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More Talks for David Kirby

16 Jun

According to his HuffPo blog David is giving some more talks. This time not in the uninterested UK but in the NE US.

David says:

I sincerely encourage any and all vaccine-autism skeptics, critics, agnostics and cynics living in the northeastern US to please consider attending one of these talks, armed with all of your most pointed, difficult and critical questions.

I have some questions which, had family circumstances allowed, I would’ve liked to have asked David when he was over here. What I hope is that NE US skeptics who might be attending, will ask some of the following questions.

1) Given your book is subtitled ‘mercury in vaccines and the autism epidemic’, do you feel it has now been scientifically established that mercury in vaccines does not cause autism? If not, what peer reviewed journal published science touching on mercury in vaccines do you believe supports your books subtitle?

2) You say that during the talk(s) you will discuss ‘The Poling Case – in which the government conceded that vaccines induced autism in one little girl…’. Could you read out the statement from the government where they provide this concession – that vaccines induced autism – and also tell us where we can read it for ourselves, including the location of the source document.

3) Do you agree with Professor Sander Greeland (PSC witness for the families in the continuing Omnibus Autism Procedings) that if vaccines did cause autism and were responsible for ‘an autism epidemic’ that would be detectable in the epidemiological literature? If so, how do you account for all peer reviewed journal published science not establishing an autism epidemic?

4) IN 2005, you said in a FAIR Autism Media interview: ‘It’s now 2005…..[W]e should see fewer cases entering the system [cdds] this year than we did last year.’ – was that the case? If not, does this explain why you then said in a reply to blogger Citizen Cain: ‘if the total number of 3-5 year olds in the California DDS system has not declined by 2007, that would deal a severe blow to the autism-thimerosal hypothesis…..total cases among 3-5 year olds, not changes in the rate of increase is the right measure.’. Do you consider a severe blow has been dealt to the autism-thiomersal hypothesis?

5) Do you consider yourself a fair and impartial journalist on this issue? If so, could you explain how Wendy Fournier of the National Autism Association built your website? Could you further explain to us where you feel the vaccines-autism hypothesis falls down?

6) You state in your literature that a ‘former NIH director’ has stated autism is an epidemic. Is this Bernadine Healy, former member of The Advancement of Sound Science Coalition who are lobbyists for Phillip Morris and Lorillard Tobacco (amongst others) and claim that second hand smoking is not dangerous? Do you feel comfortable with her stance on medical science issues?

What about you Dear Reader? What skeptical questions would you like to ask – or have someone ask – David?

Omnibus Autism hearing: Dr. Lord on autism and regression

16 Jun

Dr. Catherine Lord is widely viewed as the world’s foremost expert on autism diagnosis. The Department of Justice lawyer who examined Dr. Lord in the thimerosal portion of the Omnibus hearing spent what seemed to me to be a very long time just going over Dr. Lord’s credentials and accomplishments as they are considerable.

I was listening to the recording of her testimony yesterday, again, and was reminded of how much I had learned from listening to Dr. Lord’s testimony about what is now known about the early months and years of autistic children. I already knew the basics of what she was explaining but there were some fascinating details that I didn’t know. Links to two audio clips that contain the following testimony are found at the end of this blog entry. Once again, I did the transcribing of the audio, and once again I’m guessing the Dept. of Justice lawyer is Ms. Ricciardella:

Ms. Ricciardella: Does any of your research or research of others support a distinct subtype of regressive autism?

Catherine Lord: No. I mean as especially as we have looked at the toddlers… it’s clear that even, even these very large studies where we felt like we were asking parents many, many questions in great detail probably do not get at what the essence of what happens in those early months because the changes are more subtle and our ability to observe them is so much dependent on the context. It dependent on when do you see a child and what are you looking for. So I think that that has that has moved us, and I think much of the field, toward a sense that there isn’t a regression or not a regression the question is the degree and type of worsening that occurs, how long it lasts and how many skills a child has before that occurs.

Ricciardella: Now in terms of the clinical outcome of a 5 or 6 year old with autism. Is there any marked difference in the clinical outcome of a child who had what I’ll term “early onset autism” versus a child who did indeed have regression.

Lord: Most studies have found no difference at all. The studies that have found differences have found these relatively small differences in verbal skills.

Ricciardella: Now you touched on earlier doctor that you are continuing to research the phenomenon of regression is that correct?

Lord: That’s right

Ricciardella: And you are conducting a longitudinal study. Is that correct?

Lord: That’s right.

Ricciardella: And what information is emerging from that study with regard to regression?

Lord: With that study we have been doing is seeing children who are at risk for having autism, either because they have a sibling with autism, so they may not have any behaviors associated with autism but they have a sibling and their parents are eager to have somebody follow them, or something has occurred, or something has has been seen, often identified by parents, but sometimes by a pediatrician, for example the child has had seizures in the first year of life and so someone is concerned that this child might develop autism.
And we see the children once a month, have parents fill out the same forms each month and then we do standardized assessment, a toddler version of the ADOS. So we do a standardized observation of the child’s social behavior with us and with the parents every month.

What has come out of this is that the trajectories are much less clear than we would have thought from retrospective descriptions years later of what the children are like, and when we have tried to sort that out, I think that there a number of implications. One is that different skills are changing at different rates and at different times. So that you have, for example, eye contact is typically getting worse for almost all of the children for from 12 month to 24 months. And social engagement responsiveness to someone trying to get the child to interact with them typically is getting worse in children who have autism diagnoses say by the time they are 2 1/2.

So those things are changing but they actually cycle back around, so they get worse for a while and then for some children they start getting better again.

We also have other skills, for example response to joint attention, or response to somebody pointing, or trying to get the child to look at something, and that for a number of kids gradually gets better even at the same time that some of these social skills are getting worse.

So I think what we’ve realized is it’s just much more complicated changes in development than we thought.

And that these things we used to think only happened in kids who had regressions are actually happening in almost everybody who has autism, because there are some children who look very different from typical children at 12 months, but those are few and far between, and in fact in our follow up study that is not necessarily predictive.

The kids who are not making eye contact at 12 months are not the most autistic kids at age 3. So many things change during that toddler period and I think our conceptualizations of what regression is are partly based retroactive trying to figure out what happened and didn’t happen, which is quite different than when we can see it happening right before our very eyes.

…
(the second audio clip)
Ricciardella: Doctor are you are aware of any evidence showing that the etiology of regression in autism is different from that in “non-regression” for lack of a better word.

Lord: No. And I think again that the idea that there aren’t these clear patterns makes it much harder to draw conclusions about etiology. Because basically could arbitrarily divide these kids up in millions of different ways. So far, … people have tried to divide them up and haven’t found differences in etiology. But it’s not even clear that we know how to divide them up, or that they can be divided up.

Ms. Ricciardella: Doctor before this litigation had you ever read in any published literature that thimerosal containing vaccines cause regressive autism only.

Dr. Lord: I had not.

Ricciardella: Are you aware of any study that has ever suggested that hypothesis?

Dr. Lord: No.

Ricciardella: Doctor did you review the report submitted by Dr. Marcel Kinsbourne in this litigation?

Lord: Yes.

Ricciardella: On page 14 of his report, he states that the, “late onset of the regressive subtype and the subsequent remission or relapses become more understandable if autism is due to disease than if it is the aftermath of congenital maldevelopment.” Do you agree with this statement?

Lord: No

Ricciardella: Why not?

Lord: There are many different disorders where the onset occurs later on. We have Huntington’s disease and schizophrenia and sickle cell anemia and all kinds of disorders… where in some cases we know are genetic, but which occur later on. So I think we can’t make a simple inference that because something emerges later that means that somehow someone has caught a disease or had some kind of particular environmental event that caused it.

Ricciardella: Dr. Kinsbourne also draws a distinction between what he terms as classical or congenital autism and regressive autism. Is this a proper distinction?

Lord: I think the term congenital autism means nothing. Because, I mean, as I said it’s a developmental process. We can’t diagnose autism in a brand new baby. And so in all cases something is developing that would lead us into autism. So to make this distinction between congenital and regressive is a false dichotomy.

Ricciardella: … Dr. Kinsbourne has also describe what he terms his “over-arousal model” as an explanation for autistic behavior. Does his over-arousal model accurately describe what is known about autistic behavior?

Lord: I don’t believe so, I mean the over-arousal model has been around for 40 or 50 years and used to describe many different disorders. I think one of the hard things is that it’s becomes very circular. And children with autism do respond to being over-stimulated as do many other kids, and children with autism may respond in more conspicuous ways, and may have a lower threshold. But the problem is that often the behaviors are used to say that a child is responding by over-arousal, for example by flapping or getting very physically excited, or distracted, are the same behaviors that occur when the child is under-aroused. You know, we can get children who have a lot of self-stimulatory behaviors to do these behaviors by putting them in a situation where there’s nothing to do. We also see children do these behaviors when they are very happy or when they are not so happy. So that the behaviors that used to define over-arousal are behaviors that occur in many different contexts.

Ricciardella: Thank you. That’s all I have.

…

PSC Lawyer, Tom Powers: … I do have some questions to ask you as you might imagine based on the report you filed and the testimony you gave today. …Your testimony … is that there’s no phenotype for regressive autism. … Regression within autism is not a distinct phenotype with in autism spectrum disorder, is that correct?

Lord: Yes.

Powers: You’ve also describe regression in autistic children as a striking phenomenon. … How would you describe the difference between a phenotype and striking phenomenon?

Lord: My point about the striking phenomenon is that it is a remarkable experience to watch a child who has been able to do things not be able to do those things. Or to watch a child who has been relatively socially engaged become less engaged and be more and more difficult to engage or attract. But I think that is different from a phenotype because a phenotype implies that there are a cluster of behaviors that are associated with each other, and that there’s something unique about that cluster of behaviors. I think regression is a real phenomenon in autism, but there’s a continuum of regression. … And we can create a phenotype, I can say, well I’m only putting kids who lost words into this group and I’m going to call it the Lord phenotype. But there has been no, nobody has been able to show that that phenotype is associated with anything other than the characteristics which I used to define the phenotype.

Powers: And that would be because, as I understand it, is because autism diagnostically is entirely a symptomatic diagnosis that is there’s not a biomarker … is that correct?

Lord: It’s not, the problems with defining the phenotype aren’t because autism is defined by purely by behavior, it’s because we haven’t been able to find an association between any of these particular phenotypes that people have pulled out, and the ways in which people have pulled out the phenotype.

I realize now that if my own (now adult) ASD child been a part of Dr. Lord’s baby siblings study that they would have been able to document a “regression” because, basically all autistic children regress, depending on how strictly you define “regression”. I remember my ASD child as an infant apparently losing the ability to respond to the sound of his/her name, and then regaining that ability. Looking back, I doubt that I could isolate the dates when this “regression” started and when it ended, since is was just aggravating to me at the time and not something I brought to the attention of our family doctor.

(Edited to fix some errors my transcribing. Also, I just listened to the second clip I uploaded to boomp3.com and realized that it is a little shorter than I thought.)

Click here for the first clip.

Click here for the second clip.
For some reason I can only embed one “player” and it must be at the very end of the post. This plays the second clip:
http://static.boomp3.com/player.swf?song=by6i9hwl7_0<a style=”font-size: 9px; color: #ccc; letter-spacing: -1px; text-decoration: none” target=”_blank” href=”http://boomp3.com/listen/by6i9hwl7_0/lord-2″>boomp3.com</a&gt;

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Mitochondria and autism:time to recalibrate

6 Jun

We all have heard a lot about mitochondria and autism in the past few months.    This message has been dominated for the most part by David Kirby.  Someone got some of the confidential court documents to him, and he leaked one to the public, and discussed another in a news story. 

So, it seems like we are stuck with the idea that “there are a lot more Hannah Polings out there” and “20% of autistics might have mitochondrial disorders” and “1 in 50” (or some such number) “are at risk.” Since the Polings aren’t releasing their information, the government isn’t releasing it’s information, the reasearchers can’t talk and haven’t submitted their paper yet,  we are sort of stuck.  There just isn’t any other specific information out there on people with mitochondria issues and autism.

Is this really the case?

As it turns out, no, this is not the case.  There are a number of descriptions of people with mitochondrial disorders and autism.   And, guess what, they present a different story than we have been fed so far.

We all know about the case study on Hannah Poling.    But, in terms of how many kids (and, presumably, adults) have mitochondrial disorders come from Dr. Oliveira’s group in Portugal.  People tend to use the estimate for autism+mitochondrial disorders from his work (about 4%), but they don’t look closely enough to see that he actually describes a few details on 11 individuals.  In addition,  Dr. DiMauro’s group discussed five individuals in their paper. Gargus of UCI discussed three brothers as well.  Most recently,  Tsao and Mendell discussed two individuals in this paper.

Total it up, and we have information on 22 individuals to consider when we ask the question, “what does autism look like in mitochondrial energy challenged individuals”?

Another way to put it, does mitochondria+autism=Hannah Poling?  Did they all undergo regression ?  Of those that regress, did they all appear normal before regression?   I want to know, because this is what we are being told: autism with mitochondrial disorders/dysfunction result in kids who look normal and then regress.

We get this from David Kirby, who makes statements like:

“That would mean some 190,000 Americans with mito issues who, after normal births and development, suddenly stopped talking and regressed into autism following some kind of childhood fever.”

He seems to be getting this from statements in Hannah Poling’s Rule 4c reports and discussions with the researcher who made them.  Statements (from the Rule 4c report) that describe Hannah Poling as having:

“an etiologically unexplained metabolic disorder that appear[ed] to be a common cause of developmental regression.” He continued to note that children with biochemical profiles similar to [Hannah Poling] develop normally until sometime between the first and second year of life when their metabolic pattern becomes apparent, at which time they developmentally regress.”

David Kirby also uses comments from the researcher stating that he is working on a study of 30 kids similar to Hannah Poling who all underwent regression.  In that as yet submitted study, only Hannah Poling is considered a definite case of vaccine injury.  There is another child whose regression did occur within 7 days of a vaccination.  Somehow, this “possible” case of vaccine injury morphs into a “definite” in the later sections of David Kirby’s blog piece.   I also find it odd that David Kirby claims that people are already preparing to challenge the idea that only 2 of the 30 are possibles.  This, even before the paper is submitted!

Given all the qeustions that are raised, I’d like to know more about what kids with mitochondrial disorders and autism look like.  Don’t you?

The Kids

Let’s first take a look at the DiMauro group paper.  DiMauro’s group discusses 5 kids.  Of those patient 5 had a fever at 14months and showed regression. “At 14 months of age, she had a viral illness with high fever, encephalopathy, regression of previous acquired skills, and significant acidosis. She gradually recovered and continued developing slowly.” Sound like Hannah Poling?  Consider however that she showed developmental delay by 6 months (along with a number of other problems). She did not appear “normal” as Hannah Poling is described before her regression.  Another big difference: Patient 5 had clear mitochondrial disorder.  She has 70% mtDNA depletion in a biopsy sample.  While she is described as “gradually recovered”, she never spoke and is significantly challenged in many areas.

And that is the closest example we get to Hannah Poling in these studies

Patient 3 in the DiMauro study is described as having “…neurologic deterioration during intercurrent illnesses and recovered gradually over several weeks.”  However, he doesn’t fit the “Hannah Poling” mold as he had clear impariments since early infancy.  

The other three patients in the DiMauro study did not have any mention of regression.   There is an Aspie, a PDD kid and a kid with excellent visual/spacial skills but delayed speech and language.

OK, so the DiMauro study doesn’t have “Hannah Polings”.  What about Oliveira?  He describes 11 kids with possible, probable or definite mitochondrial resperatory chain (MRC) disorder.   Of these 11, only 1 is noted as having an “autistic regression”.  (No, it is not noted if this was coincident with vaccination).

One interesting fact in the Oliveira paper: they were studying older kids.  All the kids (with mitochondrial disorder or not) were in the 11-14 year old ages.  Why do I find this interesting?  Because I read a lot of people postulate on the web that Hannah Poling no longer shows “biomarkers” for mitochondrial dysfunction and, thus, thet disappear with age.   People are trying to say, essentially, “A lot of older kids were probably ‘Hannah Polings’ but their tests won’t show mito dysfunction because they are too old” as in, “they were vaccine injured even though we have no proof.”   Since these same people tend to rely on Oliveira’s data to estimate the prevalence of mitochondrial disorders in autism, it seems a bit of a stretch.

In our search for more “Hannah Polings”, we seem to be striking out.  But, there are still two more papers to consider.

Tsao and Mandell describe two patients.  Both were globally delayed from “the early months of life”.  Neither child developed expressive or receptive language, and one never sat up or walked.  Again, these were not “apparantly normal” kids who went through regressions.

Gargus and Imtiaz describe three children, all siblings, who have “a weak mitochondrial defect and a recognized 15q inverted duplication” (we’ll discuss some genetics in another post). The older had poor eye contact and echolalia from early infancy. He developed stimming behavior at age 3 and, sadly, died after a one-day illness at age 5.

OK, sidetrack here.  The authors describe this as  “At age 5, after a 1-day illness, he died suddenly with respiratory arrest and shock, characteristic lethal presentation of a carnitine-deficient fatty acid oxidation”.  In other words, illness can be fatal to the energy challenged.  This is precisely why doctors recommend vaccinating people with mitochondrial disorders, or at least, their close family members.

Back to the paper, the younger twin bothers (monozygotic, monochorionic) hit their developmental milestones in their first year. However, they showed language delay and limited eye contact. One had a near-SIDS event at 4 months, and was the more “severely affected” of the two.

So, the kids in the Gargus study aren’t “Hannah Polings” either as they didn’t regress and showed signs of being “not normal” from early in life.  Now, I suspect people will latch on to the “near SIDS event” at 4 months and suggest that is connected to 4 month vaccines.  No mention of vaccination is made in the paper.

Discussion

There is a huge variation in the presentations of the individuals in the above studies, leaving one to ask, “what can we take away from all of this?”.   One answer is that the huge variation is precisely one of the take-away points: if you think that autism is a spectrum disorder, you shouldn’t be surprised that the mitochondrial energy challenged present as broad or broader of a spectrum.

Second, everyone keeps looking to mitochondria+autism=”must be regressive”.  It just isn’t so.  The “30 child paper” will apparantly concentrate on regressive kids, but the other papers already published do not.

The majority of the individuals described in the DiMauro, Oliveira, Gargus, and Tsao papers show no regression. Of those who do regress, they were not “developing normally” before the regression.

The Bottom Line

The bottom line: Hannah Poling does not appear to be a good representative of the kids with mitochondria issues and autism.   The individuals discussed in papers other than the Hannah Poling case study are very different from her.  Even the other kids in the paper that will concentrate on regressive autism are mostly not like her in one major aspect: they didn’t suffer vaccine injury.

Does that mean that we can’t and shouldn’t learn from Hannah Poling?  Absolutely not.  But, we need to have experts look at and understand all the kids with mitochondrial disorders and autism.  We need this to be a scientific investigation to arrive at real answers, not a series of public relations events to shape the public view.

In honor of the “Green our Vaccines” rally: facts from the Omnibus Autism hearing

4 Jun

The lawyers for the parents in the Omnibus Autism hearing (thimerosal portion) have been claiming that one cause of “clearly regressive” autism is thimerosal at vaccine doses, even the dose of thimerosal in one vaccine. One of their supports for this odd claim is that whatever DAN! docs do to help their patients deal with “mercury toxicity” makes the kids less autistic or healthier or something. It’s all pretty vague. Dr. Mumper spoke confidently of what chelation had done for autistic kids and the boys under discussion in this portion of the trial were chelated multiple times in spite of never having shown any elevated mercury levels in their urine tests (even their chelated urine mercury levels were what would be expected for a typical person being chelated).

So what about this claim? If you do any old treatment and you think it makes the patient better in some perhaps very vague, undefined way, is this evidence of anything? Eric Fombonne, expert in autism epidemiology and clinician who works with autistic children and adults says, “Mais non.” Well, actually he said the following

Ms. Ricciardella (?): Are there standards that are used by the medical and scientific community before a treatment is recommended?

Dr. Fombonne: Yes, there are different kinds of standards to evaluate the efficacy of interventions the rule is to rely on the evidence that is the most robust that stems from a randomized clinical trial which are usually double blind placebo controlled for this method there is no study which has been relying on this method for the practices and treatment that have been discussed this morning [by Dr. Mumper]

Ms. Ricciardella: Do you have experience with randomized clinical trials?

Dr. Fombonne: Yes actually, I do. I started my research career and did my thesis my first two publications, I think, have to with randomized clinical trials.
And I am currently, we have tested the efficacy in a randomized clinical trial of a treatment which is not which is not biomedical which is a language based intervention to improve communication skills in young children with autism.
And we did a randomized clinical trial. It’s a 12 weeks treatment and we allocated at random parents and their children to a group where they were immediately treated with this intervention and there was a waiting list for the control group and 36 families in each group so it’s quite powerful in terms of it’s statistical power.
I just wanted to share with you my, my, our findings that it’s an intervention that everybody likes, eh and when we did the trial we had all the impression that it was actually achieving some positive results. The parents were happy and were convinced that the methods were showing some efficacy, and we did too.
But as we did the study well we didn’t analyze the data before the data were finally collected and when we broke the blind and looked at the results and there is no difference between the two groups–which is breaking my heart, in some ways–but this also shows that our experience as clinicians and as parents can be misleading.
And I think the field of autism has been replete over the last 30, 40 years of treatments and interventions that practitioners engage in when the parents apply to their children. And the story has been that when you take these practices and put them to rigorous empirical test, that of a randomized clinical trial, usually the story is much more disappointing. And a case in point is the secretin trial.

I don’t know if it was Ms. Ricciardella asking the questions, but that’s my guess. After this portion he explained about how many parents and clinicians from all over the world had been so excited about secretin when it became popular, and how for about 5 years clinicians used it and had some great stories to support it’s use. But when the double blind, placebo controlled studies were completed it turned out to be no more effective than placebo. And if someone tells you that there were “responders” you can tell them that there were “responders” to the sterile-saline injections, too, so why not just go with those, since they are cheaper than secretin? Besides which there’s no reason to expect that secretin (much like sterile saline) ever would do anything for the symptoms of autism. Further, the Mead boy got one or two injections of it but the family didn’t continue with them, apparently they weren’t so great for that child. Perhaps they decided to go with worm eggs, maternal fecal implantation enemas or even Eskimo oil (possibly purchased from Dr. Green’s office) instead.

http://static.boomp3.com/player.swf?song=bjsb2fd<a style=”font-size: 9px; color: #ccc; letter-spacing: -1px; text-decoration: none” target=”_blank” href=”http://boomp3.com/listen/bjsb2fd/fombonne-randomized-control-trial”>boomp3.com</a&gt;

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Green Our Vaccines Eve – Dr Jeffrey Brent

3 Jun

On the eve of the ‘green our vaccines‘ rally, I thought it might be interesting to share a ten minute or so segment from the Autism Omnibus.

Giving evidence is Dr Jeffrey Brent:

Jeffrey Brent, M.D., Ph.D. is a sub-specialty board certified medical toxicologist. He is an active member of the medical school teaching faculty and is an attending physician on the clinical pharmacology/toxicology consultation service at the University Hospital. Currently he holds the rank of Clinical Professor of Medicine at the University of Colorado Denver. Dr. Brent has a long list of publications, virtually all related to clinical toxicology. He is senior editor of Critical Care Toxicology: The Diagnosis and Management of the Critically Poisoned Patient and serves as Editor-in-Chief of Toxicological Reviews, a major international state-of-the-art review journal devoted to human toxicology.

Dr. Brent is the former President of the American Academy of clinical Toxicology, the largest organization in the world devoted to this discipline. Currently he serves as a member of the Board of Directors of the American College of Medical Toxicology.

We pick up testimony around five and half hours into day 15. I’ve transcribed directly from the audio, so please forgive minor errors. Emphasis is Brent’s, inserts are marked [].

Q: Dr Mumper discussed today some key aspects of chelation therapy….as a medical toxicologist do you see any reason for the chelation to remove mercury from either Jordan King or William Mead in these cases?

Absolutely not….there is no test in medicine that is more valid for for assessing mercury toxicity than an unprovoked urine mercury concentration.

[For Jordan King and William Mead]…their unprovoked urine concentration is exactly in the normal range.

On the other hand, they have been chelated. And the justification for that chelation with regard to mercury comes from what you see in the right hand column where in both cases, 4 out of 5 provoked examples have been…uh…increase urine mercury. Well, you’re supposed to have increased urine mercury with provoked examples! Therefore there is absolutely no indication based here or anywhere else I saw in the medical records that suggest that there is any mercury effect in these children and therefore that was absolutely no reason to chelate them for any mercury related reason.

Q: Dr Mumper also testified today to seeing an increase in lead levels in children and that chelation may help with the adverse effects from lead. Is there any scientific or medical basis for that statement?

It is true that chelation therapy is the appropriate therapy for lead toxicity. However, the records do not reflect any lead toxicity in the case of either of the two children at issue here, Mead or King. Neither of them have had an elevated blood lead level and a blood lead level is the ‘gold standard’ test for lead toxicity. Because, contrary to testimony that was given earlier today [Dr Mumpers – KL], blood lead remains elevated and it will be elevated for years in children that have lead toxicity. It equilibrates with tissues and if there’s high tissue burden there will be high blood burden.

Q: So you disagree with Dr Mumper that the blood levels would only test for acute toxicity?

Thats absolutely wrong. So there was no indication therefore for treating these two children with a chelator for any lead effects.

Q: Is there any other accepted tests for lead toxicity, other than blood?

Blood is the ‘gold standard’ and there are no other accepted tests in medicine now that we can routinely get blood/lead levels.

Q: Was there anything about the levels you observed in the medical records [of either King or Mead – KL] post chelation that would cause you to think that these were extraordinarily high levels of excretion upon chelation?

No. You always expect to see levels in the urine bump post-chelation. It would happen to any one of us. There are no validated reference ranges post chelation, thats why they’re not used in medical practice – there is no valid way of using them and in fact if you look at these two children they had mild increases in urine/lead excretion as I recall but they were nothing different than what you would normally expect to see if you gave a chelator to them.

Q: And you’ve given chelators to a lot of children?

I’ve chelated a number of children.

A: There’s nothing here that would be out of the ordinary – from your experience – absent, even in the absence of a standard reference range.

Well, in truth we don’t (?) urine/leads because the ‘gold test’ is blood/lead so I haven’t looked at many urine/leads in children that I have chelated. So I can’t speak to that in my experience. But I have seen a number of patients now come to me because of these ‘doctor’s data‘ type of laboratories which are based on urines – chelated urines – and they always have high leads in their chelated urines and I tell them ‘well, lets just do the gold standard test, lets get a blood/lead level and so far, 100% of the time they’ve been normal.

Q: Are the post chelation mercury levels in either of these two boys in excess of what you would see…or in excess – I take it there’s no standard reference range…?

No standard reference range. You do tend to see small increases, they’ve had minor increases in their mercury excretion over the reference ranges over the non-provoked. It was certainly not very dramatic and certainly well within the range of what you would expect to see. For example if you look at the studies that I cited where they were studying chelators and they were looking at the effect of the chelator on urine/mercury excretion.

Now thats a valid time to do a post chelation mercury – if you want to study the effect of the chelator. And if you look at the normal controls in those studies, when they give them a chelator you do see some increase in the urine/mercury excretion and its a moderate increase and its really not very different than what we saw in these children [King and Mead – KL]

Q: Have you chelated children for lead or mercury toxicity?

Actually, both.

Q: And under what circumstance did you chelate for mercury toxicity?

I’ve had a number, but probably the most common and the most dramatic relates to the fact that I live in Colorado and in the Rocky Mountain area there people who are still panning for Gold…..[they extract the gold from ore using liquid mercury]…and to get rid of the mercury [afterwards] they will heat it. In their house. In their kitchen. When you volatilise mercury like that [it gets into the air]….and I’ve had a number of families have become profoundly mercury poisoned.

Q: So when Dr. Mumper said that she saw ‘mobilisation’ of heavy metals by chelation and then assumed that the chelation was beneficial – do you agree with that statement?

No, I think what you see is – you give a chelator, you look in the urine and there’s more than in the non-chelated reference range is for the metals in the urine and its what you would normally expect. It tells you nothing about mobilising stores of heavy metals.

Q: Dr Mumper also talked about supplements. And those supplement were referred to increase Glutathione to treat mercury toxicity. Do you agree that that therapy is warranted in cases?

Glutathione? No. Supplemental glutathione to treat mercury toxicity has no validity at all.

The Bernadine Healy Card

31 May

Last month, ex NIH leader, Bernadine Healy came out of her semi-retirement to weigh in on the autism/vaccine hypothesis:

….the rise of this disorder, which shows up before age 3, happens to coincide with the increased number and type of vaccine shots in the first few years of life. So as a trigger, vaccines carry a ring of both historical and biological plausibility.

It was a credulous article designed, I suspect, to have a bit of a snipe at HHS – currently embroiled in the Autism Omnibus. Why do I say that?

Well, being a UK citizen I’d never heard of Bernadine Healy so I did a bit of looking around to see if I could adequately explain to myself why such a luminary would say such plainly silly and unscientific things.

It seems that:

on 10 Feb [1993], Healy, who is known for her bluntness, went to her new boss, Health and Human Services (HHS) Secretary Donna Shalala and asked about her future. Shalala apparently matched Healy for bluntness. “She let me know it wouldn’t work out in the long term.” Said Healy.

So possibly there is some lingering resentment towards HHS. Who knows. It seems doubtful that this would entirely (if at all) explain Healy’s decision to parrot pseudo-science but – people do silly things sometimes.

What I found fascinating was that this is not the first time Healy has taken an active role in direct opposition to science and the scientific process:

…..patients are forced into a one-size-fits-all straitjacket…..EBM [evidence based medicine] carries its own ideological and political agenda separate from its clinical purpose.

Dr. Bernadine Healy, a senior writer for U.S. News & World Report and former director of the National Institutes of Health, falsely claimed that “several” neurologists who “evaluated” Terri Schiavo determined that she had “a functional mind” and was “minimally conscious.”

Dr Bernadine Healey, former director of the National Institute of Health said, “Blenderizing these diverse trials into one giant 232,606-patient-strong study to come up with a seductively simple proclamation is just silly….”

That latter was Healy’s attack on a study that highlighted the dangers of vitamins.

So we can see that Healy has a history that is peppered with leanings toward a credulous approach.

It also seems that she is first and foremost a politician, willing to sacrifice her scientific credibility to support her party (she is a Republican):

Healy was appointed director of the National Institutes of Health in 1991….when Healy assumed control, the agency was beset with problems…..[s]cientists were leaving in record numbers because of…..politicization of scientific agendas (a prime example was the ban on fetal-tissue research because the Republican administration believed it encouraged abortion)

Healy had, at that time expressed support for fetal-tissue research:

….she had been a member of a panel that advised continuation of fetal-tissue research, her appointment was also seen as a move away from politicized science.

So, it must’ve come as something of a shock to NIH scientists when:

….she lobbied against overturning the Bush Administration’s ban on fetal tissue research, despite her previous support for such research.

She also had to defend herself against charges of mishandling a scientific misconduct case:

Healy demanded that OSI (like internal affairs for the NIH) rewrite a draft report that found misconduct on the part of Popovic. The OSI report also severely criticized Gallo.

“When her order for a rewrite was refused, Dr. Healy replaced the chief investigator [Suzanne Hadley] with one more malleable,” the subcommittee report said. The resulting OSI report was “watered down,” the subcommittee document said.

……….

In 1992, the National Academy of Sciences’ panel completed its investigation and produced a report critical of Gallo.

Healy chose to ignore the findings of the NAS panel and commissioned her own ad hoc committee of top NIH scientists, whom she called her “wise men,” the report said. Healy required the members to sign a secrecy agreement.

(Full story also here).

Maybe the biggest question mark against Healy’s scientific credibility and ability to be impartial as this. She was a member of The Advancement of Sound Science Coalition:

The Advancement of Sound Science Center (TASSC), formerly the Advancement of Sound Science Coalition, is an industry-funded lobby group which promotes the idea that environmental science on issues including smoking, pesticides and global warming is “junk science”, which should be replaced by “sound science”.

Notably, TASSC promote the interests of tobacco companies:

Initially, the primary focus of TASSC was an attempt to discredit research on Environmental Tobacco Smoke [passive smoking] as a long-term cause of increased cancer and heart problem rates in the community — especially among office workers and children living with smoking parents. It subsequently advanced industry-friendly positions on a wide range of topics, including global warming, smoking, phthalates, and pesticides. Later still, they extended the role of TASSC to Europe using Dr George Carlo. TASSC used the label of ‘junk science’ to criticise work that was unfavorable to the interests of its backers.

TASSC’s funders included:

3M
Amoco
Chevron
Dow Chemical
Exxon
General Motors
Lawrence Livermore National Laboratory
Lorillard Tobacco
Louisiana Chemical Association
National Pest Control Association
Occidental Petroleum
Philip Morris
Procter & Gamble
Santa Fe Pacific Gold
W.R. Grace

More can be found here.

So, all in all, I am disposed to not trust the words, or ‘beliefs’ of Bernadine Healy very much. Anyone who campaigns against the dangers of passive smoking to children or who is prepared to block science they allegedly once supported when it is politically expedient doesn’t seem that good a judge of what constitutes good science.

Dr John Briffa is wronger than wrong on vaccines and Hannah Poling

30 May

Media nutritionism is a crowded field, but John Briffa has managed to carve out a niche for himself. And Briffa’s take on vaccines stands out, even among media nutritionists. JDC takes a broader look at Briffa’s take on autism, but I’m going to focus on Briffa’s claim that:

the US Government recently looked at such evidence relating to just one girl (Hannah Poling) and concluded that vaccination had contributed significantly to her autism.

As readers of this blog can probably spot, almost every word of that statement is inaccurate: impressive work, indeed. Continue reading →

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Dean Jones PhD- oxidative stress and the Omnibus Autism hearing

28 May

Dr. Dean Jones testified on the topic of oxidative stress in the morning of Day 9 of the Thimerosal-only portion of the Omnibus Autism Proceedings hearing. Dr. Jones is a professor at Emory University. He received a Nobel fellowship to do research in molecular toxicology in Stockholm. He is currently a peer reviewer for the journals Toxicology, Nutrition, Science, and Nature Methods. He also has been the chair of a “study section” at the NIH, as such it was his job to oversee peer review process of grant applications.

He is the recipient of grants to do research. One of his major grants for looking at oxidative stress in cell nuclei. He is one of the asst. program directors for a $22 million award from the NIH for translational research. Dr. Jones oversees two labs at Emory, one is his own research lab focusing on redox chemistry. He lectures on nutritional biochemistry, pharmacology and metabolism and has written many articles on sulfur metabolism, and he estimates that he has written over 100 original research articles on oxidative stress.

Dr. Jones testified that sulfur is the 5th most common element in biological systems and sulfur is ubiquitous in living systems. All this sulfur beneficially affects how our bodies deal with heavy metals.
The following is more of my rough transcription of what Dr. Jones said as he was examined by Ms. Renzi. Words in parentheses are my summary of what was said, the rest is more of an attempt to get what was said word-for-word. Keep in mind, there is a lot more than this. I haven’t tried to transcribe all the testimony by Dr. Jones wherein he explains a lot about what Glutathione is and details the reasons for his conclusions about Dr. Deth’s hypothesis and the idea that thimerosal in the doses contained in the vaccines given to even the tiniest babies ever could do anything vaguely like harm:

Ms. Renzi: …. Glutathione does more than just detoxify heavy metals, is that correct?

Dr. Jones: Glutathione has a very important role in metabolism. It is the major thiol. (It’s a major) sulfur containing chemical…. maybe 1/3 of the total sulfur (in the body is found in glutathione) the most abundant thiol.

Ms. Renzi: What is the role of glutathione in the body?

Dr. Jones: … The one that has probably received the most attention in the past 50 years is the function of glutathione as an anti-carcinogen. Glutathione is used to counter reactive chemicals that would otherwise cause mutations in the DNA and cause cancer. A little over 50 years ago it was recognized that many chemicals we are exposed to are activated in the body to reactive chemicals, the most central way that the body gets rid of these is by reacting these with glutathione. Glutathione is the most anticarcinogenic chemical we have in our body.

It is also an antioxidant….Hydrogen peroxide is produced in the body all the time, about a pound a day of oxygen consume, about 1% of that is converted to hydrogen peroxide– a large portion of that is eliminated by glutathione.

…there is a coenzymatic function of glutathione. One of the main ways we get rid of formaldehyde is through a catalytic action, involves using glutathione as a catalyst. The glutathione is not used up (in doing that).

Ms. Renzi: Deth’s hypothesis is thimerosal containing vaccines disrupt sulfur metabolism and causes autism. …

And Based upon your knowledge and research in the area of sulfur metabolism and glutathione do you have an opinion as to whether thimerosal at the doses administered in thimerosal containing vaccines can significantly affect sulfur metabolism.

[This is about the 22 minute mark.]

Jones: What the data show is that the dose of thimerosal (under discussion) will not affect in a significant way, sulfur metabolism.

Renzi: Why is that?

Dr. Jones: (He gives the amount of sulfur in a human body. He gives estimated total body glutathione.) 1 millimolar (is) 1000 micromolar. (He gives the amount of sulfur in sulfur containing foods a typical baby would eat: 500 micromoles per kg of body weight.) … We have a huge total thiol content in the body.

Ms. Renzi: (In your scenario that compares sulfur exposure to mercury exposure from vaccines,) how did you calculate the thimerosal dose?

I took the cumulative dose (that) was 180 mcg. I rounded it up (apparently to 200 mcg). (I calculated it as if) that were given all at once to a 1kg child, so that would be a two pound child. This is a very conservative way to look at this, the exposure would probably be six-fold lower than this. If you calculated it this way that would be equivalent to one micromole per kg of body weight. The more realistic would be 0.1 micromole per kg. The cumulative dose of thimerosal is considerably less than that daily intake of sulfur amino acids would be… 2000 fold lower than the total body thiol.

Renzi: Do food items also contain reactive materials that our body use glutathione to deactivate.

Johnson: … if we look at the amount of reactive materials in a 8 oz glass of 2% cows milk that number is 21,700 nanomoles. If you assume that a child would consume 4 oz in a serving would be the equivalent of 10 micromoles. One 4 oz serving would contain more than 10 times as much of the reactive materials (as is in the estimated 200 mcg of mercury from thimerosal.)

Renzi: The amount of reactive materials (in those common foods are) above that cumulative dose in a thimerosal normally administered over a 6 month period.
…
(1 hour 36 minutes)

Dr. Jones: (summing up) … at 4 critical sites in this scheme the pieces don’t fit together that that’s a plausible hypothesis and plausible mechanism that changes in sulfur amino acid is a cause of autism

Ms. Renzi: So, the data that Dr. Deth presented actually in formulating his hypothesis doesn’t support his hypothesis is that correct? …

Yes. … Slide 28 is Dr. Deth’s slide 41… What I think that the data show, uh, you know, to me fairly clearly in, you know, that that there really is not appropriate evidence, this is just not, the data, saying that the dose of thimerosal is enough to alter the sulfur metabolism, this is not, not established by the data. And similarly if you had a perturbation in the sulfur even if a very minor effect happened it really wouldn’t be of a magnitude that one could consider that that is the cause of oxidative stress. I think you have to conclude that this is not established, either, the second point. And finally then if you look at the subsequent aspects of that the variations, the oxidative stress, there’s a normal variation in oxidative stress and that the magnitude of effects are really not appropriate, and in fact the mechanisms that he’s drawn can not account for changes in the methionine synthase activity and the in vitro data he’s provided without in vivo data supporting it, really you have to conclude that this step in the pathway is also not established. That is the oxidative stress to the methionine synthase.

…And so from that summary, from my standpoint there really is no plausibility to this hypothesis at all. It’s what I would consider a, a scaffold without a building. there’s a lot of components to it but it really doesn’t have the strength, solidity of being solid science, of being reasonable or plausible. …

So, this is my final slide, slide 29 … I think in terms of the overall, you know, my overall consideration of this:

I think the point one is the cumulative dose of thimerosal is too low to cause the magnitude of effects on glutathione metabolism that would be required to conclude that there’s any likelihood of effect there. It’s not plausible.

Point two, the natural variations are greater than one would expect from the low dose of thimerosal that are present in thimerosal containing vaccines.

The third point, … if you did have an effect, you’d have to conclude that the low non-toxic dose would probably be protective, because that would be activating protective mechanisms that ubiquitously occur.

Fourth, the in vitro studies show that thimerosal disruption of metabolism is probably occurring under non-specific conditions–ones that were you simply have the cellular conditions set up so that you are going to be disrupting lots of things–that you are not going to be giving any specificity. That’s simply because they are at irrelevant concentrations, irrelevant amounts.

I have to conclude that the data really don’t support this hypothesis that there is an effect on the glutathione system that’s causing oxidative stress and that that’s the cause of autism.

Ms. Renzi: Thank you.

Special Master Vowell (addressing PSC lawyer, Mike Williams): Are you prepared to begin cross examination or would this be a good time for a break?

Mr. Williams: I would very much enjoy a break, if that would be alright with you.

One can only imagine how much Mr. Williams needed that break.

I’m running out of adjectives to describe how thoroughly the dead parrot hypothesis has been demolished by the Department of Justice’s experts up to this point. I would not like to be Dr. Deth or even Dr. Wally. There work in cell cultures was described as basically not worthy of publication and it puzzles experts on how it got past peer review. Even the Petitioner’s Steering Committee’s own experts are doing serious damage to their own hypotheses from my observation, via sloppy testimony, bad evidence, citing what amount to speculative essays by absolute non-scientists “published” in non-peer reviewed magazines, experts with unusual ties to unusual funding sources, shaky sources for “data” in testimony that most would consider plagiarized because the real source was not cited, self plagiarism from previous reports, inflated–bordering on fabricated–credentials, extreme lack of expertise in the area where they are testifying, lack of preparation, and a lack of agreement and coherence between the petitioners own experts’ stories. Oh, and they keep bringing up new stuff, new ideas, new papers at the very last minute, which is just not done.

And … I have to ask, if the PSC lawyers were confident in what they were presenting, would they really need to be insulting to the experts for the DoJ? Seriously. Dr. Jones started to get impatient with the way Mr. Williams was badgering him on the cross examination and acting as if he, Jones, should already know what was in a paper that Mr. Williams just handed to him a minute previously, one of those last minute introductions of “evidence” that is totally out of bounds, normally. What I keep hearing on and off from the PSC lawyers, is a tone of voice that implies, “You’re just an idiot, aren’t you? You don’t know this???” Maybe that’s how lawyers are supposed to talk, but I didn’t hear it coming from the DoJ lawyers on cross examination of the PSC experts. The Special Masters have been very generous. I hope the Special Masters can see what a flimsy structure the arguments are that the PSC has constructed.It's just sleeping!

I hope parents who buy into the whole vaccine/heavy metal causation hypothesis and its accompanying “biomed” insanity are listening to these hearings because they will see how they’ve been led around by the nose by “experts” using big words and “healers” making big promises. I also hope that people don’t ever avoid vaccinating their children just out of fear of autism or vague fears of “toxicity.” The stuff to fear is not the vaccines. The stuff to fear is the sometimes deadly germs that vaccines can help protect their children from.

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Rodier on Bernard et al. and environmental causes of autism

25 May

The idea that mercury poisoning causes autism was first put forward in a paper by Sally Bernard and others entitled Autism: a novel form of mercury poisoning.

This was published in a journal called Medical Hypotheses. As you might tell from the title, Medical Hypotheses presents hypotheses-not proven ideas. The journal has no peer review process. Instead, they basically print “…will publish radical ideas, so long as they are coherent and clearly expressed”. If you write well and pay to publish, it will likely get in. Keep that in mind with any paper from “Medical Hypotheses”.

In this paper, the put forth the hypothesis that mercury causes autism. To support this idea, they compare the symptoms of autism and mercury intoxication.

In the Autism Omnibus Proceedings, Dr. Patricia Rodier spoke on specifically the Bernard paper. Dr. Rodier has a unique position in the United States, and likely the world: she is an expert on both mercury poisoning and autism. Below is a rough transcription based on the audio recording of that testimony.

She starts out by stating that she has many criticism of the Bernard paper. She also mentioned a response to that paper had already been published by Nelson and Bauman. That paper is worth reading, and it’s free on the Pediatrics website.

Dr. Rodier then discusses the comparisons made between mercury poisoning and autism, based on her experience with both. If you want the short version: there is no comparison.

First, many of the symptoms or characteristics that are discussed in the Bernard paper are not specific to either autism or mercury poisoning. These include, nausea, vomiting, irritability and temper tantrums. Basically, these are things that happen for all of us at times.

Other symptoms are common across many disabilities: mental retardation, depression and abnormal gait. Again, these are not specific to either autism or mercury poisoning.

Almost all the symptoms used for mercury poisoning are taken from “Mad Hatter’s” disease: the result of a very high exposure to inorganic mercury vapor. Only a few symptoms listed were from ethyl mercury exposure. Since the exposure from vaccines is due to ethyl mercury (thimerosal breaks down to ethyl mercury) that would be the valid comparison.

Dr. Rodier, in her testimony, then discussed how the Bernard paper doesn’t actually do what it purports to do. The comparison isn’t valid since the actual symptoms of autism and mercury poisoning do not match up in a comparison.

She then goes on to discuss many of the comparisons made by Bernard, et al., and show that the comparisons are not valid.

1. Under psychiatric disturbances, the paper discusses depression, flat affect, depressive traits, mood swings, impaired face recognition

1a. Depression is a symptom of acrodynia. This is an exposure to inorganic mercury, not ethyl mercury. While some, possibly many, autistics suffer from depression, it is not a characteristic of autism.

1b. Mood swings are a characteristic of Mad Hatters disease. Again, this is not an autism symptom or characteristic.

1c. Flat affect is a diagnostic trait for autism but not mercury poisoning . Also, this is the opposite of mood swings, a characteristic of mercury poisoning noted in ii, above.

1d. Impaired face recognition occurs in autism, but hasn’t even been tested in any kind of mercury poisoning.

So, in this first group of four: there is no overlap for the above 4 ‘symptoms’. If it happens in mercury poisoning, it doesn’t happen in autism and vice versa.

2. Under speech and language deficits, the paper describes:
2a. Verbalizing and word retrieval. This is a problem is observed in Mad Hatters disease but not autism. But, this is compared to ecololia and word use and pragmatic errors. These never happen in mercury poisoning. It is an autism trait.
3. Again under psychiatric disturbances, the paper lists “Lacks eye contact”, and “impaired vision” under mercury toxicity, compared to “problems with joint attention” as the ‘similar’ autism trait
3a. “lacks eye contact” is a symptom of autism, but not of mercury poisoning. Likewise, impaired visual fixation is a symptom of methyl mercury poisoning-the brain control of the eye muscles are impaired which doesn’t allow you to fixate on something-but is not a symptom of autism. Joint attention has nothing to do with vision. It is not a feature of any kind of mercury poisoning. It is a social impairment, not a vision issue.

4) Under CNS structure, they compare “progressive microcephaly” for mercury poisoning with “progressive microcephaly and macrocephaly” for autism.
4a. progressive microcephally is given as a symptom of mercury poisoning. The idea of ‘progressive’ is incorrect here. Also, microcephaly is a sign of methyl mercury toxicity prenatally, not postnatal exposure. Children are born with it.
4b. Progressive macrocephally is a sign of autism. However, it has never been reported in mercury poisoning.

5) Under Neurochemistry, they list “Causes demyelinating neuropathy” under mercury poisoning.

5a. Demyelinating nerorpathy results from a chronic exposure to inorganic mercury. It is not reported in autism.

5b) They list “demyelination in brain” as a characteristic of autism, but no one has ever listed this in autism and the reference doesn’t address it.

Dr. Rodier posed the question: since the authors are trying to show a connection between thimerosal containing vaccines and autism, why don’t they compare autism and ethyl mercury poisoning? Keep in mind, there are various forms of mercury (ethyl and methyl being two types of organic mercury). In their comparison, Bernard et al. have picked from ethyl, methyl and inorganic mercury symptoms. Dr. Rodier suggest the reason they didn’t stick to purely ethyl mercury symptoms because “It doesn’t make a good story”.

1) For example, in a paper by Zhang , 41 people were exposed to ethyl mercury from tainted rice. They knew dose from how much rice they ingested. The authors documented the symptoms. Doses varied from mild to death.

1a) The three most comment symptoms documented by Zhang were:

1a.i) Muscle Weakness

1a.ii) Loss of appetite

1a.iii) Dizziness

Dr. Rodier notes that “those don’t sound much like autism”.

1b) The next 10 symptoms listed by Zhang are

1b.i) nausea

1b.ii) abdominal pain and diarrhea

1b.iii) fever

1b.iv) numbness of the extreminties

1b.v) peresthesia and ataxia

1b.vi) vomiting

1b.vii) thirst

1b.viii) unsteady gait

1b.ix) ringing in the ears

1b.x) headache

Dr. Rodier: again, none of these sound like any of the symptoms of autism that are used in diagnosis.

Dr. Rodier stresses at this point: there is really no correspondence between the symptoms of ethyl mercury poisoning and autism

The government’s attorney asked: the current hypothesis is that low levels of inorganic mercury cause oxidative stress or an inflammatory process which cause autism. Does that make sense? Dr. Rodier answered quite directly, “no”. In the opinion of that autism and mercury poisoning expert, the logic does not work.

She went on to point out that scientists try to disprove hypotheses, not just find support for their given hypothesis. (author’s note here: this is quite true. You need to test a hypothesis and make sure it doesn’t fail, not just collect the evidence that implies it is correct).

She points out that there is one piece of evidence that completely refutes the Bernard et al. hypothesis. There have been autopsy studies performed on people with acute ethyl mercury poisoning. While they indeed had high levels of organic mercury after the ethyl mercury was gone, these people recovered from the mercury toxicity symptoms after the ethyl mercury was gone and the had inorganic mercury was left.

This was the end of the discussion on the Bernard paper and mercury. It is pretty clear when an expert in both fields-mercury toxicity and autism-speaks on the comparison. Compare this to the authors who wrote the paper. Of the three, only one had a background in medicine. That is Lyndelle Redwood, a nurse. None of them are researchers, none experts in either autism or mercury poisoning.

From the above it is pretty clear: the hypothesis put forth by Bernard et al. was a poorly formed and is definitely incorrect.

In the Omnibus Proceeding, the discussion then moved away from mercury directly and into the question of environmental causes of autism. The question was posed: when does autism begin? The answer was that it almost always is determined pre birth.

This led to a discussion of known environmental factors that lead to autism. Dr. Rodier listed them and listed when the exposure has to occur to result in autism.

The known environmental causes are: Rubella, thalidomide, valproic acid, ethanol, misoprostol. All are involved during gestation. The timing of exposure to increase autism risk is:

1) Rubella (German measles): before the 9th week

2) Thalidamide: week 3 and 4

3) Valproic acid: week 3 and 4

4) Ethanol: week 3-5

5) Misoprostol: week 6

She noted that tuberous sclerosis is an example of autistic symptoms developing after birth as the tumors progress.

Terbutaline has been brought up a number of times by the plaintiffs (petitioners) in the Omnibus as an example of an environmental cause of autism. The question was raised as to why Dr. Rodier didn’t discuss this. She described that it is not an environmental cause study, but a genetic study.

Twin pairs were studied. Some were exposed to terbutaline and some were not. They compared the concordance: the rate of one twin having autism if the other did not. No significant increase was found in general in this study. So, the authors looked at a smaller subset, and still found no increase. Then, they looked only at male twins, where no autistic siblings were present in the family. In that case only, they found a significant effect.

Dr. Rodier goes on to discuss that even interpreting this part is difficult because we don’t know if the increased risk was due to the terbutaline, or the fact that the children were at risk of being born early (terbutaline is given to prevent premature delivery).

The judge (Special Master in this court) asked if this was because without the terbutaline the children would not have survived to be born. Dr. Rodier agreed and pointed out that the interpretation the plaintiffs are supplying is further confused because low birth weight is also an increased risk factor. This is from a very recent paper in Pediatrics. Since the turbutaline twins were low birth weight, that could be a factor in the increased autism risk found.

The plaintiffs lawyers have been using a study on rats as an example of a post-natal environmental exposure. The government lawyer asked if this was a valid interpretation. Could this be used to suggest a post-natal exposure could cause autism in humans? Dr. Rodier answered that this is not valid. Newborn rats are more developmentally immature than newborn humans. Newborn rats have closed eyes, no hair, and in other ways are very much more developmentally like prenatal humans. The study would compare better to late-gestation humans.

There was much more in her testimony, but that gets even farther away from the Bernard paper, so we can end this discussion here and let others pick up the rest of her testimony.

Dr. Brent – Toxicologist at the Autism Omnibus hearing

25 May

Listening to Mr. Williams (lawyer for the parents) cross examine Dr. Brent the toxicologist (from May 19, Day 6) was difficult most because after 45 minutes of discussion of the toxicokinetics of ethyl-, vs. methyl, vs. inorganic-mercury all I could hear was “Blah, blah, don’t you agree that the Charleston monkey adult brain study showedgreaterinflammationoftheinorganic glutamaturgicneuron silvergrainsBurbacherinfant paper? Blah blah and further, isn’t it true thattheVahtergroup onlygave80milligramsperkilogramsperdayofmercuricchloride because the defensereferencemasterlist 436page8 indicatesthatSeychellesIslanders spoke at the IOM?”

Nevertheless, I forced myself to listen to portions of it again and again until I thought I understood what they were talking about exactly. There were several times, maybe 8 or 10 even where it seemed obvious to me that Dr. Brent had totally demolished the point that Mr. Williams was attempting to make and Mr. Williams continued on as if it was of no consequence. I kept getting this picture of King Arthur and the Black Knight from Monty Python and the Holy Grail after King Arthur has sliced off the Black Knight’s arm:

ARTHUR:
Now stand aside, worthy adversary.
BLACK KNIGHT:
‘Tis but a scratch.
ARTHUR:
A scratch? Your arm’s off!
BLACK KNIGHT:
No, it isn’t.
ARTHUR:
Well, what’s that, then?
BLACK KNIGHT:
I’ve had worse.

.

The following is more of my rough transcribing of the audio. I have no idea what that word is that sounds like “AT-trib-ated.” If you know I’d be happy to correct my spelling of it. I believe this first paper he’s referring to is one of the Charleston or Vahter adult monkey studies where they gave very large doses of methyl mercury to the monkeys every day, orally. Click here to hear this segment of the cross examination of Dr. Brent.

.

Mr. Williams: It’s says: “the microglia population is a responsive cell type. Once damage has been repaired following activation after injury microglia are known to return to a quiescent state. However, the number of attribated (sp?) microglia remained elevated … in the monkeys of the clearance group which were kept unexposed for 6 months following 12 months of methyl mercury exposure . This group had very low concentrations of methyl mercury, but retained elevated concentrations inorganic mercury at levels comparable to the 12 month exposure group and this suggests that inorganic mercury may be the proximate species of mercury responsible for microglial activation…” a situation similar to that proposed for the cortex study we already looked at. Now, do you agree that normally microglia have a protective role, they come in and clean up whatever’s there and then they return to their quiescent state?

Dr. Brent: To the extent that I understand microglia… which is limited, I would say, yes.

Williams: And if they stay activated then they can become toxic to neurons and astrocytes.

Dr. Brent: Once again, my, my understanding of microglia is more limited than other people who will be testifying later… my understanding is that microglial activations is not necessarily a bad thing and that … the effects here are not necessarily indicative of any neuropathology.

Once again, you know, we are talking about inorganic mercury effects at the concentrations they give here, and if the inorganic mercury is causing adverse effects at the concentrations, then it’s the seafood and the chicken that people are eating and not the vaccines because that’s where the far greater exposure comes from. And that doesn’t make any sense, because everyone is eating seafood and chicken, including children who are getting mercury via breast milk, and we don’t think of breast milk as a neurotoxin!

Williams: If we go down the column on the same page to about 4 sentences above… yeah about where you have it highlighted…
It says: “Further loss of astrocytes would be expected to have deleterious effects on the neuron population, for example through a excitotoxic mechanism. You were here when Dr Kinsbourne testified that that was his … understanding of the mechanism that could likely be at work here that you would have astrocytes no longer able to take up glutamate, so yyou’d have excess of glutamate and have neurons get over excited. Right?

Dr. Brent: Once again your getting a little out of the mercury area, so my answer here is going to be quite limited, what I took away from Dr. Kinsbourne’s testimony was that he was hypothesizing it was excitotoxic mechanism, related to astrocyte effects. But here for example it says, “further loss of astrocytes,” in this study there wasn’t even that much loss of astroycytes! And certainly, uhm, well we talked about the exposure scenario, so I won’t bring that up again …

Williams: And although, you want to talk about the methyl mercury dose here, you recall that the authors of the infant monkey study made a point of saying that the levels of inorganic mercury in these adult monkeys was only 5 times higher on average than the levels they found in those infant monkey brains, right?

Dr. Brent: That’s right, and that’s very good evidence therefore, that the inorganic mercury is not acting as a neurotoxin, or else we are being poisoned every day, and we are having autism being formed every day, from breastmilk, from seafood, from chicken.

Williams: (Clears throat.)

.

I don’t know if it’s immediately obvious to those who haven’t followed the discussion closely, but basically, Mr. Williams had pointed out that inorganic mercury is the “proximate” cause of damage to brain cells. Which is to say that, it doesn’t matter if the original source of the mercury was methyl-, ethyl- or inorganic mercury, because the mercury doesn’t hang around in the brain as either methyl- or ethyl-mercury. Those forms get changed into inorganic mercury, and it’s the inorganic mercury that hangs around. Inorganic mercury (referred to sometimes in the hearing as “Hg-plus-plus,” Hg++) is the same stuff whether or not it started out as methyl-, ethyl-, thimerosol, breast milk, or chicken. And the exposure to breast milk and chicken for the infant and toddler set is much higher than their exposure to thimerosal from vaccines, now or ever. Dr. Brent had said earlier in the cross examination that over the course of 6 months and infant gets “about 250 micrograms of methyl mercury.”

macaque monkey

Besides that the PSC keeps bringing up these studies where macaques were given significantly higher doses, even massively higher doses, of mercury, either thimerosal or methyl-mercury, than babies ever got. The monkeys in the Vahter study were given 50 mcg per kilogram per day of methyl mercury, which Dr. Brent explained is the equivalent in a 70 kg person getting 3,500 mcg a day of methyl mercury. The average diet for that 70 kg person would expose him or her to 11,000 mcg a year. A year! So essentially, the monkeys got a level of mercury in 3 days what they’d get in a year if they had been eating a typical American diet. But some of the monkeys were fed like this for a year. That’s the “12 month exposure group” referred in what I transcribed (above).

And even though they had had that large continual dose of mercury for a year and many of their brain cells were pretty much impregnated with mercury, the monkeys were normal behaviorally. Even if you wouldn’t expect them to become autistic because they were exposed as adults, surely they’d show some outward sign of brain damage if that much mercury were extremely dangerous to brain function.

It was also interesting to me that Burbacher had used 3 or 4 times the amount of thimerosal to dose his infant monkeys as humans got. Had Burbacher used the equivalent amount of thimerosal in the human vaccine schedule the outcome would likely have been that the levels of mercury in the monkey’s brains would have been so low that it wouldn’t have been detectable. (Clears throat.)

There was also some fun discussion about how there’s no increased autism in the Faroe and Seychelle’s islands in spite of the fact that infants have high levels of mercury in their brains (from maternal diet). Mr. Williams stated that “fish is very good for brains” as if that was a point for his side.

Dr. Brent was the first of the respondents expert witnesses to testify in this portion of the Omnibus hearing. He also had testified in the Cedillo hearing. Some of the points about Kinsbourne’s hypothesis regarding astroglial activation, glutamate excess, and cell death were dismantled by Dr. Johnson, and by other experts who testified in the past weak. Dr. Deth’s hypothesis about autism being the result of oxidative stress was pretty much smithereened by two or three of the petitioners experts. I’m still catching up with listening to all of their testimony, but of extensive portions I’ve listened to so far, well, I think it’s looking really bad for dead parrot hypothesis.

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