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

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.

Anecdotes or Cures?

Some of the information that organisations such as the UK "National Autistic Society", "Research Autism", and Cambridge's "Autism Research Centre" aren't capable of mentioning is at this link and this one.
This is a link to a video of Polly Tommey explaining about the autism catastrophe (I don't share her ideas re mmr).

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

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

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!

Reason for false association between vaccines and autism

I'm copying in this post below from another blog here as it usefully complements my other post about vaccinations.

Please note that I do not agree with everything it says.

Correlation Not Causation

Posted by David_Pollard on 28 May 2009 at 15:12 GMT

There really is a connection between vaccination and the onset of autism, but it's not a causal relationship.

Fever reduces autistic spectrum symptoms, and vaccination can cause mild fever. Generally the symptoms of autism develop quite slowly and may pass un-noticed in the early stages. It is quite likely that, in a proportion of cases, they will first be recognised following a fever when, having been reduced by the fever, they return quite quickly as it abates. This relatively sudden return could well appear to be the initial onset, leading to the (false) conclusion that whatever caused the fever also caused the autism.

Parents in such a situation will not easily be convinced by assurances and epidemiological studies. And the assertion that there is no connection whatsoever is tantamount to calling them liars, for this is to deny the evidence of their own eyes. Not surprisingly some will dig in their heels and reject the views of authority with considerable vehemence.

Whatever the other factors may be that fuel the myth that vaccination causes autism, and there do seem to be various vested interests, this is one of the major roots. The myth will not disappear until it becomes common knowledge that anything that causes fever is likely to bring autistic spectrum symptoms to notice by briefly reducing their severity. But bringing symptoms to notice is not the same as causing the ailment.

http://www.sciencedaily.c...
https://www.thefirstpost....
http://www.sciencedaily.c...

No competing interests declared.

Note: the above are not the words of Robin Clarke myself, and I do not agree with it all.

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

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 (in the forthcoming update review paper). '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's mechanisms could only be designed 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 antiinnatia 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. In the update review I will show the compelling abundance of other (including 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 living human beings.

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

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.

P.S.: Prof Alexandre Raymond explains that the genome is more complicated than geneticists have assumed, and so we should be wary of imagining we have more knowledge and understanding than is actually the case.