Canada Speaks: No, It’s Not Vaccines

6 Jul

Pediatrics have published a new paper, *Pervasive Developmental Disorders in Montreal, Quebec, Canada: Prevalence and Links With Immunizations* authored by Fombonne et al.

Pre-empting an NAA style ad hominem attack, the authors declare their conflicts early.

In the United Kingdom, Dr Fombonne has provided advice on the epidemiology and clinical aspects of autism to scientists advising parents, to vaccine manufacturers, and to several government committees between 1998 and 2001. Since June 2004, Dr Fombonne has been an expert witness for vaccine manufacturers in US thimerosal litigation. None of his research has ever been funded by the industry.

As they don’t agree with the paper this has caused the usual suspects, notably Safe Minds and FAIR Autism Media to highlight these aspects of the paper in an attempt to claim these invalidate the papers findings. Mark Blaxill of Safe Minds says that:

According to an analysis by SafeMinds, however, the study […] should be treated with skepticism, for a number of reasons.

Whilst David Ayoub states that:

“This is just another heavily biased study by an author with a long track record of financial ties to the drug industry, and whose previous views on the epidemiology of autism have been discredited,” wrote Ayoub

So, as far as the mercury militia are concerned, the following points are an issue.

1) Fombonne’s alleged financial ties to the drug industry. One assumes he is referring to Fombonne’s pre-stated offering of advice on the epidemiology and clinical aspects of autism and the fact that he’s an expert witness for vaccine manufacturers.

Let’s cut the shit here shall we? Richard Deth is a petitioners’ expert witness in major vaccine litigation. So are the Geier’s. So are various others. They have an equal ‘special interest’. Should we dismiss their papers out of hand? Either we allow *all* or allow *none*.

2) Fombonne’s previous views on the epidemiology of autism have been discredited.

Really? They have? By who? In what journal was this ‘discrediting’ published? Lets be clear here. Ayoub uses the word ‘discredited’. He didn’t say, ‘challenged’. He didn’t say ‘contraversial’ he said ‘discredited’.

David Ayoub by contrast, thinks that Rashid Buttar – a man who’s own patients think he’s a money grabbing quack – is an industry expert:

The 2 top chelation people in the world are Gary Gordon, MD, and Rashid Buttar, MD, he adds.

It’s my opinion that anyone who thinks Rashid Buttar is ‘top’ of anything autism related needs get his head back to reality pretty quickly.

3) Mark Blaxill at least takes a stab at something substantive. He questions the study methodology on two points. Firstly, he tries to insinuate that what might be true for Canada might not be for the US. Secondly he states that some of the study subjects may have received thiomersal from other vaccine sources than those noted in the study.

Fombonne et al write that:

The findings ruled out an association between pervasive developmental disorder and either high levels of ethylmercury exposure comparable with those experienced in the United States in the 1990s or 1- or 2-dose measles-mumps-rubella vaccinations.

So the word ‘comparable’ is used. Fombonne et al never attempt to state that it is a fact that what’s true for Canada is true for the US. However, its also true that there wouldn’t seem to be any good reason for _not_ thinking that. Why would the US and Canada be different? Surely thiomersal is thiomersal?

After that weak stab at something relevant, Blaxill retreats to Ayoub’s tactics of smear and spin.

Dr. Fombonne wrongfully claims that large-population studies in the United States, England and Denmark also disprove a link between mercury and autism, and he states that “there is no autism epidemic.”

The one mention of the word ‘Denmark’ in the entire paper is this one:

Our results are entirely consistent with cohort, case-control, and other ecological studies performed in Denmark and Sweden.

Fombonne et al never claim that these studies disprove anything. They merely note that consistency between those studies and their own. I can’t locate the use of the word ‘England’, ‘UK’, ‘united kingdom’ or ‘Britian’ anywhere in this paper so I fail to see why Blaxill mentions them.

Blaxill is guilty of intellectual dishonesty many times in his ‘rebuttal’. None more so than when he states that:

He conveniently ignores the vast body of scientific evidence that has shown that environmental factors such as mercury may have caused the increased number of autism diagnoses in the US and other countries.

Fombonne et al do not at any point discuss generalised ‘environmental factors such as mercury’. They discuss the key question regarding thiomersal and MMR. It raises questions about Blaxill’s integrity that he would try and switch the focus onto something he and his group explicitly have targeted to something much more general and which Fombonne et al does not address. This is a pattern becoming more and more apparent from key members of the mercury militia. As science continues to fail to support any causative link between thiomersal, MMR and autism, these groups are becoming much more generalised in their terminology. Expect to see more of this as 2006 draws to a close.

Blaxill also claims there is an increased number of autism diagnoses yet he fails to point to evidence for this. Fombonne’s own research on this point indicates a high but stable prevalence.

Blaxill continues:

Dr. Fombonne’s actions have not historically been in the best interest of families with autism—he has declared himself an expert witness on behalf of various pharmaceutical companies in thimerosal-related litigation.

By contrast, the Geier’s actions have not been in the interests of autistic peoples. And in fact this whole point about ‘best interests’ is childish in the extreme. The _only_ interest that science should adhere to is that of honest science. To suggest otherwise leaves a question mark over the objectives of Blaxill’s actions.

Several independent federal agencies and respected scientists and researchers have received federal funds to investigate the autism epidemic and the biological
plausibility of a link between mercury and ASDs.

Why is this even mentioned? Why not wait for them to be completed? Like this one already is.

Multiple studies have indicated that there is a connection between childhood vaccines containing thimerosal and the incidence of autism.

Blaxill (maybe purposefully) doesn’t mention _who_ might’ve conducted those studies, or where they were published. I’m guessing that he means the Geier’s but that recent revalations regarding their integrity and the quality of their work, made him think twice about saying their names for the record. Can’t say I blame him.

Skeptico, Orac and Autism Diva also comment on this study.

43 Responses to “Canada Speaks: No, It’s Not Vaccines”

  1. Joseph July 6, 2006 at 14:48 #

    The responses to Fombonne’s paper have been extremely weak. As usual, the “rebuttals” don’t address the science of the paper at all, but instead focus on potential conflicts of interest, the suggestion that a conspiracy may be going on, and vague citing of non-peer-reviewed evidence to the contrary.

    The claim that Fombonne doesn’t consider prior evidence that links mercury to the incidence of autism is outrageous. Where exactly is this evidence? Is he referring to Geier & Geier? Which scientist, in their right mind, would seriously consider citing Geier & Geier at this point? And I’ve repeatedly noted what the purported link looks like.

    I hope that those who disagree with Fombonne’s findings can come and have an honest debate about why, scientifically, they think the paper might be wrong.

  2. Dad Of Cameron July 6, 2006 at 15:30 #

    “Mark Blaxill at least takes a stab at something substantive. He questions the study methodology on two points. Firstly, he tries to insinuate that what might be true for Canada might not be for the US.”

    A valid, but futile point, there is no reason not to think that they are comparable, as you point out, Thimerosal is Thimerosal.

    Additionally, while Canada looks like a large whole different peice of geography on a map, 90% of Canada’s population lives within 100 miles of the U.S. border. There is no reason not to look at the Canadian population as part of the largest northernmost concentration of inhabitants of North America right along with people living in the northern United States.

  3. anonimouse July 6, 2006 at 18:31 #

    RE: Conflicts of Interest

    The most laughable ad hominem argument ever in this whole debate is the “conflict of interest” one.

    Look, Offit and Fombonne might get compensated in some way by drug companies. Nobody knows if it’s a significant portion of their income, much less if they’re “dependent” on said income. Believe me, doctors have plenty of places to generate income and drug companies perks are only part of the income pie.

    On the other hand, you have people like the Geiers who are totally dependent on the autism-mercury theory and on the existence of class action lawsuits against drug companies. Is Rashid Buttar’s “protocol” (which generates him boatloads of money per office visit) relevant if there’s no autism-mercury connection? Heck, even the Hornig and Deths of the world will feel the pinch if they don’t have their research funded by the likes of SafeMinds.

    Speaking of SafeMinds, I think that an organization run by a woman who is suing drug companies should at no point ever claim someone else has a “conflict of interest”. I wonder if Mark Blaxill’s going to get a cut of Lyn’s settlement if it should go down.

    It’s a stupid argument that only marginally works because the tobacco companies used junk science to insinuate that smoking wasn’t bad for you. But guess what? Even with all their money and power and influence, they ultimately weren’t successful because they were wrong and real scientists knew it.

  4. MAría Luján July 7, 2006 at 01:17 #

    Hi KEvin
    In fact I would say it is not thimerosal and MMR… but I found no mention of the confounding variables he can have- and he has a lot IMHO-, in biochemical/immune mechanisms he is ruling out, in the suppressor effect he even did not mention in the analysis of his data.
    I always have the sensation that here we have to say a number 50 potential stressors to ASD- not in terms of CAUSING ASD for a NT child but to a genetically susceptible child- Epidemiologists discard correlation considering 1 or 2, and the point is 50 ( or more, we do not know for sure today). If it is the accumulation how are they going to find correlation? If it is present in a subset of population How are they going to find association?
    If the question is wrong done, why the answer is going to be useful?
    Sincerely
    Ma Luján

  5. Joseph July 7, 2006 at 03:18 #

    María: The purpose of an epidemiological study such as this one is to see if some environmental factor can be correlated with prevalence. It’s clear prevalence is increasing in Canada. You say there could be 50 environmental factors. Are you saying all 50 coincidentally are causing prevalence to increase since the early 1990s, or is it just one that is causing prevalence to increase? You know what I think causes prevalence to increase and I’ve shown you pretty clear evidence of what it is. Do you still think environmental factors are epidemic-causing or not?

  6. MAría Luján July 7, 2006 at 04:45 #

    Hi Joseph
    You say
    The purpose of an epidemiological study such as this one is to see if some environmental factor can be correlated with prevalence.

    OK, but the question in this manuscript and several related is presented in terms of causal and answered in terms of the negative.
    Given all this population of equal children-genetically, biochemically, in their brain structure, etc-, exposed to this supposed CAUSE of AUTISM- thimerosal, MMR-, CAN we found a correlation between the supposed CAUSE and the number of people diagnosed under the DSMIV measured as prevalence? Therefore the question is wrong for me, because is analyzed as IF Autism can be present by an infection and autism is different. Not equal children, not equal brain structure, not equal biochemistry, not causes , not the only cause, not easy to detect at a population level without looking at clinics-including genetics. Because no confounding variables are analyzed (if the immune system is the target why MMR/ thimerosal? Why not ALL the vaccines? How many OTHER vaccines were introduced at these times in the 1990s? What about other stressors to the immune system? Air quality? Food quality? Pb sources? Others? Why these and not the others IF the supposed target is the immune system? Because someone proposed- that is/was controversial.
    It is like saying to discard what —— say, the intention is to prove that what—say is wrong and that the proposed theory by—– is wrong, but not to analyze the underlying much more complex situation if a coherent theory is proposed and tested. Because it is considered in advance that the theory is wrong…Perhaps as it is presented in terms of CAUSE… what about alternatives?

    It’s clear prevalence is increasing in Canada. You say there could be 50 environmental factors.

    I do not know, It can be more.

    Are you saying all 50 coincidentally are causing prevalence to increase since the early 1990s, or is it just one that is causing prevalence to increase?

    I consider that no ONE alone can be assigned to this, but you know what is my thinking about- excluding the “purely genetic causes” but analyzing the polymorphismic variation: Accumulation of insults to the immune system of a child, because of the genetics of this susceptible child and the effects of his/her “autistic” genetics- that can include from 5 to 100 genes- in transcriptomics,brain structure, metabolomics and biochemistry (including the management of aminoacids/peptides/proteins). No ONE, not the same for each child, not the same effect for each susceptible child. Multi triggered and multipresentation- based on genetics. Since the early 1990s, and talking only from vaccines, there were an important increase of the number of vaccines given to children-around the world. However, I consider that my main issue about vaccines is how it is assigned to THIS as causal of autism and not as a collaborator and only under certain circunstances. I consider that also the overuse of antibiotics, the quality of the food, etc can have part of the analysis in terms of stressors. Not all at once for each child, not just one.
    As a parent the (wrong) presentation of the issue is to pick between an infectious and potentially life-threatening disease (by do not vaccinate) or the risk of neurodevelopmental problems, autism and in extreme cases, death (by to vaccinate). No parent must be pushed in this position for me. And the presentation of this dicotomy is worrisome for me because it is not true. At an individual level is possible that vaccines can do harm- and there are dozens of publications about pharmacovigilance. The main point for me is to detect what children are prone to the risk/negative reaction to avoid the potential of damage not to be pushed in the position of to vaccinate or do not vaccinate per se because this is not a solution; it is a nightmare. This is what I consider important. For me it is not to vaccinate at any cost or not to vaccinate at all. It is much more complex. By adopting extreme positions a strong damage is being done to the vaccination program and at least to my autistic child in my personal view, indeed.

    You know what I think causes prevalence to increase and I’ve shown you pretty clear evidence of what it is.
    Joseph, I want to agree with you in mutual respect in disagreement and I want to let you know this: this is not personal, it is about ideas and analysis and science and theories. It is not for me about who is right, but about what the truth is. You presented what you think is clear evidence of what causes prevalence to increase as for sure and I accept that you can not agree with me. I consider that yours is part of the view- and MUST be analyzed with care- and you did very well if you ask me- but not THE COMPLETE VIEW and not for sure, IMHO, with the information available.

    Do you still think environmental factors are epidemic-causing or not?

    First, nobody can tell that an epidemic is taking place (or not) for sure because of the data available. A real increase can not be ruled out. I am skeptic of the epidemics and of the non-epidemics. In fact, I am skeptics about everything, in advance consider that the interest conflicts must be proved beyond doubt and I am interested in the data, methodology quality, the quality of the question and the quality of the answer in published science. I agree that now there is increased awareness and better diagnosis, but this is not all, but part of the analysis.The environmental factors present are not causing for me, but collaborating in to “trigger” conditions that are also present as medical conditions (secondaries to the main- with roots in genetics) that are diagnosed under the DSMIV based only in behaviors.

    Sincerely

    María Luján

  7. Hyperion July 7, 2006 at 06:48 #

    Maria:

    Actually, epidemiological studies such as this one are actually going to be more accurate if you’re looking at multiple causative factors than lab tests like the Geiers’. The thing is, all of the children in this study were exposed to many possible environmental factors. Rather than performing a sterile lab test that would only look at thimerosal or MMR on its own, this test did actually look at them in real circumstances.

    The study showed that thimerosal use does not correlate with autism prevalence. Even if your hypothesis were that thimerosal were one of 50 causative factors, this study would still overrule that hypothesis. If there were 50 separate causative factors that together caused Autism in susceptible children (which I doubt), you would still expect that changes in thimerosal dose, and its eventual removal, would correlate with some change in autism prevalence. Ditto for MMR.

    In contrast, there are many factors which influence one’s chances of contracting lung cancer. However, epidemiological studies show a strong correlation between tobacco smoke and lung cancer. They also show a correlation between heredity and lung cancer (and other cancers as well). I would not be surprised if an epidemiological study could show that living in a high-smog area increased one’s chances when smoking and other factors are controlled for. On the other hand, I highly doubt that one could find correlation between hair color and lung cancer. Even when there may be multiple causative factors involved, it is still fairly easy for an epidemiological study to tell whether one factor or another is involved.

    However, if you push the environmental-toxin hypothesis to the point that you start looking for genetics plus 50 environmental factors which may not even be constant for everyone, then at that point you really have to look at genetics as the obvious root cause. It would be virtually impossible to find 50 different causative factors, much less remove them. If genetic factors are the main thing separating NT and autistic kids, then that should be the main focus.

    Once you find possible genetic factors involved, then it might make sense to d epidemiological studies of children with these genetic factors and see if other environmental factors impact severity of impairment. This is not unlike the recent studies on ADHD and lead, where they found that it might affect the severity for those with a mutation that causes a mild form of the disorder, but that it did not cause it in people who did not have the mutation, and did not affect severity in those who had a more severe version of the mutation. There, you had a neurodevelopmental disorder where the primary determinant was genetic, with the possibility that environmental factors might increase severity for some people. (important difference: the lead levels involved still caused negative effects for NTs even though it did not cause them to develop the disorder. There is no evidence that thimerosal or MMR cause negative effects in NTs).

    It is possible (and I think highly likely) that autism and other PDDs will turn out to be similar: primarily genetic in cause, with the possibility that environmental factors could make symptoms worse for some people.

  8. anonimouse July 7, 2006 at 14:20 #

    Hyperion is dead on. It is a mistake to minimize the impact of epidemiology when it comes to this issue. Even if there is a subset of children that are more susceptible to environmental insults which then manifests itself as autism, thimerosal exposure should skew the incidence (even if just slightly) when looking at a broad population.

  9. María Luján July 7, 2006 at 16:44 #

    Hi
    Now I can´t butI will comment at night. Thank you
    Ma Luján

  10. clone3g July 7, 2006 at 18:13 #

    Perfectly stated Hyper-ion

  11. Joseph July 7, 2006 at 20:25 #

    I consider that no ONE alone can be assigned to this, but you know what is my thinking about- excluding the “purely genetic causes” but analyzing the polymorphismic variation:

    Let me restate the question. Do you think it is likely that 50 or more environmental factors started to act in unison at the beginning of the 1990s, each contributing a little to prevalence increase?

  12. anonimouse July 7, 2006 at 23:14 #

    Do you think it is likely that 50 or more environmental factors started to act in unison at the beginning of the 1990s, each contributing a little to prevalence increase?

    The answer, of course, is no – and it’s absurd to think that way. It’s also counter to the entire premise of the mercury zombies – which is that the rise in autism in the early 1990’s was directly linked to the increase in the use of thimerosal-containing vaccines.

    (By the way, I’m not calling Maria a mercury zombie.)

    If you take that away, what you have – at most – is the possibility that thimerosal MAY (strong emphasis on that word) play some minor contributory role in the secondary physical issues some autistics have. But at that point, we should be assessing those physical issues with all children who get vaccinated, autistic or not.

    Has there ever been any legitimate inquiry, for example, that thimerosal-containing vaccines or the MMR contribute to long-term gut issues, behavioral problems or any other symptom commonly placed under the “mercury poisoning” umbrella? Forget autism – if somebody can show me THAT much, I’d listen.

  13. María Luján July 7, 2006 at 23:54 #

    Hi
    Joseph, you said
    _Do you think it is likely that 50 or more environmental factors started to act in unison at the beginning of the 1990s, each contributing a little to prevalence increase?_

    No, I do not think in 50 or more environmental factors to act in unison in all autistic people at once. I do think that SOME environmental insult have been more important than others to collaborate in the development of increased prevalence- NOT AS CAUSES, CAUSES IS/ARE GENETICS- different at an individual level- but as additional stressors to the genetic susceptibility that can trigger several medical conditions that historically have been not even tested related to ASD :
    1-Environmental contamination in general ( air, food, water). Exposures in critical steps of fetal development or child development.
    2-Overuse of antibiotics.
    3-Increase of numbers of vaccines without adequate control of composition, concentrations of vaccine components themselves and adjuvants and potential adverse reactions in sensitive genetically susceptible people. Role of the crowded schedule.
    4-Viral and bacterian infections of the mother ( previous, during pregnancy- including nutritional status)prenatal and viral and bacterian infections of the child during the first 2 years.
    5-Alcohol and drugs consumptions- of all kinds- in the mother that can potentially affect fetal development.
    6-Increase of use/abuse of prescription medicaments
    7-Pediatric management of the childhood diseases (viral and bacterian)
    8-Unknown

    Looking at the present status of epidemiology, the field that seems needed to study ASD is the genetic epidemiology, not the epidemiology in the sense of infectious diseases, as have been used.
    Some information I found extremely interesting about genetic epidemiology
    “Genetic epidemiology”:http://dorakmt.tripod.com/epi/genetepi.html
    “Populatioin based association studies”:

    Click to access casecont.pdf

    “Bias and confounding in epi…”:http://carcin.oxfordjournals.org/cgi/reprint/19/12/2063.pdf

    Some quotations
    “The pitfalls of conventional epidemiologic studies equally apply to molecular epidemiological research: selection bias, information bias and confounding (Vineis & McMichael, 1998; Campbell, 2002; Boffetta, 2003) with additional problems unique to genetic studies (Olson, 2000; Cordell, 2000; Elbaz & Alperovitch, 2002; Lee & Ho, 2003; Morimoto, 2003; Potter, 2003).
    Other hallmarks of complex diseases include known or suspected environmental risk factors; seasonal, birth order, and cohort effects; late or variable age of onset; and variable disease progression. Many complex diseases are hard to diagnose accurately; even quantitative traits such as hypertension often involve sizable measurement errors (Guo, 2000b). Ultimate analysis of complex traits requires sophisticated statistical designs incorporating all genetic and nongenetic variables, their interactions, and familial correlations. A complex disease can be modelled in two different ways: (1) an additive model, closely approximates genetic heterogeneity, is characterized by no interlocus interaction, and (2) a multiplicative model, representing epistasis (interaction) among loci (Risch, 1990a). It should be recognized that, simple genetic traits are also complex when examined closely (Estivill, 1996) (see also Rannala, 2001 for a comprehensive review of complex disease genetics and the Journal of Clinical Investigation Reviews on Complex Genetic Disorders (2005)).
    Epidemiological methods for studying genes and environmental factors in complex diseases
    The Lancet, Volume 358, Issue 9290, 20 October 2001, Pages 1356-1360
    Elizabeth J Hong, Anne E West and Michael E Greenberg

    In conclusion, we have shown that failure to take an environmental factor into account may lead to erroneous conclusions about the relation between a genetic factor and a disease, when gene-environment interactions and competing risks are involved. The bias can sometimes be substantial, and we suggest some patterns of association in favor of this bias. These findings emphasize the need for application of rigorous epidemiologic principles in association studies. Researchers conducting studies on the etiology of late-onset diseases should be aware of this bias.
    “Bias in Association Studies Resulting from Gene-Environment Interactions and Competing Risks “:http://aje.oxfordjournals.org/cgi/content/full/155/3/265
    “Selection Bias in the Assessment of Gene-Environment Interaction in Case-Control Studies”:http://aje.oxfordjournals.org/cgi/content/full/158/3/259
    “Point/Counterpoint

    Point: Population Stratification: A Problem for Case-Control Studies of Candidate-Gene Associations?”:http://cebp.aacrjournals.org/cgi/content/full/11/6/505

    anonimouse
    It is unfortunate how the words are selected to make personal attacks related to the thinking of others because of personal disagrement. In fact, I can agree with several points with you or Camille or clone3g- related to many many points-, what I disagree -very much- is the way you present disagreement about ideas. But , however, thank you for taking the care to make the clarification. This is a common situation I have faced, after near 10 months of participation in blogs/forums.
    Like you some of the defenders of the non link can react really badly the first time you say “biomed…” and they do not know you- However, almost nobody asks me about the whys, who, what and based on what information I am doing what I am doing. I can´t finish the word and automatically I am one of “them”, a poor ignorant unscientific parent (mom in my case) of an autistic child sunk in the belief that Autism= mercury poisoning and I am considered by many as something less than a rat with the brain of a mosquito in advance and mistreated in consequence: the you are so stupid argument to believe the lawyers and the quacks-or worse, you only want money. Even more if you exchange opinions by the first time and you question about autism biochemistry or epidemics data by the first time, the answer is autism is not mercury poisoning. It does not matter the question, the answer is autism is not mercury poisoning.. and the truth is that I do not agree with this NEITHER.
    Where my personal position leaves me?? in NOWHERE;
    Sorry by the explanation, but this is near the 20 000 th time that I am insulted/ excluded of the insult in 5 lines.

    BTW, I mentioned the 50 or more in terms of what we do not know today ( and I never consider that I am the owner of the truth, I have a personal interpretation of). Based on the information about genetic epidemiology and role of environmental insults I presented above. Dr Fombonne is not doing Genetic epidemiology that, being ASD of genetic root, must be considered as adequate.

    Sincerely
    María Luján

  14. María Luján July 8, 2006 at 00:51 #

    Hi anonimouse
    References I found related to the possibility of immunosuppresion by measles and concomitant gut problems.
    1- Measles virus infection in a transgenic model: virus induced immunosuppresion and central nervous system disease Cell 1999,Sep 3. 98 (5), 629-640.
    2-Measles virus infection causes transient depletion of activated T cells from peripheral circulation J. Clin, Virol. 1999, 12 (3), 201: 10 Nanan R, Chittka B, Kreth H. W
    3-Changes within T cell receptor B subsets in infants following measles vaccination Clin. Immunol Immunopathol 1996 May 79 (2) 163-170. Auwaerter PG, Hussey GD, Hughes J. Goddard EA, Ryon JJ, Strebel PM, Beatty D, Griffin DE-from John Hopkins
    4-Pathogenesis of measles virus infection: an hypothesis for altered immune responses J Infect Dis 1994 Nov 170 Suppl 1 S 24-31. Griffin DE, Ward BJ , Esolen L. M: John Hopkins
    The immune response that is effective in clearing virus and in establishing long term resistance to reinfection.. “ is associated with immune suppression, autoimmune encephalomyelitis and increased susceptibility to secondary infections”. This apparent paradox may be explained in part by preferential long term activation of type 2 CD4+Tcells by measles virus infection. Preferential stumulation of type 1CD4+Tcells by inactivated virus vaccines is hypothesized to play a role in subsequent development of atypical measles,
    5-Measles virus induced immunosuppresion in vitro is associated with deregulation of GI cell cycle control proteins J Gen Virol 1999, Jul 80 (7), 1599-1608 Engelking O, Fedorov LM. Lilischkis R, ter Meulen V, Schneider-Schaulies S
    6-Measles virus infects human dendritic cells and blocks their allostimulatory properties of CD4+Tcells J Exp Med 1997, Sept 15; 186 (6) 801-812.
    7- The pathogenesis of Crohn´s disease J Gastroenterol 1994, Jul 29 Suppl 7 11-15.Pounder R. E
    The author considers that the main problem is the mesenteric blood supply
    “Viral particles have been identified within the vascular endothelium, with the appeareance of para myxoviridae. In situ hybridization and other studies suggests that these particles are measles virus”
    8-Colonic CD8 and gamma delta T cell infiltration with epithelial damage in children with autism LJ Pediatrics 2001 Mar 138 (3) 366-372 Furlano e al.
    Neuroreport. 2004 Jan 19;15(1):27-32.

    Morbillivirus has been related to MS
    Search for morbillivirus proteins in multiple sclerosis brain tissue.

    Geeraedts F, Wilczak N, van Binnendijk R, De Keyser J.

    Department of Neurology, Academisch Ziekenhuis Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands. f.c.g.geeraedts@med.rug.nl

    We investigated brain samples of patients with multiple sclerosis (MS) and controls with immunohistochemistry using monoclonal antibodies (MoAbs) against canine distemper virus (CDV) and measles virus (MV) proteins. All stained negative except for MoAb F3-5, which recognises a conserved epitope on the fusion protein of morbilliviruses. F3-5 immunostaining was found in 8/9 MS plaques and 2/5 herpes simplex virus encephalitis brain samples, but not in six controls or four patients with ischaemic stroke. Using RT-PCR we found no evidence for the presence of MV in MS plaques. The F3-5 epitope may represent a protein that is upregulated during inflammation or point to a yet unrecognised morbillivirus in the human central nervous system that might be implicated in MS pathogenesis.

    About thimerosal and MMR from pharmacovigilance of vaccines
    Autoimmunity. 2005 May;38(3):235-45.
    Infection, vaccines and other environmental triggers of autoimmunity.

    Molina V, Shoenfeld Y.

    Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel.

    The etiology of autoimmune diseases is still not clear but genetic, immunological, hormonal and environmental factors are considered to be important triggers. Most often autoimmunity is not followed by clinical symptoms unless an additional event such as an environmental factor favors an overt expression.Many environmental factors are known to affect the immune system and may play a role as triggers of the autoimmune mosaic.Infections: bacterial, viral and parasitic infections are known to induce and exacerbate autoimmune diseases, mainly by the mechanism of molecular mimicry. This was studied for some syndromes as for the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and more. Vaccines, in several reports were found to be temporally followed by a new onset of autoimmune diseases. The same mechanisms that act in infectious invasion of the host, apply equally to the host response to vaccination. It has been accepted for diphtheria and tetanus toxoid, polio and measles vaccines and GBS. Also this theory has been accepted for MMR vaccination and development of autoimmune thrombocytopenia, MS has been associated with HBV vaccination.Occupational and other chemical exposures are considered as triggers for autoimmunity. A debate still exists about the role of silicone implants in induction of scleroderma like disease.Not only foreign chemicals and agents have been associated with induction of autoimmunity, but also an intrinsic hormonal exposure, such as estrogens. This might explain the sexual dimorphism in autoimmunity.Better understanding of these environmental risk factors will likely lead to explanation of the mechanisms of onset and progression of autoimmune diseases and may lead to effective preventive involvement in specific high-risk groups.So by diagnosing a new patient with autoimmune disease a wide anamnesis work should be done.

    Eur J Dermatol. 2004 Mar-Apr;14(2):86-90.
    Autoimmune diseases and vaccinations.

    Vial T, Descotes J.

    Centre Antipoison et Centre Regional de Pharmacovigilance, 162, avenue Lacassagne, 69424 Lyon, France. thierry.vial@chu-lyon.fr

    The potential association between vaccination and autoimmune diseases has been largely questioned in the past few years, but this assumption has mostly been based on case reports. The available evidence derived from several negative epidemiological studies is reassuring and at least indicates that vaccines are not a major cause of autoimmune diseases. However, there are still uncertainties as to whether a susceptible subpopulation may be at a higher risk of developing an autoimmune disease without causing an overall increase in the disease incidence. Based on selected examples, this review highlights the difficulties in assessing this issue. We suggest that a potential link between vaccines and autoimmune diseases cannot be definitely ruled out and should be carefully explored during the development of new candidate vaccines.
    Toxicology. 2004 Mar 15;196(3):211-6.
    Autoimmunity, environmental exposure and vaccination: is there a link?

    Ravel G, Christ M, Horand F, Descotes J.

    MDS Pharma Services, 69210 St Germain sur l’Arbresle, France. guillaume.ravel@mdsps.com

    Although the wide clinical experience shows that vaccines are generally safe, concern has been expressed for a causal link between vaccines and autoimmune diseases. Even though the mechanisms of autoimmunity are ill-elucidated, the role of pre-existing risk factors including genetic predisposition and environmental factors is largely accepted. The present study was undertaken to test the hypothesis that vaccines can promote autoimmunity in genetically-prone individuals when simultaneously exposed to a chemical known to induce autoimmune reactions. Female lupus-prone (NZB x NZW) F(1) mice were given 1 microg or 10 microg of a hepatitis B vaccine at 2-week intervals in conjunction with 40 microg of mercuric chloride three times per week for 6 weeks. A marked increase in serum IgG levels and a slight increase in anti-nuclear autoantibody (ANA) levels were seen in the mice given 10 microg of the vaccine plus mercuric chloride. No straightforward conclusion can be drawn from these results because of the extreme experimental conditions of this study. Nevertheless, the results tend to support the hypothesis that vaccination could enhance the risk of autoimmunity in genetically susceptible individuals when exposed to certain environmental chemicals.

    Ann Allergy Asthma Immunol. 2003 Jun;90(6 Suppl 3):34-40.
    Neuroimmunology and inflammation: implications for therapy of allergic and autoimmune diseases.

    Frieri M.

    Division of Allergy Immunology, Department of Medicine, Nassau University Medical Center, State University of New York at Stony Brook, East Meadow, New York 11554, USA. Mfrieri@numc.edu

    OBJECTIVES: To review concepts of neuroendocrinoimmunology and provide an overview of the role of immune dysregulation, stress, and the understanding of the pathogenesis and treatment of allergic and autoimmune diseases. DATA SOURCES: Articles include original research papers, review articles, and references identified from the bibliographies of pertinent articles. RESULTS: Neuroendocrine hormones triggered during stress may lead to immune dysregulation or altered or amplified cytokine production, resulting in atopic, autoimmune diseases or decreased host defense. Various types of transmitter substances of the neuroendocrine-immune (NEI) network include epinephrine, norepinephrine, acetylcholine, substance P, vasoactive intestinal peptide, glucagon, insulin, cytokines, growth factors, and numerous other mediators. The stress response and induction of a dysregulation of cytokine balance can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Disorders in which abnormalities in immune function are mediated by the NEI network include allergic diseases: allergic rhinitis, atopic dermatitis, and gastro-intestinal allergies and asthma through overproduction of neuropeptides and cytokines. The multiple roles of Th2 cells in maintaining allergic inflammation and altering the balance between Th1 and Th2 responses are important mechanisms for allergic inflammation and tissue damage. In addition, several autoimmune diseases mediated by NEI network such as rheumatoid arthritis, systemic lupus erythematosus, and diabetes mellitus can be attributable to immune dysregulation. CONCLUSIONS: Understanding the NEI network will contribute to novel treatments for immediate and late allergic reactions. Chronic stress or depression could lead to decreased host defenses, decreased response to vaccines, viral susceptibility, or malignancy. Treatment of allergic, autoimmune diseases and asthma should include stress management and behavioral intervention to prevent stress-related immune imbalances.

    Curr Opin Neurol. 2002 Jun;15(3):333-8.

    Neurological adverse events associated with vaccination.

    Piyasirisilp S, Hemachudha T.

    Division of Neurology, Department of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. spiyasir@mail.med.cmu.ac.th

    Public tolerance to adverse reactions is minimal. Several reporting systems have been established to monitor adverse events following immunization. The present review summarizes data on neurologic complications following vaccination, and provides evidence that indicates whether they were directly associated with the vaccines. These complications include autism (measles vaccine), multiple sclerosis (hepatitis B vaccine), meningoencephalitis (Japanese encephalitis vaccine), Guillain-Barre syndrome and giant cell arteritis (influenza vaccine), and reactions after exposure to animal rabies vaccine. Seizures and hypotonic/hyporesponsive episodes following pertussis vaccination and potential risks associated with varicella vaccination, as well as vaccine-associated paralytic poliomyelitis following oral poliovirus vaccination, are also described. In addition, claims that complications are caused by adjuvants, preservatives and contaminants [i.e. macrophagic myofasciitis (aluminium), neurotoxicity (thimerosal), and new variant Creutzfeldt-Jakob disease (bovine-derived materials)] are discussed.

    Vaccination and autoimmunity-‘vaccinosis’: a dangerous liaison?

    J Autoimmun. 2000 Feb;14(1):1-10.

    Shoenfeld Y, Aron-Maor A.

    Department of Internal Medicine B, Sheba Medical Center, Tel Hashomer, Israel. shoefel@post.tau.ac.il

    The question of a connection between vaccination and autoimmune illness (or phenomena) is surrounded by controversy. A heated debate is going on regarding the causality between vaccines, such as measles and anti-hepatitis B virus (HBV), and multiple sclerosis (MS). Brain antibodies as well as clinical symptoms have been found in patients vaccinated against those diseases. Other autoimmune illnesses have been associated with vaccinations. Tetanus toxoid, influenza vaccines, polio vaccine, and others, have been related to phenomena ranging from autoantibodies production to full-blown illness (such as rheumatoid arthritis (RA)). Conflicting data exists regarding also the connection between autism and vaccination with measles vaccine.So far only one controlled study of an experimental animal model has been published, in which the possible causal relation between vaccines and autoimmune findings has been examined: in healthy puppies immunized with a variety of commonly given vaccines, a variety of autoantibodies have been documented but no frank autoimmune illness was recorded. The findings could also represent a polyclonal activation (adjuvant reaction). The mechanism (or mechanisms) of autoimmune reactions following immunization has not yet been elucidated. One of the possibilities is molecular mimicry; when a structural similarity exists between some viral antigen (or other component of the vaccine) and a self-antigen. This similarity may be the trigger to the autoimmune reaction. Other possible mechanisms are discussed.Even though the data regarding the relation between vaccination and autoimmune disease is conflicting, it seems that some autoimmune phenomena are clearly related to immunization (e.g. Guillain-Barre syndrome).The issue of the risk of vaccination remains a philosophical one, since to date the advantages of this policy have not been refuted, while the risk for autoimmune disease has not been irrevocably proved. We discuss the pros and cons of this issue (although the temporal relationship (i.e. always 2-3 months following immunization) is impressive).

    Clin Rev Allergy Immunol. 2003 Jun;24(3):263-76.

    Adverse reactions to vaccines.

    Martin BL, Nelson MR, Hershey JN, Engler RJ.

    Allergy-Immunology Department, Walter Reed Army Medical Center, Washington, DC, USA. Bryan.martin@NA.AMEDD.ARMY.MIL

    (The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.) Immunization healthcare is becoming increasingly complex as the number and types of vaccines have continued to expand. Like all prescription drugs, vaccines may be associated with adverse events. The majority of these reactions are self-limited and not associated with prolonged disability. The media, Internet and public advocacy groups have focused on potentially serious vaccine-associated adverse events with questions raised about causal linkages to increasing frequencies of diseases such as autism and asthma. Despite a lack of evidence of a causal relationship to a variety of vaccine safety concerns, including extensive reviews by the Institute of Medicine, questions regarding vaccine safety continue to threaten the success of immunization programs. Risk communication arid individual risk assessment is further challenged by the public health success of vaccine programs creating the perception that certain vaccines are no longer necessary or justified because of the rare reaction risk. There is a need for improved understanding of true vaccine contraindications and precautions as well as host factors and disease threat in order to develop a patient specific balanced risk communication intervention. When they occur, vaccine related adverse events must be treated, documented and reported through the VAERS system. The increasing complexity of vaccination health care has led the Center of Disease Control and Prevention (CDC) to identify Vaccine Safety Assessment and Evaluation as a potential new specialty.

    If it is needed the clarification, I want vaccines safer. I am not antivaccines. I almost died from measles when I was 1 year old- and probably affected my hearing for a while- because I almost had meningitis- no vaccine available.
    I would want a different treatment of individualities; I would want more doctors researchers to hear calmly and productively parents; I would want more adequately done science-whatever the “side”; I would want more ethics and concerns about autistic people health-emotional, phsycological and physical-in the consideration of each human being as valuable and important.
    María Luján

  15. María Luján July 8, 2006 at 01:05 #

    Hi anonimouse
    I have several citations about both questions you mentioned. Please if you are interested on them ( there are many) contact me by e-mail because we are going off-topic- and the post will be long ( I have some problem with the one I prepared; do not know if Kev has it in his list to approve it).
    María Luján

  16. Joseph July 8, 2006 at 02:50 #

    So what you’re saying María is that there could be 50 or more factors which theoretically could be implicated. Your list could include French Fries, could it not? Or even TV watching, DVD players, video games, computers, vitamin supplements, food additives, and so on. But doesn’t it seem unlikely to you that more than one factor contributes to prevalence increase?

    One thing you need to consider is that autism prevalence increase is really a phenomenon of the 1990s. There’s no evidence of prevalence increase before that, despite some claims you might have read about. In the 1960s the prevalence of Kanner autism was already known to be 4.5 in 10,000. This did not change up until around the time the movie Rain Man came out and the broad autism spectrum concept was invented. How is it that none of the 50 factors were epidemic-causing before?

  17. María Luján July 8, 2006 at 04:29 #

    Hi Joseph
    No,There is no biologically plausible mechanism following french fries consumption that can be thought to be involved in some kind of collaboration in the ASD CAUSE. Perhaps ,if there is allergy to the vegetal oil some kind of negative reaction localized in gut can be present, or because of disaccharidases defficiencies some kind of negative gut reaction can be present due to the disaccharides derivated from potatoes.

    You say
    Or even TV watching, DVD players, video games, computers,
    Not plausible and off topic

    vitamin supplements, food additives, and so on.
    Overuse of vitamin supplementation is a bad election for everybody, autistic or not.Overuse of vitamin A in pregnancy is contraindicated. Food aditives or presence of some compounds in water- if there is some metabolic imbalances related for examples to phenol or nitrates managements, it can have negative impact , mainly in children (Nitrates has been studied as you know- “Blue baby syndrome”).

    But doesn’t it seem unlikely to you that more than one factor contributes to prevalence increase?
    No, it doesn´t

    You say
    One thing you need to consider is that autism prevalence increase is really a phenomenon of the 1990s.
    Well , what I have been told modern epidemiology begun in the 60s…
    There’s no evidence of prevalence increase before that, despite some claims you might have read about.
    Because of lack of data, changes in diagnosis criteria, changes in broadener awareness to the conditions simply we do not know for sure. There are a lot of non-diagnosed ASD adult people.

    In the 1960s the prevalence of Kanner autism was already known to be 4.5 in 10,000. This did not change up until around the time the movie Rain Man came out and the broad autism spectrum concept was invented.
    Joseph I am sorry but do you really consider this? Following the history of epidemiology/diagnosis/pshychiatry in the field last 50 years it is not so simple for me.

    How is it that none of the 50 factors were epidemic-causing before?
    Because you are still considering CAUSES and I am trying to explain you that they are insults for me.
    Autism has been linked to near 5 to 100 different genes ( following recent published science). From what I have read , we are talking in the ASD from only a few polymorphisms ( not more than 4/5) to a lot of concomitant polymorphisms ( or talking in other words a lot of concurrents changes in only one base in a gene of the DNA). When complete portions of a gene in a chromosome- hundreds or thousands of bases are changed/altered more severe conditions are present ( Rett, Fragile X for example).
    I consider that this genetics has been present since several generations ago to now. What has changed , and mainly in the last century, is how we change our environment and how many potential stressors we include to this.
    Genetics involves transcriptomics, metabolomics, biochemistry, physiology AND regulation since the brain structure to the regulation networks in the body. We have since DNA repair systems to biofeedbacks systems to several biochemistry cycles coupled- sometimes in a very very very intrincated way. As Ian mentioned recently in another blog, I also think that the broader autism phenotype (BAP) is really broad and diverse.
    Again, please read my post above. As never in the last 50 years in history we use drugs for every bacterian infections, sometimes with concomitant viral infections in children in their first years of life, As never the last 30 years there has been a lot of new vaccines-not only for children-, as never the prescription drugs are being overused- Sometimes but more and more; as never we have environmental problems, as never the environmental contamination is widespread, the air quality has been deteriorating, and so on.
    I was born in 1964. I received not more than 6 vaccines. My children received near 18 before the 2 years of life. They were treated with 3 different kinds of antibiotics- strong-, without any kind of support for GI, when they were ill with bacterian infections. I was given tetracyclines for my childhood infections- that produced some collateral effects. And these are minor differences Yes, Joseph things have changed a lot last 40 years, but mainly last 20 years about how childhood pediatric diseases are managed, about what new antibiotics are given, about what quality of food is presented and so on.
    I am not telling you for sure that this or that CAUSED increase of prevalence; what I am saying is
    1-there is not genetic epidemiology published in ASD at the best of my knowledge. Epi is still being done such as it is for any bacterian/viral disease
    2- there is no knowledge of the impact the 5 to 100 polymorphisms/ partial complete changes genes linked to ASD affects at a systemic and individual level the physiology, brain structure AND answer to individual environmental insult in terms of individual circunstances of exposure and individual genetics.
    3-there are no analyzed theories about the mechanisms that explain the secondary medical conditions to the ASD.
    Because of all this about your question
    How is it that none of the 50 factors were epidemic-causing before?
    Can not be answered
    We do not know if a REAL increase is present
    We are aware that it is very difficult to support a theory for the environment to CAUSE ASD without genetic susceptibility
    We do not know for sure- there are some clues about some-the biochemical mechanisms that can be related to the ASD biochemistry as a whole that can produce the secondary medical conditions that can be present.

    María Luján

  18. Hyperion July 8, 2006 at 08:15 #

    One important thing about the paper you cited:

    “These findings emphasize the need for application of rigorous epidemiologic principles in association studies. Researchers conducting studies on the etiology of late-onset diseases should be aware of this bias.”

    If he’s discussing late-onset diseases, he’s not talking about autism or any other PDD or neurodevelopmental disorder. Those are all childhood-onset and result from changes during neurological development. Late-onset neurological diseases are things like Alzheimer’s, Parkinson’s, possibly schizophrenia could be included, I suppose.

    However, let’s look at Alzheimer’s for a second, just to illustrate an important point:

    As you may have noticed, Alzheimer’s cases have certainly increased dramatically over the past few decades. One could certainly ask if this increase might be due to environmental factors, just as you ask whether the increase in autism prevalence could be linked to environmental factors. However, looking at the specifics of Alzheimer’s, there’s a much more parsimonious explanation: people are living longer. At age 65, 1 in 10 people will have the disorder. At age 85, it’s 1 in 2. We have more people living to advanced ages, which will cause an increase in total diagnoses. So an increase in diagnoses or in prevalence doesn’t necessarily have to equate to environmental changes. It’s important to look to other reasons.

    One possible reason for an increase in autism prevalence might be that parents who carry the genes are more likely to have children now than they might in the past. This might make sense if the parents might have some mildly autistic traits, or perhaps a separate neurodevelopmental disorder, and such parents are more likely to find economic and reproductive success now than they might have in the past. This would be an explanation for how a purely genetic effect could cause the data we’re seeing.

    However, given the short time-period during which you see the increase in prevalence, and given that some of these increases come from within the same cohort (ie kids being diagnosed at later ages), and given that it happened to really take off right after the DSM-IV was published, along with changes in how school districts had to report disabilities, it seems very likely that increased reporting is responsible. Prior to then, it may have been more likely for a school system to shove an autistic kid into special-ed classes and just forget about him. When schools were required to fill out IEPs for special-ed students, and list specific diagnoses, and maintain documentation for all students, it created a situation where kids who were already autistic to begin with were simply more likely to receive a diagnosis and have it reported.

    The thing with environmental causes is that the burden of proof is really on those who wish to make such a claim. Twin studies have shown pretty good evidence for a genetic cause (if I remember correctly, autism is the only disorder that had a higher correlation on twin studies than ADHD, which is considered by many to be the disorder with the most genetic evidence found to date). With environmental causes, I guess I’m not seeing why they would have to exist. I suppose if I saw good evidence that certain environmental factors influenced severity of symptoms in autistic kids, I’d be willing to accept that it might be involved, but absent evidence to show involvement, I can’t really buy the argument that there is some reason why environmental factors would have to be involved. It is especially disturbing to hear speculation about vaccines and antibiotics, though. There is little or no evidence linking them to autism beyond the fact that their use has increased lately, which could really apply to just about anything. However, vaccines and antibiotics save hundreds of thousands of lives each year. You may talk fondly of the days before they were widely used, but you may wish to look up child mortality rates for that period to familiarize yourself with the reasons why those medicines are so widely used today. In fact, it is entirely possible that autistic kids could be more susceptible to those childhood diseases, or that they could be more fatal in autistic kids who had difficulty getting medical attention because of communication difficulties. In that situation, vaccines could be responsible for an increase in autism in a completely non-causative manner: by allowing autistic kids to live through infancy and early childhood.

    Finally, don’t be so sure that there must be a large number of different genes to explain the variety of autistic behavior. While this is certainly possible, and would not surprise me, it is equally possible for complex behaviors to arise from relatively simple mutations. In fact, this is often more likely, as multiple serious mutations can often lead to an inviable fetus. The human brain is a complex machine, and very small changes in the genes that regulate its development can have profound impacts.

  19. María Luján July 8, 2006 at 10:33 #

    Hi Hyperion
    Thank you for your comment about my former post.

    I will comment about , after the quotation of your words

    My intention was to present the approach of genetic epidemiology as important to take into account the genetic plus the environmental contribution in the analysis of potential collaborators in symptoms/triggers/causes and to be open minded to explore all the possibilities. I am not saying that for sure and without doubt there are environmental contributions for all cases- perhaps for subgroups, depending on individual susceptibility.

    _One possible reason for an increase in autism prevalence might be that parents who carry the genes are more likely to have children now than they might in the past. This might make sense if the parents might have some mildly autistic traits, or perhaps a separate neurodevelopmental disorder, and such parents are more likely to find economic and reproductive success now than they might have in the past. This would be an explanation for how a purely genetic effect could cause the data we’re seeing_
    I have never excluded this kind of contributions to the increase in the reported data. I only have pointed out that the situation is enough complex to not discard contributors.

    _However, given the short time-period during which you see the increase in prevalence, and given that some of these increases come from within the same cohort (ie kids being diagnosed at later ages), and given that it happened to really take off right after the DSM-IV was published, along with changes in how school districts had to report disabilities, it seems very likely that increased reporting is responsible_
    Partially, I agree with you. I have made some additional considerations, very long to include here. Perhaps you are interested on my analysis. Please contact me

    _Prior to then, it may have been more likely for a school system to shove an autistic kid into special-ed classes and just forget about him. When schools were required to fill out IEPs for special-ed students, and list specific diagnoses, and maintain documentation for all students, it created a situation where kids who were already autistic to begin with were simply more likely to receive a diagnosis and have it reported_
    Sure, I consider that this kind of situations have collaborated in the present educational data.

    _The thing with environmental causes is that the burden of proof is really on those who wish to make such a claim_
    Fair enough.

    _Twin studies have shown pretty good evidence for a genetic cause (if I remember correctly, autism is the only disorder that had a higher correlation on twin studies than ADHD, which is considered by many to be the disorder with the most genetic evidence found to date)_
    But there are some interesting recent published data about the contribution of environmental impact, depending on individual.
    Ian Parker has written very well about the point in
    “Autism is not always natural variation”:http://a-shade-of-grey.blogspot.com/2006/03/autism-its-not-always-natural.html

    _With environmental causes, I guess I’m not seeing why they would have to exist_
    Genetics only is not the point for me, the consequences in transcription, metabolism and biochemistry and the potential impact of environment modulating genes ( epigenetics) are all important for me.
    _I suppose if I saw good evidence that certain environmental factors influenced severity of symptoms in autistic kids, I’d be willing to accept that it might be involved, but absent evidence to show involvement, I can’t really buy the argument that there is some reason why environmental factors would have to be involved_
    I have never considered that the work is done. What I am is open minded to the idea and I think that there are a lot of clues published- not from the most controversial sources, but from many other fields that ASD research itself.The shift of the analysis of ASD from a purely pshycological disorder to other analysis, based on biology, is too recent.

    _It is especially disturbing to hear speculation about vaccines and antibiotics, though. There is little or no evidence linking them to autism beyond the fact that their use has increased lately, which could really apply to just about anything. However, vaccines and antibiotics save hundreds of thousands of lives each year. You may talk fondly of the days before they were widely used, but you may wish to look up child mortality rates for that period to familiarize yourself with the reasons why those medicines are so widely used today. In fact, it is entirely possible that autistic kids could be more susceptible to those childhood diseases, or that they could be more fatal in autistic kids who had difficulty getting medical attention because of communication difficulties. In that situation, vaccines could be responsible for an increase in autism in a completely non-causative manner: by allowing autistic kids to live through infancy and early childhood_
    I am very aware of the importance of vaccines and antibiotics. However, what I am talking about is in the possibility of individual susceptibility in the early childhood to the actual composition and crowded schedule of vaccines, COMBINED with a certain methodology of approach to the management of the childhood diseases. I live in a country where childhood diseases are very important to control and I am conscious of the importance of tools to control infectious diseases. However, in my family there are antecedents of allergy to the penincillin, that at least 2 times occasionated life- threatening situations.
    Pharmacovigilance of vaccines must be enough strong to avoid the change of one kind of disease for another in susceptible individuals. These ideas about vaccination- and about antibiotics mainly in terms of overuse- are more and more present in the open literature. Again , if you are interested I can provide you a lot of references about .
    I have presented this in another blog but I consider that you can understand me better with this:
    As a parent the (wrong) presentation of the issue is to pick between an infectious and potentially life-threatening disease (by do not vaccinate) or the risk of neurodevelopmental problems, autism and in extreme cases, death (by to vaccinate). No parent must be pushed in this position for me. And the presentation of this dicotomy is worrisome because it is not true in this terms. At an individual level is possible that vaccines can do harm, and also antibiotics, as I presented above. The main point for me is to detect what children are prone to the risk/negative reaction to avoid the potential of damage not to be pushed in the position of to vaccinate or do not vaccinate per se because this is not a solution; it is a nightmare. This is what I consider important. For me it is not to vaccinate at any cost or not to vaccinate at all. It is much more complex. By adopting extreme positions a strong damage is being done to the vaccination program and at least to my autistic child in my personal view, indeed. I am very related to my personal experience about. If you are interested about more, please contact me.

    _Finally, don’t be so sure that there must be a large number of different genes to explain the variety of autistic behavior. While this is certainly possible, and would not surprise me, it is equally possible for complex behaviors to arise from relatively simple mutations. In fact, this is often more likely, as multiple serious mutations can often lead to an inviable fetus. The human brain is a complex machine, and very small changes in the genes that regulate its development can have profound impacts_
    I do not discard this point, however the published evidence at hand presents another situation. I had the idea of from 5 to 20 genes involved, but recent research mentions up to 100. I think that , because of the change of only one base in the gene structure, viability is probably not in risk. Viability, I imagine, is at risk at many many thousands of replacements/alterations in the DNA.

    María Luján

  20. Joseph July 8, 2006 at 16:11 #

    No,There is no biologically plausible mechanism following french fries consumption that can be thought to be involved in some kind of collaboration in the ASD CAUSE.

    Pehaps you haven’t read about trans fats at autismfries.com. Diet is probably more important than anything else, environmentally, in neurodevelopment.

    “Or even TV watching, DVD players, video games, computers,” Not plausible and off topic

    How come? Are you familiar with the studies that link TV watching to ADHD? Why do environmental triggers have to be only poisons, injuries or viruses?

  21. Joseph July 8, 2006 at 16:17 #

    María: You also seem to disagree on the epidemiology. Is there a study, from before 1990, that finds a Kanner autism prevalence considerably higher than 4.5 in 10,000 in Europe or the U.S. ? Better yet, is there any one study, ever, that finds a prevalence considerably higher than 4.5 in 10,000 using Kanner’s autism criteria?

  22. María Luján July 8, 2006 at 22:50 #

    _Perhaps you haven’t read about trans fats at autismfries.com. Diet is probably more important than anything else, environmentally, in neurodevelopment._

    Joseph, we were talking about French fries. I know about trans fats and importance of diet and I consider that Neurodevelopment is much affected by diet( as you say).In my list of concerns is in the firt place.
    You can find here
    “Nutrients, neurodevelopment, and mood”:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15538990&query_hl=1&itool=pubmed_docsum
    a very interesting paper about

    _How come? Are you familiar with the studies that link TV watching to ADHD? Why do environmental triggers have to be only poisons, injuries or viruses._

    I am thinking in a measurable biochemical impact that you can quantitatively measure, compare and analyze.
    “Disentangling the relation between television viewing and cognitive processes in children with attention-deficit/hyperactivity disorder and comparison children”:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16585479&query_hl=4&itool=pubmed_docsum

    “There is no meaningful relationship between television exposure and symptoms of attention-deficit/hyperactivity disorder.”:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16510645&query_hl=4&itool=pubmed_docsum

    I would include stress to your list of poisons, viruses and bacterian infections- because of the effects in the immune system-, but not TV, Cellular Phones, antennas or electromagnetic radiation _for now , and until convincing data about some kind of correlation to be present and a plausible biologically, logical coherent, biochemicaly correct explanation to be presented_

    _You also seem to disagree on the epidemiology. Is there a study, from before 1990, that finds a Kanner autism prevalence considerably higher than 4.5 in 10,000 in Europe or the U.S. ? Better yet, is there any one study, ever, that finds a prevalence considerably higher than 4.5 in 10,000 using Kanner’s autism criteria?_

    As I told you, I consider the epidemiology of relative value because of the confounding variables (Kannerian autism, “regresive” autism , “ stagnant autism” “primary vs secondary”, etc- I know that several of them are not explicitly in the DSMIV but also atypical autism I have heard. I remember David was very kind to clarify me that explicitly exists only very few “different “ autism following the DSMIV). We exchange opinions about this and the BAP some months ago.It seems to me that there is a higher number of regressive/stagnant autism than Kannerian autism than before, but the distintion is only “apparent “ in terms that the “regresive” subgroup can present very mild symptoms before regression. I remember you mentioned near 50 % (but please confirm). Even more, the epidemiology has been done as it is done for viral/bacterian diseases- and ASD it is not. It seems to me that the field of genetic epidemiology is more adequate to analyze ASD in terms of procedures, analysis of bias , braodener criteria and awareness and analysis of conclussions, with specific consideration to avoid errors that are specific of this field because of the need of consideration of Genetics PLUS Environment. With all the information we have about the changes in phsychology, but also in parenting and medicine, how can we compare studies done 40 years ago with now? About even 15 years ago the open research analyzed the same paradigms and protocols , in the case of studies of ASD, using the DSM IV-. I think I will not find it ( the study with higher reports in Kanner´s autism) before 1990 for a number of reasons- and even if not reported nobody can say than in fact they were higher/ or not. However, a kannerian autism- since birth- is for me very difficult to “miss” and therefore I do not think that this kind of autism has increased at all (in true numbers) but always this is related to some published literature I have read- and you are very well informed about, surely more than me in this field.My point is that this does not involve directly that a higher number was not/ was present for sure of other kind of presentations due to the BAP.
    Ma Luján

  23. Hyperion July 8, 2006 at 23:21 #

    Tsk tsk tsk, Joseph, you’re almost as bad.

    “Diet is probably more important than anything else, environmentally, in neurodevelopment.”

    Actually, diet may be the least important environmental factor, at least assuming that the diet contains no known toxins (ie lead) or serious deficiencies. Diet is one thing that almost universally varies from culture to culture, and even from region to region within a culture. And while diet can contribute to such diseases as hypertension or diabetes, it’s just not that big of a factor with neurodevelopmental disorders. If it were, we’d see huge differences in prevalence rates for neurodevelopmental disorders across different regions. I mean far more so than we do now, to an extent that it would be blatantly obvious. This wouldn’t be just a few percentage points, this would be a situation where you’d be finding differences of several orders of magnitude between, say, fish eating populations in the American Northeast, and the grain-eating populations in the American Midwest, to use one example.

    “Are you familiar with the studies that link TV watching to ADHD?”

    Yes, they show that there is no causative effect.

    http://pediatrics.aappublications.org/cgi/content/abstract/117/3/665

    This is actually directly relevant to the discussion at hand: in that incidence, simple correlation turned out to be an illusion. Similarly with vaccines and autism, the supposed correlation turned out to be an illusion.

    This is why it’s important to check and double check the data, because false positives can pop up.

    “Is there a study, from before 1990, that finds a Kanner autism prevalence considerably higher than 4.5 in 10,000 in Europe or the U.S. ? Better yet, is there any one study, ever, that finds a prevalence considerably higher than 4.5 in 10,000 using Kanner’s autism criteria?”

    Here’s the problem: You wish to sample prior diagnoses using one set of criteria, and then compare it to later diagnoses using different criteria. Do you understand why this is completely irrelevant?

    This is pointless. Look, one thing that might help everyone involved would be to study the neuroscience involved in developmental disorders. It might help illuminate why genetic causes are considered the most likely culprit, because the specific neurological issues don’t really resemble what you would see from blunt trauma from environmental factors, it’s a lot more subtle, it involves the “wiring” involved in interneural communication. Environmental toxins just produce dead neurons, but that kind of damage isn’t consistent with what you see with developmental disorders.

  24. María Luján July 9, 2006 at 01:06 #

    Hi Hyperion
    For me the analysis of Joseph, even if I disagree with him, even strongly, deserves consideration and respect. Same yours. Can we agree in mutual respect in disagreement?
    You said
    _This is actually directly relevant to the discussion at hand: in that incidence, simple correlation turned out to be an illusion. _
    …because there is not biological plausibility and also there is not a logical coherent, biochemicaly correct explanation to be presented, even as an hypothesis, to produce the changes that are supposed to take place in ADHD at different levels (Brain, second messengers, BRain physiology, etc.
    You said
    _Similarly with vaccines and autism, the supposed correlation turned out to be an illusion._
    Because the epidemiology is not genetic, because the mechanisms (potential and there are a lot of published clues about negative effects of vaccines related to autoimmunity for example- and others) have not been explored enough ( in terms of Genetics plus Environment) yours is an opinion, valid in considering the available published science,- what has been done- but not well founded in terms of what has not been done- that is a lot.

    You said
    It might help illuminate why genetic causes are considered the most likely culprit, because the specific neurological issues don’t really resemble what you would see from blunt trauma from environmental factors, it’s a lot more subtle, it involves the “wiring” involved in interneural communication. Environmental toxins just produce dead neurons, but that kind of damage isn’t consistent with what you see with developmental disorders._
    Well I would be glad to discuss this point. Do you know this manuscript for example:

    “Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms”:http://ehp.niehs.nih.gov/members/1999/suppl-5/767-775el-fawal/el-fawal-full.html

    I have researched about the issue. Perhaps you are interested about. Please let me know.
    Sincerely
    María Luján

  25. Joseph July 9, 2006 at 01:30 #

    Actually, diet may be the least important environmental factor, at least assuming that the diet contains no known toxins (ie lead) or serious deficiencies.

    I doubt that toxins are the only important factor. There’s considerable evidence about the effects of malnutrition on brain development; fatty acids, iron and so on.

    Of course, I don’t believe this is related to autism in any significant way, but I was just trying to make a point about María’s innumerable environmental factors.

    Here’s the problem: You wish to sample prior diagnoses using one set of criteria, and then compare it to later diagnoses using different criteria. Do you understand why this is completely irrelevant?

    You apparently did not understand my question. I was trying precisely to argue that in order to determine that there has been an increase in prevalence since the 1960s, we should look at studies that use the same criteria as those in the 1960s. Unfortunately, there are none, and if there were, they would no doubt show prevalence to be around 4.5 in 10,000.

    Check out my blog. I discuss autism prevalence in many posts.

  26. Hyperion July 9, 2006 at 06:18 #

    My bad, I thought you were trying to compare 60’s Kanner diagnoses with 90’s DSM diagnoses, and didn’t get that you were illustrating the difference between the two.

  27. lenexa July 9, 2006 at 06:41 #

    From NAA’s press release today, on Fombonne: “‘It is only appropriate that his partnership with pharmaceutical companies be revealed,’ says Claire Bothwell, Board Chair of NAA.”

    Mysteriously omitted from that document: “‘It is only appropriate that I disclose that I was a plaintiff in the very first vaccines-cause-autism tort case and worked as a paralegal soliciting cases for the law firm that filed it,’ adds Bothwell, Board Chair of NAA.”

  28. Joseph July 9, 2006 at 15:04 #

    What I find odd is the implication that the existence of autistic Canadian kids who have not received any thimerosal might depend on Fombonne’s “conflicts of interest”.

  29. David H July 10, 2006 at 15:34 #

    I just read the NAA newsletter which includes the key points of SafeMinds critique of this study. Strangely, none of these points are mentioned by anyone here. The key points are as follows:

    – “The study looked at 27,749 students in grades kindergarten through 12th grade in a Montreal school district and found 187 cases of autism.”

    – “The vast majority of these cases (more than 90%) were born in years in which thimerosal vaccines were widely used for infants in Quebec, as they were in the US.”

    – “Only a tiny fraction of the autism students were born when thimerosal-free DTP and Hib vaccines were given, and these students may have been exposed to thimerosal from the Hepatitis B vaccine newly recommended for infants of foreign-born parents, which made up over one fourth of the greater Montreal population.”

    If those 3 points are true, it seems like Fombonne is relying on a very small sampling of children born when thimerosal free vaccines were given – and then there is the problem of 25% of those children receiving TCV’s because of their parents immigrant status.

  30. anonimouse July 10, 2006 at 16:23 #

    David,

    If you read the study, and not the SafeMinds Cliff Notes version as you seem to often do, you’ll see that Mark Blaxill’s points are poorly taken:

    – The sampling, while relatively small, is statistically significant. The rate of autism in the 1996-1998 birth cohort was higher than the rate of earlier ones.

    – The 90% number is completely irrelevant. Fombonne’s looking at rate of autism among a birth cohort.

    – When was the Hepatits B recommendation made and what was the immunization rate during that time period? I believe the requirement for Hep B vaccination in Quebec is grade 4, so I’d suggest uptake on a “recommneded” vaccine for immigrants was pretty nominal at best..

    Sallie and friends are either too stupid to realize their points are irrelevant or they’re just intentionally being dishonest. At this point, I’m leaning slightly towards the latter.

  31. David H July 10, 2006 at 18:38 #

    Anonimouse,

    OK, you don’t like the 90% number so lets ignore the percentages. It seems to mean that Fombonne used a sample size of something like 2700 children who didn’t receive TCV’s. Do you think that’s enough children? If Generation Rescue was able to compare children receiving vaccines to children receiving no vaccines and the number of children they studied who didn’t receive a vaccine was 2700 would that be enough for you?

    Kev,

    “Canada Speaks: No it’s not vaccines”

    Talk about your false advertising. Even if you accept this study as gold the best you could say is something like:

    “No, it’s not an increase in thimerosal”

    I would love to see a study on whether vaccines played a role in autism – this ain’t it.

  32. clone3g July 10, 2006 at 19:26 #

    Killerjabs said: lets ignore the percentages.

    Yes, let’s ignore the…….oh, I see you’ve started without us.

  33. anonimouse July 10, 2006 at 21:15 #

    “Do you think that’s enough children? If Generation Rescue was able to compare children receiving vaccines to children receiving no vaccines and the number of children they studied who didn’t receive a vaccine was 2700 would that be enough for you?”

    Yes, if the study had sound methodology and you could derive statistically significant results from it.

    Next question.

  34. Joseph July 10, 2006 at 23:44 #

    Ok David, I did the math. Given that the odds of a child not being autistic are 0.994, the odds that none of 2700 children would be autistic are 8.7 x 10^-8, an impossibility. It gets more complicated if you want to calculate “at most 1” and so on.

  35. Joseph July 11, 2006 at 00:16 #

    An interesting bit is the Kindergarten prevalence of 107 in 10,000. If it weren’t for the fact that these are the kids least likely to have received thimerosal, there’d be a huge outcry about the tsunami of autism that is upon us.

    I’ve claimed before that the prevalence of ASD is actually 150 in 10,000 or so. Looks like recognition could very well catch up to this reality.

  36. Hyperion July 11, 2006 at 04:35 #

    Maria:

    The paper which you cite discusses neurodegenerative disorders, which are diseases such as Alzheimer’s, Parkinsons, CJD, etc. These disorders are very different from neurodevelopmental disorders…in fact, they’re the exact opposite.

    neurodegenerative disorders: neural systems develop as normal and subject appears outwardly normal for most of life. Eventually, an environmental or endogenous factor causes neural degeneration and a loss of neural function, leading to outwardly disordered behavior. The condition progresses with continuing loss of neural function and deterioration of outward behaviors, usually culminating in death.

    neurodevelopmental disorders: neural systems develop differently from the get-go (AutismDiva has a great post on this subject called “When We Were Small – Very Small”). Changes in the neurological makeup are endogenous to the organism, and subject displays outwardly disordered behavior, which may progress towards more neurotypical behavior over the lifetime, or may not.

    Huge difference.

    David:

    A: 90% of the children in the study as a whole received thimerosal. Therefore it is irrelevant whether 90% of those diagnosed received thimerosal. This is basic statstical analysis. Actually, no, this is even more basic than that, this is simple arithmetic.

    B: While Joseph’s numbers seem more correct, even your estimate of 2,700 is more than adequate as a sample size. In the USA, Presidential polling data regularly uses sample sizes of ~1,000 to extrapolate the political preferences of the entire country. They can do this to within a confidence interval of a few percentage points with 95% validity. A sample of 2,700 would be perfectly valid. After all, it’s 2,688 more than the Geiers used.

  37. María Luján July 11, 2006 at 05:44 #

    Hi Hyperion
    Child Neurol. 2004 Jun;19(6):413-7.
    Polymorphisms in xenobiotic metabolism genes and autism.
    Serajee FJ, Nabi R, Zhong H, Huq M.
    Department of Pediatrics, Wayne State University, Detroit, MI, USA.
    Autism is a neurodevelopmental syndrome defined by deficits in social reciprocity and communication and by unusual repetitive behaviors. Although there is an underlying genetic predisposition, the etiology of autism is currently unknown. A recent increase in prevalence suggests that genetically determined vulnerability to environmental exposure might contribute to the causation of autism. We performed family-based association studies of polymorphisms in metal-regulatory transcription factor 1(MTF1), a multispecific organic anion transporter (ABCC1), proton-coupled divalent metal ion transporters (SLC11A3 and SLC11A2), paraoxonase 1 (PON1), and glutathione S-transferase (GSTP1) genes in 196 autistic disorder families. There was deviation from the expected pattern of transmission for polymorphisms in MTF1 (Single nucleotide polymorphism database reference identification number, dbSNP rs3790625, P = .02) and divalent metal ion transporter SLC11A3 (dbSNP rs2304704, P = .07) genes. Although these results might represent chance finding, further investigations of genetic variations of metal metabolism in autism are warranted.
    There are several mansucripts About specific differences for example in neurotrophic factors in ASD:
    Brain-Derived Neurotrophic Factor (BDNF) and Autoantibodies to Neural Antigens in Sera of Children with Autistic Spectrum Disorders, Landau-Kleffner Syndrome, and Epilepsy
    Biological Psychiatry
    Background
    Brain derived neurotrophic factor (BDNF) elevation in newborn sera predicts intellectual/social developmental abnormalities. Other autoantibodies (AAs) to endothelial cells (ECs) and myelin basic protein (MBP) are also elevated in some children. We tested relationships between BDNF, BDNF AAs, and other AAs in children with these disorders.

    Selected neurotrophins, neuropeptides, and cytokines: developmental trajectory and concentrations in neonatal blood of children with autism or Down syndrome • ARTICLE
    International Journal of Developmental Neuroscience, In Press, Phillip G. Nelson, Thea Kuddo, Eun Young Song, James M. Dambrosia, Shawn Kohler, Gowri Satyanarayana, Cassandra VanDunk, Judith K. Grether and Karin B. Nelson
    Using a double-antibody immunoaffinity assay (Luminex) and ELISA technology, we measured concentrations of certain neurotrophins, neuropeptides, and cytokines in pooled samples (one to three subjects per sample) eluted from archived neonatal blood of children with later-diagnosed autism, Down syndrome, very preterm birth, or term control infants. We also measured analytes in blood from healthy adult controls. Case or control status for infant subjects was ascertained by retrospective review of service agency medical records. We observed inhibitory substances in eluates from archived bloodspots, especially marked for measurement of BDNF. Concentrations in control subjects differed by age: BDNF rose markedly with age, while NT-3 and NT-4/5 concentrations were lower in adults than in newborn infants. IL-8 concentrations were higher in newborn infants, preterm and term, than in adults. Considered by diagnostic group, total protein was higher in Down syndrome than in either autism or control subjects. In infants with Down syndrome, concentrations of IL-8 levels were higher than in controls, whether or not corrected for total protein; NT-3 and CGRP were lower and VIP higher. In samples from autistic subjects, NT-3 levels were significantly lower than controls and an increase in VIP approached statistical significance. Concentrations of NT-4/5 and CGRP were correlated in infants with autism but not in Down syndrome or controls. Some of these results differ from earlier findings using a single-antibody recycling immunoaffinity chromatography (RIC) system. We discuss interrelationships of VIP, NT-3 and IL-8 and their potential relevance to features of the neuropathology of autism or Down syndrome
    Associations of BDNF with susceptibility to HM
    Neurotoxicol Teratol. 2005 Nov-Dec;27(6):781-96.
    Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function.
    Echeverria D, Woods JS, Heyer NJ, Rohlman DS, Farin FM, Bittner AC Jr, Li T, Garabedian C.

    Toxicol Sci. 2004 Oct;81(2):354-63. Epub 2004 Jul 14.
    Chronic low-level mercury exposure, BDNF polymorphism, and associations with self-reported symptoms and mood.
    Heyer NJ, Echeverria D, Bittner AC Jr, Farin FM, Garabedian CC, Woods JS.

    Am J Med Genet B Neuropsychiatr Genet. 2005 Jan 5;132(1):96-9.
    Mutation screen of the brain derived neurotrophic factor gene (BDNF): identification of several genetic variants and association studies in patients with obesity, eating disorders, and attention-deficit/hyperactivity disorder.

    Friedel S, Horro FF, Wermter AK, Geller F, Dempfle A, Reichwald K, Smidt J, Bronner G, Konrad K, Herpertz-Dahlmann B, Warnke A, Hemminger U, Linder M, Kiefl H, Goldschmidt HP, Siegfried W, Remschmidt H, Hinney A, Hebebrand J.

    J Neurosci. 2004 May 5;24(18):4401-11.
    Variant brain-derived neurotrophic factor (BDNF) (Met66) alters the intracellular trafficking and activity-dependent secretion of wild-type BDNF in neurosecretory cells and cortical neurons.

    Chen ZY, Patel PD, Sant G, Meng CX, Teng KK, Hempstead BL, Lee FS.

    Do you know the work of Dr JS Woods? You can find it in Pubmed. I am not saying that HM can produce autism, what I am saying is that because of all the differences since we were small- that can be found in autistic people comparing to NT development linked to genetics-even unnoticed since birth, HM toxicity CAN be higher than thought before, in terms of accumulation.
    There is not ONE genetic epidemiology study on ASD (Including epistasis- interactions of several genes at once- or susceptible population and the correct amount of potential stressors to the immune system-for example).
    That´s also a Huge problem for me.
    The toxicology of mercury has been revisited:
    Med Pr. 2001;52(1):45-51.
    Genetic polymorphism of glutathione s-transferase as a factor predisposing to allergic dermatitis]
    Lutz W, Tarkowski M, Nowakowska E.
    In the inductive phase of contact allergic dermatitis, simple chemical compounds (haptens) produce together with epidermic proteins adducts presented by Langerhans cells to T lymphocytes. Binding to protein carrier is a necessary condition of transforming a low-molecular allergen into immunogenic one and evoking immunological reaction. The production of allergen adducts with proteins is conditioned by the presence of electrophilic groups in their molecules, or their acquiring during biotransformation phase I. Active allergen metabolites undergo further alterations during biotransformation phase II which leads most frequently to the decline in their chemical activity and more rapid excretion from the body. The number of reactive metabolites (reactive allergens) available for producing adducts with proteins keeps the balance between activation and deactivation reactions. Glutathione S-transferases play a particular role in the allergens (or their metabolites) deactivation process in biotransformation phase II. These enzymes catalyse reactions responsible for the declined electrophilic potential of allergens (or their metabolites), and thus for the decrease in the number of allergen molecules able to produce protein covalent bindings (adducts). Glutathione S-transferases, occurring in the human cellular cytoplasm belong to five classes: alpha(GST A), mu(GST M), theta(GST P), pi(GST T) and Z(GST Z), as well as to one class present in microsomes. The study indicated the presence of isoenzymes GST T1 and GST M1 in the skin. Both isoforms participate in the process of low-molecular allergen biotransformation. Carriers of defective genes GST T1 and/or GST M1 are more vulnerable to allergenic effect of some allergens, e.g. thimerosal, which is associated with the absence of or decrease in the activity of isoenzymes GST T1 and GST M1.
    And there is a study linking GSTM1 to ASD.
    In Contact Dermatitis 2005 53:324-326, Thimerosal Is it Irrelevant? Several considerations are presented about individual susceptibility.
    Discussion about what is innate and what is adquired is very active in general, in several fields. ASD is not different in this sense.
    I apologize to include some long abstracts but I felt that they presented- even partially- the point.
    Ma Luján

  38. Kev July 11, 2006 at 06:43 #

    _”Talk about your false advertising. Even if you accept this study as gold the best you could say is something like:”_

    With all due respect David, I really don’t think that someone who’s nom-de-plume used to be ‘killerjabs’ is in a position to call anyone else to task over vaccines.

    I’m assuming you are discounting thiomersal as a sole trigger? This puts you at odds with just about every anti-thiomersal autism group out there. OK, fair enough – so, considering the poor standard of science for the thiomersal connection, what exactly leads you to believe anything else may be implicated, exactly what else do you believe may be implicated and how do these things fit/not fit with the thiomersal hypothesis?

  39. David H July 11, 2006 at 21:41 #

    “With all due respect David, I really don’t think that someone who’s nom-de-plume used to be ‘killerjabs’ is in a position to call anyone else to task over vaccines.”

    Powerful (ad hominem) argument Kev. I fail to see how my interest in boxing has anything to do with this topic. I’m more of an MMA (mixed martial arts) fan now anyway.

    “I’m assuming you are discounting thiomersal as a sole trigger?”

    I’m having a deja vu but yes, I do believe that we need to study vaccines as a whole as a potential cause of autism and not focus on a single ingredient. And I would also like to point out that I highly doubt thimerosal was completely removed in Canada due to its presence in the vaccine manufacturing process.

    “what exactly leads you to believe anything else may be implicated, exactly what else do you believe may be implicated and how do these things fit/not fit with the thiomersal hypothesis?”

    I believe that autism is an immune disorder caused, at least in part, by vaccines. There are many studies showing immune disorders in autistic children. I’ve posted several links to studies from the most recent IMFAR in the past illustrating this. There are also studies showing how vaccines and vaccine ingredients can cause immune disorders. I don’t think this puts me at odds with the anti-thimerosal groups because I am strongly against mercury in vaccines, as opposed to the mercury proponents at the AAP, CDC and presumably some of your biggest fans.

    I actually have a scientist in my family (ok, my wife’s side) with whom I would discuss this topic during family visits over the past few years. I don’t think he took my views seriously but he was always polite and always listened to me. He apparently conducted his own research and informed me last year that he believed vaccines were responsible for the autism epidemic. His feelings are too many vaccines at too young of an age causing autoimmunity. But he doesn’t believe thimerosal is the culprit – at least he didn’t last time I saw him which was several months ago.

    His company is in the business of developing cures and he is now working on one for autism. Last I heard he was testing a drug on pigs, which apparently have an immune system similar to people. I believe he is looking into down regulating the inflammatory cytokines such as gamma interferon but I’m not able to follow much of what he says.

  40. Hyperion July 12, 2006 at 00:56 #

    Maria:

    I could be wrong, but I believe that metal ion transporters refers to the voltage-gated Na+ and Ca+ channels. While these channels are an essential part of neurotransmission, and thus these findings may shed new light on the neuroetiology of autism, you should understand that the term “metal” here is different from mercury.

    With regards to the neonatal protein study, the comparison to Down’s Syndrome children is interesting, just not for the reason you believe. Down’s Syndrome is known to be genetic in origin and its genetic cause – an extra chromosome in the 22nd pair – is well documented. That autistic children may have similar protein issues as Down’s kids is actually good evidence that something genetically interesting may be going on.

    With the final study, all I can say is that contact dermatitis is a skin rash. While I don’t need to tell you that a skin rash is very different from autism, this actually might help explain why some people erroneously link autism and vaccines. If autistic kids are more likely to have a harmless dermatologcal reaction to a vaccine, that might cause parents to take more notice of their kids right at the age when autism often expresses its first symptoms in all kids, even unvaccinated ones, and cause them to erroneously link autistic symptoms to vaccinations.

    David:

    Why do you believe that vaccines must be responsible? After all, plenty of children have immune disorders without developing autism, and many children have all kinds of allergies without developing autism. Of course, the vast majority of children are immunized without developing autism as well.

    Furthermore, children born infected with HIV (due to maternal transmission) do not, to my knowledge, have an increased prevalence of autism. And yet these children are as immunocompromised as one can get. Young children are often given cancer treatments which cause immunosuppression, and yet they do not develop autism.

    Ok, though, maybe you’re not saying that it’s damage to the immune system, but the immune system going into overdrive as with allergies. Ok, then why don’t anti-histamines or mast-cell stailizers “cure” autism? Why are there so many children with serious allergies who do not develop autism? Why is it that you cannot point to a specific allergen (other than supposedly vaccinations) that are involved? Finally, by what process would an immune system dysfunction cause the symptoms seen in ASDs?

    I mean, c’mon, if you’re so sure of this hypothesis, where is your evidence? Surely you didn’t come to the conclusion first and now are searching for evidence, right? Surely you looked over available evidence that led you to an informed conclusion, right? So where is your evidence?

  41. María Luján July 12, 2006 at 01:51 #

    Hi Hyperion
    You said
    I could be wrong, but I believe that metal ion transporters refers to the voltage-gated Na+ and Ca+ channels. While these channels are an essential part of neurotransmission, and thus these findings may shed new light on the neuroetiology of autism, you should understand that the term “metal” here is different from mercury.

    Hyperion , I know that metals here are different from mercury – I assure you (don´t be worried about please). If you want we can have a discussion about periodic properties, but I want to point out Two things
    1- Ca channels disturbances have been found and reported in ASD. I have a lot of references about and if you are interested I can e-mail to you ( the review involves 25 pages more or less)
    2- No, I am talking about Metal +2 transporters, talking about this kind of transporters:

    J Pharmacol Exp Ther. 2005 Nov;315(2):896-904. Epub 2005 Aug 4
    Handling of the homocysteine S-conjugate of methylmercury by renal epithelial cells: role of organic anion transporter 1 and amino acid transporters.

    Zalups RK, Ahmad S.

    Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.

    Recently, the activity of the organic anion transporter 1 (OAT1) protein has been implicated in the basolateral uptake of inorganic mercuric species in renal proximal tubular cells. Unfortunately, very little is known about the role of OAT1 in the renal epithelial transport of organic forms of mercury, such as methylmercury (CH(3)Hg(+)). Homocysteine (Hcy) S-conjugates of methylmercury [(S)-(3-amino-3-carboxypropylthio)(methyl)mercury (CH(3)Hg-Hcy)] have been identified recently as being potentially important biologically relevant forms of mercury. Thus, the present study was designed to characterize the transport of CH(3)Hg-Hcy in Madin-Darby canine kidney (MDCK) cells (which are derived from the distal nephron) that were transfected stably with the human isoform of OAT1 (hOAT1). Data on saturation kinetics, time dependence, substrate specificity, and temperature dependence demonstrated that CH(3)Hg-Hcy is a transportable substrate of hOAT1. However, substrate-specificity data from the control MDCK cells also showed that CH(3)Hg-Hcy is a substrate of one or more transporter(s) that is/are not hOAT1. Additional findings indicated that at least one amino acid transport system was probably responsible for this transport. It is noteworthy that the activity of amino acid transporters accounted for the greatest level of uptake of CH(3)Hg-Hcy in the hOAT1-expressing cells. Furthermore, rates of survival of the hOAT1-transfected MDCK cells were significantly lower than those of corresponding control MDCK cells when they were exposed to cytotoxic concentrations of CH(3)Hg-Hcy. Collectively, the present data indicate that CH(3)Hg-Hcy is a transportable substrate of OAT1 and amino acid transporters and, thus, is probably a transportable mercuric species taken up in vivo by proximal tubular epithelial cells.

    Toxicol Sci. 2005 Dec;88(2):630-44. Epub 2005 Sep 14.
    Role of organic anion and amino acid carriers in transport of inorganic mercury in rat renal basolateral membrane vesicles: influence of compensatory renal growth.

    Lash LH, Hueni SE, Putt DA, Zalups RK.

    Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
    Susceptibility to renal injury induced by inorganic mercury (Hg(2+)) increases significantly as a result of compensatory renal growth (following reductions of renal mass). We hypothesize that this phenomenon is related in part to increased basolateral uptake of Hg(2+) by proximal tubular cells. To determine the mechanistic roles of various transporters, we studied uptake of Hg(2+), in the form of biologically relevant Hg(2+)-thiol conjugates, using basolateral membrane (BLM) vesicles isolated from the kidney(s) of control and uninephrectomized (NPX) rats. Binding of Hg(2+) to membranes, accounted for 52-86% of total Hg(2+) associated with membrane vesicles exposed to HgCl(2), decreased with increasing concentrations of HgCl(2), and decreased slightly in the presence of sodium ions. Conjugation of Hg(2+) with thiols (glutathione, L-cysteine (Cys), N-acetyl-L-cysteine) reduced binding by more than 50%. Under all conditions, BLM vesicles from NPX rats exhibited a markedly lower proportion of binding. Of the Hg(2+)-thiol conjugates studied, transport of Hg-(Cys)(2) was fastest. Selective inhibition of BLM carriers implicated the involvement of organic anion transporter(s) (Oat1 and/or Oat3; Slc22a6 and Slc22a8), amino acid transporter system ASC (Slc7a10), the dibasic amino acid transporter (Slc3a1), and the sodium-dicarboxylate carrier (SDCT2 or NADC3; Slc13a3). Uptake of each mercuric conjugate, when factored by membrane protein content, was higher in BLM vesicles from uninephrectomized (NPX) rats, with specific increases in transport by the carriers noted above. These results support the hypothesis that compensatory renal growth is associated with increased uptake of Hg(2+) in proximal tubular cells and we have identified specific transporters involved in the proce

    Toxicol Lett. 2006 Mar 1;161(3):210-8. Epub 2005 Oct 10.
    Behavioral changes in metallothionein-null mice after the cessation of long-term, low-level exposure to mercury vapor.

    Yoshida M, Watanabe C, Kishimoto M, Yasutake A, Satoh M, Sawada M, Akama Y.

    Department of Biochemistry, Division of Chemistry, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki 261-8511, Japan.

    The neurobehavioral changes in wild-type and metallothionein (MT)-null mice after the cessation of long-term, low-level exposure to Hg(0) were investigated. MT-null and wild-type females were continuously (24h/day) exposed to mercury vapor (Hg(0)) at 0.055mg/m(3) (range: 0.043-0.073mg/m(3)), which was similar to the current threshold limit value (TLV), for 29 weeks. The effects on behavior, such as locomotor activity in the open field (OPF), learning ability in the passive avoidance response (PA) and spatial learning ability in the Morris water maze (MM) were examined immediately and 12 weeks after the cessation of exposure. Immediately after the exposure had ceased, total locomotor activity in OPF was decreased in the both strain of mice, although the MT-null mice appeared to show more distinct effect. In the PA test, the exposed animals of both strains showed learning impairment as compared to un-exposed mice. Twelve weeks after the cessation of exposure, the locomotor activity in OPF was elevated in the exposed mice of both strains, while the learning ability in the PA test appeared normal in both strains. Spatial learning ability was not affected at all. Immediately after the exposure had ceased, the brain mercury concentration of the exposed wild-type mice was 1.75mug/g, twofold of that in the MT-null mice. In 12 weeks, brain mercury levels decreased to approximately 1/20 of those in immediately after the exposure in both of the strains. These results for the first time indicated that long-term, low-level exposure to Hg(0) could exert neurobehavioral effects, which were not reversible even after a long exposure-free period. Whereas the effects on learning ability were presumably transient, the effects on spontaneous behavior as evaluated in OPF were persistent. Finally, the MT-null mice seemed more susceptible to Hg(0)-induced neurotoxicity than the wild-type mice, confirming our previous results.

    J Toxicol Environ Health B Crit Rev. 2006 Jan-Feb;9(1):63-85.

    The speciation of metals in mammals influences their toxicokinetics and toxicodynamics and therefore human health risk assessment(1).

    Yokel RA, Lasley SM, Dorman DC.

    Pharmaceutical Sciences, College of Pharmacy, and Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, KY, 40536-0082, USA.

    Chemical form (i.e., species) can influence metal toxicokinetics and toxicodynamics and should be considered to improve human health risk assessment. Factors that influence metal speciation (and examples) include: (1) carrier-mediated processes for specific metal species (arsenic, chromium, lead and manganese), (2) valence state (arsenic, chromium, manganese and mercury), (3) particle size (lead and manganese), (4) the nature of metal binding ligands (aluminum, arsenic, chromium, lead, and manganese), (5) whether the metal is an organic versus inorganic species (arsenic, lead, and mercury), and (6) biotransformation of metal species (aluminum, arsenic, chromium, lead, manganese and mercury). The influence of speciation on metal toxicokinetics and toxicodynamics in mammals, and therefore the adverse effects of metals, is reviewed to illustrate how the physicochemical characteristics of metals and their handling in the body (toxicokinetics) can influence toxicity (toxicodynamics). Generalizing from mercury, arsenic, lead, aluminum, chromium, and manganese, it is clear that metal speciation influences mammalian toxicity. Methods used in aquatic toxicology to predict the interaction among metal speciation, uptake, and toxicity are evaluated. A classification system is presented to show that the chemical nature of the metal can predict metal ion toxicokinetics and toxicodynamics. Essential metals, such as iron, are considered. These metals produce low oral toxicity under most exposure conditions but become toxic when biological processes that utilize or transport them are overwhelmed, or bypassed. Risk assessments for essential and nonessential metals should consider toxicokinetic and toxicodynamic factors in setting exposure standards. Because speciation can influence a metal’s fate and toxicity, different exposure standards should be established for different metal species. Many examples are provided which consider metal essentiality and toxicity and that illustrate how consideration of metal speciation can improve the risk assessment process. More examples are available at a website established as a repository for summaries.

    Guang Pu Xue Yu Guang Pu Fen Xi. 2005 Oct;25(10):1688-92.
    Study on Hg2+ distribution and speciation in different tissues of rats]

    [Article in Chinese]

    Shen JC, Huang ZY, Zhuang ZX, Wang XR, Frank LS.

    Department of Chemistry, The Key Laboratory of Analytical Sciences of the Ministry of Education, Xiamen University, Xiamen 361005, China.

    Mercury is one of the important pollutants that threaten people health greatly in environment. The purpose of this paper was to determine mercury distribution and mercury binding proteins in different tissues of rat fed orally with mercuric chloride by ICP-MS and SEC-UV-ICP-MS. The result showed that liver and kidney induced large amount of metallothioneins that was found to bind to mercury, copper and zinc after mercury intake in stomach and intestines. The metallothioneins induced may be prior to combine the mercury so that it would decrease mercury binding with the other proteins that would disable their normal function.

    J Phys Chem A Mol Spectrosc Kinet Environ Gen Theory. 2006 Jan 19;110(2):452-62.
    Computational studies of the coordination stereochemistry, bonding, and metal selectivity of mercury.

    Tai HC, Lim C.

    Department of Chemistry, National Tsing Hua University, Hsinchu 300, Taiwan.

    Knowledge of the bonding and selectivity of organic mercury, [H3C-Hg]+ (MeHg+), and inorganic Hg2+ for protein and DNA functional groups is important for understanding the mechanism of heavy metal poisoning. Herein, we elucidate (1) the differences between inorganic Hg2+ and organic MeHg+ in their interactions with different ligands of biological interest, (2) the protein and DNA functional groups that Hg2+ and MeHg+ target in aqueous solution, and (3) the likelihood of “soft” Hg2+ displacing the “borderline” Zn2+ bound to “harder” nitrogen/oxygen-containing side chains such as His and Asp/Glu. The results reveal that, relative to Hg2+, the lower positive charge on MeHg+ results in a longer and weaker bond with a given ligand, in accord with the observed kinetic lability of MeHg+ complexes. They also indicate that negatively charged or polar amino acid side chains containing S-/O-/S/N donors could coordinate to both organic MeHg+ and inorganic Hg2+. In addition, Gua and Cyt could also coordinate to MeHg+ and disrupt Gua…Cyt base pairing. A key novel finding is that Hg2+ is a far better electron acceptor than Zn2+, and can thus accept more negative charge from the Zn ligands than the native Zn2+, thus enhancing Hg-ligand interactions and enabling Hg2+ to displace the native cofactor from zinc essential enzymes and “structural” Zn proteins. The results herein support several possible mechanisms for Hg poisoning. Ways that mercury poisoning could be prevented in cells are discussed.
    In the management of xenobiotics, factors affecting the toxicity of reactive metabolites are
    1-Levels of activating enzymes
    2-Levels of conjugating enzymes
    3-Levels of cofactors or conjugating chemicals. Glutathione depletion potentiates covalent binding and hepatotoxicity…Reduced glutathione plays an important protective role rapping electrophilic metabolites and preventing binding to hepatic proteins and enzymes.
    There is an entire chapter in the “Textbook of Modern Toxicology” from Hogson-2004- dedicated to Chemical and Physiological influence on xenobiotics metabolism.: Nutritional effects, Development (Phase II reactions are age dependent: for example glucuronidation, glycine levels are low the first 8 weeks in human, Transcripted “Glutathione conjugation may also be impared, because of defficiency of available glutathione”) In this book there is a figure of how there is a developmental pattern of glutathione S-transferase activity in female rats from 1 to 140 days life ( from near 5 nmoles/minml to 75 nmoles /minml).. The chapter (163-202) concludes:
    The toxic sequelae will vary with developmental stage, nutritional status, health or physiological previous status:

    In sequence, from the reaction between a xenobiotic and glutathione, several enzymes are involved: glutathione S transferase-(GSM), gama glutamyl transpeptidase, cisteynil glicinase, N acetyl transferase and finally conjugates with mercapturic acid is formed. This sequence needs adequate levels of essential amino acids, pantothenic acid for Coenzyme A and phosphorus for the synthesis of ATP.
    So I wonder if besides/ beyond glutathione , that needs aminoacids , the transformation to mercapturic acid somewhat can be hindered because of problems in some of these enzymes or nutritional problems affected by genetics and epigenetics in ASD? Nobody has published never a study on ASD children about this..
    All the complete system of detoxification, including phase I and phase II in liver must be working to detoxify efficiently.
    There are many biochemical steps that can be altered to have the findings that many researchers have in ASD.
    I do think that in autism there is certain combination of polymorphisms that are present, not only one. The key for me is the combination of genetics/epigenetics and the environment in an individual basis (A+B+C…+Z). A NT person can have A or P but this genetically different person than ASD only will present the problem related. If he/she carries the specific polymorphism he/she will have a personal/individualized presentation of. A NT person can have Hg poisoning (for example from contaminated fish consumption) but after detection and treatment the problem will solve because the Hg is showed up-in urine, blood or feces. A NT person with a polymorphism related would have a strong effect. For an ASD child the effect can be VERY strong, avoiding excretion and producing Hg/Al sequestering in tissues, coordinated to S. Only this way is explained the levels of Hg, Al, Pb, As, Cd that many children-not tested in commercial labs but repeated in trustable labs- I have first hand experience- have, because of blocking of the excretion routes and bioaccumulation.
    In the case of Hg susceptibility, there is a wide distribution of resistance in NT people. Some people have no evidences with very high blood values and other have with low
    blood values. Clarkson manuscripts present very well the issue:

    “The review of Thomas Clarkson on mercury”:http://www.ehponline.org/members/2002/suppl-1/11-23clarkson/clarkson-full.html

    and also the lap time between exposure and symptoms

    “Silent Latency Periods in Methylmercury Poisoning and in Neurodegenerative Disease”:http://www.ehponline.org/members/2002/suppl-5/851-854weiss/weiss-full.html
    I do think that they (BNDF, GMST, CPOX) deserves further studies or consideration under the studies of the Dr Woods. Also the kind of medical studies related to oxidative stress and changes in several enzymes that are cited lastly in this review.
    Remember please that some subgroups of children with ASD tested possitive for oxidative stress and mitochondrial problems.

    With regards to the neonatal protein study, the comparison to Down’s Syndrome children is interesting, just not for the reason you believe. Down’s Syndrome is known to be genetic in origin and its genetic cause – an extra chromosome in the 22nd pair – is well documented. That autistic children may have similar protein issues as Down’s kids is actually good evidence that something genetically interesting may be going on.

    Yes, this is my point. Autistic children, at least a subgroup, present from the birth differences in proteins- and proteins are of paramount importances in the management of xenobiotics for example. If there is this kind of alteratioins in this kind of proteins, what about others related to what I am pointing out? Not studied yet….

    With the final study, all I can say is that contact dermatitis is a skin rash. While I don’t need to tell you that a skin rash is very different from autism, this actually might help explain why some people erroneously link autism and vaccines. If autistic kids are more likely to have a harmless dermatologcal reaction to a vaccine, that might cause parents to take more notice of their kids right at the age when autism often expresses its first symptoms in all kids, even unvaccinated ones, and cause them to erroneously link autistic symptoms to vaccinations

    No Hyperion. For me if the child is dermatologically sensitive to thimerosal, what about injected thimerosal? All mercury is different: inhalated, injected or ingested are all managed differently and you can NOT compare the one way of exposure and to conclude something so easily for me. What is the genetic polymorphism related to this sensitivity? What if Autistic children have it? How concomitant differences are present that can make different Hg injected from inhalated from ingested? BTW, thimerosal is not A CAUSE of autism for me. FOR ME it can not be managed and can not be excreted properly in a subgroup of autistic children- because of genetics/epigenetics, as it can happens also with the inhalated ( from air Hg is ubiquos) and so on.

    Sincerely
    María Luján

  42. David H July 12, 2006 at 03:06 #

    Hyperion,

    “Why do you believe that vaccines must be responsible? ”

    Well, I do not believe that autism is strictly a genetic disorder and I believe the numbers are increasing (although I accept that part of the increase is likely due to increased awareness). Given the timing of the vaccine schedule change and the increase in autism numbers and vaccines are an suspect. The word “must” is a bit strong although I can see why you would think I feel that way. I have to admit that the strong feelings written by people like Kev tend to get me riled up and I let emotions get the best of me. What I’m trying to say is that I’m not 100% convinced that vaccines are the cause. It’s probably more in the range of 99.8%. But the only thing that would convince me otherwise would be a study comparing an unvaccinated population to a vaccinated one.

    “I mean, c’mon, if you’re so sure of this hypothesis, where is your evidence? Surely you didn’t come to the conclusion first and now are searching for evidence, right? Surely you looked over available evidence that led you to an informed conclusion, right? So where is your evidence?”

    I could ask the same question of you. Where is the evidence that vaccines do not cause autism? The epi studies looking at a single ingredient don’t even come close to cutting it. But I don’t want to answer your question with a question. You obviously know I don’t have evidence but a good article to read is here: http://www.usautism.org/PDF_files_newsletters/herbert_autism_brain_or_affecting_brain_final.pdf

  43. Kev July 12, 2006 at 05:44 #

    _”Powerful (ad hominem) argument Kev. I fail to see how my interest in boxing has anything to do with this topic. I’m more of an MMA (mixed martial arts) fan now anyway.”_

    OK, ten points for making me laugh.

    _”I’m having a deja vu but yes, I do believe that we need to study vaccines as a whole as a potential cause of autism and not focus on a single ingredient.”_

    So, discounting the theory that thiomersal is the sole vaccine ingredient at fault, what leads you to believe vaccines cause autism? Do you also believe that the groups that _do_ say mercury is the sole issue have behaved somewhat irresponsibly?

    _”I believe that autism is an immune disorder caused, at least in part, by vaccines. There are many studies showing immune disorders in autistic children. I’ve posted several links to studies from the most recent IMFAR in the past illustrating this. There are also studies showing how vaccines and vaccine ingredients can cause immune disorders. I don’t think this puts me at odds with the anti-thimerosal groups because I am strongly against mercury in vaccines, as opposed to the mercury proponents at the AAP, CDC and presumably some of your biggest fans.”_

    Two separate issues David. Issue one – can autism be an immune disorder? Of course it _can_ but is it? There’s some very interesting stuff going on in that respect but unfortunately, your dogged determination to link these possibilities to vaccines is clouding the issue for you. Issue two – being strongly against mercury in vaccines has no bearing in causation.

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