On the aetiology of autism

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A DIFFERENT VIEW
On the aetiology of autism
John J Cannell (jcannell@ash.dmh.ca.gov; jjcannell@vitamindcouncil.org)
Atascadero State Hospital – Psychiatry, Atascadero, CA, USA
Correspondence
John J Cannell, Atascadero State Hospital – Psychia-
try, 10333 El Camino Real, Atascadero, CA 93423,
USA.
Tel: +805 468 2061 |
Fax: +805 439 1073 |
Email: jcannell@ash.dmh.ca.gov;
jjcannell@vitamindcouncil.org
Received
26 March 2010; accepted 10 May 2010.
DOI:10.1111/j.1651-2227.2010.01883.x
Re-use of this article is permitted in accordance with
the Terms and Conditions set out at http://www3.
interscience.wiley.com/authorresources/
onlineopen.html.
I have suggested that the primary environmental trigger for
autism is not vaccinations, toxins or infections, but
gestational and early childhood vitamin D deficiency (1,2).
Subsequently, the title of an article in Scientific American
recently asked, ‘What if vitamin D deficiency is a cause of
autism?’ (3) Since then, an article on vitamin D and autism
in Acta Paediatrica (4) and the accompanying commentary
(5) have added to the accelerating suspicion that vitamin D
deficiency – either during pregnancy or early childhood –
may be an environmental trigger for the genetic disease of
autism.
I will not repeat the evidence from my original 2007
paper and I am well aware that evidence consistent with a
theory is not proof of that theory. Instead, I concentrate on
papers either published since my paper, or on evidence I
overlooked when researching the original paper. Finally, I
explain my reasons why this theory deserves immediate
attempts to disprove it.
Simultaneous with the above two Acta Paediatrica publi-
cations, a paper elsewhere reported that among 117 adult
psychiatric outpatients is Sweden with various diagnoses,
the 10 patients with autism had the lowest vitamin D levels
of any of the groups studied, a mean of 12 ng ⁄mL (31 nM),
approaching the osteomalacic range for adults and the
rachitic range for children (6). Even more interesting, some
of the patients seemed to improve when treated with an
average dose of about 4000 IU of vitamin D ⁄day. The
authors did not say if the improvement occurred in the aut-
ism group.
A 2008 review detailed the devastating effect gestational
vitamin D deficiency has on developing mammalian brains
(7). Unfortunately, the tiny 10 lg (400 IU) dose in prenatal
vitamins is virtually irrelevant in preventing the current epi-
demic of gestational vitamin D deficiency (8). For this rea-
son, in 2007, the Canadian Paediatric Society cautioned
pregnant women they may require not 400 IU ⁄day but
2000 IU ⁄day, or more, to prevent gestational vitamin D
deficiency (9).
If adequate amounts of vitamin D prevent autism, one
would expect children with rickets to have an increased risk
of autism. To my knowledge, the neuropsychiatric symp-
toms of rickets have not been studied in the modern era.
However, at least two old papers have addressed it (10,11),
both published before Kanner described autism in 1943.
Both papers describe ‘weak mindedness,’ ‘feeble minds,’
‘mental dullness,’ unresponsiveness and developmental
delays. Even more intriguing, both papers report that the
mental condition in rickets improved with vitamin D.
Another of the mysteries of autism is the apparent
increased incidence of autism in the children of richer col-
lege-educated parents, especially women, a finding
announced a few months ago (12). Actually, this is not a
new finding. As I discussed in my original paper, this has
been known since the early 1980s but was dismissed as
being because of ascertainment bias. This very recent report
correlates well with a 2007 CDC report (13), which found a
similar increased risk for the wealthy and well-educated,
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findings the authors tried but could not dismiss as being
because of ascertainment bias. If the vitamin D theory is
true, autism should be more common in richer well-edu-
cated mothers, who are more likely than other mothers to
practice sun avoidance and use sunblock (1,2).
In his invited commentary, Dr. Eyles asked, ‘Does skin
colour modify the risk’ of autism, noting melanin in the skin
is an effective sunblock. Such studies are difficult as they
raise sensitive social issues. Nevertheless, three of four
recent U.S. studies found a higher incidence of autism in
black children, sometimes appreciably higher (1,2). As
Fernell et al. report, the Somali immigrants in Sweden call
autism the ‘Swedish disease’ and Somali immigrants in Min-
nesota call it the ‘American disease,’ but in equatorial
Somalia, autism has no name.
Toxins delivered by water or air pollution appear to dam-
age the genome of the vitamin D deficient (14). If exposure
to such toxins were the main contributors to autism inci-
dence, then we should have seen an autism incidence pat-
tern in the US that mirrored air and water pollution with a
dramatic increase in the 1950s, a peak in the 1960s and then
a progressive decline by the early 1980s, coincident with
enactment and enforcement of the US clean air and clean
water acts of the 1960s.
Another possibility is that air pollution from Eastern Eur-
ope, India and China, which has been increasing in the last
20 years, has engendered the current crop of autism. How-
ever, why would foreign air pollution of today do what
American air pollution of the 1950s and 60s could not?
Another paper published after my original paper found
that autistic boys have unexplained reductions in metacar-
pal bone thickness (15). At some time in their life, these
children laid down less cortical bone than normal children,
a finding consistent with undetected and untreated child-
hood or even intrauterine vitamin D deficiency.
Yet another recent paper reported that the prevalence of
autism in three U.S. states was higher in areas of higher
precipitation and clouds (16). The 2005 autism prevalence
rate among school-aged children, after controlling for dif-
ferences in population size, demographic characteristics,
per capita income and state, was higher in cloudy areas.
The association of autism prevalence and the mean annual
precipitation received by a county between 1987 and 2001
was positive and significant (p = 0.0034; 95% confidence
interval, 0.0018–0.0050). Clouds and rain retard vitamin
D-producing ultraviolet B light from penetrating the atmo-
sphere.
Surprisingly, high maternal seafood consumption, of the
type known to be contaminated with mercury, has been
associated with fewer – not more – autistic markers in the
offspring (17). Lower maternal seafood intake during preg-
nancy was associated with low verbal intelligence quotient,
suboptimum outcomes for prosocial behaviour, fine motor,
communication and social development scores. While the
omega-3 and mercury content of fish is well known, less
well known is the fact that fish is one of the few foods with
significant amounts of vitamin D, which, as referenced
earlier, protects the genome from damage by toxins.
While the urban ⁄rural gradient in rickets is well known
and was one of the keys to discovering that sunlight pre-
vented rickets, less well known is a meta-analysis showing a
twofold urban ⁄rural gradient for autism (18). Similar to
rickets, city life affords less vitamin D, because of tall build-
ings, indoor occupations and increased urban air pollution,
all of which block ultraviolet B light from penetrating the
atmosphere.
Finally, a 2008 paper reported that autism was more com-
mon among mothers who took antiepileptic drugs (19). A
comment to the authors (20) detailed the evidence that an-
tiepileptic drugs are one of the few classes of drugs that con-
sistently and significantly interfere with vitamin D
metabolism, lowering 25(OH)D levels.
I agree with Dr Eyles’ comment that the vitamin D the-
ory is ‘highly parsimonious.’ Indeed, it was love of
parsimony that led me to first hypothesize that vitamin D is
intimately involved in the pathology and epidemiology of
both autism and influenza (21). Some have speculated that
the excess of winter births in autism is explained by
wintertime maternal viral infections. Obviously, another,
and more parsimonious explanation, is that vitamin D is
involved in all three.
The vitamin D theory of autism does not diminish genetic
contributions to autism occurrence. Indeed, without the
genetic tendency for autism, I suspect that severe maternal
or early childhood vitamin D deficiency may cause bone
abnormalities, as referenced above, with no evidence aut-
ism. All that the current epidemic of maternal and early
childhood vitamin D deficiency does, with its resultant neu-
ral deficiency in the pluripotent neurosteroid calcitriol, is to
allow the genetic tendency for autism to express itself.
If this theory is true, the path towards effective preven-
tion – and perhaps a treatment effect if adequate physio-
logical doses of vitamin D are given – is so simple, so safe,
so inexpensive, so readily available and so easy, that it
defies imagination. Seventeen vitamin D experts recently
stated, ‘In our opinion, children with chronic illnesses such
as autism, diabetes and ⁄or frequent infections should be
supplemented with higher doses of sunshine or vitamin
D3, doses adequate to maintain their 25(OH)D levels in
the mid-normal of the reference range [65 ng ⁄mL
(162 nmol ⁄L)] – and should be so supplemented year
round.’ (22)
Finally, if true, a darker side of the theory emerges. To
some real but unknown extent, autism is an iatrogenic dis-
ease, caused by governments, organizations, committees,
newspapers and physicians who promulgated the current
warnings about sun-exposure for pregnant women and
young children without any understanding of the tragedy
they engendered.
DISCLAIMER
Dr Cannell is founder and executive director of the non-
profit educational organization, the Vitamin D Council. He
also receives remuneration from Purity Products, a supple-
ment manufacturer.
Aetiology of autism Cannell
2ª2010 The Author/Journal Compilation ª2010 Foundation Acta Pædiatrica/Acta Pædiatrica

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Cannell Aetiology of autism
ª2010 The Author/Journal Compilation ª2010 Foundation Acta Pædiatrica/Acta Pædiatrica 3