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.
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