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"Psychological Risk Factors [Shyness] for HIV Pathogenesis" A Result Caused by the Cortisol to DHEA Ratio?

James Michael Howard jmhoward at arkansas.net
Wed Dec 17 13:40:05 EST 2003


"Psychological Risk Factors [Shyness] for HIV Pathogenesis"  A Result Caused by
the Cortisol to DHEA Ratio?

Copyright 2003, James Michael Howard, Fayetteville Arkansas, U.S.A.

This is my explanation of the findings of Cole, et al., Biological Psychiatry.
2003 Dec 15; 54(12): 1444-56.  The abstract of which is found below.  In my
response, I mention another journal article, J Med Virol. 2004 Jan;72(1):174-9,
the abstract of which is also found below.  Here is my response which was sent
to Biological Psychiatry.

"In 1985, I first suggested low dehydroepiandrosterone (DHEA) causes
vulnerability to the AIDS virus.  (The term "HIV" did not exist at the time.)
Since 1985, I decided that low DHEA should result in vulnerability to all
infections.  The first report of low DHEA in AIDS appeared in 1989 and low DHEA
has been connected to low CD4+ lymphocytes.  It is my opinion that the symptoms
of AIDS actually represent pathology resulting from loss of DHEA.  Numerous
articles regarding protective effects of DHEA against numerous types of
infections appeared later as well as articles connecting low DHEA with HIV
symptomatology.
 
Also in 1985, I suggested cortisol evolved to antagonize the effects of DHEA.  I
think this is the basis of the "fight or flight" mechanism and is the basis for
basic personality traits.  That is, the ratio of cortisol, the stress hormone,
to DHEA is important to personality responses to stress and infections.
Therefore, increased stress should also increase infections.
 
I suggest this may be the basis of the findings of Cole, et al.  That is,
individuals who express a higher cortisol to DHEA ratio are more vulnerable to
the effects of the HIV.  

J Med Virol. 2004 Jan;72(1):174-9 reports essentially identical data.  That is,
varicella zoster virus was increased due to stress.  I suggest the same
mechanism, the ratio of cortisol to DHEA, is occurring in both studies."


Here are the two abstracts:

Biological Psychiatry. 2003 Dec 15; 54(12): 1444-56. 
	
Psychological risk factors for HIV pathogenesis: mediation by the autonomic
nervous system.

Cole SW, Kemeny ME, Fahey JL, Zack JA, Naliboff BD.

Department of Medicine, University of California, Los Angeles, (SWC, JAZ), Los
Angeles, California
Epidemiologic studies have identified psychological risk factors for specific
physical diseases, but the biological mechanisms mediating these relationships
remain poorly defined.Social inhibition and autonomic nervous system (ANS)
activity were assessed on multiple occasions in 54 gay men with asymptomatic
human immunodeficiency virus (HIV) infection. Following baseline ANS assessment,
plasma HIV-1 viral load and CD4+ T cell levels were monitored for 12-18 months
to assess relationships between ANS activity and HIV pathogenesis.We confirmed
the previously reported relationship between socially inhibited temperament and
vulnerability to viral pathology. Plasma viral load set-point was elevated
eight-fold in socially inhibited individuals, and these individuals showed
poorer virologic and immunologic response to initiation of highly active
antiretroviral therapy (HAART). Effects were independent of duration of
infection, HAART regimen, demographic characteristics, and health-relevant
behavior. Neurophysiologic assessments documented elevated ANS activity in
socially inhibited individuals, and mediational analyses showed that such
differences could account for 64%-92% of the covariance between social
inhibition and virologic parameters.These data provide the first clinical
evidence that differential neural activity mediates relationships between
psychological risk factors and infectious disease pathogenesis. Such findings
also suggest novel targets for adjunctive therapy in long-term control of HIV-1
disease.


J Med Virol. 2004 Jan;72(1):174-9. 	
Stress-induced subclinical reactivation of varicella zoster virus in astronauts.

Mehta SK, Cohrs RJ, Forghani B, Zerbe G, Gilden DH, Pierson DL.

Enterprise Advisory Services Inc., Lyndon B. Johnson Space Center, Houston,
Texas.

Varicella zoster virus (VZV) becomes latent in human ganglia after primary
infection. VZV reactivation occurs primarily in elderly individuals, organ
transplant recipients, and patients with cancer and AIDS, correlating with a
specific decline in cell-mediated immunity to the virus. VZV can also reactivate
after surgical stress. The unexpected occurrence of thoracic zoster 2 days
before space flight in a 47-year-old healthy astronaut from a pool of 81
physically fit astronauts prompted our search for VZV reactivation during times
of stress to determine whether VZV can also reactivate after non-surgical
stress. We examined total DNA extracted from 312 saliva samples of eight
astronauts before, during, and after space flight for VZV DNA by polymerase
chain reaction: 112 samples were obtained 234-265 days before flight, 84 samples
on days 2 through 13 of space flight, and 116 samples on days 1 through 15 after
flight. Before space flight, only one of the 112 saliva samples from a single
astronaut was positive for VZV DNA. In contrast, during and after space flight,
61 of 200 (30%) saliva samples were positive in all eight astronauts. No VZV DNA
was detected in any of 88 saliva samples from 10 healthy control subjects. These
results indicate that VZV can reactivate subclinically in healthy individuals
after non-surgical stress. Copyright 2004 Wiley-Liss, Inc.

James Michael Howard
www.anthropogeny.com 



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