A systematic review of cytokines in CFS/ME/SEID (2019) Corbitt et al

Systematic review of cytokine studies by NCNED team.

Results: A total of 16,702 publications were returned using our search terms. After screening of papers according to our inclusion and exclusion criteria, 15 studies were included in the review. All the included studies were observational case control studies. Ten of the studies identified measured serum cytokines in CFS/ME/SEID patients, and four measured cytokines in other physiological fluids in CFS/ME/SEID patients. The overall quality assessment revealed most papers included in this systematic review to be consistent.

Conclusions: Despite the availability of moderate quality studies, the findings of this review are inconclusive as to whether cytokines play any definitive role in CFS/ME/SEID, and consequently, they would not serve as reliable biomarkers. Therefore, in light of these results, it is recommended that further efforts towards a diagnostic test and treatment for CFS/ME/SEID continue to be developed in a range of research fields.

Paper: https://protect-au.mimecast.com/s/nKM7C5QZJlI1qRNrCyQaOc?domain=em.rdcu.be

 

CFS and ME organizations will fund four of these studies within the next year, minimum - against these recommendations.

 

Can you please explain further? What are the recommendations you are talking about?

 

Sorry for my English - I believe they are recommending that other avenues be pursued outside cytokines.

"CureME is committed to patient participation, and ensures that its research is always informed by and for the benefit of people with ME/CFS. We have contributed to highly significant research in immunology (including on NK and T cells and cytokine profiles)"

CureME team at The London School of Hygiene & Tropical Medicine is delighted to announce the award of $2.1m (£1.57m) of grant funding from the United States National Institutes of Health."

Serum findings are completely inapplicable if it is neuroinflammation, restricted and localized to basal ganglia.The brain has lymphatic communication that is not represented by the blood either, you would miss any lymphoid biomarker.

Some do correlate, like IL-1, but the two reservoirs function independently.

Such localized damage is, based on current interventions, so incredibly difficult to solve - a cytokine study is probably the easiest analysis you could do and that's why 1500 of them exist. The complexity of fatigue makes them just worthless, not deleterious, because no other branch of molecular biology has been able to tackle the problem either. Equally implausible is any peripheral metabolic variance just from a phenomenological perspective - people with ATP dysfunction do not have fatigue as their primary symptom.

 

Paper is also available as open access here, https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-019-1433-0

 

Fatigue being labelled as the primary symptom is the issue that has helped muddy the waters for years.
Its fatiguability not fatigue.