Jason 2010: Kindling and Oxidative Stress as Contributors to ME/CFS

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Fred Springfield posted this to co-cure today

(if: my bolds and spacing)

Kindling and Oxidative Stress as Contributors to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Journal: Journal of Behavioral and Neuroscience Research, 2009, Vo1. 7, 1-17

AuthorsL L. A. Jason [1, *], N. Porter [1], J. Herrington [1], M. Sorenson [1], & S. Kubow [2]

Affiliations:
[1] DePaul University and
[2] McGill University
[*] Corresponding author: DePaul University, Center for Community Research, 990 W. Fullerton Ave., Chicago, Il. 60614.

Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS) is one of the more complex illnesses involving multiple systems within the body. Onset of ME/CFS frequently occurs quickly, and many patients report a prior exposure to a viral infection. This debilitating illness can affect
the immune​
neuroendocrine​
autonomic,​
and neurologic systems.​


Abnormal biological findings among some patients have included
aberrant ion transport and ion channel activity,​
cortisol deficiency,​
sympathetic nervous system hyperactivity,​
EEG spike waves,​
left ventricular dysfunction in the heart,​
low natural killer cell cytotoxicity,​
and a shift from Th1 to Th2 cytokines.​

We propose that the kindling and oxidative stress theories provide a heuristic template for better understanding the at times conflicting findings regarding the etiology and pathophysiology of this illness.

Key Terms: Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, Kindling, Oxidative Stress

[Note: The full text of this article is available for free in PDF at
http://strose.edu/academics/academi...roscienceresearch/journalcontents/article3255
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Dolphin

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Interesting paper.

I found some of the reviews of areas useful e.g. neurology where I can get confused or have difficulty keeping up with the results.

A couple of small corrections/points:
(I) Technically, although de Lange et al (2008) claimed their study showed that CBT increases grey matter volume, they did not have a CFS control group so the results could simply be due to the passage of time in people with CFS (there might be a big drop at the start of the illness and then the brain gradually recovers). Two letters making this point were published (Bramsen, 2009 and Kindlon, 2009).

(II) Vollmer-Conna (2008): they do not explain well what was found in the study. This study related to cytokine polymorphisms (i.e. genetic/inherited factors) but they don't say this. Here is the abstract of the study:

Clin Infect Dis. 2008 Dec 1;47(11):1418-25.

Cytokine polymorphisms have a synergistic effect on severity of the acute sickness response to infection.

Vollmer-Conna U, Piraino BF, Cameron B, Davenport T, Hickie I, Wakefield D, Lloyd AR; Dubbo Infection Outcomes Study Group.

Collaborators (8)

School of Psychiatry and 2Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, Sydney, Australia.

BACKGROUND: Functional polymorphisms in immune response genes are increasingly recognized as important contributors to the marked individual differences in susceptibility to and outcomes of infectious disease. The acute sickness response is a stereotypical set of illness manifestations mediated by the proinflammatory cytokines induced by many different pathogens. The genetic determinants of severity of the acute sickness response have not previously been explored.

METHODS: We examined the impact of functional polymorphisms in cytokine genes with critical roles in the early immune response (tumor necrosis factor-alpha, interleukin-6, interleukin-10, and interferon-gamma) on the severity and duration of illness following acute infection with Epstein-Barr virus, Coxiella burnetii (the causative agent of Q fever), or Ross River virus.

RESULTS: We found that the interferon-gamma +874T/A and the interleukin-10 -592C/A polymorphisms significantly affected illness severity, cytokine protein levels, and the duration of illness. These cytokine genotypes acted in synergy to potentiate their influence on disease outcomes.

CONCLUSIONS: These findings suggest that genetically determined variations in the intensity of the inflammatory response underpin the severity of the acute sickness response and predict the recovery time across varied infections.