The following is further to my discussion in my update review paper.
I hold a uniquely "privileged" position of lack of bias in relation to this dispute. I have no personal connection whatsoever with autism, with no family or friends affected by autism. As a chronically disabled person (devastated by "harmless" dental amalgams since age 17) I have all these years obtained my income only from the Department of Work and Pensions which couldn't give a damn what I write about health. As a thus consistently independently-based researcher there is no pressure on me to go along with any particular institutional position. As a chronically mentally disabled person I had and have absolutely zilch research career prospects to exert bias on my pronouncements. (And I'm certainly no great admirer of health "authorities".) My only connection with autism is that many years ago I discovered and later published the uniquely unchallenged, comprehensive, theory of autism, long before there was any talk of an increase let alone the slightest linking of it with vaccines or even mercury. Furthermore, autism is just one of my numerous great theories, so I am not here gripped by all-eggs-in-one-basket ego syndrome either.
As exclusively a theorist, I have all my cards on the public table. The only cards I bring to this debate-table are such objectivity, accuracy and logicality as I can manage (plus perhaps a bit more "ingenuity" than most). I subscribe to the view that intellectual excellence is revealed not by dogged consistency in the face of new evidence, but rather by the flexibility to acknowledge if one has been mistaken and to thereby advance with new learning.
From this background, I and the antiinnatia theory really don't give a hoot as to whether or not any vaccine causes autism. We will just follow the facts wherever they lead us.
We must distinguish between two questions. Namely:
Have vaccines caused the autism increase (mainly or in part)? and
Have vaccines played any part in causing any autism?
We must also remember that evidence that mercury is involved in autism in no way constitutes evidence that vaccines are involved too - my theory update review shows that the mercury comes mostly (and probably all) from dental amalgams instead.
I see substantial evidence that vaccines have played at most only a minor part in causing the increase. Somewhere between zero% and, at a credibility-straining push, up to 5%-10%.
For want of any better terminology I'll use the term "vax-blamers" to indicate those who reckon there is evidence of causation.
Within epidemiological evidence we can distinguish what I will call time-series data, the familiar sort of graphs showing autism rates sloping up or down between particular years.
The vax-blamers commonly assert that time-series epidemiological evidence is inferior to clinical or lab evidence. But it depends which of those two questions you are asking. If vaccinations were a major cause of the increase, then their effects really should be readily visible in the time-series data studies, insofar as they were honestly and competently conducted. Some outstandingly defective papers were published by the pro-vaxxers, which rightly undermined people's confidence in the honesty of those involved. But as I explain in my pages about corruption, I think it extremely unlikely that anyone actually falsified the source data records or their reporting in even the most abusive of these studies. (The one exception I would make is that of Prof Brent Taylor who was accused by the late Bernard Rimland of falsifying his data, not without some reason. Taylor's data does bizarrely stand utterly out of line with all the other time-series if you plot them together in a graph. But it is not a significant part of the whole anyway.)
In my update review I make my own consolidated review of this time-series data and explain how I fail to see any impact of vaccines therein. This does not of course rule out the posssibility that a minority of cases are vaccine-caused.
Vax-blamers have also paraded various clinical and lab studies as supposedly strong evidence of causation. But I don't find this evidence very persuasive. For instance the tests of monkeys injected with thimerosal. They used a schedule four times faster than the human schedule, and yet mercury reactions and metabolism do not happen four times faster in monkeys. And the inference from one species to another is too speculative. Such data is suggestive, but not adequately probative.
Finally there is a third class of data, which is epidemiological but not time-series. I see two notable examples of this sort, both relating to thimerosal, namely the secret Simpsonwood reports and this published study:
Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years. Toxicological and Environmental Chemistry, September 2008, Carolyn Gallagher and Melody Goodman.
These have both involved substantial numbers and both shown some compelling statistical associations of thimerosal with disabilities. That's even though there is perhaps a question regarding the Gallagher and Goodman study as to how much of that disability was actually autistic-type.
At this point I have to get some of those autism jigsaw puzzle pieces back out of the box I dumped them in many years ago, because these two weighty non-time-series studies seem so discrepant from the huge weight of the time-series data.
The puzzle here is that if the results of those two studies were to be taken as meaning what they appear to be, then there really ought to be a massive visibility of the vaccine causation in the time-series charts too. And yet there is none at all.
My position on this conflict of evidences is as follows. There are improbable hypotheses, such as (1) some crooks have elaborately fiddled the official records behind those time-series in several countries, or (2) probability has played a whopping trick on us and just by stupendous fluke some very misleading results came out, or (3) at exactly the same time (and volume) as the thimerosal was upped and downed, some other mysterious factor caused an exactly opposite downing and upping, such that it ended up looking like just level. While I can't rule out these three, I consider them to be extremely improbable.
A more likely explanation is that the time-series data do give us the true picture, and the other two studies are misleading us in some way. There are indeed various very valid questions as to whether one or more confounders could have unbalanced the results. Not least there is some reason to suspect a high correlation between vaccine mercury acceptance and dental mercury acceptance.
My bottom line is that there remains a possible anomaly requiring an explanation here, but I don't consider it a very desperately nagging anomaly. These studies suggest some possible involvement of vaccines, but not compellingly enough to draw any firm vax-blaming conclusions at this time.
Meanwhile there are many parents who insist that they know that vaccines were causal because their child was fine until they immediately that same day/week/month/year suddenly became autistic. What they fail to understand is that regressive autism tends to begin at the same age anyway as when millions are vaccinated. So it would be actually expected that just by fluke a fair number of those millions would develop autism the same day and so on. Such observations have no evidential value about causation whatsoever.
P.S. Some people are claiming that some vaccine court judgments somehow prove that vaccines cause autism. Firstly, court judgments, whatever their other merits, do not usually constitute scientific evidence or even conclusions beyond reasonable doubt. Secondly, cases involving severe encephalitis such as the Hannah Poling case really do not have much in common with cases where "mere" autism results. You can cause severe loss of communication and social functioning by bashing your child hard enough on the head but it doesn't follow that head-bashing is sensibly considered a cause of autism.
A bit more of my thoughts about the vaccine evidence can be found at my page about Dr Wakefield.
Fallacy about acrodynia (pink disease)
On the leftbrainrightbrain blog, "daedalus" asked:
Pink disease has zilch to do with my explanation of any autism causation, or the data I will be citing in relation to mercury. The key causal variable posited in my update review is constant inhalation of elemental mercury vapor. It matters little how many tons of mercurous chloride were applied to infants, as Hg2Cl2 is a very different chemical from mercury vapor. The former is a substantially stable solid, whereas the latter is a highly reactive gas. Indeed it’s well-known that chlorine (gas) strongly counteracts the toxicity of mercury gas, rendering it far less toxic to the workers in chlor-alkali plants. It does so by reacting with the mercury to produce mercury-chlorine salts such as the same Hg2Cl2 that was involved in Pink disease.
Indeed "daedalus" above states that:
Furthermore, the mercurous chloride was put in the babies' mouths. It's well-known that even elemental mercury has little or no toxic effect, is neglibly absorbed, when swallowed. And furtherfurthermore, those teething powers were of course not applied except at teething age (apologies for dazzling you with this rocket science here!), whereas the causality described in my update review requires continuous sustained intake.
To which I reply:RPC, why don’t you read up on what was called Pink Disease. It was a serious disease of children in the first half of the 20th century. It was a leading cause of death, with about 23% of child deaths attributed to it. Eventually it was realized that it was actually mercury poisoning from teething powders. Many of the teething powders that were produced and sold had a grain of mercurous chloride in them. Yes, a grain. If you don’t have the conversion factor handy, that is 65,000 micrograms per dose. Yes, 65,000 micrograms of mercurous chloride per dose, and many children were given multiple doses. Many tens of millions of doses were sold, with a single company reporting sale of 30,000,000 doses in one year.
Many tens of millions of children received many thousands of times more mercury from teething powders than ever received from vaccines. Mercury from teething powders gave many children pink disease and killed over a thousand. Where is the autism from the first half of the 20th century when children were given so much mercury that over a thousand were killed by it?
Pink disease has zilch to do with my explanation of any autism causation, or the data I will be citing in relation to mercury. The key causal variable posited in my update review is constant inhalation of elemental mercury vapor. It matters little how many tons of mercurous chloride were applied to infants, as Hg2Cl2 is a very different chemical from mercury vapor. The former is a substantially stable solid, whereas the latter is a highly reactive gas. Indeed it’s well-known that chlorine (gas) strongly counteracts the toxicity of mercury gas, rendering it far less toxic to the workers in chlor-alkali plants. It does so by reacting with the mercury to produce mercury-chlorine salts such as the same Hg2Cl2 that was involved in Pink disease.
Indeed "daedalus" above states that:
Many tens of millions of doses were sold, with a single company reporting sale of 30,000,000 doses in one year.and yet only:
over a thousand were killed by itwhich indicates a death rate of something like only one in a million, not exactly the most deadly formula in history.
Furthermore, the mercurous chloride was put in the babies' mouths. It's well-known that even elemental mercury has little or no toxic effect, is neglibly absorbed, when swallowed. And furtherfurthermore, those teething powers were of course not applied except at teething age (apologies for dazzling you with this rocket science here!), whereas the causality described in my update review requires continuous sustained intake.
Hertz-Picciotto et al 2010 very misleading about mercury
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.
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.
Confusion about "forms of mercury"
The following may be considered elementary chemistry but it may not be elementary child psychiatry so it still has a place here.
There is a lot of talk of mercury as though it is one thing. We could make a false comparison with some other toxic substance, for instance methanol. If I've understood my chemistry correctly, all methanol molecules are the same arrangement of one carbon atom, one oxygen and four hydrogens. The word specifically means that arrangement, that molecule. There are no "forms" of methanol, except in the trivial sense that a collection of such molecules could also be gas or solid.
But mercury is not a chemical arrangement, but rather is an element (that is, consists of atoms each having x protons and y neutrons)*. Mercury atoms can feature as part of numerous different molecules, for instance so-called "methylmercury" and "ethylmercury". But those are not mercury!
(*Though due to mercury poisoning I don't remember the values of x and y there.)
To clarify this, consider chlorine which is also an element. Chlorine is a deadly poisonous gas. When it is combined with sodium (which is also very harmful) it forms the sodium chloride better known as the salt that goes on your food and without which you would be dead very quickly. And if it is reasonable to talk of "methylmercury" as a "form of mercury" then it could be thought equally reasonable to talk of table salt as "sodylchlorine" and as a "form of chlorine".
However, we must now step back from making an absolute equivalence there. That is because mercury atoms are relatively rare and have effects disproportionate to their numbers. And those other "forms of mercury" do have some practical equivalence to elemental mercury for the reason that in everyday life they function as important carriers of those same mercury atoms around to and from your body and brain. Just do not forget that the notion of these other substances being "forms of mercury" is still a significantly misleading concept.
There is a lot of talk of mercury as though it is one thing. We could make a false comparison with some other toxic substance, for instance methanol. If I've understood my chemistry correctly, all methanol molecules are the same arrangement of one carbon atom, one oxygen and four hydrogens. The word specifically means that arrangement, that molecule. There are no "forms" of methanol, except in the trivial sense that a collection of such molecules could also be gas or solid.
But mercury is not a chemical arrangement, but rather is an element (that is, consists of atoms each having x protons and y neutrons)*. Mercury atoms can feature as part of numerous different molecules, for instance so-called "methylmercury" and "ethylmercury". But those are not mercury!
(*Though due to mercury poisoning I don't remember the values of x and y there.)
To clarify this, consider chlorine which is also an element. Chlorine is a deadly poisonous gas. When it is combined with sodium (which is also very harmful) it forms the sodium chloride better known as the salt that goes on your food and without which you would be dead very quickly. And if it is reasonable to talk of "methylmercury" as a "form of mercury" then it could be thought equally reasonable to talk of table salt as "sodylchlorine" and as a "form of chlorine".
However, we must now step back from making an absolute equivalence there. That is because mercury atoms are relatively rare and have effects disproportionate to their numbers. And those other "forms of mercury" do have some practical equivalence to elemental mercury for the reason that in everyday life they function as important carriers of those same mercury atoms around to and from your body and brain. Just do not forget that the notion of these other substances being "forms of mercury" is still a significantly misleading concept.
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.
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.
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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