Gulf War Syndrome
Gulf War syndrome (GWS), affecting a number of men and women who served in the Persian Gulf War, represents a group of medical and psychological complaints, including fatigue, respiratory illness, muscular pain, spasms, skin rash, memory loss, dizziness, peripheral numbness, and sleep disturbances. A 1996 VA study (Kang et al. 1996) reported that Gulf War veterans were 50% more likely to die in a motor vehicle accident than military personnel not sent to the Gulf War. Robert W. Haley, University of Texas Southwestern Medical Center, Dallas, reported similar findings but added in an article published by the Associated Press that the Gulf War veteran also has a higher rate of depression and suicide. Haley correlated these findings medically with individuals who have sustained brain injuries (Haley 1997; 1998; Haley et al. 1997a; 1997b).
Between August 1990 and March 1991, the U.S. deployed more than 697,000 troops in Operation Desert Shield and Operation Desert Storm. The majority of the troops were stationed in Saudi Arabia, Kuwait, or aboard ships in the Red Sea. Of these, more than 100,000 (one in seven) have reported serious health concerns to the Department of Veterans Affairs or the Department of Defense. Unfortunately, some family members of those stricken gradually display signs and symptoms of the syndrome as well, suggesting an infectious explanation of the illness.
Speculative Causes of GWS
When causative factors are obscure and not unilaterally accepted, as in GWS, speculation oftentimes overrides a precise explanation. This appears true in GWS. Suppositions are many in regard to the contributory sequence that terminated in the physical and psychological symptoms familiar to veterans diagnosed with GWS.
The postulations being most scrutinized are exposure to toxins in the environment (such as oil fires), chemical and biological weapons, low-level uranium exposure, an immune reaction to a drug administered to protect against attacks of Soman (a nerve gas), dust, and even the immunizations (specifically, the anthrax vaccine and polio booster) given to the troops prior to deployment. Any of these theories could explain a state of unwellness when imposed upon a vulnerable host.
Nutritionally oriented clinicians subscribe to the rationale, "If you can't eat it, don't smell it." This caveat was not possible to heed in the Gulf War environment. More than 500 oil well fires were burning in Kuwait during June 1991, emitting extremely high levels of particulate matter. Detections of sarin, a potentially fatal nerve gas, tabun, a neuroparalytic toxic agent, and sulfur mustard gas were reported during the period of January 19-21, 1991. Troops responsible for cleaning up Iraqi ammunition dumps may have been exposed to depleted uranium, a form of uranium used in munitions because of its density and metallurgical properties. Korenyi-Both et al. (1992) reported that the combination of Saudi dust and pigeon droppings ignited an acute hyperallergic reaction that has come to be known as Desert Storm pneumonitis or Al Eskan disease. There are those who question whether the very preventative measures--drugs and vaccinations--employed to protect the troops from chemical or biological warfare may be the agents provoking the illness. Confounding the inquest, manifestations of the syndrome are unpredictable. Just as cancer can occur long after exposure to the causative factor, the complications arising from GWS can be just as unpredictable.
Extended Health ConcerNS
The illnesses apparent in the Gulf War veterans are not just nuisance complaints, but represent concern for vulnerability to catastrophic disease. Thousands of U.S. soldiers have died of infectious diseases, chemical exposure, and other causes resulting from Operation Desert Storm.
On April 6, 2000, the Associated Press reported that the VA announced a year-long study to determine whether there is a higher incidence of Lou Gehrig's disease--amyotrophic lateral sclerosis or ALS--among the veterans of the Gulf War. It appears that at least 28 Gulf War veterans have been diagnosed with this deadly disease. Researchers are interested in locating other veterans diagnosed with ALS or other motor neuron diseases who were actively serving duty between August 2, 1990, and July 31, 1991, regardless of location. Those who did not go to the gulf area will serve as part of the control group. Eligible veterans may call (877) 342-5257.
Dr. Bob Garry of Tulane University tested 400 veterans for antibodies to squalene and found that 95% of those individuals with GWS had high levels of the antibody (Asa et al. 2000). Though a participant in metabolic processes, squalene, found in shark liver oil, some vegetable oils, and the human liver, can also be incorporated into a vaccine to accelerate, enhance, or prolong a specific immune response. Mystifying the sleuthing process, information currently available states that squalene, though once considered an immunologic potentiator, was never used as an adjuvant in the vaccines administered to the Gulf War veterans. Because the antibody to squalene is commonly found in individuals plagued by GWS, applying the Antisqualene Antibody Assay to stricken veterans may prove a valuable tool in diagnosis. It has been hypothesized that GWS is a result of an autoimmune reaction, in which the immune system inappropriately turns on its own natural supply of squalene. The assay is available through Autoimmune Technologies, LLC, of New Orleans, LA.
Mycoplasmal Infections and GWS
Rare germs called mycoplasmas are often evidenced in individuals with GWS. Mycoplasmas are bacteria-like organisms that cause atypical pneumonia in confined groups, such as military personnel. They are small, free-living, self-replicating organisms that can cause a respiratory, flu-like illness that can progress to systemic chronic fatigue syndrome-like or fibromyalgia syndrome-like illness, sometimes advancing to multiple sclerosis-like, amyotrophic lateral sclerosis-like, and arthritis-like symptoms. Researchers found that slightly less than half of very ill Gulf War veterans with signs of chronic fatigue-immune deficiency syndrome (CFIDS) or fibromyalgia syndrome (FMS)--that is, fatigue, depression, joint pain, cognitive disturbances, burning muscles, faltering speech, headache, incontinence, alimentary disorders, sore throat, tinnitus, or loss of libido--involved mycoplasma infections. Although these microorganisms do not directly cause CFIDS, FMS, GWS, or rheumatoid arthritis (RA), mycoplasmas appear to encourage their progression and exacerbation.
Most microorganisms like mycoplasmas are not considered important human pathogens when they are found at superficial sites, such as the oral cavity or intestines, as symbiotic gut flora, but some species, such as M. fermentans, M. penetrans, M. pneumoniae, M. genitalium, M. pirum, and M. hominis, have the capability to penetrate blood circulation and colonize various tissues. The study was reported by Rawadi et al. (1996).
Sexual Impairments and Birth Defects
Whether Gulf War personnel have an increased incidence of infants born with birth defects compared to nondeployed personnel is unclear. Of the 75,414 infants born in military hospitals during the study period, seven presented with some of the ocular, aural, or cardiac impairments associated with a condition commonly referred to as Goldenhar syndrome. Only five of the seven babies, however, were born to Gulf War veterans (34,069 births), although the remaining two infants were born to nondeployed military personnel. Some affirm that birth defects are not alarmingly disproportionate among Gulf War veterans; others angrily argue that the incidence is much higher than among the nonmilitary population, with some incidences of infantile defect not being appropriately recorded. Sexual malperformance, such as impotence, has been reported among service personnel participating in the Gulf War.
Why Not EveryoNE?
Researchers observed illnesses resembling GWS in laboratory animals exposed to a mixture of cholinesterase inhibitor insecticides and pyridostigmine; soldiers in the Persian Gulf War have been exposed to both agents.
Before addressing the impact that such toxins could have upon exposed individuals, it is important that the autonomic nervous system be briefly explained to the reader. The autonomic nervous system, regulating involuntary functions, consists of two divisions, referred to as the sympathetic and the parasympathetic nervous system. Each division performs functions within the body that influence cardiac muscle, smooth muscle, and glandular activity.
Individuals are born with a sympathetic, parasympathetic, or balanced nervous system, referred to as a metabolic type. Our metabolic type identifies us individually and contributes to the personality that we display to society. Passivity, aggression, right brain/left brain preeminence, sleep patterns, etc., are but a few of the characteristics metabolic dominance influences. But, diet, exercise, supplements, exposure to toxic materials, and stress can make more virulent the responsiveness of the already dominant division. The body is healthiest when neither of the two divisions holds supremacy, but rather when balance prevails.
Cholinesterase inhibitors can turn the volume up on the parasympathetic nervous system by allowing acetylcholine, a neurotransmitter, to accumulate at the cholinergic receptor, thus producing effects similar to excessive stimulation of cholinergic receptors throughout the central and peripheral nervous systems. An already parasympathetic dominant individual could, after sufficient exposure to cholinesterase inhibitors, display a heightened parasympathetic expression.
Dr. Nicholas Gonzalez (www.dr-gonzalez.com), a New York physician, specializing in cancer treatment, has many times insightfully explained the disease-promoting role of the autonomic nervous system, when the two divisions become unbalanced. Dr. Gonzalez explains that the protective closure around a cell and the nucleus that controls the exchange of materials between the cell and its environment is referred to as the membrane. The membrane protects the contents of the cell with the same fervor that a solicitous parent extends to a child. It is when the membrane loses its worthiness, a process enacted by excessive calcium loss, that the cell becomes flimsy and unprotected. If toxic materials gain entry into the nucleus, the genetic control center of the cell, damage to the cell's DNA can occur quite rapidly. Should this happen, serious destruction has befallen the host.
The membrane of the cell is different in the sympathetic and the parasympathetic individual. The sympathetic dominant individual tends toward a tighter membrane that stores waste accumulations quite well. It takes longer for toxic materials to migrate into the nucleus because the tightness of the nuclear membrane is embracing and, thereby, protective. But when the maximum load in the nuclear area has been reached, anomalies, such as tumors, may become apparent.
By contrast, the cellular and nuclear membrane, according to the work of Dr. Gonzalez, in a parasympathetic individual tends to be weak and leaky, allowing noxious materials ad libitum entry into cells. The entry of contaminants is met with slight opposition, as the cell membrane exercises sparse resistance against the invader. Noxious materials, as well as viruses, find little hindrance passing through the membrane and gaining entry into the cell.
This bit of neurophysiology may best explain the poisoning that appears to have occurred in several of the Gulf War veterans. Which of the theories, i.e., exposures to low-level uranium, oil fires, chemicals of warfare, etc., is accurate when defining the causative factor in GWS? It may not matter, because, in reality, any of the theories or all of the theories may be accurate. Any noxious exposure was too much for some of the veterans. Metabolic dominance may have made some more immediately vulnerable to the exposures; for others, the appearance of Gulf War illnesses may be longer in appearing. The effects of the exposure may take several twists before full understanding of the depth of the devastation is reached, but the cell membrane appears to be a principal player in all of the scenarios.
Dr. Jeffery Bland, Ph.D., of the Institute for Functional Medicine, reported that the first signs of chronic toxicity may appear as neuro- and immunotoxicity. Dr. Michael R. Lyon, M.D., of the Oceanside Functional Medicine Research Institute, Nanaimo, British Columbia, stated that the nervous and immune systems are highly sensitive to oxidative stress and xenobiotics, that is, drugs and organic poisons. He points out that both the nervous and immune systems have a powerful memory, which means they have tremendous capacity for recalling exposure to substances to which they have become sensitive. They become increasingly sensitized to these agents as their immune system builds antigenic memory.
Classic studies involving rats showed that exposure to a poison and a simultaneous whiff of camphor later produced serum sickness or autoimmune crisis when the animals were exposed to only a sniff of camphor. The immune system was so hypervigilant in protecting against the poison that even the scent of the camphor signaled an alert. Too many of us have, either by neglect or happenstance, been exposed to environmental pollutants that may be damaging either to the nervous or the immune system. Dr. Lyon warns that attention deficit disorder, FMS, and CFIDS are going to force society into looking at these disorders from a toxicological perspective.
Hair analysis, if properly conducted, can be a dependable assessment tool in determining toxicity from heavy metals. Detection of chemical toxicity can be made by urinary organic acid analysis and by measuring blood and fatty tissue for suspected chemicals. Concurrently, the liver should be tested in regard to serum bilirubin and enzyme levels.