Gulf war syndrome (GWS)is now officially a disease. It shares many of the symptoms of chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity and post traumatic shock syndrome. In other words, GWS is the body’s response to neurotoxins (acetylcholinesterase inhibitors) under inflammatory conditions.
The nervous system has to detect external signals, transmit the sensory information to the brain, process the information, transmit signals to peripheral organs/muscles, and stimulate responses in peripheral organs/muscles. At the molecular level, all of this detection and transmission of signals is accomplished by small molecules binding to and changing the shape/function of proteins. Disrupting the interaction between the small signal molecules (neurotransmitters) and their protein receptors is used throughout nature as an attack on the most vulnerable animal characteristic, the nervous system. Examples of nerve system attackers include mushroom toxins, plant alkaloids (atropine), spider/insect/frog/snake venoms, organophosphate/chloride pesticides, and mustard/nerve gas.
During the Gulf War, several chemicals that mimic neurotransmitters were used with the intent to protect soldiers. The neurotransmitter mimicked was acetylcholine, which is the signal used between peripheral nerves and muscles. Nerve gas targets acetylcholine signaling by blocking the enzyme, acetylcholinesterase, that sits in the space between the nerve and muscle and destroys the acetylcholine in preparation for the next signal. I have illustrated a model of the acetylcholine enzyme and have an inhibitor (grey and red) bound in the cavity of the active site of the enzyme. The active site is lined with hydrophobic tryptophan (yellow) and tyrosine (orange) amino acids.
The pesticid
es used by the soldiers were designed to kill or repel insects, but they also act as acetylcholine mimetics and bind to acetylcholinesterase. These include Lindane (left), Permethrin (right) and DEET (lower left).
The American soldiers were also forced to take a chemical to protect them from nerve gas. This compound, pyridostigmine (lower right)
bind reversibly to acetylcholinesterase and since nerve gas is very reactive, presumably the pyridostigmine will protect some of the acetylcholinesterase until the nerve gas is depleted.
Unfortunately it appears that both the insecticides and the pyridostigmine had a permanent impact on the nervous systems of many of the Gulf War soldiers. Soldiers from other countries did not use the same chemicals on their soldiers, so they were not similarly affected.
It is now fairly well established that pesticides and pyridostigmine were involved in causing Gulf War Syndrome, but very little research has been performed to explain how these chemicals cause the damage or what therapy can reverse the damage.
It appears to me that GWS occurs in similar manner to related illnesses, e.g. chronic fatigue syndrome, multiple chemical sensitivity, fibromyalgia, which can also be induced by organophosphate pesticide exposure. Two insults to the body appear to be needed: acetylcholine signal disruption and inflammation. The acetylcholine mimetics (pesticides, pyridostigmine) disrupted the nervous system and numerous immunological, infectious, chemical and emotional stresses generated a high level of chronic inflammation. The vaccine against anthrax and exposure to burning oil wells may have contributed to inflammation.