Hi, all.
Beatrice Golomb, at the Univ. of California--San Diego medical school, has just published a paper
in Nature on the above subject. I'm very happy to see this, and have written her to that effect.
The full paper can be found here, and the abstract is pasted below:
http://precedings.nature.com/documents/6847/version/1/files/npre20126847-1.pdf
Note that Dick Deth's autism model paper is cited as reference 103, and Sarah Myhill's CFS mitochondrial
paper is cited as reference 172.
I met Beatrice some years ago at meetings of the U.S. Gulf War Illness research advisory
committee in Wash., D.C. and spoke to them about glutathione depletion at that time. She is
also known for her work on studying the adverse effects of statin drugs.
I think this is an important paper, which hopefully will attract more attention in the research
community to oxidative stress and mito dysfunction in CFS and the other disorders she discusses.
Oxidative stress and mito. dysfunction are important elements of the Glutathione Depletion--Methylation
Cycle Block hypothesis, which I have proposed to explain the pathogenesis and pathophysiology of ME/CFS.
More on that can be found in the General Wiki section of these forums, and in the video and
pdf slides (available below the video) at this website:
http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D
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.
Best regards,
Rich
Beatrice Golomb, at the Univ. of California--San Diego medical school, has just published a paper
in Nature on the above subject. I'm very happy to see this, and have written her to that effect.
The full paper can be found here, and the abstract is pasted below:
http://precedings.nature.com/documents/6847/version/1/files/npre20126847-1.pdf
Note that Dick Deth's autism model paper is cited as reference 103, and Sarah Myhill's CFS mitochondrial
paper is cited as reference 172.
I met Beatrice some years ago at meetings of the U.S. Gulf War Illness research advisory
committee in Wash., D.C. and spoke to them about glutathione depletion at that time. She is
also known for her work on studying the adverse effects of statin drugs.
I think this is an important paper, which hopefully will attract more attention in the research
community to oxidative stress and mito dysfunction in CFS and the other disorders she discusses.
Oxidative stress and mito. dysfunction are important elements of the Glutathione Depletion--Methylation
Cycle Block hypothesis, which I have proposed to explain the pathogenesis and pathophysiology of ME/CFS.
More on that can be found in the General Wiki section of these forums, and in the video and
pdf slides (available below the video) at this website:
http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D
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.
Best regards,
Rich
