mostly by Aaby and/or his team (many of the “et al”s include Aaby) and so are not independent, and some of them argue against Aaby’s conclusions. None of Aaby’s studies that find adverse non-specific effects are properly controlled, they all suffer from methodological problems of one sort or another. That’s the nature of working in developing countries with high mortality, it is difficult, and we should be careful of coming to premature conclusions. I even wonder if it might have been a mistake withdrawing the high titer measles virus, as it is very effective, and the adverse effects associated with it may have been methodological artifacts or related to the timing of subsequent vaccinations, not due to the HTMV itself.

    I wasn’t suggesting that there are no non-specific effects in developed countries, we were specifically discussing Aaby’s findings of an increase in mortality after certain vaccines/vaccine combinations that he only found in areas with high mortality. I’m sure I remember learning about non-specific effects of BCG decades ago so this isn’t a new idea and, as we have mentioned before, actual infection also has non-specific effects.

    Look it’s hard changing your mind set about these types of issues. If you can’t … well you can’t.

    I don’t see how I am supposed to change my mind, based on what you have presented. I agree that non-specific effects of vaccines are interesting and we should continue to study them. I don’t think the current evidence justifies abandoning any vaccines or even changing vaccination schedules. You seem very excited about this, and seem to think that something that should be done hasn’t been done. What is that exactly, and how would it save millions of lives?

    Anyway, you might find this review study interesting Do childhood vaccines have non-specific effects on mortality? It includes a discussion of the methodological problems in this area. In particular I found the discussion of the effects of DTP vaccination on SIDS interesting. Initial studies found that DTP reduced SIDS, but then subsequent studies looking at the timing of DTP in relation to SIDS found no effects, suggesting that earlier results were due to selection bias. This is the sort of methodological problem that makes these kinds of studies so difficult to interpret, and those studies were carried out in developed countries where studies like this are much easier – fewer epidemics, civil wars, migrations of refugees etc.

    Of the non-specific effects of measles vaccine, the review concludes, “The data reviewed suggest that measles vaccine delivers its promised reduction in mortality, but there is insufficient evidence to suggest a mortality benefit above that caused by its effect on measles disease and its sequelae”. It calls for studies that don’t suffer from the methodological limitations I mentioned which I think that would be a good idea. Premature certainty is a dangerous thing.

  176. #176 Krebiozen
    January 14, 2012

    High titer measles vaccine I meant, not virus, obviously.

  177. #177 W. Kevin Vicklund
    January 14, 2012

    Something that struck me while reviewing some of the Aaby reviews: the female mortality was highly variable (.5 to 2.3 relative to normal titre), and the excess mortality was restricted to 2-year-old girls. Infants, 1-year-olds, and 3-year-olds all had the same mortality as normal titre.

  178. #178 Krebiozen
    January 15, 2012

    W. Kevin Vicklund,
    Interesting – what could make 2-year-old girls susceptible, or is this just a random bit of noise? I noticed that the data is extremely noisy, with highly variable mortality from group to group, and the other studies that supported the higher female mortality didn’t achieve statistical significance. The WHO abandoned the HTMV on the basis of this, which was probably wise on the precautionary principle, but I do wonder if it was the right decision.

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