New paper on ox. stress and mito. injury in CFS, Gulf War Illness, autism, etc.

[Guest guest]

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

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 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