Vitamin D during first year reduces schizophrenia for males; possible explanation

kpaulc kpaulc at earthlink.net
Thu Mar 4 20:50:08 EST 2004


[There is no need for a response, but
feel free to do so if you wish.]

An Opposed position:

My comments are only superficially 'in-
reply' to James' post. They are actually
addressed to =ALL=.

It strikes me that you're artificially cross-
correlating the well-known phenomenon
in which onset of 'schizophrenai' often
occurs during Adolesence with the fact
that Pubesence also occurs during Adol-
esence - creating an illusory 'link' between
sex hormones and 'schizophrenia'.

If it were as you say, there'd be a skewing
of occurrence of 'schizophrenia' by deprived
experiential conditions [because their diets
would be relatively-deficient in stereotypical
ways - kind of like the correlation between
dietary routines on Guam and ALS], but it's
well-known that a Child's interaction with a
single robustly-caring Adult virtually 'innoc-
ulates' the Child against the onslaught of ex-
periential newness that occurs during Adol-
escence.

Such Caring experience does, of course,
act upon neural dynamics, right down to
the molecular 'level', but all of that is 'normal',
and noting molecular-'level' dynamics that
result from one experiential circumstance,
or the other, in no way implicates the molec-
ular dynamics as being 'causitive'.

With respect to the vitamin-D consideration,
it could be that all that is is an indicator that
there's a Caring Adult in-the-mix, with the
vitamin-D deficit indicating the absence of
a Caring Adult [the Child exists in an envir-
onment in which Caring does not exist].

The fact is that, absent the experiential
'anchor' provided by at least one robustly-
caring Adult, the experiential newness that's
routinely encountered during Adolescence
occurs in a way that imposes disorder [TD
E/I(up)] within neural dynamics, and, if that
disorder is not somehow, otherwise, eliminated,
the result is, matter-of-factly, 'schizophrenia'.

Forgive me, Please, but the absence-of-
understanding with respect to the =FACT=
that experientially-determined neural activation
tunes neural dynamics right down to the mol-
ecular 'level' is another thing that has to be
eliminated.

Studies that do not cross-correlate to ex-
perience cannot possibly disclose anything
with respect to neural functioning.

Yes, there are Genetically-Determined deficits,
but these are all stereotypically self-disclosing.

When such stereotypy is not observable, ex-
perience =must= be cross-correlated.

Absent such experiential cross-correlation,
anything can be attributed to any observable
experientially-driven 'adjustment' within the
neuropharmacology - but the 'adjustment'
is =just= what nervous systems do to seek
'homeostasis' with respect to the environ-
mental conditions with which it has had to
cope.

It doesn't do to ignore the facts of a Child's
experience, and, then, long after the fact of
of the Child's nervous system's descent into
disorder, say that this or that correlate of the
Child's nervous system's struggle to achieve
TD E/I-minimization 'means' anything that
does not derive in the Child's Ravaging
experience.

Get it?

If you do, then, detune the position I've dis-
cussed, here, because I've deliberately stat-
ed it in-extremum - because saying it less
'forcefully' has not seemed to get-through
to folks.

Experience =matters=.

I'm =Sorry= for having to do this in reply
to your post. But it just Needs to be done.

Folks treat Children like 'inanimate objects',
and 'think' they're actually doing stuff that
can make a difference, when it cannot, un-
less experience is cross-correlated.

Cheers, James, ken [K. P. Collins

"James Michael Howard" <jmhoward at arkansas.net> wrote in message
news:dpcf409ok982lh079aser971qi2f8t54hc at 4ax.com...
> A Possible Explanation for: "Vitamin D supplementation during the first
year of
> life and risk of schizophrenia: a Finnish birth cohort study,"
Schizophrenia
> Research 2004; 67: 237-245
>
> Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.
>
> I have developed an explanation of schizophrenia which may explain the
findings
> of McGrath, et al.  It is my hypothesis that low dehydroepiandrosterone
(DHEA)
> prenatally and/or postnatally reduces brain growth and development.  (My
> principal hypothesis is that DHEA evolved because DHEA optimizes
replication and
> transcription of DNA. Therefore, all tissues, especially neural tissues,
are
> affected by availability of DHEA.) Early lack of DHEA would produce brain
> structures of less robust growth which would be vulnerable to adverse
phenomena
> later in life; this is the "early neurodevelopmental insult." Following
growth
> and development, DHEA acts to maintain and activate the brain. It is known
that
> DHEA exerts very positive effects on neural structures.
>
> I also suggest the hormones cortisol and testosterone (in men and women)
> adversely affect availability of DHEA. These may combine to precipitate a
> "schizophrenia episode."  That is, a precipitating, stressful event
(cortisol)
> near/around puberty (testosterone) will combine to adversely affect the
> availability of DHEA and adversely affect brain function. (It is my
hypothesis
> that cortisol, in fact, evolved to counteract the effects of DHEA; this is
my
> explanation of the "fight or flight" response.) Since it is known that
cortisol
> is a neurotoxin, cortisol would adversely affect function and structure,
> especially in a person of low DHEA. The early lack of development due to
low
> DHEA would produce weak structures. Continued exposure to cortisol and
> testosterone would eventually cause degenerative changes in easily
affected
> structures, with more robustly built structures succumbing later.
(Therefore,
> symptoms would appear sequentially, the type dependent upon brain
development.
> So, the same mechanism could explain various kinds of differential
destruction
> of brain structures and the timing of such.)
>
> McGrath, et al., report that "Vitamin D supplementation during the first
year of
> life is associated with a reduced risk of schizophrenia in males."  In a
study
> of the vitamin D receptor (VDR), Zofka, et al., reported that "The study
shows
> that the VDR gene predicts synthesis and/or metabolism of sexual steroid
> precursor DHEA in parallel with bone mineral density (BMD). The results
indicate
> that DHEA production and bone mass share a common genetic control through
VDR."
> In this case the vitamin D receptor is directly involved in positive
effects of
> DHEA on bone.  I suggest the same mechanism may be involved in the
connection of
> supplemental vitamin D and protection from schizophrenia, reported by
McGrath,
> et al.  I have thought for some time that the extra steroid sulfatase
located on
> the extra X chromosome of women should increase the conversion of DHEA
sulfate,
> the large supply of DHEA in the blood, to DHEA.  Both steroid sulfatases
on the
> X chromosomes are active.  (In fact I suggest this difference may have
been the
> beginning of sexual differences evolving from the evolution of XX and XY
> differences.)  It has been reported that "The metabolic conversion of
DHEAS to
> DHEA was significantly greater in women than in men." (J Clin Endocrinol
Metab.
> 2000 Sep; 85(9): 3208-17).  Therefore, females produce more DHEA than
males and
> this slight difference may account for the lack of a positive effect of
vitamin
> D on female children.  That is, the increase in DHEA provided by
stimulation of
> the vitamin D receptor and its positive effect on DHEA production may
increase
> protection of males to that of the level of female children who naturally
> produce more DHEA.
>
> I suggest the findings of McGrath, et al., that vitamin D provides some
> protection from schizophrenia results from increases in availability of
DHEA.
>
> James Michael Howard
> www.anthropogeny.com
>





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