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New Support for "A Hypothetical Explanation of Panic Disorder," German Journal of Psychiatry, 2001

Peter F. effective_spamblock at ozemail.com.au
Thu Dec 11 18:03:32 EST 2003


Yes, amongst else it *ought* to become much more commonly recognized that
psychological and somatic distress (distressors) has common chemical
"denominators" (consequences)!
P

"James Michael Howard" <jmhoward at arkansas.net> wrote in message
news:0eqhtv4vklbitqe8rvq3td39fk8ug3i29o at 4ax.com...
> Further Support of An Explanation of Panic Disorder:
>
> "A Hypothetical Explanation of Panic Disorder," German Journal of
Psychiatry
> 2001; 4: 40-42.
>
> Panic Disorder may result from reduced dehydroepiandrosterone (DHEA) and
is
> Analogous to Acquired Immune Deficiency Syndrome
>
> Copyright 2003, James Michael Howard, Fayetteville, Arkansas, U.S.A.
>
> Panic disorder is characterized by hyperprolactinemia and increased
cortisol
> among some other characteristics.  In my 2001, explanation of panic
disorder
> (PD) I used these characteristics to demonstrate that PD may result from
reduced
> DHEA.  I had also produced an explanation of acquired immune deficiency
syndrome
> (AIDS) also dependent upon pathogenesis resulting from low DHEA.  I did
not
> think to compare similarities in PD and AIDS at the time.  Because I have
> recently revisited my explanation of AIDS (2003), these similarities have
> attracted my attention.  These similarities support my explanation of
both.
> Here are how they supported my explanation of each other.
>
> It is my hypothesis from 1985 that vulnerability to the AIDS virus results
from
> low DHEA.  (The term "HIV" did not exist at that time.)  DHEA is, indeed,
very
> low in AIDS.  The first mention of low DHEA in AIDS appeared in 1989.
> Furthermore, I soon suggested that I think the symptoms of AIDS actually
result
> from loss of DHEA; I suggest "acquired immune deficiency syndrome" should
be
> "HIV-induced DHEA deficiency syndrome."  AIDS is characterized by low
numbers of
> CD4+ lymphocytes, hyperprolactinemia, and increased cortisol and so is
panic
> disorder.
>
> According to my explanation of panic disorder, hyperprolactinemia results
from
> lack of feedback of sufficient levels of DHEA to inhibit prolactin
production.
> Prolactin is known to stimulate DHEA, so it occurred to me that, perhaps,
DHEA
> inhibited prolactin when DHEA reached certain levels.  Now, the background
> source of DHEA, DHEA sulfate (DHEAS) is quite high in panic disorder.  So,
I
> made the hypothesis that DHEA is not being made from DHEAS so prolactin
remains
> high during panic attacks.
>
> DHEA and DHEAS reach very low levels in AIDS so feedback inhibition of
prolactin
> should also fail in AIDS.  Hyperprolactinemia is frequently reported in
AIDS and
> is sometimes connected with severity of AIDS.  I will not explain this in
detail
> here, but the ratio of cortisol to DHEA is very important.  (In 1985, I
> suggested that cortisol evolved to counteract the effects of DHEA.  I
think this
> ratio determines the "fight or flight" mechanism.)  Cortisol produces
negative
> effects, especially when prolonged and in excessive amounts.  Cortisol is
high
> in panic disorder and AIDS.  Fasting significantly increases DHEAS and
cortisol
> and reduces CD4 cells and "The percentage of CD4 cells was negatively
correlated
> with cortisol concentrations during fasting." (Am J Clin Nutr. 1997
> Jul;66(1):147-52).  Fasting should increase the probability of panic
disorder
> and this is the case.  Fasting increases cholecystokinin which is known to
> trigger panic disorders and increase cortisol.
>
> AIDS is characterized by low levels of CD4+ cells.  Panic attacks are also
> characterized with significantly lowered CD4+ cells compared to normals
> (Neuropsychobiology. 1992;26(1-2):23-6).  I suggest the similarity here is
> significant.  CD4+ cells are reduced in situations that reduce DHEA,
increase
> cortisol, and prolactin.  These pathologies, as well as fasting, produce
> similarities in response.  This response, if prolonged or profound, may be
the
> basis of significant morbidity and mortality.  I suggest these are all
> subordinate disturbances in dehydroepiandrosterone homeostasis.
>
> This is also available at www.anthropogeny.com/research.html





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