THE FAUCI FILES: Fauci's Gulf-War Syndrome

[fred]

THE FAUCI FILES: Fauci's Gulf-War Syndrome 
October 19, 1999

As Director of the NIH institute NIAID, Director Anthony Fauci was
at the top "of the loop" for NIH vaccine approvals involving the
military. 

The Rand Corporation revealed in today's New York Times (page one) that 
pyridostigmine bromide -- given to military personnel during the Gulf 
War -- was the probable CAUSE OF GULF WAR SYNDROME.

First, the very existence of the disease was covered up. Then 
they LIED as they proceeded to distort the statistical 
data to obscure the extent of the symptomatic presentation.
Many of those who suffered were told this disease was "psychological".
They were DELIBERATELY LIED TO!

As with the AZT, IL-2 and Cocktail Treatment Hoaxes that CONTINUE TO
MURDER TENS OF THOUSANDS OF HEALTHY PEOPLE WHO WERE HIV-POSITIVE
AND WITHOUT SYMPTOMS, the Gulf-War Syndrome cover-up has Fauci's 
corrupt fingerprints ALL OVER IT!

Fauci's IL-2 patent is owned by the U.S. government but the
manufacturing license was granted to the Chiron Corporation.
It is estimated that Fauci has received up to $1 million in royalties
so far (Fauci claims to donate this money to "charity" but
refuses to identify the charity). Fauci's NIAID/NIH refuses 
to disclose NIAID Director's Fauci's deals with Chiron Corporation 
(Freedom of Information requests for financial data are 
summarily denied by NIH attorneys). NIH Attorney Robert Lanman
has LIED about the transfer of IL-2 research from Fauci's NIAID
to the National Cancer Institute -- this has NOT happened.

What was Chiron's FINANCIAL dealings with Fauci at the time of the 
approval of pyridostigmine bromide AND Chiron's squalene for use in the
pills used by Gulf-War military personnel for protection against
nerve gas agents?

By the way, with NIH Director Varmus leaving, Fauci's name was one of 
two names publicly mentioned last week as candidates to replace Varmus. 
(See the July 30, 1999 Elton John Edition of THE FAUCI FILES for the
prediction of Varmus' involuntary removal from the NIH).

fred


The following was offered by Billi Goldberg, who posted her findings 
of pyridostigmine bromide's causative role in Gulf-War Syndrome OVER
TWO YEARS AGO:

-----------
According to Myers in the 10/19/99 New York Times, in a Rand Corporation

study financed by the Defense Department, pyridostigmine bromide is 
implicated in Gulf War Syndrome: "The drug, pyridostigmine bromide, or 
P.B., was distributed to 250,000 to 300,000 of the nearly 700,000 
American troops sent to the Persian Gulf in 1990 and 1991 as a 
"pretreatment" for potential Iraqi attacks with the nerve agent soman. 
While the drug has been used since 1955 to treat a rare neurological 
disorder, its use as an antidote to soman is still regarded as 
experimental."

Following the New York Times article, is my Gulf War Hypothesis 
including scientific references (first posted 8/17/97 and updated 4/99) 
concerning possible involvement of pyridostigmine bromide (along with 
the vaccine adjuvant squalene) as a causative factor of GWS.

=================================

New York Times, Tuesday, October 19, 1999

Survey Links Gulf War Syndrome to Nerve-Gas Antidote

By STEVEN LEE MYERS

WASHINGTON -- A scientific survey underwritten by the Pentagon has 
concluded that an experimental drug given to American troops during the 
Persian Gulf war to protect against a nerve gas may be responsible for 
the chronic illnesses afflicting tens of thousands of veterans. 
 
The report, to be released at a news conference on Tuesday, is the first

commissioned by the Pentagon to identify a possible cause for the 
illnesses, which have collectively come to be known as gulf war 
syndrome. It sharply contradicts two earlier Government studies -- by a 
Presidential commission and by the Institute of Medicine -- that ruled 
out the drug as a cause. 
 
The drug, pyridostigmine bromide, or P.B., was distributed to 250,000 to

300,000 of the nearly 700,000 American troops sent to the Persian Gulf 
in 1990 and 1991 as a "pretreatment" for potential Iraqi attacks with 
the nerve agent soman. While the drug has been used since 1955 to treat 
a rare neurological disorder, its use as an antidote to soman is still 
regarded as experimental. 
 
More than 100,000 veterans have reported experiencing symptoms 
associated with gulf war syndrome, including chronic fatigue, muscle 
pain, memory loss and sleep disorders. But because of the Pentagon's 
acknowledged shoddy record keeping in the war, it may be impossible to 
know how many of those took the drug and in what quantities. 
 
After years in which the Pentagon has systematically discounted possible

explanations for the ailments, including stress, exposure to oil-well 
fires and depleted uranium used in American bombs, the report is 
something of a breakthrough. 
 
Wary of the reaction of veterans' groups and their supporters in 
Congress, Pentagon officials Monday played down the findings of the 
survey, which was conducted over two years by the Rand Corporation, a 
nonprofit research organization financed by the Defense Department. 
 
"This is not a Eureka," said Dr. Sue Bailey, a physician who is the 
Assistant Secretary of Defense for Health Affairs. Dr. Bailey and other 
officials said they accepted the report's findings but added that more 
studies were needed before a direct scientific link could be 
established. They also said the Pentagon would continue to keep the drug

in its arsenal of vaccinations and antidotes for troops who might face 
attacks with chemical and biological weapons, even though the survey's 
conclusions also raise questions about its effectiveness against soman. 
 
The report, which runs 385 pages and was written by Dr. Beatrice 
Alexandra Golomb, is based on the findings of scores of medical studies 
on pyridostigmine bromide. Dr. Golomb is a professor at the University 
of California at San Diego and a physician at the Veterans Affairs 
medical center in San Diego. 
 
Her report cites studies that have linked the drug to side effects 
similar to those experienced by some veterans. One study, by Hebrew 
University in Israel, linked the drug to neurological disorders in mice.

Another, by the University of Texas and Duke University, concluded that 
when mixed with other chemicals it could cause nerve damage. 
 
Dr. Golomb's report goes on to suggest that the drug's short-term 
effects can become chronic because it causes abnormal levels of the 
nerve-signaling chemical acetylcholine. The chemical is involved in many

important functions, including sleep, muscular activity, memory and 
pain, which have all been cited as problems for ill veterans. 
 
The report said research showed that individual reaction to the drug 
depended on different factors, including stress, physiology and exposure

to other agents, including pesticides and even nicotine and caffeine. 
That would explain why only some veterans have reported illnesses. 
 
"One cannot rule out the possibility that long-term effects of P.B. 
might occur and might participate in the production of 
neuropsychological and other deficits reported by some" veterans, Dr. 
Golomb concludes. 
 
Scientists and veterans' advocates have long pointed to pyridostigmine 
bromide, as well as other experimental drugs given to troops in the 
gulf, as one of the possible culprits in the still unexplained illnesses

attributed to gulf war syndrome. Separate reports by the House and 
Senate identified it as such and called for further research into the 
drug's effects. 
 
Dr. Bernard D. Rostker, the Under Secretary of the Army who is the 
Pentagon's senior official overseeing gulf war illnesses, said the 
Pentagon had strongly supported several studies on pyridostigmine 
bromide, including Rand's, because of those concerns. He said the 
Pentagon was already spending $20 million on additional research into 
the possible links considered in Rand's report. 
 
"That does not mean we have made a direct relationship between the two,"

he said, referring to the drug and the syndrome. "It means we don't have

enough information." 
 
The initial reaction on Capitol Hill was harsh. Representative 
Christopher Shays, a Connecticut Republican who is one of the most 
outspoken critics of the Pentagon's handling of the issue, accused the 
Pentagon of moving slowly to study the drug and of "restating the 
obvious need for aggressive research." 
 
"The sad news is how little has been learned in eight years about 
organophosphate poisoning and the delayed neuropathies that appear to 
play a role in the illnesses suffered by gulf war veterans," Shays said.

 
Under a special waiver from the Food and Drug Administration, the 
Pentagon distributed thousands of packets of pyridostigmine bromide to 
the troops as they deployed to Saudi Arabia in 1990 following Iraq's 
invasion of Kuwait. Troops were ordered to take three flat white tablets

each day as long as they were in the region, although it appears they 
did so erratically. 
 
Pyridostigmine bromide is the only known treatment for soman, a deadly 
gas developed by the Soviet Union. Although Iraq is known to have made 
weapons with other nerve agents, including sarin, no evidence has 
surfaced to suggest Iraq ever made weapons with soman. 
 
Dr. Golomb also reported that some studies on animals suggested that the

drug might not be very effective against soman at the doses given and 
may in fact increase susceptibility to other chemical weapons. 
 
The drug has not been given to troops since the gulf war, but Dr. 
Rostker said the findings would not change the Pentagon's policy to use 
it whenever commanders determine that an enemy might have soman. 
 
"Its continued use is warranted given the fact that an exposure to soman

would result in almost immediate death," Dr. Rostker said. 
 
------------------------------------------------------------------------
------------------------------------------------------------------------

GULF WAR SYNDROME HYPOTHESIS (org. 8/17/97; upd. 4/22/99)

by Billi Goldberg


Is there the possibility that Gulf War Syndrome (GWS) is very real and 
caused by different initiating and contributing factors?

For example (1) actual exposure to nerve gas causing all sorts of 
problems especially CNS, (2) pyridostigmine crossing the blood-brain 
barrier under stressful conditions causing CNS problems, and (3) strong 
Th2/antibody response caused by vaccines with squalene-containing 
adjuvants causing immune system dysfunction by suppressing Th1/cellular 
immunity.

And, of course, there probably were other conditions particular to the 
Gulf War that would result in health problems.

As concerns the following, Berezuk stated in a 1992 article that 
"Determinations were made that informed consent was not feasible for two

products: pyridostigmine bromide 30 mg tablets and botulinum toxoid 
vaccine. Pyridostigmine bromide (Mestinon) was a well-known medication 
used to treat the symptoms of myasthenia gravis. Botulinum toxoid 
vaccine has been used to immunize at-risk laboratory personnel for many 
years. These were not the only investigational products fielded in 
support of Operation Desert Storm. The other products were to be used 
only with informed consent."

I. PYRIDOSTIGMINE BROMIDE (PSB)

In the Gulf War, an carbamate acetylcholinesterase (AChE) inhibitor 
(AChEI), "Pyridostigmine bromide, 30 mg orally, was self-administered 
every 8 hours while under the threat of nerve agent attack (for 1 to 7 
days)" (Keeler et al., 1991). Organophosphates, which include nerve 
gases, are also AChEIs, and the anticholinergic agent atropine sulfate 
is the treatment for exposure/overdose of nerve gas and AChEIs (Bohm et 
al., 1997). 

In a 1991 Israel study, Sharabi et al. stated "In a series of animal 
studies it was found that pre-treatment with PSB prior to 
organophosphate (OP) intoxication improves the post-exposure survival 
achieved by the antidotal treatment. The proposed mechanism of the 
protective effect of PSB is by shielding AChE from the OP molecule, thus

restoring the enzyme activity following spontaneous decarbamylation. The

desired level of AChE inhibition is 20-40%, produced by oral 
administration of 30 mg PSB every 8 h. The elimination half-life of PSB 
is 100 min. Inhibition of AChE is expected to result in cholinergic and 
parasympathetic effects." 

They concluded that "No correlation was found between levels of 
cholinesterase and type of severity of complaints. Anxiety, which 
accompanies wartime, may have contributed to the appearance of 
significant symptoms" (Sharabi et al., 1991). 

In a 1996 Israel study, Friedman et al. determined that PSB could cross 
the blood-brain barrier (BBB) in mice under stressful conditions. They 
concluded with "These findings suggest that peripherally acting drugs 
administered under stress may reach the brain and affect centrally 
controlled functions." 

These findings concerning pyridostigmine bromide were further supported 
in a 5/28/98 Nature study by Kaufer et al. that found: "Acute traumatic 
stress may lead to post-traumatic stress disorder (PTSD), which is 
characterized by delayed neuropsychiatric symptoms including depression,

irritability, and impaired cognitive performance. Curiously, inhibitors 
of the acetylcholine-hydrolysing enzyme acetylcholinesterase may induce 
psychopathologies that are reminiscent of PTSD." As concerns the 
connection between PSB and GWS, Shen has strongly suggested that a more 
serious investigation be undertaken (Shen, 1998).

Keeler et al. concluded their report on PSB use under threat of nerve 
agent attack by stating "The pyridostigmine regimen followed by soldiers

under wartime conditions caused a higher incidence of adverse 
physiologic events than had been reported in earlier peacetime 
evaluations. It seems possible that the combined stresses of anticipated

combat, sleep deprivation, and life in the field may well have affected 
or modified many of these responses. Based on our observations, we 
conclude that the pyridostigmine regimen can be administered to 
virtually all soldiers under wartime conditions without impairment of 
military performance."

As for a connection between ACh and immune responses, Fujino et al. 
determined that "In this study, we found that muscarinic ACh receptors 
[G protein-coupled receptors] exist in both CD4- and CD8-positive 
lymphocytes and that activation of the receptors enhances TCR/CD3 
complex-induced mRNA expression of IL-2 and IL-2 receptor subunits, 
production of IL-2, and cell proliferation." Therefore, interference 
with ACh signalling could result in immunosuppression.

II. SQUALENE (SQ)

In a piece of sensationalist journalism, Paul M. Rodriguez reported in 
the 8/11/97 "Washington Times" that "Antibodies for this synthetic 
squalene were discovered in laboratory tests on hundreds of blood 
samples taken from Gulf war soldiers, some who became sick after the 
conflict and others who have not." 

A review of the literature showed that an experimental Chiron 
Corporation vaccine adjuvant "MF59 consists of stable droplets (<250 nm)

of the metabolizable oil squalene and two surfactants, polyoxyethylene 
sorbitan monooleate and sorbitan trioleate, in an oil-in-water emulsion.

In humans, MF59 is well tolerated and enhances the immunogenicity of 
recombinant protein subunit or particle vaccines" (Granoff et al., 
1997). 

MF59 was recently used in an experimental HIV vaccine that was given to 
sero-negative individuals (Keefer et al., 1996). An investigational 
botulinum toxoid vaccine was given to service members involved in 
Operation Desert Shield/Storm (Berezuk, 1992). Some lots of this vaccine

could have contained the MF59 adjuvant.

Valensi et al. in a 1994 study determined that "In naive mice, the MF59 
adjuvants induced serum cytokine profiles that are consistent with a 
primarily Th2-type response, whereas the Quil A LTC induced cytokines 
associated with both Th1 and Th2 responses."

Rook & Zumia in a 1997 Lancet article determined that "A systemic shift 
in the Th1/Th2 balance towards Th2 will lead to an increase in: diseases

that are exacerbated by diminished Th1; diseases mediated by increased 
Th2; and mood disorders attributable to neuroendocrine changes. These 
effects can explain the diverse nature of Gulf War syndrome, because the

signs of the syndrome will vary between individuals and will also depend

on other genetic and environmental factors."

___________________________________________________________
___________________________________________________________

REFERENCES

Berezuk GP, McCarty GE. Investigational drugs and vaccines fielded in 
support of Operation Desert Storm. Mil Med 1992 Aug;157(8):404-406. 

Human Use Review and Regulatory Affairs Office, Fort Detrick, Frederick,

MD 21702. 
______________________

Bohm SK, Grady EF, Bunnett NW. Regulatory mechanisms that modulate 
signalling by G-protein-coupled receptors. Biochem J 322( Pt 1):1-18 
(Feb 1997). 

Page 3: As previously noted, inhibition of acetylcholinesterase has 
profound effects, emphasizing its importance in regulating cholinergic 
neurotransmission. Inhibition prolongs synaptic transmission, which 
ultimately desensitizes cholinergic receptors and results in paralysis 
and death due to respiratory failure. Indeed, nerve gases such as Sarin 
are acetylcholinesterase inhibitors. Acetylcholinesterase activity may 
also be affected in disease states. Myasthenia gravis (severe muscle 
weakness) is an autoimmune disorder that is caused by the production of 
antibodies to the nicotinic receptor. However, some forms of the disease

are associated with the absence of acetylcholinesterase from 
postsynaptic membranes.
______________________

Friedman A, Kaufer D, Shemer J, Hendler I, Soreq H, Tur-Kaspa I. 
Pyridostigmine brain penetration under stress enhances neuronal 
excitability and induces early immediate transcriptional response. Nat 
Med 1996 Dec;2(12):1382-1385 

Department of Biological Chemistry, Life Sciences Institute, Hebrew 
University, Jerusalem, Israel. 
______________________

Fujino H, Kitamura Y, Yada T, Uehara T, Nomura Y. Stimulatory roles of 
muscarinic acetylcholine receptors on T cell antigen receptor/CD3 
complex-mediated interleukin-2 production in human peripheral blood 
lymphocytes. Mol Pharmacol 1997 Jun;51(6):1007-1014. 

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido

University, Sapporo, Japan. 
______________________

Granoff DM, McHugh YE, Raff HV, Mokatrin AS, Van Nest GA. MF59 adjuvant 
enhances antibody responses of infant baboons immunized with Haemophilus

influenzae type b and Neisseria meningitidis group C oligosaccharide- 
CRM197 conjugate vaccine. Infect Immun 1997 May;65(5):1710-1715. 

Chiron Vaccines, Emeryville, California 94608, USA. 
______________________

Kaufer D, Friedman A, Seidmanm S, Soreq H. Acute stress facilitates 
long-lasting changes in cholinergic gene expression. Nature 1998 May 28;

393:373. 
______________________

Keeler JR, Hurst CG, Dunn MA. Pyridostigmine used as a nerve agent 
pretreatment under wartime conditions. JAMA 1991 Aug 7;266(5):693-695. 

US Army Medical Research Institute of Chemical Defense, Aberdeen Proving

Ground, Md. 21010-5425. 
______________________

Keefer MC, Graham BS, McElrath MJ, Matthews TJ, Stablein DM, Corey L, 
Wright PF, Lawrence D, Fast PE, Weinhold K, Hsieh RH, Chernoff D, Dekker

C, Dolin R. Safety and immunogenicity of Env 2-3, a human 
immunodeficiency virus type 1 candidate vaccine, in combination with a 
novel adjuvant, MTP-PE/MF59. NIAID AIDS Vaccine Evaluation Group. AIDS 
Res Hum Retroviruses 1996 May 20;12(8):683-693 

Department of Medicine, University of Rochester School of Medicine and 
Dentistry, New York 14642, USA. 
______________________

Rodriguez PM. Anti-HIV mix found in Gulf veterans. Washington Times (Aug

11 1997). 
______________________

Rook GAW, Zumia A. Gulf War syndrome: is it due to a systemic shift in 
cytokine balance towards a Th2 profile? Lancet 349:1831-1833 (Jun 21 
1997).

Department of Bacteriology (Prof G A W Rook MD), and Academic Infectious

Diseases Unit (A Zumia FRCP), Department of Medicine, University College

London Medical School, London W1P 6DB, UK
______________________

Sharabi Y, Danon YL, Berkenstadt H, Almog S, Mimouni-Bloch A, Zisman A, 
Dani S, Atsmon J. Survey of symptoms following intake of pyridostigmine 
during the Persian Gulf war. Isr J Med Sci 1991 Nov;27(11-12):656-658. 

Israel Defense Forces Medical Corps, Petah Tikva. 
______________________

Shen Z.-X. Pyridostigmine bromide and Gulf War syndrome. Medical 
Hypotheses 1998; 51:235-237. 
______________________

Valensi JP, Carlson JR, Van Nest GA. Systemic cytokine profiles in 
BALB/c mice immunized with trivalent influenza vaccine containing MF59 
oil emulsion and other advanced adjuvants. J Immunol 1994 Nov 
1;153(9):4029-4039. 

Chiron Corporation, Emeryville, CA 94608. 
______________________