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passionless Drone
Tallahassee, FL
I've got that sunny bunny feeling.
Recent Activity
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passionless commented on the article |Hello friends -
This is so sad to me because it will do exactly that the mainstream medical community is so afraid of; drive more parents of children with autism to alternative practioners. How many parents will seek out the internet for help when their regular pediatrician tells them to ignore the 24/7 reality of their childs condition based on a small epidemiology study from children born as long as thirty years ago?
My son had chronic problems with alternating diarehhea and constipation, but never got a diagnosis on it. In fact, I'd be amazed if it warranted a scribble in his folder by his pediatrician. If he were included in this study, he would show up in the 'no' group, but the reality of his situation wouldn't change.
We have a large array of clinical evidence that tells us that the children with autism generate an immune response to proteins in wheat and dairy at much more robust levels than their non diagnosed peers. I'm not certain that diagnostic code based chart reviews of a different generation of children is sufficient to rethink the findings from applied research.
- pD
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passionless commented on the article |Hi Kristina -
Studies on genetics can seem very distant; some raise questions about why research efforts (and dollars) are not devoted to studies about treatments that might have a direct (as in immediate) impact on people's lives.
While I'm generally not a big fan of pharmaceutical intervention, it does likely help some subset of children (or adults) with autism; genetic studies like this are the underpinnings of finding out how and why some drugs might be able to help.
The problem, as I see it, is that other interventions more likely to work that aren't based on biological intervetion are much more likely to be very expensive because they are highly individually tailored and involve near constant human supervision. You may have learned that too harsh of lighting affects Charlie adversely. It wouldn't suprize me.
But there isn't an effective way of developing a treatment that solves that via environmental modification; we can't expect everyone to change their lighting, and some children might be bothered by too little light.
I guess I'm OK with the notion of applying resources for 'better' and more immediate treatments, but I don't see a roadmap to them that make sense.
Of course, if we could understand the genetic and/or neurochemical processes involved with sensory perception that drives some people to be bothered by harsh lighting, that might be a step forward. But that is neither cheap nor immediate.
- pD
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passionless commented on the article |Hi Christopher Wyatt -
I'd seen that news story previously I think, and while it may be accurate, I think we need to be careful to put too much weight behind it; the irony of treating a news report as if it represnted quality analysis is not lost on me, particularly on this site.
I won't argue about the complexity involved with such a study however. If we were to assume that the LA times story were representative of unvaccinated children (a big if), I could just as easily argue that we have confounders in the other direction. For example, I might say that wealthier parents are more likely to be college graduates, and therefore older, increasing the likelyhood of having a child with autism. Or I might argue that wealthier parents are more likely to have careers similarly associated with autistic children, such as mathemeticians and engineers.
However, just because something is technically daunting, doesn't necessarily mean we shouldn't try to achieve it.
Studies are a nightmare to design, sure to be critiqued, and unlikely to settle anything in the public debate.
This may be partially correct, thogh I imagine you might be able to affect the public debate somewhat. What really bothers me about this line of argument is the implicit notion that we can never perform a study of the long term outcomes a more aggressive vaccine schedule; with literally dozens of vaccines in development are we really clever enough to keep on building on this policy without a true evaluation of its impacts?
- pD
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passionless commented on the article |
Hi Christopher Wyatt -
The unvaccinated are not, in any way, representative of the larger population. They do tend to come from higher-income, college-educated households. They tend to have better diets, better housing situation, and parents with more free time. To compare these children to a random sample of U.S. youth would be problematic.
Could you provide some links to validate this characterization of unvaccinated populations? I'm often seen it argued that we don't have enough unvaccinated children to make such a study work at all; I'd be interested to see some research indicating they have better diets, or indeed, parents with more free time than their vaccinated peers.
For example, the Madsen paper, a foundational paper in the case against MMR involvement seems to show no significant differences in socio economic status or maternal educational achievement.
Here is the table from Madsen that shows economic status:
http://content.nejm.org/content/vol347/issue19/images/large/03t1.jpeg
There is very little difference between the groups in terms of socio economic status of mothers education.
In Madsen, and every other study involving a single vaccine, the authors were able to successfully stratify based on socio economic and a variety of other factors. Why shouldn't we be able to do something similar based on a history of vaccination, as opposed to a single one?
Perfect is the enemy of very good.
I am generally in agreement with your assessment regarding the utility of a centralized data source for this type of analysis.
- pD
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passionless commented on the article |
Sorry for the H-T-M-L fail folks. My apologies.
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passionless commented on the article |
Hi John Ruch -
Your comments are well articulated and I find myself largely in agreement with you. Very nicely done.
Your concerns over creation of antibodies in the mother with unintended consequences may have profound implications for the upcoming plans to vaccinate everyone for H1N1; or indeed, past flu vaccinations depending on particular epitope used when creating the vaccine. Here's why:
In 2008, it was found that mothers of children with autism had antibodies to brain tissue with a very specific molecular weight.
Autism: maternally derived antibodies specific for fetal brain proteins.
Autism is a profound disorder of neurodevelopment with poorly understood biological origins. A potential role for maternal autoantibodies in the etiology of some cases of autism has been proposed in previous studies. To investigate this hypothesis, maternal plasma antibodies against human fetal and adult brain proteins were analyzed by western blot in 61 mothers of children with autistic disorder and 102 controls matched for maternal age and birth year (62 mothers of typically developing children (TD) and 40 mothers of children with non-ASD developmental delays (DD)). We observed reactivity to two protein bands at approximately 73 and 37kDa in plasma from 7 of 61 (11.5%) mothers of children with autism (AU) against fetal but not adult brain, which was not noted in either control group (TD; 0/62 p=0.0061 and DD; 0/40 p=0.0401).</blockquote>
Further research involving primates and the transfusion of IgG from human mothers into monkeys revealed startling changes in the offspring compared to monkeys whose mothers were given transfusions of IgG from mothers without these antibodies.
Stereotypies and hyperactivity in rhesus monkeys exposed to IgG from mothers of children with autism
To provide evidence for this hypothesis, four rhesus monkeys were exposed prenatally to human IgG collected from mothers of multiple children diagnosed with ASD. Four control rhesus monkeys were exposed to human IgG collected from mothers of multiple typically developing children. Five additional monkeys were untreated controls. Monkeys were observed in a variety of behavioral paradigms involving unique social situations. Behaviors were scored by trained observers and overall activity was monitored with actimeters. Rhesus monkeys gestationally exposed to IgG class antibodies from mothers of children with ASD consistently demonstrated increased whole-body stereotypies across multiple testing paradigms. These monkeys were also hyperactive compared to controls. Treatment with IgG purified from mothers of typically developing children did not induce stereotypical or hyperactive behaviors.</blockquote>
What does this have to do with the flu, and specifically H1N1? It turns out, in 1998, researchers found that some strains of influenza also cause creation of antibodies at that same molecular weight that react with brain proteins.
Influenza viruses induce autoantibodies to a brain-specific 37-kDa
Immunization of rabbits with certain H1N1 influenza viruses, including the neurotropic strains NWS/33 and WSN/33 and the New Jersey/76 strain, resulted in the production of autoantibodies to a brain-specific protein of 37 kDa that is present in various species, including humans</blockquote>
Of course, getting the virus would likely result in the same thing, and the specific protein structures seem to be highly influenza strain specific. Whether or not we have included these particular epitopes in previous concoctions of influenza vaccine is difficult to determine, though there may be tools at our disposal that I'm not competent enough to comment on.
One thing is certain, we have no analysis to guide us one way or the other. Some would prefer to keep it that way. Oh well.
- pD
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passionless commented on the article |Hi Nancy Nally -
Lupus was among the values that were analyzed; apparently a significant relationship was not observed.
- pD
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passionless commented on the article |Hello friends -
Nature is completely unconcerned with whatever societal constructs we have in place that reward putting off childbirth; it is a fundamental shift in the most basic biological operation in place across every animal species. To express surprize when we find that changing that operation, no matter how convenient, is not necessarily congruent with a the best outcomes is a stunning disconnect.
- pD -
passionless commented on the article |Hi Kristina -
Speaking of panic, I found a pretty startling paper this weekend. It turns out, researchers were able to permenantly increase the succeptibility to seizures in rats by the initiation of a single mild inflammatory response during critical developmental timeframes in an animal model.
Postnatal Inflammation Increases Seizure Susceptibility in Adult Rats
From the discussions section
The most exciting finding of the present study is that a mild inflammatory response evoked by LPS during a critical period of development causes a long-lasting increase in hippocampal excitability in vitro, and enhanced seizure susceptibility to the convulsants LI-PILO, KA, and PTZ in vivo. The latter effect was observed over a range of mildly inflammatory doses of LPS and was only evident if administered during the second postnatal week (P7 and P14), and not before (P1) or after (P20) this time. Importantly, inactivation of the proinflammatory cytokine TNF with an intracerebroventricular TNF antibody blocked the long-term changes to seizure susceptibility induced by LPS, whereas intracerebroventricular administration of rrTNF alone mimicked the effect of LPS on seizure susceptibility. These novel results indicate that a single transient inflammatory episode during development can modify the brain through a TNF-dependant mechanism, making it more susceptible to generate seizures in adulthood.
Amazingly horrifying stuff! Getting a single immune response during critical timeframes can cause sustained neurological outcomes into adulthood. It need not necessarily be a distinctly powerful response either. The researchers were able to get identical results by injecting inflammatory cytokines directly, and were able to block results by concurrently providing antibodies to the same cytokine. Despite the fact that all of the animals were exposed to everyday bacteria and viruses; all of which generated immune challenges to one extent or another, only those animals that got injections of bacteria cell proteins were adversely affected. At this point, can we not say with some certainty that there are some fundamental difference between everyday bacteria exposure and exposure that comes from a needle?
We also know that this doesn't have anything to do with the bacteria itself; the rats didn't get sick, they just got the protein walls of bacteria injected; essentially analogous to the bacterial proteins used during immunization to generate a memory of the bad bugs. If such a relationship existed between vaccination in humans and altered neurological outcomes, our existing suite of thimerosal research into the subject would be completely blind to this; as we have never bothered to measure the effects of the immune response, only the presence or absence of thimerosal. Likewise, MMR studies analyze only a snippet of our vaccine schedule, and indeed, one that exists at a relatively late timeframe of development compared to things like Hep B, DTAP, and Hib. You only learn about what you study, and the impact of stimulating an immune response at early ages simply hasn't been studied all that well.
It is also of particular interest that tnf-alpha is a critical component towards seizure generation, considering that we have several studies showing increased levels of tnf-alpha in the cns of those with autism, at least two studies showing that children with autism have been observed to generate increased amounts of tnf-alpha in response to stimulation by a vareity of proteins. Anyone interested could take a look at Elevated immune response in the brain of autistic patients, Elevation of tumor necrosis factor-alpha in cerebrospinal fluid of autistic children, Innate immunity associated with inflammatory responses and cytokine production against common dietary proteins in patients with autism spectrum disorder, and Preliminary evidence of the in vitro effects of BDE-47 on innate immune responses in children with autism spectrum disorders Other factors known to be markers of succeptibility to seizures, such as IL-10 and IL-1beta have been observed in ratios that are suggestive of additional risk to seizure in some studies. I could post those if anyone is interested, but this post is getting pretty lengthy as it is.
It just so happens that having a seizure early in life has been found to increase succeptibility to later neurologic injury by causing chronic glial activation. Glial activation links early-life seizures and long-term neurologic dysfunction: evidence using a small molecule inhibitor of proinflammatory cytokine upregulation.. Here researchers found that if seizures were initiated in young rats, the animals went on to display behavioral abnormalities, chronically activated microglia cells, and increased succeptibility towards epilepsy later in life. All three of these findings have parallels to what has been observed in autism.
Boiled down, we know that a single immune response during early life has been shown to result in permenant changes to brain functioning into adulthood in animal models. Those changes include increased succeptibility to exaggerated neural excitation, the consequences of which can include behavioral, physiological, and neurological changes similar to what is observed in many cases of autism. If an increasingly aggressive vaccination schedule with its consequent immune responses earlier and earlier in our children's lives is having a similar impact, we would never know based on our existing set of research.
We are doomed.
- pD
[PS - I am hopeful the embedded links will work; posting the entire string for pubmed references was just not rendering very cleanly.] -
passionless commented on the article |Hi Andrew DelAntonio -
"Do tendencies toward autistic neurology before a "regression" automatically invalidate the contention that the "regression" had an external trigger?""
Perfectly stated!
Of all of the false dichotomies in autism discussions, the notion that because someone is 'wired differently', this different wiring is the one and only thing that is affecting development, and that we can therefore ignore any external mechanisms, is one of the most widespread, and indeed, dangerous for our children. It frequently also smacks of extreme disingenuousness, considering how frequently the notion of an vaccine causation has been termed a quest for the 'simple answer' by the same people who would explain all autism behavior as 'different wiring'.
One of the big problems, of course, is that designing an appropriate epidemiological study to detect subtle, but none the less real, changes in development in already affected individuals as a result of external triggers is exceptionally difficult; and may well be beyond our means for some time (or forever). This is especially true of a condition with as much diagnostic ambiguity as autism.
Your well reasoned statements are welcomed here. Well, at least by me.
- pD
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