New Support of Schizophrenia Caused by Low Dehydroepiandrosterone (DHEA)

Caram starple at carmata.new
Thu Dec 18 23:01:17 EST 2003


James, your DHEA theories > http://www.anthropogeny.com < are
interesting and worthy of serious consideration. But what bothers me
is impression that you seem to think DHEA is THE ONE answer to too
many things. What I've come to appreciate over the years is how in
biology, and especially neurology, problems are rarely reducible to
one component. Neurological systems are highly integrated and thus low
DHEA levels may be correlated to a wide range of conditions but not
necessarily, and moreover not likely, the continuous causal mechanism
behind those conditions. 

To reason as you seem to that "DHEA levels are lower in condition X,
therefore low DHEA levels are the cause of X" strikes me as a gross
over simplification that tends to run roughshod over the extreme
interconnected complexities of neuro-biological systems. 

My two cents.


On Thu, 18 Dec 2003 17:07:31 -0600, James Michael Howard
<jmhoward at arkansas.net> wrote:

>
>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."




More information about the Neur-sci mailing list