Reply #79: Okay, here we go -- a fair amount of background info

[tpsbmam]

From Gulf War and Health: Volume 1. Depleted Uranium, Pyridostigmine Bromide, Sarin, and Vaccines

Gulf War soldiers were exposed to sarin, cyclosarin and other toxic chemicals at the same time. (And, of course, depleted uranium.)

The drug pyridostigmine bromide (PB) is pharmacologically similar to sarin and other organophosphates, but it is a member of a different chemical class, the carbamates. Both PB and sarin exert their effects by binding to and inactivating the enzyme acetylcholinesterase (AChE). The binding of sarin to AChE is irreversible, whereas the binding of PB is reversible.

Since AChE is responsible for the breakdown of the neurotransmitter acetylcholine (ACh), the inactivation of this enzyme results in a dramatic elevation of ACh levels at cholinergic synapses.

Widespread overstimulation of muscles and nerves induced by excessive levels of acetylcholine is primarily responsible for the acute cholinergic syndrome triggered by exposure to sarin and other organophosphate (OP) nerve agents.

Okay, now, the paragraphs below are from Gulf War Illness and the Health of Gulf War Veterans: Scientific Findings and Recommendations (2008).

A fair amount of the research has looked at the effects of stress/extreme stress coupled with chemical exposures, e.g.:

Neurotoxicologists at Duke University have conducted extensive research evaluating interactive effects of Gulf War-related exposures using protocols designed to parallel levels actually encountered by Gulf War veterans in theater, in the presence and absence of stress. This has included studies of the combined effects of low-level exposures to PB, permethrin, and DEET together—both with and without concurrent exposure to a moderate level of restraint stress. Results indicated that combined exposure to PB, DEET, and permethrin, in combination with stress, produced disruption of the blood brain barrier and neuronal cell death in four specific brain regions—the cingulate cortex, the dentate gyrus, the thalamus, and the hypothalamus.6 The combination of chemicals plus stress also produced reduced AChE activity in the forebrain. These effects were not observed with either stress or low-dose chemicals alone. A second report indicated that, in areas of the brain where there was no apparent disruption of the blood brain barrier, AChE activity was decreased in the midbrain, brainstem, and cerebellum. Significant neuronal cell death and evidence of glial cell activation were also observed in the cerebral cortex and hippocampus. Again, these changes were observed only following combined exposure to stress and low-level exposure to the three chemicals, and not as a result of stress or chemicals alone.

<snip>

Taken together, human and animal studies indicate that extreme and/or sustained stressful experiences can precipitate short term somatic health problems as well as sustained psychiatric illness. There is no evidence indicating whether more moderate stressors, of limited duration, is associated with the development of the types of symptom complexes associated with Gulf War illness, particularly symptoms that persist for an extended period—17 years—after cessation of the stressful experience. Questions also remain concerning the potential for stressors in theater to have altered or amplified the biological effects of some chemical exposures encountered in the Gulf War. Early suggestions that stress allows PB to enter the brain through a general disruption of the blood brain barrier have not been supported, but more recent studies have suggested that stress may exacerbate effects of PB in more delineated ways, for example, enhancing its effects on autonomic regulation. Animal studies have also demonstrated biological effects resulting from stress in conjunction with combined chemical exposures—effects that exceed those of chemicals or stress alone. Human studies that have evaluated effects of stress in relation to low-level exposure to PB, permethrin, and DEET for short periods have found no significant effects on cognitive or physical performance.

From a summary on research:

Studies indicate that the large majority of Gulf War veterans with chronic multisymptom illness do not have psychiatric disorders. It is therefore important that healthcare, research, and policy decisions concerning ill Gulf War veterans not be based on unsupported assumptions that Gulf War illness is primarily a psychiatric condition or that it was caused by psychological stressors during deployment. However, some veterans with Gulf War illness are also affected by psychiatric disorders, and it is important that those veterans are properly diagnosed and treated for those conditions.

There's way more at the report link. I'm exhausted, dizzy and not at all sure I provided the most pertinent or informative paragraphs. But the research is out there!