Peter, thank you for your correct insight.
JMH
On Fri, 12 Dec 2003 10:03:32 +1100, "Peter F."
<effective_spamblock at ozemail.com.au> wrote:
>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
>