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.