The latest pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

There are few health problems that are subject to the level of controversy that ME/CFS is in the medical community and from allopathic doctors.


Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling clinical condition characterized by unexplained and persistent post exertional fatigue accompanied by a variety of symptoms related to cognitive, immunological, endocrinological, and autonomous dysfunction. [1]

I thought it would be wise to dedicate an entire blog post to highlighting and discussing what the latest science is actually saying on the prospective pathophysiology of ME/CFS.

Not what your psychiatrist believes is the cause of ME/CFS or your yoga instructor or your bartender, but what the actual scientists are finding on the pathophysiological mechanisms of ME/CFS

Dispelling the Psychogenic ME/CFS Myth

For years allopathic doctors, psychiatrists and medical professionals have heavily tried to build a false narrative surrounding ME/CFS that the condition is of psychogenic origin and nothing more than a psychological disorder or mental illness.

However, absolutely no scientific research currently even remotely suggests that Myalgic Encephalomyelitis/Chronic Fatigue Syndrome as being of psychogenic origin or even hints at ME/CFS being a psychological or mental health disorder.

These are persistant out-dated myths and non evidence-based false narratives that are being built by psychiatrists, allopathic doctors and the psychosocial lobby so that they can prescribe now proven ineffective “treatments” such as CBT or anti-depressant medications to ME/CFS patients for their own gain.

Infact Natelson et al recently stated in their study that “psychiatric status is not an important causal contributor to CFS” and that the presence of co-existing psychiatric diagnoses does not impact on any aspect of the phenomenology of ME/CFS. [2]

It is high time for allopathic medical professionals to stop inflicting significant patient harm on the ME/CFS community, not only through complete medical neglect from not actually treating this complex serious multi-systemic illness adequately or properly, but by continually enabling this out-dated, pseudo-scientific false narrative that ME/CFS is a mental health disorder, when the science does not find or state this period.

ME/CFS as a “multi-systemic metabolic-inflammatory disorder”

Despite these challenges, modern research demonstrates a tangible biomedical basis for the disorder across many body systems.

This evidence is mostly comprised of disturbances to immunological and inflammatory pathways, autonomic and neurological dysfunction, abnormalities in muscle and mitochondrial function, shifts in metabolism, and gut physiology or gut microbiota disturbances. [3]

As someone who has read the mountains of growing biomedical science that is there on ME/CFS, it continues to blow me away that a condition that has shown so many different multi-system physiological abnormalities consistently over many different studies is still wrongly villainized by doctors to be a psychosomatic condition.

The false narrative that ME/CFS is a mental health condition is highly detrimental to both the reputation of evidence-based medicine and to patient well-being at this point.

ME/CFS patients are often treated appallingly by medical professionals, gaslighted, told their highly debilitating physical symptoms either don’t exist or are exaggerated, or co-morbid disorders such as POTS, fibromyalgia and the likes of ehler danlos syndrome are routinely misdiagnosed as anxiety and psychological disorders or just dismissed completely as being “medically unexplainable symptoms”, when they are infact not medically unexplainable in the slightest.

The whole allopathic approach when it comes to “treating” patients with these type of complex illnesses is a complete farce and has to be addressed.

The Infection Elicited Autoimmunity Model Of Me/CFS

A study published in 2018 claimed that a solid understanding of ME/CFS pathogenesis is emerging.

In this study, we compiled recent findings and placed them in the context of the clinical picture and natural history of the disease. A pattern emerged, giving rise to an explanatory model.

ME/CFS often starts after or during an infection. A logical explanation is that the infection initiates an autoreactive process, which affects several functions, including brain and energy metabolism.

According to our model for ME/CFS pathogenesis, patients with a genetic predisposition and dysbiosis experience a gradual development of B cell clones prone to autoreactivity. Under normal circumstances these B cell offsprings would have led to tolerance.

Subsequent exogenous microbial exposition (triggering) can lead to comorbidities such as fibromyalgia, thyroid disorder, and orthostatic hypotension.

A decisive infectious trigger may then lead to immunization against autoantigens involved in aerobic energy production and/or hormone receptors and ion channel proteins, producing postexertional malaise and ME/CFS, affecting both muscle and brain.

In principle, cloning and sequencing of immunoglobulin variable domains could reveal the evolution of pathogenic clones.

Although evidence consistent with the model accumulated in recent years, there are several missing links in it. Hopefully, the hypothesis generates testable propositions that can augment the understanding of the pathogenesis of ME/CFS. [4]

References

[1] Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Comprehensive Review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787585/

[2] The Effect of Comorbid Medical and Psychiatric Diagnoses on Chronic Fatigue Syndrome.

https://www.ncbi.nlm.nih.gov/pubmed/31642345

[3] Pathological Mechanisms Underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787592/

[4] Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: An Explanatory Model

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818468/

The information in this article has not been evaluated by the FDA and should not be used to diagnose, cure or treat any disease, implied or otherwise.

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