Could people with fibromyalgia, ironically, be less suceptible to covid-19 and the worst of its effects than the rest of the population? A new study (Interleukin Deficiency Disorder Patient Responses to COVID-19 Infections, Journal of Advances in Medicine and Medical Research, 2021) suggests so and when I read about it today in this article, I just had to share.
Its seems that those who test positive for fibromyalgia are deficient in two particular cytokines, IL-6 and IL-8, and those two cytokines happen to be the same ones that rage out of control during severe COVID-19 infections, their immune system overreacting to overproduce them until the lungs get flooded by these compounds, leading to life-threatening pneumonia.
From the article: “During a screening, only 82 out of 2,195 fibromyalgia patients tested positive for COVID-19 antibodies. And only one of those 82 individuals was hospitalized and placed on a ventilator for severe COVID-19 infection.” The new study states “When screened for evidence of past COVID-19 infections, these patients experienced an extremely low incidence of COVID-19 infections based upon antibody testing, there were no mortalities, and the level of morbidity was significantly below what has been reported in general populations.”
In the UK,the offcial line is that there is still no blood test to confirm fibromyalgia and from what I read about the FM/a blood test (as it is called) developed in 2012 by biomedical firm EpicGenetics, which tests the concentration of cytokines within your blood sample, “more clinical tests need to be done” to confirm its efficiency. However, the original study showed promise, concluding “the aberrant responses of levels of a large number of cytokines of in vitrostimulated PBMC using the methodology in this study is significantly correlated with the clinical diagnosis of FM” (Unique immunologic patterns in fibromyalgia, BMC Clinical Pathology, 2012).
There has been a further study (Cytokine and chemokine profiles in fibromyalgia, rheumatoid arthritis and systemic lupus erythematosus: a potentially useful tool in differential diagnosis – Rheumatology International 2014), which flagged up limitations in the study and called for more targetted studies to take the idea further. This did draw the conclusion that the cytokine trait likely applied to chronic sensitization syndromes as a whole: “In all probability, chronic sensitization syndromes (which includes FM) are associated with a milieu whereby responses to sympathetic, hormonal, cytokine and chemokine stimulation are diminished”. This interests me very much as it has been my area of self-study over all the many years I have had to pretty-much self diagnose with fibromyalgia whilst pieced together the bewildering mystery as to how it is related to central sensitivity, hormone dysfunction, various issues with sympathetic nervous system function and stress. It would be great if studies could reach a conclusion as to how these are all related and the cytokine factor is a promising one.
While the article may sound very cut-and-dry, we are a long way from knowing what, if any, part cytokine levels play in fibromyalgia and, perhaps, it is too soon to draw a final conclusion if we are to take into consideration other, contradictory sounding, studies. For instance, this one states (emphasis added by me): “Plasma IL-6 levels are reportedly higher in patients with CFS than in healthy controls [19, 24, 36]. Plasma IL-6 levels exhibit a dose–effect relationship with CFS severity…Moreover, IL-6 reportedly plays an important role in the main symptoms of CFS, such as hyperalgesia, fatigue, sleep impairment, and depression. Wallace et al. reported that increased IL-6 levels contribute to the pathogenesis of fibromyalgia, the main symptoms of which are chronic diffuse muscle pain, fatigue, and skin sensitivity …IL-6 reportedly induces excessive daytime sleepiness or disturbed non-refreshing sleep in patients with CFS. Increased IL-6 levels are associated with worse sleep quality [3, 40].” (The clinical value of cytokines in chronic fatigue syndrome – Journal of Translational Medicine, 2019). These are all extremely familiar symptoms to me and I am well aware, from my own health and that of others I cross paths with, that the line between fibromyalgia and CFS is an extremely hazy one, so knowing if those cytokines are “down” or “up” will be utterly key before any therapuetic approaches (to increase or lower them) can safely be considered!
While more studies are certainly needed, this article (from ProHealth, the same source as the covid-FM article) declares that the FM/a test is making a huge impact on fibromyalgia studies and that is now being used in genetic studies with a view to reversing the cytokine shortfall (thus, in theory, “curing” fibromyalgia) using a vaccination to increase those missing cytokines. That protocol is, of course, now being questioned in light of the new study. Nobody wants to reverse fibromyalgia and at the same time increase susceptibility to covid so this is an interesting conundrum and a piece of topical news that I found far too interesting not to share.
Meanwhile, I can’t help wondering if syndromes such as FMS and CFS have more to do with variable (even, erratic) cytokine behaviour, rather than a fixed pattern of shortfall or excess; and, therefore, whether their behaviours are just a down-stream effect driven by other factors, such as stress (fight or flight), state of mind and emotions (belief systems, residual emotional trauma), and learned behaviours by the body (a faulty “loop in the brain” that can be neuroplastically rewired), etc and can therefore be modulated using the kind of methods harnessed by The Gupta Program. So, as interesting as the new study is, all routes seem to lead me back there, to redouble my efforts at treating it all as “a loop in the brain”.
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