{"id":32204,"date":"2021-10-28T09:27:19","date_gmt":"2021-10-28T08:27:19","guid":{"rendered":"https:\/\/wames.org.uk\/cms-english\/?p=32204"},"modified":"2021-10-28T09:27:19","modified_gmt":"2021-10-28T08:27:19","slug":"hypothesis-me-cfs-as-an-immune-oxidative-stress-disorder","status":"publish","type":"post","link":"https:\/\/wames.org.uk\/cms-english\/hypothesis-me-cfs-as-an-immune-oxidative-stress-disorder\/","title":{"rendered":"Hypothesis: ME\/CFS as an immune & oxidative stress disorder"},"content":{"rendered":"

The reification of the clinical diagnosis of myalgic encephalomyelitis \/ chronic fatigue syndrome (ME\/CFS) as an immune and oxidative stress disorder: construction of a data-driven nomothethic network and exposure of ME\/CFS subgroups<\/a>, by Michael Maes, Marta Kubera, Kristina Stoyanova, Jean-Claude Leunis in<\/span> Current Topics in Medicinal Chemistry<\/em>, Vol 21 , Issue 16 , 2021 [DOI : 10.2174\/1568026621666210727170147]<\/h3>\n

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Article abstract:<\/strong><\/h3>\n

The approach towards myalgic encephalomyelitis \/ chronic fatigue syndrome (ME\/CFS) remains in a permanent state of crisis with fierce competition between the psychosocial school, which attributes ME\/CFS to the perception of effort, and the medical approach (Maes and Twisk, BMC Med, 2010,8,35).<\/p>\n

The aim of this paper is to review how to construct a nomothetic model<\/a> of ME\/CFS using Partial Least Squares<\/a> (PLS) path analysis and ensembling causome (bacterial) translocation as assessed with IgM\/IgA responses to LPS), protectome (lowered coenzyme Q10), adverse outcome pathways (AOP) including increased lysozyme, CD38+ T cell activation, cell-mediated immune activation (CMI), and IgM responses to oxidative specific epitopes and NO-adducts (IgM OSENO).<\/p>\n

Using PLS, we trained, tested and validated this knowledge- and data-driven causal ME\/CFS model, which showed adequate convergence, construct and replicability validity. This bottom-up explicit data model of ME\/CFS objectivates the descriptive narratives of the ME\/CFS phenome, using causome-protectome-AOP data, whereby the abstract concept ME\/CFS is translated into pathways, thereby securing the reification of the ME\/CFS phenome.<\/p>\n

We found that 31.6% of the variance in the physiosomatic symptom dimension of ME\/CFS was explained by the cumulative effects of CMI and CD38+ activation, IgM OSENO, IgA LPS, lysozyme (all positive) and coenzyme Q10 (inversely).<\/p>\n

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Cluster analysis<\/a> performed on the PLS-generated latent vector scores of all feature sets exposed three distinct immune groups of ME\/CFS, namely:<\/p>\n