Marco
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This is a very interesting paper which I would urge everyone to read.
Currently it appears on Nature Precedings as a pre-publication manuscript (to stimulate discussion etc). I can only hope it is subsequently published.
While written from the perspective of Gulf War Illness, she proposes similar physiological processes underlying a range of 'overlap' illnesses with non-specific and protean symptoms including ME/CFS.
Predisposition to oxidative stress, stressor triggers, inflammation/oxidative stress, mitochondrial dysfunction etc will be very familiar I'm sure.
While this may at first sight appear to be a slightly controversial 'think piece', Beatrice Golomb is a very experienced researcher and 'mainstream' as evidenced by her CV :
http://cnl.salk.edu/~bgolomb/
It would be great to get her 'onboard' with ME/CFS research.
Currently it appears on Nature Precedings as a pre-publication manuscript (to stimulate discussion etc). I can only hope it is subsequently published.
While written from the perspective of Gulf War Illness, she proposes similar physiological processes underlying a range of 'overlap' illnesses with non-specific and protean symptoms including ME/CFS.
Predisposition to oxidative stress, stressor triggers, inflammation/oxidative stress, mitochondrial dysfunction etc will be very familiar I'm sure.
http://precedings.nature.com/documents/6847/version/1/files/npre20126847-1.pdfOxidative Stress and Mitochondrial Injury in Chronic Multisymptom Conditions:
From Gulf War Illness to Autism Spectrum Disorder
Beatrice Alexandra Golomb, MD, PhD
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.
While this may at first sight appear to be a slightly controversial 'think piece', Beatrice Golomb is a very experienced researcher and 'mainstream' as evidenced by her CV :
http://cnl.salk.edu/~bgolomb/
It would be great to get her 'onboard' with ME/CFS research.