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."
