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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Sorry but the silence, in terms of lack of evidence for any association between borrelia and ME, seems to be particularly deafening!
Sorry, Dr. Edwards, but when discussing any possible link between Lyme and ME and all the noise associated with both, you opined "...I think we have to assume that some other researchers have looked in to this..."
I cannot say what has been published. But it's common practice in the US at least to take someone who had been diagnosed and treated for Lyme, and who remained symptomatic, but eventually turned sero-negative (or not), and re-brand that individual with ME/CFS.
The thing is, perhaps that old case of Lyme HAS morphed into ME/CFS. Right? Like EBV or an enterovirus, Bb triggered ME/CFS. There is no reason to believe this would be any less a valid occurrence.
Perhaps Lyme lingers but diagnostics fail. The patient tests negative via the CDC's 2T system. It happens. So, Borrelia, in stealth mode, sickens the patient, while clinicians diagnose that individual with ME/CFS, because until SEID has been accepted, it is still primarily a diagnosis of exclusion. Or, maybe, in an ultimate twist, an individual meets the requirements for BOTH diseases - I know at least a few of the members of this forum are a part of that fraternity.
However you approach these possibilities, Borrelia assumes more than just a tad of a correlation, and coincidence does not factor in at all.
.......We found a significantly increased level and frequency of IgG anti-neural antibody reactivity in the PTLDS patients (41 of 83; 49.4%) both in comparison to patients who had been treated for Lyme disease previously but did not have residual symptoms (5 of 27; 18.5%) and to healthy controls who never had Lyme disease (3 of 20; 15.0%) (p < 0.01 for both compar- isons). The anti-neural antibody response in the patients with PTLDS was independent of serologic positivity for antibodies to Borrelia burgdorferi (the etiologic agent of Lyme disease).
.In contrast to the findings of our prior study on PTLDS patients (Chandra et al., 2010), we found no significant difference in the prevalence of anti-neural antibody reactivity between ME/CFS patients (4 of 51; 7.8%) and healthy controls (7 of 53; 13.2%) (p = 0.5).
Further inquiry into B cell activation mechanisms and autoantibody response may be useful to gaining a better understanding of differences between PTLDS and ME/CFS, and might provide potential markers for the identification of disease subsets.
@voner Can you tell us how big was the study? And did they test blood and/or spinal fluid? Which kind of labs/tests did they use?
In a previous study published in BBI, we developed a semi- quantitative immunoblot assay to compare antibody reactivity to neural antigens in a group of PTLDS patients and controls (Chandra et al., 2010)
A third possibility is that this correlation was clinically observed recently (it was), and that publication is underway. Dr de Meirleir seems to be pretty good about publishing whatever he finds, and very recently gave a presentation which was not put online due to containing material due to be published soon. I wouldn't be surprised if his upcoming publication is exactly about the correlation between ME diagnosis and the presence of Lyme.The fact that nobody has published a study showing a correlation, despite having treated patients as if there were some correlation either means that nothing could be found even with twisting the statistics as much as possible and so nothing was published because it would be rather embarrassing, or the people involved were too lazy to even gather the data.