wigglethemouse
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Loved the video @Belbyr. Thanks for posting. However in his paper on the work in 2012 he presented thisThe article mentions IL-6 and IL-10 being higher in the chronically ill.
Gordon around 16:30 to 20:00 talks about IL-6 and IL-10 being 'running hotter' in CFS patients after infectious mononucleosis, in the video posted above. This guy is really on to something!
Cytokine expression profiles of immune imbalance in post-mononucleosis chronic fatigue
Link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3480896/
Results
I'd have to rewatch the video to see it what specific context he mentions IL6 and IL10. From Figure 1 in the paper the effect of IL6 looks small compared to the cytokines 8 and 23Standard comparative analysis indicated significant differences in IL-8 and 23 across subject groups. In constructing a linear classification model IL-6, 8 and 23 were selected by two different statistical approaches as discriminating features, with IL-1a, IL-2 and IFN-γ also selected in one model or the other. This supported an assignment accuracy of better than 80% at a confidence level of 0.95 into PI-CFS versus recovered controls.
This study by Broderick et al looked at Cytokine signatures in ME/CFS and GWI and found males and females behaved differently. Exercise also changed cytokine expression significantly.
A comparison of sex-specific immune signatures in Gulf War illness and chronic fatigue syndrome
Link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3698072/
Montoyas 2017 study added a correction factor for gender but did not present results separated. IL6 and IL10 were not mentioned in the abstract
Cytokine signature associated with disease severity in chronic fatigue syndrome patients
https://www.pnas.org/content/114/34/E7150
So it seems it's more complicated......................
ETA: In Broderick's 2012 paper he says this and provides examples of differences in other studies.
When comparing this work with results from other studies it is important to remember the type of sample and the specific patient population studied.
In an attempt to address some of these questions, this secondary analysis has focused specifically on a group of female adolescents diagnosed PI-CFS as the result of a uniform and known pathogen, namely EBV.
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