Abstract

Abstract : Gulf War Illness (GWI) is one of many post-war syndromes with different ostensible origins. Several investigators have pointed out that GWI symptoms are similar to the symptoms of such disorders as chronic fatigue syndrome (CFS), post-traumatic stress disorder (PTSD), fibromyalgia, and neutrally mediated hypotension (NMH), all of which are thought to arise from disorders of the autonomic nervous system. This project tests the hypothesis that autonomically-mediated GWI is not synonymous with PTSD, CFS or NMH, but shares a number of autonomic symptoms that are common to these conditions. Our hypothesis is that individuals who are autonomically hyperresponsive are more likely to develop GWI when exposed to the stresses of war, and that alteration in the function of neural pathways that use acetylcholine is an important element in such autonomic dysfunction. We are testing our hypotheses via two interconnected studies. The first will attempt to confirm the findings of Lockridge (1999) who found a predominance (10:1) of carriers of specific butyrylcholinesterase (BChE) variants among symptomatic Gulf War veterans compared to veterans without symptoms. The second study will examine autonomic reactivity, BOhE genotype, and ex vivo carbamate affinity for BChE and acetylcholinesterase. We expect to find a higher incidence of autonomic hyperresponsiveness in the cases and in the heterozygote BChE variant carriers compared to either of the controls.

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