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.