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What is Gulf War Syndrome (GWS)? |
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General Information
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Etiology (Causation) |
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The NO/ONOO- cycle is implicated by Pall as being a plausible etiology for Multiple Chemical Sensitivities (MCS), Fibromyalgia (FM), Chronic Fatigue Syndrome (CFS), Post-Traumatic Stress Disorder (PTSD), and Gulf War Syndrome. Peroxynitrite (ONOO-) is oxidized from nitric oxide. Excess peroxynitrite depletes energy stores, which is perceived to cause extreme fatigue (Pall, ND). Of more interest to those who suffer from MCS is the fact that peroxynitrite breaks down the blood brain barrier and excess levels allow greater access to the brain (Pall, ND). This greatly increases the effects of chemicals on the brain. Essentially a non-MCS person has a barrier that protects the brain from damage from low-level chemical exposure, however a person who suffers from MCS has little or no barrier making the brain subject to increased damage and reactivity with minute exposures most people do not react to. The key effect of nitric oxide (NO) is that it inhibits cytochrome P-450 activity and slows degradation of hydrophobic organic chemicals (Pall, ND). This means that excess nitric oxide slows down the body’s natural detoxification processes leaving MCS patients subject to the effects of chemical exposure longer than non-sufferers. Between a reduced blood-brain barrier and increased time to naturally detoxify the body, MCS patients are subject to permanent and long-term brain and nervous system damage which includes toxic encephalopathy.
“The only etiologic mechanism proposed for each of these is a vicious cycle mechanism involving elevated levels of nitric oxide and its oxidant product, peroxynitrite. This cycle may be initiated by a variety of diverse short-term stressors, including viral organic solvent exposure, and exposure to three classes of pesticides, organophosphorus/carbamate pesticides, organochlorine pesticides and pyrethroid pesticides). Each of these short-term stressors are known to be able to trigger responses that lead to increases in nitric oxide levels. Indeed, other initiating short-term stressors, including a protozoan infection, carbon monoxide exposure, thimerosal exposure and ciguatoxin exposure are also known or thought to act to increase nitric oxide levels, as well” (Pall, 2006). |
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Prevalence |
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Callender, TJ, et al. (1995). Evaluation of chronic neurological sequelae after acute pesticide exposure using SPECT brain scans. Journal Toxicology & Environmental Health. 41:275-284.
Caress, S., & Steinemann, A. (2003). A Review of a Two-Phase Population Study of Multiple Chemical Sensitivity. Environmental Medicine. 111, 1490 - 1497.
Davidoff, L. (1989). Multiple Chemical Sensitivities (MCS). The Amicus Journal. Winter.
Ferrie, H. (October 2003). Multiple Chemical Sensitivity: Government and Medical Science Finally Recognize Crippling Effects of MCS. Vitality, Retrieved May 17, 2006, from http://www.vitalitymagazine.com/node/112 Gibson, P. (2005). Understanding & Accommodating People with Multiple Chemical Sensitivity in Everyday Living. Independent Living Research Utilization.
Haley, RW, Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3):227-33.
Heuser, G, et al. (1994). Neurospect findings in patients exposed to neurotoxic chemicals. Toxicology & Industrial Health. 10:561-571.
McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji, V (2004). Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR]. International Journal of Epidemiology 33, 1-8.
Meggs WJ, Dunn KA, Bloch RM, Goodman PE, Davidoff AL (1996). Prevalence and nature of allergy and chemical sensitivity in the general population. Archives of Environmental Health. Jul-Aug;51(4):275-82.
Meggs, WJ (1999). Mechanisms of allergy and chemical sensitivity. Toxicology and Industrial Health. 15:3-4, 331-338.
Multiple chemical sensitivity: a 1999 consensus. Arch Environ Health. 1999 May-Jun;54(3):147-9.
Pall, M. (ND). Multiple Chemical Sensitivity: The End of Controversy. Washington State University School of Molecular Biosciences, Retrieved May 18, 2006, from: http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm
Pall, M (2006). The NO/ONOO- Cycle as the Cause of Fibromyalgia and Related Illnesses: Etiology, Explanation and Effective Therapy. Washington State University School of Molecular Biosciences.
Pall, M (2003). Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism. Environmental Health Perspectives. 111:12, 1461-1464.
Pall, M. (2001). Multiple Chemical Sensitivity - The End of Controversy. Washington State University, School of Molecular Biosciences, Retrieved May 17, 2006, from http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm
Schnackenberg,E. et al (2007). A cross-sectional study of self-reported chemical-related sensitivity is association with gene variations of drug-metabolizing enzymes. Environmental Health.
Ziem, G (2001). Medical Evaluation and Treatment of Patients with Chemical Injury and Sensitivity. National Institute of Environmental Health Sciences.
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Treatment |
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The following agents have been predicted to be useful by Dr. Pall and Dr. Ziem (Pall, 2006) in the Pall/Ziem protocol to down-regulate the NO/ONOO- cycle biochemistry:
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References |
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Nebulized Inhaled Reduced Glutathione (RX Only) Nebulized Inhaled Hyroxocobalamin (RX Only) Mixed Natural Tocopherols Buffered Vitamin C Magnesium as Malate Four Different Flavonoid Sources: Ginkgo Biloba Extract, Cranberry Extract, Silymarin, & Bilberry Extract Selenium as Selenium-Grown Yeast Coenzyme Q10 Folic Acid Carotenoids Including Lycopene, Lutein and Alpha-carotene Alpha-Lipoic acid Zinc (modest dose) Manganese (low dose) Copper (low dose) Vitamin B6 in the Form of Pyridoxal Phosphate Riboflavin 5’-Phosphate (FMN) Betaine (Trimethylglycine) Green Tea Extract Acetyl L-Carnitine
For more information on treatments for MCS, see Medical Treatment. |
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