Schizophrenia and Increased Schizophrenia in Males in Winter 
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 Schizophrenia and Increased Schizophrenia in Males in Winter

Schizophrenia and Increased Schizophrenia in Males in Winter

Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that schizophrenia results from low dehydroepiandrosterone
(DHEA) in utero and/or early infancy.  I suggest low DHEA results in reduced
growth and development of affected structures which are vulnerable later in life
to events which reduce DHEA availability.  Cortisol and testosterone should
adversely affect DHEA.  This combination of an associated stressful event
(cortisol) and puberty (testosterone) around the time of the beginning of the
natural decline of DHEA, around age twenty, may explain a preponderance of onset
of schizophrenia in the late {*filter*}s and early twenties.  (DHEA is low in
schizophrenia.  DHEA is known to positively affect growth of neuronal
structures.)

My principal hypothesis is that DHEA was selected by evolution because DHEA
optimizes replication and transcription of DNA.  Therefore, all tissues,
especially the brain, are affected by levels of DHEA.  Subordinately, the other
major, adrenal steroid hormone, cortisol, evolved to counteract the effects of
DHEA and produces the "fight or flight" mechanism.  Too much cortisol will
adversely affect neural structures poorly developed by low DHEA.  (It is known
that excessive cortisol over prolonged periods damages neural structures.)
Testosterone interferes with availability of DHEA and this adversely affects
neural structures which have developed poorly because of low DHEA.

I recently had the necessity to explain seasonal affective disorder (SAD)
(depression) of winter.  In so doing, I found that testosterone interferes with
the conversion of DHEAS (sulfate), the reserve form of DHEA, to DHEA, the active
form.  It is also my hypothesis (1985) that depression may result from low DHEA
in vulnerable individuals.  (It has since been determined that DHEA is low in
depression and that the ratio of cortisol to DHEA is involved.)  Testosterone
increases in fall and winter, therefore, the conversion of DHEAS to DHEA is
reduced by testosterone during these seasons.  This may explain SAD.

A study in 2003 reported that "Only male cases of schizophrenia and
schizophreniform disorder showed a significant seasonal distribution to dates of
onset of symptoms, with a peak in August (winter)." (Psychol Med. 2003
Jan;33(1):163-7).  I suggest the same mechanism is occurring in this study as in
SAD but is affecting different liabilities produced during growth and
development of the brain.  That is, it is testosterone, the increase in
testosterone in winter, and the effects of testosterone on the conversion of
DHEAS to DHEA that are causing the "significant seasonal" peak of schizophrenia
in the winter.



Mon, 16 Oct 2006 01:14:46 GMT
 
 [ 1 post ] 

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