Autism Causes .info

Autism did not begin only in the 1930s

noreply@blogger.com (Robin P Clarke) — Wed, 01 Sep 2010 21:07:00 +0000

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 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.

Vitamin D, sunshine, skin color, migration, and autism

noreply@blogger.com (Robin P Clarke) — Sat, 21 Aug 2010 22:01:00 +0000

Others have pointed to evidence suggesting that autism is associated with migration to less sunny countries, especially by darker-skinned people. For instance according to Autism, ethnicity and maternal immigration.
Keen DV, Reid FD, Arnone D.:

"Maternal immigration is associated with substantial increased risk of autism-spectrum disorders with differential risk according to different region of birth and possibly ethnicity."

There's the notable "epidemic" among Somalian immigrants. This could conceivably have something to do with (I guess) higher selenium levels in Somalian diet (due to lower rainfall, different geology, or the high fish content of the local diet). People moving to a diet of less selenium than they had evolved for could be more vulnerable to the antiinnatia effect of mercury, in absence of less antidoting selenium.

But while I don't rule out that possibility, a more likely process appears to involve vitamin D deficiency. Indeed a theory of causation by vitamin D deficiency has already been published in Medical Hypotheses (before that journal's editorial decisions recently became subject to non-editorial interventions by the owner, the publisher of supposedly scientific journals Elsevier).

This vitamin D deficiency thesis would tie in solidly with the antiinnatia theory, for the reason explained by the popular health writer Joseph Mercola:

"In fact, there’s compelling evidence that vitamin D is in fact KEY for proper gene expression." "Each cell in your body has its own ‘DNA library’ that contains information needed to deal with virtually every kind of stimulus it may encounter, and the master key to enter this library is activated vitamin D."

In other words, Mercola is here stating that vitamin D deficiency is something of an antiinnatia factor. So of course it would tend to cause autism (at critical developmental periods). Indeed, I indicated in my 1993 paper (and indeed all versions from 1982 onwards) that deficiencies of nutrients could obviously be antiinnatia factors.

Questions now arise as to how much contribution to antiinnatia (autism etc) is made by vitamin D deficiency, and whether the relationship with mercury, antiinnatia genes, etc is additive or synergistic.

Of course using vitamin D deficiency to raise one's infant's IQ would have certain major downsides, probably even worse than dosing them with extra mercury vapor; so farbeit from me to recommend it as a sort of "smart" drug.

P.S.: Vitamin D deficiency as an antiinnatia factor could also be the basis of recent observations of seasonal variation of autism incidence (by birthdate).

One might next predict that if D deficiency is indeed an antiinnatia factor, then IQ should also be season-of-birth dependent. It looks like that may not be the case. But then quite possible reasons for that could be that in the populations studied there was not much sunlight exposure anyway, and schoolchildren were routinely supplied with cod liver oil and orange juice (as in the uk for many years) such as would prevent substantial deficiency.

Fetal testosterone, “extreme-male-brain” and “developmental instability”

noreply@blogger.com (Robin P Clarke) — Sun, 01 Aug 2010 21:15:00 +0000

A conception of autism as extreme-male-brain (EMB) has attracted much publicity, with many persons being led to assume that it is the only remotely meritable contemporary understanding of autism.

There is indeed good reason to believe that fetal testosterone (FT) affects the development of the fetus, such that the brain remains thereafter more “male”; and this then manifests in more tendency towards “systematising” (as involved in science or engineering) and less towards empathising or emotional sensibility.

A questionable extension from this is the notion that FT increases some “autistic traits” and that in extreme those traits amount to autism, with autism being understood as being effectively identical to EMB. This “autism = EMB” thesis depends on overlooking the substantial evidence which does not fit with it. Autism (pre-increase) had strong associations with high social class and high parental IQ [1], and it is far from clear why extreme-male-brain would have. Likewise unclear is how it could credibly account for the symmetry data or the physical stigmata [1], or why it would involve such un-male but classic autism characteristics as shyness, hand-flapping/posturing, echolalia of whole sentences, lack of dizziness after spinning, intense resistance to change, toe-walking, etc [1].

EMB also struggles to explain the famous increase of autism, invoking at best a notion of a hypothesised increase of assortative mating of geeks. It is difficult to see any credible calculation of how assortative mating could have so rapidly increased autism tenfold within 20 years. And it would suggest that the autism increase in Silicon Valley would be conspicuously far greater still, whereas in practice the increase seems much the same everywhere. And EMB also fails to account for the stark change of ratio of age of onset.

On the one hand those numerous facts clash with the autism-as-EMB and geek assortative mating conceptions, while on the other hand there is the fully satisfactory alternative explanation presented here and in the 1993 paper.

These considerations show that EMB has inadequate merit as a candidate for being the central theoretical concept of autism. It can however be seen to be a part of the story, as I will now explain.

Innate programming has a more substantial role in the behaviour of female mammals than of males, for pregnancy management and nurturing (for instance empathy, theory of mind, communication). So the biologically optimum level of antiinnatia is lower for females. (In addition they would tend to have stronger genetic endowments of these predispositions, more resistant to antiinnatia factors.) Meanwhile, “systematising” is what brains do as a matter of default in the absence of specific pre-programmed reactions being evoked. Consequently the relatively “blank slate” mind of high antiinnatia tends to look like “male brain” in some respects. Or they even tend to actually be the same thing. Males would have a higher optimal level of antiinnatia, and so the characteristically male hormone testosterone would advantageously tend to raise antiinnatia somewhat (or in other words FT would tend to be something of an antiinnatia factor).

If FT were the sole or principal non-environmental antiinnatia factor, then women would be concentrated at the low end of the scales of IQ, health, body symmetry and beauty, while men would be concentrated at the high end of those scales. But that rather obviously is not the case, and that tells us that FT cannot be more than a relatively minor antiinnatia factor.

See also the explanation in the sex differences section of my original paper.

The associated concept of “developmental instability” presumes that organisms have “correct”, “intended”, “normal” courses and outcomes of development from which “maldevelopment” deviates. But they do not. There is no blueprint in DNA; rather, development just happens blindly and aimlessly in interaction with varying environment, just as natural selection does. And already in the 1993 paper I had indicated two respects in which even erraticness (‘instability’) of phenotypic outcome can be biologically advantageous (i.e. ‘intended’).

The correct concept—the oxygen to this phlogiston of developmental science—is antiinnatia, now more evidentially-suppported than ever.

The "Imprinted Brain" theory of Badcock and Crespi

noreply@blogger.com (Robin P Clarke) — Thu, 29 Jul 2010 22:29:00 +0000

Many years after I thought of this gene-expression theory of autism, another gene-expression theory of autism was published by Christopher Badcock and Bernard Crespi. It is rather more of a brain-strain than my own, in that it is based on the not-so-basic concept of genomic imprinting. And it leaves unexplained many things about autism which the antiinnatia theory easily embraces within its commanding logic.

I think it very likely that this imprinted brain theory may play some valid part in the understanding of autism, but I think it quite certain that it in no way can replace antiinnatia as the central explanatory concept. I won't review it any further here for the simple reason that I haven't found much need for it, and why complicate things unnecessarily? Isn't the antiinnatia theory quite enough already?

Meanwhile there are some faults I find in their notion of autism as imprinted brain. They consider that the opposite of autism is schizophrenia. Having myself fully worked out the definitive theory of schizophrenia (but unable to finish writing it up due to my severe mercury amalgam poisoning disabilities; my outline theory of manic-depressive I did publish though), I can understand why they have made that mistake. That's because one of the key things of schizophrenia is over-expression of certain innatons, whereas the very essence of autism is under-expression of innatons. But I had already explained in my 1993 paper (and unpublished section about IQ) that the opposite of autism is common-or-garden low IQ. Of course that would seem impossible as autism itself often involves low IQ, but well that's life, full of such tricks to catch the insufficiently deep thinkers of this world!

Hertz-Picciotto et al 2010 re blood levels of mercury

noreply@blogger.com (Robin P Clarke) — Sat, 17 Jul 2010 08:55:00 +0000

This study appears to be competently done in terms of methodology etc. It is just misguided in terms of its theoretical background assumptions.

They found that fish consumption raised blood mercury. Which is not surprising as blood mercury has been well-known to reflect recent mercury intake. But they didn't take any measurements of blood selenium. Almost all fish has mercury content more than cancelled out by selenium, which is why the Seychelles studies contradicted the Faroes ones. Mercury in fish is already reacted, compounded with proteins or whatever, which greatly reduces its harmfulness, whereas the mercury vapor emerging from dental amalgams is unreacted until it hits your own proteins (hormones, receptors, etc) and reacts with them.

They found no association of mercury blood levels with autism, and no association of fish-eating with autism. Which is not surprising as the autism would be caused not by mercury in blood but in brain cells. It's long been known that blood levels of mercury are near-useless as an indicator of body burden of mercury and mercury poisoning.

Ask the wrong questions and you'll get the wrong answers. 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 Hertz-Picciotto's one requiring going round sucking blood from children rather than just counting their mothers' fillings! (So should Ms Hertz-Picciotto be hauled before the Americans' GMC on charges of needlessly abusing children?)

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.

Why mercury supposedly could not get to DNA to cause antiinnatia!

noreply@blogger.com (Robin P Clarke) — Thu, 01 Jul 2010 19:53:00 +0000

Wegener's collossal epoch-making discovery of continental drift was dismissed with derision by the community of professional geologists for 50 years, apparently merely because he was unable to show any mechanism by which the continents might drift. That was even though his deriders were in no position to show anything that would prevent the continental drift. And was even though volcanos have long made it reasonable to believe there is a layer of molten rock under the Earth's crust.

A similar situation exists in respect of the incorporation of environmental mercury into the antiinnatia theory. 'Skeptical' nitpickers could say that there is no demonstrated means by which mercury ions could reach the DNA in order to attach to it as per the theory. They would point out that the DNA is in working normal life not loosely and openly floating around in body fluids but instead is confined to a very controlled environment of proteins such as histones and secluded away inside the protective membrane of the cell's nucleus which in turn is some way in from the cell's lipid bilayer outer membrane. They would further point out that the DNA is to a large extent tightly curled up in condensed inactive form, further inhibiting unconstrained access by rogue mercury atoms. They would claim that mercury would have already bound with sulphydryls of proteins before it could get to the DNA. They would claim that mercury is bound much more strongly to other things than to DNA (though not sure if there's any real evidence on that).

Those who dismissed Wegener's continental drift theory could not show any videos or even photos from under the Earth to substantiate their assertions. And likewise those who would dismiss the idea of mercury getting to the DNA can't actually show any proof that mercury never gets to it. And despite even some of those queries listed above being true, they do not genuinely undermine the case, as I will now explain.

The antiinnatia theory does not entail a notion that most or even a high proportion of gene-expression is suppressed by antiinnatia. If it were then it would surely result in non-life or at the very least a being that had little resemblance to a human. On the contrary, antiinnatia theory entails only a very small proportion of gene-expression being suppressed, perhaps 1/1000th or less to produce an autism diagnosis condition. Furthermore it is not being suggested that all children exposed to mercury become autistic, rather only a small minority. And even they only become affected by the mercury after 18 months or so, in accordance with the evidence shown in the update paper.

Furthermore there is the fallacious notion that mercury is absolutely a "bad" "toxic" thing such that the organism must have only mechanisms to keep it out. On the contrary, the whole point of the antiinnatia theory is that antiinnatia is highly advantageous provided it does not reach the excessive levels which manifest as autism.

And so, at lower levels, mercury as an antiinatia factor would not be opposed by the organism but actually positively selected for. There would be natural selection positive selection of processes (or 'faults') which passively or even actively admit mercury to access the DNA. I don't mean flooding the DNA with mercury, but merely allowing just a very few atoms of Hg to sprinkle themselves sparsely on the DNA. DNA strands are rather complex molecules. It is quite conceivable that there are occasional locations among all that complexity at which a mercury atom could find itself relatively welcome and unrepelled.

That is clearly a far from unreasonable concept. Everyone is free to choose their own reckoning of the burden of proof in this matter, but it looks to me like the common-sense burden of proof lies with any "skeptics" to show that the mercury could not even occasionally, even after 18 months constant exposure, even in very modest doses get to the DNA, rather than the burden being to show that it does.

Should I say that "absence of evidence is not evidence of absence"? No, because there is not an absence of evidence. I see a compelling abundance of other (i.e. non biochemical) evidence that mercury is an antiinnatia factor. That's what gives me faith in the unseen, faith that the binding to DNA that has been decisively shown in vitro also occurs in vivo.

Copy number variations are at best only marginal to autism causation (which is in accordance with antiinnatia theory)

noreply@blogger.com (Robin P Clarke) — Tue, 15 Jun 2010 02:51:00 +0000

The main importance of this study in Nature lies in what it has not found. It has involved a huge amount of time and effort expended on seeking for pathological genetics underlying this so-called 'disease' or 'disorder' (ASD), and yet such pathology as it has found can account for only about three percent of all the autism-related cases under study. That doesn't surprise me at all. It is entirely in accordance with the still-unchallenged antiinnatia theory. Therein, I agreed with those who reckoned that autism was a polygenetic condition just as IQ genetic variance was polygenetic. The vast majority of genetic variations genuinely associated with autism would be the very same "normal", non-pathological, variations that contribute to IQ differences -- for the reasons the theory explained.

These authors are scraping the bottom of the wrong barrel, looking for the wrong things, and as a result they find the wrong things which then lead them away from the main story of autism causation. So-called ASD is a very rough and broad empirical diagnosis which is liable to include quite a number of cases who do not really belong in the true autism broad syndrome but just have some genetic twirks that make them behave rather similarly (like a bee misleadingly resembles a wasp). All the vast media/discussion hype then goes on to assume, falsely, that the study results really are about autism per se rather than such false trails. Their study could have had more hope if it had used narrowly-defined core autism as its cases.

But the people there are working to a pre-set paradigm, within what we might call the disease model. This presumes that something has "gone wrong" with these individuals and seeks out that "wrong". Furthermore they assume it is genetic! It may be significant that their 90% genetic stat is supported only by a reference that is 15 years old. In my 1993-published theory I indicated conditions in which autism would change from being mainly genetic to being mainly environmental. And exactly that has now happened in the last 2 decades.

Their pre-set paradigm is to find what has "gone wrong" and then find a drug to "put it right" and voila! a profitable patent emerges (they hope).

Huge publicity is being given to these marginal fringe findings, while the real central ressearch is all but completely hidden by this hype. For instance the Autism Research Institute's evidence that DMSA chelation to remove mercury can cure about 70% of cases, as documented by online videos of the cured children. But that doesn't generate profits for big corporations, or jobs for the 170 researchers listed here. So it is ignored, despised and even persecuted just as was Semmelweiss's immense discovery, inter many alias. Or they could have just spent a little time more enlighteningly reading my 1993 paper. But then Wegener's continental drift had to wait through 50 years of professional derision so perhaps I'm calling time a little prematurely here.

There's reason to suspect there's already a fairly good genetic test for autism, namely whether both parents have Mensa-level IQs. An even better test is how many non-gamma-2 dental amalgams the parents have, and how little outdoor air. But why follow the facts when you can follow the crowd that's following the money instead?

Edit: There's now appeared a much more detailed (but far longer) critique by Mark Blaxill. My only reservation about it is that the claim in the title that it "proves that inherited genes don't cause autism" is absolutely unfounded.

Good review of autism increase question

noreply@blogger.com (Robin P Clarke) — Sun, 25 Apr 2010 22:29:00 +0000

A notable review of the debate on whether or not autism has increased can be found here. Interestingly, it leads to the same conclusion as myself - that the increase was real - even though not raising what I would consider the trump card fact presented in my update review. But then, no one else besides myself has noticed that point yet.

Gradual regression notably in line with the theory's gradual causation

noreply@blogger.com (Robin P Clarke) — Fri, 26 Feb 2010 09:51:00 +0000

It has this month been reported that the regressive form of autism does not tend to have an abrupt start (as commonly perceived, especially by those blaming vaccines for causing a sudden start of the condition). Instead the condition develops gradually from age 6 months up to 3 years (and possibly onwards as the study stopped there).

This is of course very compatible with the causation proposed in the update review of the antiinnatia theory, because that causation itself does not strike suddenly (like a vaccination shot) but instead builds up gradually with the infant's cumulating constant inhalation [breathing in] of the mother's dental mercury vapor.

The accompanying observation that parents tend to under-perceive their child's abnormality can be simply understood in terms of the universal natural reluctance to believe bad news. Which for a parent who already has an autistic child, is even badder news.

Flawed study of adult autism in UK

noreply@blogger.com (Robin P Clarke) — Sat, 13 Feb 2010 09:42:00 +0000

The NHS has recently published a study of the extent of adult autism in the UK ("Autism Spectrum Disorders in adults living in households throughout England - Report from the Adult Psychiatric Morbidity Survey 2007").

It supposedly shows that there has not been any real increase of autism over recent decades. This is the same NHS that's just made a huge scare-campaign in support of the swine-flu scam, and that gives its endorsement to the fraudulent SCENIHR report as supposedly proving the safety of dental amalgams, even despite numerous people pointing out the falsities of that report.

This autism report is also unacceptably flawed. Some of the flaws are detailed at this campaigning website (at which some of the other content is itself flawed wishful-thinking):
http://childhealthsafety.wordpress.com/2010/02/10/uksurveyautismlink/.

I myself had dismissed the NHS report for the simpler reason that there is no way indicated of establishing comparability of a test applied to children and a test (even if the same one) applied to adults. But I now welcome the additional critiques raised by childsafetyhealth. Another critical review can be found in issue 34 of The Autism File.

"Whose side is Robin P Clarke on?"

noreply@blogger.com (Robin P Clarke) — Sat, 13 Feb 2010 03:19:00 +0000

Since the publication of the theory, three entrenched factions have appeared in the autism causation world. A first faction believes autism can never be a problem, so cannot need curing or be a disorder. A second faction believes that vaccines, either MMR or mercury-containing thimerosal (or latestly Hep-B) have caused autism to increase. A third faction is the corporate medical establishment which promotes the idea that autism is a primarily genetic disorder and that the increase is not real but just the effect of increased awareness or diagnosis.

My involvement in autism research pre-dates all these factions and I partly disagree with all of them, but also partly agree with them all. I see some sound work from all of them and also some abysmally unsound work from all of them. I'm not in the business of taking sides. I judge publications on their reasoning and evidence rather than the partisanship of the conclusions or authors. In my experience as exclusively a theorist, I have to conclude that it is very rare for even biased parties to actually falsify their raw data; if they did so it would be impossible for my theories to so comfortably accommodate them as they do. Meanwhile, far too many people insist on following the false "logic" that "there's no smoke without fire". A crooked institution arranges a cover-up even if there is in reality not some catastrophe genuinely there to be covered up anyway.

My guess is that these factional differences will melt into history just as the silly confrontation of "Wagnerians" versus "Brahmsians" did.

Why Bernard Rimland made just one mistake

noreply@blogger.com (Robin P Clarke) — Mon, 18 Jan 2010 18:27:00 +0000

Bernard Rimland's contribution to autism research has been unequalled. To him belongs the credit for debunking Bettleheim's theory of "refrigerator mothers", and replacing it with the modern understanding of autism as genetic/biochemical in nature.

He had much responsibility for the discovery of the benefits of vitamin B6 and magnesium. He was one of the first to discern that autism was increasing. And he recognised that mercury was involved in causing it.

He made just one mistake (as I see it), namely taking the view that vaccines were the cause of the autism increase [note: cause of the increase]. I think part of the reason for that mistake was a situation of having one's nose too close to the grindstone, so-to-speak. This is liable to lead into that other metaphor of the frog not bothering to jump out of the slowly heating water.

Given the assumptions that:

autism was increasing;
mercury was involved;
the increase was in second-year onsets;
vaccinations were the only noticeable input of infant mercury;
vaccinations had increased at ~sort-of~ the same era as the autism increase;
parents were increasingly reporting autism onset "immediately" after vaccinations;
the only other notable source of mercury, dental amalgams, had been in use for 150 yrs before the increase, and not in infants anyway;
the medical establishment were engaged in their usual conspiracy tricks, publishing misleading studies about vaccines, hiding their Simpsonwood data, and persecuting those who challenged them;

Given these observations, it was not unreasonable to become convinced that vaccinations were the cause of the autism increase.

Myself? As a fatigue-disabled person, struggling to just survive, and with much wider interests than Dr Rimland's focus on autism, it was not within my capabilities to keep up with all the details of the dispute about the increase. And as my "excellent" "fine work" 1993 paper had been totally pretended into non-existence by all but a tiny elite anyway, there seemed little point in taking such an interest in a dispute of no practical importance to myself.

It was only by fluke that I got involved again. I began to wonder if my decades of severe disability (not autism; since age 15) had been caused by dental mercury. I now had, for the first time, increasing billions of webpages that I could search on the subject. I gradually became more informed and more suspicious. Then I read that mercury binds to DNA and thereby inhibits gene-expression at doses far lower than producing other effects. This rang a bell because it was exactly what I had said would cause autism, in my 1993-published paper. I also learnt that the type of amalgam had switched from the 1970s to non-gamma-2 which emit 30-50 times more mercury vapour into the air. Thanks to my autism theory (which everyone else was ignoring) I also knew that the process was like holding the genes hostage rather than like a shattering hammer blow. I also understood that amalgam delivers its poison through the air, and thus can be breathed in by the (post-natal) infant as well as the parent.

Dr Rimland didn't know these facts, so the idea that dental amalgam could have caused the increase would have rightly seemed daft to him. How could a non-increasing source cause an illness increase in people who aren't even having it installed in them? In 2006 I sent to Dr Rimland a draft of my update review but I got a reply from Dr Edelson that Dr Rimland was too ill to read it. I'm sure that if I had not been delayed by the callous harassment conspiracy www.2020housing.co.uk I would have been able to persuade Dr Rimland that it was dental mercury that was the main cause of the increase.

Do von Economo neurons produce bigotry?

noreply@blogger.com (Robin P Clarke) — Sat, 16 Jan 2010 01:21:00 +0000

There is occasionally a scientific paper that stands out with its joining of the dots. One such is that of John Allman et al in respect of von Economo neurons (vens):
Allman JM, Watson KK, Tetreault NA, Hakeem AY: Intuition and autism: a possible role for Von Economo neurons. Trends Cogn Sci 2005, 9:367-73.

His paper could have been even hotter if it had managed to mention how various of its elements had already been raised long ago in my 1993-published paper. For instance the idea that features that are recent in phylogeny (evolutionary history) are more liable to be impaired, and that that is what gets lost in autism (both key concepts in antiinnatia theory). And the antiinnatia theory had started out in its first minutes with the concept of "autism = deficiency of innate prejudices", which is strikingly close to some of the notions therein.

What is rather curious about his von Economo paper though, is the standard values-laden language it contains. We are told that autism is a "disorder" in which these rapid decisions about people are "impaired". I would beg to suggest that the characterisation of the vens as enabling rapid crude decisionmaking about whether or not to view people as friends is a description of bigotry. So perhaps it would be better to consider normal neurotypical to be a "disorder" and autism to involve freedom from an "impairment" which might be advantageous to the knee-jerker but harmful (in excess) to community cohesion. I guess Dr Allman would agree about this now that I have pointed it out.

More evidence on the autism increase

noreply@blogger.com (Robin P Clarke) — Sun, 27 Dec 2009 23:13:00 +0000

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

Shallow critiques of the Holmes and Bradstreet studies of mercury

noreply@blogger.com (Robin P Clarke) — Wed, 23 Dec 2009 12:20:00 +0000

The Holmes and Bradstreet studies have been supposedly demolished by critiques in the book Defeating Autism by Michael Fitzpatrick. In reality his critiques read self-damningly in the context of his having a whole chapter titled “Being appropriately critical”.

A widely cited study published in 2003 examined the mercury content of babies’ ‘first haircut’ samples from 94 children with autism and 45 controls and found levels significantly lower in the autistic children (and the more severe the autism the lower the mercury level)(Holmes et al. 2003). The authors interpreted these findings as suggesting that children with autism do not excrete mercury into their hair — and that the mercury burden remains active and toxic, within the bodies of children with autism. There were, however, a number of reasons to be sceptical about these findings {Institute of Medicine 2004: 133-134). Firstly, the study was funded by Safe Minds, a militant, parent-led, anti-mercury campaigning group.

But so what? Almost all other studies are funded by immensely-wealthy corporate-dominated interests such as pharma manufacturers and the institutions they dominate. Applying that objection evenhandedly rather than with Fitzpatrick’s peculiar selectivity would result in there being virtually no studies at all recognised as legitimate in the last century of medical research.

Secondly, its authors included only one recognised scientist, the Kentucky [[University!]] chemist [[Professor!]] Boyd Haley, well known for blaming mercury in dental amalgam and from other environmental sources for a range of disorders, including chronic fatigue syndrome and Alzheimer’s disease. Another author, Amy Holmes, is a doctor with an autistic child; she is a campaigner against vaccination and a provider of chelation therapies. Another, Mark Blaxill, has a business school MBA.

Here Fitzpatrick employs ad-hominem insinuation, which is widely condemned by scientists as meritless, albeit being popular in the unscientific circles at which his book is aimed. And he deploys it with extremely prejudiced selectivity, because one might just as reasonably dismiss all or most professional (hence “recognised”) scientists on the basis of their money-making connections to corporatised, institutionalised and career-ised operations. Applying his argument with any diligence would leave little or nothing standing in the scientific record. And even such greats as Copernicus, Newton, Darwin, Mendel, Faraday and Einstein were not “recognised” scientists, until retrospectively so recognised.

Thirdly, there were concerns about selection bias: autistic subjects were recruited from Holmes’s clinic and controls via the internet.

But so what? Quite how could any such selection bias account for that finding of 8-fold difference with very high statistical significance, p&lt0.000004.

Fourthly, though the hair samples were described as ‘first haircut’, they were taken at a median age of over 17 months, rather than at birth, so the implications of their mercury content for prenatal exposures (for example, to RhoD immunoglobulin containing thimerosal, given to Rhesus negative mothers during pregnancy) were unclear.

But my own theory of the increase involves postnatal exposure to mercury rather than prenatal, so even if that objection had any real soundness it would still not apply to that amalgam theory.

Fifthly, infant exposures to other sources of mercury were not ascertained.

But again, in terms of the study being merely evidence of a mercury-autism connection, so what?

Most importantly, the authors presented no direct evidence for their hypothesis that low hair levels of mercury reflect persisting toxicity in children with autism.

But so what? Has anyone presented any evidence against that hypothesis?

A subsequent study comparing children with autism and controls in Hong Kong, found no difference in mercury levels (Ip et aI. 2007). The authors concluded that their results showed that there was ‘no causal relationship between mercury as an environmental neurotoxin and autism’.

But that Ip et al. study has been absolutely discredited and shown to actually corroborate Holmes et al. rather than challenge it: http://www.ageofautism.com/2007/12/the-ip-blip-and.html. And it anyway concerns 7-year-olds (and in the context of Dr Fitzpatrick’s own nit-picking of a mere 17 months delay above).

Though numerous anecdotal reports and testimonials claim dramatic improvements in symptoms of autism following chelation therapy to remove mercury and other heavy metals believed to be toxic, it is impossible to find independent confirmation of these benefits.

But those “numerous anecdotal reports and testimonials” are “independent confirmation”. Except that when Dr Fitzpatrick uses the word “independent” he in reality means “corporate-establishment-dependent”. And those corporate-institutionalised groups had not found any confirmation for the simple reason that they did not carrry out any studies because they did not want to find any such confirmation.

However, one study of chelation has been widely cited in support of the mercury-autism theory. In this study, conducted jointly by the Florida DAN! doctor Jeffrey Bradstreet and the Geiers, more than 200 children with autism were found to have excreted significantly more mercury in their urine than 18 controls (apparently healthy children whose parents had sought chelation treatment because of worries about heavy metal toxicity) (Bradstreet 2003). Apart from revealing a frightening willingness of parents to subject their children to chelation therapy, it is difficult to draw any conclusions from this study.

That study found more than 3 times higher mercury in autistics, with a huge significance level of p&lt0.0002. But Dr Fitzpatrick indeed could not draw the mercury-acquitting conclusion he wished to from those brief numbers so he did not find even a tiddler of space for them in his book (perhaps because it was required for his closing masterclass about “Being appropriately critical” instead).

Apart from revealing a frightening willingness of parents to subject their children to chelation therapy,

....in the context that no-one has ever been killed by DMSA chelation, in stark contrast to the lethal drugs that Dr Fitzpatrick routinely prescribes. But then his book also didn't find the little space to mention that it was DMSA rather than EDTA in the study (and this in a book that opens with a shock-horror anecdote narrative about a unique EDTA case).

The non-mysteries of savant syndrome and synaesthesia

noreply@blogger.com (Robin P Clarke) — Mon, 21 Dec 2009 10:47:00 +0000

Savant syndrome is rare, and I haven't studied it much, but I will just put here my thoughts about it.

Some people think it is somehow puzzling that an individual can have such extraordinary ability in some obscure form of calculation or calendar-memorising or such-like. Especially if they are not particularly high IQ. I don't find it particularly suprising myself, at least not more so than the already amazing things that the brain of the average person is capable of anyway.

For instance if you have any experience of cheapo binoculars you will know that the human visual system has an ability to coordinate two misaligned images into one. And indeed it does this all the time even when binoculars are not involved and even when stereoscopics and other factors make the images disalike. This effortless merging of binocular images must take some rather substantial hardwired computing power.

A second less obvious example came to my attention after I was attacked by a thug and left for dead. A few weeks later I was amazed to find that my right ear was hearing sounds half a semitone sharper than my left ear. Which causes all music to sound very unmusical indeed. This problem, the technical name of which I have forgotten, resolved itself on the 13th day just before it had driven me completely bonkers. But again, it shows that the auditory brain must be likewise effortlessly mapping together the disparate sounds from the two ears, even while our attention is concentrated on other things such as understanding or appreciating the sounds in question.

These high-power computations are performed without effort in the brains of even the most average of people. Let us combine that fact with the observation that in normal development, some neurons have to "migrate" their axons and dendrites significant distances to establish connections with other parts of the brain or body. Under certain conditions it can be expected that such migrations will get misdirected, and this would in respect of sensory neurons quite credibly produce the mix-up of sensations that is synaesthesia.

Meanwhile there could occasionally be another sort of misdirected migration-connection, in which an area which would normally be innately-assigned to one of those complex innate functions such as binocular vision or hearing gets connected to some other inputs and outputs and thereby recruited for some other task instead. And would thereby produce, rarely, one or other savant syndrome ability.

The history of suppression of scientific genius

noreply@blogger.com (Robin P Clarke) — Sun, 20 Dec 2009 12:11:00 +0000

Excerpts from Eysenck's book Genius (1995)

"The list is truly endless ..." "Nothing has changed"
(except that genius is now totally invisible)

[One of the cases which Eysenck did not mention here was that of Ludwig Boltzmann, whose outstanding discovery of statistical thermodynamics was ridiculed by university professors for ten years till he took his life.]

[page 147:] Less often remarked, but possibly even more insidious, is the resistance by scientists to scientific discovery [.....]
[page 148:] Planck's experience with other leading physicists was no different. .... 'I found no interest, let alone approval, even among the very physicists who were cleary connected with the topic. Kirchoff expressly disapproved. I did not succeed in reaching Clausius. He did not answer my letters, and I did not find him at home when I tried to see him in person in Bonn. I carried on a correspondence with Carl Neumann, of Leipzig, but it remained totally fruitless' (Planck, 1949, p.18). ' .... a new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.'
.... even after the publication of De Revolutionibus most astronomers retained their belief in the central position of the Earth; even Brahe (Thoren, 1990) whose observations were accurate enough to enable Kepler (Caspar, 1959) to determine that the Mars orbit around the sun was elliptical, not circular, could not bring himself to accept the heliocentric view.
Thomas Young proposed a wave theory of light on the basis of good experimental evidence, but because of the prestige of Newton, who of course favoured a corpuscular view, no-one accepted Young's theory (Gillespie, 1960). ....
Similarly, William Harvey's theory of the circulation of the blood was poorly received, in spite of his prestigious position as the King's physician, and harmed his career (Keele, 1965). Pasteur too was hounded because his discovery of the biological character of the fermentation process was found unacceptable. Liebig and many others defended the chemical theory of these processes long after the evidence in favour of Pasteur was conclusive (Dubois, 1950). Equally his micro-organism theory of disease caused endless strife and criticism. Lister's theory of antisepsis (Fisher, 1977) was also long argued over, and considered absurd; so were .... .... Priestley (Gibbs, 1977) retained his views of phlogiston as the active principle in burning, and together with many others opposed the modern theories of Lavoisier, with considerable violence. Alexander Maconochie's very successful elaboration and application of what would now be called 'Skinnerian principle' to the reclamation of convicted criminals in Australia, led to his dismissal (Barry, 1958).
Another good example is Wegener's continental drift theory, which was given short shrift when he first announced it (Wegener, 1915), but which is now universally accepted. .... most geologists rejected it out of hand. Many of them refused to take it seriously and simply ignored it. ....
The list is truly endless, and is continued in Barker's (1961) article. Here I will rather cite in a more detailed manner a particularly interesting case, that of Ignaz Philipp Semmelweis (Slaughter, 1950). .... An almost ten-fold reduction in mortality might have been expected to provoke praise, interest and imitation. Nothing of the kind. .... Professor Klein, his boss, driven by jealousy, ignorance and vanity, put all sorts of obstacles in Semmelweis's way, underhandedly prevented his promotion, and finally drove him from Vienna.
Another victim of mindless medical orthodoxy was the great Andreas Vesalius, who pioneered modern anatomy 450 years ago. .... Embittered by the harsh condemnation of his work, Vesalius gave up scientific work, burnt his notes, .... Vesalius was made to undertake a pilgrimage to Jerusalem .... he was shipwrecked and perished.
.... it would be quite wrong to imagine that this is the sort of thing that happened in ancient, far-off days, and that nowadays scientists behave in a different manner. Nothing has changed, and I have elsewhere described the fates of modern Lochinvars who fought against orthodoxy and were made to suffer mercilessly (Eysenck, 1990a). .... It is odd that books on genius seldom if ever mention this terrible battle that originality so often has when confronting orthodoxy.

From HJ Eysenck, Genius (Cambridge University Press, 1995) pp. 147-152.

Increasing support for the handflapping explanation

noreply@blogger.com (Robin P Clarke) — Tue, 15 Dec 2009 11:19:00 +0000

When working up the details of the antiinnatia theory, it very soon became apparent that some features of autism could not be credibly explained as due to loss of innatons. This led me to think of the idea of prehuman innnatons being suppressed by later changes, and indeed I thereafter learnt that this concept was already well-established and called atavisms. I explained the handflapping and posturing as a re-emergence of the sort of behaviour regularly seen in wild rats, squirrels and birds in the wild. Fuller details are in the 1993 paper.

Nowadays with the internet it is vastly easier to research things than it was back in the 1980s and 90s. I have now learnt that we did indeed have a rat-like prehuman ancestor, for 163 million years! As described in this video of your granny (which be warned is rather 'exciting' by the way):
http://www.youtube.com/watch?v=y0iSf4yISDA
same as at:
http://animal.discovery.com/videos/animal-armageddon-purgatorius.html

Age of Onset graph

noreply@blogger.com (Robin P Clarke) — Sat, 14 Mar 2009 21:00:00 +0000

First graph is from the Autism Research Institute (though named "Institute for Child Behavior Research" during most of this graph). Second is my re-working to show the changing ratio of age of onset. How easily is this data compatible with no increase?

The Neurodiversity / Autism Pride movement

noreply@blogger.com (Robin P Clarke) — Fri, 06 Feb 2009 14:07:00 +0000

Since I published that first paper, one development that has been enabled by the emergence of the www (and blogs in particular) has been the neurodiversity or autism pride movement. This rightly says that many autistics (or at least people with a moderate degree of the autistic/Asperger syndrome) are perfectly happy and functional as they are and do not want to be "cured" of their personality. Indeed they rightly point out the shortcomings of mere "neurotypicals".

They reasonably reject the notion that they have a "disorder".

So far so good, but some then go on, like all good fanatics, to take a dogmatically exaggerated position. Supposedly autism is never really a problem, and no autistics need curing. And not being a problem it (supposedly logically) "therefore" cannot be caused by a toxin such as mercury. Their fanaticism thus leads them to devote their lives (perhaps subsidised by vaccine mfrs) to half-baked nitpicking of everything that evidences mercury or an increase of autism.

They then go on to make out that the great scientists who have done so much to help the problem of autism, namely those involved in DAN! (defeat autism now) are a load of evil greed-driven liars.

All this is a pathetic unnecessary exhibition of black-white stereotyping by these attitude-driven fanatics. Many people are not handicapped by their autisticness. But meanwhile there are many who are severely devastated by it. There is room in the world for both these facts to be true simultaneously. None of the heroic DAN! practitioners have ever said that any autistics must be forced to accept treatment.

And no one wanting to get rich would choose to do so by clashing head-on against the medical establishment.

"Offensive" / " inappropriate" language about autism

noreply@blogger.com (Robin P Clarke) — Fri, 06 Feb 2009 12:51:00 +0000

When I first started sending manuscripts to journals, I once got back a reply that it was offensive to use the term "autistics". Instead one has to ramble on about "children with autism" (which is probably why so many people assume that autism is confined to children, and is something that one either "has" or does not "have"). Meanwhile it has become the standard practice of the same people to refer to autism and related conditions as "autism spectrum disorder", or ASD. There's even a journal called the Journal of Autism and Developmental Disorders. Now I may be just a twit but I would have thought that referring to autism as being a disorder must be genuinely offensive, given that so many autistics do not want to be "cured" of the "disorder" they supposedly have. And meanwhile let's not be big hypocritical babies unable to usefully call a spade anything shorter than "tool for digging".

Persons with femaleness.
Persons with generosity.
Persons with racism.
Persons with Britishness.
Persons with Protestantism.
Persons with degrees.
Persons with professorships.
Persons with elderliness.
Autistics with childness.

In addition, the terminology of "autistic spectrum" I find very unhelpful, because it gives a false impression of having only one dimension of variability. In reality the autistic syndrome is a rather multidimensional thing, which would be best referred to as just that. It naturally includes those diagnosed as Aspergers and also those with just one or two features of the syndrome (such as the communication disabilities noted in siblings of the Rutter/Folstein twin study).

(Just images of my Rimland quotes)

noreply@blogger.com (Robin P Clarke) — Sun, 15 Jun 2008 09:52:00 +0000

Yet another theory of ageing!

noreply@blogger.com (Robin P Clarke) — Mon, 11 Feb 2008 11:03:00 +0000

This is nothing to do with autism but, oh well anyway.

Some peculiar facts. Children conspicuously indulge in energy-wasting exercises with great enthusiasm. They see fences and walls as things to climb up, and buildings as things to run round two or three times. Adults by contrast increasingly tend to the opposite. As they age they get less and less enthusiastic about even just running along their chosen route. They are conspicuously very unenthusiastic about taking even a fraction of the exercise they need to keep healthy. They get overweight and unfit and start complaining about being cold, indeed become hypothyroid, whereas younger people think nothing of going out in the frost only half-dressed.

Some will tell you that the adults' reducing activity is due to their ageing. And yet in certain pre-industrial societies the adults carry on working well beyond 100, till they drop from genuine old age (at about 120 years). Some will tell you that the feeling cold and hypothyroid is likewise a symptom of the normal degradations of time. I disagree. Just about anyone's "hypothyroid" can be cured instantly by chasing them up the stairs to my 20th floor apartment. They'll then be complaining about being too hot instead.

Like all my medical theories, this new theory of ageing has a basis in evolution by natural selection. In evolutionary history, people have had to do a lot of hard physical work merely to survive. And have had to avoid getting injured. For these reasons, adults have evolved innate predisposition towards using their energy with high efficiency, avoiding unnecessary indulgence in work, and avoiding indulgence in unnecessarily hazardous activities.

Meanwhile, children have had less pressure of survival-work to do but do have to engage in the process of growing up which includes an expanding repertoire of physical capabilities needed for adulthood, such as being able to run and climb rather than just crawl. So young children are innately predisposed to engage in that physical training. Some sporty types retain such predisposition into later youth, but most eventually succumb to "age".

My view of all the above is that there is a new "ageing" syndrome which has arisen due to the reduced need for physical work in adulthood. The innate predisposition to efficient physical behaviour, what we might call laziness, now results in adults getting far less exercise (aerobic and strength training) than they need for good health. This in turn leads to their becoming obese, and to their becoming hypothyroid simply due to underactivity.

The cure for this new syndrome could be to introduce a new force of Exercise Police to chase all the adults round the block a few times a day. Any better suggestions? (Apart from banning cars until proven safe.)

Causes of autism - update of unchallenged theory

noreply@blogger.com (Robin P Clarke) — Thu, 28 Dec 2006 14:29:00 +0000

This is a website relating to the unchallenged theory of autism, IQ and genius (the antiinnatia theory). An update review paper is being prepared for publication. Meanwhile you can download the original 1993 publication here . Be sure to print it out rather than trying to read on screen.

I cannot put the update paper on a website before it has been accepted by a journal. But in the interim I can send you a copy by email if you email a request for it to rpclarke [at] autismcauses[dot]info .