The purpose of this website is to provide material supplementary to the update review (not yet published) of the 1993-published autism theory paper (linked in header above). All the posts here serve that purpose in one way or another, but some are more worthwhile or necessary than others. So here is a brief guide to the contents here.

Click here to read discussion of whether there is a relationship of vaccines to autism.

"Skeptical" people will generate plenty of supposedly clever reasons for rejecting the whole basis of the antiinnatia theory. That's despite the fact that any such "skeptics" must therefore be instead gullibly taking seriously one of a handful of utterly absurd alternative theories as explained in the update paper.

An answer to one of these "skeptical" notions is this one about being supposedly impossible for mercury to get to the DNA. And this one about supposedly the history of Pink Disease (acrodynia) proving that mercury doesn't cause autism. But perhaps you're a sheep?

Autism research is now becoming seriously distorted by official charlatanism similar to that of which the proof is shown here. And that distortion directly affronts the truths to which this theory relates. One of the leading sources of extreme misinformation is the book by Paul Offit, which is being distributed free to parents of victims via the American Academy of Pediatrics.

The myths:

1. that there has been no autism increase,
2. that mercury is not associated with autism, and
3. that removal by chelation cannot help,

are all addressed in the articles linked above and therefrom (and more fully in conjunction with the update review paper).

Turning to less militarised corners of the autism research field, I'll first point out that theories are often not in conflict even when they superficially may appear to be.

And there is only one autistic/ASD/etc syndrome, not several or many "autisms".

You can find the link to the spectacularly-predicted Purgatorius video here, along with some further evidence relating to my explanation of the hand-flapping.

Some other peoples' excellent graphs of the increase in the US can be found here, particularly the ones with multiple differently-coloured curves. They basically confirm my interpretation of the California DDS data as essentially a simple exponential-shaped increase.

Here is a link to my comment on close-spaced pregnancy findings of Keely Cheslack-Postava, Kayuet Liu, and Peter S. Bearman.

I've added yet another amazing new prediction, that the Flynn Effect (rising IQs increase) affects non-human animals as well.

Mitochondrial dysfunctions could be caused by antiinnatia (both within and without the brain), or they could be a non-antiinnatia "side effect" of mercury toxication. They could be part of some processes whereby antiinnatia affects neuronal function. So the reports about mitochondria appear to give neither support nor challenge to antiinatia theory.

Data on a "photoninthedarkness" blog leads me now to thinking that the increase has involved some diagnostic substitution, but not in the way that is assumed by pro-vaxxers. More later, but I reckon when there was a rapid real increase of autism c. 1985-1995, much of it was incorrectly diagnosed as non-autistic retardation. Thereafter the diagnoses substituted to the correct autism diagnoses. This leads me to suspect that the autism increase actually stopped increasing about ten years ago and since then it's just been an artifact of substitution.

“We’re finding that the immune system seems to function at a lower level in autism,” says Hertz-Picciotto. Which could be because the dental mercury that caused the autism increase is well-known to also impair immune functioning.

July 2011: Powerful yet further evidence of mercury involvement in autism - 6-fold increased autism in children whose grandparents survived Pink Disease.

(I'll continue work on this intro menu in due course, so be sure to check back later.)

There is only one autistic/ASD syndrome!

There are many thousands of autistics, and each one is unique.

But I resolutely reject the notion suggested by some, that there are "many autisms", for the following reasons.

The world has been aware of the autistic syndrome/Asperger syndrome for nearing 70 years now. Many people have spent much time trying to delineate separate subdivisions within that syndrome. The result has been a resounding lack of finding any such subdivisions. Even attempts to show any certain distinction between "Aspergers" and "high-functioning autism" have drawn a blank [as per Tony Attwood's review linked at end here].

Meanwhile there are certainly great variations in how autism manifests. And there is much reason to believe that the etiological (causal) factors can be quite different in different cases.

Years ago when I was first writing down the antiinnatia theory of autism I wrote a paragraph which explained about this. But because the paper (as published in 1993) was already rather long, I cut that paragraph out before publication. I'll now reinstate it here, in concept at least (as I don't remember the original wording).

Autism(/ASD etc) is like a tree. Just as a tree has many roots, so autism has many causes. Just as a tree has many branches, so autism has many characteristics and signs (notwithstanding the dumbing-down to a "triad of impairments"). But also, just as a tree has only one trunk, so autism/ASD/Aspergers/etc has only one central causal, definitional mechanism/concept, namely antiinnatia.

We can elaborate this metaphor of a tree by thinking of it as grounded in some rather peculiar soil. At the northwest corner there is a lot of (say) uranium in the soil, whereas at the southeast corner there is none at all. In consequence of this the leaves of one corner of the tree contain a lot of uranium while at the opposite corner there is little or none. But all are part of the same tree.

But....!
Notwithstanding the above, it would be wise for autism research to recognise various distinctions, such as male/female, and late/early onset. And another distinction I would suggest to be particularly important.

The evidence concerning this is is more fully elaborated in my update review, but I will briefly outline it here. According to my update of the theory, the autism increase has been caused by mercury (from non-gamma-2 amalgams); whereas the pre-increase autism had generally minimal involvement of mercury. (But it couldn't be zero as no-one has ever lived in a zero-mercury environment.)

It follows that within contemporary autism/ASD/Aspergers/etc we are looking at two substantially different things. On the one hand the minority (10-20%?) who would have been autistic/etc even if the increase had not taken place. These would be the "true" autism/etc, so to speak. On the other hand, those cases caused by mercury intake. These latter are very likely to have a variety of mercury-specific symptoms accompanying their antiinnatia-caused symptoms.

It follows that any research that just lumps together both these groups is liable to learn little about either. Indicators towards distinguishing between the two are likely to include: age of onset, number of maternal amalgams, level of indoor mercury vapor, results of porphyrin tests or hair mercury tests. Meanwhile, mercury levels in blood or urine are most unlikely to be worthwhile distinguishers.

It may be possible to discern the two categories in bimodal distributions and or scattergrams, getting beyond overly simple averaging of the whole autistic category.

Review of Asperger's/Autism relationship by Tony Attwood.

More evidence on the autism increase

Uta Frith is one of the most notable names in what we might call the autism research 'establishment'. She has recently stated [1] that autism in earlier decades was usually of the classic, severe variety, whereas nowadays most or many cases are of the mild to moderate or high-functioning variety. Putting that in the context of my view that there has been a major global increase due to a certain identified environmental factor, her observation poses the question of why that environmental factor should have produced generally less extreme autism than the preceding "genetic" form did.

And that is a question that is very happily answered by my explanation of the increase. Because the cause I invoke accumulates postnatally, it only impacts at a later age, whereas the classic genetic causation would impact from long before birth. And so one would indeed expect the new causation to commonly be less severe than the earlier variety.
1. Uta Frith, Autism: A very short introduction, OUP 2008