Contrary to widely-promoted assertions, the Hertz-Picciotto et al 2010 study does not in the slightest constitute evidence that mercury has not been involved in causation of autism.
They found no association of mercury blood levels with autism. Which is not surprising as the autism would be caused not by mercury in blood but by mercury in brain cells. It's been known for decades that blood levels of mercury are near-useless as an indicator of body burden of mercury and chronic mercury poisoning.
“The distribution of mercury into the body tissues is highly variable and there appears to be little correlation between levels in urine, blood or hair and toxic effects.” —NIDH/ADA Workshop on Biocompatibility of Metals, Journal of the American Dental Association 109 (September 1984).
Further references for the uselessness of blood mercury levels can be found in the critique by Joachim Mutter of the fraudulent SCENIHR report, and in Mutter, Naumann, Guethlin. Comments on the Article "The toxicology of mercury and its chemical compounds". Crit Rev Toxicol 2007 37:537-549.
Even my mere common-or-garden general practitioner ("family doctor") was able to tell me years ago that a blood test of mercury would be worthless for diagnosing chronic mercury poisoning.
A great way to get the wrong answers is to ask the wrong questions. A far more right question to have asked would have been whether there is an association between number of mothers' amalgams (i.e. a cause) and autistic behaviors (i.e. the key effect of interest). Some such studies have already been done and found significantly positive results. They are far easier to carry out than this one requiring going round sucking blood from children rather than just counting their mothers' fillings.
Another right question would be the association of lack of outdoor air with autism, and again significantly positive results have been found by Waldman & Adilov.
More advanced understanding of antiinnatia; this post is not for beginners here!
Don't start your reading here, first study the 1993 paper and the home page here.
It is mainly about concepts. Sound science cannot be founded on concepts alone, but science gets in a muddle if the concepts are not properly clarified. So this can be important.
The nature of the autistic syndrome.
An expression "the autistic spectrum" has become popularised. This is regrettable because it promotes a fallacy that autism variation is all or mostly on one dimension from mild to severe. A more reasonable concept is that autism, Aspergers, and related things such as dyslexia, are all part of the autistic syndrome, that is tendency to clustering together of certain characteristics. This clustering is many-dimensional, with the number of dimensions being equal(ish?) to the number of characteristics whose expression can be affected by antiinnatia. In practice, as generally found with factor analysis, there would be a smaller number of main/most important dimensions (such as predisposition to allocating attention to the behaviors of others), some mediumly important ones, and a lot of less important ones.
The inclusion of such things as dyslexia (or what might otherwise be called language disabilities) is warranted by the finding of these being found associated in twin studies, and their symptoms falling within the same theoretical framework of suppression of innatons.
The nature of antiinnatia factors
The 1993 paper indicated that both environmental and genetic factors would be antiinnatia factors. We might add that perhaps epigenetic, genomic imprinting or mitochondrial factors could also have antiinnatia effect.
In any case, there is no reason to suppose a yes/no distinction between variables that are antiinnatia factors and those that are not. Instead, like autism itself it is a matter of degree with no clear cutoff.
And one would expect some antiinnatia factors to be "purer" (more non-specific) than others. This can arguably be seen in the social class differential graphs of my 1993 paper (graphs of table 1 added in author's reprint). The "pure" would be due to the purer antiinnatia, while the "complicated"/"organic" would be due to the less pure causing what we might call side-effects. (I discussed this variable purity of antiinnatia factors already in the 1993 paper itself.)
The numerous antiinnatia genes in combination would act as a relatively pure, general antiinatia factor, even though any one of those genes taken in isolation might have some idiosyncratic side-effects.
One would expect some grossly injurious process such as an untimely bash on the head, or a severe infective brain inflammation of viral encephalitis would have substantial side effects.
I would reckon that mercury, while a relatively pure antiinnatia factor, would be less pure than the 'portfolio' of antiinnatia genes, due to its interference with thiol-dependend enzymes, and its tendency to generate oxidative stress.
One can then go on to reasonably expect that there would be some other factors which have more or less of antiinnatia factor effect. And obviously any gene specifically related to language function is going to tend to be a factor in suppression of at least language function, and hence favour outcomes with a bit of resemblance to autism even though arguably not properly considered a true antiinnatia factor.
It is mainly about concepts. Sound science cannot be founded on concepts alone, but science gets in a muddle if the concepts are not properly clarified. So this can be important.
The nature of the autistic syndrome.
An expression "the autistic spectrum" has become popularised. This is regrettable because it promotes a fallacy that autism variation is all or mostly on one dimension from mild to severe. A more reasonable concept is that autism, Aspergers, and related things such as dyslexia, are all part of the autistic syndrome, that is tendency to clustering together of certain characteristics. This clustering is many-dimensional, with the number of dimensions being equal(ish?) to the number of characteristics whose expression can be affected by antiinnatia. In practice, as generally found with factor analysis, there would be a smaller number of main/most important dimensions (such as predisposition to allocating attention to the behaviors of others), some mediumly important ones, and a lot of less important ones.
The inclusion of such things as dyslexia (or what might otherwise be called language disabilities) is warranted by the finding of these being found associated in twin studies, and their symptoms falling within the same theoretical framework of suppression of innatons.
The nature of antiinnatia factors
The 1993 paper indicated that both environmental and genetic factors would be antiinnatia factors. We might add that perhaps epigenetic, genomic imprinting or mitochondrial factors could also have antiinnatia effect.
In any case, there is no reason to suppose a yes/no distinction between variables that are antiinnatia factors and those that are not. Instead, like autism itself it is a matter of degree with no clear cutoff.
And one would expect some antiinnatia factors to be "purer" (more non-specific) than others. This can arguably be seen in the social class differential graphs of my 1993 paper (graphs of table 1 added in author's reprint). The "pure" would be due to the purer antiinnatia, while the "complicated"/"organic" would be due to the less pure causing what we might call side-effects. (I discussed this variable purity of antiinnatia factors already in the 1993 paper itself.)
The numerous antiinnatia genes in combination would act as a relatively pure, general antiinatia factor, even though any one of those genes taken in isolation might have some idiosyncratic side-effects.
One would expect some grossly injurious process such as an untimely bash on the head, or a severe infective brain inflammation of viral encephalitis would have substantial side effects.
I would reckon that mercury, while a relatively pure antiinnatia factor, would be less pure than the 'portfolio' of antiinnatia genes, due to its interference with thiol-dependend enzymes, and its tendency to generate oxidative stress.
One can then go on to reasonably expect that there would be some other factors which have more or less of antiinnatia factor effect. And obviously any gene specifically related to language function is going to tend to be a factor in suppression of at least language function, and hence favour outcomes with a bit of resemblance to autism even though arguably not properly considered a true antiinnatia factor.
Abstract of the draft of the update review of the antiinnatia theory
While I cannot post here the actual full paper (as that can breach the pre-publication policies of some journals), I think it will be ok to put here just the abstract (summary), as currently drafted. It's important to understand that this abstract has space only to merely assert the conclusions therein stated, but the full paper presents the evidence and reasoning through which those conclusions are reached.
The causes of autism: A theory now further supported by four predictions;
why dental amalgams caused increased autism;
and why mercury pollution caused the Flynn effect IQ increase
The gene-expression theory of autism and IQ (antiinnatia theory) is further supported via others’ findings relating to four predictions:
1. Correlation of body symmetry with IQ.
2. In autism, rationality less reduced by innate predispositions.
3. Autism being caused by molecules which erratically, dose-dependently bind to DNA and thereby reduce gene-expression (e.g. mercury).
4. Shared causality of raised IQ (the Flynn effect) and autism.
The hitherto-puzzling Flynn effect is explained in terms of varying atmospheric mercury. The Flynn effect has reversed because mercury pollution has reversed. Mercury pollution is probably causing harm additional to that currently recognised. Fetal testosterone is only a minor antiinnatia factor. Autism partially coincides with “extreme-male-brain”. The concept of “developmental instability” is unsound.
Summary of the amalgam case:
· Autistic behaviours are shown to have increased about tenfold in Western capitalist countries.
· Mercury was definitely involved.
· Mercury vapor from amalgams is the main source of mercury in the body.
· No other tenable sources of the mercury are available.
· Non-gamma-2 amalgams emit 30-50 times more mercury vapor, which is highly absorbed by lungs and infant brain.
· Exponential increase started promptly after the introduction of non-gamma-2 amalgams.
· A marked change of ratio of age of onset coincided closely with the increase. Yet the ratio remained low in Poland, where data did not show any increase either.
· Number of maternal amalgams is a risk factor for autism in the US, but maybe not in Poland.
· The antiinnatia theory had unknowingly pre-explained how mercury would cause autism.
· Accords with the antiinnatia theory causality of maintained suppression rather than knockout blow.
· The late onset is explained as due to accumulation when infants regularly inhale the vapor.
· The new ventilation prediction has already been supported by correlation of rainfall/snowfall with autism.
I cannot put this update paper on a website in advance of it being accepted by a journal. But in the interim I can send you a draft copy by email if you email a request for it to rpclarke{att]autismcauses{dott]info .
The causes of autism: A theory now further supported by four predictions;
why dental amalgams caused increased autism;
and why mercury pollution caused the Flynn effect IQ increase
The gene-expression theory of autism and IQ (antiinnatia theory) is further supported via others’ findings relating to four predictions:
1. Correlation of body symmetry with IQ.
2. In autism, rationality less reduced by innate predispositions.
3. Autism being caused by molecules which erratically, dose-dependently bind to DNA and thereby reduce gene-expression (e.g. mercury).
4. Shared causality of raised IQ (the Flynn effect) and autism.
The hitherto-puzzling Flynn effect is explained in terms of varying atmospheric mercury. The Flynn effect has reversed because mercury pollution has reversed. Mercury pollution is probably causing harm additional to that currently recognised. Fetal testosterone is only a minor antiinnatia factor. Autism partially coincides with “extreme-male-brain”. The concept of “developmental instability” is unsound.
Summary of the amalgam case:
· Autistic behaviours are shown to have increased about tenfold in Western capitalist countries.
· Mercury was definitely involved.
· Mercury vapor from amalgams is the main source of mercury in the body.
· No other tenable sources of the mercury are available.
· Non-gamma-2 amalgams emit 30-50 times more mercury vapor, which is highly absorbed by lungs and infant brain.
· Exponential increase started promptly after the introduction of non-gamma-2 amalgams.
· A marked change of ratio of age of onset coincided closely with the increase. Yet the ratio remained low in Poland, where data did not show any increase either.
· Number of maternal amalgams is a risk factor for autism in the US, but maybe not in Poland.
· The antiinnatia theory had unknowingly pre-explained how mercury would cause autism.
· Accords with the antiinnatia theory causality of maintained suppression rather than knockout blow.
· The late onset is explained as due to accumulation when infants regularly inhale the vapor.
· The new ventilation prediction has already been supported by correlation of rainfall/snowfall with autism.
I cannot put this update paper on a website in advance of it being accepted by a journal. But in the interim I can send you a draft copy by email if you email a request for it to rpclarke{att]autismcauses{dott]info .
Abnormalities of the "resting network" and of language lateralisation
In my most recent draft of the update review of the theory, I wrote:
Firstly the "resting network", which in neurotypicals activates while not concentrating on a task, and becomes inactive when task-engaged. Whereas in autistics it tends to just have a similar level of activity in both circumstances. Ref: Failing to deactivate: Resting functional abnormalities in autism. Daniel P. Kennedy, Elizabeth Redcay and Eric Courchesne
Secondly, here is Dr Courchesne speaking before the ASF's 2010 meeting:
“We discovered that autistic infants and toddlers displayed a pronounced abnormality of language activation and cortical development.” “At each age studied from infancy to young childhood, most autistic subjects had greater activation on the incorrect side, namely, the right temporal cortex, compared to the left side and this incorrect activation pattern did not change or “normalize” even by 3 or 4 years of age. The abnormal pattern was strong in a substantial percentage of autistic infants and toddlers....".
Pisula (2010) lists numerous areas of the brain which are known to be normally (and by implication innately) associated with specified psychological functions, and which function abnormally in autism. She notes that these findings cannot be adequately accounted for in terms of “theory of mind” or “executive dysfunction” or “lack of central coherence”. But they all rather obviously fall very clearly within the concept of innatons being affected by excessive antiinnatia. So Pisula’s review can be re-read in retrospect as even further testimony to the empirical soundness of the antiinnatia theory...."I'd now add to that list two more instances of a similar kind.
Firstly the "resting network", which in neurotypicals activates while not concentrating on a task, and becomes inactive when task-engaged. Whereas in autistics it tends to just have a similar level of activity in both circumstances. Ref: Failing to deactivate: Resting functional abnormalities in autism. Daniel P. Kennedy, Elizabeth Redcay and Eric Courchesne
Secondly, here is Dr Courchesne speaking before the ASF's 2010 meeting:
“We discovered that autistic infants and toddlers displayed a pronounced abnormality of language activation and cortical development.” “At each age studied from infancy to young childhood, most autistic subjects had greater activation on the incorrect side, namely, the right temporal cortex, compared to the left side and this incorrect activation pattern did not change or “normalize” even by 3 or 4 years of age. The abnormal pattern was strong in a substantial percentage of autistic infants and toddlers....".
Head size, simplex/multiplex autism, and IQ
A number of reports have been published indicating that head size in the first year of life has been found to be several percent greater in autistics, such as this latest one.
Media report linked here.
This is important and substantially competent research by this team. But there's some room for improvement.
Like most researchers they presume that autism is a "disorder" for which they are trying to find out what has "gone wrong". And so even when something good is found it has to be labelled as "overgrowth" of the brain.
And yet a remarkably similar progression of "overgrowth" has been found to be characteristic of high-IQ children (Gale, O'Callaghan, Bredow, Martyn 2010). And the 1982 published 1993 antiinnatia theory explained that whatever in low doses causes high IQ in higher doses causes autism.
You can see a very good presentation to the IACC about this "overgrowth", by the founder of this line of evidence, Eric Courchesne (between minutes 130-162 plus discussion to 174). He explains that it involves substantially higher numbers of neurons particularly in prefrontal. And that it is characteristic of "simplex" autism rather than of "multiplex" autism (defined as autism cases occurring more than once in a family). And furthermore, the advance over normal growth comes to level off after the first couple of years and indeed may be followed by a decline to below normal.
I've not looked into this research in great depth, but would provisionally suggest the following as reasonable explanations of these findings.
Multiplex autism could usually be due to a family sharing an indoor mercury vapor pollution problem from (mainly maternal) dental amalgams. EC notes that multiplex is much more common, which is in line with my conclusion that dental mercury- induced autism now accounts for 80% or more of all autism.
So it would be the simplex autism that is more a matter of too many antiinnatia genes, that is genes for high IQ, and which would also be genes favouring large heads and more neurons, which is in line with these observations. (The larger heads and more neurons would not cause the higher IQ but would be correlated with it.)
The subsequent decline would be readily explained by two processes. Firstly anyone with even fleeting acquaintance with autism can see that it soon leads to the autistic experiencing a substantially understimulating environment compared to neurotypicals. Such an understimulating environment can reasonably be expected to lead to the brain waning away somewhat. And meanwhile, for those autism cases caused by mercury, the mercury would continue to accumulate due to the defective detoxification, and the brain would consequently lose neurons due to that neurotoxin accumulation.
Media report linked here.
This is important and substantially competent research by this team. But there's some room for improvement.
Like most researchers they presume that autism is a "disorder" for which they are trying to find out what has "gone wrong". And so even when something good is found it has to be labelled as "overgrowth" of the brain.
And yet a remarkably similar progression of "overgrowth" has been found to be characteristic of high-IQ children (Gale, O'Callaghan, Bredow, Martyn 2010). And the 1982 published 1993 antiinnatia theory explained that whatever in low doses causes high IQ in higher doses causes autism.
You can see a very good presentation to the IACC about this "overgrowth", by the founder of this line of evidence, Eric Courchesne (between minutes 130-162 plus discussion to 174). He explains that it involves substantially higher numbers of neurons particularly in prefrontal. And that it is characteristic of "simplex" autism rather than of "multiplex" autism (defined as autism cases occurring more than once in a family). And furthermore, the advance over normal growth comes to level off after the first couple of years and indeed may be followed by a decline to below normal.
I've not looked into this research in great depth, but would provisionally suggest the following as reasonable explanations of these findings.
Multiplex autism could usually be due to a family sharing an indoor mercury vapor pollution problem from (mainly maternal) dental amalgams. EC notes that multiplex is much more common, which is in line with my conclusion that dental mercury- induced autism now accounts for 80% or more of all autism.
So it would be the simplex autism that is more a matter of too many antiinnatia genes, that is genes for high IQ, and which would also be genes favouring large heads and more neurons, which is in line with these observations. (The larger heads and more neurons would not cause the higher IQ but would be correlated with it.)
The subsequent decline would be readily explained by two processes. Firstly anyone with even fleeting acquaintance with autism can see that it soon leads to the autistic experiencing a substantially understimulating environment compared to neurotypicals. Such an understimulating environment can reasonably be expected to lead to the brain waning away somewhat. And meanwhile, for those autism cases caused by mercury, the mercury would continue to accumulate due to the defective detoxification, and the brain would consequently lose neurons due to that neurotoxin accumulation.
Adult-onset autism
In the update review of the antiinnatia autism theory I explain why dental amalgam mercury vapor causes autism in infants but not in adults. Namely because beyond a certain age the behaviours associated with the innatons become established as learnt habits, skills, knowledge, as the elaborated connectivity of the brain, and as crystallised intelligence in place of fluid intelligence.
There might be thought to be a valid objection to this in terms of three case reports of autism beginning at later ages, 11, 14, and 31 years.
It is notable that all three cases resulted from herpes encephalitis. In respect of the 31-year-old, he was in a coma for more than 14 days, and from having been a university lecturer was permanently transformed to having a mental age of less than 2 years. We can thus see that it was only in the context of an extreme level of brain damage that the characteristics of autism resulted. So we can interpret his case as being one where even the established habits, skills and so on were wiped out, by a condition substantially more severe than (for instance) mercury poisoning. (Not that mercury poisoning should be considered non-serious itself.)
There might be thought to be a valid objection to this in terms of three case reports of autism beginning at later ages, 11, 14, and 31 years.
It is notable that all three cases resulted from herpes encephalitis. In respect of the 31-year-old, he was in a coma for more than 14 days, and from having been a university lecturer was permanently transformed to having a mental age of less than 2 years. We can thus see that it was only in the context of an extreme level of brain damage that the characteristics of autism resulted. So we can interpret his case as being one where even the established habits, skills and so on were wiped out, by a condition substantially more severe than (for instance) mercury poisoning. (Not that mercury poisoning should be considered non-serious itself.)
Autism did not begin only in the 1930s
In two weeks time there will be published a new book:
The Age of Autism: Mercury, Medicine, and a Man-made Epidemic
By Dan Olmsted, Mark Blaxill
I've not read it (yet) but I can anticipate that I would agree with the authors that autism has increased and involved mercury but would be unpersuaded by their reckoning that vaccinations have been a major factor in the increase.
Here I shall just comment on this first sentence of a preview extract circulated by Safeminds:
Reference: Down, J.L. Mental Affections of Childhood and Youth, 1887 originally, re-issued as Classics in Developmental Medicine, No. 5, 1990 Mac Keith Press, London
It was discussed in the 2006 Awares conference. This is a link to the paper by Darrold Treffert.
I also suggest that the concept of the "holy fool" such as portrayed in the play and opera Boris Godunov corresponds with mild autism: a person who speaks the truth that others cannot. And bear in mind that the rare autistic individuals would be likely to have had a hard time surviving in earlier ages; even mildly autisticky people might have had a hard time sufficient to prevent them producing children.
Furthermore, there is the important consideration that a rare condition such as autism pre-1970 would only come to the attention of a person once there is a sufficient level of cosmopolitanism, due to urbanisation and transport, enabling one person to "survey" a sufficiently large sample of people. Down made his observation in 19th century England after the railways were established in the world's first modernised country. Thereafter, the US and Austria started to catch up industrially and so autism came to attention there too. That's not to say that the personal links to mercury stated in the AoA book cannot be also part of the story.
The Age of Autism: Mercury, Medicine, and a Man-made Epidemic
By Dan Olmsted, Mark Blaxill
I've not read it (yet) but I can anticipate that I would agree with the authors that autism has increased and involved mercury but would be unpersuaded by their reckoning that vaccinations have been a major factor in the increase.
Here I shall just comment on this first sentence of a preview extract circulated by Safeminds:
"We believe that autism was newly discovered in the 1930s for the simple reason that it was new."But this first sentence can be shown to be mistaken. Dr Down of Down Syndrome fame had already in the 19th century given good descriptions of both infantile autism and regressive autism.
Reference: Down, J.L. Mental Affections of Childhood and Youth, 1887 originally, re-issued as Classics in Developmental Medicine, No. 5, 1990 Mac Keith Press, London
It was discussed in the 2006 Awares conference. This is a link to the paper by Darrold Treffert.
I also suggest that the concept of the "holy fool" such as portrayed in the play and opera Boris Godunov corresponds with mild autism: a person who speaks the truth that others cannot. And bear in mind that the rare autistic individuals would be likely to have had a hard time surviving in earlier ages; even mildly autisticky people might have had a hard time sufficient to prevent them producing children.
Furthermore, there is the important consideration that a rare condition such as autism pre-1970 would only come to the attention of a person once there is a sufficient level of cosmopolitanism, due to urbanisation and transport, enabling one person to "survey" a sufficiently large sample of people. Down made his observation in 19th century England after the railways were established in the world's first modernised country. Thereafter, the US and Austria started to catch up industrially and so autism came to attention there too. That's not to say that the personal links to mercury stated in the AoA book cannot be also part of the story.
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