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New Support of Schizophrenia Caused by Low Dehydroepiandrosterone (DHEA)

Psi-Clone nospam at nospam.net
Mon Jan 5 02:26:30 EST 2004


do you understand multi-perz and schizo... o what a tangled web we weave
just dont forget who *u* r. u speak differently to your grandparents than to
your parents then to your kidZ. you have to have a lot of balls to not be
multi-personality. they'll kill you. i saw some info on dhea... i say leave
the endocrine sys to vishnu[allagory] if i get a response i will
elaborate.... tired,,, ZZZzzzz

Psi-Clone


"James Michael Howard" <jmhoward at arkansas.net> wrote in message
news:iec4uvs40k4rbvii4k54grsl3e6vt4cjac at 4ax.com...
>
> New Support of Schizophrenia Caused by Low Dehydroepiandrosterone
>
> Copyright 2003, James Michael Howard, Fayetteville, Arkansas, U.S.A.
>
> The following was written in response to Psychiatry Research 2003; 120:
211-218
> "Increased levels of serum basic fibroblast growth factor in
schizophrenia"
> (abstract at end of this treatise)
>
> 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; this is the "early
> neurodevelopmental insult" of schizophrenia.
>
> Furthermore, it follows from my hypothesis that DHEA acts to maintain and
> activate the brain, following growth and development.  It is known 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.  Therefore, a precipitating, stressful events near puberty 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 in
> schizophrenia.
>
> Hashimoto, et al., report "elevated bFGF levels in the serum of patients
with
> schizophrenia, especially in earlier age-of-onset cases considered to have
more
> neurodevelopmental insults."  Hasdai, et al., found that "serum levels of
bFGF
> are elevated in patients with ischemic heart disease." (Int J Cardiol.
1997; 59:
> 133-8).  While Osorio, et al., disagree as to cause, they found
significant
> reductions in DHEA-S in ischemic heart disease (Horm Res.
2002;57(5-6):165-9).
> DHEA is known to be low in schizophrenia (Biol Psychiatry 1973; 6: 23)
>
> I suggest the findings of Hashimoto, et al., may be interpreted to support
my
> hypothesis that low DHEA is involved the etiology of schizophrenia.
>
> James Michael Howard
> www.anthropogeny.com
>
>
>
> Here is the abstract of Psychiatry Research 2003; 120: 211-218:
>
> "Basic fibroblast growth factor (bFGF) is a multifunctional growth factor
that
> has been implicated in a variety of neurodevelopmental processes. The aim
of the
> present study was to examine whether bFGF contributes to the
pathophysiology of
> schizophrenia. Serum bFGF levels in 40 patients with schizophrenia (15
> drug-naive and 25 medicated patients) and in 40 age- and sex-matched
healthy
> normal controls were measured. Serum bFGF levels were significantly higher
in
> the medicated patients than in the normal controls. Analysis of partial
> correlation coefficients showed that the increased bFGF levels might not
be
> attributable to antipsychotic medication. Although there was no
significant
> overall difference in bFGF levels between drug-naive patients and normal
> controls, the bFGF levels in these patients significantly correlated with
the
> severity of negative symptoms. Furthermore, we found a significant
negative
> correlation between serum bFGF levels and the age of onset in the entire
patient
> group. Our finding of elevated bFGF levels in the serum of patients with
> schizophrenia, especially in earlier age-of-onset cases considered to have
more
> neurodevelopmental insults, suggests that bFGF abnormalities may be
involved in
> the pathophysiology of schizophrenia."





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