CoQ10Dr. Beatrice Golomb, Author of First Successful GWI Treatment Study, Publishes GWI Disease Progression Hypothesis

Current hypotheses related to Gulf War Illness (GWI) suggest it is a chemically-caused neurological disorder with ongoing immune/auto-immune dysfunction.  Rather than a stable injury, evidence suggests GWI may be a progressive disease, with at least one component of the progression cellular oxidative stress and mithochondrial dysfunction (OSMD).

Dr. Beatrice Golomb (M.D., Ph.D.) of the University of California-San Diego has published a preliminary research paper related to this hypothesis with Nature Precedings.  Dr. Golomb's CDMRP-funded study based on this hypothesis discovered the first successful treatment to lessen some GWI symptoms, Coenzyme Q10 (CoQ10).  

Another CDMRP-funded study related to mitochondria and GWI is ongoing in Atlanta, and is continuing to recruit Gulf War veterans who meet GWI diagnostic criteria.  

An overview follows, with a link to the full article thereafter.  

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Oxidative Stress and Mitochondrial Injury in Chronic Multisymptom Conditions: 

From Gulf War Illness to Autism Spectrum Disorder

Beatrice Alexandra Golomb, MD, PhD

University of California, San Diego

Department of Medicine

Department of Family and Preventive Medicine

Running Title: Gulf War and Mitochondria


Abstract

Background: Overlapping chronic multisymptom illnesses (CMI) include Chronic Fatigue
Syndrome (CFS), fibromyalgia, irritable bowel syndrome, multiple chemical sensitivity, and
Gulf War illness (GWI), and subsets of autism spectrum disorder (ASD). GWI entails a more
circumscribed set of experiences that may provide insights of relevance to overlapping
conditions.

Objectives: To consolidate evidence regarding a role for oxidative stress and mitochondrial
dysfunction (OSMD), as primary mediators in CMI, using GWI as a departure point.
Methods: Exposure relations, character, timecourse and multiplicity of symptoms, and objective
correlates of GWI are compared to expectation for OSMD. Objective correlates of OSMD in
GWI and overlapping conditions are examined.


Discussion: OSMD is an expected consequence of known GWI exposures; is compatible with
symptom characteristics observed; and accords with objective markers and health conditions
linked to GWI, extending to autoimmune disease and infection. Emergent triangulating evidence
directly supports OSMD in multisymptom “overlap” CMI conditions, with similarities to, and
diagnosed at elevated rates in, GWI, suggesting a common role in each.

Conclusions: GWI is compatible with a paradigm by which uncompensated exposure to
oxidative/nitrative stressors accompanies and triggers mitochondrial dysfunction, cell energy
compromise, and multiple downstream effects such as vulnerability to autoantibodies. This
promotes a profile of protean symptoms with variable latency emphasizing but not confined to
energy-demanding post-mitotic tissues, according with (and accounting for) known properties of
multisystem overlap conditions. This advances understanding of GWI; health conditions
attending GWI at elevated rates; and overlap conditions like CFS and ASD, providing prospects for vulnerability assessment, mitigation of progression, treatment, and future prevention – with
implications germane to additive and excessive environmental oxidative stressor exposures in the
civilian setting.

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The full pre-publication/preliminary findings paper, published at Nature Precedings, is available online at:  http://precedings.nature.com/documents/6847/version/1/files/npre20126847-1.pdf