CHOMSKY Archives

The philosophy, work & influences of Noam Chomsky

CHOMSKY@LISTSERV.ICORS.ORG

Options: Use Forum View

Use Monospaced Font
Show Text Part by Default
Show All Mail Headers

Message: [<< First] [< Prev] [Next >] [Last >>]
Topic: [<< First] [< Prev] [Next >] [Last >>]
Author: [<< First] [< Prev] [Next >] [Last >>]

Print Reply
Subject:
From:
Robert Napier <[log in to unmask]>
Reply To:
The philosophy, work & influences of Noam Chomsky
Date:
Tue, 10 Sep 2002 21:24:47 -0000
Content-Type:
text/plain
Parts/Attachments:
text/plain (859 lines)
If you guys can cope with the occasional biblical reference and the detail, you will find this
to be a devastatingly accurate account of what will bring the US down if nothing else does.

Copyright 2001
Final Diagnosis: Environmental Toxic Pathway Analysis and Immune System Cytokine Modality
Provide Key Insight into Chronic Fatigue Syndrome Mechanism and Etiology of Varied Pathogen
Driven Illnesses.

By: J. E. Phelps
Abstract:


T he cytokine signature of chronic fatigue syndrome (CFS) is similar to that seen in chemical
injury, Gulf War Syndrome, and Human Immunodeficiency Virus. CFS is shown to have a Th2 cytokine
humoral modality from the shut down of the Th1 cellular defense. Th2 is an allergic antibody
biased mode that takes precedence as the Th1 cellular mode that regulates pathogen infection
internal to cells is exhausted. Illnesses for Department Of Energy gas diffusion plant workers
have this modality and many similarities to CFS due to similar toxic exposures. This report
investigates the stance that toxic materials drive disease and presents an underlying common
mechanism that has been overlooked and more recently suppressed. The report will show that there
are new highs in toxic induced immune damage that lead to a proliferation of unregulated
pathogens that further damage health. Analysis of the toxic pathways of nuclear industry toxic
metals point to cytokine signatures that offer key insight into progression of these cytokine
activations leading to long term CFS. Beryllium metal cytokine factors are presented as a model
for other toxic metals and chemicals that form insoluble products in the lymph nodes that lead
to long term cytokine triggering and shutting down the macrophage pathogen destruction function.
The beryllium model is then expanded into a general model for other toxic metals and fluorides
that share biological concentration of cytokine triggering toxic materials in the lymph nodes.
This effect leads to continual cytokine triggering and toxic damage to the macrophage cells that
perform pathogen destruction and antigen presentation function. The discussion also takes into
account the time line of scientific discoveries that have allowed these insights into CFS since
its recent popularized discovery in the mid 1980's. This report is a comprehensive and broad
based discussion illustrated with practical examples and referenced to peer reviewed scientific
journals used to show the key effect in CFS and human immune health.
______________________________________________

T he human immune system is a complex system of dynamic cells with many cytokine feedback
factors that have been explored in the last decade to reveal many of the mechanisms for illness.
The immune defense takes on two distinct modes as set up by the stimulation of T helper cells,
as triggered from the lymph nodes. The cellular Th1 immune system profile is one designed to
control pathogens internal to cells and the humoral Th2 system response controls external cell
pathogens. [1] Study of the cell factors and cytokine signaling yields an understanding of how
these factors lead to and control many illnesses, including chronic fatigue syndrome (CFS). This
report outlines a cellular mechanism and a toxic pathway for damage to the immune system by
analysis of the cellular cytokine response from toxic damage, which then leads to more
progressive disease factors from loss of pathogen regulation.

This discussion will time line the discovery of CFS, correlate toxic environmental factors with
CFS, and connect the cell mechanisms to the prime factors driving the CFS immune dysfunction
process. The nuclear weapon materials research offer key insight into the toxic pathways and
cellular responses that lead to these theories and conclusions. This report reflects my research
into viral and immune system effects since 1980, with direct experience from the Oak Ridge,
Tennessee nuclear site. I, as an ORNL Sr. Staff, was the first to propose that fluorides had an
insoluble precipitate effect in the lymph nodes due to calcium affinity, similar to what is
reported for metal oxides. This key effect has not been reported by ORNL and suppressed since
1986 due to Oak Ridge liabilities from toxic emissions. Presenting a key finding on fluoride
toxic effect and its cumulative mechanism in a public forum is the purpose of this report.

This report is principally concerned with the lymph system, its cytokine signaling, and how it
responds to toxic exposure. Cell and lymph system response is nothing new as even snake venom
toxin drives cytokine response and nitrogen oxide (NO) generation. [2] Snake bites require light
tourniquet pressure to prevent circulation of snake venoms in the lymph system and around the
body leading to death in some cases. Many biological toxins are handled well by the lymph
system, but many toxic materials enter the same pathways and cause serious problems due to
insolubility problems of mineralization or turning to stone in these critical zones.. Oddly
enough, it has been suggested that the symbolic imagery connected with the Virgin Mary icon
standing with foot placed on a snake emanating from the Earth and the snake biting the apple as
symbolism for contamination from the Earth's lower regions connected to disease and illness.
Religion symbolism from Noah is connected to the largest land mass volcano on the Earth and the
toxic emanations to health effect on man and animals. This report will take a multi-disciplined
investigation, using vulcanology, history, religion, nuclear plants, wars, and toxic research to
look more deeply into these health effects.

From the nuclear weapons production, Oak Ridge is one of the most chemically impacted industry
sites in the U.S. and many toxic linked illness patterns are evident. The toxic material
research studies from the nuclear industry and Oak Ridge health problems provide a clear and
unique view for some of the mechanisms for toxic driven immune activation in illnesses. These
studies, that are well known in the nuclear plants, will be used to illustrate and prove the
process of toxic induced immune illnesses. Toxic material pathways into the human body, how they
retain or concentrate with time, and vector to different organ systems play pivotal roles in
disease etiology. Some of these toxic material pathways directly affect the immune system
resistance and lead to viral disease etiology. Examining these patterns and how they overlap CFS
is the focus of this report.

The term CFS (CFIDS) made its national appearance in the mid 1980's with the investigations of
Dr. Paul Cheney concerning sick persons in the area of Lake Tahoe, on the California and Nevada
border. Most of these CFS persons were fine one day and came down with a mononucleosis like
illness the next, with flu like symptoms persisting. In 1999, Cheney described the illness as
one that depleted glutathione, used much ATP, and showed a very significant up regulation in an
enzymatic pathway known as the 2-5A RNase L.[3] Looking for toxic exposure factors, the waters
of Lake Tahoe are pristine, but the area has volcanic origin that contaminate some wells and
soils with volcanic materials. Well waters are often contaminated with higher levels of arsenic,
manganese, radium, radon, and fluoride than surface waters. South Lake Tahoe has public water
supplies from wells that have metal contamination, often associated with volcanic zones or
mining. South Lake Tahoe water reports have specific caution for immune compromised persons
because of these pollutants. [4]

Cheney's CFS Tahoe cluster diagnosis was made possible by detection of new chemical bio-markers,
but CFS is not new as it appears to be symptomatically reported in 1750 and in other terms in
earlier periods. [5] It is also speculated that the biblical story of Jesus healing the person
by the well is even earlier evidence of the illness. The Cheney / Tahoe mononucleosis like
illness is associated with swollen lymph node from activation of EBV, HHV-6, and other viral
pathogens that are associated with follow on disease factors, like MS. [6, 7] Glutathione (GSH)
depletion is associated with the cellular oxidant repair process and detoxification of tissues
and it is lowered by chemical and pathogen damage to mitochondria of cells that manufacture ATP.
[8, 9] Lowered GSH can hasten cell apoptosis and is an indicator in chronic disease, cancer,
arthritis, and rapid aging. [10 ,11, 12, 13, 14, 15] Glutathione is important in liver
detoxification and in maintaining the mucosa cells that line the intestine. [16, 17] Glutathion
depletion drives shifts in cytokine mode from Th1 to Th2. [18] The 2-5A RNase L enzyme is part
of the activation process for the Th1 interferon cytokine that inhibits viral replication in
cells.[19] 2-5A RNase L is also important in the control of HIV replication. [20] These
bio-markers point out that control of viral pathogens in the body have been compromised. The
mechanism from just these indicators is not well defined, but these are indicators of immune
cell toxic effects..

Cheney's patients were from an extinct volcanic zone with contaminates in well water. From the
study of vulcanology, we know volcanic zones have many of the toxic fluorides and metals
problems associated with mining and operation of Department Of Energy (DOE) plants that emit
metals and fluorides. [21, 22, 23] Volcanos have more explosive power than nuclear weapons and
produce toxic fallout and contamination problems with acids, toxic metals, and toxic halogen
compounds [i.e.: calcium fluoride, hydrogen fluoride, hydrogen chloride]. Meteor events also
present toxic emissions like those from volcanoes and these same factors play dominate roles in
species survival. The Earth, for many millennia, was bathed in distilled waters from the heat of
the sun that produced a thin layer of less toxic soils on the planets surface and clean surface
waters. Mining, industry, and well drilling often compromise this natural toxic isolation
process and lead to health problems in man.

Toxic emissions from volcanoes have been associated to bio-markers such as porphirine and
porphyrins, which are diagnostic indicators of toxic cell damage effects from metals and
chemicals. [24] Persistent toxic gas emissions of volcanos kill animals and cause long term
defoliation of downwind areas. Mining and smelting operations often cause similar problems with
acid run off contaminating soil and water with metals and fluoride. It should be noted that
centuries earlier volcanic zones were connected with rapid spread of disease. An example is the
Hawaiian islands and their native residents weakened immune resistance to measles, syphilis, and
other diseases, as Europeans traded and socialized with them. It is noted in history that in
this population disease spread incredibly fast and devastated the islands inhabitants, which
suggested their immune resistance was degraded by their volcanic environment. Volcanic eruptions
are even postulated to have caused the downfall of the Egyptian city of Memphis from massive
plagues. It was these early associations that connected toxic material to the weakening of the
immune protection system making persons vulnerable to opportunistic infection and endogenous
viruses in the body, as well as exogenous viral transmission. These early observations suggested
CFS had environmental and industrial linked toxic contamination origins.

In other centuries toxic metals such as arsenic, lead, and mercury were associated with health
effects. Lead was connected to the neurological hearing illnesses that Beethoven experienced and
even associated with the demise of the Roman empire due to the lead food storage methods.[25]
Lead promotes a Th1 type cytokine response and tumor necrosis factor alpha (TNFa) that will
activate the macrophage's and pull particulate into the lymph nodes. [26] The leading Th1
cytokine called TNFa promotes macrophage activation. Persistent triggering of Th1 inflammatory
cytokines by toxic materials is linked to CFS factors like headache, fever, myalgia, fatigue,
and are toxic in high doses. Here the pathway was via food supply with absorption via stomach
and gut and retention of metal oxides in the local lymph nodes. Toxic metal retention and damage
to the immune system is associated with cancer vulnerability.[27, 28, 29] The effects of arsenic
in well water are associated with the rising cancer rates in India. It was attempted to improve
the biologically polluted, surface public water supplies in India via drilling wells, but this
resulted in high arsenic public water. Arsenic is well connected to lung, bladder, and skin
cancer, but is a treatment for liver cancer that impairs the mitochondria of cancer cells. [30,
31] A similar attempt to avoid biologically contaminated surface water in Africa presented wells
with high fluoride content. How these toxic materials distribute in the body organs and inner
cell effect is important to immune resistance.

A metal oxide analogy from the mining industry is connected to the mechanism of a controversial
anti-cancer drug called laetrile. In special mining practices, cyanide chemicals are combined
with insoluble metal oxides in a process called in-situ mining to form extractable soluble metal
products. The cyanide radical makes metal oxides soluble via replacement of the oxygen radical.
The cyanide radical is unique in its ability to render metal oxides soluble and the effect is
used in mining for various metals and in the electroplating process. Some enzyme processes mimic
this effect in human chemistry. Cyanide radicals are also drawn into the lymph nodes, where the
increased probability to react with metal oxides may reduce their concentration. Lessening the
lymph node concentrations of insoluble metals then linked to the anti-cancer effect by restoring
lymph node cell function. It is suggested that the biblical symbolism of turning to stone is a
version of these metal oxide ore minerals forming stone and impairing the lymph system. The
function of the immune system is central to the control of cancer viruses, yet many studies are
done with only the cancer tumor cells in mind. The laetrile studies omit the immune system
effects and the metal loading effects in the lymph nodes. Many B vitamins are also cyanide
involved compounds that may play a role in the metal detoxification process. Vitamin B-17 and
laetrile share the cyanide radical. Many grains contain B-17 and over processing of foods tends
to denature these natural beneficial content. Food processing and cooking often deplete food of
vitamins and cyanide compounds. In the last 50 years, the industrial dominance of metals in
immune damage has been replaced by more dominate chemicals, such as fluorides. [32, 33] This
makes the effects of laetrile of lesser benefit in cancer treatment.

These simple observations began my thesis for the mechanism for disease from the impact of toxic
metals on cells in the early 1980's. These observations qualify that many toxic metals are
linked to disease, now it remains to determine what quantity and what processes are involved. It
was observed that many toxic heavy metals damage cells and activate immune system response. The
toxic cell damage triggers cytokine production and T-cells that kill the damaged cell with
hyper-oxygen products and trigger macrophage's, which clean up the material and process it with
hyper-oxygen reduction chemistry. [34] The process results in the accumulation of insoluble
metal oxides in the macrophage region of lymph nodes and can be seen in data from many toxic
metals. This biological accumulation of toxic metals is seen in the research data for beryllium,
silicon, plutonium, uranium, and other insoluble metal oxides. [35, 36, 37] The effect is very
clear in research for lung damage from airborne toxic metals pathways to lung that activate the
lung inflammatory immune response. Toxic materials in the lung activate the cytokine production
of TNFa that promote macrophage's, and can be seen with radiation and for toxic metals. [38, 39,
40] Cytokine TNFa is directly delivered to the mitochondria of cells and involved in apoptosis /
necrosis. [41] The mitochondria of cells play important roles in cell energy production and
hormonal and cytokine messaging.

Beryllium is the most detailed studied toxic metal and makes an excellent example for the model
of how the toxic metal activates the immune system. [42] Beryllium workers can become sensitive
to beryllium and become sensitized to breathing it as determined by a lymphocyte proliferation
test. With any addition exposures persons can acquire a fatal disease called chronic beryllium
disease, where the lungs cells are damaged by continual inflamation. This is often mediated with
steroid inhaler medication. The disease is often mis-diagnosed as asthma initially due to
similarity of symptoms. Beryllium is taken into the lymph nodes via the action of macrophage's
and as the lymph concentration builds it triggers the lymph nodes to make T-cells and
B-lymphocytes in response to the toxic beryllium metal. [43] As the concentration in the lymph
nodes builds the insoluble metal oxides retain long term and keep the local lung lymph system
triggered long term in the Th1 inflamation mode. In this Th1 state the lung uses much
glutathione for cell repair processes. [44] Since this is an effect local to the lungs, the
glutathione is not depleted in the whole body. The air pathway for beryllium used in the nuclear
weapons business is a well developed model for the immune activation process, and shows a local
process that is highly related to indicators seen in CFS. Sensitization to beryllium compounds
happens after cells in the lymph nodes undergo blast cell transformation. It is clear that
beryllium concentrations of beryllium toxic metal in lymph nodes set up the cytokine triggering
of the immune system.

Other toxic metals cause the same problems at concentrations lower than that needed to kill the
cells directly, as long term cytokine activation causes serious health problems. [45] As the
metals concentrations build in the lymph nodes the TNFa cytokine causes necrosis of the
macrophage and other lymph nodes cells and continual generation of activated T and B cells. If
the lymph node concentrations get too high this disables the pathogen destruction function of
macrophage's. Beryllium oxide particles principally involves the local lung lymph nodes, but
other toxic metals that are more soluble and enter the body via air or food chain can impair
lymph nodes near the intestine or all the lymph nodes at once. As the macrophage's are disabled
it leaves cell fragment products scattered around the tissues that then bias the system toward a
Th2 response in the long term. Th2 modality excretes IL-10 which further shuts down the
macrophage function and exasperates the effect. This leaves the body vulnerable to inner cell
viruses and other pathogens such as mycoplasma.

Metal prosthetic joints in the body further illustrate the effect of metal particulate
concentrating into the lymph nodes and this triggering inflammatory cells that loosen the bone
with high levels of peroxides. [46, 47] Metal particles of less than 1 micron can be carried
into the lymph nodes via the macrophage's and concentrate there. [48] The lungs are sensitive to
many different metal particles that can also set up the Th1 inflamation mode. The effect is
intensified if the particles from airborne exposure have an acid like coating that is insoluble.
Regulations have attempted to mediate these toxic particle exposures, but has made further poor
choices. Gasoline refining eliminated lead in the 1980's because of this effect on the
population and replaced it with hydrogen fluoride (HF), which has even worse cumulative factors
and time integral dose effect on the macrophage function. Rising levels of pesticides in food
and water, rising industrial emissions of HF all combine to contribute to effects that trigger
the cytokines and lead to CFS cytokine Th2 modality in the long term. The worsening
environmental metal effects can be seen in even the surface waters of the Great Lakes with their
increasing levels of toxic metals that can damage the immune system, produce allergy, increases
susceptibility to disease, and autoimmune disorders. [49] Even pollution of rivers from
fluorides added to public water supplies harm salmon. [50] Animals and man can be highly
affected by toxic metals and their phagocytosis cell ability severely impaired by low
concentrations of metals, while NK cell activity is not impaired. [51] It is these poorly
controlled pollutants that drive increasing rates of CFS, cancer, and many immune linked
illnesses.

The key etiology of the toxic accumulation effect can be anticipated by the function of oxygen
based chemistry of stationary macrophage's in the lymph nodes acting with the mobile
macrophage's carrying toxic cell material from around the body to these local lymph zones. This
is an often overlooked important and key effect to have build up of insoluble toxic material
directly in the critical signaling network of lymph nodes that keeps the immune system cytokine
triggered and supply high oxidative stress directly in the lymph nodes. This effect can lead to
toxic metals damaging the ability of the body to control pathogens and even to rising viral
presence in the body from endogenous and exogenous sources. [52, 53] For air pollutants the
lungs nodes are most affected and for food and water pollution the stomach and intestine nodes
are the principle effect zones. A pivotal role is carried by the proper function of the lymph
node pathogen regulation mechanism. Simple local inflammatory activation of the immune system
results in increased glutathione to aid in DNA repair, and long term global activation results
in depletion of glutathione. Decreased levels of glutathione promote cell apoptosis / necrosis.
Toxic's that damage the liver cause a lack of glutathione for DNA repair.

The importance of a cell organelle called the mitochondria was better defined with respect to
disease mechanisms in the mid 1980's with its critical role as the cell energy mechanism and the
source of ATP. [54] These organelles were small cells within cells with bacterial like DNA that
were vulnerable to oxidation effect, metals, and oxidative halogens.[55] GSH plays a strong role
in the production of ATP and mtDNA repair from oxidative damage. [56, 57] CFS is well connected
to lowered ATP levels. [58] Mitochondrial damage is connected to nerve damage and aging. [59,
60] Mitochondria is how the body converts stored fat into energy and damage to these areas of
cells is linked to weight gain and obesity factors that are high in the US. Fluorides have the
capacity to affect the thyroid T-3 hormone production and modify cellular ATP production
throughout the body as well as diminish mitochondrial numbers in cells. [61] Depletion of ATP is
connected to the Th1 to Th2 switch seen in CFS and other diseases. [62] High concentrations of
toxic metals and fluorides in the lymph nodes will highly impact the mitochondria of these
cells. This leave little doubt that the worst case for mitochondria damage due to toxic
concentrations is the lymph nodes and that this process is directly connected to CFS and other
immune dysfunction illnesses.

Toxic metal and fluoride releases are connected to the Oak Ridge K-25 gas diffusion plant and a
number of workers were noted to be affected by symptoms similar to chronic fatigue syndrome. Gas
diffusion plant workers with CFS like symptoms number in the hundreds. The K-25 gaseous
diffusion plant lost huge amounts of toxic hydrogen fluoride (HF) to the air of the plant and
region and was discovered by questioning workers about processes and releases. Other HF releases
from the X-10 Molten Salt Reactor and the Y-12 UF-4 "Salt Shop" operations provided similarly
affected workers and correlation to HF toxic effect due to cumulative low level exposures. The
large losses of the K-25 plant exposed not only workers, but downwind residents of the plant to
fluorides. Fluorides were highly suspected as area pine trees, which are very vulnerable to
fluorides, were showing impact. There was both air / lung pathway effects, soil contamination /
food pathways into the gastrointestinal system, and ground and surface water pathways into
communities. These pathways for fluorides connected them with the CFS like symptoms and asthma
seen in workers and communities. The workers had high levels of calcium that is indicative of
fluoride exposure. [63] They also had high retention of metals and high porphyrin. Fluorides
tend to be accumulated (integrated) over a lifetime and the same net dose occurs from a ten unit
dose over one year or that of a one unit dose over ten years.

Fluorides cause some of the worst damage to the immune system with very low concentrations.
Industrial fluorides emission in Germany in the late 1800's was perhaps the first chemical to
produce worker and community health problems. Fluoride is connected to renal stone formation via
insoluble calcium fluoride formation, much like what happens with metals in lymph nodes. [64]
Veterinarians warn against using fluoride tooth pastes on animals and with the knowledge of the
lymph node effects fluoride tooth pastes and fluoridated public water become dangerous to public
health. Industrial fluoride emission was linked to asthma and to arthritis. [65, 66, 67]
Fluoride workers also show their cytokine response biased toward the Th2 in the long term. [68]
Fluorides impair the macrophage's at very low concentrations and the effect is strongest in the
lymph nodes from the insoluble product effect that is often combined with metals and free
radical synergy effects. [69, 70, 71, 72] Fluorides cause swelling of the mitochondria
indicating damage to ATP processes. [73] Hydrogen fluoride sets off inflamation in lungs. [74,
75] Fluorides toxic effects set up the same mechanism as seen in the beryllium model. Fluorides
are pulled into the lymph nodes and the affinity of fluoride for calcium produces an insoluble
precipitate that is similar to the effects caused by the insoluble metals. The effect sets up
TNFa and hyper-oxygen damage that locally lowers glutathione in the lymph cells. TNFa promotes
viral RNA replication. Increasing viral infection in the type I macrophage's promotes more TNFa
and this is multiplied by the repeating effect of cells in the lymph system. This activation of
the Th1 process also sets up a switch to Th2 mode slowly as the macrophage's stop working and
foreign cell products accumulate in the tissues that trigger the Th2 mode. Th2 suppressor
effects on Th1, impaired ATP, glutathione, and other effects contribute to the mode switch. [76]
Th2 mode involves IL-10 that further depresses and shuts down the macrophage action and locks in
the Th2 mode.

This lymph node / mitochondria impact thesis became a toxic pathway mechanism for immune
dysfunction in 1986 that explained the process for all immune linked diseases and even aging /
longevity factors. The thesis was that insoluble toxic material, metal oxides and fluorides
predominately, accumulated in the lymph nodes and disabled this pathogen destruction mechanism
and the toxic presence set up a continuous cytokine response in the lymph system that keeps the
immune system triggered and allows pathogen presence. [77] In the early stages of viral
activation, a Th1 profile with TNFa is often seen and in a normal immune response these levels
control the virus. [78] Internal cell viruses such as EBV, CMV, HHV-6, mycoplasma, cancer
viruses, HIV, and etc. can run out of control with a system biased toward Th2. The toxic
material concentrations triggered the inflamation effects that cause cell apoptosis, necrosis,
consume glutathione, etc. Add in pathogenic components and the outcome is further modified. HIV
spends cell energy and promotes TNFa and IL-10, which helps in the demise of T-cells as the
disease progresses due principally to the loss of macrophage activity from the IL-10. [79]

The 1991 Gulf War exposed thousands of veterans to various toxic materials that have long
retention in the body and set up the same conditions as the toxic metal effects in the lymph
nodes. Many of these Gulf War Veterans experience the symptoms of CFS and multiple chemical
sensitivity (MCS). [80] They also are biased toward the Th2 profiles because of the similarity
to the industrial pollution that drives CFS. They were exposed to toxic metals in the form of DU
and mercury preservative in Th2 promoting vaccines. They were exposed to halogens in the form of
bromine from PB tablets, excessive chlorides from water treatment, various pesticides, and
fluorides from nerve gases.[81] Recent studies have shown that those exposed to chemicals have
brain damage. [82] CFS affected persons also show brain damage. [83] Gulf War Syndrome (GWS)
persons also have fibromyalgia similar to CFS. [84] It is not a single chemical factor analysis
that solves the illness toxic driven equation, but various toxins acting in the same pathway to
disable the lymph system that best explains GWS. This war was the toxic equivalent of hell that
dosed many there with 30 years of industrial and environmental pollutants that aged them with
health effects to 60 years old females. There is one central etiology mechanism involving
insoluble compounds in the lymph nodes triggering the cytokine response. The immune dysfunction
comes from multiple contaminates acting via a common mechanism that allow varied illness
outcomes as determined by exogenous and endogenous viral predispositions and other opportunistic
pathogens.

Food processing and preparation play a strong role in the vitamin and free radical effects in
the intestine that affect these cells and their local lymph nodes. Food processing and cooking
destroy most of the nutrients in food. Raw and uncooked living vegetable foods supply more
vitamins, as compared to cooked vegetables or fried food. [85, 86, 87] Cooked food has long been
associated with delivery of free radicals from food stuffs to the stomach and intestines and
this effect causes some excess production of white blood cells, called digestive leukosis. High
temperature fried food supplies the most free radical content and highest toxic exposure due to
bio-concentration in the food chain. Raw and uncooked foods don't produce these free radical
effects and provide better delivery of enzymes and vitamins, as well as fiber to detoxify the
system. Raw food diets aid in mediation of CFS, cancers, and other immune illnesses because of
these vitamin and reduced free radical factors.

The raw food verses cooked food is also involved with the biblical issues of Genesis. Animal
foods add a level of bio-concentration of toxic material from airborne contamination of the
animal food chain. Cooking vegetables or animal products produces free radicals from the
pollutants and pesticides that can retain more easily in the body. Vegan diets also make the
intestine more basic, which results in less immune activation and less absorption of toxic
metals. Because of these effects, the raw uncooked vegan diet is connected toward effective
intervention for fibromyalgia, rheumatoid, heart, and cancer. [88, 89, 90, 91, 92, 93] Vegan
diets also alter the fecal bacteria levels and bacterial fatty acid generation. [94, 95] The
toxic load and nutrient supply in the intestines is highly associated with immune illnesses and
long term effects result in leaking gut syndromes. The quick heating pasteurization of milk also
produces toxic effect. [96] Raw food diets promote illness recovery.

There is more that supports the conclusion that the toxic loading in the lymph nodes shut down
the monocytes / macrophage's and is the pivotal problem with HIV. [97] HIV transmission and
infections appear most prevalently in the intestine and its local lymph system. Here the toxic
load of the food and water chain come into play with cytokine factors and lymph node effect. The
intestinal region is the most affected from cooked food free radicals and the uptake of toxic's
in the food and water chain. Regions in Africa with the highest fluoride in well water and food
have the largest problem with HIV transmission. [98, 99, 100, 101, 102, 103] Many of the high
fluoride regions follow the east African Rift Valley zone that is lined with volcano and seismic
zones. In many of these areas the persons have frosty white teeth from dental fluorosis and many
are disabled by age 40. This is significant because fluoride toxic effects set up cytokine
profiles that HIV transmission and growth require with TNFa in the lymph nodes and loss of
macrophage / monocyte performance driving Th2 bias in the intestines and body as a whole. [104]
The TNFa cytokine promotes the viral proliferation of HIV. [105]

HIV as it infects more cells in the body sets up its own cytokine signatures that become the
additional factors on top of the toxic effects that keep it from being regulated. HIV also
produces IL-10, which suppresses macrophage action. [106] Impaired monocyte / macrophage
function is highly associated to HIV progression and pathology for other viral infection. [107]
Rising IL-10 levels that suppress macrophage action directly connect to the loss of CD-4+ T
cells. [108] These T-cells are preferentially attacked due to the gp120 bonding site on T-cells
that promotes HIV cellular transmission into these cells. The early AZT treatment acted more to
destroy cell mitochondria than to oppose HIV replication. [109, 110] HIV always involves
activation of other viruses and these can worsen the cytokine activations and AIDS progressions.
[111] HHV-7 is often activated in HIV infected persons and the lymph nodes are seen to be the
site of reactivation. [112] This leaves little doubt that the failing lymph node effect play a
central role in HIV proliferation. This can also be seen in the case of cancer viruses where the
failing lymph node cellular regulation allow cancer metastasis of lymph nodes and helps to
spread the cancer viral infection. The same effect also spreads HIV and other viruses, rather
than regulate and destroy them. The HAART treatment for HIV lowers the AZT dose and avoids using
TNFa mechanisms that promotes HIV transcription and this has almost rendered HIV a chronic
survivable disease, with many having near normal life-span with non-detectable HIV in their
blood. The principle problem with HIV and the immune system is that TNFa triggers it, but it is
the monocytes and macrophage's that play the pivotal role in controlling the viral destruction
and proliferation of HIV. The key factor is macrophage and monocyte performance for regulation
of HIV, with the exposure to fluorides dominating this performance in many countries.

In Conclusion, immune system diseases are caused by poor environmental, industrial, and
agricultural practices bringing toxic material into contact with the air, food and water chain
leading to animals and humans. The principle toxic offenders are fluorides and its halogen
family relatives, closely followed by toxic metals, and chemicals that impact GSH. The leading
damage vector is via damage to the cell mitochondria of lymph node macrophage cells of the Th1
driven cellular defense immune system. The failing macrophage's leave cell products from killed
cells in the body that drive Th2 mode and this drives a lock in process into Th2 seen in
chemical plant workers, CFS, GWS, MCS, and HIV. The critical or processional pivotal event
leading to this is the accumulation of insoluble toxic products in the lymph nodes. This effect
produces the net aging effect of the body, as it sets the net cellular degradation from
unregulated pathogens.

______________________________________________________


References:

1. Kuby, J., (1994) Immunology, W. H Freeman and Co., ISBN 0-7167-2643-2 p 297-321.

2. Petricevich, V. L., Teixeira, C. F., Tambourgi, D. V., Gutiérrez, J. M.,. (2000) Increments
in serum cytokine and nitric oxide levels in mice injected with Bothrops asper and Bothrops
jararaca snake venoms. Toxicon, 2000 09, 38: 9, 1253-1266.

3. CFS Radio Program February 28th, 1999 Roger G. Mazlen, M.D., Host withDr. Paul Cheney, WEVD
Radio New York City, Transcribed by Carolyn Viviani.

4. South Lake Tahoe Public Utility District, 1999 Annual Water Quality Report.

5. Manningham, R., (1750) The symptoms, nature, causes and cure of the febricula or little
fever: commonly called the nervous or hysteric fever; the fever of spirits; vapours, hypo, or
spleen. 2nd edition. J Robinson, London, pp 52-53.

6. Hernán1, M. A., Zhang, S. M., Lipworth, L., Olek, M. J.., Ascherio, A., (2001) Multiple
Sclerosis and Age at Infection with Common Viruses, Epidemiology 2001;12:301-306.

7. Ablashi, D. V., Eastman, H. B., Owen, C. B., Roman, M. M., Friedman, J., Zabriskie, J. B.,
Peterson, D. L., Pearson, G. R., Whitman, J. E., Frequent HHV-6 reactivation in multiple
sclerosis (MS) and chronic fatigue syndrome (CFS) patients. J Clin Virol, 2000 05, 16: 3,
179-191.

8. Valentine, W. N., Paglia, D. E. (1980), Syndromes with increased red cell glutathione,
Hemoglobin, 1980 01, 4:5-6, 799-804.

9. Parke, D.V., (1982), Mechanism of chemical toxicity-a unifying hypothesis, Regul Toxicol
Pharmacol, 1982, 12, 4, 267-286.

10. Slater, A. F., Stefan, C., Nobel, I., Van den Dobbelsteen, D. J., Orrenlus, S., (1995),
Signaling mechanisms and oxidative stress in apoptosis, Toxicol Lett, 1995 12, 82-83, 149-153.

11. Lang, C. A., Mills, B. J., Mastropaolo, W., Liu, M. C., (2000), Blood glutathione decreases
in chronic diseases, J Lab Clin Med, 2000-05, 135:5, 402-405.

12. Pawowicz, Z., Zachara, B. A., Trafikowska, U., Maciag, A., Marcheluk, E., Nowicki, A.,
(1991), Blood selenium concentration and glutathione peroxidase activities with breast cancer
and with advanced gastrointestional cancer, J Trace Elem Electrolytes Health Dis., 1991 12, 5:
4, 275-277.

13. Tarp, U., Hansen, J. C., Overvad, K., Thorlling, E. B., Tarp, B. D., Graudal, H., (1987),
Glutathoine peroxidase activity in patients with rhumatoid arthritis and in normal subjects:
effect of long-term selenium supplementation, Arthritis Rheum, 1987 10, 30: 10, 1162-1166.

14. Hazelton, G. A., Lang, C. A., (1980), Glutathione contents of tissues in the aging mouse,
Biochem J, 1980 00, 188: 1, 25-30.

15. Hussain, S., Slikker, W. Jr, All, S. F., (1995), Age-related changes in antioxidant enzymes,
superoxide dismutase, catalase, glutathione peroxidanse and glutathione in different regions of
the mouse brain, Int J Dev. Neurosci. 1995 12, 13: 8, 811-817.

16. Batt, A. M., Ferrari, I., (1995), Manifestation of chemically induced liver damage, Clin
Chem, 1995 12, 41: 12 Pt 2, 1882-1887.

17. Naito, Y., Yoshikawa, T., Boyu, Y., Fujii, T., Masui, Y., Tanaka, Y., Fujita, N., Yoshida,
N., Kondo, M., (2000), Protective role of glutathione against nitric oxide-induced necrosis in
rat gastric mucosal cells, Aliment Pharmacol Ther., 2000 04, 14 Suppl 1: 145-152.

18. Peterson, J., Proc Natl Acad Sci., March 1998, Immunology Magazine.

19. Suhadolnik, R. I., Peterson, D. L., O'Brien, K., Cheney, P. R., Herst, C. V. T.,
Reichenbach, N. L., Kon, N., Horvath, S. E., Iacono, K. T., Adelson, M. E., De Meirleir, K, De
Becker, P., Charubala, R., Pfleiderer, W., {1997) Biochemical Evidence for a Novel Low Molecular
Weight 2-5A-Dependent RNase L in Chronic Fatigue Syndrome, Journal of Interferon and Cytokine
Research, 17:377-385 (1997).

20. Sobol, R.W., (1992) A structural and functional characterization of the 2-5A synthesis/RNase
L antiviral pathway and its role in HIV-1 regulation: the pivotal role of 2-5A, Diss Abstr Int
52(7):3590 1992.

21. McGee, K. A., Doukas, M. P., Kessler, R., Gerlach, T. M., (1997) Impacts of Volcanic Gases
on Climate, the Environment, and People, U.S. Geological Survey Open-File Report 97-262, May
1997.

22. Rubin, C. H., Noji, E. K., (1994). Evaluating a Fluorosis Hazard After a Volcanic Eruption,
Archives of Environmental Health, Sep/Oct94, Vol. 49 Issue 5, p395, 7p, 2 charts, 3 graphs
Health, September, 1994.

23. Independent Investigation of the East Tennessee Technology Park, Volume 1 (October 2000).
DOE Office of Oversight, Environment, Safety and Health.

24. Podkletnov, N. E., Markhinin, E. K., (1981) New data on Abiogenic synthesis of prebiological
compounds in volcanic processes, Orig Life 1981 12, 11:4, 303-315.

25. Yamawaki, M., Ariga, T., Gao, Y., Tokuda, A., Yu, J. S., Sismanis, A., Yu, R.K.. (1998)
Sulfoglucuronosyl glycolipids as putative antigens for autoimmune inner ear disease. J
Neuroimmunol 1998 Apr 15;84(2):111-116.

26. Krocova, Z., Macela, A., Kroca, M., Hernychova, L., (2000) The immunomodulatory effect(s) of
lead and cadmium on the cells of immune system in vitro. Toxicol Vitr, 2000 02, 14: 1, 33-40.

27. Axelson, O., (1980) Arsenic compounds and cancer. J Toxicol Environ Health, 1980 00, 6: 5-6,
1229-1235.

28. Dodd, N. J., Silcock, J. M., (1976) Electron spin resonance study of changes during
development of solid yoshida tumour. II. Paramagnetic metal ions. Br J Cancer, 1976 11, 34: 5,
556-565.

29. Germolec, D. R., Yoshida, T., Gaido, K., Wilmer, J. L., Simeonova, P. P., Kayama, F.,
Burleson, F., Dong, W., Lange, R. W., Luster, M. I., (1996) Arsenic induces overexpression of
growth factors in human keratinocytes. Toxicol Appl Pharmacol, 1996 11, 141: 1, 308-318.

30. Shen, Z. Y., Shen, J., Cai, W. J., Hong, C., Zheng, M. H., (2000) The alteration of
mitochondria is an early event of arsenic trioxide induced apoptosis in esophageal carcinoma
cells. Int J Mol Med, 2000 02, 5: 2, 155-158.

31. Akao, Y., Yamada, H., Nakagawa, Y., (2000) Arsenic-induced apoptosis in malignant cells in
vitro. Leuk Lymphoma, 2000 03, 37: 1-2, 53-63.

32. Bryson, C., (1998) The Donora Fluoride Fog: A Secret History of America's Worst Air
Pollution Disaster Fall 1998 Earth Island Journal

33. Glasser, G., (1998) - Fluoride And The Phosphate Connection, Earth Island Journal Special
Report "Fluorides And The Environment", (1998)

34. Clark, W. R., (1986) The Experimental Foundation of Modern Immunology, John Wiley and Sons.
p 418-421.

35. Harley, N. H., Foulkes, E. C., Hilborne, L. H., Hudson, A., Anthony, C. R., (1999). A Review
of the Scientific Literature As It Pertains to Gulf War Illness, Volume 7, Depleted Uranium.
RAND report.

36. Kniazhev, V. A., Umnikova, N. M., (1975), Toxicology of high-fired beryllium oxide inhaled
by rodents. II. Metabolism and early effects, Arch Environ Health 30(11): 546-551.

37. Kathren, R. L., Strom, D.J., Sanders, C. L., Filipy, R. E., McInroy, J. F., Bistline, R. E.,
(1993) Distribution of Plutonium and Americium in Human Lungs and Lymph Nodes and Relationship
to Smoking Status, Radiation Protection Dosimetry, Vol. 48(4): p 307-315.

38. McKinney, L. C., Aquilla, E. M., Coffin, D., Wink, D. A., Vodovotz, Y., (October 1998).
Ionizing radiation potentiates the induction of nitric oxide synthase by IFN-g and/or LPS in
murine macrophage cell lines: role of TNF-a. Journal of Leukocyte Biology, Volume 64 459-466.

39. Morales, A., Miranda, M., Sánchez Reyes, A., Biete, A., Fernández Checa, J.C., (1998)
Oxidative damage of mitochondrial and nuclear DNA induced by ionizing radiation in human
hepatoblastoma cells. Int J Radiat Oncol Biol Phys, 1998 Aug, 42:1, 191-203.

40. Tinkle, S. S., Schwitters, P. W., Newman, L. S., (1996). Cytokine Production by
Bronchoalveolar Lavage Cells in Chronic Beryllium Disease. Environ Health Perspect 104(Suppl
5):969-971.

41. Ledgerwood, E. C., Prins, J. B., Bright, N. A., Johnson, D. R., Wolfreys, K., Pober, J. S.,
O'Rahilly, S., Bradley, J. R., (1998). Tumor Necrosis Factor Is Delivered to Mitochondria Where
a Tumor Necrosis Factor-Binding Protein Is Localized. Lab Invest 1998, 78:1583-1589.

42. Deodhar, S.D., Barna, B.P., (1991) Immune mechanisms in beryllium lung disease. Cleve Clin J
Med, 1991 Mar, 58:2, 157-160.

43. Sawyer, R.T. Kittle, L.A., Hamada, H., Newman, L.S., Campbell, P.A., (2000)
Beryllium-stimulated production of tumor necrosis factor-alpha by a mouse hybrid macrophage cell
line. Toxicology, 2000 00, 143: 3, 235-247.

44. Comhair, S.A., Lewis, M. J., Bhathena, P. R., Hammel, J. P., Erzurum, S. C., (1999)
Increased glutathione and glutathione peroxidase in lungs of individuals with chronic beryllium
disease. Am J Respir Crit Care Med, 1999 Jun, 159:6, 1824-1829.

45. Slifka, M. K., Whitton, J. L., (2000) Clinical implications of dysregulated cytokine
production. J Mol Med, 2000 01, 78: 2, 74-80.

46. Tucci, M., Baker, R., Benghuzzi, H., Hughes, J., (2000) Levels of hydrogen peroxide in
tissues adjacent to failing implantable devices may play an active role in cytokine production.
Biomed Sci Instrum, 2000 01, 36: , 215-220.

47. Urban, R. M., Jacobs, J.J., Tomlinson, M. J., Gavrilovic, J., Black, J., Peoch, M., (2000)
Dissemination of wear particles to the liver, spleen, and abdominal lymph nodes of patients with
hip or knee replacement, J Bone Joint Surg Am, 2000 04, 82: 4, 457-476.

48. Azuma, Y., Kaji, K., Katogi, R., Takeshita, S., Kudo, A., Tumor necrosis factor-alpha
induces differentiation of and bone resorption by osteoclasts. J Biol Chem, 2000 00, 275: 7,
4858-4864.

49. Bernier, J., Brousseau, P., Krzystyniak, K., Tryphonas, H., Fournier, M., (1995)
Immunotoxicity of heavy metals in relation to Great Lakes. Environ Health Perspect, 1995 12, 103
Suppl 9: , 23-34.

50. Foulkes, R. G., Anderson, A. C., (1994), Impact of Artificial Fluoridation on Salmon Species
in The Northwest USA and British Columbia, Canada, Fluoride Vol.27 No.4 220-226 1994.

51. De Guise, S., Bernier, J., Lapierre, P., Dufresne, M. M., Dubreuil, P., Fournier, M., (2000)
Immune function of bovine leukocytes after in vitro exposure to selected heavy metals. Am J Vet
Res, 2000 03, 61: 3, 339-344.

52. Christensen, M. M., Ellermann Eriksen, S., Rungby, J., Mogensen, S. C., (1996) Influence of
mercuric chloride on resistance to generalized infection with herpes simplex virus type 2 in
mice. Toxicology, 1996 00, 114: 1, 57-66.

53. Soltýs, J., Borosková, Z., Dvoroznáková, E., (1997) Effects of concurrently administered
copper and mercury on phagocytic cell activity and antibody levels in guinea pigs with
experimental ascariasis. J Helminthol, 1997 12, 71: 4, 339-344.

54. Graff, C., Clayton, D. A., Larson, N.G., (1999) Mitochondrial medicine-recent advances, J
Intern Med., 1999 Jul, 246:1, 11-23.

55. Treem, W. R., Sokol, R. J., (1998) Disorders of the mitochondria, Semin Liver Dis., 1998,
18:3, 237-253.

56. Morales, A., Miranda, M., Sanchez, Reyes A., Biete, A., Fernandez Checa J. C., (1998)
Oxidative damage of mitochondrial and nuclear DNA induced by ionizing radiation in human
heptoblastoma cells, Int J Radiat Oncon Biol Phys, 1998 Aug, 42:1, 191-203.

57. Yakes, F. M., Van Houten, B., (1997) Mitochonrail DNA damage is more extensive and persists
longer than nuclear DNA damage in human cells following oxidative stress, Proc Natl Acad Sci
USA, 1997 Jan, 94:2, 514-519.

58. J. Alexander Bralley, J. A., Lord, R. S., (1994). CFS, Journal of Applied Nutrition,
46(3):74-78.

59. Tritschler, H. J., Packer, L., Medori, R., (1994) Oxidative stress and mitochondrial
dysfunction in neurodegeneration, Biochem Mol Biol, 1994 Aug, 34:1, 169-181.

60. Lenaz, G., (1998) Role of mitochondria in oxidative stress and ageing. Biochim Biophsy Acta,
1998 Aug, 1366:1-2, 53-67.

61. Bachinskii, P. P., Gutsalenko, O. A., Naryzhniuk, N.D., Sidora, V. D., Shliakhta, A. I.,
(1985) Action of the body fluorine of healthy persons and thyroidopathy patients on the function
of hypophyseal-thyroid the system, Probl Endokrinol (Mosk) 1985 Nov-Dec;31(6):25-29.

62. Hasko, G., Kuhel, D. G., Salzman, A. L., Szabo, C., (2000) ATP suppression of IL-12 and TNFa
release from macrophages. Br J Pharmacol, 2000 03, 129: 5, 909-914.

63. Hynczak, A. J., Adamowicz, A., Fabisz, L., Kosmider, K., Suska, M., Wnuczynaki, K., Wozniak,
Z., (1980), Calcium and magnesium in the blood serum of workers exposed to fluoride compounds,
in relation to age and duration of employment, Med Pr. 1980 01, 31:5, 345-349.

64. Trace Elements in Human and Animal Nutrition (Fifth Edition) Edited by Walter Mertz, U. S.
Dept. of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center,
Beltsville, Maryland, 1987 p371.

65. Waldbott George L, (1998) The Preskeletal Phase of Chronic Fluoride Intoxication, Fluoride
31(1) 1998, pp 13-20.

66. Fluoride, The Aging Factor, Dr. John Yiamouyiannis, Health Action Press, 1993.

67. Roholm, K., (1937) Fluorine Intoxication, A Clinical-Hygiene Study, With a Review of the
Literature and Some Experimental Investigations. H.K. Lewis & Co., Ltd., London, 1937.

68. Balabolkin, M.I., Mikhailets, N.D., Lobovskaia, R. N., Chernousova, N. V., (1995), The
interrelationship of the thyroid and immune statuses of workers with long-term fluorine exposure
Ter Arkh, 1995, 67:1, 41-42.

69. Curnette, J., et al (1979) Fluoride-mediated Activation of the Respiratory Burst in Human
Neutrophils, Journal of Clinical Investigation, Vol. 63, pp. 637-647.

70. Zhan, Y., Du, L., Zhan, C., (1995) A study on human dental embryology in an endemic high
fluorosis region, Zhonghua Bing Li Xue Za Zhi 24(1):36-8 (1995) (www.ncbi.nlm.nih.gov
id=7781114) Department of Histology and Embryology, Guiyang Medical College.

71. Gabler, W. L., Leong, P. A., (1979) Fluoride Inhibition of Polymorphonumclear Leukocytes,
Journal of Dental Research, Vol. 48, No. 9, pp. 1933-1939.

72. Gabler, W. L., et al. (1985) Effect of Fluoride on the Kinetics of Superoxide Generation by
Fluoride, Journal of Dental Research, Vol. 64, p. 281.

73. Kozlyuk, A. S., et al. (1987) Immune Status of Children in Chemically Contaminated
Environments, Zdravookhranenie, Issue 3, pp. 6-9.

74. Lund, K., Boe, J., Refsnes, M., Sandström, T., Söstrand, P., Kongerud, J., (1996) Acute
inflammatory markers in bronchoalveolar lavage fluid from subjects exposed to hydrogen fluoride
European respiratory journal, vol. 9, suppl. 23, 1996, s. 438s ; ISSN 0106-433 9.

75. Lund, K., Boe, J., Refsnes, M., Söstrand, P., Schwarze, P., Sandström, T., (1996)
Experimental hydrogen fluoride exposure induces airway inflammation in normal subjects American
journal of respiratory and critical care medicine, vol. 153, no. 4, pt 2, 1996, s. A484 ; ISSN
1073-449X

76. Visser, J.T., De Kloet, E.R., Nagelkerken, L,. (2000). Altered glucocorticoid regulation of
the immune response in the chronic fatigue syndrome. Ann N Y Acad Sci 2000;917:868-875.

77. Nosik, N.N., (2000) Cytokines in viral infections Vopr Virusol, 2000 00, 45: 1, 4-10.

78. Rentenaar, R.J., Gamadia, L.E., van DerHoek, N., van_Diepen, F.N., Boom,R., Weel, J.F.,
Wertheim van Dillen, P.M., van Lier, R.A., ten Berge, I.J., (2000) Development of virus-specific
CD4(+) T cells during primary cytomegalovirus infection. J Clin Invest, 2000 02, 105: 4,
541-548.

79. Lane, B. J., Provost, Craig, M. A., Resting energy expenditure in asymptomatic HIV-infected
females. J Womens Health Gend Based Med, 2000 04, 9: 3, 321-327.

80. Reid, S., Hotopf, M., Hull, L., Ismail, K., Unwin, C., Wessely, S., (2001) Multiple chemical
sensitivity and chronic fatigue syndrome in british gulf war veterans. Am J Epidemiol 2001 Mar
15;153(6):604-609.

81. Roland, P. S., Haley, R. W., Yellin, W., Owens, K., Shoup, A. G., (2000) Vestibular
dysfunction in Gulf War syndrome. Otolaryngol Head Neck Surg, 2000 03, 122: 3, 319-329.

82. Haley, R.W., Marshall, W.W., McDonald, G.G., Daugherty, M.A., Petty F., Fleckenstein, J.L.,
(2000) Brain abnormalities in Gulf War syndrome: evaluation with 1H MR spectroscopy. Radiology,
2000 06, 215: 3, 807-817.

83. Cook, D. B., Lange, G., DeLuca, J., Natelson, B.H., (2001) Relationship of brain and mri
abnormalities and physical functional status in chronic fatigue syndrome, Int J Neurosci 2001
Mar: 107 (1-2): 1-6.

84. Buskila, D., Fibromyalgia, (2000) chronic fatigue syndrome, and myofascial pain syndrome.
Curr Opin Rheumatol, 2000 03, 12: 2, 113-123.

85. Rauma, A.L., Torronen, R., Hanninen, O., Verhagen, H., Mykkanen, H., (1995) Antioxidant
status in long-term adherents to a strict uncooked vegan diet. Am J Clin Nutr, 1995 Dec,
62(6):1221-1227.

86. Rauma, A. L., Torronen, R., Hanninen, O., Mykkanen, H., (1995) Vitamin B-12 status of
long-term adherents of a strict uncooked vegan diet ("living food diet") is compromised. J Nutr,
1995 Oct, 125(10):2511-2515.

87. Donaldson, M.S., (2000) Metabolic vitamin B-12 status on a mostly raw vegan diet with
follow-up using tablets, nutritional yeast, or probiotic supplements, Annals of Nutrition &
Metabolism. 44(5-6):229-234, 2000 Sep-Dec.

88. Rauma, A.L., Nenonen, M., Helve, T., Hanninen, O., (1993) Effect of a strict vegan diet on
energy and nutrient intakes by Finnish rheumatoid patients. Eur J Clin Nutr 1993
Oct;47(10):747-749.

89. La Puma, J., (1999) Vegan Diet and Rheumatoid Arthritis. Internal Medicine Alert, April 15,
1999 v21 i7 p52(1).

90. Nenonen, M.T., Helve, T.A., Rauma, A.L., Hanninen, O.O., (1998) Uncooked, lactobacilli-rich,
vegan food and rheumatoid arthritis. Br J Rheumatol 1998 Mar;37(3):274-281.

91. Peltonen, R., Nenonen, M., Helve, T., Hanninen, O., Toivanen, P., Eerola, E., (1997) Faecal
microbial flora and disease activity in rheumatoid arthritis during a vegan diet. Br J Rheumatol
1997 Jan;36(1):64-68.

92. Hanninen, O., Rauma, A. L., Kaartinen, K., Nenonen, M., (1999) Vegan diet in physiological
health promotion. Acta Physiol Hung 1999;86(3-4):171-180.

93. Kaartinen, K., Lammi, K., Hypen, M., Nenonen, M., Hanninen, O., Rauma, A.L.,. (2000) Vegan
diet alleviates fibromyalgia symptoms. Scand J Rheumatol 2000;29(5):308-313

94. Ling, W.H., Hanninen, O., (1992) Shifting from a conventional diet to an uncooked vegan diet
reversibly alters fecal hydrolytic activities in humans. J Nutr 1992 Apr;122(4):924-930.

95. Peltonen, R., Ling, W-H., Haenninen, O., Eerola, E., (1992) An uncooked vegan diet shifts
the profile of human fecal microflora: Computerized analysis of direct stool sample gas-liquid
chromatography profiles of bacterial cellular fatty acids. Applied and Environmental
Microbiology [APPL. ENVIRON. MICROBIOL.], vol. 58, no. 11, pp. 3660-3666, 1992.

96. "Milk - The Deadly Poison" (1998) Robert Cohen , Argus Publishing, Inc., ISBN 0-9659196-0-9.

97. Mabondzo, A., Le Naour, R., Le Grand, R., Vaslin, B., Benveniste, O., Cheret, A., Raoul, H.,
Romet Lemonne, J.L., Dormont, D., (1995) Functional consequences of macrophage infection by
human immunodeficiency virus: bispecific antibody targeting of HIV-1-infected cells to Fc gamma
RI expressing effector cells. J Hematother, 1995 12, 4: 6, 579-585.

98. Grobler, S. R., van Wyk Kotze, T. J., Cleymaet, R., (1991) Fluoride concentration in
drinking water in small villages in the Cape province, J Dent Assoc S Afr, 1991 12, 46: 12,
571-574.

99. Ibrahim, Y. E., Affan, A. A., Bjorvatn, K., (1995) Prevalence of dental fluorosis in
Sudanese children from two villages with 0.25 and 2.56 ppm fluoride in the drinking water. Int J
Paediatr Dent, 1995 12, 5: 4, 223-229.

100. Walvekar, S.V., Qureshi, B. A., (1982) Endemic fluorosis and partial defluoridation of
water supplies - A public health concern in Kenya. Community Dent Oral Epidemiol, 1982 Jun,
10:3, 156-160.

101. Olsson, B., (1979) Dental findings in high-fluoride areas in Ethiopia. Community Dent Oral
Epidemiol, 1979 Feb, 7:1, 51-56

102. Tobayiwa, C., Musiyambiri, M., Chironga, L., Mazorodze, O., Sapahla, S., (1991) Fluoride
levels and dental fluorosis in two districts in Zimbabwe. Cent Afr J Med, 1991 Nov, 37:11,
353-361.

103. Zietsman, S., (1991) Spatial variation of fluorosis and fluoride content of water in an
endemic area in Bophuthatswana. J Dent Assoc S Afr, 1991 Jan, 46:1, 11-15

104. Altfeld, M., Addo, M. M., Kreuzer, K.A., Rockstroh, J.K., Dumoulin, F.L., Schliefer, K.,
Leifeld, L., Sauerbruch, T., Spengler, U., (2000) T(H)1 to T(H)2 shift of cytokines in
peripheral blood of HIV-infected patients is detectable by reverse transcriptase polymerase
chain reaction but not by enzyme-linked immunosorbent assay under nonstimulated conditions. J
Acquir Immune Defic Syndr, 2000 00, 23: 4, 287-294.

105. Beretta, A., Clerici, M., Hasson, H., Fumagalli, L., Trabattoni, D., Lillo, F., Ferrante,
P., Saniabadi, A.R., Adachi, M., Lazzarin, A., (2000) Ex-vivo purging of circulating monocytes
results in immunovirologic improvement in partially HAART responder HIV-infected patients. J
Biol Regul Homeost Agents, 2000 00, 14: 1, 27-31.

106. Blazevic, V., Heino, M., Lagerstedt, A., Ranki, A., Krohn, K.J., (1996) Interleukin-10 gene
expression induced by HIV-1 Tat and Rev in the cells of HIV-1 infected individuals. J Acquir
Immune Defic Syndr Hum Retrovirol, 1996 00, 13: 3, 208-214.

107. Smith, P. D., Chura, K., Masur, H., Lane, H. C., Fauci, A. S., Wahl, S. M., (1984) Monocyte
function in the acquired immune deficiency syndrome. Defective Chemotaxis., J Clin Invest, 1984
12, 74: 6, 2121-2128.

108. Srikanth, P., Castillo, R. C., Sridharan, G., John, T. J., Zachariah, A., Mathai, D.,
Schwartz, D. H., (2000) Increase in plasma IL-10 levels and rapid loss of CD4+ T cells among
HIV-infected individuals in south India, Int J STD AIDS, 2000 01, 11: 1, 49-51.

109. Bialkowska, A., Bialkowski, K., Gerschenson, M., Diwan, B. A., Jones, A. B., Olivero, O.
A., Poirier, M. C., Anderson, L. M., Kasprzak, K. S., Sipowicz, M. A., (2000) Oxidative DNA
damage in fetal tissues after transplacental exposure to 3'-azido-3'-deoxythymidine (AZT).
Carcinogenesis 2000 May;21(5):1059-1062.

110. Lamperth L; Dalakas MC; Dagani F; Anderson J; Ferrari R; (1991) Abnormal skeletal and
cardiac muscle mitochondria induced by zidovudine (AZT) in human muscle in vitro and in an
animal model. Lab Invest. 1991 Dec;65(6):742-751.

111. Crowley Nowick, P.A., Ellenberg, J.H., Vermund, S.H., Douglas, S.D., Holland, C.A.,
Moscicki, A.B., (2000) Cytokine profile in genital tract secretions from female adolescents:
impact of human immunodeficiency virus, human papillomavirus, and other sexually transmitted
pathogens. J Infect Dis, 2000 03, 181: 3, 939-945.

112. Kempf, W., Müller, B., Maurer, R., Adams, V., Campadelli Fiume, G., (2000) Increased
expression of human herpesvirus 7 in lymphoid organs of AIDS patients. J Clin Virol, 2000 05,
16: 3, 193-201.


Author:
The author formed and directs the Magnum-Opus Project to correct and expose the wrongs the
Manhattan Project and the abuses of openness in national security. He is former Senior
Development Staff of Oak Ridge National Laboratory and has direct experience with some of the
most toxic materials from the nuclear industry. He worked on toxic site remediation, radiation
detection, invented the USRADS survey system, and won ORNL significant event award. He
discovered high levels of hydrogen fluorides emissions from the gas diffusion plants and noticed
the link to CFS like illnesses in the worker and local community populations. He defined the
basic mechanism for CFS and HIV in national security circles in the 1980's. He claims his
inspiration for the discovery came from the icon imagery of vulcanism connected to the story of
the Ark and the environmental imagery associated with Mary controlling the venom from the Earth
entering the food chain. Author says insoluble lymph mechanism information was suppressed for
more than a decade by industry control of research, negligence on the part of CDC, ATSDR, and
EPA, and criminal cover up on the part of the DOE. He purposely chose public publication of his
work to express the need for preventive and alternative medicine to take a more balanced stance
against AMA and pharmaceutical based dominance and excessive profiteering in medicine. Return to
main page

ATOM RSS1 RSS2