A DOE Watch Exclusive Report

The serious health problems that arose from the Gulf War and its chemical poisons leading to heavy metals poisoning.


The Governments covered up environmental and health problems.

Gulf War Illness and its prime causation factors---GSH and SOD

Gulf War Illness Explained in the Simplest Terms

By: Jim Phelps
Copyright 2005

The 1991 Persian Gulf War still affects hundreds of thousands of American Veterans from the "toxic soup" that cut some 30 years off many of their life-spans. There has been much discussion of the toxic soup's components that have taken the terrible toll on those exposed. The significant toxic exposures were aluminum and mercury in vaccines, the Depleted Uranium from munitions, the oil well fires, the nerve gases that hydrolyses to hydrogen fluoride, DEET, PB, high chlorine in drinking water, methanol from "Nutrasweet" soft drinks, and other insecticides.

All these varied toxic materials leave many people mystified as to what are the main components driving the long term illnesses showing up in many of the hundreds of thousands of people sent into the Gulf War zone and others that never entered the war zone who also became sick from only the vaccines. The question becomes what is the common factor that connects all these persons leading to this similar illness pattern. There were some immediate effects due to consumption of high amounts of Nutrasweet beverages in the hot climates that put many soldiers well over the safe levels of methanol, which began some of the nervous system damage. This was made worse by damage to repair enzymes like SOD, due to varied chemical exposures that lowered this essential enzyme.

The common factor that connects to all the illness is not a mystery and is a well known effect, but one that is suppressed. The common mechanism is the loss of enzymes in the human body and the main two involved are glurathione (GSH) and SuperOxide Dimutase (SOD). Glutathione is the main enzyme that clears many toxic metals from the body and without it being at full potential toxic metals concentrations rise in the body leading to increases in free radical damage to cells via reactive oxygen damage (ROS). SOD is responsible for repair of the ROS damage to the cells. So, the main problem is both the loss of the mechanism that clears the toxic material and the loss of the mechanism that repairs the damage due to rise in the toxic materials driving high rates of ROS damage.

The other key enzyme is one called RNase L which is damaged by the high free radical effects from the toxic metals interaction with cell mitochondria. The RNase L enzyme is the key one that controls viral infections (and also mycoplasma, bacteria) within cells. High radiation generation of free radicals also damages this same enzyme class and results in viral infections that are typically controlled with these enzymes. Inner cell infections like mycoplasmas can appear that require antibiotics to control.

GSH and SOD also care for the brain and pass easily into the brain tissues. The GSH clears the brain of toxic metals, like mercury and lead, and the SOD tries to heal the damage caused by the toxic metals substituting into cell processes that lead to ROS damage. The "brain fog" or "foggy thinking" that associates with Gulf War Illness is a direct result of lowered levels of GSH and SOD in the body and is a first order sign for this type mechanism being of prime importance.

The prime causes of reduced GSH and SOD are toxic materials like HF (hydrogen fluoride), AlFx, DEET, mercury, PCB, chlorine, insecticides, and a lack of vegetables and fruits in diets. Everyone in the US today has some degree of GSH and SOD suppression and the problem worsens with age. Many of these toxic materials highly retain in the body and the leading problems come from mercury, PCBs, and fluorides. The mercury component and the bad diets lead many vets to get many of the Gulf War Illness symptoms just due to the many killed vaccines they received that employed mercury.

The reduction of the clearance of toxic metals due to GSH is easily observed in the population as it plays a direct role in why hair turns gray. Grey hair is caused principally by rising levels of Hg or mercury in the body being incorporated into the hair follicles causing the loss of pigment from the higher cellular ROS problems. Grey hair has higher levels of mercury in it than pigmented hair strands and the effect helps to pull some mercury from tissues. Grey hair for many people begins in areas of the chin and face, where the highest concentrations of mercury tend to accumulate in tissues from mercury dental fillings. With increasing age the gray hair can affect most of the head's hair. This is a common example of the effects of reduced GSH and SOD enzymes that happens with age and rise of internal retention of PCB, pesticides, HF, and Hg that act to damage GSH and SOD production.

The enzyme GSH removes toxic metals from the brain and tissues by combining the toxic metals with sulfur and then an excretion pathway via the bile into the feces and out of the body. As GSH levels in the body fall from chemical poisoning effects it places more of a load on the kidney pathway of excretion. The toxic metals loading on the kidney can become too large easily and damage the renal tubule cells leading to less excretion rate and an acid shift of the blood that enhances the toxic metals retention problems. The failure of the GSH pathway to remove metals from the body and the damage of the kidney pathway to remove metals from the body produces a rise in toxic metal retention in the body, high ROS levels, and very high risk for cancer and all the immune linked illnesses. The failure of the kidney pathway to remove toxic metals generally shows with porphyria in the urine.

Vets that came to the war zone were exposed to HF from nerve gas demolition plumes of hydrogen fluoride enzyme system poisons drifting into their breathing air space that damaged the GSH and SOD levels. Vets were also exposed to DEET, oil hydrocarbons, and insecticide sprays the also damaged GSH and SOD levels. The net result of this long term poisoning effect is a slow rise in the toxic metals (Hg, Pb, Al, Cd, etc.) concentrations in the body and a slow decline of the beneficial trace metals (Zn, Mg, Se, Cu, etc.) in the body that support the formation of GSH and SOD. One can even look at the recovery regimen that GWI researcher named Dr. Garth Nicholson recommends and find he recommends minerals and other factors that boost these beneficial trace elements and GSH and SOD. Nicholson was the first to spot mycoplasma effects in GWI, and the mycoplasma problems are also common to radiation exposures due to high levels of ROS damage to RNase L cellular enzymes in the body generated by high radiation.

This basic mechanism for illness is common to the Chronic Fatigue Syndrome (CFS) and the illnesses of the DOE gas diffusion plant workers. The most damage to the GSH and SOD in these cases is due to the rise of fluoride and HF exposures that lead to the upset of the metals metabolism in the body. The health damage is due to high levels of ROS that lead to health problems that look like they are caused by internal radiation free radical damage. The rise of the toxic metals and the acid pH shifts in the blood lead to kidney cell damage that has the appearance of DU type heavy metals poisoning. When the body's pH goes into the acid domain the metals retention is high and the ROS damage to cells extreme and usually results in cancer virus activation.

In areas like Oak Ridge where high levels of chemicals like HF kill off the GSH and SOD enzyme clearance of mercury from the body one finds higher rates of thyroid damage. High levels of mercury are well associated with hypothyroidism and Hashimoto's Thyroiditis. Sometimes the thyroid effects in Oak Ridge have the appearance of hyperthyroidism when there is too much cadmium and the high free radical damage due to loss of SOD. It is a very similar effect that damages the kidneys that potentiates toxic metals retention.

The worst effect from GWI comes from the fluoride and aluminum vaccine effects that spontaneously form AlFx compounds that mimic the pituitary hormone TSH. The AlFx compound then determines the levels of thyorid gland and liver T-3 and T-4, which program the energy levels in the mitochondria of every cell in the body. It is this effect that results in the depletion of the GSH levels needed in all the cells of the body. This effect causes the night sweats that are common to both people with CFS and GWS. It also causes the loss of restful sleep and the inability to sleep because the cells won't power down like they would under the control of the pituitary gland.

It is this thyroid hormone mimic problem that lies at the very heart of GWI, because so little of a chemical can cause such a global effect on all cells in the body. The effect that is produced is like that of hyperthyroidism, which leaves people very tired, often sleepless, and will little cellular GSH. The standard thyroid test using TSH results in misdiagnosis of hypothyroidism because these persons will test low for TSH and be uncommonly tired. This effect leads to the confusion on GWS by many doctors and it also leads to ways to cover up the health problems by testing only for TSH. Only the Thyroid Panel tests begin to show the T-3 and T-4 high level problems that the AlFx compound causes in the GWI equation.

The key to the AlFx TSH hormone mimic effect is that AlFx compounds don't follow the night and day amplitude and pulse fluctuations of the normal pituitary TSH. The AlFx compounds have drastically different bonding characteristics to TSH receptor sites of cells due to the fact that highly electronegative fluorine is involved in the site bonding. This effect results in a nearly permanent bond to the receptor sites for TSH, which highly upsets the normal thyroid hormone regulation process. It is this effect that depletes the GSH in every cell in the body and why the Al and F contamination effects are often the worst on GSH levels and the illness processes.

The bottom line is that 10 days of war took 30 plus years off the lives of hundreds of thousands of US soldiers that entered this conflict. Hundreds of thousands of Vets were exposed to some of the most retained chemical poisons on the planet that killed their GSH and SOD levels leading to health problems about like those of a 60-year-old female. Some have brain injury so severe from the toxic metals effects on the brain that look like the seizures of Minimata Disease. Gone was their prime of life and health and 20-30 year old people were suddenly given the health of life outlook for an elderly person. If one considers the typical life span these days as being 75 years, then the loss of 30 years from the life span of each of the 800,000 people in the Gulf War means 400,000 people effectively died from this toxic soup war zone.

The American Government appears interested in offering up DU as the principle reason for all the rise of cancers in Iraq after the war. This benefits the US because it conceals the main issue of wide ranging chemical damage effects from blown up oil wells and oil refineries that used HF and the oil products that damage the GSH and SOD in the human body. There is no possible way that the use of DU in Iraq has caused the wide spread illness effects in the civilian populations. On the other hand, there is little doubt that DU is directly involved in affecting the health of persons that cleaned up DU hits on vehicles, those that stirred up the DU dusts hunting war souvenirs, and some of the Iraq population in close proximity to high level DU contamination. DU oxide dusts of the nano-meter size particles easily gain entry to the body via skin and via lung and has toxic characteristics similar to mercury. The DU issue is being politicized to hide the very much larger problems of chemical effects on GSH and SOD. The chemical damage factor to GSH and SOD causes the DU retention time in the body (or the biological half-life) and ROS damage to be greater, and the same effect applies to all other toxic metals.

All of the studies for DU's biological half life is done on healthy animals with normal levels of GSH and SOD, and without the mercury toxicity effect on renal cells. When chemical damage to the GSH and SOD levels in the body is included for the increased toxic metals damage to kidney calls, the biological half-life of DU and other metals is made much longer. The use of mercury in vaccines helped to impair kidney cells and the damage is high as mercury also suppresses GSH and SOD. All the GWI studies that use the single challenge DU exposure for the biological half-life numbers that don't include the chemical damage to the enzyme clearance of toxic metals are in error. With the reduction of GSH and the bile pathway comes high loading of the renal cells with DU, Hg, and other toxic metals that damage these cells and set up higher levels of toxic metals retention in the body due to highly impacted losses of the two main clearance mechanisms.

The DU armor on US tanks is sandwiched between sheets of aluminum and when the material is hit, not only DU dusts come off but Aluminum dusts do also. The aluminum dusts pose an even worse health risk than the DU, because they form the AlFx compounds in the body that upset the TSH pituitary regulation process and the prime factor that triggers GWS via GSH depletion. These exposures would add on top of the aluminum in the vaccine exposures.

The War in Iraq also is one of political affectations, rather than any real threats against the US. Bush-41 holds a huge interest in the Kuwait oil fields and he was the first US operation to open up Kuwait's oil fields. Iraq was considered a threat to Israel and the Jews. Government engineered the Iraq conflicts for Israel's interests and not those of the US. In so doing, persons have killed some 400,000 effective lives in the US and cost the US trillions of dollars for the interests of a foreign power that has little interest in the US other than trickery to promote their own group aggrandizement interests. Big oil person Condi Rice, who was trained by Madeline Albright's father in Denver, Co., is part of the Jewish problems. Oil is being used by Israel to leverage US into doing their bidding. Even the 911 event was about Israel's agents helping to facilitate the WTC attacks and helping the Arab factions pull off the attacks. The pattern that has gone on since the times of JFK's death fits the Mossad Logo that Reads: "By Way Of Deception Thou Shalt Do War"

The Persian Gulf Wars are all about the concepts of deceit and treachery and this method is being used to conceal the main health effects of GSH and SOD damage via chemical effects on enzymes. The effect is most pronounced for hydrogen fluoride systemic poisoning effects on enzymes using metals. This simple and very basic of effects is the principle damage vector to most all persons health in the US and the very roots of the system of profits for the AMA based medical system. When this very basic system for cause and effect on health becomes exposed, large parts of the medical system in the US will be tossed aside as being too expensive and insensible. Again, the main cause of Gulf War Illness and the very war itself is about politics and money and not about any mystery causation.

The very roots of the GOP dominated industry is on the very verge of being found out for the degrees to which they have abandoned citizens health to favor making uranium, aluminum, and other strategic metals to gain control via wars. Long ago the US decided to cover up this major cause of ill health in the US and use AMA medicines to mask the symptoms and control the damage factors. The Rockefeller based AMA and big oil is right in the middle of the cover-ups. Even religion, which is highly GOP oriented, is being used to help cover up the health associations from toxic emissions that appear in the biblical times.

The very same diversion tactics have been used in Oak Ridge to conceal the HF dominated health damage to workers and area residents health. In Oak Ridge radiation and heavy metals are played up as the direct cause for what is causing everyone's health problems. The real problem is a two step progression due to chemical damage from HF, PCB, and Hg to enzymes GSH and SOD leading to factors that look like radiation damage effects to cell enzymes that regulate viruses and cause the rise of toxic metal retention. Oak Ridge uses deception to protect themselves from the massive lawsuits and the Govt. payout for the health damage their operations have caused to a large area in and around Oak Ridge. The local medical system uses the large-scale cover up of the problems as a reason to make great profits treating all the additional illnesses and dispensing large amounts of drugs to those affected. Oak Ridge has long had an understanding with the local medical community that they won't disclose the main causes of illnesses or diseases, if they associate in any way to the DOE operations in Oak Ridge. It is this same system of ultimate deceit and treachery used to fool the citizens that has been extended to those veterans of the Gulf Wars and the people of Iraq and other sites where the toxic soup factors have become extreme.

Both GSH and SOD are liver oriented enzymes and required in every cell to work properly. GWI's prime cause and effect leads off with chemical damage to the liver's production of GSH and SOD. When this liver enzyme system is chemically poisoned the body's toxic metal load begins to increase and as this occurs these toxic metals interact with the cell mitochondria that then causes the increase in the ROS levels within the cells. It makes perfect since that these two areas would become the first affected, as these are the most vulnerable areas for chemical and metal poisoning effects on the body. The very same effect occurs with aging, as levels of these enzyme poisons rises in the body with age.

Even the factors of high rates of ALS seen in the GW vets is directly associated with the GSH and SOD enzymes. ALS is associated with upsets of copper and manganese that form these enzymes. The problems of Mad Cow and Prion linked illnesses are caused by these same factors. Mad Cow effects come from a systemic shift toward Mn-SOD from the Cu-Zn-SOD, and loss of Mn dependent enzymes that cleave viral RNA within cells. When sulfur bearing compounds like DMSO are applied to Mad Cow affected brain tissues, the plaques dissipate, and DMSO appears to act as GSH in supplying the sulfur to remove the toxic metals from the brain that attract the SOD needed for myelin repair.

For those of you who want to look more deeply into the issues of how GWI and CFS are well association let me recommend reading this better documented piece at:
"http://www.doewatch.com/cfs.html"
and see this for more fluorine details:
"http://www.doewatch.com/f.html"

This health problem's main vector from damage to GSH and SOD has been long known back in time and is part of the story of Prometheus and damage to the liver from exposure to volcanic emissions, HF. Hercules rescued Prometheus from liver damage problems is the heart of this same health damage vector. If one notes, the Prometheus figure is part of Rockefeller Center in New York City, and this same mechanism is what makes the doctors of the Rockefeller AMA based system their wealth. The main problem of GWI is the greed of GOP oriented system of AMA profiteering by suppression of how industry poisons the GSH and SOD liver enzymes leading to immune related illnesses in the population.

The Prometheus story is the Greek version of health effects from nature's emission of toxic materials, but versions of the same theme carry back in time to the stories of Noah and Moses, and their very similar volcanic associated health effects. The major problem blocking the real story on GWI being told by the US Govt. is all about near total corruption in US politics and the US version of religion based on alterations from the truths of the old biblical narratives.

This is an effort to make the real story public, as we survive in each other's care. The real story here is about being dutiful toward the people of the US and not its corrupted operations that attempt to deceive the people from the truth. It is these untruths in religion and cover ups in health that are at the very roots of the terrorism equation, which Israel and the GOP exploit to the harm of every citizen in the US.

The People of America have never been so disenfranchised from control of their Govt. nor the US Constitution as threatened as now from this corrupted political and religion process. The entire US system is at risk from these cover-ups in health linked to industry emissions and racketeering process used to hide the massive problems.

REFERENCE CITATIONS:

Title
Role of glutathione and hepatic glutathione S-transferase in the biliary excretion of methyl mercury, cadmium and zinc: a study with enzyme inducers and glutathione depletors.

Author
Gregus Z; Varga F

Source
Acta Pharmacol Toxicol (Copenh), 56(5):398-403 1985 May

Abstract
The effect of hepatic glutathione (GSH) depletion and enzyme induction on hepatic glutathione S-transferase (GST) activity, biliary excretion of GSH, methyl mercury, cadmium and zinc was studied in rats. The GSH depletors, methyl iodide and diethyl maleate, did not influence hepatic GST activity but, depending on the substrate used, benzo(a)pyrene, phenobarbital, pregnenolone-16 alpha-carbonitrile (PCN) and trans-stilbene oxide (TSO) increased it by 16-33, 44-89, 53-97 and 208-279%, respectively. GSH depletors decreased (-88%), benzo(a)pyrene and TSO did not affect, phenobarbital and PCN increased (+113 and +149%) the transport of GSH into bile. The biliary excretion of methyl mercury, cadmium and zinc was reduced by GSH depletors (-97, -74 and -93%), and enhanced by phenobarbital (+139, +280 and +220%) and PCN (+150, +121 and +160%). Treatment with benzo(a)pyrene and TSO did not affect the excretion of methyl mercury and zinc into bile, but decreased that of cadmium. These results do not provide evidence for the role of hepatic GST but strongly support the importance of biliary GSH excretion in the hepatobiliary transport of methyl mercury, cadmium and zinc. It is assumed that phenobarbital and PCN enhance the biliary excretion of these metals by increasing the transport of GSH, the carrier molecule, from liver to bile.

Title
Effect of lipoic acid on biliary excretion of glutathione and metals.

Author
Gregus Z; Stein AF; Varga F; Klaassen CD Address Department of Pharmacology' University Medical School of P]ecs' Hungary.

Source
Toxicol Appl Pharmacol, 114(1):88-96 1992 May

Abstract
Several metals are excreted in bile as glutathione complexes' and their biliary excretion is facilitated by increased hepatobiliary transport of glutathione. The present study analyzed the effect of lipoic acid (LA; thioctic acid; 37.5-300 mumol/kg' iv)' an endogenous disulfide which can be reduced in vivo to a dithiol' on the hepatobiliary disposition of glutathione-related thiols and the biliary excretion of metals (10 mumol/kg' iv) in rats. Administration of LA enhanced the biliary excretion of reduced glutathione in a dose-dependent fashion. Despite increasing glutathione output' LA (150 mumol/kg' iv) did not increase' but rather decreased' the biliary excretion of methylmercury' cadmium' zinc' and copper' which are transported into bile in a glutathione-dependent manner' as indicated by a marked reduction in their biliary excretion after diethyl maleate-induced glutathione depletion. In contrast' biliary excretion of inorganic mercury' which is minimally affected by glutathione depletion' was dramatically enhanced (12- to 37-fold) by LA administration. Following inJection of LA' the concentrations of endogenous disulfides in arterial blood plasma (e.g.' cystine' glutathione disulfide' cysteine-glutathione' protein-cysteine' and protein-glutathione mixed disulfides) were considerably diminished' while the levels of endogenous thiols (e.g.' glutathione and cysteine) were increased. This finding indicates that LA' probably after enzymatic conversion to dihydrolipoic acid' can reduce endogenous disulfides to thiols. It appears that LA induces the transport of glutathione into bile by the temporary formation of dihydrolipoic acid-glutathione mixed disulfide' which after being translocated into bile is cleaved to LA and reduced glutathione. Because the glutathione molecule thus transported into bile cannot complex metals at the thiol group' this might be the mechanism for the observed failure of the LA-induced increase in biliary excretion of glutathione to enhance the hepatobiliary transport of metals that are transported into bile as glutathione complexes (i.e.' methylmercury' cadmium' zinc' and copper). The observations also raise the possibility that endogenous dihydrolipoic acid' by forming a stable complex with mercuric ion' may play the role of a carrier molecule in the hepatobiliary transport of inorganic mercury.

Title
Biliary secretion of glutathione and of glutathione-metal complexes.

Author
Ballatori N; Clarkson TW

Source
Fundam Appl Toxicol, 5(5):816-31 1985 Oct

Abstract
As bile is the main route of elimination of many metals, a large number of studies have been directed toward the characterization of the hepatobiliary transport of both endogenous and exogenous metals. Although some progress has been made, we still know little of the basic mechanisms involved in the hepatocellular uptake of metals, in their intracellular translocation and metabolism, or in their transport into bile. Our recent studies have focused on the last step in the hepatobiliary transport of mercury, namely, the secretion of the metal from liver cells into bile. The rate of secretion of methyl and inorganic mercury into bile was low in suckling rats and rapidly increased to adult rates soon after weaning. These changes closely followed similar developmental changes in the biliary secretion of reduced glutathione (GSH). When GSH secretion into bile was completely inhibited, without changing hepatic levels of GSH or mercury, mercury secretion was also completely blocked. mercury secretion paralleled individual and sex-related differences in GSH secretion. At the same time, the secretion of mercury was independent of bile flow, of the thiol and mercury concentration gradients between bile and liver cells, and of those between bile and plasma. Our results, therefore, indicate a close coupling between the secretion of mercury and that of GSH. These in vivo findings, along with in vitro studies by others in vesicles isolated from the canalicular membrane of the liver cell, indicate a carrier-mediated transport system for GSH, but the nature of the linkage of this transport system with mercury secretion is not yet fully established. Our data and those in the literature are consistent with the involvement of at least two steps in the movement of mercury from liver cells to bile--the formation of a mercury-glutathione complex in the liver cell, followed by the secretion of this complex through a process closely linked to GSH secretion. The identification of GSH as an endogenous complexing agent in the transport of metals between tissues and body fluids now permits the design of therapeutic strategies aimed at exploiting this transport vehicle to effect the removal of metals via physiological routes of excretion. The present discussion considers the role of GSH in the hepatobiliary transport of metals. In doing so, a brief review is given of current understanding of hepatic GSH metabolism and transport.