Read the most advanced science of autism causes here. Bypass the commenterati and go direct to the science. Don't waste your time at the sites which pretend "no-one" knows what causes (or what sometimes cures) autism.
This is a website relating to the unchallenged theory of autism, IQ and genius, Personality and Individual Differences 14:459-482 (1993) by Robin P Clarke (the antiinnatia theory). An update review paper is being prepared for publication. Meanwhile you can download the original 1993 publication (presentationally revised) here, and the original 1993 publication (author's reprint) here . (the journal site version is here:, but without added charts of social class and you may have to pay Elsevier $31.)

Do vaccines cause autism?

Vaccines as alleged cause of autism or of the autism increase.

There exist two widely contrasting views, both expressed with absolute confidence, on whether vaccines have contributed to causing any autism. 
On the one hand, many personnel of what is sometimes called the medical establishment absolutely dismiss all possibility of causation of autism by vaccines.  The book  “Autism’s False Prophets” (Offit, 2008) has been a prominent player in this viewpoint.
There are many serious problems with that book, but of relevance to the present question is Dr Offit's statement on page 111 that “even if thimerosal in vaccines accounted for only 1 percent of autism—one in 15,000 children—epidemiological studies would have found it.”.  His basis for that conclusion comes from his preceding sentence stating that “Problems caused by vaccines as rare as one in 100,000 have been readily detected by epidemiological studies”.  He in turn reckons to have justified that statement with three examples of vaccine adverse effects, namely causation of the rare problems of intussusception, thrombocytopenia, and Guillaine-BarrĂ© syndrome, all of which were identified from epidemiological studies.  
But that reasoning is unsound.  Those rare consequences were discernable only because they were (i) definitively diagnosable conditions, and (ii) rare conditions whose occurrence would be readily distinguishable from the background level.  By contrast, autism is not only hard to diagnose and impossible to clearly enumerate, but also sufficiently common and widely varying in prevalence of diagnosis that any causation less than a few percent would be impossible to discern among the statistical “noise” variation.  It is consequently my opinion that there does not exist sufficiently clear data to justify the extreme position advanced by Offit in those sentences. 
Meanwhile many thousands of non-professionals are equally absolutely convinced of a concept of “vaccine-damaged children” (by which they mean autistic children), combined with the notion that vaccines have caused a huge increase of autism. 
One part of what persuades them is the “direct experience” of thousands of parents of so-called “vaccine-damaged” autistic children.  We are told that we should respect the testimony of those who have seen the direct experience for themselves.  And as there are thousands of them, “therefore” it must be a major cause.  But their direct experience is only that their own one or more children became autistic after a vaccine.  Their direct experience does not extend to what happened to all the many other autistic children before they became autistic.  And this comes in the context that just about all the children were being vaccinated anyway (and at that age), so logically just about all those who became autistic would be expected to have been vaccinated at that age anyway, even if no vaccine-autism causation ever occurred.
These “vaccine-blamers” also err in assuming that the clear evidence of a mercury-autism causal link constitutes clear evidence of a thimerosal-autism causation.  They err here because they incorrectly dismiss any involvement of mercury from dental amalgam instead (which can easily account for the entire autism increase data).  
A third, most important, factor underlying the vaccine-blamers’ convictions has been the confusing gradual growth of information about the subject.  Most notable in this is this graph in Figure A1 which was presented to the world by Mark Blaxill (2001).
 Figure A1:  Blaxill’s 2001 alignment of autism and vaccines
Looking at that graph in 2001 one might reasonably have seen it as reasonable grounds to suspect causation of the autism increase by vaccine mercury.  A more sophisticated reader might have appreciated that the fall at the end of the autism series was only an artifact of delayed diagnosis, and also appreciated that seven selected years are too few for very firm conclusions.  And yet it is still rather suggestive, especially in the context of the Bernard et al. (2001) review which had suggested the plausibility of causation by mercury, and with the lack of any obvious other sharply increasing mercury sources impacting on infants.
However, we can now substitute more up-to-date and fuller autism data into Blaxill’s 2001 graph, as follows (and autism has continued to increase even to recent years).
  Figure A2: Blaxill’s vaccine mercury data placed alongside updated and more extensive autism data
This fuller data should make it obvious that the increase cannot remotely be accounted for in terms of vaccine mercury.  The increase has continued surging further upwards for more than 17 years since the vaccine mercury started to decline.  And it can be seen that the increase was of a form of a progressive exponential, accelerating through the whole of the 1980s and not just during the period focused on by Blaxill’s chart.  The curve can be completely understood in terms of increasing numbers of the non-gamma-2 amalgams introduced from the mid-1970s.  The vaccine mercury data just happened to run parallel with the autism data for four or five years.  But it appears not to have made any discernable impact on that already-existing exponential increase.  From looking at this data it is difficult to conclude that anything more than a handful of percent of the autism increase can have been due to vaccine mercury.  And data from other countries is even less supportive.  Safeminds (2011) have tried to argue that the data from Denmark in reality shows a decrease following discontinuation of Thimerosal, but that is predicated on an assumption that the inpatient/outpatient ratio did not change over some years when autism was apparently rapidly increasing.  But it is highly probable that a rapid increase of autism would cause the inpatient ratio to rapidly fall as well, as inpatient resources would fail to keep up with the unexpected demand.)
A further unsound argument for blaming vaccines was presented by McDonald and Paul (2010).  The authors reckoned that they could usefully analyse the autism increase curve by making an approximation of it in terms of two straight lines.  They then pointed out that the junction of the two lines, the "changepoint", at which they suggest the autism increase began, was about 1988-9 (i.e. just at the start of Blaxill’s vaccine mercury data).

But in reality, just about any curve of roughly exponential increase form can have a couple of straight lines imposed on it such as to passably plausibly account for the entire data set.  Especially if you set the time axis long enough so the increase will look like an abrupt event rather than a gradual one.  Nice correlations can be found for each line with its corresponding part of the data, and impressively high significance levels pointed out.  But it does not follow that the increase is usefully understood in terms of such pairs of lines.

McDonald and Paul featured remarkably small graphs of the increase, which tend to give the impression that there was no increase before their "changepoint". And they use a whopping 50-year timespan.  It would be better to have larger (taller) graphs around the critical period so we can examine the end of the "level" section more closely.
It should be quite obvious from Figure A2 here (and Figures 3, 4 and 6 in the main text) that there was not some abrupt changepoint around 1988-9, and not around any other year either.  It is entirely an artifact of their flawed methodology which imposes a “changepoint” on the data whether appropriately or not.
In 2011, Safeminds published a rebuttal review of the evidence that was alleged to prove vaccines do not cause autism (Safeminds, 2011).  It is important to understand that lack of proof of absence does not constitute proof of presence, and so that rebuttal review does not constitute any sort of proof that vaccines actually do cause any autism.
Another popular fallacy is that court judgments constitute evidence or even proof of causation of autism by vaccines.  Court judgments are not scientific evidence, but merely non-scientists’ opinions of probability based on the scientific evidence presented as related to the particular cases.  
There have also been suggestions that the data discussed at the Simpsonwood conference, later radically reformulated into the paper of Verstraeten et al., constitutes glaring proof of vaccine-caused autism.  But there were severe methodological deficiencies even in the earlier “generations” of that study.  As discussed in the Safeminds (2011) review, there was a very large under-ascertainment and high likelihood of biased selection of cases.  And if the findings of 7-fold or even 2-fold relative risk were sound, then one would expect to see that clearly reflected in the Figure A2 herewith, but on the contrary I can’t even see a 1.1-fold bulge there.
Some vax-blamers also sometimes cite this 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.   Part of the problem with the vaccine-autism theorists is that they keep jumping between theories.  At first it was the triple MMR to blame, then it became mercury-containing vaccines, then a combination of both, and then again maybe it was Hib or Hep-B.  In reality there's scant real evidence that any of these have caused the increase (which was well underway long before 1989 and the increase just carried on rather than changed in some way at that point)..
In conclusion, neither of the strongly asserted positions are justified by the evidence.  There is no good evidence that vaccine mercury never causes autism, and yet neither is there any good, publicly-visible clear proof that it has caused any autism.  And it certainly did not cause the autism increase.  And that increase is meanwhile easily and fully accountable for in terms of the changeover to non-gamma-2 dental amalgams from 1976. 


 Blaxill M: Rising incidence of autism: association with Thimerosal. In: Institute of Medicine. Thimerosal-containing vaccines and neurodevelopmental disorders. Washington DC: National Academy Press; 2001:49–50.
Bernard S, Enayati A, Redwood L, Roger H, Binstock T: Autism: a novel form of mercury poisoning. Med Hypoth 2001, 56:462-471.
McDonald ME, Paul JP: Timing of increased autistic disorder cumulative incidence. Environ Sci Technol 2010, 44:2112-2118
Offit PA: Autism’s false prophets. Columbia University Press; 2008.
Safeminds: Vaccines and autism – what do epidemiological studies really tell us? 2011.

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 thus consistently independently-based researcher there is no pressure on me to go along with any particular institutional position.  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.

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.

Fallacy about acrodynia (pink disease)

On the leftbrainrightbrain blog, "daedalus" asked:

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?

To which I reply:

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 it
which 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.

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.

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 .

Abnormalities of the "resting network" and of language lateralisation

In my most recent draft of the update review of the theory, I wrote:

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.

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.)

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:
"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.